ACTIVITY -1

DEMONSTRATION AND PRACTICE OF PHYSIOTHERAPY

EVALUATION FOR PATIENTS WITH CARDIAC
REHABILITATION
 World Health Organisation (WHO) defines Cardiac rehabilitation (CR) as "The sum of activity
and interventions required to ensure best possible physical, mental, and social conditions so that
patient with chronic or post-acute cardiovascular disease may, by their own efforts, preserve or
resume proper place in society and lead an active life". (WHO, 1993)

CR is a comprehensive model of care comprising core components, (Grace et al., 2016) of

structured exercise, psychosocial counselling, patient education, risk factor reduction and
modification in behaviour, with a goal of optimizing patient's quality of life and helping to
reduce the risk of future heart problems.

The recommendations of CR programs are governed by the American Heart Association,

American College of Cardiology and the European Society of Cardiology. The timely medical
and physiotherapeutic evaluation is useful in prognosis.

CR is beneficial :

 A Cochrane review of 147 studies portrayed that for myocardial infarction and heart failure
patients, cardiovascular mortalityreducesby25%andreadmissionratesby20%.Arecentnetwork
meta-analysis, where the complex components of CR were better considered, showed significant
decrease in all-cause mortality with CR. (Kabboul et al.,2018).

 CR is associated with improved quality of life, (Francis et al., 2019) better psychosocial well-
being, cardiorespiratory fitness.

 CR is cost-effective. There is no difference in outcomes between supervised and home-based

programs, and cost remains the same (Anderson et al., 2017)

 The American Heart Association (AHA) guidelines provides a useful framework for
evaluation, management and prevention guidelines(Smith et al., 2011).

 This information is stratifies the patient in two ways:

⁃ It establishes risk for progression of atherosclerosis in patients and the likelihood of

cardiac events in future.
⁃ It establishes risk for adverse cardiac events in prescribed exercise training, as well as
contraindications and, if not, the level of monitoring and supervision recommended during
the initial training period.

MEDICAL HISTORY COMPONENTS:

1. Medical diagnoses: A variety of diagnoses are reviewed, including, cardiovascular disease,

existing coronary artery disease, history of MI, angioplasty, angina, and hypertension; pulmonary
 disease, such as asthma, emphysema, and bronchitis, cerebrovascular disease, cancer; peripheral
arterial disease; diabetes, anemia, phlebitis, or emboli; pregnancy; musculoskeletal imbalances
and neuromuscular and joint disease; osteoporosis.
2. Symptoms: Angina including discomfort (pressure, pain, tingling,, heaviness, burning,
numbness) in the chest, arms, jaw, or neck, or; light-headedness, dizziness, or fainting; shortness
of breath; palpitations, if associated with physical activity, eating a large meal, exposure to cold
or emotional upset.
3. Risk factors for atherosclerotic disease progression: It includes hypertension, diabetes,
dyslipidemia, Smoking, obesity and physical inactivity. Recent illness, surgical procedure or
hospitalization.
4. Medication dose, schedule and drug allergies. Other habits such as alcohol or illicit druguse.
5. Exercise history: Information on usual habits of activity, such as frequency, duration, intensity,
and type of exercise.
6. Work history: Estimated time to return towork.
7. Psychosocial history: The living conditions, marital and family status, transportation needs;
familyneeds,
8. Depression, anxiety, domestic and emotional problems; or other psychological disorders.

 A list of medications, dosing intervals, and compliance with the drug regimen is reviewed,
because these may affect the response to exercise.

 Comorbid conditions such as pulmonary, endocrine, and neurological illnesses and behavioral
and musculoskeletal conditions is evaluated. The social and occupational histories yield valuable
information and allow the tailoring of exercise training and goals to meet individual needs.

 Family and community resources that can assist patients with family concerns and returning to
work shouldbe considered.

PHYSICAL EXAMINATION

The initial physical examination shall be performed by trained and qualified health care provider
under the physician who is actively involved in routine care of patients with cardiovascular
disease (CVD). The components includes the following. (Fletcher, 2001)

1. Body weight, height, BMI, waist-to-hip ratio, waist circumference at the level of the umbilicus
2. Pulse rate
3. Resting blood pressure
4. Lungs Auscultation , with attention to uniformity of breath sounds (absence of rales, wheezes,
and abnormal breath sounds)
5. Heart Auscultation, with attention to murmurs and rubs
6. Auscultation and Palpation and of carotid, abdominal, and femoral arteries
7. Palpation and inspection of lower extremities for skin integrity (particularly in those with
diabetes),
8. Edema and presence of arterial pulses.
9. Absence or presence of xanthoma
10. Examination related to orthopedic, neurologic, or other conditions.
11. Examination of the leg wounds and chest after coronary bypass surgery or percutaneous coronary
revascularization

Figure 1.1 Lung auscultation Figure 1.2

Figure 1.3 Heart Auscultation Figure 1.4

-A resting standard 12-lead electrocardiogram (ECG) is useful in assessing heart rate (HR),
rhythm, conduction abnormalities, and evidence of prior MI. It serves as an important reference
for future comparison, particularly if the patient develops new signs or symptoms suggestive of
ischemia, infarction, or dysrhythmias.

Figure 1.5 Mason Liker lead placement

-Musculoskeletal complaints and injury are common, especially when a patient is beginning an
exercise program. Musculoskeletal function is assessed before exercise training begins.

-Assessment of lower extremity strength, flexibility, and balance is performed to prevent

injuries related to weight-bearing exercise. CR staff assesses posture and alignment to determine
history of musculoskeletal injury.

-Those patients who have undergone coronary artery bypass surgery through median
sternotomy, it is needed to evaluate sternal stability by identifying any pain, movement in
the sternum, clicking, or popping.

Sternal bone healing is usually achieved by 8 weeks.(Sargent et al., 1991) In about 2% to 5%

of cases infection, nonunion, and instability occur and are predisposed by clinical factors such as
immunosuppression, diabetes mellitus, obesity,, advanced age, and osteoporosis.(Losanoff et al.,
2002)
 RISK STRATIFICATION FOR CARDIAC EVENTS DURING EVALUATION:

The risk stratification do not consider comorbidities (insulin-dependent diabetes, morbid obesity,
severe pulmonary disease, complicated pregnancy, or neurological or orthopedic conditions) that
may constitute a contraindication to exercise during exercise training sessions.

Characteristics of patients at lowest risk (all characteristics listed must be present for
patient to remain at lowest risk)
 Absence of complex ventricular dysrhythmia during exercise testing and recovery
 Absence of angina or other significant symptoms (e.g., unusual shortness of breath, light-
headedness, or
 dizziness during exercise testing and recovery)
 Presence of normal hemodynamics during exercise testing and recovery (i.e., appropriate
increases and
 decreases in heart rate and systolic blood pressure with increasing workloads and recovery)
 Functional capacity ≥7 metabolic equivalents(METs)

Non exercise testing findings:

 Rest ejection fraction≥50%
 Uncomplicated myocardial infarction (MI) or revascularization procedure
 Absence of complicated ventricular arrhythmias at rest
 Absence of congestive heart failure(CHF)
 Absence of signs or symptoms of post event or post procedure ischemia

Characteristics of patients at moderate risk (any one or combination of these findings

places a patient at
moderate risk)
 Presence of angina or other significant symptoms (e.g., unusual shortness of breath, light-
headedness, or dizziness occurring only at high levels of exertion[<7METs)
 Mild to moderate level of silent ischemia during exercise testing or recovery (ST-segment
depression<2mm
 from baseline)
 Functional capacity<5METs.

Non exercise testing findings:

 Rest ejection fraction = 40% to49%

Characteristics of patients at high risk (any one or combination of these findings places a
patient at high
risk)

 Presence of complex ventricular arrhythmias during exercise testing or recovery

 Presence of angina or other significant symptoms (e.g., unusual shortness of breath, light-
headedness,or
 dizziness at low levels of exertion [≥5 METs] or during recovery)
 High level of silent ischemia (ST-segment depression ≥2 mm from baseline) during exercise
testing or recovery
 Presence of abnormal hemodynamics with exercise testing (i.e., chronotropic incompetence or
flator
 decreasing systolic BP with increasing workloads) or recovery (i.e., severe post exercise
hypotension)

Non exercise testing findings:

 Rest ejection fraction
 Presence of signs or symptoms of post event or post procedure ischemia
 Presence of clinical depression
 Complex dysrhythmias at rest
 Complicated MI or revascularization procedure
 Presence of CHF

Contraindications for Exercise Training:

Absolute Contraindications to Exercise Training (Gibbons et al., 2002)

 Recent change in resting ECG suggesting significant ischemia, recent MI, or other acute cardiac
event
 Unstable angina and Uncontrolled cardiac arrhythmias
 Symptomatic severe aortic stenosis or valvular disease
 Symptomatic decompensated heart failure
 Acute pulmonary embolus or acute noncardiac disorder that may affect exercise performance
 (e.g., infection, thyrotoxicosis)
 Acute myocarditis , pericarditis orthrombophlebitis

Relative Contraindications to Exercise Training (Gibbons et al., 2002)

 Electrolyte abnormalities, tachyarrhythmias or bradyarrhythmias

 High-degree atrioventricular block or atrial fibrillation with uncontrolled ventricular rate or
known aortic dissection
 Hypertrophic obstructive cardiomyopathy with peak resting left ventricular outflow gradient of
>25mmHg
 Severe resting arterial hypertension(systolic blood pressure>200mm Hg and diastolic BP >110
mmHg)
 Mental impairment leading to inability to cooperate with testing
 precludes safe and adequate exercise performance
SAFETY AND PERSONNEL:

The safety of exercise testing is well documented, and the overall risk of adverse events is very
low. Among large series of subjects with and without known CVD, the rate of major
complications (including MI and other events requiring hospitalization) is <1 to as many as 5 per
10000 test and rate of death is <0.5 per 10000 tests and adverse events depends on study
population. (Balady et al., 2010)

The AHA has described the required supervision for exercise testing. (Myers et al., 2009) The
level of supervision depends on the type of patients being tested. For higher risk patient (recent
MI, heart failure, or arrhythmia), the supervising physician determines the necessity. In other
cases, trained health care professionals conduct the test and directly monitor patient status
throughout testing and recovery. (Rodgers et al., 2000)

Appropriate emergency equipment, establishment of a workable emergency plan, and regular

practice of the plan (with critiques) are fundamental to ensuring the safety of a CR program.

Emergency equipment should be immediately available to all exercise areas and should include the
following:

 Telephone and medical alert signal to call for paramedics or code team as applicable.
 Portable battery-operated defibrillator with ECG printout and monitor that may have external
pacemaker capability should be available for programs with moderate- to high-risk patients
participating. Direct current (DC) capability in case of battery failure should be available for the
defibrillator, monitor, and ECG printout.
 Depending on the individual facility’s policies, an automatic external defibrillator (AED) may be
used in place of a manual defibrillator. The availability of an AED is especially useful for
programs serving low-risk patients. Rhythm analysis and shock administration with an AED may
result in prolonged interruptions in chest compressions.”
 Portable oxygen and tubing, with nasal cannula, and facemasks.
 Adult oral and nasopharyngeal airways in various sizes should be standard equipment on all
emergency carts as well as bag valve mask and pocket face masks.

Intubation equipment including air adjuncts such as Combitube or laryngeal mask airway. If
intubation equipment is available for use, personnel who are certified and licensed to perform
intubation and continuous quantitative waveform capnography should be accessible.

Additional equipment for medical emergencies and maintenance policies includes:

 -Portable suction equipment.+
 -Intravenous access and administration equipment and fluids.
 -BP measurement equipment (sphygmomanometer and stethoscope).
 -Cardiac board.
 -Personal protective equipment—gloves, masks, gowns, face shields.
 -General medical supplies.

Emergency documentation forms.

 The emergency equipment and medications should be appropriately stored, locked, and secured
 out of reach of the general public.
 Biomedical engineering check of equipment for maintenance performed every 6 months.
Documentation of such maintenance is required.
 Defibrillators checked daily for discharge capability

MEDICATION:

The diagnostic exercise tests typically are performed with medications withheld to better assess
any underlying ischemic response, functional testing performed before entrance into a CR program
should occur with the patient taking medications as prescribed.

For example, withholding beta-blockers before exercise testing will interfere with HR prescription
for exercise training. Under ideal conditions, the functional exercise test should be administered at
a time when the patient normally exercises and following normal medication ingestion time.

EXERCISE TESTING

Exercise test is a key component of the assessment made before a patient begins with the exercise
program.

-Graded exercise tests are used to assess ability to tolerate increased physical activity. ECG,
hemodynamic, and symptomatic responses are monitored for manifestations of myocardial ischemia,
dysrhythmias, or other exertion-related abnormalities.

-The exercise test is used for diagnostic, prognostic, and therapeutic applications.The test is also a
motivational tool for patients as well as verification of patient improvement.

-Apart from a diagnostic tool, exercise tests are useful to staff as a functional tool. The test is useful
in assessing cardiorespiratory fitness and developing an exercise prescription. It is used to measure
functional changes over time to assess exercise training outcomes.
-Exercise tests and simulated work tests helps determine an individual’s ability to return to work.
(Wilke et al., 1993). Not every patient referred for CR services are candidates for exercise testing
and patients should not be denied participation.

Absolute Contraindications to Exercise Testing (Gibbons et al., 2002)

 Acute MI -within 2 days) and high-risk unstable angina
 Uncontrolled cardiac dysrhythmias causing hemodynamic compromise
 Symptomatic severe aortic stenosis or valvular disease
 Symptomatic decompensated heart failure
 Acute pulmonary embolus or acute non cardiac disorder that may affect exercise performance(e.g.,
 infection, thyrotoxicosis)
 Acute myocarditis , pericarditis orthrombophlebitis
 Physical disability that will preclude safe and adequate exercise performance
 Inability to obtain consent

Relative Contraindications to Exercise Testing (Gibbons et al., 2002)

 Left main coronary stenosis or moderate stenotic valvular heart disease

 Electrolyte abnormalities, tachyarrhythmias or bradyarrhythmias
 Atrial fibrillation with rapid ventricular rate, for example >150bpm
 Hypertrophic cardiomyopathy
 Mental impairment leading to inability tocooperate.
 High-degreeatrioventricularblockorsevererestingarterialhypertension(systolicBP>200 mmHg and
diastolic BP >110mmHg)

EXERCISE TEST MODALITY AND PROTOCOL

Exercise tests may be submaximal or maximal according to the effort required.

-Submaximal exercise testing has a predetermined end point: a specific peak HR such as 120
bpm, a percentage of predicted maximum HR such as 70%, an arbitrary metabolic equivalent
(MET) level such as 5 METs, or a submaximal rating of perceived exertion (RPE) such as 13 to
15.

-Submaximal tests are used before hospital discharge at 4 to 6 days after acute MI. (Gregoratos et
al., 2002). This low leveltest provides sufficient data for evaluation of activities of daily living,
physical activity, and serves as baseline for early ambulatory exercise prescription.

-Symptom-limited tests are designed to continue till the patient demonstrates signs and symptoms
that requires termination of exercise. (Gibbons et al., 2002) These are selected when testing is
performed more than 14 days after acute MI. “Minimum Requirements for Measures Assessed
During Exercise Testing.” are as follows

Minimum Requirements for Measures Assessed During Exercise Testing

Pretest procedures and assessments

 Minimum of 5 min of rest before initial measures are taken and Informed consent
 Demonstration of equipment use and explanation of maximal effort or desired endpoint
 Explanation of rating scales
 12-lead ECG in supine and in position of exercise and every minute.
 Blood pressure in supine and in position of exercise
 Assessment of medications, when last taken
 12-lead ECG during last minute of each stage, or at least every 3 min if single stage test is
administered
 Bloodpressureandperceivedexertionduringlastminuteofeachstage,oratleastevery3 min if single stage
test is administered
 Other rating scales as appropriate

Post test procedures and assessments

 Minimum of 6 min in sitting or supine position, or until near-baseline measures are reached. A
period of active cool-down may be included in the 6 min recovery period; for functional exercise
tests, a 1 to 3 min cool-down is recommended, depending on the level of exertion, to minimize post
exercise effects of venous pooling.
 Blood pressure immediately after exercise, then every 1 or 2 min until normotensive or near-
baseline measures are reached.
 Ratingofsymptomseachminuteaslongastheypersistafterexercise.Patientsshouldbe observed until all
symptoms have subsided and the ECG is within acceptable limits as determined the supervising
clinician.

-Several exercise testing protocols are available for both treadmill and stationary cycle ergometers,
summarized by the ACSM (ACSM’s Guidelines for Exercise Testing and Prescription, 2018) , is
selected according to the individual patients estimated physical fitness (age, underlying disease,
and current activity level.)

-Work rate increments during staged protocols vary from 1 to 2.5 METs (1 MET = 3.5 mL
kg−1 · min−1 oxygen uptake), whereas those of ramp protocols designed to useless
abrupt increments.

-Treadmill testing provides more common form of physiological stress (i.e., walking), with subjects
likely to attain a higher oxygen uptake and peak HR whereas cycling is preferable in orthopedic
condition which limits ability to walk or bear weight. Cycling is also smaller, quieter, and less
expensive
-When a mechanically braked ergometer is used, pedal rpm is constant, for example at 50 rpm.

-After a zero-load warm-up of 1 to 2 min, use 25 W or less increments for patients who are
deconditioned.50 W increments for more fit or heavier patients. Stages set at a minimum of 2 min in
duration, increasing the load by25 W

-The most frequently used stepped treadmill protocols are the Bruce, the modified Bruce, and the
Naughton. Ramp protocols are designed in stages no longer than 1 min and for the patient to attain
peak effort within 8 to 12 min and is individualized to patient effort .

The energy requirement (oxygen uptake) of non–weight-bearing activity is inversely proportional to

body weight. So, at the same workload, the higher the body weight, the lower the oxygen uptake.
Symptom Rating are used by patients.

Symptom Rating Scales :

Before exercising, patients are familiarized with the symptom rating scales.
5-grade angina scale

0- No angina
1 - Light, barely noticeable
2 - Moderate, bothersome
3 - Severe, very uncomfortable
4 - Most pain ever experienced

5-grade dyspnea scale

0 - No dyspnea
1 - Mild, noticeable
 2 - Mild, some difficulty
3 - Moderate difficulty, but can continue
4 - Severe difficulty, cannot continue

10-grade angina/dyspnea scale

0- Nothing
0.5- Very, very slight
1. Very slight
2. Slight
3. Moderate
4. Somewhat severe
5. Severe
6.
7. Very severe
8.
9.
10. Very, very severe

Intermittent Claudication Rating Scale

0 No claudication pain
1 Initial, minimal pain
2 Moderate, bothersome pain
3 Intense pain
4 Maximal pain, cannot continue

Cardiopulmonary Exercise Testing

It uses ventilatory gas exchange analysis during exercise and is a useful tool for assessment of
patients with CVD. (Rhodes et al., 2013) Gas exchange primarily include oxygen uptake (V . O2 ),
carbon dioxide output (V . CO2 ), minute ventilation, and ventilatory threshold among which oxygen
uptake at peak exercise is considered the most reliable measure of cardiorespiratory function and
aerobic capacity. (Balady et al., 2010)

-Importance of CPX
 Evaluationofexercisecapacityinselectedpatientswithheartfailuretoassistinthe estimation of prognosis
and assessing the need for cardiac transplantation
 Assistance in the differentiation of cardiac versus pulmonary limitations, cause of exercise-
 induced dyspnea or impaired exercise capacity, when the etiology is uncertain
 Evaluation of the patient response to specific therapeutic interventions in which the
 improvement of exercise tolerance is an important goal
 A precise determination of the appropriate intensity for exercise training through identification of
the ventilator threshold.

Exercise training intensities to maintain and improve health and fitness among individuals with or
without heart disease is derived from direct measurements of peak oxygen uptake. (Arena et al.,
2007) . It is the most useful when the HR response to exercise is not a reliable indicator of exercise
intensity (e.g.in patients with atrial fibrillation).
DIAGNOSTIC UTILITY

Abnormalities in HR, BP ,exercise capacity, and exercise ECG are important findings. Cardiac
events are likely to occur in patients with lower exercise capacities and in exercise- induced
hypotension. Other markers of adverse prognosis are abnormal HR recovery with HR drop of
st
<12bpm within 1 minute of recovery (Cole et al., 1999) ,frequent ventricular ectopy (Frolkis
et al., 2003) and inability to acheive 85% of maximum predicted HR (Gauri et al., 2001) .
-The most common ECG definition of a positive test is a horizontal or downsloping(ST
depression that is greater than or equal to 1 mm for at least 60 to 80 ms after end of the QRS
complex). (Gibbons et al., 2002)
-Stress test ECG finding is interpreted in the context of clinical information regarding the baseline
ECG, the patient’s cardiovascular history, and the presence or absence of symptoms.
Typical angina (substernal chest discomfort which may begin in, or radiate into, the arms or jaw) is
provoked by exertion or emotional stress and is relieved by rest and nitroglycerin. It affects men
older than 50 years and women older than 60 years, making the pretest probability of disease so
high that the test result does not dramatically change the probability of the presence of coronary
disease.
Atypical angina (chest discomfort which may include discomfort other than in the chest, arms, or
jaw, shortness of breath) all of which complicates the diagnosis. It particularly occurs in men older
than 30 years and women older than 50 years. (Gibbons et al., 2002)
-Sensitivity is the percentage of patients with disease(as e.g., ≤50% lesion of at least one major
coronary artery) who will have an abnormal test.
-Specificity is the percentage of patients free of disease who will have a normal test.

The specificity and sensitivity of exercise ECG each are approximately 70% and are affected
based on the subgroup of patients being evaluated.

ALTERNATIVES FOR EVALUATING PHYSICAL ACTIVITY STATUS

-Six-Minute Walk Test-The 6-minutewalktest(6MWT) can be used as a surrogate measure of

exercise capacity if standard treadmill or cycle testing is not available. It is best used to evaluate
changes in exercise capacity with training over time and is not useful in the objective determination
of myocardial ischemia.

- Clinician–Patient Interview and Questionnaires

The interviews and surveys are not a substitute for exercise testing, we may obtain rough estimation
of exercise tolerance by using MET tables and questioning patients about activities which induce
fatigue (Medicine, 2012). A number of physical activity surveys are used to quantify activity.
(Kriska et al.,1997)

-Controlled Job Simulation

The data from an exercise test can be compared to the available MET tables to assist in
recommending safe vocational and vocational activities. (Morris et al., 1993)

The mechanical efficiency, specific job-task requirements, and environmental and psychological
stressors alters the response measured in the laboratory. Controlled simulation of physical tasks can
aid employers and physicians in determining whether a patient can safely return to work (Wilke et
al., 1993)
 ACTIVITY-2
DEMONSTRATION AND PRACTICE OF EVALUATION OF
PERIPHERAL VASCULAR DISEASES (ARTERY/VEIN/LYMPHATIC)
Peripheral Vascular Diseases or PVD is a general term used to describe any disorder that
interferes with arterial and venous blood flow of the extremities.

 In PVD blood vessels become narrowed and blood flow decreases .This can be due to
arteriosclerosis or hardening of the arteries or it can be caused by blood vessel spasm.

 PVD typically causes pain, fatigue, often in your legs and especially during exercise
.The pain usually improves with rest.

 It can also affect the vessels that supply blood and oxygen to your arms, stomach,
intestine and kidneys

PERIPHERAL ARTERIAL DISEASE

Arterial insufficiency refers to a lack of adequate blood flow to a region or regions of the body
.Many different disorders may arise from arterial insufficiency and can be classified by variety of
descriptors

• PAD is the result of systemic atherosclerosis. The underlying disease process that affects the
blood vessels is common to patients with coronary artery disease (CAD), stroke and diabetes
mellitus. For example, many people undergoing coronary angiography have previously
unrecognized PAD.

• Health care professionals working in rehabilitation or medical fitness programs need to

understand the common coexistence of CAD, cerebrovascular disease and PAD, how
exercise therapy can benefit program participants with PAD.

FACTORS THAT LEADS TO PAD OWING TO ARTERIAL INSUFFICIENCY

 AGE: The striking increase in both the incidence and prevalence of PAD with increasing
age is apparent.

 GENDER: The prevalence of PAD, symptomatic or asymptomatic, is slightly greater in

men than women, particularly in the younger age groups. In patients with IC, the ratio of men
to women is between 1:1 and 2:1. This ratio increases in some studies to at least 3:1 in more
severe stages of the disease, such as chronic CLI. Other studies have, however, shown a more
equal distribution of PAD between genders and even a predominance of women with CLI.

 SMOKING: The relationship between smoking and PAD has been recognized since 1911,
when Erb reported that IC was three-times more common among smokers than among non-
smokers. Interventions to decrease or eliminate cigarette smoking have, therefore, long been
advocated for patients with IC. It has been suggested that the association between smoking
and PAD may be even stronger that between smoking and coronary artery disease (CAD).

 DIABETES MELLITUS: Many studies have shown an association between diabetes

mellitus and the development of PAD. Overall, IC is about twice as common among diabetic
patients than among non-diabetic patients. In patients with diabetes, for every 1% increase in
hemoglobin A1c there is a corresponding 26% increased risk of PAD (Brinaz et al,2010)
 HYPERTENSION: Hypertension is associated with all forms of cardiovascular disease,
including PAD. However, the relative risk for developing PAD is less for hypertension than
diabetes or smoking.

 DYSLIPIDEMIA: In the Framingham study, a fasting cholesterol level greater than 7

mmol/L (270 mg/dL) was associated with a doubling of the incidence of IC but the ratio of
total to high-density lipoprotein (HDL) cholesterol was the best predictor of occurrence of
PAD. Although some studies have also shown that total cholesterol is a powerful
independent risk factor for PAD, others have failed to confirm this association.

 INFLAMMATORY MARKERS: Some recent studies have shown that C-reactive

protein(CRP) was raised in asymptomatic subjects who in the subsequent five years
developed PAD compared to an age-matched control group who remained asymptomatic. (
Skirtz et al,2009)

The damage caused by these factors is reflected in structural changes in the walls of the
arteries, causing abnormal blood flow because of the following disorders.

 Areteriosclerosis

 Atherosclerosis.

 Arteriosclerosis obliterans.

 Thromboanginitis obliterans.

 Raynaud’s disease.

 Ulceration.

• Between 10 and 25 percent of LE ulcers are caused by arterial diseases ( Valencia et

al,2001).

• The incidence of arterial diseases and LE ulceration is less than venous diseases and
ulceration however arterial diseases may lead to loss of limb and even death.

INCIDENCE AND PREVALENCE OF ASYMPTOMATIC PERIPHERAL ARTERIAL

DISEASE

• Total disease prevalence based on objective testing has been evaluated in several
epidemiologic studies and is in the range of 3% to 10%, increasing to 15% to 20% in
persons over 70 years.(Criqui et al,1985;Hiatt et al,1995;Selvin et al,2004)

INCIDENCE AND PREVALENCE OF SYMPTOMATIC PERIPHERAL ARTERIAL

DISEASE

• The prevalence of IC would appear to increase from about 3% in patients aged 40 to 6%

in patients aged 60 years.. In the relatively younger age groups, claudication is more
common in men but at older ages there is little difference between men and women.
• A surprising finding in population screening studies is that between 10% and 50% of
patients with IC have never consulted a doctor about their symptoms ( Bruitz et al,2012)

CLINICAL PRESENTATION

 Most frequently located on LE’s :lateral malleoli , dorsum of feet and toes.

 When wounds are present on ischaemic limb atherosclerotic occlusion of the peripheral
vasculature is almost present.

 The majority of patients with arterial insufficiency also have diabetes.

 Trophic changes are present and include abnormal nail growth ,decreased leg and foot
hair dry skin.

 Skin is cooled upon palpation.

 Wounds are painful and patient may also describe pain the leg or feet.

 Wound base is necrotic and pale lacking granulation tissue.

 Other signs include decreased pulses, pallor on elevation and rubor when dependant.

 Rest pain relieved by resting or medication.

 Intermittent claudication-Painful sensation in the calf muscles because of narrowing of

vessels if atheroma is present.Pain is increased by walking ( Susan B O’Sullivan)
Buerger’s test

Figure 2.1 Elevated Pallor Figure 2.2 Dependent Rubor

Figure 2.3 (VASCULAR FOUNDATION AND AACVPR 2016)

DIAGNOSTIC EVALUATION OF PATIENTS WITH PERIPHERAL ARTERIAL

DISEASE (L. Norgren and W. R. Hiatt et al, 2007)

Ankle pressure measurements (ankle-brachial index)

• Measuring the pressure in the ankle arteries has become a standard part of the initial
evaluation of patients with suspected PAD.
• A common method of measurement uses a 10-12 cm sphygmomanometer cuff placed just
above the ankle and a Doppler instrument used to measure the systolic pressure of the
posterior tibial and dorsalis pedis arteries of each leg.

• These pressures are then normalized to the higher brachial pressure of either arm to form
the ankle-brachial index (ABI). The index leg is often defined as the leg with the lower
ABI. The ABI provides considerable information.

• A reduced ABI in symptomatic patients confirms the existence of hemodynamically

significant occlusive disease between the heart and the ankle, with a lower ABI indicating
a greater hemodynamic severity of occlusive disease.

Figure 2.4 Figure 2.5

TREADMILL EXERCISE TESTING

 Treadmill exercise testing is an accepted method of evaluating walking capability in

patients with claudication.

 Performing treadmill tests before and after an intervention can provide an objective
assessment of change in this important measure.

 There are several protocols commonly used to document outcomes in research and
clinical care, but each has some common elements.

 The test is performed on a motorized treadmill

 Patient is asked about claudication symptoms at regular intervals (i.e., every 30 seconds)

 The claudication onset time (the time when the first claudication symptoms begin) and
maximum walking time (the time when the patient can go no farther and needs to stop)
are documented .
 With each protocol, the participant continues walking until he or she cannot walk any
longer

Figure 2.6 Treadmill exercise testing

STANDARD GRADED PROTOCOLS INCLUDE ( Vascular foundation 2016)

 Gardner-Skinner Protocol (Gardner et al, 1991)

⁃ Treadmill speed is held constant at 2 mph

⁃ Treadmill grade begins at 0 percent and increases 2 percent every 2 minutes

 Hiatt Protocol (Hiatt et al, 1990)

⁃ Treadmill speed held constant at 2 mph

⁃ Treadmill grade begins at 0 percent and increases by 3.5 percent every 3 minutes.

 Bronas/Treat-Jacobson Protocol (Treat-Jacobson et al,2009)

⁃ Treadmill speed begins at 2 mph

⁃ Treadmill grade begins at 0 percent and increases by 3.5 percent every 3 minutes through
10.5 percent grade (12 minutes, stage 4)

⁃ Beginning with stage 5, the treadmill grade is kept constant at 10.5 percent and the speed
increases by 5 mph every 3 minutes

Global Outcomes Questionnaires

1. SF-36 (especially the physical function and vitality sub-scales)

2. Sickness Impact Profile (SIP)
3. Functional Status Questionnaire

Disease-Specific Questionnaires

1. Walking Impairment Questionnaire (WIQ):

• Developed by Regensteiner JG, Hiatt WR. Copyrighted, permission required prior to use

• Title: Regensteiner JG, Steiner JF, Hiatt WR. Exercise training improves functional status
in patients with peripheral arterial disease.

2. Peripheral Artery Questionnaire (PAQ):

• Developed by Spertus J, Jones P, Poler S, and Rocha-Singh K

• Title: The peripheral artery questionnaire: a new disease-specific health status measure
for patients with peripheral arterial disease

3. Vascular Quality of Life Questionnaire (VascuQol)

• Developed by Morgan MB, Crayford T, Murrin B, and Fraser SC

• Title: Developing the Vascular Quality of Life Questionnaire: a new disease-specific

quality of life measure for use in lower limb ischemia.

4. Low Level Physical Activity Recall Questionnaire

• Title: Regensteiner JG, Steiner JF, Hiatt WR. Exercise training improves functional
status in patients with peripheral arterial disease. Citation: J VascSurg 1996:23;104-115

Alternative stress tests for patients who cannot perform treadmill exercise

 Certain patient populations should not be asked to undergo treadmill testing as previously
described, including those who have severe aortic stenosis, uncontrolled hypertension or
patients with other exercise limiting co-morbidities, including advanced congestive heart
failure or chronic obstructive pulmonary disease.

 Patients who cannot perform treadmill exercise can be tested with active pedal plantar
flexion. Active pedal plantar flexion has demonstrated excellent correlation with
treadmill testing, and should be considered an appropriate alternative to treadmill testing.

 A second alternative is to inflate a thigh cuff well above systolic pressure for 3 to 5
minutes, producing a similar degree of ‘‘reactive’’ hyperemia.

 The decrease in ankle pressure 30 seconds after cuff deflation is roughly equivalent to
that observed 1 minute after walking to the point of claudication on a treadmill.
Unfortunately, many patients do not tolerate the discomfort associated with this degree
and duration of cuff inflation and, in modern vascular laboratories, this is rarely
performed.

PHARMACOTHERAPY FOR INTERMITTENT CLAUDICATION

 Patients with IC should all receive drug and lifestyle treatment for their cardiovascular
risk factors and coexisting diseases to prevent cardiovascular events (myocardial
infarction, stroke and death) associated with atherosclerosis.

Drugs with evidence of clinical utility in claudication

 Cilostazol

 Naftidrofuryl

 Carnitine and Propionyl-L-Carnitine

 Lipid lowering drugs

 Isovolemic hemodilution

 Anti-throbetic agents.

 Vasodilators.

 L-Arginine.

 Prostaglandins ( Hiatt et al,2014)

Figure 2.7 FUNCTIONAL CONSEQUENCES OF PAD

EFFECTS OF EXERCISE TRAINING IN PAD

• Exercise training has been incorporated into current guidelines for the management of
PAD. Multiple societal guidelines including American College of Cardiology/American
Heart Association 2005 Practice Guidelines for the Management of Patients With
Peripheral Arterial Disease, American Association of Cardiovascular and Pulmonary
Rehabilitation 2004 Guidelines for Cardiac Rehabilitation and Secondary Prevention
Programs, Intersociety Consensus for the Management of PAD (TASC II), and American
College of Sports Medicine 2010 Guidelines for Exercise Testing and Prescription all
 recommend supervised exercise training in the treatment of claudication symptoms in
PAD (Paramenter et al,2010;Perkins et al,2011; Gardner at al,2010)

• Supervised exercise programs have been recommended as first-line therapy for treatment
of claudication. Recent evidence demonstrates benefits of exercise training even among
those patients with PAD who do not have claudication ( Bras et al,2004)

The goals of comprehensive prevention strategies, including exercise, are 3-fold:

(1) To reduce limb symptoms;

(2) To improve exercise capacity and prevent or lessen physical disability; and

(3) To decrease the occurrence of cardiovascular events.

 Exercise training markedly improves walking ability in PAD patients with intermittent
claudication.

 A meta-analysis performed in 1995 that included uncontrolled trials suggested clinical

efficacy of exercise in ameliorating claudication symptoms, indicating that supervised
exercise increased painfree walking distance by 180%. ( Brias at al,2011)

 A rigorous systematic review including only controlled clinical trials encompassing 22

studies with 1200 participants conducted by the Cochrane group in 2008 compared
supervised exercise programs with usual care in the treatment of claudication. Exercise
produced clinically relevant increases in walking time (5 minutes) and walking distance
(100 m).

 Differences in exercise intensity as well as adherence to exercise programs may account

for the observed variability in treatment effect.

 In randomized trials of exercise rehabilitation in patients with claudication, exercise has

been shown to increase daily activity levels measured by accelerometer (Duscha et
al,2011)and patient-perceived health-related quality of life ( Askew et al,2005)

 Increased physical activity may translate to slower functional decline and potentially to
reduced cardiovascular risk (Crowther et al,2012;Tendera et al,2011)

 McDermott and colleagues conducted a randomized trial of supervised treadmill

exercise compared with strength training and usual care in 156 PAD patients. The
symptom pattern corresponded to the observed distribution in clinical practice: 18% had
claudication, and 82% had atypical symptoms or were asymptomatic. At 6 months,
patients in the treadmill exercise group increased exercise performance as evidenced by
a longer 6-minute walk distance (20.9 m) compared with a decline in the control group
(15 m).

 Lower-extremity resistance training improved leg strength as well as maximum treadmill

walking time without an increase in 6-minute walk distance. Both treadmill and
 resistance exercise training improved physical functioning–associated quality of life
measures.

 The exercise prescription should be based on exercise sessions that are held three times a
week beginning with 30 minutes of training but then increasing to approximately 1 hour
per session.

Thus, the findings support

(1) Recommending supervised exercise programs for all patients with PAD regardless of
symptom status and

(2) The notion that exercise training can interrupt functional deterioration in PAD.

Table 2.1 EXERCISE PRESCRIPTION FOR SUPERVISED ENDURANCE

TRAINING IN PATIENTS WITH INTERMITTENT CLAUDICATION (Bronas et
al,2009)

FREQUENCY 3-5 DAYS/WEEK

MODALITY TREADMILL WALKING

INTENSITY Exercise at the given work rate at which the patient experiences the
onset of claudication, continue walking untill the patients has
ischaemic leg pain symptoms score of mid to moderate (3-4 of
maximum 5 points),then stop until pain completely subsides ,resume
exercise again at similar intensity ,repeat rest/exercise bouts .Progress
to a higher workrate when the patients is able to walk for 8 minutes
bouts without the need to stop for leg symptoms.
DURATION Total exercise time including rest periods should equal 50
minutes/day

Table 2.2 EXERCISE AND SPORTS SCIENCE AUSTRALIA (ESSA) 2013

 Table 2.3 EXERCISE PRESCRIPTION FOR PAD( ACSM GUIDELINES )

TYPE INTENSITY SESSION DURATION FREQUENCY

Weight-bearing aerobic Moderate intensity 30–60 min·d-1, but Weight-bearing
exercise, such as walking, and (i.e., 40% to <60% initially some patients aerobic exercise
non–weight-bearing activity, that allows the may need to start with 10- 3–5 d·wk-1;
such as arm ergometry. patient to walk minute bouts and exercise Resistance
Cycling may be used as a until he/she reaches intermittently to exercise at least
warm-up, but should not be a pain score of 3 accumulate a total of 30– 2 d·wk-1
the primary type of activity. (i.e., intense pain) 60 min·d-1
Resistance training is on the 4-point pain 2 to 4 sets with 8 to 12
recommended to enhance and scale . per set with a rest interval
maintain muscular strength Patients lift weights of 2 to 3 minutes between
and endurance. Elastic bands ≥50% one sets .
Light cuff and hand weights repetition
Light free weights maximum (1-RM).
Wall pulleys etc

SPECIAL CONSIDERATIONS (ACSM GUIDELINES)

 The optimal work-to-rest ratio has not been determined for individuals with PAD. The
work-to-rest ratio may need to be adjusted for each patient.

 A cold environment may aggravate the symptoms of intermittent claudication; therefore,

a longer warm-up may be necessary (Long et al,2004)

 Encourage patients to stop smoking if they are current smokers.

 For optimal benefit, patients should participate in a supervised exercise program for a
minimum of 5 to 6 months. Following exercise training programs of this length,
improvements in pain-free walking of 106% to 177%, and 64% to 85% in absolute
walking ability, may occur (Couzin et al,2011)

VENOUS INSUFFICIENCY AND ULCERATION

 Inadequate drainage of venous blood form a body part ,usually resulting in edema or skin
abnormalities or ulceration.

 Chronic venous Insufficiency refers to venous insufficiency that persists for long period
of time .CVI is the most common cause of leg ulcers .

 The incidence of venous ulceration is much higher than that of arterial ulceration. In,fact
80% of all leg ulcers are caused by venous diseases.

 Aging, lack of exercise ,obesity ,pregnancy, long hours of standing or sitting and heredity
will predispose an individual to venous hypertension and subsequent CVI.

CLINICAL PRESENTATION
 Swelling of unilateral or bilateral LEs relieved in early stages by elevation.

 Complaints of itching, fatigue , aching ,heaviness in involved limb .

 Skin changes including haemosiderine staining and lipodermatosclerosis.

 Fibrosis of the dermis.

 Increase in skin temperature of lower legs.

 Wounds- most commonly located in LE proximal to medial malleolus. Granulation tissue

is usually present around the wound.

 Tissue is wet typically from large amount of drainage exudate .

 Signs and symptoms of lymphedema may be present.

 Minor dull leg pain relieved with elevation ( Susan B O’Sullivan)

SPECIAL TEST FOR VENOUS INSUFFICIENCY

 TRENDELENBURG TEST-To measure the competence of the veins. It measures the

time requires to refill the veins in the dorsum of the foot .Lower extremity is elevated to
allow venous blood to empty. Torniquet is applied on the thigh to prevent the back flow.
After 1 minute the patient is made to stand .If veins fully distend within 5 seconds before
torniquet is released ,vascular incompetence in deep veins is suspected. If distension
occurs after 5 seconds after torniquet is released Incompetence in superficial veins is
suspected.

 VENOUS FILLING TIME- The extremity is elevated and then lowered into
dependantposition .The time it takes for the veins on the top of the foot to refill is
recorded.

 Normal filling time is 15 seconds

 ˃15 seconds indicate arterial disease.

 ˂15 seconds indicate venous diseases.

SEMMES WINSTON MONOFILAMENT TESTING

 Sensory test done when symptoms are long standing includes complain of numbness,
burning and tingling sensations.

 It is a non-invasive test to evaluate the pressure and touch sensation using a nylon
monofilament to measure cutaneous pressure sensation in the feet. The filament consists
of varying size each mounted on a handle.

 The filament is applied to skin until it bends .The patient is asked to report with eyes
closed whether filament is touching a body part .Each monofilament supplies a specific
amount of force when it is placed on a test area and gently bend.
 The monofilaments are available in a largest but most testing can be accomplished using
few filaments. An individual has normal sensation when 4.17 monofilaments (1gm) of
force can be applied.

Figure 2.8 Semmes Winston monofilament testing

INTERVENTION

 Venous leg ulcers can be prevented by compression therapy .

 Treatment will also include exercise to increase mobility and positioning to support and
enhance venous blood flow.

 For individuals with diagnosis of venous diseases or mixed (mild) arterial/venous disease
,a combination of therapeutic measures will accelerate the results.

 These include compression bandaging , Manual lymphatic drainage, ROM exercises.

 Wound care should avoid whirlpool use owing to the risk of dependant positioning, cross
contamination, cytotoxic additives and unnecessary costs.

 Pressure ulcers can be relived by the use of PRDs pressure mapping to determine
pressure loads , positioning or turning and education of the patient, family and care
givers.

 Other factors that contribute to ulceration such as shear, friction, mobility, sensation,
moisture, nutrition, age and underlying medical conditions should also be addressed .

 With appropriate wound care, control of pressure and attention to risk factors, a wound
should progress through the phase of wound healing ,showing signs of improvement
within weeks.

 Partial thickness wounds typically takes 1 to 2 weeks while clean full thickness wounds
can take 2 to 4 weeks.
 PRESSURE MAPPING

Figure 2.9

WOUND MANAGEMENT

Figure 2.10 MAGGOT THERAPY FOR CAVITY Figure 2.11 WOUND CLEANSING WITH NON
WOUND FORCEFUL IRRIGATION
Figure 2.12 PULSATILE LAVAGE WITH Figure 2.13 PROVAND WOUND CLOSURE
SUCTION SYSTEM

LYMPHEDEMA Compression is an essential intervention, pressures that are too high

will occlude superficial lymph capillaries and prevent the initial step of fluid absorption
and need to control edema and lymphedema.

The current recommended course of care is a 2 week programme of complete

Decongestive Therapy (CDT).

 Phase I intensive includes skin care, elevation, MLD, lymphedema bandage exercise and
compression garment.

 Phase II (self management) includes skin care ,compression garment during the day
,exercise ,lymphedema bandaging at night, MLD as needed ( Susan B O’ Sullivan)
Table 2.4 RECENT RESEARCH EVIDENCES

TITLE JOURNAL METHODOLOGY CONCLUSION

Effect of Low- JAMA, 325(13), Both exercise groups were The 6MWD changed from
Intensity vs High- (McDermott et asked to walk for exercise in 332.1 m at baseline to 327.5
Intensity Home- al., 2021) an unsupervised setting 5 times m at 12-month follow-up in
Based Walking per week for up to 50 minutes the low-intensity exercise
Exercise on Walk per session wearing an group and from 338.1 m to
Distance in Patients accelerometer to document 371.2 m in the high-intensity
With Peripheral exercise intensity and time. exercise group. The 6MWD
Artery Disease: The The low-intensity group changed from 328.1 m at
LITE Randomized walked at a pace without baseline to 317.5 m at 12-
Clinical Trial ischemic leg symptoms. The month follow-up in the
high-intensity group walked at nonexercise control group
a pace eliciting moderate to which was not significantly
severe ischemic leg symptoms. different from the change in
the low-intensity exercise
group

Impacts of aquatic Journal of The AQ group performed Aquatic walking exercise

walking on arterial applied walking and leg exercises in can decrease arterial
stiffness, exercise physiology (Park waist-to-chest-deep water. Leg stiffness and improve
tolerance, and et al., 2019) arterial stiffness [femoral-to- exercise tolerance,
physical function in ankle pulse wave velocity cardiorespiratory capacity,
patients with leg )], R, , ankle-to- and muscular strength in
peripheral artery brachial index ), o2max, patients with PAD. This
disease: a 6MWD, physical function, training demonstrates
randomized clinical muscular strength, body relatively high exercise
trial composition, RMR, and adherence in this population
flexibility were measured and may be a useful
before and after 12 wk. therapeutic intervention for
improving physical function
in patients with PAD.
 ACTIVITY 3
DEMONSTRATION AND PRACTICE OF INTERPRETATION
OF ELECTROCARDIOGRAPHY IN HEART DISEASE
THE ELECTROCARDIOGRAM

The electrocardiogram (ECG) provides a graphic depiction of the electrical forces generated by
the heart. The ECG graph appears as a series of deflections and waves produced by each cardiac
cycle.

Significance of ECG Deflections

Electrical Components
Deflection Description
P Wave
First wave seen
Small rounded, upright (positive) wave indicating atrial
depolarization (and contraction)
PR Interval Distance between beginning of P wave and beginning of QRS
complex
Measures time during which a depolarization wave travels from
the atria to the ventricles
QRS Interval Three deflections following P wave Indicates ventricular
depolarization (and contraction)
Q Wave: First negative deflection R Wave: First positive
deflection
SWave:FirstnegativedeflectionafterRwave
ST Segment Distance between S wave and beginning of T wave
Measures time between ventricular depolarization and beginning
of repolarization
T Wave Rounded upright (positive) wave following QRS
Represents ventricular repolarization
QT Interval Measured from beginning of QRS to end of T wave.
Represents total ventricular activity.
U Wave Small rounded, upright wave following T wave
Most easily seen with a slow HR. Represents repolarization of
Purkinjefibers.

Fi

Figure 3.1: The normal ECG deflections

Normal Sinus Rhythm Parameters

 Rate 60 - 100bpm
 Regularity Regular
 Pwaves Normal
 PRinterval 0.12 - 0.20s
 QRSduration 0.04 - 0.12s

Types of ECGs

The two types of ECG recordings are the 12-lead ECG and a rhythm strip. Both types give
valuable information about heart function. A 12-lead ECG records information from 12 different
views of the heart and provides a complete picture of electrical activity. These 12 views are
obtained by placing electrodes on the patient‘s limbs and chest. The limb leads and the chest, or
precordial, leads reflect information from the different planes of the heart. A rhythm strip, which
can be used to monitor cardiac status, provides information about the heart‘s electrical activity
from one or more leads simultaneously. Chest electrodes pick up the heart‘s electrical activity for
display on the monitor. The monitor also displays heart rate and other measurements and allows
for printing strips of cardiac rhythms.

INTERPRETATION OF THE ABNORMAL ECG

1. Since the P wave represents atrial activity and the QRS ventricular activity the ECG can be
used to determine heartrhythm.
2. Damage to the conducting tissue will alter the pathways of the activation and may alter The
QRSmorphology.
3. Increased muscle mass will alter the amplitude and duration of P and QRS waves and this
allows recognition of hypertrophy of the muscle in different chambers of theheart.
4. Loss of muscle mass alters QRS and allows recognition of myocardialinfarction.
5. Many factors can alter the patterns of repolarisation and these can be suspected from changes
in the ST -segment and Twaves.

CARDIAC ARRHYTHMIAS

 Sinus node arrhythmias

 Atrial arrhythmias
 Junctional arrhythmias
  Ventricular arrhythmias
 Atrioventricular blocks

Sinus Arrhythmia
In sinus arrhythmia, the pacemaker cells of the SA node fire irregularly. The cardiac rate stays
within normal limits, but the rhythm is irregular and corresponds with the respiratory cycle.
Sinus arrhythmia can occur naturally in athletes and children, but it rarely occurs in infants.
Conditions unrelated to respiration may also produce sinus arrhythmia, including inferior wall
myocardial infarction (MI), advanced age, use of digoxin (Lanoxin) or morphine, and conditions
involving increased intracranial pressure.
Sinus Arrhythmia
The SA node dischargesirregularly.
The R-R interval isirregular.

Rate: Usually normal (60–100 bpm); frequently increases with inspiration and
decreases with expiration
Rhythm: Irregular; varies with respiration P Waves: Normal (upright and
uniform) PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)
♥ Clinical Tip: The pacing rate of the SA node varies with respiration,
especially in children and elderly people.

Sinus Bradycardia
Sinus bradycardia is characterized by a sinus rate below 60 beats/ minute and a regular rhythm. It
may occur normally during sleep or in a person with a well-conditioned heart—an athlete, for
example.
 Sinus Bradycardia
■ Results from slowing of the SAnode.

Rate: Slow (<60 bpm)

Rhythm: Regular
P Waves: Normal (upright and uniform) PR
Interval: Normal (0.12–0.20 sec) QRS: Normal
(0.06–0.10 sec)
Clinical Tip: Sinus bradycardia is normal in athletes and during sleep. In acute
MI, it may be protective and beneficial or the slow rate may compromise
cardiac output. Certain medications, such as beta blockers, may also cause
sinusbradycardia.

Sinus tachycardia
Sinus tachycardia in an adult is characterized by a sinus rate of more than 100 beats/ minute. The
rate rarely exceeds 160 beats/ minute except during strenuous exercise; the maximum rate
achievable with exercise decreases with age.

Sinus Tachycardia
■ Results from increased SA nodedischarge

Rate: Fast (>100 bpm)

Rhythm: Regular
P Waves: Normal (upright and uniform) PR
Interval: Normal (0.12–0.20 sec) QRS: Normal
(0.06–0.10 sec)
♥ Clinical Tip: Sinus tachycardia may be caused by exercise, anxiety, fever,
hypoxemia, hypovolemia, or cardiac failure.

Sinus Arrest
A disorder of impulse formation, sinus arrest is caused by a lack of electrical activity in the
atrium, a condition called atrial standstill. During atrial standstill, the atria aren‘t stimulated and
an entire PQRST complex will be missing from the ECG strip.
The SA node fails to discharge and thenresumes.
Electrical activity resumes either when the SA node resets itself or when a lower
latent pacemaker begins todischarge.
The pause (arrest) time interval is not a multiple of the normal P-Pinterval.

Rate: Normal to slow; determined by duration and frequency of sinus pause

(arrest)
Rhythm: Irregular whenever a pause (arrest) occurs
P Waves: Normal (upright and uniform) except in areas of pause (arrest)
PR Interval: Normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)
♥Clinical Tip: Cardiac output may decrease, causing syncope or dizziness.

Wandering pacemaker
A wandering pacemaker is an irregular rhythm that results when the heart‘s pacemaker changes
its focus from the SA node to another area above the ventricles. The origin of the impulse may
wander beat-to-beat from the SA node to other atrial sites or to the AV junction. The P wave and
PR interval vary from beat to beat as the pacemaker site changes.
Wandering Atrial Pacemaker (WAP)
■ Pacemaker site transfers from the SA node to other latent pacemaker sites in

the atria and the AV junction and then moves back to the SAnode.

Rate: Normal (60–100 bpm)

Rhythm: Irregular
P Waves: At least three different forms, determined by the focus in the atria
PR Interval: Variable; determined by focus
QRS: Normal (0.06–0.10 sec)
 Premature Atrial Contraction (PAC)
Premature atrial contractions (PACs) originate outside the SA node and usually result from an
irritable spot, or focus, in the atria, which take over as pacemaker for one or more beats. The SA
node fires an impulse, but then an irritable focus jumps in, firing its own impulse before the SA
node can fire again.
Premature Atrial Contraction (PAC)
Asinglecomplexoccursearlierthanthenextexpectedsinuscomplex.
After the PAC, sinus rhythm usuallyresumes.

Rate: Depends on rate of underlying rhythm

Rhythm: Irregular whenever a PAC occurs
P Waves: Present; in the PAC, may have a different shape
PR Interval: Varies in the PAC; otherwise normal (0.12–0.20 sec)
QRS: Normal (0.06–0.10 sec)
♥Clinical Tip: In patients with heart disease, frequent PACs may precede
paroxysmal supraventricular tachycardia (PSVT), A-fib, or A-flutter.

Atrial Fibrillation
Atrial fibrillation, sometimes called A-fib, is defined as chaotic, asynchronous, electrical activity in
atrial tissue. The ectopic impulses may fire at a rate of 400 to 600 times/ minute, causing the atria to
quiver instead of contract.
Atrial Fibrillation (A-fib)
Rapid, erratic electrical discharge comes from multiple atrial ectopicfoci.
No organized atrial contractions aredetectable

Rate: Atrial: 350 bpm or greater; ventricular: slow or fast

Rhythm: Irregular
P Waves: No true P waves; chaotic atrial activity
PR Interval: None
QRS: Normal (0.06–0.10 sec)
♥Clinical Tip: A-fib is usually a chronic arrhythmia associated with
underlying heart disease.
Atrial Tachycardia
Atrial tachycardia is a supraventricular tachycardia, which means the impulses driving the rapid
rhythm originate above the ventricles. Atrial tachycardia has an atrial rate from 150 to 250 beats/
minute. Three types of atrial tachycardia exist: atrial tachycardia with block, multifocal atrial
tachycardia, and paroxysmal atrial tachycardia (PAT).
Atrial Tachycardia
ArapidatrialrateoverridestheSAnodeandbecomesthedominantpacemaker.
Some ST wave and T wave abnormalities may bepresent.

Rate: 150–250 bpm

Rhythm: Regular
P Waves: Normal (upright and uniform) but differ in shape from sinus P waves
PR Interval: May be short (<0.12 sec) in rapid rates
QRS: Normal (0.06–0.10 sec) but can be aberrant at times

Atrial Flutter
Atrial flutter, a supraventricular tachycardia, is characterized by an atrial rate of 250 to 350 beats/
minute, although it‘s generally around 300 beats/ minute. Originating in a single atrial
focus,thisrhythmresultsfromcircusre-entryandpossiblyincreasedautomaticity.Thewave blend
together in a saw-toothed appearance and are called flutter waves, or f waves. These waves are the
hallmark of atrial flutter.
Atrial Flutter (A-flutter)
AV node conducts impulses to the ventricles at a 2:1, 3:1, 4:1, or greater ratio
(rarely1:1).

Degree of AV block may be consistent orvaria

Rate: Atrial: 250–350 bpm; ventricular: slow or fast
Rhythm: Usually regular but may be variable
P Waves: Flutter waves have a saw-toothed appearance
PR Interval: Variable
QRS: Usually normal (0.06–0.10 sec), but may appear widened if flutter waves
are buried in QRS
Clinical Tip: Signs and symptoms depend on ventricular response rate.

Premature Junctional Contraction

A premature junctional contraction (PJC) is a beat that occurs before a normal beat and causes an
irregular rhythm. This ectopic beat occurs when an irritable location within the AV junction acts as
a pacemaker and fires either prematurely or out of sequence
 Premature Junctional Contraction (PJC)
Enhanced automaticity in the AV junction producesPJCs

Rate: Depends on rate of underlying rhythm

Rhythm: Irregular whenever a PJC occurs
P Waves: Absent, inverted, buried, or retrograde in the PJC
PR Interval: None, short, or retrograde
QRS: Normal (0.06–0.10 sec)
♥ Clinical Tip: Before deciding that isolated PJCs may be insignificant, consider
the cause.

Accelerated Junctional
An accelerated junctional rhythm is caused by an irritable focus in the AV junction that speeds up to
take over as the heart‘spacemaker

Accelerated Junctional Rhythm

Rate: 61–100 bpm

Rhythm: Regular
P Waves: Absent, inverted, buried, or retrograde
PR Interval: None, short, or retrograde
QRS: Normal (0.06–0.10 sec)
♥ Clinical Tip: Monitor the patient, not just the ECG, for clinical improvement.
.

Junctional Tachycardia
In junctional tachycardia, three or more PJCs occur in a row. This supraventricular tachycardia
occurs when an irritable focus from the AV junction has enhanced automaticity, overriding the
S node to function as the heart‘s pacemaker.
Junctional Tachycardia

Rate: 101–180 bpm

Rhythm: Regular
P Waves: Absent, inverted, buried, or retrograde
PR Interval: None, short, or retrograde
QRS: Normal (0.06–0.10 sec)
♥ Clinical Tip: Signs and symptoms of decreased cardiac output may be seen in
response to the rapid rate.

Junctional Escape
A junctional escape rhythm is a string of beats that occurs after a conduction delay from the atria.
The normal intrinsic firing rate for cells in the AV junction is 40 to 60 beats/ minute. The AV
junction can take over as the heart‘s pacemaker if higher pacemaker sites slow down or fail to
fire or conduct. The junctional escape beat is an example of this compensatory mechanism.
Because junctional escape beats prevent ventricular standstill, they should never be suppressed.
Junctional Escape Beat

Anescapecomplexcomeslaterthanthenextexpectedsinuscomplex.
Rate: Depends on rate of underlying rhythm
Rhythm: Irregular whenever an escape beat occurs
P Waves: None, inverted, buried, or retrograde in the escape beat
PR Interval: None, short, or retrograde
QRS: Normal (0.06–0.10 sec)
 Premature Ventricular Contraction (PVC)
A premature ventricular contraction (PVC) is an ectopic beat that may occur in healthy people
without causing problems. PVCs may occur singly, in clusters of two or more, or in repeating
patterns, such as bigeminy or trigeminy. When PVCs occur in patients with underlying heart
disease, they may indicate impending lethal ventricular arrhythmias.

Premature Ventricular Contraction (PVC)

Usually PVCs result from an irritable ventricularfocus.
PVCsmaybeuniform(sameform)ormultiform(differentforms).
ThepausefollowingaPVCmaybecompensatoryornoncompensatory.

Rate: Depends on rate of underlying rhythm

Rhythm: Irregular whenever a PVC occurs P Waves: None associated with the
PVC PR
Interval: None associated with the PVC
QRS:Wide(>0.10sec),bizarreappearance
♥ Clinical Tip: Patients may sense the occurrence of PVCs as skipped beats.
Because the ventricles are only partially filled, the PVC frequently does not
generate a pulse.

Ventricular Tachycardia
In ventricular tachycardia, commonly called V-tach, three or more PVCs occur in a row and the
ventricular rate exceeds 100 beats/ minute. This arrhythmia may precede ventricular fibrillation
and sudden cardiac death, especially if the patient isn‘t in a health care facility. entricular
tachycardia is an extremely unstable rhythm. It can occur in short, paroxysmal bursts lasting
fewer than 30 seconds and causing few or no symptoms. Alternatively, it can be sustained,
requiring immediate treatment to prevent death, even in patients initially able to maintain
adequate cardiac output.
Ventricular Tachycardia (VT): Monomorphic
QRScomplexesinmonomorphicVThavethesameshapeandamplitude.

Rate: 100–250 bpm

Rhythm: Regular
P Waves: None or not associated with the QRS
PR Interval: None
QRS: Wide (>0.10 sec), bizarre appearance

♥ Clinical Tip: It is important to confirm the presence or absence of pulses

because monomorphic VT may be perfusing or nonperfusing.
♥ Clinical Tip: Monomorphic VT will probably deteriorate into VF or unstable
VT if sustained and not treated.

Ventricular Fibrillation
Ventricular fibrillation, commonly called V-fib, is a chaotic pattern of electrical activity in the
ventricles in which electrical impulses arise from many different foci. It produces no effective
muscular contraction and no cardiac output. Untreated ventricular fibrillation causes most cases
of sudden cardiac death in people outside of a hospital.
Ventricular Fibrillation (VF)
Chaotic electrical activity occurs with no ventricular depolarization
orcontraction.
The amplitude and frequency of the fibrillatory activity can be used to define the
type of fibrillation as coarse, medium, orfine.

Rate: Indeterminate
Rhythm: Chaotic
P Waves: None PR Interval:None
QRS:None
♥ Clinical Tip: There is no pulse or cardiac output. Rapid intervention is critical.
The longer the delay, the less the chance of conversion.
Asystole
Asystole is ventricular standstill. The patient is completely unresponsive, with no electrical
activity in the heart and no cardiac output. This arrhythmia results most commonly from a
prolonged period of cardiac arrest without effective resuscitation. Asystole has been called the
arrhythmia of death. The patient is in cardiopulmonary arrest. Without rapid initiation of CPR
and appropriate treatment, the situation quickly becomes irreversible.
Heart Rate Rhythm P Wave PR Interval QRS
(sec.) (Sec.)

None None None None None

Heart Block
Atrioventricular (AV) heart block results from an interruption in the conduction of impulses
between the atria and ventricles. AV block can be total or partial or it may delay conduction. The
block can occur at the AV node, the bundle of His, or the bundle branches.

First Degree Heart Block

First-degree AV block occurs when impulses from the atria are consistently delayed during
conduction through the AV node. Conduction eventually occurs; it just takes longer than normal.

First-Degree AV Block

Rate: Depends on rate of underlying rhythm

Rhythm: Regular
P Waves: Normal (upright and uniform)
PR Interval: Prolonged (>0.20 sec)
QRS: Normal (0.06–0.10 sec)
♥Clinical Tip: Usually AV block is benign, but if associated with an acute MI,
it may lead to further AV defects.
Second Degree Heart Block, Mobitz Type I
(Wenckebach)
It occurs when each successive impulse from the SA node is delayed slightly longer than the
previous impulse. That pattern continues until an impulse fails to be conducted to the ventricles,
and the cycle then repeats.
Second-Degree AV Block
Type I (Mobitz I or Wenckebach)
P-
RintervalsbecomeprogressivelylongeruntilonePwaveistotallyblockedandprod
uces
noQRS.Afterapause,duringwhichtheAVnoderecovers,thiscycleisrepeated.

Rate: Depends on rate of underlying rhythm

Rhythm: Irregular
P Waves: Normal (upright and uniform)
PR Interval: Progressively longer until one P wave is blocked and a QRS is
dropped
QRS: Normal (0.06–0.10 sec)
♥ Clinical Tip: This rhythm may be caused by medication such as beta blockers,
digoxin, and calcium channel blockers. Ischemia involving the right coronary
artery is another cause.

Second Degree Heart Block, Mobitz

Type II (Classical)
It is less common than type I but more serious. It occurs when occasional impulses from the SA
node fail to conduct to the ventricles.
Type II (Mobitz II)
Conductionratio(PwavestoQRScomplexes)iscommonly2:1,3:1,or4:1.
QRScomplexesareusuallywidebecausethisblockusuallyinvolvesbothbundleb
ranches.

Rate: Atrial rate (usually 60–100 bpm); faster than ventricular rate
Rhythm: Atrial regular and ventricular irregular
P Waves: Normal (upright and uniform); more P waves than QRS
complexes
PR Interval: Normal or prolonged but constant
QRS: Usually wide (>0.10 sec)

Clinical Tip: Resulting bradycardia can compromise cardiac output and lead
to complete AV block. This rhythm often occurs with cardiac ischemia or an
MI.

Third Degree Heart Block (Complete)

Also called complete heart block, third- degree AV block occurs when impulses from the atria
are completely blocked at the node and can‘t be conducted to theventricles.
Third-Degree AV Block
Conduction between atria and ventricles is absent because of electrical block
at or below the AVnode.
“Complete heart block” is another name for thisrhythm.

Rate: Atrial: 60–100 bpm; ventricular: 40–60 bpm if escape focus is

junctional, <40 bpm if escape focus is ventricular
Rhythm: Usually regular, but atria and ventricles act independently
P Waves: Normal (upright and uniform); may be superimposed on QRS
complexes or T waves
PR Interval: Varies greatly
QRS: Normal if ventricles are activated by junctional escape focus; wide if
escape focus is ventricular
Angina
Peaked or flattened T wave, T-wave inversion, and ST-segment depression with or Without
T-wave inversion
Bundle-branch block
 QRS complex: Width increases to greater than 0.12 second with bundlebranchblock
 Lead V1 (to right of heart) and V6 (to left of heart): Used to determine whether block is in right or
left bundle
RBBB:
T-wave inversion in lead V1 and widened S wave and upright T wave in lead V6

LBBB:
Wide S wave (which may be preceded by a Q wave or small R wave) and small positive T wave in
lead V1; tall, notched R wave or slurred R wave and T-wave inversion in lead V6.

Myocardial infarction
Three pathologic changes on ECG — ischemia, injury, and infarction
Pathologic ECG changes
 Zone of ischemia: T-wave inversion
 Zone of injury: ST-segment elevation
 Zone of infarction: Pathologic Q wave in transmural MI

Locating the MI

 Anterior wall: Leads V2 to V4; involves LAD artery

 Septal wall:V1 to V2; involves LAD artery
 Inferior wall: Leads II, III, aVF; involves right coronary artery
 Lateral wall: Leads I, aVL, V5, V6; involves left circumflex artery
 Posterior wall: Leads V7, V8, V9; involves right coronary or left circumflex arteries
 Right ventricular wall: V4R, V5R, V6R; involves right coronary artery

.
 ACTIVITY NO. 4
DEMONSTRATION AND PRACTICE OF SECONDARY
PREVENTION AND RISK FACTOR IDENTIFICATION AND
REDUCTION
Coronary artery disease (CAD) is the leading cause of death, with more than 1 million new and
recurrent cardiovascular events occurring each year, and its prevalence and impact are expected to
grow. Advances in treatment have improved survival after the initial event, but persons with
established CAD have a high risk of future cardiovascular events. Recent clinical studies show that
persons with CAD can reduce their risk of subsequent cardiovascular events through effective
secondary prevention, which reduces mortality and improves quality of life.

SECONDARY PREVENTION

Physical Activity

Regular physical activity is an important component of secondary prevention of CAD; it increases

exercise capacity, treats co-morbid risk factors, and improves quality of life. Exercise-based cardiac
rehabilitation has been shown to reduce all-cause and cardiac mortality compared with usual care.
The goal for all patients is 30 to 60 minutes of moderate-intensity physical activity (e.g., brisk
walking, biking) on most, if not all, days of the week. Consistent physical activity improves
cardiovascular risk factors, especially total cholesterol and triglyceride levels—and systolic blood
pressure. Exercise-based cardiac rehabilitation programs may be initiated shortly after an acute
coronary syndrome or revascularization procedure. Hospital-based cardiac rehabilitation has not been
shown to be superior to home-based cardiac rehabilitation for low-risk patients. Before patients begin
a rigorous exercise program, physicians should assess their cardiovascular status by taking a physical
activity history or performing an exercise test.

Weight and Dietary Management

Obesity is associated with increased CAD mortality and adversely affects cardiac function and
comorbid CAD risk factors. Obesity is classified using the body mass index (BMI). Weight loss is
indicated for patients who are classified as overweight or obese according to their BMI. The
American Heart Association (AHA) recommends measuring BMI at each office visit, then providing
objective feedback and consistent counselling on weight loss strategies. Long-term weight
maintenance is best achieved through a balance of physical activity and moderation of caloric intake;
improvements in cardiac risk factors are commonly observed with even modest weight loss (i.e., 10
percent of baseline weight). Insufficient evidence exists to determine whether weight reduction
decreases cardiovascular mortality in persons who areobese.
 Figure 4.1 BMI classification

Tobacco Cessation

Tobacco cessation has been shown to reduce all-cause mortality in patients with established CAD. In
a recent Cochrane review, investigators concluded that persons who quit smoking after a myocardial
infarction (MI) or cardiac surgery reduce their risk of death by at least one third, and that
discontinuing smoking is at least as beneficial as modifying other risk factors. Physicians are
encouraged to ask about tobacco use at each office visit, and to extend a clear recommendation to quit
to every patient who smokes. If a patient is willing to try to quit, physicians can assist with cessation
through counselling and pharmacotherapy, which are most effective when combined. Providing
behaviour therapy, telephone support, and self-help materials for at least one month can help patients
with CAD to quitsmoking.

Hypertension

The AHA recommend treating hypertension (i.e., blood pressure greater than 140/90 mm Hg, or
greater than 130/80 mm Hg for persons with diabetes mellitus or chronic kidney disease) for the
secondary prevention of CAD. Lifestyle modifications involve weight management, regular physical
activity, prudent alcohol consumption, and a low-sodium diet. The JNC 7 and the AHA recommend
initial treatment of hypertension after an MI with beta blockers or angiotensin-converting enzyme
(ACE) inhibitors, with additional medications added in a stepwise fashion to achieve goal blood
pressure. Beta Blockers
have shown that beta-blocker therapy can reduce recurrent MI, sudden cardiac death, and mortality in
patients after MI, even in those who are normotensive. Consequently, the AHA has recommended
that a beta-blocker regimen be initiated and maintained indefinitely for the secondary prevention of
CAD in all patients after having an MI, unless contraindicated. There is no clear consensus as to
which beta blocker is the safest or most effective. ACE Inhibitors Two large randomized trials have
demonstrated the benefits of ACE inhibitors in the secondary prevention of CAD. The Heart
Outcomes Prevention Evaluation (HOPE) study showed that 10 mg per day of ramipril (Altace)
reduced cardiovascular death and MI in those who were at high risk of or had established vascular
disease without heart failure. The European Trial on Reduction of Cardiac Events with Perindopril in
Stable Coronary Artery Disease (EUROPA) revealed a 20 percent reduction in cardiovascular
mortality and MI in patients with stable CAD without heart failure who were treated with perindopril
(Aceon). Investigators who performed a combined analysis of several studies concluded that there is
strong evidence for consistent cardiovascular protection with ACE-inhibitor therapy by improving
survival and reducing the risk of major cardiovascular events in patients with vasculardisease.

Management of Patients with Diabetes

The mortality rate of CAD is higher in patients with diabetes than in those without diabetes.
Controversy exists regarding appropriate glucose control for diabetes management. Several guidelines
recommend treatment to reduce A1C levels to less than 7 percent; however, recent randomized
clinical trials have not demonstrated reductions in cardiovascular events or mortality with intensive
glucose control. Studies have shown inconsistent improvement with intensive glucose control in
microvascular complications, including nephropathy, but increased adverse effects were observed,
including weight gain, fluid retention, and symptomatic hypoglycemia. The largest recent trial
investigating cardiovascular outcomes with intensive glucose control was discontinued early because
of a 22 percent increased risk of all-cause mortality in the group treated toward an A1C goal of 6
percent compared with less-intensive glucose control. In summary, recent randomized clinical trials
have not shown significant reductions in cardiovascular events or mortality with intensive glucose
control. Secondary prevention of CAD in patients with diabetes also includes treatment of comorbid
hypertension, dyslipidemia, and hypercoagulability. Treatment of diabetes with statins reduces
vascular morbidity and mortality regardless of cholesterol values, and a 2008 meta-analysis reported a
proportional reduction in major vascular events, with a reduction in low- density lipoprotein (LDL)
cholesterol levels in those with diabetes. A multifactorial approach to diabetic care that includes
glucose control; blood pressure management with renin-angiotensin system blockers; aspirin therapy;
and lipid management with statins has been shown to reduce vascular complications and
cardiovascular mortality.
Antiplatelet Agents
Antiplatelet agents are recommended in all patients for the secondary prevention of CAD. In a large
meta-analysis, antiplatelet therapy reduced recurrent vascular events by one fourth in patients with a
previous vascular event. Aspirin treatment (81 to 162 mg per day) should begin immediately after
diagnosis of CAD and continue indefinitely unless contraindicated. Clopidogrel (Plavix) is an
effective alternative in patients who cannot take aspirin, and the AHA recommends using clopidogrel
in combination with aspirin for up to 12 months after an acute cardiac event or percutaneous coronary
intervention (PCI) with stent placement.

Lipid Management
Recent clinical trials have demonstrated that reducing cholesterol levels decreases the risk of
recurrent coronary events, and evidence based cholesterol-lowering guidelines have been established
by the National Cholesterol Education Program Adult Treatment Panel III (ATP III). The AHA and
ATP III recommend that all patients with CAD initiate lipid management through therapeutic lifestyle
changes. For the secondary prevention of CAD, ATP III recommends LDL levels of less than 100 mg
per dL (2.59 mmol per L), with an optional goal of less than 70 mg per dL (1.81 mmol per L); if the
LDL level is greater than 130 mg per dL (3.37 mmol per L), cholesterol-lowering medications are
indicated in addition to lifestyle changes. Statins should be the initial medication choice; however,
additional agents may be considered if the LDL goal is not reached through statin therapy alone.
Recent studies have shown intensive statin therapy reduces all-cause mortality in patients after acute
coronary syndromes compared with standard therapy; consequently, some have encouraged statin use
in all patients who have CAD. For every sustained 2 mg per dL reduction in LDL cholesterol, statin
therapy has been shown to reduce major coronary events, coronary revascularization, and stroke by 1
percent. The AHA suggests that physicians consider advising patients to increase dietary intake of
omega-3 fatty acids to improve cholesterol levels, but a Cochrane review found insufficient evidence
to recommend for or against supplementation.

EXERCISE PRESCRIPTION FOR MAXIMIZING FITNESS (AHA)

Maximizing Fitness Exercise training programs generally are designed to improve aerobic fitness and
include the prescriptive components of intensity, duration, frequency, progression, and modality. For
patients with CVD, intensity usually is determined on the basis of results from the baseline exercise
test by any of the following methods: 40% to
80%ofpeakexercisecapacitywiththeHRreserve;inpatientswhohaveperformeda
Cardio-pulmonary exercise testing, 40 to 80 measured Vo2 reserve, or peak Vo2.The intensity may be
further modified by using the subjective RPE scale of 12 to 16 on a scale of 6 to 20. Among patients
with an ischemic response during exercise, the intensity should be prescribed at an HR just below the
onset of ischemic symptoms by ≈10 beats). The ischemic threshold is most often determined as the R
at which typical angina begins to occur. The goal duration of exercise at the prescribed intensity is
generally 30 to 60 minutes per session. AIT involves alternating 3- to 4-minute periods of exercise at
very high intensity (90%–95% HRpeak) with 3-minute intervals at a moderate intensity (60%–70
Rpeak). Such training for ≈40 minutes 3 times per week has been shown to yield greater
improvements in peak Vo2 than those seen with standard continuous, moderate-intensity exercise.
Although AIT has long been used in athletic training and appears to have promise in patients with
CVD, AIT cannot yet be broadly recommended for such patients until further data on safety and
efficacy are available.
 ACTIVITY 5
DEMONSTRATION AND PRACTICE OF ADL AND FUNCTIONAL
EVALUATION IN CARDIAC PATIENTS.
 Aims of cardiac patients functional evaluation

 Reproducible assessment of patient’s exercise capacity

 Prescription of endurance training intensity
 Evaluation of response to endurance training
 Evaluation of response to therapeutic interventions (drugs, ventricular resynchronization,
etc.) affecting exercise capacity
 Evaluation of the O2 transport and utilization system efficiency (ventilatory,
hemodynamic, and metabolic components)

Two categories of assessment

1. Cardiovascular function

• Assessing Peak Oxygen Consumption from Exercise Tests

• Assessing Cardiovascular Functional Capacity Without Exercise Tests

2. Muscular function.

• 1-repetition maximum test (1-RM).

• Handgrip dynamometer.

• Short Physical Performance Battery

Assessing Peak Oxygen Consumption from Exercise Tests

• Recent guidelines and scientific statements are available that provide comprehensive
recommendations for procedures for clinical exercise testing.

• Exercise testing can be performed with various exercise modes; however, the 2 most
common choices are cycle ergometers and treadmills.

Table 5.1
• There are 2 types of cycle ergometers; Mechanically braked and electrically braked.

• Work rates on mechanically braked cycle ergometerscan be varied by both the rate of
pedaling and the resistance to pedaling. This requires a fixed pedal rate of typically 50 or
60 rpm to achieve the desired fixed work rate.

• Electrically braked cycle ergometers are designed to automatically change the resistance
on the pedal as the pedal rate varies to maintain a desired fixed work rate.

• Exercise tests are administered according to specified protocols with multiple variations
possible.

• The duration of an exercise test should require at least 6 minutes but no more than 15
minutes, with an ideal time of 10 minutes.

• The first decision in selecting a protocol is between a fixed incremental or ramp style.

• A fixed incremental protocol uses a specific work rate either in watts on a cycle ergometer
or by a combination of speed and elevation on a treadmill for a set period of time (stage) of
1, 2, or 3 minutes.

• One of the most desirable features of fixed incremental protocols is that the VO2 of each
stage can be estimated (standard error of estimate [SEE] 7%) using equations provided by
the American College of Sports Medicine.(Pescatello et al., 2014)

• There are many standardized incremental treadmill protocols. The Bruce protocol was
commonly used in routine cardiac diagnostic assessments; however, the relatively high first
work rate of approximately 5 metabolic equivalents (METs; 1 MET = 3.5 mL O2kg-1min-
1) and the large stage increments of 2 to 3 METs makes it unsuitable for patients with HF.
Preferred options for this population are either the modified Naughton or a modified Balke
protocol.

• For cycle testing, few standardized protocols exist because the maximal watt level varies
directly with the total body weight (muscle mass) of the patient. Certainly, some clinics use
a number of standardized incremental protocol options for cycle testing to achieve different
expected maximal watt levels.

Bruce and modified Bruce protocols

• The Bruce treadmill protocol is the most widely used exercise protocol in the United States
(Bruce et al., 1973; Hermansen&Saltin, 1969) due to physician familiarity, availability of
equations to predict functional capacity (Foster et al., 1984; McConnell et al., 1991; Myers
&Bellin, 2000) and efficiency of time utilization for both the clinician and patient.
 • The aerobic requirements (~5 METs) associated with the first stage of the Bruce protocol
and the large increases (~3 METs) between stages may make it less than optimal for
persons with a low functional capacity.

• In addition, the Bruce protocol encourages extensive handrail support, which results in
over estimation of the patient’s peak exercise capacity askell et al., 1982; McConnell et
al., 1991).

• In response to these limitations, modifications of the Bruce protocol and many other
treadmill and cycle protocols have been developed, including patient specific ramping
protocols (Myers &Bellin, 2000). A common recommendation is to choose a protocol that
will result in test duration of 8–12 minutes (Arena et al., 2007).

• The Bruce protocol consists of multiple 3-minute stages that begin at a walking pace of 1.7
mph 45.6 m ∙ min−1) and a 10% grade. Every stage, the speed and percent grade is
increased. In the second stage (fourth to sixth minutes), the grade is increased to 12% and
the speed is increased to 2.5 mph 67 m ∙ min−1). n subsequent stages, the grade is
increased by 2% and the speed by either 0.8 or 0.9 mph 21.4 or 24.1 m ∙ min−1). O2max
prediction equations have been developed utilizing the Bruce treadmill protocol in active
and sedentary men and women, patients with CVD, and older adults.

Figure 5.1 Mason Liker Lead placement Figure 5.2 Treadmill exercise testing

• The modified Bruce protocol (Lerman et al., 1976) is more appropriate for high-risk or
older adults. The protocol is similar to the standard Bruce with the exception of the first
two stages. Stage 1 starts at 0% grade and 1.7 mph 45.6 m ∙ min −1) and progresses to a
5% grade while maintaining the same speed. In stage 3, the speed is maintained, but the
grade is increased to 10%. At this point, the remainder of the protocol follows the standard
Bruce.

Table 5.2 Bruce protocol

Table 5.3 Modified Bruce protocol

Bruce protocol

Population –

Active and sedentary men

VO2max =14.76 – 1.379 time) + 0.451 time2) −0.012 time3)SEE = 3.35 Ml ∙ kg−1
∙min−1

Active and sedentary women

O2max = 4.38 time) −3.90 SEE = 2.7 Ml ∙ kg−1 ∙min−1

 Patients with cardiac problem and older adults

VO2max = 2.282 (time) +8.545 SEE =4.9 Ml ∙ kg−1 ∙min−1

Modified Bruce High-risk, elderly

VO2 = 3.5 + (S × 0.1) +(S × G × 1.8)

• This equation is used only for treadmill walking while holding the handrails.

• To estimate O2 for the modified Bruce, the ACSM metabolic equation for walking can be
used, where S is speed in m ∙ min−1 1 mph = 26.8 m ∙ min−1) and G is the percent grade
expressed as a decimal (e.g., 10% = 0.10).

Balke Protocol

• The Balke and Ware (Balke& Ware, 1959) protocol is a multistage protocol consisting of
1-minute stages that begin at a speed of 3.4 mph 91.1 m ∙ min−1) at a grade of 0% during
the first minute. The speed is maintained throughout the entire test, but the grade is
increased by 1% every minute. Using the alke equation, the individual’s O2max can be
estimated.

• The modified Balke is a well-accepted treadmill protocol that keeps the speed constant and
increases workload by increasing grade. Speed in the modified Balke is 3.0 mph, which is
0.4 mph slower than the standard Balke, if one takes into account the shorter stride of
women. At this speed, women can walk fast but do not need to break stride into a run; thus,
stress on weight-bearing joints is minimized. Grade is increased from 0% to 2% after 1 min
and then 1% every minute until the test is terminated.(Pollock et al 1984)

• Active and sedentary men VO2max = 1.444 (time) +14.99 SEE = 2.5 Ml ∙ kg−1 ∙min−1

• Active and sedentary women VO2max = 1.38 (time) +5.22 SEE = 2.2 Ml ∙ kg−1 ∙min−1

• For women, the Balke protocol begins at 3.0 mph and 0% grade for 3 minutes, increasing
2.5% every 3 minutes.

Table 5.4 Balke protocol

 Modified Naughton Protocol

• The Naughton (Foster et al., 1983) is another protocol that is best used for patients with
CVD and patients who are high risk. The Modified Naughtonprotocol consists of 2-minute
stages starting at an initial speed of 1.0 mph 26.8 m ∙min−1) and 0% grade.

• The second stage is at a 0% grade, but the speed is increased to 1.5 mph 40.23 m ∙ min−1).
ereafter, each stage increases by 2 mph 53.6 m ∙ min−1) and a grade of 3.5%.

• Male cardiac patients O2max = 1.61 time) +3.6 SEE = 2.60 mL ∙ kg−1 ∙min−1

Table 5.5 Modified Naughton Protocol

• Alternatively, both standardized and individualized ramp-style protocols can be used.

• Individualized ramp protocols can be derived using software options with metabolic
systems, which require setting a starting and maximal speed of walking (or fixed speed)
and an estimate of the functional capacity of the patient in METs. The software then
generates the increments in speed and elevation to obtain the estimated MET level in a
targeted test time (usually 10 minutes). A similar process is used for cycle testing, setting a
starting and expected watt level and then computing the rate of increase in watts to be
obtained in alinear fashion over a 10-minute period of time.

• Determination of peak VO2 during a CPX requires collecting ventilatory expired gases
during the test. The 3 primary variables measured during the test are the total ventilation
and the fractional concentrations of expired oxygen and carbon dioxide.

• As mentioned, additional CPX variables can also be measured, which have prognostic and
diagnostic utility.

• CPX measurements require specialized equipment and trained personnel, which can be a
limiting factor, because these resources may not be readily available.
• However, as more academic programs have developed for training individuals to
administer these tests and the costs of the equipment are relatively fixed (i.e, the primary
cost is the purchase of the equipment, the costs per test are minimal) the opportunities for
obtaining a measured peak VO2 are growing.

• The next best option for assessing cardiovascular functional capacity is from a maximal
exercise test, performed without ventilatory expired gas measurements. This option is
commonly available in cardiology clinics and practices.

• These tests are primarily performed for diagnostic purposes with routine monitoring of the
exercise electrocardiogram, along with blood pressure, heart rate, and signs and symptoms.
These tests also require specifically trained personnel.

• Cardiovascular functional capacity can be estimated from either a prediction equation

using maximal test time with standardized protocols or from the maximal work rate
obtained during the test.

• With use of any prediction equation, there is some degree of error associated with the
estimation. Prediction equations using test time typically have reported error ranges of
approximately 3 to 5 mL O2kg-1min-1.

• Estimations from maximal work rate are derived using the American College of Sports
Medicine equations. However, it is important to recognize that this creates some issues,
because these equations were developed for steady-state submaximal work rates (not
maximal). Thus, the estimates may result in greater error ranges than those reported for the
submaximal level (ie, more than 7%).

• A third option for assessing cardiovascular functional capacity is from a submaximal

exercise test. These procedures rely on having a reasonable estimation of maximal heart
rate, commonly estimated using age. A heart rate to VO2 (predicted from work rate)
relationship is established at 2 submaximal levels and then a linear line is extrapolated to
derive an estimated maximal value.

• Advantages of submaximal testing are that it requires less training from staff, takes less
time, and because the patient’s effort is submaximal has lower associated risks.

• However, because many patients with HF are prescribed b-blocker medications,(Yancy et

al., 2013)prediction of maximal heart rate is compromised. Thus, this method may not be
viable for many patients with HF.
 Table 5.6

Assessing Cardiovascular Functional Capacity without Exercise Tests

• The 6-minute walk test (6MWT) has gained acceptance in the clinical community as a
feasible option to obtain an estimate of cardiovascular functional capacity in disease-based
populations known to experience exercise intolerance.

• In most clinical settings, this can be done in a hallway that is at least 30 m long. However,
it should be mentioned that the length and type (oval vs back-and-forth) may result in
slight differences in performance. Attempts to perform this test on a treadmill have not
been found to be successful.(Lenssen et al., 2010)
• Other assessments have been studied. Some investigators have determined the ability of a
shuttle walk test (SWT) to evaluate chronic disease patient populations.(Lewis et al.,
2001; Morales et al.,1999; Singh et al.,1992)This test requires patients to walk back and
forth around 2 markers on a 10-m course (each 10m51 shuttle) at a pace dictated by audio
signals recorded on a cassette tape or CD. The speed is initially set at 0.5 m/s and increased
by 0.17 m/s every minute.
• The test is terminated when the patient cannot complete a shuttle in the required time
interval. As with the 6MWT, it is recommended that only standardized comments (no
encouragement) be provided and that the SWT is repeated at least twice to account for a
learning effect.

• The major distinguishing characteristic between the 6MWT and SWT is the incremental
nature of the SWT. Proponents of the SWT suggest this should result in a greater level of
effort, compared with the self-pace nature of the 6MWT, and thus provide a better
indicator of cardiovascular functional capacity. Although this test may have merit, to date,
the research evidence base is lacking to recommend it be used in place of the 6MWT.

Muscle function

• The gold standard method to assess muscular strength is the 1-repetition maximum test (1-
RM). The resistance for the lifting can be either free weights or resistance exercise
machines.

• Although a 1-RM can be obtained from any weight lifting exercise, the 2 most common
lifts are the bench press (for upper body strength) and the leg press (for lower body
strength). The American College of Sports Medicine guidelines provide a set of normative
values derived from an adult population that was free from chronic disease.(Pescatello et
al., 2014)

• Unfortunately, there are no definitive standards for interpreting 1-RM performance in

patients with HF. One of the major issues with performing 1-RM assessments is the time
requirement, especially if patients need to be familiarized with using the free weights or
machines. Other issues are the need for specialized equipment and trained personnel and
the risks associated with maximal effort.
• A second option for performing muscular function assessments is to use a handgrip
dynamometer.
• This test has been used for many years as a physical fitness measure in school-aged
children. It does require a handgrip dynamometer; however, these devices are relatively
inexpensive (<$400) and are durable.

• The procedure is simple, only requiring the patient to squeeze the handle of the
dynamometer as hard as they can for 3 seconds.

• After a short rest, the test is repeated 2 more times, with each hand being tested. Although
normative values specific for patients with HF do not exist, large population standards are
available. (Spruit et al., 2013) These tests are starting to be administered in the HF
population and seem to have some merit.(Izawa et al., 2009; Sunnerhagen et al., 1998)

• There are also indirect measures of muscular strength that can be used as indicators of
muscular functional ability. The origins for many of these evaluations came from work
with geriatric populations. The method that seems to be gaining the most acceptance is the
Short Physical Performance Battery.(Pavasini et al., 2016)

• This functional test includes assessments of gait speed (4 m), strength (sit to stand,
repeated 5 times), and balance (standing position). A composite score is formulated, with
higher scores indicating better functional ability.

Evaluation of Activities of Daily Living Instruments in Cardiac Patients

The following eight different types of instruments were identified:

1. Barthel Index (BI),

2. Functional Independent Measurement (FIM),

3. Canadian Occupational Performance Measure (COPM),

4. The Kansas City Cardiomyopathy Questionnaire (KCCQ),

5. Daily Activity Questionnaire in Heart Failure (DAQIHF),

6. Performance Measure for ADL-8 (PMADL-8),

7. Klein-Bell Index, and

8. PULSES Profile.

BARTHEL INDEX OF ACTIVITIES OF DAILY LIVING

• The Barthel Scale/Index (BI) is an ordinal scale used to measure performance in activities
of daily living (ADL). Ten variables describing ADL and mobility are scored, a higher
number being a reflection of greater ability to function independently following hospital
discharge. The Barthel Index measures the degree of assistance required by an individual
on 10 items of mobility and self care DL. “ arthel scale,” n.d.)

• Producer and year of publication–(Mahoney &Barthel, 1965)

• Number of items - 10

• Duration (in minutes) - 25

• Scoring – (0-100) Proposed guidelines for interpreting Barthel scores are that scores of 0-
20 indicate “total” dependency, 21-60 indicate “severe” dependency, 61-90 indicate
“moderate” dependency, and 91-99 indicates “slight” dependency.

• Activity - Bowels, bladder, grooming, toilet use, feeding, transfer, mobility, dressing,
stairs, bathing

• Validity - Convergent = 0.73-0.77

• Reliability -Test-retest = 0.89 Inter-rater = 0.95

 Functional Independence Measure (FIM)

• The Functional Independence Measure (FIM) is an 18-item measurement tool that explores
an individual's physical, psychological and social function.(Linacre et al., 1994) The tool
is used to assess a patient's level of disability as well as change in patient status in response
to rehabilitation or medical intervention.(Heinemann et al., 1993)

• Producer and year of publication- UDSMRR, (1990)

• Number of items-18

• Duration (in minutes) -45

• Scoring – rating on a 7- point scale ranging from fully dependent (1) to independent with
no aids (7). The maximum total score is 126, indicating functional independence, and the
lowest score 18, suggesting complete functional dependence.

• Activity-Self-care, locomotion, mobility, sphincter control, cognitive emphasis involving

communication and social cognition

• Validity, reliability and sensitivity to change: Good construct and concurrent validity has
been established. FIM® scores discriminate between disabilities and levels of severity of
impairment (Heinemann et al., 1994); correlate with the time taken for care (Disler et al.,
1993); and correlate highly with Barthel Index scores in people with stroke (Fricke
&Unsworth, 1996). High internal consistency has been reported Cronbach’s α = 0.93–
0.95, Ravaud et al., 1999).
• Ottenbacher et al. (1996) performed a meta-analysis of 11 papers investigating reliability
of the FIM® and reported median correlations coefficients between total scores equal to
0.95 for inter-rater reliability, 0.95 for test retest reliability, and 0.92 for equivalence
reliability. The minimum detectable change score of 90% has been reported to be 23 points
(Stineman et al., 1996).

• Predictive usefulness: An admission FIM® score > 70 has been associated with achieving
non-dependence by discharge whereas those with an admission score < 50 remained
dependent (Ween et al., 2000).

Canadian Occupational Performance Measure (COPM)

• The COPM was developed as a client-centred tool to enable individuals to identify and
prioritize everyday issues that restrict or impact their performance in everyday living. One
of the strengths of the measure is its broad focus on occupational performance in all areas
of life, including self-care, leisure and productivity, taking into account development
throughout the lifespan and the personal life circumstances.

• Producer and year of publication-Law, (1994)

• Number of items-5

• Duration (in minutes)-30-40

• Scoring-0-10

• Activity- Self-care, productive, and leisure

• Reliability- Inter-rater: For performance = 0.63-0.89 For satisfaction: 0.76-0.88

 The Kansas City Cardiomyopathy Questionnaire (KCCQ),

• The Kansas City Cardiomyopathy Questionnaire (KCCQ) is a 23-item self-administered

questionnaire developed to independently measure the patient’s perception of their health
status, which includes heart failure symptoms, impact on physical and social function, and
how their heart failure impacts their quality of life (QOL) within a 2-week recall period.

• Producer and year of publication-Green, (2000)

• Duration (in minutes)-4-6

• Scoring- 0-100

• Activity- Dressing yourself, showering/bathing, walking 1 block on level ground, doing

yard work, housework or carrying groceries, climbing a flight of stairs without stopping,
hurrying or jogging.

• Validity- Construct = 50.9, 60, 83.3

• Reliability-Test-retest = 0.14

• The KCCQ tool quantifies the following six (6) distinct domains and two (2) summary
scores:

• KCCQ Symptom Domain quantifies the frequency and burden of clinical symptoms in
heart failure, including fatigue, shortness of breath, paroxysmal nocturnal dyspnea and
patients’ edema/swelling. n overall symptom score is generally used in analyses; subscale
scores for both frequency and severity are also available.

• KCCQ Physical Function Domain measures the limitations patients experience, due to
their heart failure symptoms, in performing routine activities. Activities are common,
gender-neutral, and generalizable across cultures, while also capturing a range of exertional
requirements.

• KCCQ Quality of Life Domain is designed to reflect patients’ assessment of their quality
of life, given the current status of their heart failure.

• KCCQ Social Limitation Domain quantifies the extent to which heart failure symptoms
impair patients’ ability to interact in a number of gender-neutral social activities.

• KCCQ Self-efficacy Domain quantifies patients’ perceptions of how to prevent heart

failure exacerbations and manage complications when they arise. This scale is not included
in the summary scores.

• KCCQ Symptom Stability Domain measures recent changes in patients’ symptoms; their
shortness of breath, fatigue or swelling. It is compares patients frequency of heart failure
symptoms at the time of completing the KCCQ with their frequency 2 weeks ago. As a
measure of change, it is most interpretable as a baseline assessment of the stability of
patients’ symptoms at the start of a study and shortly thereafter, as a measure of the acute
response to treatment. This domain is not included in the summary scores.

• Clinical Summary Score includes total symptom and physical function scores to
correspond with NYHA Classification.

• Overall Summary Score includes the total symptom, physical function, social limitations
and quality of life scores.

Daily Activity Questionnaire in Heart Failure (DAQIHF),

• A questionnaire composed of 82 questions and subquestions dealing with seven main
dimensions of everyday life with added specific consideration for autonomy and/or
perceived exertion.

• Producer and year of publication- Garet, (2004) (Garet et al., 2004)

• Duration(in minutes)-15-20

• Activity- The seven main dimensions considered were sleeping and resting periods, basic
everyday activities (eating, washing, toilet), housework activities, leisure time physical
activities, physical activity at work or way of being occupied, moving about and
miscellaneous activities. Autonomy and/or perceived exertion addressed specific
information about the amount of help provided by a third person for an activity and if
interruption was needed systematically, sometimes or never while doing a specific activity.

• Validity - Construct = 88%

• Reliability-Test-retest = 0.82-0.98 Inter-rater = 0.82-0.94

Performance Measure for ADL-8 (PMADL-8)

• PMADL-8 is an 8-item, self-administered questionnaire that quantifies functional

limitations in activity of daily living for patients with HF. PMADL-8 was measured with a
4-category response scale (i.e., 1 = very easy; 2 = somewhat easy; 3 = somewhat hard; and
4 = very hard), which had a total score that ranged from 8 to 32 points, in which higher
scores indicated severe functional limitations.

• Producer andyearofpublication-Shimiza, (2009)

• Activity-Getting up and off from the floor without instruments, washing your body and
hair, going up a flight of stairs without a handrail, vacuuming your room, pulling and
closing a heavy sliding door, getting into and out of a car, walking at the same speed with
someone of the same age, walking up a slight slope for 10 min.

• Validity- Construct = 68.2 Convergent = 69%

• Reliability-Test-retest = 0.96

Klein-Bell Index

• Producer and year of publication- Bell and Klein, (1982)

• Tool Description - generic instrument that can be used with persons with or without
disability. Developed to measure basic activities of daily living (ADL) independence in
both adults and children.

• Items are divided into 6 sub-dimensions:

1)Mobility
2)Emergency Communication
3)Dressing
4)Elimination
 5)Bathing/Hygiene
6) Eating.

• The majority of items measure ADLs and others measure body function (bladder/bowel
emptying and incontinence, chewing/swallowing food and liquids, verbalizing telephone
messages).

• Number of Items:170

Brief Instructions for Administration & Scoring

• Administration:

• clinician-administered interview

• measures degree of patient independence

• Administration of the scale takes from 1-3 hours.

• Equipment: items typically used in basic activities of daily living (ex. toilet, bed, etc.)

• Scoring:

• Task weights of 1, 2, or 3 are assigned to each task.

• In developing the weights, four factors were considered, including: importance to health,
difficulty for non-disabled persons, time required to perform the task, and the burden of
care-giving.

• Items are summed (each task is multiplied by its weight)

• Overall independence scores range from 0 to 313 (0%-100%).

• Validity-Construct = have** (number was not reported)

• Reliability-Test-retest = 0.98 Inter-rater = 0.92

PULSES Profile

• The PULSES Profile was designed to evaluate functional independence in ADLs of

chronically ill and elderly institutionalized populations. The profile is used to predict
rehabilitation potential, to evaluate patient progress, and to assist in program
planning.(Moskowitz, 1985).

• Producer and year of publication-Maccann and Maskowitz, (1957)

• Number of items- 6

• Duration(in minutes)-5-10

• Scoring- 24
• The components of the PULSES acronym are: P = physical condition U = upper limb
functions L = lower limb functions S = sensory components (speech, vision, hearing) E =
excretory functions S = mental and emotional status

• In 1979, Granger proposed a revised version of the PULSES Profile with slight
modifications to the classification levels and an expanded scope for three categories. This
is now considered the standard version. (Granger et al., 1977)

• Reliability- Test-retest = 0.87 Inter-rater = 0.95

 ACTIVITY -6

DEMONSTRATION AND PRACTICE OF RESPONSE OF

EXERCISE TO HEMODYNAMICS
 Exercise is a structured and systematic physical activity, to which the human body responds
through a series of integrated changes in function that involve most physiologic systems.
Cardiopulmonary system plays an integral role in it.Exercise results in a marked increase in
oxygen consumption. This increase is accomplished by a significant increase in heart rate and
peripheral oxygen extraction and, to a lesser extent, by an increase in stroke volume. There is a
small increase in mean systemic and pulmonary artery pressures and marked decrease in
systemic and pulmonary resistances with exercise. The result of changes in focal vasomotor tone
is that a greater percentage of the cardiac output is directed to the working muscles.( Hossack,
1987)

Hemodynamic parameters

• The primary hemodynamic parameters include

• heart rate (HR) and blood pressure (BP),
• while the advanced hemodynamic parameters include
• stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) (Alhashemi et al.,
2011)

Hemodynamic responses to Exercise- The cardiovascular system, composed of the heart, blood
vessels, and blood, responds predictably to the increased demands of exercise. With few
exceptions, the cardiovascular response to exercise is directly proportional to the skeletal muscle
oxygen demands for any given rate of work, and oxygen uptake (VO2) increases linearly with
increasing rates of work.

• Heart Rate-The immediate response of the cardiovascular system to exercise is an increase

in heart rate due to a decrease in vagal tone. This increase is followed by an increase in
sympathetic outflow to the heart and systemic blood vessels. During dynamic exercise, heart
rate increases linearly with workload and o2.

• Cardiac Output-(Scruggs et al., 1991) (Gledhill et al., 1994).Cardiac output (Q) is the total
volume of blood ˙ pumped by the left ventricle of the heart per minute. It is the product of heart
rate (HR, number of beats per minute) and stroke volume (SV, volume of blood pumped per
beat). The arterial-mixed venous oxygen (A-- vO2 ) difference is the difference between the
oxygen content of the arterial and mixed venous blood. person’s maximum oxygen uptake
O˙ 2 max) is a function of cardiac output Q) multiplied by the ˙ -vO2 difference. Cardiac
output thus plays an important role in meeting the oxygen demands for work. As the rate of work
increases, the cardiac output increases in a nearly linear manner to meet the increasing oxygen
demand, but only up to the point where it reaches its maximal capacity (Q max).

-To visualize how cardiac output, heart rate, and stroke volume change with increasing rates of
work, consider a person exercising on a cycle ergometer, starting at 50 watts and increasing 50
watts every 2 minutes up to a maximal rate of work (Figure 3-1 A, B, and C). In this scenario,
cardiac output and heart rate increase over the entire range of work, whereas stroke volume only
increases up to approximately 40 to 60 percent of the person’s maximal oxygen uptake O˙ 2
max), after which it reaches a plateau.

- Recent studies have suggested that stroke volume in highly trained persons can continue to
 increase up to near maximal rates of work (Scruggs et al., 1991) (Gledhill et al.,1994).

• Blood Flow - The pattern of blood flow changes dramatically when a person goes from resting to
exercising. At rest, the skin and skeletal muscles receive about 20 percent of the cardiac output.
During exercise, more blood is sent to the active skeletal muscles, and, as body temperature
increases, more blood is sent to the skin. This process is accomplished both by the increase in
cardiac output and by the redistribution of blood flow away from areas of low demand, such as
the splanchnic organs. This process allows about 80 percent of the cardiac output to go to active
skeletal muscles and skin at maximal rates of work (Rowell 1986). With exercise of longer
duration, particularly in a hot and humid environment, progressively more of the cardiac output
will be redistributed to the skin to counter the increasing body temperature, thus limiting both the
amount going to skeletal muscle and the exercise endurance (Rowell 1986).

• Blood Pressure(Rowell et al., 1993) (Isea et al., 1994). -Mean arterial blood pressure increases
in response to dynamic exercise, largely owing to an increase in systolic blood pressure, because
diastolic blood pressure remains at near-resting levels. Systolic blood pressure increases linearly
with increasing rates of work, reaching peak values of between 200 and 240 milli meters of
mercury in normotensive persons. Because mean arterial pressure is equal to cardiac output times
total peripheral resistance, the observed increase in mean arterial pressure results from an
increase in cardiac output that outweighs a concomitant decrease in total peripheral resistance.

-This increase in mean arterial pressure is a normal and desirable response, the result of a
resetting of the arterial baroreflex to a higher pressure. Without such a resetting, the body would
experience severe arterial hypotension during intense activity (Rowell et al., 1993).

-Hypertensive patients typically reach much higher systolic blood pressures for a given rate of
work, and they can also experience increases in diastolic blood pressure. Thus, mean arterial
pressure is generally much higher in these patients, likely owing to a lesser reduction in total
peripheral resistance. For the first 2 to 3 hours following exercise, blood pressure drops below
pre-exercise resting levels, a phenomenon referred to as post-exercise hypotension (Isea et al.,
1994).

-The specific mechanisms underlying this response have not been established. The acute changes
in blood pressure after an episode of exercise may be an important aspect of the role of physical
activity in helping control blood pressure in hypertensive patients.
 Figure 6.1

 Oxygen Extraction - The A- vO2 difference increases with increasing rates of work and results
from increased oxygen extraction from arterial blood as it passes through exercising muscle. At
rest, the A-vO2 difference is approximately 4 to 5 ml of O2 for every 100 ml of blood (ml/100
ml); as the rate of work approaches maximal levels, the A-vO2 difference reaches 15 to 16
ml/100 ml of blood.

Figure 6.2

 Coronary Circulation - The coronary arteries supply the myocardium with blood and nutrients.
The right and left coronary arteries curve around the external surface of the heart, then branch
and penetrate the myocardial muscle bed, dividing and subdividing like branches of a tree to
form a dense vascular and capillary network to supply each myocardial muscle fiber. Generally
 one capillary supplies each myocardial fiber in adult humans and animals; however, evidence
suggests that the capillary density of the ventricular myocardium can be increased by endurance
exercise training. At rest and during exercise, myocardial oxygen demand and coronary blood
flow are closely linked. This coupling is necessary because the myocardium depends almost
completely on aerobic metabolism and therefore requires a constant oxygen supply. Even at rest,
the myocardium‘s oxygen use is high relative to the blood flow. bout 70 to 80 percent of the
oxygen is extracted from each unit of blood crossing the myocardial capillaries; by comparison,
only about 25 percent is extracted from each unit crossing skeletal muscle at rest. In the healthy
heart, a linear relationship exists between myocardial oxygen demands, consumption, and
coronary blood flow, and adjustments are made on a beat-to-beat basis. The three major
determinants of myocardial oxygen consumption are heart rate, myocardial contractility, and
wall stress. Acute increases in arterial pressure increase left ventricular pressure and wall stress.
As a result, the rate of myocardial metabolism increases, necessitating an increased coronary
blood flow. A very high correlation exists between both myocardial oxygen consumption and
coronary blood flow and the product of heart rate and systolic blood pressure (SBP) (Jorgensen
et al. 1977). This so called double product R • S ) is generally used to estimate myocardial
oxygen and coronary blood flow requirements. During vigorous exercise, all three major
determinants of myocardial oxygen requirements increase above their resting levels. The
increase in coronary blood flow during exercise results from an increase in perfusion pressure of
the coronary artery and from coronary vasodilation. Most important, an increase in sympathetic
nervous system stimulation leads to an increase in circulating catecholamines. This response
triggers metabolic processes that increase both perfusion pressure of the coronary artery and
coronary vasodilation to meet the increased need for blood flow required by the increase in
myocardial oxygen use.

 Rate pressure product (RPP )- Rate pressure product (RPP), calculated by multiplying SBP
and HR, is a valid non-invasive surrogate measure of myocardial oxygen consumption.

-Typically, an increase in HR during exercise is a sign that more blood and oxygen is travelling
to the working muscles, while elevated BP indicates more blood gets pumped to the heart.Both
HR and SBP are the most important variables determining changes in myocardial oxygen
consumption between rest and exercise (Robinson, 1967).

-HR, SBP and RPP increases with the increase workload on the heart to provide the adequate
blood supply to the active myocardium during exercise. As reported earlier also, there was
significant increase in SBP, HR and RPP with exercise, due to increase in sympathetic discharge
(Nagpal et al., 2007).

 Peripheral Circulation-The rising metabolic demands in the exercising muscles require

increasing blood flow to that regional bed. Two major compensatory mechanisms occur: a
threefold in¬ crease in the arteriovenous oxygen extraction and a fourfold rise in skeletal blood
flow. The latter change is due to an elevation in aortic pressure and a reduction in muscle
vascular resistance, which is mediated by metabolic end products of exercise.

-Another factor causing the increased blood flow to the exercising muscles is a redistribution of
the cardiac output. The blood flow to the renal, splanchnic, and cutaneous circulations decreases,
whereupon it can then be shunted to the exercising muscles.

-The mechanism for this reduction is mediated in part by stimulation of the sympathetic nerves
to the mesenteric and renal vessels, leading to vasoconstriction. The percentage of the cardiac
output delivered to the exercising skeletal muscles increases from 20% at rest to 80% during
 maximal exercise; the coronary blood flow increases fivefold, and the cerebral blood flow
remains unchanged during maximal exercise. (Zelis et al., 1975)

CLINICAL MEASURES – Three types of exercise can be used to stress the cardiovascular
system: (1) isometric, (2) dynamic and (3) both combined. Static or isometric exercise imposes a
disproportionate pressure load on the left ventricle relative to the body‘s response to supply
oxygen. Dynamic exercise initiates a more appropriate increase of cardiac output and air
exchange. Since the delivered work load can be accurately calibrated and the physiologic
response easily measured, dynamic exercise is the favoured modality for clinical testing. Using
progressive work loads of dynamic exercise, patients with coronary disease can be protected
from sudden and dangerous increases in myocardial oxygen requirements. Maximal and sub-
maximal exercise can be used, but maximal testing yields the most useful and accurate
diagnostic information. A true maximal exercise test is achieved when measured oxygen
consumption the body‘s oxygen requirement for doing work) reaches a plateau and will not
increase despite an increase in work load.

Hemodynamic evaluation (Vincent et al., 2011) (Blauwet et al., 2013)

• Comprehensive hemodynamic evaluation is one of the many tools our highly skilled doctors use
to evaluate your cardiovascular health. Hemodynamics is the method used to study blood
pressure and how well your body transports oxygen in your blood to the tissues of your
body.(Blauwet et al., 2013)
• Hemodynamic assessment allows us to
• Early detection of impending cardiovascular decompensation Identification of critical illness
• Selection of appropriate treatment modalities
• Monitoring of therapeutic interventions (Vincent et al., 2011)

Treadmill Exercise Stress Testing –

SKIN PREPARATION
Proper skin preparation is essential for the performance of an exercise test. The areas for
electrode application should be marked with a felt-tip pen, the ink serving as a guide for removal
of enough of the superficial layer of skin. The marked areas are then cleansed with an alcohol-
saturated gauze pad.
ELECTRODES
The only suitable electrodes are constructed with the metal interface sunken so that there is a
column that can be filled with either an electrolyte solution or by a sponge soaked with
electrolyte solution.
 Figure 6.3 Lead placement Figure 6.4 Lead systems for exercise testing
Mason- Liker modification

BLOOD PRESSURE MEASUREMENT

Blood pressure should be taken at least at the mid-portion of each exercise stage and with the
appearance of chest pain. We prefer the following equipment to available automated blood pressure
devices. Treadmill side rail when blood pressure is taken. The test should usually be stopped if the
systolic blood pressure has a sustained drop, especially if this drop is accompanied by chest pain.

Table 6.1 Exercise protocol

APPLICATIONS OF EXERCISE TESTING

To DIAGNOSE CHEST PAIN

The exercise test can be used to evaluate patients with chest pain or other findings suggestive, but not
diagnostic, of coronary artery disease. The results of exercise testing can help establish the probability of
such patients having heart disease. Exercise testing can also be used to evaluate asymptomatic patients
with ECG abnormalities which could be due to coronary artery disease, including ST segment
depression, right bundle branch block and patterns suggestive of myocardialdamage.

To DETERMINE PROGNOSIS
The exercise test can be used to determine the prognosis of individuals with coronary artery disease. It
can establish the risk for mortality and morbidity of patients after an acute myocardial infarction and
those with angina pectoris. Exercise-induced hypotension and persistent ST segment depression
beginning at a low heart rate are predictive of diffuse coronary artery disease in men. The functional
capacity as determined by the work load achieved can be used to estimate the prognosis and surgical
survivability of patients with coronary artery disease.

EVALUATION OF FUNCTIONAL CAPACITY

The exercise test can be used to evaluate the functional capacity of patients. Maximal oxygen
consumption is the best non-invasive measurement of the functional capacity of the cardiovascular
system. Exercise testing can more accurately measure the degree of cardiac impairment than the
physician‘s assessment of functional classification. atients with mild cardiac impairment are usually
found to have a maximal oxygen consumption less than 22 cc O,/kg/min, while in those who consider
themselves severely limited, the maximal oxygen consumption is 16 cc O,/kg/min or less. The
determination of a patient‘s functional capacity affords an objective measurement of the degree of
cardiac impairment and may be useful in patient management.

EVALUATION FOR EXERCISE PROGRAMS

The exercise test can be used to evaluate the safety of participating in an exercise program and can help
formulate an exercise prescription. Though aerobic exercise training has not been demonstrated to have
a beneficial effect on the atherosclerotic process, its beneficial effects on the cardiovascular system and
on cardiovascular hemodynamics have been demonstrated. In certain individuals, it would be
advantageous to objectively evaluate their response to exercise in a monitored situation prior to having
them embark on an exercise program.
Table 6.2 RECENT RESEARCH EVIDENCES

TITLE JOURNAL METHODOLOGY CONCLUSION

Cardiopulmona European Subjects underwent pre- Selected CPET parameters
ry exercise heart journal; randomization treadmill CPET, relate to severity of angina
testing and Ganesananth dobutamine stress symptoms and quality of life,
efficacy of an et al., echocardiography (DSE) and only an oxygen-pulse plateau
percutaneous 2022 symptom assessment. These detects the severity of
coronary assessments were repeated at the myocardial ischaemia and
intervention: a end of a 6-week blinded follow- predicts the placebo-controlled
substudy of the up period. efficacy of PCI in patients with
ORBITA trial single-vessel CAD.

Adoption of BMC Fifty CHD patients after RT training can reduce

the Cardiovascul percutaneous coronary postoperative blood lipid and
cardiopulmona ar disorder intervention (PCI) were recruited quantitative load levels in CAD
ry exercise test Wang et al., and randomly enrolled into the patients and improve adverse
in the exercise 2024 control (Ctrl) group and mood. Furthermore, it can
ability and intervention (Int) group. Routine improve patients'
cardiopulmona health education and health cardiopulmonary function,
ry function education combined with RT cardiopulmonary fitness,
rehabilitation training were carried out for the exercise ability, and quality of
of coronary two groups. Blood lipid levels life.
artery disease and lung function were
(CAD) patients compared between the two
groups after intervention.
Cardiac function was evaluated
by Doppler ultrasonography, and
cardiopulmonary fitness and
exercise ability were evaluated
by a cardiopulmonary exercise
test (CPET). The self-rating
anxiety scale (SAS) and self-
rating depression scale (SDS)
were employed to evaluate
negative emotions. The 36-item
short-form (SF-36) was adopted
to evaluate quality of life.
 ACTIVITY 7

EVALUATION OF FATIGABILITY IN

CARDIOVASCULAR DISEASES
FATIGUE
A very noticeable symptom in most cardiac and pulmonary conditions is fatigue (Nordgren and Sörensen
2003). It is present in up to 69% to 82% of patients with cardiac disease and up to 68% to 80% of patients
with pulmonary disease (Skilbeck et al., 1998)

Fatigue is defined as an internal homeostasis breakdown caused by an increase in energy production

demanded by an external stimulus. Fatigue can be generally defined as a decrease in physical
performance related to a rise within the real/perceived difficulty of a task or exercise, as well as the
inability of the muscles to keep up with the specified level of strength during exercises (Abd-Elfattah et
al., 2015).

FATIGUE AND CARDIOVASCULAR DISEASE

➢ It is defined as an unpleasant feeling of inability to perform physical or intellectual efforts (physical

fatigue, mental fatigue), occurring prematurely during activity and resulting in an alteration of the
subject’s usual performances and quality of life (Wilson et al., 1984).

➢ It is a key symptom in the course of cardiovascular disease although its real prevalence has not been
clearly established, essentially due to the difficulty of quantifying fatigue (Lewis and Wessely,
1992).

➢ It is particularly frequent in heart failure and is often associated with a 50% reduction of physical
capacities, but it is also observed during coronary artery disease without ventricular dysfunction
(Liang et al., 1992).

CLASSIFICATION OF FATIGUE

➢ The distinction between physical fatigue and mental fatigue appears to be more appropriate than
the classification between peripheral fatigue and central fatigue (Bigland-Ritchie and Woods, 1984).

➢ This approach, based on physical and mental dimensions, facilitates correlations with the clinical
reality of cardiovascular disease.

▪ PHYSICAL FATIGUE

➢ Physical fatigue corresponds to loss of efficiency of the effector muscle.

➢ It can be due to very diverse causes in the context of cardiovascular disease, as several steps of
energy production can be altered, resulting in real exercise intolerance (Casillas et al., 2006).
▪ MENTAL FATIGUE

➢ Mental fatigue usually corresponds to a feeling of loss of vitality, lassitude, and the term
“asthenia” is often used. A depressive tendency is predominant (Casillas et al., 2006).

• CNS FATIGUE can be defined as a decrease in the voluntary activation of muscles, directly related
to a decrease in the frequency and synchronization of motoneurons, and a reduced drive from the
motor cortex (Zajac et al., 2015).

• PERIPHERAL FATIGUE is the decrease in the contractile strength of muscle fibers with changes
in the mechanisms underlying the transmission of muscle action potentials (Zajac et al., 2015).

PATHOGENESIS OF FATIGUE IN CARDIOVASCULAR DISEASE

WHAT HAPPENS INSIDE THE MUSCLE? Apart from these physiological changes that occur
because of peripheral fatigue, there are metabolic, neuromuscular, and mechanical consequences in
muscle cells that originate from fatigue. These are related to three main factors: (i) Failure in energy
metabolism as the myocyte cannot continue resynthesizing ATP. (ii) Inefficiency in the contraction
coupling mechanism due to an impairment in the number or functionality of the actin and myosin cross-
bridges. (iii) Metabolic acidosis produced by the intramuscular accumulation of Pi and hydrogen ions.

Figure 7.1: Factors affecting Governor Fatigue Theory (Tornero-Aguilera et al., 2022)
CAUSES OF PHYSICAL FATIGUE

MISMATCH OF CARDIAC OUTPUT TO THE BODY’S NEEDS:

➢ It may be due to heart failure related to disorders of contractility (systolic heart failure), and left-
ventricular filling (diastolic heart failure) (Smart et al., 2005).

PERIPHERAL MUSCLE DECONDITIONING:

➢ This is inducing poor adaptation to exercise. This form of exercise intolerance is dominated by
alteration of muscle oxidative metabolism.

➢ It has been demonstrated the consequences of muscle deconditioning with premature acidosis
associated with creatine phosphate depletion during exercise and an abnormally long creatine
phosphate resynthesis time during the recovery phase (Cottin et al., 1996).

➢ These abnormalities are particularly marked in patients with heart failure, also associated with
impaired muscle aerobic metabolism leading to premature lactic acidosis during exercise (Mancini
et al., 1992; Drexler and Coats, 1996).

METABOLIC DISEASES:

➢ It is associated with cardiovascular diseases (dyslipidemia, diabetes, obesity) can worsen exercise
intolerance, and insulin resistance is particularly involved in muscle deconditioning associated with
heart failure (Coats & Anker, 2000).

ALTERATION OF ENDOTHELIAL FUNCTION:

➢ It is also responsible for disorders of microcirculatory adaptation in cardiovascular disease.

➢ Exercise capacity is limited according to the degree of alteration of NO-dependent vasodilatation
(Rush et al., 2005).
➢ The combination of muscle metabolic disorders and perfusion disorders during chronic heart failure
plays a predominant role compared to insufficient cardiac output in the pathogenesis of exercise
intolerance.

NEUROENDOCRINE DISORDERS

➢ It is especially stimulation of the sympathetic nervous, renin-angiotensin-aldosterone and arginine-

vasopressin systems, are increasingly incriminated in the pathogenesis of cardiovascular disease,
particularly heart failure.
➢ These disorders are responsible for numerous harmful effects that impair exercise capacity:
vasoconstriction, increased peripheral resistances, increased blood volume, ventricular re-modelling
(Re, 2004).

RESPIRATORY IMPAIRMENT

➢ It is frequent in severe heart failure, related to abnormalities of the ventilation/perfusion ratio and
responsible for harmful reflex hyperventilation probably due to excessive activation of muscle
chemoreceptors and ergo-receptors (Scott et al., 2000).
➢ Fatigue is then aggravated by dyspnea, which is usually correlated with increased pulmonary artery
pressure. Respiratory failure can be related to chronic obstructive pulmonary disease associated with
cardiovascular disease, as both diseases share a major risk factor, smoking.

CAUSES OF MENTAL FATIGUE

Advanced forms of mental fatigue essentially present in two ways:

1. VITAL EXHAUSTION

➢ It is an entity associating unusual and persistent fatigue, loss of energy, a feeling of dejection and
irritability.

➢ It represents a risk factor for cardiovascular morbidity and mortality comparable to dyslipidaemia and
can be at least partially explained by an abnormal lipid profile or decreased fibrinolytic capacity
(Koertge et al., 2003; Appels & Otten, 1992).

➢ The type of personality plays an important role in development of this syndrome. Patients presenting
anxiety and social inhibition are the most frequently affected (Appels & Mulder, 1989).

2. DEPRESSION

➢ The sadness, apathy and psychomotor retardation are characteristic of depression which are often
associated with fatigue and irritability.

➢ It is frequent in the course of cardiovascular disease. It affects about 50% of post-infarction patients
(Frasure-Smith et al.,1993).

➢ Also, it represents an independent risk factor that significantly increases the morbidity and mortality
(Frasure-Smith et al., 1995).

➢ The reduction of heart rate variability, reflecting a hyperadrenergic state, predisposing to arrhythmias,
 and correlated with depression in coronary patients, partly explains this impact (Vigo et al., 2004).

➢ Depletion in cerebral neurotransmitters, essentially serotonin, is involved in this autonomic

dysregulation (Anderson et al.,1992).

DIAGNOSTIC APPROACH (Casillas et al., 2006)

1. Distinguish between fatigue and dyspnea.

2. Eliminate another cause for fatigue.
▪ The first step consists of distinguishing physiological physical fatigue occurring after intense or even
unusual exercise. In these circumstances, evaluation of exercise capacity is particularly useful to
eliminate real exercise intolerance.
▪ An associated disability (neurological, orthopedic, etc.) able to explain or at least worsen exercise
intolerance by the excess energy expenditure that it induces, must be excluded; early cognitive
disorders may present in the form of mental fatigue and are frequent in chronic heart failure. Impaired
intellectual performance can be secondary to cerebrovascular disease or decreased cerebral blood
flow, which can be induced by exercise.
▪ Impaired cognitive performance can be detected by psychometric tests eliminating an etiology other
than cardiovascular disease (infection, cancer, inflammatory syndrome, neuromuscular disease, etc.)
by complementary investigated guided by clinical findings.
3. Evaluated Fatigue related CV disease.
▪ When a cardiovascular origin is considered to be probable, fatigue must be quantified and its physical
or mental dimension must be specified, as physical and mental factors are usually interrelated.

A. Circumstances of onset: T h i s can help to guide the diagnosis:

➢ In favour of an organic cause: Fatigue increasing during the day, stable, without major mood
disorders, related to exercise and improved by rest.
➢ In favour of a psychological origin: starts in the morning, associated with apathy, sleep disorders and
sexual disorders, loss of appetite, variable over time, not improved by rest. Finally, the search for
stressful of life events (bereavement, work stress, retirement, etc.) also appears to be necessary, due
to the intricate relations between these events, depression and cardiovascular disease (Rafanelli et al.,
2005).
B. Generic scores:

➢ The use of a fatigue score would appear to be the simplest and least expensive methodology.
However, it is insufficient as it is unable to discriminate between the mental and physical components,
 and it is not correlated with objective physical parameters such as the exercise test in patients with
coronary artery disease or peak VO2 in chronic heart failure (Wilson, 1996).

➢ Most generic scores validated in French are designed to evaluate fatigue correlated with cancer. They
investigate the behavioral, physical, cognitive and affective dimensions (Fillion et al., 2003).
➢ Rhoten’s score is one of the simplest to use, as it is composed of a visual analogue scale from 0 (no
fatigue) to 10 (total exhaustion) and is correlated with the Multidimensional Fatigue Inventory
comprising 20 items evaluating physical and mental aspects (Fillion et al., 2003; Schneider 1998).
➢ It is similar to the visual analogue scale developed by Krupp for multiple sclerosis (Krupp et al.,1988).
➢ Dutch Fatigue Scale has been validated in patients with heart failure (Tiesinga et al., 1998).

ASSESSMENT OF PHYSICAL FATIGUE (Casillas et al., 2006)

In practice, this assessment is based on clinical interview and demonstration of objective signs of fatigue.

SPECIFIC QUESTIONNAIRES

As the patient’s description of his or her feelings of fatigue is insufficient and as generic scores are
inappropriate, two reproducible methods adapted to large numbers of patients are proposed:

➢ Borg’s score:

▪ This score is used to measure the perception of the level of activity during exercise and therefore the
physiological intensity of this exercise.
▪ It comprises 15 levels on a scale ranging from 6 (very mild activity) to 20 (very strenuous activity),
and the extreme physical fatigue preceding discontinuation of the exercise corresponds to the highest
levels.
▪ Borg’s score is validated to define the intensity of work during retraining, especially when heart rate
cannot be used (arrhythmia, drug-induced chronotropic effect), as the desired level of exercise is
usually situated between 12 and 16.
▪ Borg’s score is also useful to guide physical activity in patients with stabilized heart disease (Ilarraza
et al., 2004).
▪ However, this score presents a marked interindividual variability for equivalent levels of exercise. It
also appears difficult for patients to distinguish between feelings of fatigue and dyspnoea (Wilson et
al., 1993)
 Figure 7.2: Rate of Perceived Exertion (RPE) Scale

➢ The New York Heart Association (NYHA) classification:

▪ It represents the international reference for functional evaluation of chronic heart failure based on the
circumstances of onset of dyspnea (Fisher, 1972).

▪ The symptoms with strenuous activity;

▪ The symptoms with moderate activity (rapid walking, flights of stairs, etc.);

▪ The symptoms with mild activity (dressing, personal hygiene, etc.);

▪ The symptoms with the slightest activity or at rest.

 Figure 7.3: New York Heart Association (NYHA) Scale

FUNCTIONAL QUANTIFICATION (Casillas et al., 2006)

▪ Observation of the usual symptoms of physical fatigue (muscle weakness, tremors, cramps, disorders
of the coordination, etc.) is not sufficient to assess the severity of fatigue and to guide treatment
decisions.

▪ Other objective parameters of exercise capacity must be used: Measurement of muscle strength and
endurance, maximum muscle strength is reduced during cardiovascular disease especially in the
presence of left ventricular dysfunction.

▪ Correlations between electromyographic parameters and decreased endurance and muscle strength are
also observed in patients with heart failure (Schulze et al., 2005). Similar alterations demonstrated in
peripheral artery disease have been shown to be reversible in response to physical reconditioning.

➢ CPET:
▪ The most conventional method to assess decreased physical performance in the context of
cardiovascular disease, as fatigue constitutes the usual limiting factor during this test (Wilson, 1996).
▪ Data obtained from the patient’s clinical history and fatigue scores also frequently underestimate the
data provided by exercise tests for the evaluation of fatigue symptoms (Wilson et al., 1999).

▪ Measurement of gas exchanges during the exercise test allows investigation of the entire chain of
oxygen binding, transport and utilization, essential for oxidative phosphorylation. It is a validated
criterion of cardiopulmonary and metabolic performance.

▪ When a plateau is reached during a progressive exercise test, it usually means that the patient’s
maximum capacities have been reached (Taylor et al., 1955). In subjects with cardiovascular disease,
this plateau is generally not reached and, in these subjects, the peak VO2 is determined, as it reflects
maximum oxidative capacities and therefore the highest degree of physical fatigue.

▪ Ventilatory threshold: It provides complementary information to peak VO2. (It can be defined as the
point beyond which there is a non-linear increase of the ventilatory equivalent for oxygen (VE/VO2),
with no concomitant elevation of the ventilatory equivalent for carbon dioxide (VE/VCO2).

▪ In contrast with peak VO2, it is a submaximal parameter independent of patient motivation (Noonan
& Dean 2000). It corresponds to a well-tolerated level of exercise (preceding onset of physical fatigue)
and effective in terms of physical reconditioning especially in the case of heart failure (Meyer et al.,
2005).

Figure 7.4: Cardiopulmonary Exercise Testing (CPET)

➢ Walk tests:
▪ It is a complement or even an alternative to the exercise test for the analysis of exercise capacity. A
standardized walk test can therefore be proposed in order to confirm the reality of physical fatigue.

▪ The 6-minute walk test is the most extensively validated test and the most widely used in the context
of cardiovascular disease, especially in patients with heart failure (Guyatt et al., 1985)
▪ It constitutes a prognostic factor for morbidity and mortality and is correlated with aerobic capacities
and NYHA classification (Bittner et al., 1993).
▪ It is reproducible and particularly adapted to elderly patients who are unable to perform a maximum
exercise test (O'Keeffe et al.,1998).
▪ Physical activity is reduced in the case of chronic fatigue and quantification of physical activity is
part of the evaluation of the global functional repercussions.

▪ Usual methods are based on the use of specific scores or accelerometric methods (Casillas et al., 2005).

Figure 7.5: Six-minute Walk tests (6-MWT)

➢ Surface EMG for assessment of fatigue:

▪ The surface electromyography (s EMG) is the main method to record and study the muscles functions,
by recording the electrical signal of the muscles during voluntary, involuntary, or stimulated
contraction.
▪ After performing contractions for a long period of time, the nerve's signal is normally reduced in
frequency and the force generated by the contraction diminishes which in turn results in muscle
fatigue.
▪ Fatigue is not a physical variable. Therefore, its assessment requires the definition of indices based on
physical variables that can be measured. Those indices can be extracted from the acquired surface
EMG signals.

Procedure
• The single most relevant determination of fatigue is done through the measurement of force or power
measurement, which is produced during the course of a voluntary effort of maximum intensity,
maximal voluntary contractions (MVCs) test.
• In general, when the subject performs the task of interest or the fatigue task continuously, at the pre-,
post- time point, brief MVC tests will be conducted to register the drop of maximal force output from
particular muscle.
• This will quantify the muscle fatigue pattern in relation to the task performed. The force output decline
rate measured in these MVCs tests will indicate the muscle fatigue pattern.
• Although the drop of maximal voluntary contractions output directly indicates the presence of muscle
fatigue. However, the surface electrodes have the ability to record up the superficial muscle layer’s
electrical transmissions, after which it magnified and ultimately the determination of the signal power
spectrum is done when the response produced in sEMG.

Processing

• The EMG signals that are collected from the muscles by the electrodes will have noise. Thus, the EMG
signal must be filtered in a proper manner to remove any noise.
• The frequency of noise contaminating the EMG signal may be low or high.
• Low-frequency noises usually come from an amplifier's direct current offsets. Normally this noise can
be avoided with the use of a high pass filter.
• The interference of high frequency comes from computers, radio broadcasts and can be removed by
using a low pass filter.
• The high pass filter is used to eliminate the low ranged frequencies that result at the electrical signal
 collection. The frequencies that are passed with a filter transmission as a band are known as a
passband. The frequencies that cannot be passed with a filter are known as stop band.
• In general, surface EMG signals can be processed in three domains:
Time
Frequency
Time-frequency
✓ Time domain
• The fatigue is related to the increment of the EMG amplitude.
• The muscle fatigue detection in the time domain can be estimated by extracting features like root
mean square (RMS) and mean absolute value (MAV).
✓ Frequency domain
• The most common procedure is to monitor the relative changes in the mean (MNF) and median
power frequencies (MDF) and to relate these measures to the initial value or non-fatigue state
mean and median power frequencies.
• Kaljumae & Hänninen (2003) used the phenomena of the shift of sEMG, MNF and MDF towards
lower frequencies under the isometric condition to document the change of fatigability of vastus
lateralis (VL) and vastus medialis (VM) after 10 weeks of bicycle ergometer training program in
male subjects
✓ Time frequency domain when amplitude increase and spectrum decrease that’s mean fatigue.

Extraction
• Muscle fatigue is recognized by the EMG signal as long as there is a mutual decline in parameter
examined in the frequency domain and time-frequency domain, and an increment in the parameter
evaluated in the time domain.

Figure 7.6: The increment in the pattern of RMS and decline in the pattern of MDF features for the
EMG signal during muscle fatigue (Yousif et al., 2019)
EVALUATION OF MENTAL FATIGUE
Table 1
Summary of Self-Reporting Questionnaires used to detect Mental Fatigue.

NAME OF DESCRIPTION STRENGTHS WEAKNESS

QUESTIONNAIRE

Occupation fatigue 15 items, classify and distinguish Robust and Only detects
exhaustion recovery three subscales of mental fatigue embodies a gender three domains
(OFER) scale (i.e., chronic work-related fatigue bias and work-status of mental
(Winwood et al., traits, acute and end-of-shift states, free psychometric fatigue.
2005) and effective fatigue recovery characteristic.
between shifts).

Visual analog scale 18 items, l00-mm lines in the case Uses semantic Frequent
to evaluate fatigue of visual analogue lines between differential scale reluctance of
severity (VAS-F) two extremes “not at all tired” to which gives a individuals to
(Lee, Hicks & Nino- “extremely tired”. unique bipolar use the
Murcia, 1991) ordinal scale format highest and
that captures a lowest
person’s feelings extremes.
about a given item.

Fatigue assessment 10-items, evaluates symptoms of It was found to be Four items

scale (FAS) chronic fatigue. Half the items the most promising appeared to
(Michielsen, De measure physical fatigue and the fatigue measure be gender
Vries & Van Heck, other half measures mental fatigue. when compared to bias women
2003). It is a unidimensional scale five other fatigue tended to
measuring fatigue independently questionnaires. score
from depression. significantly
higher than
men.
NAME OF DESCRIPTION STRENGTHS WEAKNESS
QUESTIONNAIRE

Multidimensional 20 items, dimensions covered: Good internal Has not been

fatigue inventory General Fatigue, Physical Fatigue, consistency validated
(MFI) (Smets et al., Mental Fatigue, Reduced (Cronbach’s Alpha with mentally
1995) Motivation and Reduced Activity. = 0.84). fatigued
individuals.

Fatigue severity 14 items, evaluates multiple aspects Validated with both Does not
inventory (FSI) of fatigue such as perceived female and male correlate with
severity, frequency, and cancer patients with mental fatigue
interference with daily functioning an age range of 18– in the MFI
(Donovan & Jacobsen, 2011). 24. It has an internal (Lou et al.,
consistency of 0.94 2001).
(Hann, Denniston &
Baker, 2000).

CLINICAL APPROACH TO FATIGUE IN DEPRESSION (Casillas et al., 2006)

▪ Several clinical features can sometimes be helpful to identify mental fatigue in major depression,
starting with the typical chronology with very severe symptoms at the beginning of the day
(where even the slightest activity becomes an effort), classically followed by improvement in the
evening.

▪ Mental fatigue corresponds to the concept of psychomotor retardation in depression, ranging

from moderate loss of vitality (minimal lethargy) to major asthenia, when the patient is constantly
bedridden.

▪ The depressed subject may complain of a simple lack of energy, then suffer from a massive loss
of motivation (abulia), and finally present major psychomotor inhibition.
 ▪ The mental component of fatigue in the course of major depression therefore takes on very
specific clinical forms that should be recognized and quantified by means of validated measuring
instruments.

Assess the repercussions on the patient’s independence and quality of life

▪ This is the most global dimension of the evaluation, designed to assess the efficacy of therapeutic
intervention on fatigue related to cardiovascular disease.

▪ Generic disability scales can be used to assess independence when the functional repercussions
of this fatigue are severe, essentially advanced heart failure in the elderly, who frequently present
multiple disabilities.

▪ The most widely used quality of life scales are generic scales allowing comparison with other
types of diseases. This is essentially

▪ MOS SF-36 (Medical Outcome Study 36-item Short Form),

▪ Specific quality of life scales is available, essentially designed for chronic heart failure: the
MLwHF (Minnesota living with Heart Failure), validated in French, is the scale most frequently
applied (Leidy et al., 1999).

MINNESOTA LIVING WITH HEART FAILURE QUESTIONNAIRE

1. The HRQoL of patients with HF are an important outcome as it reflects the impact of HF on their
daily lives. HF patients experience high levels of physical, functional and emotional distress
(Gonzalez-Saenz de Tejada et al., 2019).
2. It is one of the most widely known and used is the Minnesota Living with Heart Failure Questionnaire
(MLHFQ).
3. It is a self-administered disease-specific questionnaire for patients with HF, comprising 21 items.
4. It provides a total score as well as scores for two domains, physical and emotional. The questionnaire
has been translated into and validated in Spanish.
Table 2
Minnesota Living With Heart Failure Questionnaire

QUESTIONNAIRE MINNESOTA LIVING WITH HEART FAILURE

QUESTIONNAIRE

Description Patient self-assessment of how heart failure affects his or her daily life

Administration Self

Time to complete 5-10 minutes

Number of items 21

Domains and Content reflects most frequent and important ways heart failure affects
Categories patient’s lives. Overall score with 2 (physical and emotional)
dimensions designed to describe two important aspects to quality of life.

Scaling of items All items same 0 to 5 Likert scale

Scoring Sum of item responses for total and dimension scores

Reliability Test-retest/reproducibility: r = 0.87

Internal consistency: Cronbach’s alpha for all items = 0.92

MCID 5 points on total score. 8

Estimated standard error of the measure is 6-7 points.

Responsiveness Randomized controlled trials have detected significant effects of ACE

inhibitors, positive inotropic agents, cardiac resynchronization, exercise
training and disease management programs.
MANAGEMENT OF FATIGUE IN THE COURSE OF CARDIOVASCULAR
DISEASE PHYSICAL FATIGUE

PHYSICAL RECONDITIONING FOR PHYSICAL FATIGUE

▪ Cardiac Function: Increased myocardial perfusion due to improvement of coronary endothelial

function (Hambrecht et al., 2000). This allows an improvement of cardiac output during exercise in
patients with stable coronary artery disease and an increased ejection fraction in patients with heart
failure, although this does not appear to be constant (Hambrecht et al., 1998).
▪ A mean increase of 20% of maximum aerobic capacities due to a predominant impact on muscle
oxidative metabolism: increase of oxidative enzyme performances and capillary density in striated
muscle fibres in patients with coronary artery disease, and occlusive peripheral artery disease (Ades
et al., 1996)
▪ Reduction of peripheral resistance by improvement of endothelial dysfunction resulting in more
effective muscle perfusion (Gokce et al., 2002). Reduction of peripheral resistance, together with
reactivation of NO-dependent vasodilatation, participates in improvement of aerobic performances
in patients with coronary artery disease or heart failure (Brendle et al., 2001). Reduction of the
hyperadrenergic state with restoration of autonomic regulation associated with increased heart
rate variability and an antiarrhythmic effect in patients with coronary artery disease without
ventricular dysfunction and in patients with heart failure (Lucini et al., 2002).
▪ Metabolic Impact: improvement of dyslipidaemia, control of obesity, reduction of insulin resistance
(Zinman et al., 2003)
▪ Improvement of ventilatory capacities in patients with heart failure with improvement of
alveolocapillary diffusion, contributing to resolution of dyspnoea (Guazzi et al., 2004).
▪ These effects of physical reconditioning result in lowering of the fatigue threshold with improvement
of exercise capacity in patients with heart failure or stable coronary artery disease (Belardinelli et
al., 1999). The effects of physical reconditioning in patients with stable coronary artery disease
are superior to those observed after angioplasty (Hambrecht et al., 2004).
▪ In patients with intermittent claudication, the claudication distance is improved by an average of
150% after physical reconditioning (Leng et al., 2000).
▪ Ergonomic measures (Casillas et al., 2006)
▪ Activity management education (distribution of tasks and rest periods to avoid reaching an excessive
level of fatigue), domotic devices, technical aids, and domestic help will be necessary when the
severity of the fatigue affects the patient’s independence.
▪ These compensatory measures are essentially used in severe heart failure, and are primarily
designed to maintain the patient at home.

PHYSICAL RECONDITIONING FOR MENTAL FATIGUE

✓ Various modalities of management of mental fatigue have been proposed: psychotherapy,

behavioral stress management techniques, relaxation, pharmacological treatments.

✓ Psychological management can improve vital exhaustion and reduce the associated cardiovascular
morbidity (Appels et al., 1997).

✓ In the context of depression, serotonin reuptake inhibitors can improve heart rate variability after
acute coronary syndrome, reflecting correction of the autonomic equilibrium in favour of the
parasympathetic system. They are also present a better cardiovascular safety than tricyclic
antidepressants (Jiang & Davidson, 2005).

✓ Multifactorial treatment of depression is now an integral part of the global management of patients
during retraining (Barth et al., 2005).

✓ Relaxation techniques are effective, particularly on mood disorders and somatic symptoms of
cardiovascular disease (Van Dixhoorn & White, 2005).

GLOBAL MANAGEMENT OF FATIGUE

✓ It corresponds to optimal control of risk factors and is designed to slow the progression of
atherosclerosis while limiting the symptoms of cardiovascular disease.

✓ Cardiac rehabilitation, due to its multidisciplinary intervention, integrates both personalized

secondary prevention measures and physical reconditioning. It helps to limit progression of coronary
artery disease (Niebauer et al., 1997).

✓ The clinical efficacy of physical reconditioning has been confirmed demonstrating a 20% to 25%
reduction of cardiovascular mortality after retraining in patients with coronary artery disease or heart
failure (Piepoli et al., 2004; O'Connor et al., 1989).

✓ The improvement of quality of life in response to cardiac rehabilitation has been demonstrated in
these patients and after rehabilitation for peripheral artery disease with or without intermittent
claudication (McDermott et al., 2004; Suzukiet et al., 2005).
RECENT EVIDENCES:

Table 3
Summary of Self-Reporting Questionnaires used to detect Mental Fatigue.

JOURNAL/
TITLE OBJECTIVE METHODOLOGY RESULT
AUTHOR/YEAR
Annals of Rehabilitation To investigate A block-randomized The recruitment and
Rehabilitative Intervention feasibility of controlled trial delivery of the
Medicine for Individuals recruitment, involving 23 adults, interventions were
With Heart tablet use in blinded to their feasible. Activity
(Kim et al., 2019) Failure and intervention group assignment, Card Sort may not
Fatigue to delivery, and use in a rural southern be appropriate for
Reduce of self-report area in the United this study
Fatigue outcome States. Individuals population due to
Impact: A measures and to with heart failure recall bias. The
Feasibility analyze the effect and fatigue received interventions
Study of Energy the interventions for warrant future
Conservation 6 weeks through research to reduce
plus Problem- videoconferencing fatigue and decrease
Solving Therapy or telephone. participation in
versus Health Participants were sedentary activities.
Education taught to solve their
interventions for fatigue-related
individuals with problems using
heart failure- energy conservation
associated strategies and the
fatigue. process of Problem-
Solving Therapy or
educated about
health-related
topics.
Annals of Extended To investigate 914 patients with Extending cardiac
Rehabilitative cardiac the effects of two acute coronary rehabilitation with a
Medicine rehabilitation behavioral syndrome were face-to-face
improves lifestyle randomized to (1) 3 behavioral group
(Hoeve et al., aerobic interventions months of standard intervention was
2018) capacity and integrated into cardiac successful in
fatigue: A cardiac rehabilitation (CR- sustaining aerobic
randomized rehabilitation on only); (2) CR-only capacity gains for
controlled trial aerobic capacity, with additional face- up to 12 months and
fatigue, and to-face physical for reaching long-
participation in activity group term goals for
society and to counseling sessions improvements in
explore plus 9 months of fatigue. The
mediating effects after-care with benefits in aerobic
of physical general lifestyle capacity seem to be
activity group counseling mediated by
(CR + F); or (3) improvements in
CR-only plus 9 daily physical
months of after-care activity. A
with individual, telephonic
general lifestyle behavioral
telephone intervention
counseling sessions provided no
(CR + T). Aerobic additional benefits.
capacity (6-minute
walk test), fatigue
(FSS), and
participation in
society (USER-P)
were measured at
randomization, 3
months, 12 months,
and 18 months.
Frontiers in Fatigue is The cross- After controlling for In CAD patients
Physiology Associated sectional study baseline levels of after ACS, fatigue
with investigated 142 cardiovascular was linked with
(Gecaite- diminished CAD patients measures, age, diminished
Stonciene et al., Cardiovascular within 2-3 weeks gender, education, cardiovascular
2021) Response to after recent heart failure function during
Anticipatory myocardial severity, arterial anticipation of a
Stress in infarction or hypertension, mental stress
Patients with unstable angina smoking history, challenge, even
coronary pectoris. Fatigue use of nitrates, after inclusion of
artery disease symptoms were anxiety and possible
measured using depressive confounders.
Multidimensional symptoms, Type D Further similar
Fatigue Personality, studies exploring
Inventory 20- perceived task other
items. difficulty, and psychophysiological
Multivariable perceived task stress responses are
linear regression efforts, warranted.
analyses were cardiovascular
completed to reactivity to
evaluate anticipatory stress
associations was inversely
between fatigue associated with both
and global fatigue and
cardiovascular mental fatigue as
response to well as total fatigue
TSST, while
controlling for
confounders.
 ACTIVITY-8
DEMONSTRATION AND PRACTICE OF AUSCULTATION
OF HEART SOUNDS
INTRODUCTION
Auscultation is the art of listening to sound produced by the body, usually using a stethoscope.
Auscultation is performed for the purposes of examining the circulatory system and respiratory system
(heart sounds and breath sounds), as well as the gastrointestinal system (bowel sounds). It is an integral
part of physical examination of a patient and is routinely used to provide strong evidence in including or
excluding different pathological conditions that are manifested clinically in the patient.
Skill in auscultation is dependent on the following factors:

1. A functional stethoscope

2. Proper technique

3. Knowledge of the different categories of heart sounds and murmurs

STETHOSCOPE

The stethoscope comprises a bell and a diaphragm. The bell is most effective at transmitting lower
frequency sounds, while the diaphragm is most effective at transmitting higher frequency sound. In other
words, the bell is designed to hear low pitched sounds and the diaphragm is designed to hear high pitched
sounds. They are connected via rubber tubing to the ear pieces. These should be worn facing forward as
the ear canals run anteriorly.

AUSCULTATION PERFORMANCE
Ensure the room is warm and quiet, that privacy can be maintained during examination and that you will
not be interrupted.
1) Prior to performing the procedure, introduce self and verify the client's identity using agency protocol.
Explain to the client what you are going to do, why it is necessary, and how he or she can cooperate.
Discuss how the results will be used in planning further care or treatments.
2) Perform hand hygiene and observe appropriate infection control procedures.
3) Provide for client privacy. In women, drape the anterior chest when it is not being examined.
4) Inquire if the client has any history of the following: family history of illness, including cancer,
allergies, tuberculosis; lifestyle habits such as smoking & occupational hazards (e.g. inhaling fumes);
medications being taken; current problems (e.g. swellings, coughs, wheezing, pain).
CARDIAC EXAMINATION

It should be noted that auscultation comes after palpation, the patient is normally lying comfortably at 45
degrees angle with their chest region fully exposed. There are four main regions of interest for
auscultation, and a brief knowledge in human anatomy is crucial to pin point them.

The 4 pericardial areas are examined with diaphragm including:

1) AORTIC REGION (between the 2nd and 3rd Intercostal spaces at the right sternal border)
(RUSB- right upper sternal border).

2) PULMONIC REGION (between the 2nd and 3rd Intercostal spaces at the left sternal border)
(LUSB-left upper sternal border).

3) TRICUSPID REGION (between the 3rd, 4th, 5th, and 6th intercostal spaces at the left sternal
border) (LLSB – left lower sternal border).

4) MITRAL REGION (near the apex of the heard between the 5th and 6th intercostal spaces in
the mid- clavicular line) (apex of the heart).

The four pericardial areas relate to the heart sounds and can detect various abnormalities in the heart such
as the valve stenosis or incompetence which are diagnostic for many diseases in the cardiovascular system.
However, there are specific maneuvers done for further investigation, and some of these would include:

Figure 8.1: Heart Auscultation regions

Figure 8.2 a) Aortic Area Figure 8.2 b) Mitral/Apex Area

Figure 8.2 c) Tricuspid Area Figure 8.2 d) Pulmonic Area

Figure 8.2: Heart Auscultation regions

STEP ACTION

1. Observe for general signs of heart or respiratory disease.

2. Ask the patient to lower the gown. Indicating patient in control of exposure.

INSPECT the chest for asymmetry, deformity, injury, scars, skin color, lifts/heaves or
3.
pulsations, and increased or decreased antero-posterior chest diameter or use of accessory
muscles.
Observe rate, rhythm, depth and effort of breathing, noting if expiratory phase is prolonged
4.
or any bulges or retractions present. Record findings.

PALPATE the ribs and sternum noting any

5.
tenderness, muscle spasm, surgical emphysema. Helps to
distinguish traumatic chest pain from lung or cardiac
pain.

Confirm that the trachea is near the midline. Unilateral

6.
change in pressure in the chest may result in displacement
of the trachea.
 Assess chest expansion and symmetry by placing hands on
7.
patient ‘s back at the level of and parallel to 10th ribs, with
thumbs sliding together at the midline to raise loose skin
folds and ask client to breathe deeply.
Note any lag / asymmetry/ pain /amount of movement and
elasticity of chest wall.

Check for tactile fremitus by asking patient to say 99

8.
with either the ballor ulnar surface of one hand against the
posterior chest in the pattern shown

Asking the patient to cross arms across front of chest,

9.
PERCUSS the intercostal spaces on posterior chest in the
pattern shown. Note the symmetry, location and quality of
percussion note and locate diaphragmatic dullness on
both sides.
 Estimate diaphragmatic excursion by comparing the level
10.
of dullness on full expiration and full inspiration normally
a distance of about 5-6cm.

AUSCULTATE the posterior chest, with the stethoscope

11.
diaphragm, asking the patient to breathe deeply through
open mouth to identify breath sounds Follow the same
pattern as for percussion, listening through at least one full
breath a teach location. Note quality of sounds and
location and timing in cycle of breathing or any
adventitious (additional) sounds.

Assess Jugular Venous Pressure Position patient

12.
at 45-degree angle with head supported by pillows to allow
for a natural zero-point from which to measure the vertical
height. To distinguish from arterial pulsation, observe that
JVP: Is visible but not palpable and as a more pronounced
inward movement it is usually seen to flutter twice with
every cardiac cycle (in normal sinus rhythm) when applying
light pressure to the base of the neck it will disappear and
return from the top.
 Moving to anterior chest, INSPECT, PALPATE as
13.
before, assessing expansion and fremitus as shown.

PERCUSS the anterior and lateral chest in pattern as shown,

14.
noting any abnormal notes. Expect dullness over heart at 3rd
to 5thinterspace on left.

AUSCULTATE using same pattern, noting intensity of sounds

15.
and variation from normal.
If indicated, listen for transmitted voice sounds as before.
16.
 Position patient supine with head slightly elevated and
17.
examining from the right INSPECT and PALPATE for
apical impulse. Normally located in 4th or 5th intercostals
space, medial to midclavicular line. If location is difficult ask
patient to exhale and hold breath. Note location, diameter,
amplitude and duration. Positioning patient on the left side
increases the intensity of the apical beat.
Once you have found the apical
impulse, make finer assessments
with your fingertips, and then
with one finger.
AUSCULTATE with the diaphragm of stethoscope at right
18.
2nd interspace at the sternal border (aortic area), left 2nd
interspace (pulmonic area), then left 3rd, 4th and 5th
interspaces (tricuspid area) and at the apex 5th interspace at
midclavicular line (mitral area). Intensity, rhythm and
splitting of sound on each event of the cardiac cycle should
be noted.

Positioning patient over onto left side, AUSCULTATE

19.
with the bell of stethoscope at apex (mitral area). Low
pitched sounds of S3 and S4 and murmur of mitral
stenosis are heard more easily.
 Asking patient to sit up, lean forward and hold breath in
20.
exhalation, listen with diaphragm of stethoscope along left
sterna border and at apex, pausing periodically for patient to
breathe. Accentuates aortic murmurs. Pericardial friction rub
may be heard.

Ask the patient to hold their breath, AUSCULTATE for

21.
bruits using the bell of the stethoscope over the carotid
arteries in turn. Indicates arterial narrowing.

HEART SOUNDS
S1 /first heart sound / lub: Softer than 2nd sound at right and left 2nd interspace and often (but not
always) louder at apex.

Variations: Accentuated in tachycardia, short PR intervals, exercise, anemia, mitral regurgitation,

mitral stenosis. Diminished in first degree heart block, congestive heart failure or coronary heart
disease. Varying in complete heart block, atrial fibrillation.

S2/second heart sound / dub: Listen at 2nd and 3rd interspace with patient breathing more deeply.
Physiological split usually disappears on expiration. Pathological split occurs during expiration.

Variations: Wide split or persistently single may indicate ASD, Heart block or disease of valve.
Persistent splitting results from delayed closure of pulmonic valve or early closure of aortic valve.
 INTENSITY (EXPRESSED AS A FRACTION ON 6-POINT SCALE)

Table 1
Gradation of Murmurs
GRADE DESCRIPTION

1. Very faint and may not be heard in all positions

2. Quiet but heard immediately stethoscope placed on chest

3. Moderately loud

4. Loud

5. Very loud. Heard even when stethoscope partly off chest

6. May be heard with stethoscope entirely off chest

Auscultation Finish

• PATIENT
Check with the patient that they are comfortable and understand the outcome of the examination
and any necessary follow-up and/or self-care advice.
• DOCUMENTATION
Murmurs should be described in terms of timing, shape, location of maximal intensity, radiation
or transmission from this location, intensity, pitch and quality.
• SELF Wash your hands
 ACTIVITY 9:

DEMONSTRATION AND PRACTICE OF INTERPRETATION OF

RADIOLOGICAL INVESTIGATIONS

(ECHO, ANGIOGRAPHY)
ECHOCARDIOGRAPHY
Echocardiography (echo or echocardiogram) is a type of ultrasound test that uses high-pitched sound
waves to produce an image of the heart. The sound waves are sent through a device called a transducer
and are reflected off the various structures of the heart. These echoes are converted into pictures of the
heart that can be seen on a video monitor. Ultrasound gel is applied to the transducer to allow
transmission of the sound waves from the transducer to the skin. The transducer transforms the echo
(mechanical energy) into an electrical signal which is processed and displayed as an image on the screen.
The conversion of sound to electrical energy is called the piezo-electric effect.

CONVENTIONAL ECHO
The modalities of echo used clinically are:
1. IMAGE ECHO
▪ Two-dimensional echo (2-D echo)
▪ Motion-mode echo (M-mode echo).

2. DOPPLER ECHO
▪ Continuous wave (CW) Doppler
▪ Pulsed wave (PW) Doppler.

Different echo modalities are not mutually exclusive but complement each other and are often used
together.

DELIVERY ROUTES

1. Transthoracic window:
Left parasternal
Apical
Subcostal
Right parasternal
Suprasternal
Posterior thoracic
2. Transesophageal window

3. Intravascular: Intracardiac Intracoronary

4. Epicardial

TRANSTHORACIC ECHO
A standard echocardiogram is also known as a transthoracic echocardiogram (TTE), or cardiac ultrasound.
The subject is asked to lie in the semi recumbent position on his or her left side with the head elevated.
The left arm is tucked under the head and the right arm lies along the right side of the body. Standard
positions on the chest wall are used for placement of the transducer called Echo windows.

Figure 9.1 TTE (Trans-thoracic Echocardiography)

Figure 9.2 2-D Echocardiography

Figure 9.3 TTE (Trans-thoracic Echocardiography)
STANDARD ECHO WINDOWS
Standard locations on the anterior chest wall are used to place the transducer, which are called echo
windows. These are:

✓ Left parasternal
✓ apical
✓ subcostal
✓ right parasternal
✓ suprasternal

PARASTERNAL LONG-AXIS VIEW (PLAX VIEW)

Transducer position: left sternal edge; 2nd–4thspace
Marker dot direction: points towards right shoulder.
Structures seen:
✓ Proximal aorta

✓ Aortic valve

✓ Left atrium

✓ Mitral valve

✓ Left ventricle

✓ IV septum

✓ Posterior wall

✓ Right ventricle

✓ Pericardium.

✓ Most echo studies begin with this view. It sets the stage for subsequent echo views.
 Figure 9.4: PLAX view

PARASTERNAL SHORT-AXIS VIEWS (PSAX VIEWS)

Transducer position: left sternal edge; 2nd–4th space
Marker dot direction: points towards left shoulder (90° clockwise from PLAX).
By tilting the transducer on an axis between the left hip and right shoulder, short-axis cuts
are obtained at different levels, from the aorta to the LV apex. This angulation of the
transducer from the base to apex of the heart for short-axis views is known as bread-loafing.
Short Axis Levels:
✓ Pulmonary artery
✓ aortic valve level
✓ mitral valve level
✓ papillary muscle
✓ Left ventricle.

Figure 9.5: PSAX view: mitral valve (MV) level

APICAL 4-CHAMBER VIEW (A4-CH VIEW)
Transducer position: apex of the heart
Marker dot direction: points towards left shoulder.
Structures seen:
✓ right and left ventricle
✓ right and left atrium
✓ mitral, tricuspid valves
✓ IA and IVseptum
✓ left ventricular apex
✓ lateral wall left ventricle
✓ free wall right ventricle

Figure 9.6: Apical 5-Chamber View (A5CH view)

The A5CH view is obtained after the A4CH view by slight downward tilting of
the transducer.
The 5th chamber added is the left ventricular outflow tract (LVOT).

• Transducer position: as in A4CHview.

• Marker dot direction: as in A4CHview.
Structures seen: As in A4CH view. Additionally:
✓ LV outflow tract
✓ Aortic valve
✓ proximal aorta
 SUBCOSTAL VIEW

o For subcostal view, the position of the subject is different from that used to obtain parasternal and
apical views.

o The subject lies supine with the head held slightly low, feet planted on the couch and
the knees slightly flexed.
o Better images are obtained with the abdomen relaxed and during the phase of inspiration.

o Transducer position: under the xiphisternum

o Marker dot position: points towards left shoulder.

o Structures seen: As in A4CHview.

SUPRASTERNAL VIEW
o For suprasternal view, the subject lies supine with the neck hyperextended by placing a pillow
under the shoulders. The head is rotated slightly towards the left.
o The position of arms or legs and the phase of respiration have no bearing on this echo window.

o Transducer position: suprasternal notch.

o Marker dot direction: points towards left jaw.

o Structures seen:

▪ Ascending aorta
▪ Pulmonary artery.

RIGHT PARASTERNAL VIEW

o For right parasternal view, the subject lies in the semi-recumbent position on the right side. The
right arm is tucked under the head and the left arm lies along the left side of the body.
o In other words, this position is the mirror-image of that used for the left parasternal view.

o Transducer position: right sternal edge; 2nd–4thspace

o Marker dot direction: points towards left shoulder.

o Structures seen:

o Aortic valve
o Aortic root.
CARDIAC STRUCTURE AND FUNCTION:
✓ LV and RV function
✓ LV and RV wall thickness
✓ Valvular function(stenosis/regurgitation)
✓ Cardiac devices (artificial valves, closure devices)
✓ Cardiac masses (clots, tumors)

Figure 9.7: Right Parasternal View

Figure 9.8: Echocardiography Report
CORONARY ANGIOGRAPHY

DEFINITION:
It is an invasive examination involving injection of contrast media after selective cannulation of the
coronary arteries with image acquisition in multiple projections. Coronary angiography remains the
gold standard for detecting clinically significant atherosclerotic coronary artery disease.

INDICATIONS:

✓ Known or suspected CAD

✓ Patients With Nonspecific Chest Pain

✓ Patients With Unstable Acute Coronary Syndromes

✓ Patients With STEMI

✓ Patients With Post-Revascularization Ischemia

✓ Perioperative Evaluation Before (or After) Non cardiac Surgery

✓ Patients With Valvular Heart Disease

✓ Patients With Congenital Heart Disease

✓ Patients With CHF

RELATIVE CONTRAINDICATIONS:
There are no absolute contraindications to cardiac catheterization
✓ Coagulopathy
✓ Decompensated congestive heart failure
✓ Uncontrolled Hypertension
✓ CVA
✓ Refractory Arrythmia
✓ GI Haemorrhage
✓ Pregnancy
✓ Inability for patient cooperation
✓ Active infection
✓ Renal Failure
✓ Contrast medium allergy
CORONARY ANATOMY

➢ The left and right coronary cusp give rise to their respective coronary arteries
➢ The major epicardial vessels are the left main coronary artery that divides into the Left
anterior Descending artery and Left Circumflex Artery, and the Right Coronary artery.

ANGIOGRAPHIC VIEWS

✓ Anatomic landmarks formed by the spine, catheter and diaphragm provide information to discern
the tomographic view from which the image is obtained.

 Left Anterior Oblique (LAO): Image intensifier is angled above the left side of the patient
‘s chest, visualizing the heart from the left side.
 Right Anterior Oblique (RAO): Image intensifier is angled above the right side of the patient’s
chest, visualizing the heart from the right side.
 Anterior Posterior (AP): Image intensifier is angled directly above the patient ‘s mid-
chest, visualizing the heart from front to back
 Lateral Image intensifier is angled at a 90° angle from the patient ‘s midline, visualizing the
heart from the far left side.

✓ Cranial Image intensifier is angled toward the patient’s head, visualizing the heart from above.
✓ Caudal Image intensifier is angled toward the patient’s feet, visualizing the heart from below.

Left Main AP, LAO cranial, LAO caudal

Proximal LAD LAO cranial, RAO caudal

Mid LAD LAO cranial, RAO cranial, Lateral
Distal LAD AP, RAO cranial, Lateral

Diagonal LAO cranial, RAO cranial

Proximal circumflex RAO cranial, LAO caudal

Intermediate RAO caudal, LAO caudal

 Obtuse marginal RAO caudal, LAO caudal, RAO cranial
Proximal RCA LAO, Lateral
Mid RCA
Distal RCA
PDA
Posterolateral

ANGIOGRAM-INTERPRETATION
A systematic interpretation of a coronary angiogram would involve:
Evaluation of the extent and severity of coronary calcification just prior to or soon after
contrast opacification
Lesion quantification in at least 2 orthogonal views:
1. Severity
2. Calcification
3. Presence of ulceration/thrombus
4. Degree of tortuosity
5. ACC/AHA lesion classification
6. Reference vessel size
• Grading TIMI flow
• Grading TIMI myocardial perfusion blush grade
• Identifying and quantifying coronary collaterals

ACC/AHA LESION CLASSIFICATION

➢ Type A Lesion: Minimally complex, discrete (length <10 mm), concentric, readily accessible, non-
angulated segment (<45°), smooth contour, little or no calcification, less than totally occlusive, not
ostial in location, no major side branch involvement, and absence of thrombus
➢ Type B Lesion: Moderately complex, tubular (length 10 to 20 mm), eccentric, moderate
tortuosity of proximal segment, moderately angulated segment (>45°, <90°), irregular contour, moderate
or heavy calcification, total occlusions <3 months old, ostial in location, bifurcation lesions requiring double
guide wires, and some thrombus present.
➢ Type C Lesion: Severely complex, diffuse (length >2 cm), excessive tortuosity of proximal
segment, extremely angulated segments >90°, total occlusions >3 months old and/or bridging
collaterals, inability to protect major side branches, and degenerated vein grafts with friable lesions.
 LESION LENGTH
Measured―shoulder-to-shoulder in an shortened view
✓ Discrete Lesion length < 10mm
✓ Tubular Lesion length 10–20mm
✓ Diffuse Lesion length ≥ 20mm

LESION ANGULATION:
Vessel angle formed by the centerline through the lumen proximal to the stenosis and extending beyond
it and a second centerline in the straight portion of the artery distal to the stenosis
✓ Moderate: Lesion angulation ≥ 45degrees
✓ Severe: Lesion angulation ≥ 90 degrees

CALCIFICATION:
Readily apparent densities noted within the apparent vascular wall at the site of the stenosis.
✓ Moderate: Densities noted only with cardiac motion prior to contrast injection

✓ Severe: Radiopacities noted without cardiac motion prior to contrast injection

TIMI FLOW GRADES:

✓ TIMI 0 flow: absence of any antegrade flow beyond a coronary occlusion.

✓ TIMI 1 flow: (penetration without perfusion) faint antegrade coronary flow beyond the
occlusion, with incomplete filling of the distal coronary bed.
✓ TIMI 2 flow: (partial reperfusion) delayed or sluggish antegrade flow with complete
filling of the distal territory.
✓ TIMI 3 flow: (complete perfusion) is normal flow which fills the distal coronary bed completely.
Figure 9.8a: Normal Coronaries (LCA)

Figure 9.8b Normal Coronaries (RCA)

Figure 9.8c Blockage

COMPUTERISED TOMOGRAPHY (CT)

A computed tomography (CT) scan of the heart is an imaging method that uses x-rays to create
detailed pictures of the heart and its blood vessels. This test is called a coronary calcium scan when
it is done to see if you have a buildup of calcium in your arteries. It is called CT angiography if
it is done to look at the arteries that bring blood to your heart. This test evaluates if there is narrowing
or a blockage in those arteries. The test is sometimes done in combination with scans of the aorta or
pulmonary arteries to look for problems with those structures.

TYPES OF CT
1. EBCT (Electron beam CT)

2. MDCT (Multidetector CT)

The most notable technical advance is progressive increase in the number of detector rows (or slices).
Each row is a narrow channel, approximately 0.625 mm in width, through which x-rays are detected on
scintillation crystals. The number of detector rows aligned in an array has increased from a single detector
to 4, 16, and 64 (present standard technology) and now on to wide detectors of 256 to 320 rows.

SCAN MODES
There are two basic scan modes in cardiac CT, helical (spiral) and axial (sequential, step & shoot) scanning.

Helical (spiral) scanning: Most current MDCT scanners use spiral, retrospectively gated acquisition
techniques. Helical scanning involves continuous radiation exposure and table movement (the patient is
moved through the rotating x-ray beam), during which the detector arrays receive projection data from
multiple contiguous slices of the patient.

Axial (sequential, step & shoot) scanning: axial imaging involves sequential scanner snapshots, in
between which the x-ray tube is turned off and the table is moved to a different position for the
next image to be acquired.
INDICATIONS:
➢ Evaluation of chest pain in patients at low to intermediate pretest probability of disease and
persistent chest pain after an equivocal stress test.

➢ Suspicion of coronary artery anomalies. MDCT has very high sensitivity and specificity for
coronary anomalies.
➢ Pulmonary vein evaluation can be performed, often before or after pulmonary vein isolation for
atrial fibrillation.
➢ Evaluation of cardiac masses when other modalities such as TTE, TEE, or MRI are unrevealing.

➢ Evaluation of pericardial disease when other modalities such as TTE, TEE, or MRI are unrevealing.

➢ Assessment of anatomy in complex congenital heart disease. Presurgical evaluation, particularly

before redo open heart surgery. MDCT can aid in describing prior bypass graft location, identifying
safe sites for surgical approach.
➢ Assessing graft patency after prior bypass surgery is feasible in many cases, though sometimes
limited by artifacts related to calcium and surgical clips.
➢ Evaluation of aortic disease. MDCT is the test of choice for evaluating aortic aneurysm and suspected
aortic dissection.
➢ Evaluation of suspected pulmonary embolism

CONTRAINDICATIONS:
➢ Unlike with cardiac MRI, few absolute contra indications exist for cardiac CT. However, there are
important risks associated with radiation and/or contrast exposure that must be weighed against the
benefits of the scan.

ABSOLUTE CONTRAINDICATIONS:
➢ Renal insufficiency. Given the potential for contrast nephropathy, patients with significant renal
insufficiency (i.e., Cr > 1.6 mg/dL) should not undergo contrast-enhanced CT unless the information
from the scan is critical and therisks/benefits are thoroughly discussed with the patient.

➢ Known history of anaphylactic contrast reactions A prior anaphylactic response to contrast is

generally felt to be an absolute contraindication to intravenous iodinated contrast administration at
many institutions.
➢ Pregnancy
➢ Clinical instability
RELATIVE CONTRAINDICATIONS

➢ Contrast (iodine) allergy. Patients with allergic reactions to contrast should be pretreated with
diphenhydramine and steroids before contrast administration.

➢ Recent intravenous iodinated contrast administration. Patients who have received an

intravenous dose of iodinated contrast should avoid contrast-enhanced CT scanning for 24 hours
to reduce the risk of contrast nephropathy.
➢ Hyperthyroidism. Iodinated contrast is contraindicated in the setting of uncontrolled
hyperthyroidism due to possible precipitation of thyrotoxicosis.
➢ Atrial fibrillation or any irregular heart rhythm, is a contraindication to coronary CT angiography
due to image degradation from suboptimal ECG gating.
➢ Inability to breath hold for at least 10 seconds. Image quality will be significantly reduced due to
respiratory motion artifact if the patient cannot comply with breath hold instructions.
➢ Morbid obesity
➢ Severe coronary calcium

CLINICAL APPLICATIONS:
CORONARY CALCIUM SCORING
Coronary calcium is a surrogate marker for coronary atherosclerotic plaque. Coronary artery calcium
score is directly proportional to the overall extent of atherosclerosis, although typically only a
minority (approximately 20%) of plaque is calcified. Complete absence of coronary artery calcium
makes the presence of significant coronary luminal obstruction highly unlikely and indicates a very
low risk of future coronary events.

THE AGATSTON CORONARY ARTERY CALCIUM (CAC) SCORE is the most frequently
used scoring system. It is derived by measuring the area of each calcified coronary lesion and
multiplying it by a coefficient of 1 to 4, depending on the maximum CT attenuation within that lesion.

VOLUME SCORE MASS SCORE

A coronary calcium coverage score: multivessel coronary calcium, the number of calcified
lesions and diffuse spotty pattern (small foci <3 mm) are associated with a higher clinical risk.
 The CAC score can be classified into five groups:
➢ zero, no coronary calcification;
➢ 100, mild coronary calcification;
➢ 100 to 399, moderate calcification;
➢ 400 to 999, severe calcification;
➢ 1000, extensive calcification.

CORONARY CT ANGIOGRAPHY: The primary clinical application of cardiac CT is the

performance of noninvasive coronary CT angiography among patients with symptoms suggestive of
myocardial ischemia. The overall accuracy of 64-row CT angiography included a sensitivity of 87%
to 99% and specificity of 93% to 96%.
Coronary CT angiography for evaluating CAD is most useful in low- to intermediate-risk patients
with angina or anginal equivalent. The negative predictive value of coronary CT angiography is
uniformly high in studies, approaching 93% to 100%; in other words, coronary CT angiography is an
excellent modality for ruling out coronary disease.

CARDIAC MRI
Cardiac magnetic resonance imaging (MRI) has a wide range of clinical applications. Many of these
applications are commonly employed in clinical practice—for example, in the evaluation of
congenital heart disease, cardiac masses, the pericardium, right ventricular dysplasia, and hibernating
myocardium.

IMAGING PLANES
The main cardiac imaging planes are oblique to one another. As the cardiac imaging planes are also
at arbitrary angles with respect to the scanner, they are called―double oblique planes. The 3 main
cardiac imaging planes are the short axis, as seen in the first image below; the horizontal long axis,
as seen in the second image below; and the vertical long axis, as seen in the third image below
(the long axis is the line from the center of the mitral valve orifice to the left ventricular apex).

CARDIAC FUNCTION
Cardiac function is evaluated using cine gradient echo sequences often known as ―bright blood‖
sequences (see the image below). Steady-state free precession (SSFP) gradient echo sequences have
largely replaced spoiled gradient echo sequences for this purpose. Different trade names for these
SSFP sequences are True FISP (True Fast Imaging with Steady-state Precession; Siemens), Field
Echo; Phillips). These sequences are typically used in conjunction with segmented k-space
acquisition.

MORPHOLOGY
Fast spin echo sequences often known as ―black blood sequences are typically used (see the image
below). Multiple options are available, but half-Fourier, single-shot, fast spin echo (SS- FSE)
sequences are the fastest. Different trade names for these half-Fourier single shot sequences are
HASTE (Half-Fourier Acquired Single- shot Turbo spin Echo; Siemens) and SS-FSE (GE, Phillips).

PERFUSION
Magnetization-prepared gradient echo sequences are used to assess myocardial perfusion (see the
image below). The magnetization preparation pre pulse can be a saturation or inversion recovery
pulse and is used to improve T1-weighted contrast. Different trade names for these sequences are
Turbo FLASH (Fast Imaging using Low Angle Shot; Siemens), Fast SPGR (Spoiled Grass [Gradient
Recall Acquisition using Steady States]; GE), and TFE (Turbo Field Echo; Phillips). Echoplanar
sequences can also be used.

VIABILITY/INFARCTION
Contrast-enhanced MR evaluation of myocardial viability utilizes inversion recovery gradient echo
sequences, with the inversion time set to null viable myocardium. Either spoiled gradient echo or
SSFP sequences can be used in conjunction with the inversion recovery pre pulse. These sequences
typically utilize segmented k-space acquisition.
ANGIOGRAPHY
Many different sequences have been used to image the coronary arteries. These sequences are
typically used in conjunction with segmented k-space acquisition. Two-dimensional (2D),
segmented, gradient echo sequences can be used to evaluate coronary artery anomalies. Three-
dimensional (3D) techniques are used to evaluate the arteries for stenosis. Images can be acquired
during breath-holding or free breathing. Images can be obtained with or without intravenous contrast.
A 3D, segmented SSFP sequence without intravenous contrast is well suited to evaluate the coronary
arteries. If intravenous contrast is employed, intravascular contrast agents are the most useful.
Standard 3D, spoiled gradient echo sequences with intravenous contrast are used to evaluate the aorta
and great vessels.
.

ACTIVITY 10

DEMONSTRATION AND PRACTICE OF METHODS OF

CALCULATING TRAINING HEART RATE
The intensity of an aerobic activity is the energy required to perform that activity relative to its
maximum metabolic cost, i.e. the maximum oxygen uptake (VO2 max). Therefore, to obtain a desired
training intensity VO2 or some equivalent index must be measured. Given below are some different
techniques frequently used to determine an appropriate training intensity for a cardiac patient.

Methods of calculating training heart rate: There are methods of calculating training heart rate:

OBJECTIVE METHOD:

They are used during Phase II, III, IV of Cardiac Rehabilitation.

➢ Method 1: Age Adjusted Method: THR= % Intensity*HRmax

220-Age = HR max (maximum heart rate)

164-Age*0.7 = HR max (For patients on Beta-Blockers)
Case 1 Age=34
70%-80% of HRmax
By using formula: 220-34= 186.
186 x .70 (70% of max) = 130
186 x .80 (80% of max) = 148
The target heart rate zone for this person would be 130 to 148 bpm.

➢ Method 2: THR = % Intensity * HR peak

➢ Method 3: Karvonen formula: THR= (HR max-HR rest) % Intensity + HR rest

The Karvonen Formula is a mathematical formula that helps to determines target heart rate
zone. The formula involves using patients maximum heart rate (MHR) minus his/her age to come up
with a target heart rate range (which is a percentage of his/her MHR). Staying within this range it will
help us to work most effectively during cardiac rehabilitation.

BELOW ARE THE CALCULATION OF HEART RATE MAINLY PREFERRED FOR PATIENTS
WHO ARE ON BETA-BLOCKERS: (AACVPR)
They are used during Phase II, III, IV of Cardiac Rehabilitation.

➢ Method 4: Percentage of Maximal METs: THR= (MET peak-MET rest) % Intensity + MET
rest, MET rest is taken as 1.
➢ Method 5: THR = HR at VO2 that is a specific percentage of VO2 max. This formula plots the
relationship between HR and VO2. THR may then be chosen from HRs that corresponds to VO2
values of 50% to 85%of VO2 max achieved.

➢ Method 6: THR = % Intensity * VO2 max

➢ Method 7: THR = % Intensity * VO2 peak

➢ Method 8: THR = % Intensity * VO2 reserve = (VO2max-VO2rest) % Intensity + VO2rest

➢ Method 9: THR = % Intensity * Work Rate (WR) peak (in watts)

➢ Method 10: THR = HR at VO2 at AT (Anaerobic Threshold)

VT1: Below VT1 is refers as Low Intensity.
VT2: Above VT2 is refers as High Intensity.
Between VT1 and VT2 is refers as Moderate Intensity.

➢ Method 11: THR= Resting HR+10-20bpm

It is used for patients during Phase I of Cardiac Rehabilitation.

SUBJECTIVE METHOD:

Talk Test:
It is an unreliable method, mainly used for home based cardiac rehabilitation. Here, patient has to
maintain an exercise intensity where conversation which is comfortable. The exercise intensity where
the talking becomes difficult during exercise is a mark for the 2nd Ventilatory Threshold (VT2) has
crossed. This method is not suitable for guiding low exercise intensity exercise (AACVPR).

Borg Scale/ RPE:

It is a 0-10- or 6-20-point scale. It is popularly used for Atrial Fibrillation, cardiac transplant patients,
and for patients who are showing chronotropic incompetence.
Figure 10.1: RPE Scale
 ACTIVITY -11

DEMONSTRATION AND PRACTICE OF EXERCISE TESTING

AND INTERPRETATION FOR CARDIOVASCULAR DISEASE
EXERCISE STRESS TESTING
Cardiac stress testing is a means to diagnose coronary artery disease in the presence of anginal symptoms,
and is important in evaluating patients with symptoms of chest pain. Stress testing can answer the
question: "Are the patient's symptoms caused by occlusive coronary disease?" Significant prognostic
information can be obtained as well, especially using the well-validated Brue Treadmill Score.

How to Stress the Heart

Stress can be induced on the heart in one of two ways: exercise stress testing or drug-induced
(pharmacological stress testing). Pharmacological stress testing can be done using either regadenoson
(Lexiscan, Astellas) or dobutamine.

EXERCISE STRESS TESTING:

INDICATIONS:
✓ Assessment of cardiovascular risk
✓ Detection of coronary artery disease (ischemic heart disease)
✓ Evaluation of CAD
✓ Assessment of therapeutic response: Exercise test can be used to assess the effects of medications or
interventions such as PCI, CABG etc.
✓ Exercise prescription
✓ Determine degree of impairment

ABSOLUTE AND RELATIVE CONTRAINDICATIONS TO EXERCISE TESTING

ABSOLUTE CONTRAINDICATIONS
● Acute myocardial infarction (MI), within 2 days (48 hours): due to risk of aggravating the infarction
and developing ventricular arrythmias
● Ongoing unstable angina: due to risk of developing acute MI and VA
● Uncontrolled cardiac arrhythmia with hemodynamic compromise
● Active endocarditis: due to risk of embolization
● Symptomatic severe aortic stenosis: due to risk of syncope
● Decompensated heart failure
● Acute pulmonary embolism, pulmonary infarction, or deep vein thrombosis
● Acute myocarditis or pericarditis
● Physical disability that precludes safe and adequate testing
RELATIVE CONTRAINDICATIONS
● Known obstructive left main coronary artery stenosis
● Moderate to severe aortic stenosis with uncertain relation to symptoms
● Tachyarrhythmias with uncontrolled ventricular rates
● Acquired advanced or complete heart block
● Hypertrophic obstructive cardiomyopathy with severe resting gradient
● Recent stroke or transient ischemic attack
● Mental impairment with limited ability to cooperate
● Resting hypertension with systolic or diastolic blood pressures >200/110 mm Hg

SUBJECT PREPARATION
Preparations for exercise testing include the following:

➢ ● The purpose of the test should be clear in advance to maximize diagnostic value and to ensure
safety. If the indication for the test is not clear, the referring provider should be contacted
➢ for further information.
➢ ● The subject or patient should not eat for 2-3 hours before the test. Routine medications may be
taken with small amounts of water. Subjects should dress in comfortable clothing and wear
comfortable walking shoes or sneakers.
➢ ● The subject or patient should receive a detailed explanation of the testing procedure and purpose
of the test, including the nature of the progressive exercise, symptom and sign end points, and
possible complications.
➢ ● When exercise testing is performed for the diagnosis of ischemia, routine medications may be
held because some drugs (especially β-blockers) attenuate the HR and blood pressure responses to
exercise. If ischemia does not occur, the diagnostic value of the test for detection of CAD is limited.
No formal guidelines for tapering or holding medications exist, but 24 hours or more could be
required for sustained-release preparations, and the patient should be instructed to resume
medication if rebound phenomena occur. Many exercise test evaluations occur while patients are
taking usual medications, which should be recorded for correlation with test findings.
➢ ● A brief history and physical examination are required to rule out contraindications to testing.
The goal during exercise stress test is to achieve a specific target heart rate in order to induce an
adequate level of stress to detect flow-limiting coronary stenosis. This has been determined to be 85%
of the age-predicted maximum heart rate using the simple equation below:
Maximum Heart Rate
Men= 208- (0.7*age in years)
Women=206- (0.88*age)
CAD on beta blockers= 164-age*0.7

When a patient is not able to exercise adequately to achieve 85% of the age-predicted maximum heart
rate, or when beta-blockers are inhibiting the heart rate increase which is needed, the sensitivity of the
stress test to detect coronary stenosis will be reduced and pharmacologic stress testing should be
considered.

ECG Lead placement

(By mason Lekers lead placement method)

Adequate skin preparation.
Extremity electrodes moved to the torso to minimize motion and muscle artifact.
Arm electrodes- lateral aspects of infraclavicular fossae.
Leg electrodes-above the anterior iliac crest and below the rib cage.

Figure 11.1: Mason-Likar’s Lead Placement

➢ The STANDARD BRUCE PROTOCOL on a treadmill is most commonly utilized to increase
the heart rate with exercise and is summarized below. This uses 3-minute stages with progressive
increases in speed and incline.

Measuring VO2 Max With the Bruce Protocol

Men: 14.8 - (1.379 x T) + (0.451 x T²) - (0.012 x T³)
Women: 4.38 x T - 3.9
➢ MODIFIED BRUCE PROTOCOL

➢ BALKE PROTOCOL
For women the treadmill speed is set at 3.0 mph, with the gradient starting at 0%, and increased by
2.5% every three minutes.
Estimating VO2 max from Balke protocol
Male = 1.444* time + 14.99 (Pollock et al., 1976)
Female = 1.38* time + 5.22 (Pollock et al., 1982)
Note that exercise should be terminated if any of the following occur (ACC/AHA Guidelines):

1. Severe hypertension (systolic blood pressure > 200/110 mmHg before test or > 250/115 mmHg
during exercise);
2. Hypotension (decrease in SYSTOLIC blood pressure > 10 mmHg);
3. Exercise limiting chest pains;
4. Sustained ventricular tachycardia;
5. Central nervous system symptoms (ataxia, severe dizziness, near-syncope);
6. Signs of poor perfusion (cyanosis or pallor); and
7. Patient's desire to stop.
8. Intolerable dyspnea and fatigue
Table 1
Interpretation of responses to graded exercise testing

VARIABLE CLINICAL SIGNIFICANCE

ST-segment depression An abnormal ECG response is defined as ≥1.0 mm of horizontal or

(ST↓) downsloping ST ↓ 60–80 msec beyond the J point, suggesting
myocardial ischemia.

ST-segment elevation (ST ↑) ST elevation (ST ↑) in leads displaying a previous Q-wave MI almost
always reflects an aneurysm or wall-motion abnormality. In the absence
of significant Q waves, exercise-induced ST ↑ often is associated with a
fixed high-grade coronary stenosis.

Supraventricular Isolated atrial ectopic beats or short runs of SVT commonly occur
dysrhythmias during exercise testing and do not appear to have any diagnostic or
prognostic significance for CVD.

Ventricular The suppression of resting ventricular dysrhythmias during exercise

dysrhythmias does not exclude the presence of underlying CVD; conversely, PVCs
that increase in frequency, complexity, or both do not necessarily
signify underlying ischemic heart disease. Complex ventricular ectopy,
including paired or multiform PVCs, and runs of ventricular
tachycardia (≥3 successive beats) are likely to be associated with
significant CVD and/or a poor prognosis if they occur in conjunction
with signs and/or symptoms of myocardial ischemia or in patients with
a history of sudden cardiac death, cardiomyopathy, or valvular heart
disease. Frequent ventricular ectopy during recovery has been found to
better predictor of mortality than ventricular ectopy that occurs only
during exercise.
Heart rate (HR) The normal HR response to progressive exercise is a relatively linear
increase, corresponding to 10 ± 2 beats·MET-1 for inactive subjects.
Chronotropic incompetence may be signified by:
1. A peak exercise HR that is >2 SD (≈20 beats·min-1) below the
age predicted maximal HR or an inability to achieve>85% of
the age-predicted maximal HR for subjects who are limited by
volitional fatigue and are not taking β blockers.
2. A chronotropic index (CI) <0.8 ; where CI is calculated as the
percentage of heart rate reserve to percent metabolic reserve
achieved at any test stage.

Heart rate An abnormal (slowed) HRR is associated with a poor prognosis. HRR
recovery (HRR) has frequently been defined as a decrease ≤12 beats/min at 1 min
(walking in recovery), or ≤22 beats/min at 2 min (supine position in
recovery).

Systolic blood The normal response to exercise is a progressive increase in SBP,

pressure (SBP) typically 10 ± 2 mm Hg·MET-1, with a possible plateau at peak
exercise. Exercise testing should be discontinued with SBP values of
>250 mm Hg. Exertional hypotension (SBP that fails to rise or falls
[>10 mm Hg]) may signify myocardial ischemia and/or LV
dysfunction. Maximal exercise SBP of<140mmHg suggests a poor
prognosis.

Diastolic blood The normal response to exercise is no change or a decrease in DBP. A

pressure (DBP) DBP of >115 mm Hg is considered an endpoint for exercise testing

Anginal Can be graded on a scale of 1 to 4, corresponding to perceptible but

symptoms mild, moderate, moderately severe, and severe, respectively. A rating of
3 (moderately severe) generally should be used as an endpoint for
exercise testing.
Aerobic fitness Average values of VO2max expressed as METs, expected in healthy
sedentary men and women, can be predicted from the following
regressions (43): men = (57.8–0.445 [age])/3.5; women = (41.2–0.343
[age])/3.5.

Figure 11.2: Mason-Likar’s ECG Lead Placement

 Figure 11.3: Treadmill Exercise Testing (Balke/Bruce)

Figure 11.4: ECG Monitoring

 ACTIVITY- 12

DEMONSTRATION AND PRACTICE OF HEART RATE VARIBILITY IN

CARDIOVASCULAR CONDITIONS
HEART RATE VARIABILITY
Heart rate is the number of heart beats per minute. Heart rate variability (HRV) is the fluctuation in the time
intervals between adjacent heartbeats. HRV index’s neurocardiac function and is generated by heart- brain
interactions and dynamic non-linear autonomic nervous system (ANS) processes. HRV is an emergent
property of interdependent regulatory systems which operate on different time scales to help us adapt to
environmental and psychological challenges. HRV reflects regulation of autonomic balance, blood pressure
(BP), gas exchange, gut, heart, and vascular tone, which refers to the diameter of the blood vessels that
regulate BP, and possibly facial muscles. (Gevirtz RN, Lehrer PM, Schwartz MS. Cardiorespiratory
biofeedback. 4th ed (2016).

CARDIAC AUTONOMIC CONTROL

 Figure 12.1: Autonomic control

EFFECT OF ANS ACTIVITY

S Y M PATHETIC AND PARASYMPATHETIC INFLUENCE

Sympathetic stimulation, occurring in response to stress, exercise and heart disease, causes an
increase in HR by increasing the f of pacemaker cells in the heart’s sino-atrial node by the action of
noradrenaline released from postganglionic neurons (Achar 2006).

Sympathetic activity, primarily resulting from the function of internal organs, allergic reactions and
the inhalation of irritants increases the firing rate of pacemaker cells and the HR by releasing
acetylcholine from post ganglionic neurons, providing a regulates in physiological autonomic function
(Acharya et al.,2006).
 HRV

TIME DOMAIN FREQUENCY DOMAIN

TIME DOMAIN
It measures the changes in heart rate over time or the intervals between successive normal
cycles (Kleiger et al., 1992). Time domain variables (Taskforce, 1996):

➢ SDNN-Standard deviation of the RR intervals: Overall HRV

➢ SDANN-Standard deviation of the 5 min mean of RR intervals: Sympathetic activity

➢ RMSSD-Square root of the mean squared differences between adjacent RR intervals: Vagal
activity

➢ pNN50- Percentage of interval differences of adjacent RR intervals greater than 50

milliseconds derived from differences between consecutive RR intervals: Vagal activity

FREQUENCY DOMAIN
It describes the periodic oscillations of heart rate signal decomposed at different frequencies and amplitudes.
Frequency domain variables (Taskforce, 1996):

➢ Low frequency power (LF): The power in the low frequency range (0.04-0.15Hz) and reflects
a combination of sympathetic and parasympathetic input.
➢ High frequency power (HF): The power in high frequency range (0.15-0.40Hz) and reflects
vagal function.
➢ LF/HF ratio: The ratio of low frequency to high frequency and it reflects the global
sympathovagal balance (<1).
Figure 12.2: Normative values of HRV variables
HEART RATE VARIABILITY AND THE ETIOLOGY AND PROGRESSION
OF CARDIOVASCULAR DISEASE RISK (Thayer et al., 2009)

MODIFIABLE BIOLOGICAL RISK FACTOR:

➢ Hypertension:

The findings from large, epidemiological studies provide strong evidence that vagal tone, as
measured by HRV, is lower in persons with hypertension that in normotensive. Importantly, these
studies suggest that decreases in vagal tone may precede the development of this critical risk factor
for cardiovascular disease (Liao et al., 2002, Singh et al., 1998).

➢ Diabetes:

Several indices of HRV (LF and HF power) were inversely associated with fasting glucose levels and
were significantly reduced in diabetics in those with impaired fasting glucose levels compared to
those with normal fasting glucose levels (Singh et al., 2000)

➢ Cholesterol:

Christensen et al., 1999 examined the association between 24hour HRV and cholesterol in 47 men
with heart disease and 38 healthy men. In both groups total cholesterol and low density lipoprotein
were inversely associated with 24 hour HRV.

➢ Liver cirrhosis:

Liver cirrhosis is associated with decreased HRV. Decreased HRV in patients with cirrhosis has a
prognostic value and predicts mortality. Loss of HRV is also associated with higher plasma pro-
inflammatory cytokine levels and impaired neurocognitive function in this patient population.

➢ Sepsis:

HRV is decreased in patients with sepsis. Loss of HRV has both diagnostic and prognostic value in
neonates with sepsis. The pathophysiology of decreased HRV in sepsis is not well understood but
there is experimental evidence to show that partial uncoupling of cardiac pacemaker cells from
autonomic neural control may play a role in decreased HRV during acute systemic inflammation.

➢ Tetraplegia:

Patients with chronic complete high cervical spinal cord lesions have intact efferent vagal neural
pathways directed to the sinus node. However, an LF component can be detected in HRV and arterial
 pressure variabilities of some tetraplegic patients. Thus, the LF component of HRV in those without
intact sympathetic inputs to the heart represent vagal modulation.

➢ Sudden cardiac death:

Patients’ victim of sudden cardiac death has been found to have lower HRV than healthy individuals.

PROTOCOL TO ASSESS HRV

(Taskforce of European society of cardiology and North American society of electrophysiology,
1996):

Step 1: Subject preparation:

No caffeine products, physical exercise for at least 12 hours prior to testing Nil orally for 3 hours prior
to testing.

Step 2: Recording:

10 min of supine rest at 240C and subject is instructed to close eyes and avoid talking Lead 2 ECG
recording for 20 min in supine position.

Step 3: Acquisition:

ECG signal amplified, digitized and stored in computer.

Step 4: Analysis:

Detection of R waves Elimination of ectopic beats HRV analysis of detected R wave.

PROCEDURE:
• SUBJECT PREPARATION:
Soothing and control environment should be there. Patient should relax and calm. All jewellery or
accessories should be removed. Clean skin with distilled water then place electrode

• STANDARD LEAD PLACEMENT: Negative electrode- right arm(white) Positive electrode-left

arm(black) Earthing electrode- right leg (green).

.
Figure 12.3: HRV Subject Preparation

Figure 12.4: HRV Lead Placement: Negative electrode (White-right arm), Positive electrode
(Black-left arm), Earthing electrode (Green-right leg)
• INTERPRETATION:

Figure 12.5: HRV Analysis

Fig. : 3.3Heart rate variability waveform

Figure 12.6: HRV Report

CLINICAL APPLICATIONS OF HRV

• Depression of HRV has been observed in many clinical scenarios, including autonomic neuropathy,
heart transplantation, congestive heart failure, myocardial infarction (MI), and other cardiac and non-
cardiac diseases (COPD).
• However, it is important to realize that clinical implication of HRV analysis has been clearly
recognized in:
• As a predictor of risk of arrhythmic events or sudden cardiac death after acute MI, and as a
clinical marker of evolving diabetic neuropathy.
• Recently, its role in evaluation and management of heart failure has also been recognized. As a
marker of adaptation at autonomic modulation of heart.
• It can also be used as a marker of cardiac autonomic control as well as cardiac fitness.
Table 1:

Recent Evidences

JOURNAL/
AUTHOR/Y TITLE OBJECTIVE METHODOLOGY RESULT
EAR

GeroScience HRV-guided The main objective 8-week cluster RCT Both groups
training vs was to analyze the with an HRV-based improved VO2
traditional effect of HRV- training group (HRV- max and METS.

Carrasco-Po HIIT training guided training G) and a traditional

yatos et al., in cardiac versus high HIIT group (HIIT-G).

2024 rehabilitation: intensity interval Maximal oxygen Resting SBP was

a randomized training on consumption, heart rate, lower in HRV-G.
controlled trial cardiorespiratory and blood pressure
fitness, heart rate were measured during
variability, quality the Bruce protocol
In HRV-G, the
of life, and training treadmill test. HRV was
resting DBP,
volume at high measured with the
maximal DBP,
intensity, as well as HRV4Training
SBP decreased,
exercise adherence, application, and quality
HR increased.
safety, and of life with the Mac
feasibility in New QLMI. The
ischemic patients. repeated measures
HRV-guided
ANCOVA was used
training presents a
with the age and the
better
baseline scores as
cardioprotective
covariables. Forty-six
effect than HIIT-
patients were
G at a lower high-
randomized and
intensity training
assigned either to HRV-
volume.
G (n = 23) or HIIT-G (n
= 23).
International Heart Rate To investigate Twenty-one patients There was a
Journal of Variability- whether heart rate were randomly statistically
Environment Guided variability (HRV)- allocated to the HRV- significant
al Research Training for guided training guided training group difference in the
and Public Improving improves mortality (HRV-G) or the change in weekly
Health Mortality predictors to a predefined training averaged RMSSD
Predictors in greater extent than group (PRED-G). They in favor of the
Manresa- Patients with predefined training measured their HRV at HRV-G, while no
Rocamora et Coronary in coronary artery home daily and trained differences were
al., 2022 Artery Disease disease patients. three times a week for found in the
six weeks. Resting heart remaining
rate, isolated vagal- analyzed
related HRV indices variables.
(i.e., RMSSD, HF, and
SD1), weekly averaged HRV-guided
RMSSD, heart rate training is
recovery, and superior to
maximum oxygen predefined
uptake were assessed training in
before and after the improving vagal-
training period. related HRV
when
methodological
factors are
accounted for.

Annals of Acute and We assessed acute Participants within 7 We found a trend

Physical chronic effects and chronic effects weeks after MI were for an acute
Rehabilitatio of high- of high-intensity randomly assigned to increase in HR of
n and intensity interval training HIIT or MICE groups 2.5 bpm during
Medicine interval and (HIIT) versus for a 9-week sleep after HIIT.
moderate- moderate-intensity intervention. HR and
Eser et al., intensity continuous exercise the power spectrum of We found a trend
2022 continuous (MICE) on HR and HRV were measured for a chronic
exercise on HRV in individuals pre- and post- decrease in HR
heart rate and after acute ST- intervention by using during supine and
its variability segment elevation orthostatic challenge standing position
after recent MI (STEMI). and during sleep to as well as during
myocardial assess chronic effects. sleep in the MICE
infarction: A Sleep measurements group but a trend
randomized were performed at night for an increase in
controlled trial after HIIT, MICE or no HR during supine
training to assess acute and standing
effects. Mixed models position in the
assessed time*group HIIT group.
interaction for
differences in chronic Low- and high-
and acute effects, frequency power
adjusted for beta- (LF, HF) of the
blocker dose and standing segment
number of training increased from
sessions. pre- to post-
intervention in the
MICE group but
decreased in the
HIIT group.

Annals of The effects of This study A total of 30 patients Compared with

Non-invasive aerobic investigated the with diabetic routine
ElectroCardi exercise effects of aerobic cardiovascular hypoglycemic
ology combined with exercise combined autonomic neuropathy drug therapy,
resistance with resistance (DCAN) were combining
Su et al., training on training on serum randomly divided into a aerobic exercise
2022 inflammatory inflammatory control group (n = 15) and resistance
factors and factors and heart and an exercise group training helped to
heart rate rate variability (n = 15). The control reduce the level
 variability in (HRV) in women group was treated with of blood glucose
middle-aged with type 2 routine hypoglycemic and serum
and elderly diabetes mellitus drugs, while the inflammatory
women with (T2DM). exercise group was factors in T2DM
type 2 diabetes treated with routine patients with
mellitus hypoglycemic drugs + DCAN, and
resistance training (AE improved
+ RT). The levels of autonomic nerve
fasting plasma glucose function.
(FBG), two-hour
plasma glucose (2hPG), After the
(CRP), (IL-6) and intervention, the
(TNF-α) were measured HRV time
before and after the domain and
intervention. The HRV frequency domain
was evaluated by 24-h indexes in the two
ambulatory ECG. groups were
significantly
improved
compared with
those before the
exercise
experiment.

The time-domain
indexes, i.e.,
SDNN and
RMSSD, as well
as the frequency
domain index,
were significantly
higher in the
exercise group.
 ACTIVITY 13
DEMONSTRATION AND PRACTICE OF PHASE 1 (IN PATIENT)
CARDIAC REHABILITATION PROGRAMMEFOR MI, PTCA, CABG,
VALVULAR HEART DISEASE, HEART FAILURE ETC.
PHASE 1 CARDIAC REHABILITATION:
Cardiac Rehabilitation (CR) is an interdisciplinary team approach to patients with functional
limitations secondary to heart disease. The World Health Organization (WHO) has defined CR as
the sum of activities required to favorably influence the underlying cause of the disease, as well as
the best possible physical, mental, and social conditions, so that they may, by their own efforts,
preserve or resume, as normal a place as possible inthe society.
The first line of rehabilitation after an acute cardiac event begins in the acute-care inpatient setting:

➢ The Major Objectives of Phase I Include:

• Patient and Family Education
• Preventing the Deleterious Effects of Bed rest.
• Safe Discharge to Home

➢ Phase I Goals:
• Clear the patient for any skeletal, muscle or orthopedic problems - ROM, pectus excavatum,
pectus carinatum, scoliosis, joint swelling, gross muscle weakness, etc.
• Clear the patient for any pulmonary problems that would limit activity - i.e. - thoracic
deformities, obstructive or restrictive pathologies, presence of adventitious sounds (crackles,
wheezes, bronchophony, egophony, whispered pectoriloquy, stridor), etc.
• Return the patient home and to the workplace with the patient having a clear understanding
about what are the safe activities they can participate in without reinjuring their hearts.
• Decrease the patient's pain and fear of living.
• Increase the patient's physical work capacity.
• Help the patient to modify their coronary risk factors through education.
• Give objective information back to all members of the cardiac rehab team.

➢ The following criteria recommended by the ACSM and the AACVPR should be used as
contraindications for entry in the exercise component of the phase I program:
 • Unstable angina
• Resting systolic BP greater then 200mm hg or resting diastolic BP greater than 100 mm hg
• Orthostatic BP greater than 100 mm hg
• Moderate to severe aortic stenosis
• Acute systemic illness or fever
• Uncontrolled atrial or ventricular dysrhythmias
• Uncontrolled sinus tachycardia (>120 beats/min)
• Uncontrolled CHF
• Third-degree atrio ventricular block
• Active pericarditis or myocarditis
• Recent embolism
• Thrombophlebitis
• Resting ST displacement (>3 mm)
• Uncontrolled diabetes
• Orthopedic problems that would prohibit exercise.

Inpatient Physical Activity and Education Program Schedule and Guidelines for
cardiac Patients:
Cardiac Rehabilitation/ Physical Ward Activity Patient Education
Therapy
Step 1: 1.5 METs Begin sitting in chair Orient to CVICU.
a.m. Ward TX: (when stable) several Reinforce purpose of
Sitting with feetsupported; times a day for 10-30 physical therapy and
active- assistive to active ROM to major min. deep- breathing
muscle groups, active ankle scapular exercises. Orient to
elevation/Depression, retraction/protraction, exercise component
3-5reps; deep breathing. rehabilitation program.
Monitored ambulation of 100 ft. as tolerated. Answer patient and family
p.m. Ward TX: questions regarding
sitting with feet supported; progress.
active ROM to major muscle groups, 5 reps;
deep breathing.
Monitored ambulation of 100-200 ft. with
assistance as tolerated.

Step 2: 1.5 METs Ward TX: Begin sitting in chair Orient to CVICU.
Sitting; repeat exercises from step 1 and (when stable) several Reinforce purpose of
increase reps to 5-10; deep breathing twice times a day for 10-30 physical therapy and
daily. min. deep- breathing
exercises.
Orient to exercise
component rehabilitation
program.
Answerpatient and family
questions regarding
progress.
Step 3: 1.5-2 METs Ward TX: Increase ambulation to Begin pulse-taking
Standing begins active upper- extremity and 300 ft. or instruction when
trunk exercise bilaterally without resistance approximately 3 appropriate and explain
(shoulder flexion, abduction, internal/external corridor lengths at slow RPE scale.
rotation, hyper extension, circumduction place with assistance Answer question of
backward; elbow flexion; trunk lateral flexion twice daily. patient and family.
and rotation; knee extension (if appropriate); Reorient patient and
ankle exercises, 5-10 reps, twice daily family to ICCU.
monitored ambulation of 300 ft. twice daily. encourage family
attendance at group
classes
Step 4: 1.5-2 METs Ward TX Increase ambulation to
Standing: active exercisesfrom step 3, 10-15 1 lap at slow pace with
reps, twice daily. assistance twice daily.
Monitored ambulation of 424 ft. twice daily.
Step 5: 1.5-2 METs Ward TX: Increase ambulation up Orient to ICE Continue
Standing: active exercise from step3, 15 to 3 laps (up to 1,320 instruction in pulse
reps, once daily. ft0 daily as tolerated. taking and use of RPE
Monitored ambulation for 5-10 min (424-848 Begin participating in scale. Explain value of
ft.) as tolerated. daily ADL and personal exercise. Present T-shirt
Exercise: walk to IEC for monitored ROM/ care as tolerated. and activity log.
strengthening exercises from step 3, 15 reps; Encourage chair sitting
legstretching (posterior thigh muscles, with legs crossed.
gastrocnemius), 10 reps; treadmill or bicycle
protocol) with physical approval.
Step 6; 1.5-2.5 METs Ward TX; Increase ambulation Give discharge booklet
Standing active exercises from step 3 with 1 up to 5 laps (up 1,980 and general discharge
lb. weight each upper extremity,15reps, once ft.) daily. Encourage instructions to patient
daily. independence in ADL. and family.
Monitored ambulation for 10-15 min (up to
1,980 ft.) if appropriate. Encourage chair sitting Encourage group class
Exercise center; walk to IEC for monitored withlegs elevated. attendance. Individual
ROM/ Strengthening exercises from step 5 instruction by physical
with 1 lb. weight each upper extremity, 10 therapist, nutritionist,
reps; treadmill and/or bicycle 15- 20 min; pharmacist.
and stair climbing 96-12 stairs) with
assistance.
Step 7: 2-3 METs Ward TX; Increase ambulation Discuss and initiate
Standing; active exercises from step 3 with 1 up to 8 laps (up 3,300 referral to phase II
lb. weight each upper extremity, 15 reps, ft.) daily. Encourage program if appropriate.
once daily. Monitored ambulation for 15-20 independence in ADL. Reinforce prior
min (9up to 3,300 ft.) if appropriate. Exercise teaching.
center: walk to ICE for monitored ROM/ Encourage chair sitting Give instruction in
Strengthening exercises from step 5 with 1 lb. with legselevated. home exercise program.
weight each upper extremity, 15 reps; leg Explain PD- GXT and
stretching, 10 reps; treadmill and/ or bicycle upper-limit heart rate.
20-30 min; and stair climbing (up to 14
stairs) with assistance.
Step 8: 2-3 METs Ward TX; Increase ambulation Reinforce prior
Standing; exercises from step 3 with 2 lb. up to 9 laps 9 up to teaching.
weight each upper extremity, 15 repetition, 3,746 ft.) daily.
once daily. Monitored ambulation if Encourage
appropriate. independence in ADL.
Exercise center: walk to ICE for monitored
ROM/ strengthening exercise from step 5
with 2 lb. weight each upper extremity,15 Encourage chair
reps; leg stretching, 10 repetitions; sitting withlegs
treadmill and/ or bicycle 20-30 min; and elevated
stair climbing (up to 16 stairs).
Inpatient Physical activity and educational program schedule and guidelines
for Myocardial infraction patient

Cardiac Rehabilitation/Physical Ward activity Patient education

therapy
Step1- 1.5METs Bed rest. Orient to exercise
Ward TX- Passive ROM to major May feed self. component of rehabilitation
joints, active ankle exercise, 5 reps, program.
deep breathing (supine) twice daily.
Step-2- 1.5METs Feed self. Answer patient and family
Ward TX- Active assistive ROM to Partial morningcare (washing questions regarding
major muscle group, active ankle hands and face, brushing progress, procedures,
exercise, 5 repetitions, deep teeth in bed) reasons for activity
breathing(supine/sitting) twice daily. Bedside commode. limitation.
Explain RPE scale.
Step-3- 1.5METs Begin sitting in chair for
Ward TX- Active ROM to major short periods as tolerated 2
muscle groups, active ankle exercise, 5 times daily.
reps, deep breathing (sitting) twice Bathe self.
daily. Bedside commode.
Step-4- 1.5METs Bathroom privileges.
Ward TX- Active exercise, shoulder Sit in chair 3 times daily.
flexion and abduction, elbow flexion, Up in chair for meals.
hip flexion, knee flexion, toe raises, Bathe self, dress, comb
ankle exercise, 5 reps, deep breathing hair(sitting).
(standing) twice daily.
Step-5-1. 5-2METs Bathroom privileges. Answer patient and
Ward TX- Active exercise, shoulder Up as tolerated in room. family questions.
flexion abduction and circumduction, Stand at sink to shave and Orient to ICCU phase of
elbow flexion, trunk lateral flexion, hip comb hair. recovery.
flexion and abduction, knee flexion, toe Bathe self and dress. Present discharge booklet
raises, ankle exercise each (standing) and other material (AHA).
twice daily. Monitored ambulation of
100-200ft, twice daily, with physician
approval.
Step-6- 1.5-2 METs Ward TX- Continue ward activity Instruction in pulse taking
Standing- Exercises outlined in steps 5, from step 5. and rationale.
5-10 reps once daily, Monitored Up in chair as tolerated. Explain value of exercise.
ambulation for 5min (440ft). Increase ambulation up to 1 Present T-shirt and activity
Exercise center. Transport to IEC for lap 440ft with assistance if log.
monitored ROM/strengthening exercise appropriate, twice daily. Begin discharge instruction
from step 5,5-10 reps, leg stretching Walk short distance in hall with patient and family
(posterior thigh muscles, (room and quad areas) as when appropriate.
gastrocnemius) 10 reps, treadmill or tolerated. Encourage group classes
bicycle 5min and stair climbing 2-4 attendance
stairs with physician approval.
Step 7- 1.5-2.5 METs Ward TX- Continue ward activity
Standing- exercises from step 5 and from step 5.
1lb weight each extremity, 5-10 Sit up in chair most of the
repetitions, once daily. Monitored day.
ambulation for 5-10 min (440- 1000ft). Increase ambulation up to 3
Exercise center. Transport to IEC for laps up to 1100ft daily.
monitored ROM/strengthening exercise
from step 6 with 1lb weight each
extermity,5-10 reps, leg stretching,10
rep's treadmill or bicycle 5-10min
and stair climbing.
Step 8- 1.5-2.5 METs Ward TX- Continue ward activity Give instruction in home
Standing- exercises from step 5 and from step 7. exercise program.
1lb weight each extremity, 5-10 reps, Increase ambulation up to 5 Initiate to phase
once daily. Monitored ambulation for laps up to 1980ft daily. 2 if appropriate.
10 min (up to 1980ft) if appropriate.
Exercise center. Ambulation to IEC for
monitored ROM/strengthening exercise
from step 6 with 1lb weight each
extermity,10 reps, leg stretching,10
reps’ treadmill or bicycle 10-20 min
and stair
climbing (10-12 stairs)
Step9- 1.5-2.5METs Up as tolerated in room
Ward TX- standing- exercises from andquad area.
step 5 and 2lb weight each extremity, Increase ambulation up to6
10 repetitions, once daily. Monitored laps up to 2640ft daily.
ambulation if appropriate.
Exercise center. Ambulation to IEC
for monitored ROM/strengthening
exercise from step 6 with 2lb weight
each extermity,10 reps, leg
stretching,10 rep's treadmill or bicycle
20- 25min and stair climbing (12-14
stairs).
Step10- 1.5-3METs Up as tolerated in roomand
Ward TX- standing- exercises from quad area.
step 5 and 2lb weight each extremity, Increase ambulation up to 8
10 repetitions, once daily. Monitored
laps up to 3300ft daily.
ambulation if appropriate.
Exercise center. Ambulation to IEC
for monitored ROM/strengthening
exercise from step 6 with 2lb weight
each extermity,10 reps, leg
stretching,10 rep's treadmill or bicycle
25-
30min and stair climbing (14-15 stairs).
 Inpatient Physical activity and educational program schedule and guidelines
for open heart surgery p a t i e n t

Cardiac Rehabilitation/Physical Ward activity Patient education

therapy

Step1-1.5METs Begin sitting in chair Orient to CVICU.

Ward TX- Sitting with feet supported- when stable several times Reinforce purpose of physical
Active assistive to active ROM to major a dayfor 10-30 min. therapy and deep breathing
groups, active ankle scapular May ambulate 100-200 ft exercise.
elevation/depression, with assistance, 1-2 times Orient to exercise component
retraction/protraction, 3-5 repetition, daily. of rehabilitation program.
deep breathing. Monitored ambulation of Answer patient and family
100 ft as tolerated. questions regarding
Ward TX- Sitting with feet supported- progress.
Active ROM to major muscle, 5
repetitions, deep breathing. Monitored
ambulation of 100-200 ft assistance as
tolerated.
Step2-1.5METs Continue activities Continue above.
Ward TX- Sitting- Repeat exercise from from step1
step 1 and increase repetitions to 5-10,
deep breathing twice daily. Monitored
ambulation of 200ft with assistance as
tolerated (stress correct posture) twice
daily.
Step3-1.5-2METs Increase ambulation to Begin pulse- taking
Ward TX- Standing- Begin active upper- 300ft or approximately 3 instruction when
extremity and trunk exercise bilaterally corridor lengths at slow appropriate and explain RPE
without resistance (shoulder flexion,
pace with assistance twice scale.
abduction, internal/external rotation,
hyperextension, circumduction daily. Answer question of patient
backward, elbow flexion, trunk lateral and family.
and rotation, trunk lateral flexion and Reorient patient and family to
rotation, knee extension if appropriate, ICCU.
ankle exercise, 5-10repetitions, twice Encourage family
daily. Monitored ambulation of 300ft attendance at group classes.
twice daily.
Step4-1.5-2METs Increase ambulation to 1
Ward TX- Standing- Active exercises lap at slow pace with
from step 3, 15 repetitions, twice daily. assistancetwice daily.
Monitoredambulation 424 ft twice daily.
Cardiac Rehabilitation/Physical Ward activity Patient education
therapy
Step1-1.5METs Ward TX- Begin sitting in chair Orient to CVICU.
Sitting with feet supported- Active assistive when stable several times Reinforce purpose of
to active ROM to major groups, active ankle a dayfor 10-30 min. physical therapy and
scapular elevation/depression, retraction/ May ambulate 100-200 ft deep breathing exercise.
protraction, 3-5 repetition, deep breathing. with assistance, 1-2 times Orient to exercise
Monitored ambulation of 100 ft as tolerated. daily. component of
Ward TX- Sitting with feet supported- Active rehabilitation program.
ROM to major muscle, 5 repetitions, deep Answer patient and
breathing. Monitored ambulation of 100-200 family questions
ft assistance as tolerated. regardingprogress.
Step2-1.5METs Ward TX- Continue activities from Continue above.
Sitting- Repeat exercise from step 1 and step1
increase repetitions to 5-10, deep breathing
twice daily. Monitored ambulation of 200ft
with assistance as tolerated (stress correct
posture) twice daily.
Step3-1.5-2METs Ward TX- Increase ambulation Begin pulse- taking
Standing- Begin active upper extremity and to300ft or approximately instruction when
trunk exercise bilaterally without 3 corridor lengths at slow appropriate and explain
resistance (shoulder flexion, abduction, pace with assistance twice RPE scale. Answer
internal/external rotation, hyperextension, daily. question of patient and
circumduction backward, elbow flexion, family. Reorient patient
trunk lateral and rotation, trunk lateral and family to ICCU.
flexion and rotation, knee extension if Encourage family
appropriate, ankle exercise, 5-10repetitions, attendance at group
twice daily. Monitored ambulation of 300ft classes.
twice daily.
Step4-1.5-2METs Ward TX- Increase ambulation to 1
Standing- Active exercises from step 3, 15 lap at slow pace with
reps, twice daily. Monitored ambulation 424 assistance twice daily.
ft twice daily.
Cardiac Rehabilitation/Physical Ward activity Patient
therapy education
Step1-1.5METs Ward TX- Begin sitting in chair when Orient to CVICU.
Sitting with feet supported- Active assistive stable several times a day for Reinforce purpose
to active ROM to major groups, active ankle 10-30 min. of physical therapy
scapular elevation/depression, May ambulate 100-200 ft with and deep breathing
retraction/protraction, 3-5 reps, deep assistance, 1-2 times daily. exercise.
breathing. Monitored ambulation of 100 ft as Orient to exercise
tolerated. component of
Ward TX- Sitting with feet supported- Active rehabilitation
ROM to major muscle, 5 repetitions, deep program.
breathing. Monitored ambulation of 100-200 Answer patient and
ft assistance as tolerated. family questions
regarding Progress.
Step2-1.5METs Ward TX- Continue activities from step1 Continue above.
Sitting- Repeat exercise from step 1 and
increase repetitions to 5-10, deep breathing
twice daily. Monitored ambulation of 200 ft
with assistance as tolerated (stress correct
posture) twice daily.
Step3-1.5-2METs Ward TX- Increase ambulation to300ft or Begin pulse- taking
Standing- Begin active upper- extremity and approximately 3 corridor instruction when
trunk exercise bilaterally without resistance lengths at slow pace with appropriate and
(shoulder flexion, abduction, internal/external assistance twice daily. explain RPE scale.
rotation, hyperextension, circumduction Answer question of
backward, elbow flexion, trunk lateral and patient and family.
rotation, trunk lateral flexion and rotation, Reorient patient and
knee extension if appropriate, ankle exercise, family to ICCU.
5-10repetitions, twice daily. Monitored Encourage family
ambulation of 300ft twice daily. attendance at group
classes.
 Step4-1.5-2METs Increase ambulation to 1 lap
Ward TX- Standing- Active exercises from
at slow pace with assistance
step 3, 15 repetitions, twice daily. Monitored
twice daily.
ambulation 424 ft twice daily.

Prescription Phase 1 Cardiac Rehabilitation

Frequency 2-3 times/day

Intensity MI: RHR+20, CABG: RHR+20

Duration MI: 5-20 min, CABG: 10-20 min

Activity ROM, treadmill, bike, one flight of stairs

Abbreviations: CABG= coronary artery bypass graft surgery patient, HRmax= maximal heart rate,
MI= myocardial infarction patient, RHR= resting heart rate(bpm), ROM= Range of motion

NOTE: Importance of anticoagulation therapy and precautions for exercise-related injuries and
bleeding

Precautions for upper extremity exercise and sternal healing

• Avoidance of resistance-typeexercise with severe aortic stenosis or insufficiency
➢ The ACSM provides the following guidelines to modify or terminate a phase
I exercise session for cardiac patients:

• fatigue
• failure of monitoring equipment
• Light-headedness, confusion, ataxia, cyanosis, dyspnea, nausea or any peripheral circulatory
insufficiency
• onset of angina with exercise
• symptomatic supra ventricular tachycardia
• ST displacement (3mm0 horizontal or down sloping from rest
• Ventricular tachycardia (three or more consecutive premature ventricular
contraindications [PVCs])
• Exercise-induced left bundle branch block
• Onset of second or third-degree atrio ventricular block.
• R-on-T PVC
• Frequent multifocal PVCs (30% of the complexes)
• Excessive hypotension (.20 mm hg drop in systolic BP during exercise)
• Excessive BP (>_ 110 mm hg)
• Inappropriate bradycardia 9 drop in HR greater than 10 beats/min) with an increase or no
change in workload.

➢ Difference in phase 1 cardiac rehabilitation in different cardiac conditions:

The use of upper extremity ROM exercises in an important component of the early recovery phase
from heart surgery and MI. CABG post-surgery patients are more susceptible to orthostatic
hypotension and reflex tachycardia. Prior to ambulation in these patients, the orthostatic BP
measurement should be taken to avoid possible cardiovascular complications. The rate of
progression of the training program depends upon patients age, level of fitness and health status. The
slightly slower rate of progression at the beginning of the program for the MI patients, compared to
the CABG patients. Generally, by 4 to 6 weeks the infracted region of the myocardium will develop
scar tissue and the healing process will be complete. After this time, training intensities can increase
more rapidly, equaling the rate of progression for a CABG patient.
Journal/ Title Methodology Finding
Author/
Impact
Factor
Frontiers in Efficacy of Single-center, prospective, Primary Outcome: Increased
Cardiovascula Home-Based randomized controlled, single-blind peak VO2 post-CR program.
r Medicine Cardiac clinical trial. Secondary Outcomes: Improved
Zhang et al., Rehabilitation 100 participants with LVA post-acute HRQoL (measured via EQ-5D-
2023 in Left anterior MI randomized (1:1) to CR 3L), better cardiac function, and
I.F- 3.6 Ventricular or control group. reduced MACCE incidence at 1
Aneurysm Interventions: Standard drug year.
(LVA) Post- treatment and routine education for Key findings anticipated:
Myocardial both groups; CR group received 36 Moderate-intensity CR
Infarction sessions of physician-supervised improves cardiorespiratory
Patients: The home-based CR. fitness, cardiac function,
GRACE Duration: May 2022–May 2024. HRQoL, and reduces mortality
Study Follow-up: 1 year. risk in LVA post-MI patients.
Assessments: CPET, transthoracic Home-based CR found to be a
echocardiography, D-SPECT. viable alternative to center-
Randomization using opaque sealed based programs for stable post-
envelope method. MI patients.

High Blood Cardiac Double-blind randomized controlled FCEM intervention reduced

Pressure & Rehabilitation trial conducted at Shariati Hospital in mortality rates significantly
Cardiovascula Using the Tehran, Iran (2012–2023), involving (5.7%, 11.4%, 17.1% in
r Prevention Family- 70 MI patients and their families. intervention group vs. 20%,
(Vahedian- Centered Patients were assigned to either an 37.1%, 48.9% in control group).
Azimi et al., Empowerment FCEM intervention group or a Mortality risk was four times
2024) Model is standard CR control group. Mortality higher in the control group (HR:
I.F- 3.1 Effective in rates and health-related quality of life 4.346, P = 0.003). Intervention
Improving (HRQoL) were assessed over a 10- improved HRQoL for 48
Long-term year follow-up using various months.
Mortality in questionnaires.
Patients with
Myocardial
Infarction: A
10-year
Follow-Up
Randomized
Clinical Trial
 ACTIVITY-14
DEMONSTRATION AND PRACTICE OF PHASE II (OUTPATIENT)
CARDIAC REHABILITATION PROGRAMME FOR MI, PTCA, CABG,
VALVULAR HEARTDISEASE, HEARTFAILURE
Phase II:

Outpatient Cardiac Rehabilitation

Organized, supervised outpatient cardiac rehabilitation has become an important part of the
rehabilitation process should begin when the patient in discharge from the hospital.

Timing and location

Ideally, the Phase II program should be organized as a hospital-based program, although a

community-based or h program may be implemented if an outpatient program is not available, the
outpatient phase of cardiac rehabilitation is intermediate stage, during which the patient progress
from a restricted low level of training to a less restricted, moderate level program of physical
activity.

Exercise Prescription for Phase II

During Phase II, the purpose of the exercise prescription for the cardiac patient should be the
development of functional capacity. This section addresses the principles of exercise prescription
(intensity, frequency, duration, mode of training, the rate of progression) as applied to the cardiac
patient

Determination of Intensity of Training

The intensity of an aerobic activity is the energy required to perform those activities relative to its
maximum metabolic c that is, the maximum oxygen uptake (VO2max). Therefore, to obtain a
desired training intensity, VO2 or some equivale index must be measured. In the following
paragraph, four different techniques frequently used to determine an appropriate training intensity
for a cardiac patient are discuss.

Heart Rate: The upper limit for the THR in the outpatient program may vary considerably,
depending on medical tests symptomatology, method of calculation, RPE, personal preference and
whether the patient has performed an SL-G Generally, the THR estimated for hospital discharge can
be used for the first 3 to 6 weeks of the outpatient program and patient with of SL-GXT is typically
performed to evacuate the patient ‘s medical status. The test result is used to monitor the exercise
prescription and to further define the patient ‘s risk (example the need for continued ECG
monitoring physical capacity for return to work, change in meditation etc. All three methods are
acceptable, although method I generally y significantly lower THR ‘than the other. The THR of
healthy can be calculated by method I was approximately beats/min and 13 beats/min (10 to 15%)
lower than that calculated by the other methods at 70% and 85% of maxim respectively. For cardiac
patient, the difference was, approximately 20 beats/min and 11beats/min, respectively. It is
therefore, that method I is too conservative. If it is used, several investigators have recommended
adding 10% to 15% to calculated THR in order to achieve an appropriate training response

Method II was first developed by Karvonen et al provide a sample calculation for a THR range of
60% to 80% of HRreserve. The AHA recommended starting at 50% to 60% of HRmax reserve.

Methods III plot the relationship between HR and VO2. A THR may be change from
HRsthat corresponds to V values of 50% to 89% of VO2max achieved. For patient on beta
adrenergic blocking agents the determination of the T requires special consideration. When these
drugs are administered the patient ‘s HR and BL2 are significantly redo although the relationship
between the percentage of HRmax and the percentage of VO2max is not altered. Therefore,
determination of the THR and the method of doing so are similar for patient on or off beta-blockade.

Rating of Perceived Exertion. The REP scale was conceived and introduced by Borg in the
early 1960‘s and is important adjunct to HR in monitoring the intensity of training in, cardiac
patient The original scale was a 15-gr category ranging from 6 to 20, with a description marker or
subjective physical effort at every one number. This scale modified by DR. Borg in 1985. A more
recent 10-grade category scale with ratio properties and similar very description also been
developed by Borg. Because HRmax declines with age, actual HR values and RPE do not match in
older ad RPE values are similar for both younger and older individuals. RPE values are similar for
both younger and o individuals. During the early stages of the Phase II program the recommended
RPE range (11 to 13 on the category R scale, or 4 to 6 on the category-ratio scale.
 Table 14.1 Classification of intensity of exercise based on 30 to 60 minutes of
endurance training

HRmax Vo2 max or HRmax Rating of perceived Classification of

Reserve exertion Intensity
˂35% ˂30% ˂10 Very light
35% - 59% 30%-49% 10-11 Light
60%-79% 50%-74% 12-12 Moderate
80%-89% 75%-84% 14-16 Heavy
≥90 ≥85 ˃16 Very hard

Metabolic Equivalent. The appropriate range for intensity of conditioning activities for cardiac
patient as recommended the ACSM is usually 40% to 85% of the patient ‘s maximal functional
capacity. Since data on the energy cost of activities now exist, activities that fall within the
prescribe range may provide adequate stimulation for improcardiorespiratory function.

Table 14.2 Estimated energy requirements of certain activities

ACTIVITY MET ‘S
MILD
Baking 2.0
Billiards 2.4
Canoeing 2.5
Dancing 2.9

MODERATE
Calisthenics (no weight) 4.0
Cycling 3.5
Gardening 4.4
Golf 4.9
VIGOROUS
Badminton 5.5
Chopping wood 4.9
Field hockey 7.7
Squash 12.1
Anaerobic Threshold: Cardiopulmonary exercise testing to evaluate the functional capacity of
cardiac patients has gained in popularity in recent years. A physiological characteristic of the AT is
the nonlinear rise in ventilation a carbon dioxide production (VCO2), while VO2 continues to rise in
a linear fashion .AT is an appropriate stimulus for cardiorespiratory training. Sophisticated
equipment is needed to determine AT. Training intensities should be prescribed slightly below the
HR that correspondence to the AT, ensuring that the patient is performing aerobic work. The use of
the AT method to prescribe exercise should be done only in conjunction with the standard and
accepted methods of prescription.

Frequency and duration of Training

This typically means three supervised exercise sessions in an organized outpatient program and
four additional sessions at home each week. For patient who are not stable, whose meditation are
still being adjusted, whose risk status has not been determined, or who are at high risk, the home
program would not be recommended.

The exercise session during the early stages of the Phase II program is of short duration (15 to
20min each). Depending on medical status and fitness levels, some patient may require an extra
exercise session each day during the early stage of rehabilitation if their caloric expenditure is not
sufficient. Increase in 5 min increment per week until a 45 min session is attained. Once a 45 min
duration of training has been attained, frequency of training can be reduced or maintain between 3 to
5 times/week. For most patients this may take 4 to 6 weeks.

Table 14.3 Guidelines for Exercise Prescription for Cardiac Patients as

Compared with Healthy Adults

Prescription Phase- Healthy adults

II(Dischargeto3months)
Frequency 1-2 times/day 3-5 times/week
Intensity MI: RHR+20: RPE 13 60-85% of HRmax
CABG: RHR+20: RPE 13

Duration MI: 20-60 min 20-60 min

CABG: 20-60 min
Activity ROM, treadmill (walking, jogging) ROM, treadmill (walking,
biking, arm ergometer, calisthenics, walking- jogging) biking, arm
weight training. ergometer, calisthenics,
weight training, biking,
running, swimming.
Mode of Training: There are many activities that provide adequate stimulation for improving
cardiorespiratory function. Several methods of training have been suggested for use during the
Phase II program and they include continuous (single or dual mode), (circuit training and circuit
weight training), and interval.

The continuous training method (usually walking, cycling, or a combination) imposes a

submaximal energy requirement that is maintained throughout a training period. The advantage of
this type of training is the case of prescribing exercise and the ability to monitor the patient.

Circuit training has been shown to be an excellent method of conditioning to improve both
muscular strength and cardiovascular endurance in cardiac patient. Circuit training incorporates a
combination of lower body (stationary cycling treadmill walking, and stair climbing) and upper
body exercise (rowing, light weight, and wall pulley). Patient exercise for 5 to 12 min on each
modality, alternating arm and leg activities. Circuit weight training (CWT) is a series of resistance
training exercise designed to improve both muscular strength and cardio respiratory fitness generally
circuit weight training result in significant gains in strength but only modest improvement in
VO2max in both health and patient population. As a result of these modest improvements in
cardiorespiratory fitness, it recommended that circuit weight training be utilized only in conjunction
with, rather than serve as a substitute for, regularly performed aerobic exercise.

Interval training is defined as work followed by properly prescribes relief (rest) periods. The
advantage of this metho of training is that patient with low exercise tolerance may perform a greater
amount of physical work during an exercise session.

Regardless of the method of training, the exercise prescription should include exercise that
compasses all the major muscle group of the body.

Endurance activities: The ACSM has classified endurance activities on the basis of the rate of
endurance bod expenditure. Some activities, such as walking, jogging and cycling can be easily
maintained at a constant rate of energy expenditure. Increase the energy expenditure for other
activities basketball and racquetball) are highly related t person ‘s skill level.

Walking: walking is safe from the standpoint with a cardiovascular and orthopedic risk and has
been found to be an excellent for improving aerobic fitness. The compliance to walking program is
usually high because walking requires no special skills, facilities, or equipment and can be
incorporated into most busy lifestyle. 12-step walking program that can be used in an outpatient or
home program. The patient should be stable at a step for 1-to-2-week before progressing to higher
level. One of the objectives of the program is to have patient progress to the point that the expend a
minimum of 250 to 300 kcal/session, or 1,000 kcal/week. This amount of activity improves a
participant’ aerobic capacity 15 to 30 over 4 to 6 months. Therefore, at a slow to moderate walking
speed, patient must eventually walk 45 to 60min/session, or increase the training frequency or both
to reach the required caloric expenditure. The use of hand-held weight during walking increases the
energy cost of the exercise. Walking with 3-lb weight on the wrist or the hands and using an arm-
swing up to shoulder height increase the oxygen cost by 1 MET and the HR b approximately 10 to
12 beats/min. BP response resulting from the use of hand- held weight are usually small; thus, their
general use is not contraindicated for most individual including patient with hypertension. However,
the use of hand-held weight is associated with a significant greater number of orthopedic problems
of the elbow joint.

Jogging: Cardiac patient entering a jogging program usually begin with short periods of jogging
interspersed with equal distance of walking. As they progress, they will walk less and jog more.

However, it should be noted that several investigations have shown that high-intensity effort are
associated with a greater risk for developing further cardiovascular complication. It would therefore
be sensible to consider low-impact activities which are associated with lower injury rates for many
participants.

Stationary Cycling: Stationary cycling is probably one of the best activities that can be used at
home. As with walking, stationary cycling is an excellent rhythmic, large-muscle-group activity that
simulates the metabolic a cardiovascular system. Usually, stationary cycling can be initially
tolerated at 100 to 300 kilopond meter (kpm)/min (1 to 50 W). If a patient ‘s power output cannot be
tolerated for the minimum required duration, some zero-resistance pedaling may be used or an
interval training program incorporated. For example, 1 min of zero resistance pedaling may be
followed by 1 to 3 min of a power output equal to 100 to 300kpm/min.

The patient may initially do this for a total of 10 min. As the patient adapts to the power output
exercise, interval should be gradually increased until the desired duration of exercise can be
performed.

The use of a proper cool-down period following stationary cycling is important, as postexercise
hypotension is commonly experienced symptom associated with an abrupt cessation of cycling
exercise. Thus, easy pedaling against light or no resistance should be continued for several minutes
during the cool-down period

Arm- Leg Cycle Ergometer: The use of arm-leg cycle ergometer such as the Air Dyne is a
popular mode of exercise in cardiac rehabilitation program. The Air Dyne ergometer is versatile and
allow a participant to train with legs only o arm only, or a combination of arm and legs. The arm
shoulder action is a push-pull movement that develops the muscle used in many commonly
performed work and recreational activities. Generally cycling exercise that combines upper and
lower body movement will result in less specific muscle fatigue and allow the patient to train longer
and/ or a higher VO2 than when using arms or leg alone. Rowing is also a combined upper and
lower body exercise, although it is not quite analogous to the push-pull movements performed
during Air Dyne Cycling. Typically, more emphasis it placed on the use of the trunk musculature
than on the arms and shoulder alone.

Arm Cycle Ergometer: Patients with PVD orthopedic limitations may benefit greatly from the
used of the Air Dyne o by arm training are similar to those of leg training or a combination of arm
and leg training. However, when prescribing arm exercise, calculating a THR based on the HRmax
found during the treadmill or cycle ergometer GXT may result in appropriately high exercise HRs.
Several studies comparing leg test for arm ergometer. When prescribing exercise of arm training, it
is important to remember that at any given submaximal power output, the physiological cost (HR,
BP RPP, and VO2).

Swimming: although swimming can be introduced in the Phase II program, it is not recommended
until after an SL GXT has been administered and approximately 6 weeks of rehabilitation have
been completed. This period should allow sufficient time for healing of the sternum and leg
incisions in the surgery patient and the heart tissues of the M patient. The advantage of a swimming
program is many: it is an aerobic activity involving both arms and legs; the water bouncy helps
venous returns and HR; swimming causes fewer musculoskeletal injuries; and it can be therapeutic
for patients with arthritis, intermittent claudication, limb amputation, or paralysis.

Stair climbing and Stair stepping: Because climbing stairs is a component of most people ‘s
daily routines, an because the development of new equipment’s has facilitated the use of stairs
stepping as an exercise mode, stair climbing exercise has become quite popular in Phase II program.
In general, the newer stair-stepping devices can be regulated to a low level of intensity and would be
appropriate for use in the clinical stable CAD patient. However, some precautions should be taken when
using these devices. For patient with CHF, weak thigh muscles, orthopedic problem (i.e., arthritis,
knee, and ankle problems), stair climbing device may be contraindicated. In additional, some of the
olde model is at higher risk for a-climbing machines cannot be regulated below 30 steps/min and so
may present too great aninitial exercise intensity for the low-fit or high-risk patient.

Resistance training: along with the ROM/flexibility exercise previously describes for Phase I,
resistance (1.e strength) training should be empathized during Phase II of cardiac rehabilitation.
Traditionally, cardiac patient was told avoid resistance training because it was associated with an
increased pressure load on the heart and a decrease venous return, thus placing the patient at higher
risk for a cardiac event. The increased in HR, systolic and diastolic BP, and mean arterial
pressure. The decreased venous return was the result of the absence of an active muscle pump.

However, most recent data have shown that the increase in BP with exercise is directly related to the
amount of muscles mass being used and the relative percent of maximum at which it is stimulated.
For example, when comparing static and dynamic exercise performed by hand grid and doubled-
legged knee extension, mean arterial pressure increase were found to be similar for each mode of
exercise but greater for knee extension .Thus in contrast to what some have interpreted about arm
exercise, the HR VO2 and VP responses are greater for leg exercise than for arm exercise Hasalam
et al. have shown that cardiac patient performing light to moderate intensity strength training of up
to 60% of maximal volitional contraction (MVC) were able to maintain their RPP at or below 85%
of the maximum RPP found during an SL-GXT. Other program has shown the safety of strength
training with no added incidence of ischemia dysrhythmia, or frequency and intensity of angina
pectoris.

The following criteria for abstaining from participation in resistance training have been
established by the ACSM an AACVPR-

• Abnormal hemodynamic responses with exercise.

• Ischemic changes during graded exercise testing on the ECG.

• Poor LVF.

• Uncontrolled hypertension, Or

• dysrhythmia

• Peakexercise capacity less than 6 METs.

Exercise prescription for Resistance Training: Most patients begin their resistance
training following hospital discharge with 10 to 15 repetitions of 3- to 5-lb wrist weight or
dumbbells and progress to 5- to 7-lb weight before the 6 weeks SL-GXT. Following an SL-GXT at
4 to 6 week, general restriction on lifting can be eliminated, which will allow patient to progress to
heavier weight and the use of barbells or resistance exercise machines as their medical condition
permits Several methods are available for determination of an appropriate resistance training load in
cardiac patients One method simply starts the patients with lightest weight on the weight stack At
this weight the patient perform 10 to 12 repetition or exercise up to an RPE of no greater than 13
(somewhat hand). Gradually progress the patient to the next higher weight using increment of 5 to 10
lbs. (or 3% to 5% of the previous weight) in every 1 to 2 weeks. Other method includes starting the
training load at 30% to 50% of a one repetition maximum (1RM) or the maximum weight that ca be
lifted 2 or 3 times (90% of 1RM). One RM is the maximum amount of weight that can be lifted one
time.

Rate of Progression: The rate of progression during the Phase II program should be
gradual. However, during the inital 4 to 6 weeks of rehabilitation, patients are still considered in the
starting stage of the exercise program. Exercise training should therefore be individualized and
continue to be conducted at low intensities. Patients should be progressed first by increasing the
frequency and duration of training and later the intensity of exercise. After completion of the 6-
week SL-GXT, training intensity for the low to moderate risk patient can usually increase to 70% of
HRmax reserve and continue to progress to a 250 to 300 kcal expenditure per exercise session.

Warm –Up and Cool- Down: Each exercise session should incorporate a warm-up and cool- down
period to 10 to 1 min each. This may be accomplished with low0intensity cardiovascular activities.
In addition, light ROM exercise low-level calisthenics may help prepare the muscle, joints and
ligaments for the added stress of the exercise. Proper warm-up may prevent potential
musculoskeletal injuries as well as cardiovascular complications. The importance of the cool-down
period is equal to that of the warm-up period. The major purpose of cooling down is to keep active
the primary muscle groups that were involved in the exercise. Continued activity during the cool-
down period will also reduce the risk of cardiac dysrhythmia.

Special consideration for PTCA and CABG patients

If ˂ 3 arteries are blocked then PTCA or ˃3 (CABG) In PTCA no need to do open heart surgery.
PTCA patient typically experiences re-stenosis during first 6 months after the procedure
In PTCA typically began slow ambulation and ROM exercises approx. 24 hours after the
procedure. After discharge patients should be encouraged to join the PHASE-I program. It is
important patient become knowledgeable regarding signs and symptoms of re-stenosis and when to
see medical attention. Necrosed part cannot be corrected in PTCA or CABG but by rehabilitation/
exercises the necrose part remains intact it will not act as contractile tissue.

Conditioning of surrounding muscles is important in order to take over the activity of that muscle.
PTCA patient progress very fast while in CABG patient recovery is difficult. Guidelines similar
to MI patient can be used Two weeks after discharge patient return to hospital for follow up to visit
with cardiologist.
 ACTIVITY 15
DEMONSTRATION AND PRACTICE OF PHASE III (COMMUNITY OR
HOME BASED) CARDIAC REHABILITATION PROGRAMME FOR MI
PTCA, CABG, VALVULAR HEART DISEASE, HEART FAILURE ETC.
The phase III program may be conducted in an organized and supervised community-based setting
and phase-IV denotes a long-term maintenance program that can be supervised. The phased III and
IV programs should provide the cardiac patient with an opportunity to continue the conditioning
programs of phase I and Phase II.

Objectives of Phase III Cardiac Rehab

• Functional goals

• Exercise training under supervision

• Psychosocial goals

• Return to work

• Return to hobbies and lifestyle

• Anxiety/depression management

• Secondary preventive targets

Phase III:
This phase is sometimes erroneously referred to as the Exercise ‘phase.
It incorporates
• Exercise training in combination with ongoing education and psychosocial and vocational
interventions.
• The duration of Phase 3 may vary from six to 12 weeks, with patients required to attend a
CR unit two to three times weekly for structured exercise and other lifestyle interventions.

Phase III Cardiac Rehabilitation Team;

• The Physician

• The Physical Therapist

• The Nurse

• The Occupational Therapist

• Psychologist

• The Dietician or Nutritionist

Table 15.1 Components of Training Session for Cardiac Patients;

Component Phase Duration (min)

warm-up I 15-20
II-IV 10-15
muscular conditioning II- IV 10-20
I II 5-20
aerobic exercise 10-60
III and IV
30-60
15
I-IV
cool-down

Participants in Phase III and IV have typically been out of hospital for 6 to 12 weeks. In addition,
they should be clinically stable, knowledgeable about cardiac symptom, and able to self-regulate
exercise regiments. They should have a minimum functional capacity of 5 METs. At this stage of
training, the exercise prescription is similar for both MI and CABG patient and becomes closer to
that recommended for the healthy adult. The intensity of training is based on the patient ‘s medical
and physical status and on the results of an entry SL-GXT. The initial intensity prescribed is usually
60% to 70% of the HRmax reserve. As the patient continues to progress in the program, the intensity
may reach 85% of functional capacity.

Duration of training should be between 30 and 60 min, depending on available time and the
intensity of exercise. This time range does not include the time needed for warm up, muscular
conditioning, and cool- down, Normally, the duration of training for cardiac patients is longer
than what is recommended for healthy adults because the former are training at lower intensity.

Frequency of training should be a minimum of 3 days/week and, if time is available, up to 5

days/week. As in phase II, an energy expenditure of 250 to 300 Kcal/session and 1,000 Kcal/week
are important threshold for developing and maintaining fitness.

Table 15.2 shows the wider variety of activities now available to participation of the phase III and
IV programs. The activity still depends on medical status, Functional capacity, needs and desires,
time, and available facilities. Generally, highly competitive games are not recommended for high-
risk individuals. Special preparation may be required for those patients who want to resume normal
work and leisure activities, for example, the muscles needed to perform specific tasks may need
specific training.
 Table 15.2 Guidelines for exercise prescription used in phase III and IV.

Prescription Phase III (after 3 months) Healthy adults

Frequency 3-5 times/ week 3-5 times/ week

Intensity 60-65% of HRmax 60-65% of HRmax

Duration 30-60 min 20-60 min

Activity walking, biking, jogging, walking, jogging, running,

swimming, calisthenics, weight biking, swimming, calisthenics,
training endurance sports weight training endurance sports

If local patients prefer to train at home rather than as part of a supervised program, they should
be encouraged to have periodic evaluations of their training routines. These evaluations may occur
once every two weeks to several months, depending on medical status and level of training.
Preferably these sessions are conducted in the phase II or community-based facility and should
simulate exercise conditions at home.

CONSIDERATIONS FOR SPECIAL POPULATIONS

The cardiac rehabilitation specialist should be aware of certain specific problems and needs that
may be associated with exercise prescriptions for special patient populations. The purpose of this
section is to present some patient populations that deserve such additional attention.

Percutaneous Transluminal Coronary Angioplasty Patients:

The number of percutaneous transluminal coronary angioplasty (PTCA) procedures has risen
dramatically over the past few years. Many patients who undergo a PTCA are discharged within 36
h of the procedure, leaving little time for providing then with a comprehensive in-patient program.

Because the angioplasty often results in immediate improvements in clinical status (i.e., in ECG
abnormalities, LVF and angina) and work capacity, many patients deny the need for further medical
intervention. It is therefore critical that these patients be made aware of the importance of exercise
and risk factor modification, especially since 20% to 30% of PTCA patients will experience
restenosis during the first 6 months after the procedure. Just because of the procedure was successful
does not mean that the patient should ignore fact that he or she has significant CAD.

• The PTCA patient can typically begin slow ambulation and ROM exercise approximately 24
hours after procedure.

• Prior to discharge from the hospital the patient should be encouraged to visit a
multidisciplinary phase II program. Because the re-stenosis may range from 20% to 30%, it
is important that patients become knowledgeable concerning the sign and symptoms of
restenosis and be given clear instructions about when to seek medical attention.

• If the patient is given an SL-GXT prior to or shortly after discharge, this information may be
used to prescribed exercise. Generally, the rules outlined for the CABG patient apply for
the PTCA patient, with the PTCA patient apply for the PTCA patient, with the PTCA patient
usually progressing a little faster.

• If the patient is also recovering from an MI, however, the guidelines outlined for the MI
patient should be used.

• Typically, at 2 weeks after discharge, the patient returns to the hospital for a follow-up visit
with the cardiologist.

• If the patient is not enrolled in an outpatient program it is advisable to have him or her meet
with a member of the cardiac rehabilitations staff for further instructions regarding exercise
and diet.

• At this time the patient ‘s exercise progress should be evaluated and the prescription
modified if necessary. In addition, it is helpful to review the principles of exercise and to
provide the patient with instructions on measuring HR, and on using the RPE scale.

Elderly Patients: An increasing number of cardiac patients are above the age of 65 years. These
patients are particularly susceptible to the adverse effects of bed rest so early mobilization is
especially important to return them to active and independent lifestyles. The elderly patient is often
poorly fit and may suffer from significant muscle atrophy, orthostatic intolerance, hypertension,
diabetes, mellitus, and degenerative bone disease, in addition to CAD which may further complicate
the exercise prescription.

Individualization of the exercise prescription is essential for elderly patients to minimize the risk of
cardiovascular and orthopedic complications; nevertheless, the design should follow the principles
described earlier in the chapter. Generally, the goal of physical activity is to maintain functional
capacity for independent living.

Intensity: Exercise intensity is generally prescribed using the previously described techniques.
However, recent data suggests the need to reevaluate the methods used to determine exercise
intensity in the elderly. It is generally accepted that the relative HRmax reserve correspondents to
relative VO2max. However, there may be an exception in the elderly. In this study the percent of

HRmax method more closely represented the percent VO2max and may therefore provide a more
precise estimation of exercise intensity. The elderly coronary patient generally starts with a lower
intensity of exercise because of limited functional capacity and additional medical conditions
(osteoporosis, hypertension, orthostatic hypertension) that may affect exercise performance. Exercise
training at intensities as low as 30% to 40% of Vo2max improves cardiorespiratory fitness in very
low-fit individuals. In contrast, high- intensity/high-impact exercise in elderly individuals may result
in a significant increase in the incidence of musculoskeletal injuries in addition to greater risk of
cardiovascular complications.

Duration and Frequency: The duration and frequency of exercise should also be modified for
elderly. Interval training (2to 6 min, with 1-min to 2-min rests) is often necessary for these
individuals in both the inpatient and early outpatient phase. As the patient better tolerates the
activity, the exercise time may be gradually lengthened to 30 to 60 min of continuous exercise. The
frequency of exercise should be two to three times a day during the initial stages of the program and
progressed up to 5 times per week when longer durations of exercise can be sustained.

Mode of Training: The types of activities that should be emphasized include those that involve
low impact to feet and legs and a rhythmic use of the large muscles’ groups. Walking, stationary
cycling, and a combination of arm-and leg-work are excellent activities for the elderly patient.
Swimming may be particularly beneficial to patients who, in addition to their cardiovascular
problems, suffer from arthritis or other degenerative bone diseases.

Because muscle atrophy and weakness in the elderly have been linked to recurrent falls (a major
cause of morbidity and mortality), the need for specific resistance and flexibility exercise is often
indicated. Several have shown the feasibility and efficacy of resistance training in the elderly.
• Resistance training includes the same activities as described previously for MI and CABG
patients but is typically performed with lighter weights and up to 15 or 20 repetitions.
The use of variable-resistance machines may be initiated when the patient is clinically stable.
However, because many elderly individuals have a limited ROM, it may be necessary to
double-pin machines thereby-avoiding excessive stress on muscles and joints.
• As with younger patients, the progression of exercise depends on the older adult ‘s initial
level of fitness, medical condition, and need. However, progression is generally slower for
the elderly patient. Warm-up and cool-down periods should be longer.
 • Exercise in hot environments should be avoided, since elderly patients often have
impaired mechanisms of heat dissipation.
• More constant supervision may be needed during ambulation during the early phases of
Cardiac Rehabilitation because of high incidence of orthostatic and subsequent falls.

Patients with Peripheral Vascular Disease

• Patients with PVD are often limited in their ambulation as a result of ischemic pain
(claudication) in the legs. Typically, the pain disappears upon cessation of the activity.
• Recommendations for exercise include both an interval-training method as well as daily
exercise.
• Interval training may consist of several 1 to 5 min bouts of low-level aerobic exercise
followed by 2 to 10 min of rest.
• As the patient progresses, longer periods of aerobic activity should be introduced, until the
patient can sustain 30 to 60 min of continuous aerobic activity.
• Many PVD patients find the RPE scale a useful tool in rating their peripheral discomfort.
Generally, when leg discomfort reaches 13 to 15 on the 15-point category RPE scale,
patients should stop exercising and recover.
• Other investigators suggest continuous exercise at a level slightly below the onset of
significant pain symptoms (grade II, or moderate on the angina scale). A subjective rating of
pain can be made by using the angina scale developed by the ACSM.

Grade I Definite discomfort or pain, but only of initial or modest levels.

Grade II Moderate discomfort or pain from which the patient ‘s attention can be diverted by a
number of common stimuli.
Grade III Intense pain from which the patient ‘s attention cannot be diverted, except by
catastrophic events.
Grade IV Excruciating and unbearable pain

Depending on where the lesion is located, some patients may tolerate cycling better than walking. In
this case a major portion of the exercise session should be performed on the cycle ergometer.
However, because walking remains significant form transportation, some walking is also
recommended. Alternative exercise during phases II and III may include swimming and rowing. The
progression and prescription of exercise during the initial stages of the exercise program should be
guided by the patient ‘s symptoms.
➢ Patients with Left Ventricular Dysfunction

Patients with LVD or CHF were not referred to cardiac rehabilitation programs. However, as a result
of the improved medical management of patients with CHF and recent investigations showing the
safety and efficacy of rehabilitation, more CHF patients are now enrolled in exercise programs. CHF
patient generally has a low functional capacity; investigators have reported a lack of correlation
between exercise time and the degree of LVD. Alterations in peripheral mechanism (impaired
vasodilator capacity of skeletal muscle, reduced aerobic enzyme activity, and increased pulmonary
pressures) play a significant role in these patients marked exercise intolerance. Because of these
peripherical alterations, exercise has been suggested as a therapeutic modality for the CHF patient.

The ACSM provided the following guidelines for exercise prescription for patients with LVD;

In phase I and early phase II, interval training using 2 to 6 min low-level exercise bout interspersed
with 1 to 2 min rests or lower level of training may be an appropriate method of exercise.

• An increase in the frequency of exercise may be required because of the patient ‘s low level of
fitness. Exercise prescriptions for the phase IIprogram should begin with moderate intensities of
40% to 60% of Vo2max or should be adjusted to 10 beats/min below any significant sign or
symptoms (e.g. angina, exertional hypotension or complex dysrhythmias).

• The duration of training should be gradually increases depending on the patient ‘s medical
status and tolerance of the exercise. Because of HR response to exercise in the CHF patient may
be impaired; the use of BP and ECG to monitor exercise may become more important. RPE
responses during exercise should range from 12 to 14, and the use of a dyspnea scale may be
indicated.

• ROM exercise would must often be appropriate with the CHF patient; resistance training and
stair-climbing activities may be contraindicated. Many patients with CHF receive diuretic agents
and other cardiovascular medications to control their condition.

• Chronic diuretic therapy results in alterations of electrolyte balance (hypokalemia and

hypomagnesemia) which may precipitate complex ventricular impairment, patients with CHF
are prone to develop exercise induced hypotension. Therefore, patients with LVD should be
monitored continually and have prolonged warm-up and cool-down periods.

➢ Transplant Patients

• Transplants patients provide challenges to the cardiac rehabilitation staff because of altered
hemodynamic characteristics, acute rejection episodes and markedly reduced exercise capacities.
Their low functional capacity is a result of extended periods of inactivity prior to the surgery, the
surgical procedure (denervation and low hemoglobin), and the use of immunosuppressant
drugs.
• Resting and exercise HRs in the denervated heart are elevated after surgery. The denervated
heart adjusts more gradually to an exercise lead and stays elevated longer during the recovery
period.

• At the onset of exercise, the increase in cardiac output (Q) is primarily the results of an increase
in SV augmented by the Frank-Starling mechanism. Later increases are mediated by greater
levels of circulating catecholamines.

• The impatient exercise program for the transplant patient usually starts 3 to 7 days after surgery.
The progression of the patient is usually slower, with the speed of ambulation or stationary
cycling and repetitions of ROM activities lower than for the CABG patient.

• The prevalence of rejection in the first 3 months after surgery may require the inpatient to
exercise during the low-traffic hours of the day to avoid unnecessary contact with patients,
visitors and medical staff. As a result of the slower HR response, transplant patients require a
longer warm-up period, and a more gradual increase in workload is necessary.

• Exercise prescriptions in the Phase II and III programs include a frequency and duration of
training of 3 to 5 days/week for 30 to 60 min/session. Since the HR response to exercise is
altered in the denervated heart, the use of the standard HR methods of exercise prescription
may not be appropriate. Therefore, exercise intensity should be based on the patient ‘s VO2max.
Generally, the intensity is set at 60 to 70 of the maximal METS ‘s achieved on an SL- GXT
performed after the first 4 to 6 weeks of rehabilitations. As for the patients with LVD, the use of
the RPE scale for the transplant patient is important. With the help of this scale, the exercise
prescription based on the patient ‘s maximal MET capacity can be fine-tuned.

Special points
• Stratification based on the patient ‘s prognosis for future cardiovascular events and rate of
survival during the first year following an MI or CABG is crucial. Patient stratification is a
major determinant of the design of each patient ‘s program in regard to the appropriateness
of training; the type, duration, and intensity of the exercises prescribed; and the level of
medical monitoring and supervision needed.

• Standards for exercise prescription for each phase of rehabilitation have been recommended
by the AHA, the ACSM and AACVPR. Because of the physical limitations in cardiac
patients, progression of exercise is slower, the intensity lower, the frequency greater, and the
duration longer than in programs recommended for healthy individuals.

• Training programs should be well rounded. Strength training should be included early in the
recovery process (Phase III), so that the patient may be better prepared to carry out work and
leisure activities. Additionally, ROM exercise should be implemented at each phase
rehabilitation, particularly in surgery patients.
 ACTIVITY 16:
DEMONSTRATIONAND PRACTICE OF PHYSIOTHERAPY
EVALUATION IN CARDIAC SURGERIES PRE-OPERATIVE AND POST
OPERATIVE

37
Pre- operative assessment includes:

1) ECG leads –Is the process of recording the electrical activity of the heart over a period of
time using electrode placed on the skin in conventional 12 lead ECG, 10 electrode are placed
on the patient ‘s limb and on the surface of the chest.

2) Echocardiogram –uses standard two dimensional, three dimensional and Doppler

Ultrasound to create image of the heart.

3) Cardiac catheterization –is the insertion of a catheter into a chamber or vessel of the heart.
This is done both for diagnostic and interventional purposes.

4) PFT –The primary purpose of the PFT is to identify the severity of pulmonary impairment.
PFT has a diagnostic and therapeutic role and help clinician answer some general question
about patient with lung disease.

5) 6-minute walk test –it is a pulmonary function test in which the distance a patient can walk
over a 6-minute period is measured, usually including pulse oximetry. Used for prognosis,
diagnosis, and response to therapy.

6) Endotracheal tube – is a catheter that is inserted into trachea for the primary purpose of
establishing and maintaining a patent airway and to ensure the adequate exchange of oxygen
and carbon dioxide.

7) Central lines - A central venous catheter also called a central line is a thin long flexible tube
used to give medicines, fluids, nutrients or blood products over a long period of time usually
several weeks or more. A catheter is often inserted in the arm or chest through skin into a
large vein.

8) Nasogastric tube - A nasogastric tube is a narrow bore tube passed into the stomach via the
nose. It is used for short- or medium-term nutritional support, and also for aspiration of
stomach contents - e.g., for decompression of intestinal obstruction.

9) Drains – A surgical drain is a tube used to remove pus, blood or other fluid from a wound

10) Peripheral lines –Peripheral line is a catheter placed into a peripheral vein in order to
administer medical or fluid. Upon insertion, the line can be used to draw blood.

11) Urinary catheter – It is inserted into a patient’s bladder via the urethra. Catheterization
allows the patient’s urine to drain freely from the bladder for collection.

12) Rectal temperature probe

Post-operative assessment includes:

1) Type of operation

38
 a) Pneumonectomy: The entire lung is removed.

b) Lobectomy: Any of five lobes may be removed

c) Segmental resection: A broncho-pulmonary segment is removed with its segmental artery

and bronchus

d) Wedge resection: This non-anatomical resection is used for diagnosis in open lung biopsy
and treatment of well-localized peripheral carcinomas in patients withreduced lung function.

2) Incision:

Incision used in open heart surgery:

a) Vertical approach: median sternotomy is probably is probably the commonly usedanterior

incision.

Fig 16.1Vertical approach

b) Transverse approach: this is sub-mammary and bilateral, through the 4thintercostal spaces
and a transversely divided sternum

Fig 16.2 Transverse approach

39
3) Chest radiograph: The chest x-ray is the most commonly performed diagnostic x-ray
examination. A chest x-ray produces images of the heart, lungs, airways, blood vessels and the
bones of the spine and chest.

4) Body temperature: It’s the degree of heat maintained by the body or it’s the balance between
heat produced in the tissues and heat lost to the environment. (normal: 37 degrees Celsius).

5) Pulse rate: The rate of the arterial pulse usually observed at the wrist and stated in beats per
minute.

6) Respiratory rate: normal: 14-20 breaths/minute [Adults]

30-60 breaths/minute [new born]

20-40 breaths/minute [early childhood]

15-25breaths/minute [late childhood]

7) Blood pressure: lateral pressure exerted by flowing blood on arterial wall.

Normal [systolic: 110-130]/[diastolic:60-90]

8) Heart rate: A measure of cardiac activity usually expressed as number of beats per minute.
Normal heart rates at rest:

• Children (ages 6-15) 70-100 beats/minute

• Adults (ages 18 and over) 60-100 beats/minute

9) SpO2: Oxygen saturation is defined as the ratio of oxy-hemoglobin to the total concentration of
hemoglobin present in the blood (i.e. Oxy-hemoglobin + reduced hemoglobin).

Normal: 97%-99% [in health individual]

10) Drug chart

11) Fluid chart

12) Oxygen therapy

13) Drains:

• The amount of fluid drained

• Whether or not there is an air leak

• Whether on or off suction

• In off suction, whether or not the drain is swinging.

40
 Table 16.1: Recent evidences:

Journal/ Title Methodology Finding

Author/
ImpactFactor
Anaesthesia A randomised Prospective, pragmatic, Primary outcome: No
Akowuah et controlled trial of parallel-group, randomised significant difference in
al., 2021 prehabilitation in controlled trial conducted 6MWT between groups (p
I.F- 7.5 patients at a single NHS tertiary = 0.503). Secondary
undergoing institution; patients outcomes: Significant
elective cardiac scheduled for elective improvement in maximal
surgery cardiac surgery were inspiratory pressure (p =
randomly allocated to 0.002 at 6 weeks and p =
either prehabilitation or 0.001 at 12 weeks) for
control group; primary prehabilitation group; no
outcome was functional significant improvement
exercise capacity (6MWT) in sarcopenia, quality of
and secondary outcomes life, or anxiety/depression
included inspiratory muscle scores. No safety
strength, sarcopenia, concerns were reported.
quality of life, anxiety,
depression, and safety
outcomes.
Annals of The effect of Randomized controlled The intervention group
Saudi preoperative chest study conducted at Pécs showed significantly
Medicine physiotherapy on Clinical Centre, Hungary better respiratory function
Hadel oxygenation and (2019). The intervention and oxygen saturation
Shahood et al. lung function in group received preoperative levels post-surgery
IF: 1.5 cardiac surgery chest physiotherapy, while compared to the control
patients: a the control group only group. The intervention
randomized received postoperative group also had a
controlled study physiotherapy. significantly shorter
Measurements of FVC, hospital stay.
FEV1, and oxygen
saturation (SpO2) were
taken preoperatively, and
for 7 consecutive days
postoperatively.

41
 ACTIVITY 17:
DEMONSTRATIONAND PRACTICE OF COMA PATIENTS
EVALUATION MANAGEMENT

42
Coma is a state of unarousable unresponsiveness. Alteration of arousal is a spectrum of
abnormalities that range from being alert to unresponsive (comatose). It is an acute, life-threatening
situation. Evaluation must be swift, comprehensive, and undertaken while urgent steps are taken to
minimize further neurological damage.

➢ Assessment of Coma patient comprises:

History—through friend, family or emergency medical personnel

General physical examination-
• Skin: (for example, rash, anemia, cyanosis, jaundice)
• Temperature: (fever-infection /hypothermia-drugs/circulatory failure)
• Blood pressure: (for example, septicemia/Addison's disease)
• Breath: (for example, fetor hepaticus)
• Cardiovascular: (for example, arrhythmia)
• Abdomen: (for example, organomegaly)

Neurological assessment

Fig 17.1 level of consciousness scales

43
Table 17.1 Neurological examination

Motor function Respiratory pattern

Motor response Cheyne Stokes: hemisphere Bilateral hemispheric lesions
-Increased intracranial pressure Cardiopulmonary
dysfunction
Deep tendon reflexes Central neurogenic hyperventilation
-Brain stem lesion
Muscle tone Ataxic breathing
-rapid/midbrain
-medullary lesion
Plantar Apneustic breathing:
-Rapid with pauses/lower,
- lower pontine tegmentum/ cervico medullary junction
Slow regular breathing
–Drug intoxications
-Severe hypothyroidism

Cranial Nerve findings

Pupil
• Size, shape, equality/symmetry and reactivity
• Eye movements
• Position at rest (nystagmus)
• Oculocephalic movements
• Cold caloric testing

Motor Examination:
• Observation
• Muscle tone
• Response to stimuli
• Decorticate posturing
• Decerebrate posture

Signs of Herniation in Coma

• Abnormal respiration
• Fixed or minimally reactive pupils or asymmetric dilated pupil
• Gaze deviation
• Decerebrate or decorticate posturing
• Transient hypertension
• Bradycardia

44
 Fig 17.2: Motor response of coma patient

Management of Coma patients in ICCU:

Initial Treatment:
• Airway Breathing
• Circulation
• ABC - identify and address life threatening inadequacies
• Treat rapidly progressive metabolic disorders -- hypoglycemia
• Evaluate for intracranial hypertension and imminent herniation and treat
Check vitals:
• Respiration
• Pulse, BP
• Temperature

Emergency treatment:
• Maintain ventilation-oxygenation
• Maintain circulation
• Control seizures
• Reduce ICP
• Maintain temperature
• Control hypoglycemia

Maintain ventilation:
• Insert oral airway
• Clean oropharyngeal secretions
• Insert cuffed endotracheal tube, if apnea
• Mechanical ventilation, if apnea
Maintain circulation:
If hypotension (<90mm hg systolic)
• Replace fluid
• Saline if hyperglycemia, or suspected stroke, diabetes occurs
• Dextrose saline or isolate if undiagnosed.
• Vasopressor if low systolic B.P instead of fluid.If Hypertension
• Beta blockers, nitroglycerine.

45
Physiotherapy management for comatose patient
1. Positioning
I. Positioning restore ventilation to dependent lung regions more effectively than PEEP in
unconscious patient.
II. Side lying reduces density in upper most of the lungs
III. Right side lying may be more beneficial for cardiac output.
IV. Positioning affects arterial oxygenation by improving V/Q mismatch.
Chest clearance techniques
1) Chest vibration: helps in moving loosen mucus plugs towards large airways.
2) Shaking: direct secretion towards large airway and stimulate cough.
3) Chest percussion/ clapping: dislodges and loosen secretion from lung.
i) Manual hyperinflation:
• Reverse atelectasis
• Improves oxygen saturation and lung compliance
• Improves sputum clearance
ii) Suctioning
• Secretions are accessible to catheter
• Secretions are detrimental to patient.
• Patient is unable to clear secretion by other means.
Neurophysiological facilitation
• Cutaneous and proprioceptive stimulations increase depth of breathing.
• Hasten the response through neuromuscular mechanism through proprioceptors.
Early mobilization
• Early mobilization starts right away in turning the patient in every 2 hours.
• Activity is required to maintain sensory input, comfort joint mobility.
• Physiotherapy for comatose patients involves moving their limbs and massage. It is
important that their muscles remain strong and that atrophy does not set in. It is also
important to keep their blood circulation going.
• Massaging of muscles also ensures that they will not experience atrophy.
• Compassionate physiotherapists work for hours with comatose patients, massaging their
muscles, exercising them, talking to them and trying to bring them out from their comatose
state.

46
Techniques of coma stimulation:
Approaching the Patient
• Identify yourself
• Talk to the patient slowly, and in a normal tone of voice
• Keep sentences short and give the patient extra time to think about what you've said
Visual Stimulation
• Provide a visually stimulating environment at the bedside, such as colorful, familiar objects,
family photographs (labeled), and TV 10-15 minutes at a time
• Provide normal visual orientation, by positioning patient upright in bed, in the wheelchair,
etc. This also helps decrease complications of prolonged bed rest, such as pressure sores,
breathing problems, osteoporosis, and muscle contractures.
Auditory Stimulation
• Provide regular auditory stimulation at the patient's bedside. All hospital staff should be
encouraged to speak to the patient as they work in the room or directly with the patient.
• Use radio, TV, tape recording of a familiar voice, etc. for 10-15 minutes at intervals
throughout the day
• Direct work to focusing and localizing sound and look for patient's response when youchange
the location of a sound, e.g. call the patient's name, clap your hands, ring a bell, rattle,
whistle, etc. 5-10 seconds at a time.
Smell Stimulation
• Use after shave, cologne, perfume, favored extracts, coffee grinds, shampoo, and favorite
foods
• Provide the stimuli for no more than 10 seconds
• Avoid touching the skin with the scent, because patient may accommodate the scent and be
less responsive to it.
Touch Stimulation
• Tactile input can be faciliatory (encourage a desired response) or inhibitory
(discourage/interfere with a desired response)
• Use a variety of textures, such as personal clothing, blankets, stuffed animals, lotions, etc.
• Use a variety of temperatures, such as warm and cold cloths or metal spoons dipped for 30
seconds in hot or cold water
• Vary the degree of pressure - firm pressure is usually less threatening or irritating to the
patient than light touch. Examples include grasping a muscle and maintaining the pressure

47
 for 3 -5 seconds, stretching a tendon and maintaining the stretch for a few seconds, and
rubbing the sternum.

General management of Unconscious Patient

• Care of pressure area
• Care of the mouth, eyes and skin
• Nutrition and fluid balance
• Care of bowel and bladder
• Monitoring of the CVS
• Control of infection
• Physiotherapy to protect muscle and joints
• Maintenance of adequate oxygenation, if feasible

48
 Table 17.2: Recent Evidences:

Journal/Auth Title Methodology Finding

or/ Impact
Factor
Journal of Early Retrospective study with 56 Early physiotherapy significantly
Chemical Physiothe severe TBI patients divided improved GCS scores in the
Health Risks rapy into experimental and control experimental group (mean change: 5.46
Prasad Sah et Improves groups. ± 1.47) vs. control group (mean change:
al., 2023 Consciou Inclusion Criteria: Severe 1.85 ± 0.84).
IF: 0.89 sness TBI patients with GCS scores No significant difference in GCS
Level in 3–8 and proper assessment. improvement based on diagnosis or
Severe Intervention: Experimental gender.
Traumatic group received 14 days of Importance of early rehabilitation for
Brain physiotherapy; GCS measured severe TBI recovery, with individualized
Injury on Day 1 and Day 14. approaches based on specific injuries.
Patient Analysis: Statistical analysis
using SPSS 25; ANOVA for
relationship assessment.
Exclusion Criteria: Patients
transferred, those without
consent, inability to undergo
therapy, insufficient records,
or poor follow-up.
Journal of Physiothe The article synthesizes Post-Traumatic Amnesia: Therapy
Physiotherapy rapy existing evidence on during amnesia is feasible, leveraging
Hassett et al., managem physiotherapy for moderate- procedural memory and adaptive
strategies.
2023 ent of to-severe TBI using
Spasticity and Contractures: Serial
IF: 9.7 moderate- randomized controlled trials casting provides temporary range-of-
to-severe (RCTs), systematic reviews, motion improvements; spasticity
traumatic and clinical guidelines. Key treatments, including botulinum toxin-A,
brain tools include the Glasgow yield inconsistent long-term benefits.
injury Coma Scale and Westmead Strength and Mobility Training: Task-
Post-Traumatic Amnesia specific and ballistic resistance training
improve mobility, especially in severe
Scale. It incorporates practical
cases. Overground and treadmill-based
recommendations from walking training are equally effective.
INCOG guidelines and expert Fitness Training: Aerobic programs
opinions. improve fitness and reduce depression,
but long-term benefits remain unclear.
Long-Term Outcomes: Mobility
improves post-rehabilitation, but
inactivity and high-level balance deficits
persist.

49
50
 ACTIVITY – 18

DEMONSTRATION AND PRACTICE OF EVALUATION OF

VENTILATOR DEPENDENT PATIENTS
History taking:

1. Mechanical ventilation may be required due to the dysfunction of one or several body
systems.
2. Pulmonary, cardiac, neurologic, and/or immunologic compromise are among the more
common patient issues found in today’s acute care setting.
3. The patient’s history will provide vital information that, if missed, will result in a delay in
diagnosis or cause further complications.

1. History of pulmonary systems.

1) Determine if there is a history of cough.

2) Sputum production (including color and amount) and progressive or persistent dyspnea
that may worsen with exercise or respiratory infections.
3) Exposure to risk factors such as tobacco smoke, occupational dust, and chemicals, and
smoke from home cooking and heating fuels is an important consideration.
4) The presence of less-obvious occupational exposures such as farming, pharmacy, mining,
or laboratory work.
5) Chronic obstructive lung disease is a major pulmonary cause for mechanical ventilation
and is a priority when formulating a diagnosis.
6) A travel history of the patient (including vaccinations) should also be obtained especially
in the more cosmopolitan areas where foreign travel is common. Travel in third world
countries may lead to exposure to virulent diseases such as tuberculosis and acquired
immune deficiency syndrome.
7) Drug-induced lung disease is a more obscure source of pulmonary dysfunction but is
becoming more common. Drugs such as amiodarone, angiotensin-converting enzyme
inhibitors, aspirin, and chemotherapy agents are only a few commonly used drugs that can
cause a wide range of pulmonary disorders (Ozkan et al.,2001).
2. History of Cardiovascular system

1) Signs and symptoms of cardiac disease including chest pain, shortness of breath, and
peripheral edema are reviewed in history.
2) The subtler signs such as abnormal fatigue (especially in female patients), syncope,
palpitations, and nocturia should also be addressed.
3) History of myocardial ischemia.

4) History of other heart diseases.

3. History of neurological system

1) Neurologic dysfunction can result in the need for mechanical ventilation because
neurologic control of respiration is affected.
2) Questions focused on recent behavioral changes may reveal problem areas.

3) Substance abuse must be explored with the patient and/or family even if questioning may
cause denial or discomfort with the topic.

4. History of immunological system

General signs and symptoms such as fever, chills, night sweats, weakness, and weight gain
or loss could be signs of immunologic compromise and a possible infectious process.

Chief complaints:

1. It is imperative to consider the chief complaint and try to determine a cause-and-effect

relationship. If the main problem is pulmonary in nature, try to determine if the problem is
an upper or lower airway disease process.
2. Upper airway diseases include rhinitis, sore throat, sneezing, nasal obstruction, or even
voice change.
3. With lower airway diseases, the findings include wheezing, pleuritic chest pain, cough,
sputum production, and hemoptysis.
 4. Reactive airway disease would be included here, and measurement of airflow limitation
(pulmonary function tests) may be included in history or may need to be pursued.
5. It is important to determine the major cause for the use of mechanical ventilation because
when there is some reversal of that cause, removal of mechanical ventilation should be
considered.

Observations:

1. Observations for signs of distress

1. The key factor is to observe patient-ventilator synchrony.

2. Is the patient comfortable or agitated and restless?

3. Subtle changes such as accessory muscle use can signal impending respiratory distress. It
is important to remember that the patient was placed on the ventilator to reduce the work
of breathing and should not be displaying any signs of increased work of breathing.
Although usually observed in children, nasal flaring can be an indication of respiratory
distress in adults.
4. The relationship between the chest and abdominal muscles can reveal increased work of
breathing.
5. Paradoxical abdominal movement (retraction during inspiration and protrusion on
exhalation) in the ventilated patient often indicates increased work of breathing and/or
diaphragm muscle fatigue.
6. Diaphragm fatigue can be partially assessed by increased work of the intercostals and
accessory muscles. These signs indicate that the patient and ventilator are not in synchrony,
respiratory distress is present, and intervention is needed.

2. Observations when there are no signs of distress

1. When there is no sign of distress further evaluation should start.

 2. MacIntyre et al recommend that all patients on ventilatory support must be frequently
evaluated for weaning and possible discontinuation.
3. The four criteria to be considered in this assessment are: evidence of some reversal of the
underlying cause of respiratory failure, adequate oxygenation, hemodynamic stability, and
the capability to initiate an inspiratory effort.
4. Signs and symptoms of inadequate oxygenation include agitation, tachycardia, tachypnea,
hypertension, or hypotension. If any of these signs are present, weaning should not be
considered and further evaluation of the disturbance in oxygenation is needed.

Evaluation of Aspiration

1. Aspiration is a major complication with mechanical ventilation and should be a top priority
in the differential diagnostic process.
2. In the absence of medical contraindications, the head of the patient’s bed should be elevated
to a 30 to 45-degree angle to prevent aspiration, especially from enteral feeding.

Evaluations for weaning trials

1. Evaluating the patient during a weaning trial is a common expectation.

2. Spontaneous breathing trials are used when evaluating this patient population.

3. Rapid shallow breathing is among the clinical findings that indicate the patient is going to
fail the weaning trial.
4. Yang and Tobin quantified this clinical finding into an objective parameter known as the
“rapid shallow breathing ratio” which is a simple ratio of the respiratory rate divided by
tidal volume(BOX.1).
5. A value >100 breaths/min/L may indicate that the patient will not tolerate to weaning. This
parameter can be easily calculated and trended to determine improvement and tolerance of
weaning.
 BOX.3.1 (RAPID SHALLOW INDEX)
f/VT
f = frequency or rate
VT = tidal volume in liters (L)
Examples: When the rate is 20 and tidal volume is
400 mL (.4L)
20/0.4 = 50 breaths/min/L
When the rate is 35 and tidal volume is 300 mL
(.3L)

Evaluation of delirium

1. Delirium is another common finding with the mechanically ventilated patient that can
prolong length of stay, increase morbidity and mortality, and impact outcomes. The causes
are multifactorial and can be complicated to correct.
2. Evaluate delirium accurately and consistently.
3. When considering tools to use for this purpose, you should consider the reliability and
validity of the instrument.
4. The Confusion Assessment Method in the Intensive Care Unit (ICU) is a tool that has been
tested and refined over the last decade for its use in critically ill mechanically ventilated
patient population.
5. It incorporates many aspects of delirium including onset of changes in mental status,
inattention, disorganized thinking, and altered level of consciousness. This tool can help
by increasing assessment accuracy and avoiding misleading terms such as ICU psychosis.
Table 18.1
Physical assessment and chest radiograph assessment and their correlation:

1. Auscultation, percussion, and palpation are very important skills when evaluating the
mechanically ventilated patient.
2. Proper assessment of both anterior and posterior lung fields is an essential part of the
evaluation. Because most ventilated patients spend the majority of time in the recumbent
position, failure to examine the dependent areas of the lungs can result in missed findings
(eg, atelectasis, pleural effusion).
3. The chest radiograph will demonstrate loss of lung volume and, in severe compressive
atelectasis, a mediastinal shift. More subtle radiographic signs of atelectasis include
movement of hilar structures and/or fissure toward the collapse and hemidiaphragm
elevation.
4. Another physical finding is a pleural effusion, an accumulation of fluid between the
visceral and the parietal pleura. On exam, a pleural effusion is dull to percussion with
absent breath sounds and auscultation may reveal a pleural friction rub.
5. Radiographic findings of a pleural effusion show blunting or absent costophrenic angles, a
visible meniscus, fluid tracking into the fissure, and an obscure diaphragm.
6. A large pleural effusion may appear as a complete “white out” with mediastinal shift and
complete hemidiaphragm loss. Thoracentesis is warranted if the patient is in distress or if
the cause of the effusion is unknown.
7. Evaluation of congestive heart failure (CHF) or pulmonary edema is necessary in the
mechanically ventilated patient with crackles, dyspnea, distended neck veins, and
orthopnea.
8. The radiograph reveals redistribution of the pulmonary vasculature to the upper lobes,
development of Kerley’s B lines, small right pleural effusion, and engorged pulmonary
arteries (Figure 1).
9. In most cases, the cardiothoracic ratio is increased, an indication of CHF. Symptoms of
CHF may not be realized until weaning from the ventilator because positive pressure
ventilation and positive end-expiratory pressure (PEEP) are responsible for improved
oxygenation by redistributing fluid in the alveoli.
10. Positive airway pressure increases intrathoracic pressure, decreases preload by decreasing
venous return, and increases the pressure gradient between the left ventricle and the extra
thoracic arteries.
 11. When intrathoracic pressures and PEEP are decreased during weaning, development of
CHF symptoms and pulmonary edema may result.
12. It is essential for the APN to monitor signs of fluid overload and pulmonary edema during
weaning trials to judge better extubation success when mechanical ventilation is no longer
needed.

Figure 18.1 A patient with congestive heart failure. Note the engorged pulmonary arteries (arrows),
Kerley’s B lines (block arrows), and an increased cardiothoracic ratio (double headed arrow)

• A systematic approach to the review of the chest X-ray is imperative for practice.
• In addition to anatomical and physiological data, the chest radiograph provides important
information about the technology surrounding the patient including placement of
intravascular lines and artificial tubes such as the endotracheal tube, chest tubes, feeding
tubes, and other technology.
• Careful review of the chest X-ray can serve as a learning mechanism as well as an additional
filter to ensure quality care.

Assessment of mechanical ventilation:

1. Mechanical ventilation can cause lung injury as a result of a combination of high pressure,
overdistention of the alveoli, and repetitive alveolar opening and closing. Overdistention and
cyclic inflation of injured lungs can exacerbate lung injury and promote systemic
inflammation.
2. This injury causes the release of multiple mediators that increase the micro permeability of
the alveolar sacs allowing influx of protein rich fluid, decreased compliance, and increased
lung water. The Acute Respiratory Distress Syndrome (ARDS) Network trial produced
dramatic results that demonstrated a decrease in mortality if smaller tidal volumes were used
(6-8 mL/kg). This simple adjustment in ventilator settings is thought to decrease the
overdistention of the alveoli and lessen ventilator-induced lung injury.
3. As part of the assessment, evaluates tidal volume, compliance, and airway pressures daily in
order to provide protective lung ventilation.
4. The peak inspiratory pressure (PIP) is the maximum pressure during the complete respiratory
cycle and represents the force needed to ventilate the lungs considering airflow resistance
resulting from endotracheal tube size, secretions, and other causes of obstruction. Monitoring
PIP is a valuable tool in early detection of conditions that affect compliance or resistance.
5. When the PIP is elevated, begins data collection and analysis to determine if the source of the
elevated PIP is due to increased airway resistance or decreased lung compliance. Peak
Inspiratory pressure can be an objective outcome measurement of interventions such as
bronchodilator administration or suctioning. Elevated PIPs can cause lung injury and are
monitored closely to follow trends in compliance.
6. Plateau pressure (Pplat) is the end-inspiratory airway pressure. Because this is a static
measurement, resistance in the circuit and airways is negligible and true mean alveolar
pressure is represented. Pplat is typically much higher in patients with decreased compliance
in conditions such as pneumonia, cardiogenic pulmonary edema, acute lung injury (ALI), and
ARDS. The clinical goal is to maintain Pplat<30 cm H2O to limit alveolar lung injury.
7. Compliance is defined as the ease with which the lungs fill with a positive pressure breath
and is expressed in the equation: C=Vt/(Pplat -PEEP). As the lungs become stiff in acute lung
injury and ARDS, the compliance decreases, which requires increased pressure to inflate the
lungs. Reduced compliance results in decreased ventilation. Restrictive lung diseases that
decrease compliance include atelectasis, consolidation, hyperinflation, ARDS, and
pulmonary edema. Elevated PIP and elevated Pplat with a narrowing difference between the
two (Delta PIP - Pplat) indicate decreased compliance.
8. Resistance is the ease with which gases flow through the ventilator system and the lungs.
Secretions, bronchospasm, long ventilator tubing, and narrow ET tubes all increase resistance.
Resistance is measured as pressure overflow (R = pressure/flow).
 An increase in PIP with a normal or low Pplat creates a larger gradient between PIP and Pplat.
This indicates increased airway resistance.
9. Monitors the mechanically ventilated patient for auto-PEEP. Air progressively trapped in the
lungs at the end of exhalation leads to positive alveolar pressure at end expiration. Clinical
situations that lead to the development of auto-PEEP include rapid respiratory rate, prolonged
inspiratory times, limited exhalation time, severe obstruction and small airways collapse. This
increase in pressure can impede venous return to the heart and reduce cardiac output and
pulmonary blood flow. Auto-PEEP can lead to increased work of breathing and cause patient
ventilator asynchrony if the patient is actively trying to exhale as the ventilator triggers.
Allowing longer expiratory times, decreasing minute ventilation and tidal volumes, and
increasing inspiratory flow are the preferred interventions in treating auto-PEEP.

Assessment of vital signs

a) HeartRate

1. Normal adult rate is between 60-100 beats per min (bpm). Heart rate assessment is readily
available on electrocardiograph (ECG)monitor.
2. Tachycardia – in adults is defined as HR > 100 bpm. During mechanical ventilation, some
conditions may increase patient’s HR are enumerated in the table below.
3. Bradycardia – in adults is defined as HR < 60 bpm. It often occurs with vagal stimulation
during endotracheal suctioning. Preoxygenation is often necessary to minimize the
occurrence of arterial desaturation and arrhythmias during suctioning. Since, arterial
desaturation occurs in as little as 5 seconds during suctioning, hypoxia and cardia
Complications can occur rather rapidly. When arterial desaturation occurs, endotracheal
suctioning must be stopped immediately and 100% O2 must be delivered immediate
 Table 18.2 Conditions that affect the Heart Rate
Conditions that may cause Conditions that may cause
TACHYCARDIA BRADYCARDIA
Hypoxemia Sudden hypoxia or vagal stimulation during
endotracheal suctioning
Hypovolemia Inadequate coronary blood flow
Pain Heart block
Anxiety and stress Abnormal SA node function
Fever Hypothermia
Drug Drug reaction

b) Blood-Pressure
1. Continuous BP monitoring in critically ill patients is usually done via indwelling arterial
catheter interfaced with the pressure monitor. Most common insertion site of the catheter is
radial artery. Other sites are brachial, femoral, dorsalis pedis and popliteal artery.
2. Hypertension – it is defined as when BP is higher than the normal limits, may be caused
by acute and chronic patient conditions.
3. Hypotension – is the BP lower than the normal limits. It may be due to absolute hypovolemia
(blood loss), relative hypovolemia (shock), or pump failure (CHF). Hypotension occurring
during mechanical ventilation is often associated with excessive intra-thoracic pressure,
peak inspiratory pressure and lung volumes. Hypotension is one of the complications of
Positive Pressure Ventilation (PPV) or PEEP.
Table 18.3 Conditions that affect the blood pressure:

Conditions that may affect Conditions that affect HYPOTENSION

HYPERTENSION
Fluid overload Decrease venous return due to PPV
Stress Absolute hypovolemia (e.g., blood loss,dehydration)

Anxiety Relative hypovolemia (e.g., sepsis, shock)

Pain Pump failure (e.g.,CHF)
Congestive heart failure
Cardiovascular diseases
Polycythemia (blood viscosity increase)
c) Respiratory frequency

1. Normal spontaneous respiratory frequency for adults is 10-16 breaths per min. An increased
respiratory frequency TACHYPNEA may be an early warning sign of hypoventilation or
hypoxia. In normal individuals, maximum response to hypoxia occurs below a PaO2 of 50
mmHg. If the frequency exceeds 20 bpm and is rising, the patient should be evaluated for the
cause of tachypnea.
2. Tachypnea precedes the development of respiratory failure and the use of mechanical
ventilation; tachypnea is indicative of respiratory dysfunction. When tachypnea’s and low tidal
volume are observed in a patient, successful weaning from the mechanical ventilator is not
likely.
3. Routine monitoring of the respiratory frequency of the patient is a useful method to assess the
pulmonary status of a ventilated patient. This especially holds true in the weaning process. A
sudden increase in spontaneous respiratory frequency during the weaning attempt is indicative
of moderate or severe respiratory insufficiency or hypoxia.

d) Temperature
• It can be measured routinely in intervals or continuously in intensive care settings via rectal,
oesophageal or pulmonary artery catheter.

Table 18.4 Conditions that affect the body temperature

Condition that may cause Conditions that cause

HYPOTHERMIA HYPERTHERMIA
Infection CNS problems
Tissue necrosis Metabolic disorders
Leukemia Drugs and toxins
Increase metabolic rate Induced coronary bypass surgery
Head injury
Motor assessment:

• Passive range of motion.

• Active assisted range of motion.
• Active range of motion
• Manual muscle testing

Sensory assessment:

• As with other aspects of the neurological examination, if abnormal findings or specific

symptoms then more detailed testing is indicated.

• Testing for pain sensation is best done by double simultaneous stimulation (as for trigeminal
nerve)

o To exclude CNS lesions, if testing on dorsum of hands & feet is normal no further
testing for pain is needed

• Double simultaneous stimulation with gauze or wisp of cotton wool can be used to

o Light touch is usually spared in unilateral spinal cord lesions

• Testing for :

o 2-point discrimination with paper clip ends, normal is 2-8mm on fingertips & up to
75mm on upper arm &thigh

• Proprioception is the most sensitive & easiest test for post. column pathway deficits move
great toe up or down & ask patient which way you moved (upper limb not usually needed to
be tested)

• Stereognosis is dependent on touch & position sense as well as post. column & sensory cortex
function:
 o Ask patient to identify a familiar object placed in palm (eg. key or paperclip)

• Vibration sense is often the 1st sensation lost in peripheral neuropathies such as alcoholism
or diabetic:

o Place vibrating tuning fork over DIP joint of a finger & the great toe, ask patient to tell
you when vibration disappears.
o If sense is absent, move to a more proximal joint

Assessment of reflexes:

1. Document as: 0 = absent; 1+ = diminished; 2+ = normal; 3+ = hyperactive; 4+=

hyperactive with clonus.
2. Symmetric hyporeflexia may be normal or due to sedation,hypercalcaemia
3. Asymmetric reflexes indicate neurologic or muscular dysfunction.
4. To evaluate the L4-5 nerve root (as in disc prolapse) test power of extensor hallucis
longus
5. +ve Babinski reflex (up-going plantar reflex) indicates an upper motor neuron lesion
6. Reflexes and their spinal cord levels

Coordination and balance assessment:

Cerebellar function:

• Place finger on nose test with each hand & eyes closed (or finger to examiner's finger
then to pt's nose, eyes open)
• Heel-to-shin testing with each leg (ankle to knee and backa gain)
• Rapid alternating movements eg. touch each fingertip with thumb; supinate/pronate hand;
tap floor with foot;
• Balance is a function of vision, vestibular sense and proprioception, 2 must be intact to
maintain balance:
• Romberg test - stand with feet together
 • Patient with vestibular deficit will report vertigo
• Close eyes if proprioceptive deficit, patient will sway ⇒ +ve Romberg's
• Tandem gait (heel-toe walking) is sensitive but not specific test of balance.

Assessment of laboratory data:

1. Fluid balance and anion balance

Mechanical ventilation may affect the patient’s renal function and fluid balance. As the fluid and
electrolyte concentrations are related, the anion gap may also be affected as a result of positive
pressure ventilation.

a) Fluid balance

Normal urine output is 50-60 milli L per hour. Urine output of below 20 milli L / hr is indicative
of fluid deficiency. Oliguria may be seen after bleeding diarrhoea, renal failure, shock, drug
poisoning, deep coma, or hypertrophy of the prostate.

b) Anion gap
Anion gap is the difference between cations (positive ions) and anions (negative ions) in the
plasma. The normal range is 15-20 when K+ is included in the calculation.
Anion gap = Na+ - Cl- -
HCO3 Normal range = 10-
14 mEq / L Or
Anion gap = Na+ + K+ - Cl- -
HCO3 Normal ranges = 15-20
mEq / L

c) Metabolic acidosis and anion gap

It is the presence of normal anion gap is usually caused by the loss of base. This condition is
called hyperchloremic metabolic acidosis because it is usually related to excessive chloride ions
in the plasma. Metabolic acidosis in the presence of increased anion gap is due to the increased
fixed acids.
 d) Respiratory compensation for metabolic acidosis
In mechanically ventilated patient’s metabolic acidosis, hyperventilation may occur as
compensation for metabolic acidosis. So, it must be identified and corrected and should not
assume that respiratory insufficiency is present.

e) Metabolic alkalosis

It’s important to monitor patient’s potassium levels during mechanical ventilation. Severe
potassium depletion can lead to metabolic alkalosis and compensatory hypoventilation.

2. Arterial blood gases:

ABGs provide useful information about a patient’s ventilation, oxygenation and acid base status.

Table 18.5: Blood gas parameters and normal ranges for adults

Parameters Monitoring Normal

PaCO2 Ventilatory status 35-45 mmHg
PaO2 Oxygenation status 80-100 mmHg
PH Acid-base status 7.35-7.45

Table 18.6: Interpretation of oxygen status

Parameters Criteria Interpretation

PaO2 80-100mmHG Normal
60-79mmHg Mild hypoxemia
40-59 mmHg Moderate hypoxemia
<40mmHg Severe hypoxemia
PaO2 / FiO2 <300 mmHg (PCWP < Acute lung injury (ALI)
18mmHg) ARDS
<200mmHg (PCWP <
18mmHg)
P (A-a) O2 Room air Should be less than 4 mmHg for
100% O2 every 10 years of age otherwise
hypoxemia
Every 50mmHg difference
approximates 2% shunt
PaO2/ PAO2 FiO2> 30% >75% Normal
<75% hypoxemia
3. Assessment of ventilator status

• Ventilation is defined as the movement of gases in and out of the lungs and is another common
parameter for evaluation of mechanical ventilation. The partial pressure of carbon dioxide
(PaCO2) found in an ABG is the gold standard used to assess ventilation.
• However, end-tidal CO2 (PetCO2) monitoring using capnography assesses ventilation and is
frequently used with mechanical ventilation. End-tidal CO2 monitoring may be indicated:
1) For monitoring the severity of pulmonary disease and evaluating response to therapy,

2) as an adjunct to determining the tracheal rather than esophageal intubation, and

3) for monitoring adequacy of pulmonary, systemic and coronary blood flow.

• The capnogram (graphic display of end-tidal CO2 monitoring) may be useful in detecting
obstructive pulmonary disease. The major limitation of end-tidal CO2 monitoring is frequent
calibration due to moisture in the ventilator circuit that can distort the value.

4. Complete blood test(CBC)

• The hemoglobin and hematocrit reflect oxygen-carrying capacity and need to be

monitored.
• More conservative use of blood and blood products has been recommended in recent years
due to increased mortality related to multisystem organ dysfunction and the systemic
inflammatory response syndrome.
• Ventilator-associated pneumonia (VAP) is pneumonia that occurs after 48 hours of
mechanical ventilation and is suspected with new or progressive fever, increased white
blood count, and purulent secretions.

5. Electrolyte Assessment

Electrolytes are also important to maintain proper muscle function, especially the diaphragm.
Phosphorus is particularly important to the function of the diaphragm and is monitored regularly
in patients receiving ventilation.
Maintaining proper nutrition is the most efficient method to keep phosphorus and other
electrolytes at adequate levels.
6. Sputum Assessment

Changes in the color or consistency of the sputum are considered to be an indicator of pneumonia.

7. Broncho-alveolar Lavage:

• Early in the work-up of VAP, airway secretions are obtained for culture and gram stain by
bronchoalveolar lavage (BAL) or by blind bronchial suctioning(BBS).
• The culture and gram stain may give sufficient information to identify bacteria, but different
techniques may be needed. BAL allows deep suctioning for quantitative sputum cultures and
is generally safe for patients on the ventilator.
• However, the costs associated with performing a BAL and evidence showing that BBS is as
sensitive as bronchoscopic sampling has increased the amount of noninvasive sampling to
detect VAP.

Physiotherapy management of mechanically ventilated patients and physiotherapy treatment

plans :

General goals

Weaning from mechanical ventilator and restoration to maximal functional level of activity.

Specific goals

Maintaining and improving muscle strength, endurance, joint range of motion and secretion
clearance.

Other goals

• Prevention and treatment of atelectasis and skin breakdown and maintenance of homeostasis.
• Psychological support and education to patients and family in selfcare and home activities is
additional consideration.
• The treatment program should be dynamic and flexible, responding to the patient’s needs as
ascertained through a thorough and continuing evaluation.
• Specific physiotherapy procedures may include, but are not limited to, breathing-retraining
exercises, postural drainage and manual techniques, range of motion and strengthening
exercise and ambulatory activities.
1. Breathing-retraining exercises(BRE)

• The purpose of breathing-retraining exercise (BRE) for the ventilator-dependent patient is to

maintain or improve muscle endurance, strength, coordination and rhythmicity. Although
BREs cannot be performed by all patients being mechanically ventilated, they are performed
with many. The type and appropriateness is depend on patient’s degree of respiratory failure,
associated complications and mode of ventilator.
• Coordination of breathing exercises and mechanical ventilator.

• For a better understanding of how breathing retraining exercise can be used during mechanical
ventilator, the types or categories of ventilators, the modes of ventilation, and use of positive
end expiratory pressure is essential for cardiopulmonary physiotherapists.

Deep breathing

• It is an attempt to utilize all inspiratory muscles to produce a maximum breath. It is depend

on the mode of ventilation and degree of patient’s spontaneous breathing.
• A pressure limited ventilator will permit the patient to take deep breath because the breath is
limited by the preset pressure of the ventilator. With volume or time limited ventilator, the
breath is limited by the predetermined volume limit, inspiratory time and flowrate.
• Patient receiving IMV can take deep breaths, if the IMV rate is not too high. If the rate is high,
the short-term interval between mechanical breath before the next ventilator breath
automatically occurs.
• However, SIMV permits enough time for a deep breath. Like diaphragmatic breathing
exercises, it do not perform continuously. A program of 5-10 breaths. 2-3 times a day, can be
utilized. Measurement of vital capacity with spirometer at bedside provides a form of
biofeedback.

Segmental breathing

• Emphasis specific area of chest wall during a deep breath. The anterior-apical and lateral-
basilar areas of the chest wall usually move freely with deep inspiratory efforts. The
therapist’s hands are placed over these areas, unilaterally or bilaterally, and the patient is
 instructed to inhale deeply, pushing the chest wall up against the pressure provided by the
therapist’s thumb. This manual pressure is not sustained throughout the inspiratory effort but
is released gradually as the patient continue with inspiration.
• A method of “quick release” ,however, utilizes constant pressure during inspiration with rapid
removal of the pressure at the end of the breath. This technique may facilitate a deep breath
and may locally alter intrapleural pressure causing expansion of lung segments.

• Another method is “quick stretch” a quick stretch stretching the chest wall at end expiratory
effort. It required patient and therapist excellent coordination. A pressure limit ventilator that
cycle “off” when a predetermined pressure is reached is the most compatible with this
facilitating technique. The volume-limited or time-limited ventilator permits increased
inspiratory efforts and chest wall excursion. However, the volume of each spontaneous breath
is limited by the preset volume limit of the ventilator. Patient receiving IMV mode of
ventilation can achieve greater volumes during spontaneous phase of IMV. However, they
can receive only the predetermined volume during the mechanical breaths, unless the
ventilator pressure is limited. Whatever mode or type of ventilation the patient is receiving,
segmental breathing should be attempted.
• Segmental breathing used with chest wall stretching and inspiratory muscle facilitating
techniques will help maintain chest wall compliance and accessory muscle strength.

Abdominal breathing

• Emphasis active expiration for patients who have paralyzed or extremely weak diaphragms,
but good accessory and abdominal muscle contraction to increase intraabdominal pressure
• .This increase pressure “pushes” the diaphragm to usually high position in the thorax. When
intraabdominal pressure is reduced, the diaphragm passively passively “falls” to produce
inspiration. The accessory muscles can assist with this inspiratory effort to produce a greater
tidal volume. This type of breathing can be performed mechanically with type ventilator
called “pneumo belt”.
Disadvantages:

1) Conscious effort is necessary to breath.

2) Patients must be in upright position to provide, using gravity, the maximum excursion of
the diaphragm.
 Abdominal pursed lip breathing

• Commonly used for patients with small airway diseases, e.g., emphysema. Permits patient to
maintain small airway patency during expiration by control resistance at the lip.

• It is not practical when the patient is intubated but may be useful during weaning when the
patient can breathe spontaneously through the mouth. A valve to increase the resistance in
the expiratory circuit to the ventilator can provide the purse-lip effect.

2. Chest physiotherapy

• Chest physiotherapy (CPT) is acclaimed as an important constituent of respiratory care in all

mechanically ventilated (MV) critically ill patients, even in the absence of primary or
significant lung disease (Clini et al 2005). Tracheal intubation indeed seriously impairs cough
reflex and mucociliary escalator function leading to sequestration and impaction of secretions
in the lower airways. This exposes MV patients to severe lung complications [i.e., ventilator-
associated tracheobronchitis, ventilator-associated pneumonia (VAP), and lung atelectasis],
prolongs the weaning process, and may increase mortality (Pneumatiko et al., 2009).
• One of the key tasks of the intensive care unit (ICU) physiotherapist in MV patients is to
facilitate removal of retained or profuse airway secretions aiming to reduce airway resistance,
optimize lung compliance, and decrease the work of breathing. For this purpose, the ICU
physiotherapist disposes of a diversified armamentarium of breathing methods, manual
techniques, and mechanical devices, used alone or in combination (Volsko et al., 2013).
• In spite of this theoretical benefit, CPT practice for this indication is far from standardized
varying from as-needed airway suctioning over a more intricate “multi- modality” approach
to physiotherapist-driven manipulation of the ventilator. Also, the incessant call for
protocolized medicine (e.g., creation of unit-specific VAP prevention “bundles”) as well as
concerns regarding medicolegal responsibilities must be considered when defining the role of
such “routine” daily physiotherapy (Herbetetal et ., 2017).
What are the principles, expected benefits, risks, and points for attention of the different CPT
techniques used in MV patients?

• All CPT techniques aimed to dislodge secretions and to facilitate their transport in and
removal from the airways. Body positioning and chest mobilization included frequent posture
changes, maintenance of a 30° upright position most of the time, in-bed rotations, proper chest
alignment, and passive range-of-motion limb exercises.
• Another major CPT goal was to improve gas exchange and oxygenation by enhancing
alveolar ventilation, augmenting ventilation/perfusion matching, and redistributing body
fluid on a gravitational basis. Standardized protocols for chest mobilization, however, do not
exist.
• Manual lung hyperinflation (aka “bagging” or “bag-squeezing”) promotes alveolar
recruitment by delivering larger than baseline and peak pressure-limited tidal volumes,
thereby enhancing lung compliance and gas exchange. It is also suggested that it mimics a
cough so that airway secretions are mobilized towards the larger airways (Paulus et al., 2012).
• IPV physiotherapy creates a convective gas front to the distal airways by delivering very
small bursts of tidal volume within a frequency range of 60 to 600 cycles/minute. As such,
temporary alveolar recruitment and ventilation is provided while mucus is cleared from
middle-sized airways and propelled cephalad by generating peak expiratory flows that largely
exceed inspiratory flows (Kallet at al., 2013). The effect of IPV is enhanced by adding
assisted autogenic training whereby secretions are loosened and collected at low to mid lung
volumes and subsequently expelled by the IPV expiratory flow. IPV was found to be as
effective as “standard care” CPT for improving lung function and enhancing sputum
expectoration in ambulatory older children and adults with cystic fibrosis (Varekojis et al .,
2003). ICU patients thought to benefit from IPV are those with relapsing atelectasis,
“copious” secretions, or inhalation injury.
• As long as the patient’s hemodynamic and respiratory parameters are stable before the start
of CPT, all manual techniques can be safely applied.
• Intensive chest mobilization may occasionally be complicated by endotracheal tube or
intravascular catheter disconnection, hemodynamic intolerance, increased intracranial
pressure, and cardiac arrhythmias. Manual hyperinflation and IPV physiotherapy involve
disconnecting the patient from the ventilator. Both techniques might significantly interfere
with currently used sedation and ventilation protocols and methods (e.g., low level sedation,
 sedation breaks, gas anesthesia, low tidal volume/high PEEP ventilation). Possible
physiological side effects of delivered air volume, flow rates and airway pressure must be
carefully considered. IPV, in particular, is expensive and handling requires good knowledge
of respiratory (patho)physiology because the patient is placed on a dedicated “high-frequency
ventilator” device. Driving pressure must be set appropriately and adapted to the patient’s
chest excursion. During IPV physiotherapy, the patient’s heart rate, respiratory rate, blood
pressure, pulse oximetry and end-tidal CO2 must be observed closely for signs of intolerance.
• Supplemental oxygen must be provided if needed. To minimize the risk of barotrauma, a
pressure pop off must be utilized and peak airway pressures carefully monitored. Performing
IPV on a 24/7 basis is labor-intensive and necessitates a skilled physiotherapist team
operating under close supervision of ICU physicians.
• CPT-induced changes in the patient’s general, hemodynamic or respiratory condition must
be immediately notified and anticipated conveniently.
• Specific contra-indications for any form of CPT are undrained pneumothorax, shock or severe
hemodynamic instability, recent pulmonary surgery, hemoptysis or active pulmonary
hemorrhage, unstable chest wall (e.g., multiple rib or vertebral fractures), acute
bronchospasm, and increased intracranial pressure.

3. Early mobilization

Early mobilization includes activities such as sitting, standing and ambulation, as well as passive
exercises, like range of motion exercises and ergometry (Moris et al 2008, Schweickert et al 2009,
Burtin et al., 2009).
The term “early” has yet to be defined, since among the various studies, the onset of interventions
may vary by as much as 1 week (Denehy et al., 2013; Moss et al., 2016).

Mobilization in the intensive care unit (ICU) is generally considered early. After the report by
Schweickert et al. (2009), of the effectiveness of early rehabilitation interventions on the physical
and mental functions of mechanically ventilated patients, several studies have reported similar n
results in patients hospitalized in the ICU. However, studies of active mobilization beyond the
sitting position are few (Nydahl et al., 2014, Berney et al., 2013) and a consensus has been reached
with respect to neither the timing of “early mobilization” (Yusuda et al., 2016) nor the prescription
of standardized interventions.
 Effectiveness of early mobilization:

• In a landmark study, Schweickert et al. (2009) randomly assigned 104 mechanically ventilated
patients to early physical and occupational therapy versus usual care, compared the
proportions of patients in each group who returned to independent functional status at the
time of discharge from the hospital.
• An independent functional status at hospital discharge was regained by 59 % of patients in
the intervention group, in whom early mobilization began at a mean of 1.5 days after the onset
of mechanical ventilation, compared with 35 % of patients in the control group in whom early
mobilization began at a mean of 7.4 days(P=0.02).
• Patients in the early mobilization group also suffered from shorter periods of delirium and
required fewer days of recurrent mechanical ventilation than the control group during 28 days
of follow-up.
• ICUAW is a common complication of critical illness, affecting limb and respiratory muscles,
and is associated with weaning failure (Hermans et al.,2014). Additional reasons for
ineffective cough include the cumulative effects of sedation as well as lack of patient co-
operation or effort (Smina et al ., 2003) that may be the result of delirium or cognitive
impairment, both of which are highly prevalent in the critically ill population (Ouimet et al .,
2007; Pandharipande et al ., 2013).
• Moreover, effective cough requires closure of the glottis which is prevented during
endotracheal intubation or by glottic muscle weakness (Smina et al ., 2003). Ineffective cough
leads to secretion pooling, atelectasis and respiratory tract infection which may result in
weaning failure and the need for reintubation (Goncalves et al., 2012; Salam et al.,2004;
Smina et al., 2003). Suctioning of the trachea via the endotracheal tube, may also impair
mucociliary function, and is ineffective for clearing the peripheral airways (Nakagawa et al .,
2005), further contributing to secretion pooling.

4. Cough augmentation techniques

It comprises:
1. Lung volume recruitment, (also termed air-stacking or breath-stacking),
2. Manually assisted cough,
3. and mechanically assisted cough using a mechanical insufflation-exsufflation (MI-
E)device
Lung volume recruitment (air-stacking or breath-stacking)
During lung volume recruitment, the patient inhales a volume of gas via the ventilator, or self
inflating resuscitation bag adapted with a one-way valve to facilitate gas holding. The patient
retains the inhaled volume by closing the glottis, inhales another volume of gas and then again
closes the glottis; this process is repeated until maximum insufflation capacity is reached (Toussaint
et al., 2009). Lung volume recruitment can be performed in isolation or in combination with
manually assisted cough.

Manually assisted cough

Manually assisted cough consists of a cough timed with an abdominal thrustor lateral costal
compression once maximal air-stacking is achieved and timed to glottic opening (Bach et al.,
2012).

• Costophrenic assist.
• Hemlich type (Abdominal ThrustAssist).
• Anterior chest compression assist.
• Counter rotation assist

Mechanically assisted cough using a mechanical insufflation-exsufflation (MI-E) device.

• MI-E devices such as the CoughAssist™ (Philips Respironics Corp, Millersville, PA)
alternate the delivery of positive (inflation) and negative pressures (rapid deflation) delivered
to the patient via an oronasal interface, mouthpiece, endotracheal or tracheostomy tube (Bach
et al., 2013).
• Alternation of pressure maybe manually or automatically cycled. MI-E comprises a deep,
pressure-targeted lung insufflation aimed at expanding the lungs to approximately 90% of
capacity (Gomez-Merino et a ., 2002). Insufflation is followed by vacuum exsufflation
enabling lung emptying and increasing peak cough flow. Pressures of 40 mmHg (insufflation)
to -40 mmHg (exsufflation) (54 cmH2O) are usually most effective and best tolerated by the
patient (Bach et al., 2014). Due to pressure drop off and reduced airflows, when applying
MI-E via an endotracheal or tracheostomy tube, the cuff should remain inflated and pressures
of 38 mmHg to 51 mmHg (50 cmH2O to 70 cmH2O) can be used, depending on patient
tolerance (Bach et al., 2014).
 • The duration of insufflation and exsufflation should enable maximum chest expansion and
rapid lung emptying, with two to four seconds used for adults (Bach et al ., 2010) and shorter
durations for children (Chen et al., 2014). Treatments usually comprise three to five
insufflation-exsufflation cycles followed by a short period of rest to avoid hyperventilation
Bach et al., 2012). Treatments can be repeated until no further secretions are expectorated.
MI-E can be performed in isolation or in combination with manually assisted cough.

How the intervention might work?

• The increased lung volumes generated via lung volume recruitment increase elastic recoil,
thereby increasing peak cough flow and promoting sputum expectoration (Kang et al ., 2000).
• Manually assisted cough further enhances peak cough flow, particularly for patients with
weak expiratory muscles (Kirby et al.,1966). MI-E has been shown to produce a higher peak
cough flow when compared with manual techniques (Bach et al., 1993).
• Additionally, routine suctioning does not reach the left main stem bronchus approximately
90% of the time (Fishburn et al., 1990), whereas MI-E provides the same exsufflation flows
in left and right airways, enabling more effective secretion clearance (Garstang et al., 2000).
• Multiple, primarily observational studies over the last two decades suggest that cough
augmentation techniques are safe and efficacious in managing exacerbation of respiratory
failure due to infection in patients with neuromuscular disease or spinal cord injury in the
community or long-term care setting (Bach et al., 1993; Kang et al.,2000; Kirby et al., 1966).

1. Endurance and resistance training:

• Early exercise rehabilitation of mechanically ventilated (MV) patients has been shown to be
safe and feasible. Benefits of exercise rehabilitation in MV patients in the ICU include shorter
ICU and hospital length of stay, reduced days on the ventilator, increased peripheral and
respiratory muscle strength, and increased health related quality of life (Kayambu et al.,
2013).
• Barriers to exercise in the ICU have been described as being structural, cultural or patient-
related (Dubb et al., 2016). Pain, clinical stability and level of cooperation are examples of
patient related barriers; while structural barriers can include staff experience, time constraints
or equipment issues. Cultural barriers relate to attitudes or protocols that may exist in the ICU
 (Dubb et al., 2016).

• Hodgson et al. ( 2014 ) found that the most commonly reported barriers to early exercise in
MV patients were intubation with an endotracheal tube and sedation. While consideration of
potential risks versus the possible benefits of exercise rehabilitation of MV ICU patients is
important, undue concerns regarding adverse events may lead to exercise rehabilitation being
withheld or delayed unnecessarily.

2. Inspiratory muscle training:

• More recently, it is increasingly apparent that diaphragm dysfunction is present in a high

percentage of critically ill patients and is associated with increased morbidity and mortality.
Mechanically ventilated patients, diaphragm weakness is thought to develop from disuse
secondary to ventilator-induced diaphragm inactivity and as a consequence of the effects of
systemic inflammation, including sepsis. This form of critical illness acquired diaphragm
dysfunction impairs the ability of the respiratory pump to compensate for an increased
respiratory workload due to lung injury and fluid overload, leading to sustained respiratory
failure and death. (CHEST 2018)
• Inspiratory muscle training applies a load to the diaphragm and accessory inspiratory muscles
to increase their strength and endurance. Trials of inspiratory muscle training in the ICU have
typically applied this load via devices that impose resistive or threshold loads, or via
adjustment of the ventilator sensitivity so that patients can only initiate inspiratory flow by
generating more negative intrathoracic pressure (Moodie et al., 2011).
• Inspiratory muscle strengthening that is achieved by threshold pressure training or ventilator
sensitivity adjustment can have significant benefits for patients weaning from mechanical
ventilation in ICU. These benefits include an improved breathing pattern, more successful
weaning, potential reductions in length of stay, and briefer use of non- invasive ventilatory
support after extubation. These benefits are achieved safely when the training is applied to
appropriate patients under constant supervision and with other safeguards in place (Elkin et
al., 2015).
Table 18.7 Recent Evidences

Journal/ Title Methodology Finding

Author/
Impact
Factor
Spontaneous Single-center, prospective, open- no significant benefit of
Annals of breathing trial label, randomized controlled the extensively assisted
Intensive Care with pressure superiority trial (balanced weaning strategy, which
/ support on randomization, 1:1 ratio) with two involved spontaneous
positive parallel groups. Including 98 breathing trials with
(Mezidi end‑expiratory intubated patients mechanically pressure support and
et al., pressure and ventilated for >24 h, who failed PEEP, combined with
extensive use of their first SBT using T-piece. extended post-extubation
2024) /
Comparison between SBT with
non‑invasive NIV, over the standard
pressure support (PS 7 cmH2O) +
IF : 6.925 ventilation versus PEEP (5 cmH2O) + extended NIV weaning approach using T-
T‑piece in post-extubation ("extensively piece trials and guideline-
difficult‑to‑wean assisted weaning") vs. SBT with based NIV. While both
patients from T-piece and NIV according to strategies were safe, the
mechanical guidelines ("standard weaning"). extensively-assisted
ventilation: a approach did not reduce
randomized the time to successful
controlled extubation in difficult-to-
trial wean patients. Future
research may explore
subgroups that could
benefit more from
extensively assisted
weaning strategies.

JAMA/ Effect of Pressure 1153 adults deemed ready for A spontaneous breathing
Support vs T- weaning after at least 24 hours of trial consisting of 30
(Subirà et al., Piece Ventilation mechanical ventilation at 18 minutes of pressure
2019 ) / Strategies During intensive care units in Spain. support ventilation,
Spontaneous Patients were randomized to compared with 2 hours of
IF:45.5 Breathing Trials undergo a 2-hour T-piece SBT (n T-piece ventilation, led to
= 578) or a 30-minute SBT with 8-
on Successful significantly higher rates
cm H2O pressure support
Extubation of successful extubation.
ventilation (n = 557). The primary
Among Patients outcome was successful These findings support the
Receiving extubation (remaining free of use of a shorter, less
Mechanical mechanical ventilation 72 hours demanding ventilation
Ventilation A after first SBT). Secondary strategy for spontaneous
Randomized outcomes were reintubation breathing trials.
Clinical Trial among patients extubated after
SBT; intensive care unit and
hospital lengths of stay; and
hospital and 90-day mortality.
 ACTIVITY- 19

DEMONSTRATION AND PRACTIC OF SUCTIONING IN

INTUBATED PATIENTS
Suctioning:

• Removal of these secretions can be carried out through the oropharyngeal (mouth and
pharynx), nasopharyngeal (nose and pharynx), or nasotracheal (nose, pharynx, and trachea)
routes. Artificial airways, such as an endotracheal tube (a tube inserted into the trachea
through the nose or mouth) or a tracheostomy tube (a tube inserted through a surgical
incision into the trachea), can also be used as routes for suctioning.

• Suctioning is performed on patients who have lost control of their ability to swallow and to
cough up secretions due to a stroke, unconsciousness, or disease process. The procedure
should be performed ONLY when needed. Frequent suctioning causes trauma to the
mucous linings of the respiratory tract and can result in hemorrhage and edema.
Nasotracheal suctioning can also cause hypoxemia, infections in the lungs (pneumonia),
atelectasis (collapsed lung), and cardiac arrest.

• It is desirable to have the patient manage his own secretions. Postoperative patients must
be turned and encouraged to cough and deep breath frequently (usually every two hours)
following surgery. This practice will be helpful in preventing postoperative complications
such as pneumonia and reducing the need for suctioning.

• When more than one route is used, either route may be performed first. Whenever the route
is changed, however, the used catheter and gloves are discarded, and a new catheter and
new gloves are used for the new route. Sterile technique must be used for all nasotracheal
suctioning to prevent the introduction of foreign organisms.
Suction open/closed

Open Technique of Suction

• As critically ill patients are usually intubated. regular pulmonary toilets must be applied.
• Formerly this was always through the open suction technique, that is disconnection of the
endotracheal tube, installation of the sterile catheter and application of negative pressure
• As the patient did not receive ventilation during this period, an efficient technique in less
than 15 sec is necessary.

In Line or Closed Suction

• Most ICU applies inline suction techniques whereby a sealed catheter is connected to the
endotracheal tube and suction is possible without disconnection from the ventilator.
• This technique is associated with less risk of desaturation and reduction in lung volume
(Cereda et al., 2001), fewer arrhythmias, less cardiovascular changes (Lee et al., 2001) and
less reduction of PEEP ( Moggioreetal., 2003).
• However, in pressure-controlled mode of mechanical ventilation, the negative pressure
from suction catheter may trigger ventilator breathes, and the inspiratory flow from the
ventilators may force the secretion away from the catheter tip, resulting in fewer secretions
being aspirated ( Leacocketal., 2006).
• After suctioning a lung recruitment technique such as MHI or VHI may be required to
minimize the risk of atelectasis included by the negative pressure suctioning generated by
either the open or closed system.

Mini tracheostomy:

• Is often utilized in ICU and is available for patients with secretions retention, weak cough
and contraindications to or intolerance of oral/nasopharyngeal airways.
• However as only size 10 French gauge suction catheters can be used, this may limit suction
effectiveness in some patients.

• Also mini tracheotomy is an uncuffed tube, and hence will not prevent the patient from
aspirating oropharyngeal secretions.
 Nasotracheal suction:

It is a means of stimulating cough but is an unpleasant procedure for the patient and should be
performed only when absolutely necessary.

Indications :
• Inability to cough
• Thick copious secretions
• Retained secretions
• Acute exacerbation of chronic bronchitis.
• Respiratory failure.
• Neurological disorders.
• Post-operative complications.
• Laryngeal dysfunction.

Contraindications:

• Stridor.
• Severe bronchospasm.
• Head injuries.
• Leakage of CSF into nasal passage.
• Respiratory muscle paralysis.

Airway suction causes damage to the tracheal epithelium and this can be minimized by the
appropriate choice of catheter and careful technique (Brazier et al., 1999).

A flexible catheter of suitable size, usually 12 FG in adults, should be lubricated with a water- soluble
jelly and gently passed through the nasal passage so that it curves down to the pharynx. Ocassionally,
a cough stimulated when the catheter reaches the pharynx and the suction can be applied, the
secretions aspirated, and the catheter is withdrawn.
 When suction is applied the vacuum pressure should be kept as low as possible, usually in the
range 60-150mmhg (8.0-20kpa), although this will vary depending on the viscosity of the mucus
A built-in fingertip control or Y- connector is recommended to allow a more gradual buildup of
suction pressure than it is possible by release by kinked catheter tube.

Oropharyngeal suction:

An oropharyngeal suction airway is a plastic tube shaped to fit the curved palate .It is inserted with
its tip directed towards the roof of the mouth and is then rotated so that tip lies over the back of the
tongue.

Procedure performs prior to suction

Verify Need for Suctioning.

The need for suctioning can be determined from the following sources.
(1) Physician's orders.
(2) Nursing Care Plan.
(3) The supervisor's directive.
(4) Local SOP.
(5) Personal observations.

One or more of the following observations in a patient indicate a need for suctioning:

• Increased respirations accompanied by labor or difficult breathing.

• Moist, noisy, rattling, or gurgling sounds while breathing.
• Secretions drooling from the mouth and/or nose.

• NOTE: The physician's orders, nursing care plan, or the supervisor's directive will dictate the
frequency of suctioning, usually prn (as needed).
Perform a Patient Care Handwash.

• When suctioning, every effort must be made to prevent the introduction of pathogens into
the lower airways. Clean technique and thorough handwashing are essential for
suctioning of the oral and nasal cavities.
• Sterile technique is mandatory for deep suctioning in the tracheobronchial tree and
suctioning through the endotracheal and tracheostomy tubes. Follow aseptic techniques for
all suctioning of the airway in order to minimize the spread of microorganisms that are not
normally found in the air passages.

Obtain the Necessary Equipment

Obtain the following equipment.

Disposable suction equipment set. If such a set is not available, assemble the following:

(a) Sterile, disposable suction catheters. (Catheters are sized using the French scale: the smaller
the number, the smaller the catheter. For example, 12 is smaller than 14 by this scale. These two
catheter sizes are the most commonly used for suctioning the adult patient.)
(b) Liter flask of sterile saline or water.

(c) Sterile solution basin.

(d) Sterile gloves

Suction apparatus.

• Suctioning of the airway requires a source of vacuum. Most hospitals that have piped-in
oxygen also have a piped-in vacuum source. When a piping system is not available,
portable suction units must be used. Most portable suction used in hospitals units must be
connected to an electrical source.
 • Many portable units designed for field use, however, obtain their power from
compressed gas (air, oxygen, or Freon)

Figure 19.1Suctioning apparatus Figure 19.2 Suction testing

1."Y" connectors (if applicable). "Y" connectors/ adapters are needed if the suction catheters
do not have suction ports.

Identify the Patient.

When you have orders to suction a patient, verify the patient's identity to make sure that you
perform the procedure on the correct patient.
1. If the patient is conscious, ask him his name and check his bed card and
hospital identification bracelet.
2. If the patient is unconscious, check the name on the bed card and on the
hospital identification bracelet. Make sure that the name is the same on the
card and the band.
Explain the Procedure

Explain the suctioning procedure to the patient to lessen his fears and gain his cooperation.

Provide Privacy .:

• Place a screen or curtain around the patient's area or close the door if the patient is in
a room.
Position the Patient.:

• Place the patient in a semi-Fowler's position. This position is a semi-sitting position in which
the patient manages secretions better and breathes easier.
• In some cases (such as spinal injuries), the patient will have to be suctioned without being
moved.
Check the Pressure on Suction Apparatus.

• Turn on the suction apparatus.

• Place a thumb over the end of the suction tubing and observe the pressure gauge.

1. Suction pressure is usually expressed in inches (in) of mercury (Hg) on the portable unit and
in millimeters (mm) of mercury (Hg) on the wall-mounted units. The recommended pressure
settings for adult patients are 7 to 15 inches of Hg for the portable unit and 120 to 150 mm
Hg for the wall-mounted unit.
2. If the pressure is too low, the secretions cannot be removed. If the pressure is too high, the
mucous lining may be forcibly torn away and pulled into the catheter openings.

3. If the pressure is not within the recommended limits, notify the supervisor before
continuing.
4. Turn off the suction unit after the correct pressure has been verified.

Prepare Materials.

Open the disposable suction set (if used) or prepare materials for suctioning.
(1) Open the sterile solution basin on the bedside table.

• Pour the sterile solution into the solution basin without contaminating the solution, basin, or
sterile field.

• Follow the package directions and open the suction catheter package to expose the suction
part of the catheter.
1. Open the sterile gloves package. In a disposable kit, the catheter and a sterile glove may be
wrapped together. If the gloves are wrapped separately from the suction catheter, open the
catheter package first.
Oxygenate the Patient.

• Provide additional oxygen for the patient prior to suctioning in order to prevent further
hypoxemia (oxygen deficiency in the blood).
• Suctioning removes available air and oxygen as well as removing accumulated secretions.
• If the patient is on oxygen therapy, it will increase the percentage of oxygen to 100 percent
for one minute.

• If the patient is not on oxygen, have him take a minimum of five deep breaths.

• If the patient is unable to breathe on his own, administer five breaths with a BVM system.

Put on Sterile Glove(s).

• Some suction kits provide only one sterile glove. If only one sterile glove is available, put

it on your dominant hand. Use the gloved hand to handle sterile items. The gloved hand
must remain sterile throughout the procedure.
• If two sterile gloves are available, put one glove on your non dominant hand. Then put
the remaining glove on your dominate hand. Your gloved dominate hand will be used
to handle sterile items and must remain sterile throughout the procedure. The glove on
the other hand provides protection to you and is used to handle nonsterile items.

• Remove Catheter From Package. Remove the sterile catheter from the package with the
sterile (dominant) hand. Keep the catheter coiled to prevent contamination.

• Attach Catheter to Suction Tubing. Attach the suction catheter to the tubing from the suction
apparatus (figure 4-3). When performing this step, hold the suction catheter in the gloved
dominate hand and hold the tubing from the suction apparatus in the nonsterile (ungloved) hand.

Test Patency of Catheter.

• Turn the suction apparatus on with the non-sterile hand.

 • Hold the catheter in the sterile hand and insert the tip in the basin of sterile solution.

• Place the thumb of the nonsterile hard over the suction port and observe the fluid entering
the drainage bottle. If no fluid enters the drainage bottle, the catheter is blocked. If this

• occurs, obtain another catheter and repeat the procedure.

CAUTION: Do not leave the catheter in the solution. Even antibacterial solutions can
promote the growth of certain types of bacteria.

Figure 19.3. Connecting a catheter to suction apparatus Figure 19.4.Inserting catheter using
nasotracheal route.
A. Patient sticking out tongue.
B. B. Insertion completed

suctioning the patient:

• Suctioning should not be continuous for more than 10 to 15 seconds. Suctioning removes
oxygen as well as secretions; therefore, longer periods of continuous suctioning may result in
an oxygen deprivation that is too severe for the patient.

NOTE: If you hold your breath during the suctioning period, you will be more aware of the
oxygenation level of the patient
• Gently insert the suction catheter into the nasopharynx without suctioning. (Remember, it is
usuallyeasiertoinsertthecatheterintotherightnostril.)Ifthecathetercannotbeinserted

into the nasopharynx through either nostril, remove the catheter and obtain assistance from
your supervisor or other appropriate personnel.

• Quickly and gently advance the catheter into the trachea (figure 4.4). The insertion process
may cause the patient to cough. Mild coughing is usually not a problem and may actually help
in the insertion process.

• Suction secretions by placing the thumb over the suction port. Suction the patient for
approximately 15seconds.

• Observe the patient throughout the procedure for color change or increased pulse rate. Pulse rate
increases with hypoxemia. Listen for changing breath sounds. As secretions are removed,
breathing should become quiet again. Discontinue suctioning if severe changes in color or pulse
occurs.

• After suctioning, remove your thumb from the suction port and withdraw the catheter using a
slow, rotating motion.

• Clear the catheter as required between suctioning. This is accomplished by inserting the tip

of the catheter in the sterile solution, applying suction, and allowing the solution to run
through the catheter until the catheter is clear of secretions.

• Repeat suctioning until all secretions have been aspirated. Allow the patient to rest
between suctioning and reoxygenate the patient before each suctioning.

Procedure performed after suctioning:

a) Remove Catheter and Glove.

After the suctioning is complete and the catheter has been removed, turn off the suction
apparatus and disconnect the catheter from the suction tubing. Discard the catheter into the
contaminated trash receptacle. Remove your glove(s) and discard into the contaminated
trash receptacle.
b) Make the Patient Comfortable. Provide for the patient's comfort by straightening and
tightening bed linens, placing the patient in the semi-Fowler's position, raising the bedside
rails (if indicated), and placing the call bell/light within easy reach of the patient.

c) Dispose of Used Items. Discard other disposable items into the trash receptacle. Clean and
store non-disposable items in accordance with the local SOP and replenish supplies as needed.

d) Wash Hands. Perform a patient care handwash.

e) Record Procedure in the Nursing Notes. Record the time, patient's respiration rate,
description of respirations (labored, noisy, etc.), procedure used (oral, nasopharynx, or
nasotracheal), and the type and amount of secretions obtained. If you cleared the catheter
between suctioning, remember to subtract the amount of saline solution used from the total
amount of fluid in the drainage bottle in order to arrive at the amount of secretions actually
obtained.

Fig 19.5 Process of Suctioning through tracheostomy tube

Evidence based ETT suctioning in neonates and infants:

In the NICU, ETT suctioning is a common procedure performed by nurses and respiratory
therapists. However, it is not a benign procedure.
Associated risks include:

• Cardiac dysrhythmia
• Hypoxemia
• Atelectasis
• Bronchospasm
• Infection
• Trauma to the mucosal linings
• Trauma to the cilia of the airway
• Increased intracranial pressure
(Drudgin et al,1999;Kaiser et al,2000;Rio et al,2005)

ETT suctioning of infants and children with small ETTs that have internal diameters of <4 mm
may cause an immediate decrease in dynamic compliance and expired tidal volume regardless of
lung pathology. Despite the risks associated with suctioning, failure to suction when needed can
result in a plugged ETT and the trauma of reintubation, atelectasis, and decreased oxygenation and
ventilation.

Optimal hydration and adequate warming and humidification of inspired gas maintain the normal
consistency of secretions, reducing the risk of a plugged ETT.

Clinical Indications for ETT Suctioning in Infants and Neonates. Nine of the 62 articles reviewed
addressed the clinical indications for ETT suctioning. Four out of 9 articles were expert opinon
level and addressed only adults, 1 neonatal article was expert opinion level, 2 were national
surveys, 1 article was a literature review, and 1 included the AARC Clinical Practice Guideline.
All 9 articles recommended that the decision to suction should be based on individual patient
assessment and identified the following clinical signs that may indicate the need for suctioning:

• Visible secretions in the ETT

• Audible secretions
• Coarse and/or decreased breath sounds
• Oxygen desaturations
• Decreased chest excursion
• Changes in blood gas values
• Changes in respiratory rate and pattern, Bradycardia
 • Patient agitation
• Increased proximal airway pressure on the
ventilator.
(Carroll et al., 1995; Glass et al., 2002; Young et al., 1999)

Recommended suction catheter size and insertion depth when suctioning intubated patient:

Catheter size:
• Based on reviews of five articles, including one relating specifically to infants, the size of the
suction catheter should not exceed one-half the diameter of the ETT ,providing an internal-
to-external diameter (ID:ED) ratio of0.5–0.66.
• Using this ratio ensures that air continues to enter the lungs while air is being removed
through the application of negative pressure.
• Use of this size catheter also limits mucosal trauma and atelectasis( Cardlon et
al.,1991;Hodge et al.,1992).
• It may be difficult to use a suction catheter with the recommended ID:ED ratio in the NICU
because of the small size of the ETTs used for preterm neonates. A 5 or 6 - French suction
catheter almost totally occludes a 2.5 mm ETT but approximates the desirable ID:ED ratio
with most of the other ETTs used (Young et al, 1995).

Insertion depth:
• When the suction catheter is passed beyond the ETT, stimulation of the vagus nerve may
cause bradycardia and hypotension.
• Prolonged coughing associated with suctioning increases intrathoracic pressure, causing
decreased venous blood return to the heart and hypotension ( Wood et al .,1998).
• Deep ETT suctioning may cause irritation to the respiratory epithelium, resulting in
inflammation and infection (It may also result in trauma to the mucosa and adverse effects
on the mucociliary transport mechanism of the respiratory tract).
• 41 Of the 62 articles reviewed, 11 addressed depth of catheter insertion. Three articles were
literature reviews, 4 were expert opinions, and 4 were research studies. The research studies
included experimental, animal study, retrospectives design and a randomized-controlled trial.

➢ Shallow ETT suctioning has been defined as the of a suction catheter to a predetermined depth,
usually the length of the ETT plus the adapter. In contrast, deep suctioning is the insertion of a
suction catheter until resistance is met, followed by withdrawal of the catheter by 1 cm before
application of negative pressure (Clifton et al., 2006)
Table 19.1: Recent evidence:

Journal/ Title Methodology Finding

Author/
Impact
Factor
JAMP / Comparison of Randomized controlled trial The study found no significant
(Vijaysaba the involving adult patients (>18 difference in the frequency of
ri et al ., effectiveness of years) on mechanical ventilator-associated
2024) / suctioning with ventilation for >48 hours. pneumonia (VAP) between the
4.938 closed tracheal Participants were randomized open tracheal suction system
suction and into two groups using (OTSS) and the closed tracheal
open tracheal computer-generated random suction system (CTSS), with a
suction systems numbers: p-value of 0.242. While CTSS
in adult patients • Group A: Received did not show a reduction in
receiving suctioning via an open infections caused by common
mechanical tracheal suction system VAP pathogens such as
ventilation (OTSS). Staphylococcus aureus,
• Group B: Received MRSA, or Acinetobacter
suctioning via a closed species, patients in the CTSS
tracheal suction system group had a higher frequency
(CTSS). of VAP caused by
Primary Outcome: Frequency Pseudomonas spp. However,
of ventilator-associated the CTSS group demonstrated
pneumonia (VAP). a decrease in the average
Secondary Outcome: Length of length of hospital stay
hospital stay. compared to the OTSS group.

Intensive Nasal high flow Randomized controlled trials The results of this study
Care preoxygenation include non-severely indicate that compared with
medicine/ for endotrachea hypoxemic patients requiring SMO, preoxygenation with
(Guittonet l intubation intubation in the ICU. Patients HFNC in the ICU did not
et al ., in the critically received preoxygenation by improve the lowest SpO2
2019) / ill patient: a high-flow therapy by nasal during intubation in the non-
IF: 8.610 randomized cannulae or standard bag valve severely hypoxemic patients
clinical trial mask oxygenation during rapid but led to a reduction in
sequence intubation. HFNC intubation-related adverse
was maintained throughout the events.
intubation procedure whereas
SMO was removed to perform
laryngoscopy. The primary
outcome was the lowest pulse
oximetry (SpO2) throughout
the intubation procedure.
Secondary outcomes included
drop in SpO2, adverse events
related to intubation and
outcome in the ICU
.

ACTIVITY - 20

DEMONSTRATION AND PRACTICE OF COUGH ASSIST

MACHINE
Definition:

Mechanical Insufflation-Exsufflation (MIE) or a Cough Assist Device (CAD) is the use of positive
airway pressure which rapidly changes to negative pressure to assist the patient‘s cough. Patients
for a wide variety of reasons and conditions are unable to cough or clear airway secretions
effectively due to reduced peak cough flow. These devices assist in the mobilization and clearance
of bronchial secretions by inflating the lungs. MIE is an alternative to suctioning providing
decreased mucosal trauma and increased patient comfort.

Figure 20.1 Cough assist machine

Indications for use:

• The cough assist device is to be used with patients who present with respiratory
compromise and restricted lung patterns.
• These patients present frequently with :
• Decreased lung volumes
• Retention of secretions
• Impaired or absent cough
• Increased work of breathing

Contraindications for use:

• Undrained pneumothorax
• History of bullous emphysema
• Known susceptibility to pneumothorax or pneumo-mediastinum
• Any recent barotraumas
How to adjust phase of breathing in cough assist machine?

Each phase of breathing should be set so that you can get the air in and out of your lungs
comfortable and then pause to continue coughing if needed.

1. Set the inhale time knob at 1second.

2. Set the exhale time knob at 1second.
3. Set the pause time knob at 2 second.
4. Set the inhale flow knob at the 3 squiggly arrows

How to use the Cough Assist Machine?

1. Check to make sure that the inspiratory (positive) and the expiratory (negative) pressures are
set. Start at +20/-20 and gradually increase to+40/-40.

• Remove the face mask/mouthpiece and hold the tubing firmly against a tight surface.
• Turn on the machine.
• Set the manual/auto switch to manual.
• Toggle the manual control switch between inhale and exhale a few times to ensure
that the pressures are correct and that the manometer returns to zero.

2. Set the manual/auto switch to auto. The unit will then automatically cycle from the positive
to negative pressure and back to zero for the pause.

3. Reattach the mask/mouthpiece to the tubing and place it tightly on your face/mouth so that
no air leaks out. You may need to use a nose clip to prevent air leakage.

4. Turn the machine on.

5. As you breathe in, the machine will help by giving a big breath of air. This breath will end
at the time set on your machine.

6. As you breathe out, the machine will help by sucking the air out. This will help your cough
be much stronger and it will help to remove any secretions.

7. Take a series of 4-6 breaths continuously from the cough machine and then rest for 20-
30 seconds and cough out any secretions that may have loosened up.

8. Repeat the series of breaths with a rest 4-6 times or until you no longer have any
secretions to cough out.
How to adjust the pressures?

1. Remove the face mask/mouthpiece and hold the tubing firmly against a tight surface.

2. Turn on the machine.

3. Set the manual/auto switch to manual

4. To adjust both inspiratory pressure and expiratory pressure, turn the Pressure knob
clockwise to increase the pressures and counterclockwise to decrease the pressures.

5. To adjust the INSPIRATORY PRESSURE to be less than the expiratory pressure:

• Toggle and hold the manual control lever to inhale.

• Decrease INSPIRATORY PRESSURE by turning the Inhale Pressure knob

counterclockwise to the positive pressure on the manometer that you can
tolerate.

Practice of cough assist machine

• The Cough Assist Machine helps to clear secretions from the lungs by helping you with
your breathing.

• When you breathe in (inspiration), the machine gives you air (positive
pressure) to expand your lung.

• When you blow out (expiration), the machine creates a sucking force (negative pressure)
that pulls the air out of your lungs. This rapid change in pressure during the different
phases of breathing (inspiration and expiration) helps make your cough stronger and more
effective.
Table 20.1 Recent evidences:

Journal/ Title Methodology Finding

Author/
Impact Factor
Respiratory care/ Comparison A bench study compared CPF measurements varied
of Four cough peak flow (CPF) and across devices, showing
(Terzi et al., Mechanical effective cough volume decreased CPF at the
Insufflation- (ECV) across four tracheal level and
2023 ) / IF:2.4 Exsufflation mechanical insufflation- increased CPF at the mouth
Devices: exsufflation (MI-E) devices level during airway
Effect of under simulated airway collapse.
Simulated collapse and stable
Airway conditions. Various
Collapse on inspiratory/expiratory
Cough Peak pressure pairs were tested,
Flow ranging from +20/−20 cm
H2O to +40/−70 cm H2O.
Pressure and flow signals
were recorded at 200 Hz
during automatic MI-E
cycling, with 2-second
insufflation and exsufflation
phases and a 1-second
intercycle pause. After
stabilization, data from at
least 10 cycles were
analyzed per condition.

RespirCare. / Effects of A randomized controlled trial MI-E significantly

Mechanical conducted in mechanically enhanced airway mucus
de Camillis et al., Insufflation- ventilated ICU patients to clearance reduced
2020/ Exsufflation assess the effectiveness of respiratory rate, and
IF: 2.4 on Airway mechanical insufflation- improved oxygenation in
Mucus exsufflation (MI-E) on airway mechanically ventilated
mucus clearance. Parameters
Clearance patients compared to
such as sputum production,
Among standard suctioning
respiratory rate, and
Mechanically oxygenation levels were methods.
Ventilated measured.
ICU Subjects.
 ACTIVITY - 21

DEMONSTRATION AND PRACTICE OF MECHANICAL AND

VENTILATOR HYPERINFLATION
Manual hyperinflations

Manual Hyperinflation therapy is a very common therapy performed on patients who are suffering
from some sort of respiratory distress. It is one of the technique which is used to optimize
Mucociliary Clearance, often called bag squeezing, it was developed in 1968 to improve
oxygenation, clear bronchial secretions, and achieve alveolar re-expansion. MHI increases
transpulmonary pressure and enhance collateral ventilation.(Bertijsw et al., 2012).

MHI is widely recognized as a technique that mimics the physiological mechanism of a cough,
by using a manual resuscitation bag to deliver tidal volumes (Vt) 100-150% larger than baseline
Vt and a peak airway pressure of no more than 40 cmH2O, delivering a slow inspiratory flow,
followed by a inspiratory hold and a fast expiratory flow that generates a whirlwind peak
expiratory flow. (Berney et al., 2012).
Indications

Atelectasis
Increase pulmonary secretions

Poor lung compliance

MHI may be indicated in patients requiring mechanical ventilation and self ventilating
tracheostomy patients who have Chest x-ray changes of lung collapse and/or
consolidation or by areas which are poorly ventilated on auscultation.
Contraindications
Cardiovascular Instability
Undrained pneumothorax
Very high PEEP
Recent pneumonectomy
Severe bullae
Recent lung surgery
Clamped chest drained
Haemoptysis
High frequency oscillatory ventilation – ( unless weaning)
Table 21.1: Procedure

Action Rationale
• Assess the patients vital signs • To ensure they are stable and in order to
detect changes in the
• patients condition
• Prepare the patient by giving explanation, • Minimizes any distress to the patient thus,
sedation and analgesia as required • maximizing effectiveness of
treatment
• Position the patient so that the lung to be • Optimises ventilation to the affected lung
treated is uppermost and assists with the drainage of
secretions
• Connect the 2 litre re-breathing bag to the • Prevents hypoxia and ensures safety of
02 supply and ensure the expiratory valve equipment. To prevent contamination or
is working & place a filter in the circuit the bag and/or the patients lungs Provides
between the patient and the bag and attach feedback to the operator of the airway
the Manometer pressures being delivered

• Set the 02 flow rate to15 litres per • To ensure 100% oxygen is delivered &
• minute) the bag fills Quickly
• Put the ventilator on Standby or use the • Prevents patient anxiety
preoxygenation suction facility
o to disable the alarm
• Disconnect the patient from the ventilator • To enable manual hyperinflation
and attach the re-breathe bag to the
airway via the catheter mount or the
closed suction circuit Mount

• Using a two handed technique, initially • To allow the operator to gain a feel of
deliver a tidal volume breath (watching the patients lung compliance and
the patients chest expansion) ensure an adequate Tidal Volume is
being delivered into the patients
lungs
• Then perform MHI breaths. The manual • To ensure effective manual
hyperinflation breath should be hyperinflation breaths and recruit
maintained for at least 2 seconds, but no collapsed alveoli .Limits the detrimental
more than 7 seconds at a pressure of no effects on Cardiovascular system
more than 40 cmH2O

• Release the bag sharply on expiration to • To mobilise secretions from more

simulate the Forced Expiratory technique peripheral to central Airways
• If indicated apply manual techniques • To assist secretion clearance and lung re-
such as shaking or vibration at the end expansion
of expiration and during expiration
• Repeat the procedure several times as • Effect optimal secretion clearance and
indicated recruitment of collapsed Alveoli

• Explain the procedure to the patient • Minimises stress and discomfort to the
throughout the entire process and always patient
synchronize with spontaneous ventilation

• If the patient is coughing the expiratory • Reduces the pressure built up in the lungs
pressure valve should be and reduces
• Released • the risk of barotrauma
• Perform suction if the patient coughs or • Clears secretions preventing them being
secretions are heard forced back into smaller Airways

• Continue the above procedure until no • Effect optimal recruitment of collapsed

further treatment is indicated (e.g.if no alveoli and secretion clearance
more secretions are heard or the chest is
clear on auscultation)
• Restore ventilatory support, ensuring • Re-establishes current ventilatory
that adequate tidal and minute volume support
are being achieved or re attach the
patient to their oxygen supply

• Monitor the patient's vital signs during • To ensure no adverse effects of manual
and after the procedure and check that the hyperinflation are occurring and that
expected parameters the patient is returned to a safe
• have been restored. Reauscultate the environment to evaluate the effects of
patients chest treatment
• Document on the patients chart and in the • Makes staff aware of the patients'
medical notes that Manual Hyperinflation response therefore, safeguarding
treatment has been performed. Note any the patient's well being
changes in the patient's condition adverse
or otherwise
Precautions

Premature babies and neonates

Raised ICP
High PEEP over8mmhg
Low cardiac output
Dialyzed patient
Bronchospasm
ARDS
Recent abdominal surgery

Dangers of manual hyperinflation

Increased intra-thoracic pressure

Increase intracranial pressure
Barotraumas
Patient distress
Changes in BP
Reduced cardiac output.

Ventilator hyperinflation (2017 Guidelines)

The short-term effectiveness of manual hyperinflation (MHI)in improving oxygenation and

pulmonary compliance, re-expanding areas of atelectasis, and clearing pulmonary secretions has
been widely demonstrated. However, there is controversy in whether patients ventilated on high
levels of positive end-expiratory pressure(PEEP) should be disconnected from the ventilator to
receive MHI, because disconnection would cause loss of functional residual capacity, decrease in
oxygenation and shear stress of distal lung units. To prevent adverse effects of disconnection, the
ventilator may be used to deliver increased tidal volume, a technique called ventilator
hyperinflation (VHI).
Indications

Invasively ventilated patient

Increased viscosity of respiratory secretions
Acute chest X-ray changes of lung collapse with or without consolidation. Poorly
ventilated areas of lung tissue on auscultation.
Patients who need to be more closely monitored via ventilation.

Absolute contraindications

Undrained pneumothorax
Severe bronchospasm
Head injury with ICP >25mmHg
Severe arterial hypotension
Subcutaneous emphysema of unknown cause

Figure 21.1 – Manual Hyperinflation

Table 21.2: Relative Contraindications

• Proximal Tumor/obstruction • Risk of gas trapping or causing trauma

• Emphysematous Bullae • Increases risk of pneumothorax
• Recent oesophageal or lung surgery • High airway pressure may compromise
• e.g. lobectomy/pneumonectomy the anastamosis. Check with surgeons
regarding stump pressure.

• Severe exacerbation ofchronic • Increased airway pressure will increase

obstructive pulmonary disease (COPD)/ airway irritation and inflammatory
Bronchospasm response
• Acute Respiratory Distress Syndrome • Increases risk of
• (ARDS) / contusions pneumothorax/barotraumas

• Raised intracranial pressure (ICP) • Increasing intrathoracic pressure can

compromise mean arterial pressure and
• compromise cerebral perfusion pressure
• Hypotension (Systolic <80) • Increased positive pressure in thoracic
cavity compromises venous return –
reduces cardiac output
• CVS instability/arrhythmias • Compromised venous return - further
• increases effort required to maintain
adequate tissue perfusion
• Acute Head Injury • As for raised ICP
• Unexplained Haemoptysis • May be indicative of acute trauma to the
• lung parenchyma

• High respiratory rate • Difficult to co-ordinate the technique

• Patients who are coughing vigorously on • Generates high intrapulmonary pressures
the ventilator
Table 21.3: Procedure:

Action Rationale
Assess the patients vital signs To ensure they are cardiovascular stable
and in order to detect changes in patient
condition during procedure
Note starting tidal volume and from this Patients will be on lung protective
calculate target treatment volume of 100- ventilation
150% increase of starting tidal volume Strategy with lung volume targeted at vol
of 4-8ml/kg of ideal body weight
Limited the target vol to between 100- 150%
of starting vol for VHI will limited the
pressure/vol on lung in compliance with
lung protective ventilation whiisted still
being an effective treatment(Dennis et al
2012).
The volume range will provide you with a
target volume at which treatment is
effective.
Explained the procedure and obtain the Minimize the distress to the patient and
consent foam as able or where appropriate. maximizes effectiveness of treatment.
Where consent is unable to Confirm patient willing to undertake
obtained patient will be treated in best interests. treatment if they have capacity

Optimize the patient position position for Optimises ventilation to the affected lung
maximal effectiveness of treatment( lung and assists with the drainage of secretions.
to be treated is uppermost)
Ensure pre treatment ventilation settings and Pretreatment ventilation settings need to be
observation are documented on to documented clearly so that the patients
observation chart prior to starting VHI. returned to the previous ventilation settings
• Vt/P insp once VHI treatment is completed
• PAW alarm ,PIP alarm
• T-insp
• I Eratio
Ensure The Flow And Pressure Wave foam Are Enables the operator to observe for gas
Displayed On The Ventilation trapping and bronchospasm if either of
these occurs treatment should be
Change The PAW alarm to 35cm H2O terminated.

Avoids unnecessary alarms during

treatment and alerts you to excess pressure
on the lungs.
Table 21.4: Recent evidence:

Journal/ Title Methodology Finding

Author/
Impact
Factor
PLoS One Manual and An online survey was The study provided
/ Liyanage et ventilator conducted among insights into the
al., 2024 / hyperinflation physiotherapists in Sri Lanka variability in
I.F – 2.9 parameters working in intensive care hyperinflation practices,
used by settings. The survey gathered highlighting common
intensive care data on the parameters used parameters and variations
physiotherapis for both manual and in their use among
ts in Sri Lanka: ventilator hyperinflation. physiotherapists in Sri
An online Lanka.
survey

European Study and 40 patients were studied No significant canges in

respiratory effectiveness of under prospective HR, SPO2, and lung
journal/ ventilator randomized crossover study compliance.
hyperinflation, evaluating Heart rate (HR), MAP increase 5 minutes
(Viera et al ., associated or mean arterial pressure after VH, return to the
not to manual (MAP), saturation(SPO2), baseline after 15 minutes.
2017) abdominal exhaled tidal volume (TVex),
compression, in peak expiratory flow (PEF),
Impact critically ill static compliance and
factor- patients under resistance of patients
12.24 mechanical submitted to hyperinflation
ventilation. isolated and associated with
abdominal compression
 ACTIVITY- 22

DEMONSTRATION AND PRACTICE OF MOBILIZATION

EXERCISEFOR ICU PATIENTS

Mobilization in the ICU

The effects of critical illness, and the therapies instituted, can have effects that persist long after
ICU discharge. These effects include profound and prolonged neuromuscular dysfunction. ICU-
acquired weakness (ICUAW) is common (up to 60% in some studies) and begins in the first few
days of critical illness. It is possible that early mobilization (exercising patients while they are still
receiving mechanical ventilation) may protect against ICUAW and limit long term neuromuscular
dysfunction. Other deleterious consequences of immobility may also be attenuated by mobilizing
patients in the ICU.

ICU Acquired Weakness (ICUAW)

ICU Acquired Weakness (ICUAW) includes critical illness myopathy (CIM), critical illness
polyneuropathy (CIP), or a mixture of both (myopathy is typically predominant). It is very
common in the mechanically ventilated (25-60% in those mechanically ventilated for > 7 days).
There is increasing body of evidence that ICUAW leads to poor quality of life and persistent
weakness lasting long after ICU discharge .

Pathophysiology

• Multifactorial pathogenesis may involve:

• Axonopathy, not demyelinating

• Mitochondrial dysfunction

• Micro vascular ischemia

• Sodium channelopathy

• Catabolism

• Immobility
 Figure: 22.1 Potential body/structure effects of critical illness. HR_ heart rate, DVT (deep
vein thrombosis).

Risk Factors

• Sepsis
• Systemic inflammation
• Poor glycemic control
• Steroids
• Neuromuscular blocking agents
• Immobility
• Malnutrition
• Female sex
• Pre-existing sarcopenia
Clinical Features

• Onset is typically about 1 week into a critical illness

• Sensation is preserved (deficits can be present with axonopathy; difficult to assess in icu
due oedema and coma)

• Symmetrical deficits

• Mostly proximal weakness

• Reflexes are present, though diminished

• CSF findings are normal

• Cranial nerve function and autonomic nervous system function are usually intact

• Ck may be raised if myopathy is present

• Nerve conduction studies (if performed) show normal conduction velocities with
decreased compound muscle action potentials(c maps)
• Score of <48 on the mrc sum score (mrc-ss) of muscle strength is diagnostic of
ICUAW.

Investigations

Investigations are often not necessary; however, they may be required depending on the possible
differential diagnoses and implications for management and prognosis

Laboratory

• CK (mildly elevated – and transiently so – in critical illness myopathy (not so with

critical illness neuropathy)
• UEC
• B12level
• Acetylcholine receptor antibodies (for myasthenia Gravis)
• Inflammatory markers (e.g. CRP)
• Lumbar puncture
• Imaging
• CXR (evidence of malignancy causing Eaton-Lambert syndrome)
• MRI of the brainstem and spine
Special tests

• Nerve conduction studies and electromyography: CIP shows sensorimotor axonopathy

with decreased compound muscle action potentials (CMAP) and sensory-nerve action

potentials, but preserved conduction velocities (CV). CIM shows reduced amplitude and
increased duration of CMAPs. ICUAW often is a mixture of CIP and CIM.
• Muscle biopsy if no satisfactory explanation is found.

Differential Diagnosis

• Critical illness polyneuropathy – presents around a week into a critical illness, typically
with limb weakness and atrophy, reduced tendon reflexes, loss of peripheral sensation to
touch and pain, preservation of CN function, electrophysiological studies -> motor and
sensory neuropathy, biopsies -> axonal degeneration and denervation -> atrophy of
muscles.
• Residual paralysis – exclude using peripheral nerve stimulation (minimal response to
TOF, PTc)
• Residual sedation – calculation of dose, duration and ability to clear medications
(response to antagonism; naloxone, flumazenil)
• Acute myopathy – risk factors = neuromuscular blockage and corticosteroids, motor
findings with no sensory abnormalities, CK elevated, electrophysiological testing -
>myopathy, muscle biopsy ->loss of thick filaments
• Spinal cord lesions – associated with a sensory level and hyperreflexia

• Brain stem problems – cranial nerve lesions.

• Guillain-Barre syndrome – ascending motor weakness, loss of reflexes, some peripheral

sensory deficits, pain, post-viral, high protein in CSF, responsive to Ig and plasmapheresis
 Management

• Intensive glycemic control

• Minimize use of corticosteroids and neuromuscular blockade
• Physiotherapy – consider including early mobilization
• Electrical muscular stimulation(Ems)
• Minimize sedation
• Electrolyte replacement
• Optimize nutrition
• Ventilator weaning

Prognosis

Short-term

• Increased ventilation
• Increased icu stay
• Increased mortality

• Long-term

• Most recover to be able to walk independently

• Small amounts have mild disability
• 30% have severe quadriparesis, quadriplegia or paraplegia

PHYSIOLOGY OF ICU MOBILIZATION

Benefits of positioning upright from supine

▪ ↑ Lung volumes
▪ ↑ Lung compliance
▪ ↓ Airway closure
▪ ↑PaO2
▪ ↓ Work of breathing
▪ ↑ Mobilization of secretions
▪ Benefits of mobilization
▪ ↑Ventilation
▪ ↑ V/Q matching
▪ ↑ Recruitment of lung units
▪ ↑ Surfactant production/distribution
▪ ↑ Mobilization of secretions
▪ ↑ Cardiopulmonary fitness and exercise capacity

Parameters Indicating a Lack of Readiness for Physical Therapy Interventions

Pulmonary Measures

• SaO2: <88% or patient experiences a 10% oxygen desaturation below resting SaO2

• Respiratory rate: >35breaths/min

• PEEP: >10 cmH2O
• FIO2:≥0.6

Cardiovascular Measures

• Mean arterial pressure: <65 or >120 mm Hg or ≥10 mm Hg lower than normal

systolic or diastolic blood pressure for patients receiving renal dialysis

• Resting heart rate: <50 or >140bpm

• Systolic blood pressure: <90 or >200 mmHg
• New arrhythmia developed (including frequent ventricular ectopic beats or new
onset atrial fibrillation)

• New onset angina-type chest pain

Laboratory Values

Table: 22.1

Hematocrit<25% No exercise

Hemoglobin<8 g/Dl No exercise

Platelets <20,000/mm3 No exercise

Anticoagulation INR ≥2.5–3.0 Discuss with

physician

Metabolic Measures

• Glucose levels <70 or >200mg/dL

Disadvantages

• Injury and fall risk

• Hemodynamics instability
• Neurological instability (e.g. acute agitation and pain)
• Respiratory instability (e.g. desaturation, ventilator asynchrony)
• Increased metabolic demand, VO2 andVCO2
• Risk of disconnection/ dislodging lines and tubes and subsequent complications
(e.g. endotracheal tubes, ECMO lines, central lines, IDCs)

• Early mobilization causes harm in medical stroke patients (AVERT study)

• Cost due to increased staffing and physiotherapy time demands
Table. 22.2

Rationale Example of Techniques and Approaches

Respiratory strategies

Respiratory weakness and difficulty being Costophrenic assisted cough , Pursed-lip

weaned from mechanical ventilation are breathing , Diaphragmatic breathing ,
common symptoms with this population. Scoop technique
Difficulty with clearance of secretions
may necessitate use of assisted cough
techniques.
ROM

Due to the peripheral muscle weakness, Passive ROM

patients will benefit from progression to Active ROM

active movement to regain strength. Active-assistive ROM

Resisted ROM

PNF diagonals

Patient education

New and overwhelming change in Pacing of activities

 functional capabilities and strength may Safety awareness to prevent falls

necessitate education regarding alternative Compensatory strategies to increase

ways to perform tasks and activities. efficiency of movements

Functional mobility training

Due to severe symmetrical weakness, Bed mobility

patients may be unable to perform Balance

functional tasks. Transfer training

Some patients are unable to perform the Gait

most basic tasks, and others are unable to Stair negotiation

perform more complex tasks.
Exercise prescription and training

Patients in the ICU are not able to undergo a Borg RPE Scale
traditional maximal or submaximal exercise PFIT
test. Because of this limitation, intensity of Two-Minute Walk Test
exercise and activity depends on patient self- Six-Minute Walk Test
report of fatigue and can be based upon
response-dependent management.

Fig: ROM- range of motion, PNF- proprioceptive neuromuscular facilitation, ICU- intensive

care unit, RPE- Rate of Perceived Exertion, PFIT- Physical Function in the ICU Test.

Barriers to Mobilization

These are commonly perceived barriers (they are not absolute and can often be overcome):

• Endotracheal intubation and mechanical ventilation

• ECMO
• Femoral lines
• Sedation
• Delirium
• Staffing levels
• Need for a multi-disciplinary team approach
• Respiratory stability
 • Hemodynamics stability
• Barriers to early mobilization are likely cultural (to individual icu’s) rather than
specifically related to patient factors

Early mobilization

Early mobilization refers to exercising patients while they are still receiving mechanical
ventilation

• The precise timing, combination of interventions and their intensities (step up as

tolerated‘ versus ‗step down when tiring) varies between studies and clinical
settings

• Interventions commonly include:

• Passive range of motion exercises
• Sitting
• Transfer to chair
• Standing
• Ambulation
• Bicycle ergometer

Physiotherapy in ICU

Physiotherapists are part of the multidisciplinary ICU team. The traditional focus of treatment has
been the respiratory management of both intubated and spontaneously breathing patients.
Emerging evidence of the longstanding physical impairment suffered by survivors of intensive
care has resulted in physiotherapists re-evaluating treatment priorities to include exercise
rehabilitation as a part of standard clinical practice. Physiotherapists perform an assessment that
includes the respiratory, cardiovascular, neurological, and musculoskeletal systems to formulate
treatment plans. The precise roles and indications for physiotherapy are uncertain as
physiotherapy involvement is largely based on clinical reasoning and there is a lack of high-
quality evidence supporting physiotherapy in the ICU.
Physiotherapist roles include:

• Involvement in physiotherapy devised care plans

• Optimization of cardiopulmonary function
• Weaning from the ventilator
• Early rehabilitation/mobilization programmed
• Positioning to protect joints, prevent contractures and improve muscle tone
• Promote functional independence and improve exercise tolerance
• Management of musculoskeletal pathology
• Assisting with orthotics and equipment (e.g. Fitting of cervical collars, spinal
braces, slings etc. in trauma patients; setting up TENS machines)

• Patient education (exercise, rehab etc.)

Mobilization deconditioning and musculoskeletal mobilization

• Physiotherapists have a role in maintaining joint and muscle function in those who are at
risk of contractures, for example in neurological injuries and patients with prolonged
paralysis
• There is increasing emphasis on exercise rehabilitation over respiratory management. It is
increasingly evident as survivors of a prolonged ICU stay can suffer deconditioning,
muscle atrophy, and weakness that may impact upon quality of life.
Figure 22.2 Hemodynamic monitoring parameters in ICU
Mobilization Protocol
DEVELOPING A PROGRESSIVE MOBILITY ACTIVITY PROTOCOL

Effects of Immobility

Deconditioning is a term that is used to describe the complex physiological and potentially
reversible effects that result from periods of inactivity or immobility (O‘Keefe, 2002).

Figure 22.3 Physiological changes during 1 week of bed rest. CO _ cardiac output; HR _ heart
rate; MV _ mechanical ventilation; SV _ stroke volume Based on data from De Jonghe et al.
(2007); Hamburg et al, (2007); Kortebein, Ferrando, Lombeida, and Evans (2007); McCance and
Heuther (2006); Topp, Ditmyer, King, Doherty, and Hornyak (2002); and Winkleman (2009).

Figure 22.4 Progressive mobility activity protocol steps. HOB (head of the bed).
Figure 22.5 Complications of immobility. ARDS _ acute respiratory distress syndrome; CNS _
central nervous system; CO _ cardiac output; DVT _ deep vein thrombosis; PE _ pulmonary
embolism; SV _ stroke volume; UTI _ urinary tract infection. Based on data from De Jonghe et al.
(2007); Hamburg et al. (2007); Kortebein, Ferrando, Lombeida, and Evans (2007); McCance and
Heuther (2006); Topp, Ditmyer, King, Doherty, and Hornyak (2002); and Winkleman (2009).
 TABLE 7.3 PROGRESSIVE MOBILITY ACTIVITY PROTOCOL STANDARDS OF
PRACTICE

STANDARDS OF PRACTICE—Progressive Mobility/Activity :In the care of all patients, the

RN will: Assess the patient for PMAP eligibility within 8 hours of admission and every 8 hours.

Initiate PMAP if the patient:

Is at risk for deconditioning due to immobility.

Requires orthostatic training to an upright position
Is free from contraindications.
➢ Question complete bed rest orders for prolonged periods if a legitimate reason is not
apparent. Bed rest should be a rare exception.
➢ Educate and reassure the patient about activity.
➢ Perform ROM of extremities every 8hours.
➢ Reposition patient and perform skin assessment every 2hours.
➢ Consult PT/OT and RT as appropriate for evaluation and assist with mobility.
➢ Consult lift team as appropriate
➢ Minimize sedation as per (protocol/policy) during daytime hours to allow for PMAP.
➢ Implement PMAP three times during the day and more as tolerated.
➢ Evaluate cardiopulmonary tolerance to each position change by assessing vital signs, ECG and
SpO2 before and after each activity. Allow a 5-minute equilibrium period after the position
change before determining cardiopulmonary stability.
➢ Progress each step duration 30 to 60 minutes as tolerated.
➢ If cardiopulmonary instability develops, decrease duration to 15 minutes, and if intolerance
continues, return to previous step.
➢ Repeat each step until the patient demonstrates hemodynamic and physical tolerance to state
activity/position for 60minutes.
➢ Advance to the next step.
Initiate orthostatic training three times a day by placing the patient in a reverse Trendelenburg
position if the patient demonstrates cardiopulmonary intolerance or contraindications to P MAP.
Continue to assess PMAP (re)initiation when the patient demonstrates stability with upright mobility.
➢ PMAP is to continue until the patient is ambulating independently or discharged from the
hospital.

Note. ECG _ electrocardiogram; PMAP _ progressive mobility activity protocol; PT _physical

therapist; OT _ occupational therapist; RN _ registered nurse; ROM _ range of motion; RT
_respiratory therapist; SpO2 _ oxygen saturation. Standards OF PRACTICE—Progressive Mobility
/Activity is the property of Salem Community Hospital, Salem, OH.

Progressive mobility activity protocol documentation record. BP _ blood pressure; ECG _

electrocardiogram; FiO2 = fraction of inspired oxygen; HOB _ head of the bed; HR _ heart
rate; PM _ progressive mobility; R _ respiration; ROM _ range of motion; SpO2 _ oxygen
saturation
 Table 22.3: Recent evidence:

Journal/ Title Methodology Finding

Author/
Impact
Factor
Clinical To evaluate The study was a within-patient The use of blood flow
rehabilitation/ the addition of randomized trial. Two intensive care restriction did not
(Barbalho et al., blood flow units in Belém, from September to present adverse effects
2019) restriction to October 2017.In total, 34 coma patients and seems to be a valid
IF: 2.710 passive were admitted to the intensive care unit strategy to reduce the
mobilization sector, and 20 patients fulfilled the magnitude of the rate
in patients in study requirements. All participants of muscle wasting that
the intensive received the passive mobilization occurs in intensive
care unit protocol for lower limbs, and blood care unit patients.
flow restriction was added only for one
side in a concurrent fashion.
Intervention lasted the entire patient’s
hospitalization time. main outcome
measurement was thigh muscle
thickness and circumference.
34 subjects were enrolled in the study:
11 were excluded for exclusion criteria,
3 for death, and 20 completed the
intervention (17 men and 3 women;
mean age: 66±4.3 years). Despite both
groups presented atrophy, the atrophy
rate was lower in blood flow restriction
limb in relation to the control limb (–2.1
vs. –2.8mm, respectively, in muscle
thickness; P=0.001). In addition, the
blood flow restriction limb also had a
smaller reduction in the thigh
circumference than the control limb (–
2.5 vs. –3.6 cm, respectively; P=0.001).
Journal of critical Comparison A randomized, single-blind, placebo- Most bed exercises
Care/ of exercise controlled crossover trial was carried were low-intensity
(Medrinal et al., intensity out to evaluate the effects of four bed and induced low
2018) during four exercises (passive range of movements levels of muscle work.
IF: 2.685 early (PROM), passive cycle-ergometry, FES cycling was the
rehabilitation quadriceps electrical stimulation and only exercise that
techniques in functional electrical stimulation (FES) increased cardiac
sedated and cycling) on cardiac output. Each output and produced
ventilated exercise was carried out for ten minutes sufficient intensity of
patients in in ventilated, sedated patients. Cardiac muscle work.
ICU: a output was recorded using cardiac
randomized Doppler ultrasound. The secondary
cross-over aims were to evaluate right heart
trial function and pulmonary and systemic
artery pressures during the exercises,
and the microcirculation of the vastus
lateralis muscle. The results were
analyzed in 19 patients. FES cycling
was the only exercise that increased
cardiac output, with a mean increase of
1 L/min (15%). There was a
concomitant increase in muscle oxygen
uptake, suggesting that muscle work
occurred. FES cycling thus constitutes
an effective early rehabilitation
intervention. No muscle or systemic
effects were induced by the passive
techniques.
 ACTIVITY -23

DEMONSTRATION AND PRACTICE OF HUMIDIFICATION AND

NEBULISATION FOR ICU PATIENTS
 Definition:

Nebuliser is a drug delivery device used to administer medication in the form of a mist inhaled
into the lungs. Nebulisation is a method of converting a medicine or solution into an aerosol, which
is inhaled directly into the lungs.

Fig 23.1.Nebulizer

Table 8.1. Definitions related to nebulization

Aerosol output: the mass per minute of particles in aerosol form produced by the nebulizer

Respirable particles: particles <5 lm diameter.

Respirable fraction: the mass of respirable particles expressed as a percentage of the aerosol output.

Respirable output: the mass of respirable particles produced per minute (aerosol output respirable
fraction).

Drug output: the mass of drug produced per minute as an aerosol.

Mass median diameter: the diameter of the particle such that half the mass of the aerosol is
contained in smaller diameter particles and half in larger.

Mass median aerodynamic diameter (MMAD):the diameter of a sphere of unit density that has
the same aerodynamic properties as a particle of median mass from the aerosol.
Aim of nebulizer therapy

1. The aim of treatment with nebulisers is to deliver a therapeutic dose of the drug as an
aerosol in the form of respirable particles within a fairly short period of time, usually5–
10minutes.
2. Nebulisers are useful when large doses of inhaled drugs are needed, when patients are too
ill or otherwise unable to use hand held inhalers, and when drugs are not available in hand
held inhalers.
3. The commonest indication is for the emergency treatment of asthma and exacerbations of
chronic obstructive pulmonary disease . Other indications include the long-term
bronchodilator treatment of chronic airflow obstruction ; prophylactic drug treatment in
asthma ; antimicrobial drugs for cystic fibrosis , bronchiectasis., and HIV/AIDS; and
symptomatic relief in palliative care.

4. The present British Standard (BS7711) for jet nebulisers indicates that they should provide
an aerosol with a respirable fraction of at least 50% at their recommended driving gas
flows.
5. Any combination of compressor and nebuliser needs to be assessed for a particular drug
solution and drug volume . For the commonly used bronchodilators, output data derived
from 0.9% sodium chloride can be used as a general guide.

Types of Nebuliser

1. Jet nebulisers consist of a nebulising chamber in which an aerosol is generated with a flow
of gas provided either by an electrical compressor or compressed gas (air or oxygen).
2. Ultrasonic nebulisers are self-contained electrical devices in which an aerosol is generated
by vibrating fluid placed within them. They can nebulise larger volumes of fluid and are
quiet.
3. In the sections which follow “nebuliser” means jet nebuliser unless otherwise specified
Drug Output

Unlike the output of most ultrasonic nebulisers, the aerosol output of jet nebulisers is not the same
as drug output. Measurement of aerosol output for a particular drug solution therefore gives only
a general guide to nebuliser performance. The drug output from different systems needs to be
known, particularly since many drug solutions and suspensions such as antibiotics and
corticosteroids have physicochemical properties which are quite different from 0.9% sodium
chloride (which is often used to measure aerosol output) and the commonly used bronchodilators.

Factors Affecting Drug Output:

1. Driving Gas Flow Rate

Most jet nebulisers are now designed to work at a flow rate of 6–10 l/min. Flow rates generated
by electrical compressors should be measured at the outlet of an attached nebuliser (dynamic
flow). The flow required will depend upon the nebuliser design, the dimensions of the
connecting tubing and, to a lesser extent, the drug used.

2. Nebuliser chamber design

Increasing the fraction of droplets intercepted by the internal bazesina standard jet nebuliser
will decrease particle size but increase nebulisation time. Incorporating an open vent into the
nebulizer may allow entrainment of air and a faster nebulisation rate. Breath enhanced open
vent nebulisers incorporate valve systems and utilise a patient’s inspiratory flow to in-crease
the nebulisation rate. However, they may not provide benefit to patients such as infants whose
inspiratory flow rates do not exceed the output flow rate from the compressor.
Subsidiary factors affecting choice of equipment

Compressors vary in size, shape, weight, cost, running cost and noise level. Nebuliser chambers
preferably should not contain components that can be easily swallowed.

Simple jet nebulisers should consist of a removable top and a single component
chamber. Nebulisers should be able to be easily assembled and disassembled by patients.

Using nebulisers-

Nebulisation time

The nebulisation time is the time from starting nebulisation until continuous nebulisation has
ceased. The time taken to deliver a drug is important for patient compliance. Nebulisation time for
bronchodilators should be less than 10 minutes.

Nebulisation end point

“Dryness” is a diffcult end point for patients to recognize. It may be better for patients to be advised
to nebulise for about a minute after “spluttering” occurs. Patients need to know how long this
should take when their equipment is working correctly.

Tapping

Tapping the nebuliser chamber when the solution begins to “splutter” increases the volume output.

Face masks and mouthpieces

Bronchodilator responses are the same whether masks or mouthpieces are used. The choice should
therefore depend upon convenience – for example, masks are better for emergencies and patient
preference. Face masks should be tight-fitting. Patients should breathe with an open mouth.

For ipratropium bromide, mouthpieces should be preferred to masks if there is a possibility of

glaucoma. For antibiotics, rhDNase and corticosteroids, mouth-pieces should be used.
 Fig. 23.2: Nebulisation mask Fig. 23.3: Mouth piece

Nebulisers in children

General

1. A metered dose inhaler and spacer (if necessary, with a face mask) is a cheaper and more
convenient delivery system than a nebulisers . However, some infants and children cannot
tolerate face masks and spacers, in which case nebulisers are needed.
2. Where possible, children should be encouraged to breathe through the mouth. If old
enough, they should use a mouthpiece rather than a mask.
3. A maximum time for treatment should be given to parents of children using particular
drug/nebuliser/compressor combinations. Shorter nebulisation times may improve
compliance.
Protocol for using Nebulizers in different conditions

Asthma

1. Nebulisers should be used as recommended in the British Thoracic Society guidelines on the
management of asthma (1993, updated1997).
2. For regular treatment at home alternative delivery methods such as a metered dose inhaler and
spacer, or a dry powder inhaler should first be assessed.

3. For treatment of acute exacerbations re-cognition of the severity of the illness and prompt
treatment are of paramount importance . Treatment with a metered dose inhaler and spacer
may be as effective and cheaper than nebulisation but is not yet widely undertaken.

4. In severe acute asthma frequent broncho-dilator therapy may be helpful. Doses of 1–3 mg/hour
terbutaline or 0.3 mg/kg salbutamol hourly (to a maximum 10 mg/hour) have been used in
trials so far. More randomised controlled trials are now needed to determine the optimum dose
and duration of treatment.

Bronchiolitis

1. Nebulised ribavirin may be considered in infants at high risk or those with severe disease

2. Administration is by a small particle aerosol generator containing a solution of 20 mg/ml,

operated for 12–18 hours per day for 3–7days. Ribavirin has not been shown to reduce the length
of hospital stay, or the need for oxygen or assisted ventilation. It is not used for the majority of
infants with respiratory syncytial virus positive bronchiolitis in the UK.

Bronchopulmonary dysplasia (BPD)

1. Uncontrolled data suggest that inhaled steroids may improve lung mechanics and short
term measures of outcome
2. The best dose, drug delivery device, and the optimum timing of administration are not
known.
3. The side effect profile and the long-term effects of inhaled steroids in these children.
Nebulisers in acute severe asthma

1. The use of nebulisers in acute severe adult asthma.

2. Oxygen should be used as the driving gas whenever possible. Treatment should otherwise
be given using either an electrical compressor or compressed air.

Nebulisers in chronic asthma

Nebulised bronchodilators may be given either to patients with chronic persistent asthma or those
with sudden catastrophic severe asthma (brittle asthma).

If nebulised treatment is prescribed patients must:

1. Have clear instructions from a doctor, specialist nurse, or pharmacist;

2. Be instructed not to treat acute attacks at home without also seeking help; receive an
education programme.
3. Have regular subsequent follow up, including peak flow monitoring, at an asthma clinic and
be seen by a doctor, specialist nurse, or physiotherapist.

Chronic persistent asthma

Nebulised bronchodilators should only be used to relieve persistent daily wheeze at Step 4 or
above of the BTS guidelines on the management of asthma.

The use of nebulisers should only be considered:

1. After a review of the diagnosis.

2. If the airflow obstruction is significantly reversible by bronchodilators (minimum increase in

forced expiratory volume in one second (FEV1) 0.2 l or peak expiratory flow rate (PEFR) 60
l/min).

3. After the patient has demonstrated correct use of his or her usual hand-held inhaler;

4. After a larger dose of bronchodilator – for example, 4–6 actuations of a hand-held inhaler six
hourly, with a spacer if necessary – has been tried for at least two weeks

5. If the patient is taking regular high dose inhaled corticosteroid anti-inflammatory treatment and
is complying with the pre-scribed dose and frequency.
Nebulisers in bronchiectasis

Antibiotics

1. A therapeutic trial of long-term nebulised antibiotics with careful evaluation is justified in

individual patients when background symptoms, severity of acute exacerbations, or risk of
progression warrant antibiotic therapy, provided that oral antibiotics combined with regular
postural drainage have been unsuccessful.

2. Any changes in the volume of purulent sputum and patient well-being between acute
exacerbations and the severity and frequency of exacerbations should be carefully assessed to
evaluate the efficacy of the treatment.

3. Nebulised antibiotics should usually only be used as an adjunct to regular postural drainage and,
for acute exacerbations, oral or intravenous antibiotics.

4. The doses and frequency of treatment with nebulised antibiotics are similar to those for adults
with cystic fibrosis.

Nebulisers in chronic obstructive pulmonary disease (COPD)

These recommendations refer to nebuliser treatment for chronic obstructive pulmonary disease
(COPD). The definition of the disease and degrees of severity, together with re-commendations
for overall treatment strategies, will be available in the forthcoming British Thoracic Society
guidelines for the management of COPD (1997) and are available in a similar document from the
European Respiratory Society and the American Thoracic Society.

Acute exacerbations of copd

1. If the exacerbation is relatively mild, bronchodilators should be given by a hand-held

inhaler using 200–400 lg salbutamol or 500–1000 lg terbutaline.
2. In more severe cases nebulised salbutamol (2.5–5 mg) or terbutaline (5–10 mg) or
ipratropium bromide (500 lg) should be given 4–6 hourly for 24–48 hours or until the
patient is improving clinically.
 3. Combined nebulised treatment (2.5–10 mg of a b agonist with 250–500 lg ipratropium
bromide) should be considered in more severe cases, especially if the patient has had a poor
response to either treatment given alone.

Nebulisers in palliative care

1. Nebulisers may be used for the palliation of patients with cough or breathlessness related to
advanced disease. Any prescription should be reviewed within three days to check efficacy.

2. Bronchodilators may be indicated for the palliation of breathlessness due to concurrent

reversible airflow obstruction.

3. Local anaesthetics such as 2% lignocaine (2–5 ml) or 0.25% bupivacaine (2–5 ml) are indicated
for the palliation of non-productive cough, particularly if due to large airway tumour, bronchial
stent, or diffuse lung disease. They should not be used for the palliation of breathlessness.

Nebulisers in the intensive care unit

General

Nebulised drug therapy may be less effective in patients undergoing mechanical ventilation
because ventilated patients will have more severe lung disease and aerosol deposition from
nebulisers and metered dose inhalers is reduced during mechanical ventilation compared with
spontaneous breathing. There are few published studies proving the efficacy of aerosol drug
treatments in ventilated patients, and it is often necessary to make clinical judgements on the need
for it using clinical data from spontaneously breathing subjects.

Indications

1. Severe acute airflow obstruction: beta agonists, anticholinergic drugs.

2. Respiratory syncytial virus infection in infants: tribavirin(ribavirin).
3. Bronchopulmonary dysplasia in infants: corticosteroids.
4. Adult and infant respiratory distress syndrome: surfactants (beractant, colfosceril palmitate,
poractantalpha, pumactant).
5. Pulmonary infection: antibiotics.
6. Pulmonary hypertension: epoprostenol(prostacyclin).
Methods of aerosol administration

Until further evidence becomes available, any of the following three methods of aerosol ad-
ministration appears to be appropriate for mechanically ventilated patients.

Metered dose inhaler

• The medication can be administered by metered dose inhaler into a spacer connected to the
inspiratory limb of the ventilator circuit with actuation at the onset of lung inflation.
• Humidification should be interrupted for a few minutes before administration.
• The amount of drug reaching the lungs has been estimated as 1.5–2% in infants and 4– 6%
in adults.

Fig. 23.4: Metered dose inhale

Jet nebuliser

• An inspiratory phase activated jet nebuliser connected to an aerosol holding chamber

placed in the inspiratory limb of the circuit, or at least connected to the T piece in the
inspiratory tubing no greater than 30 cm from the Y piece, can be used.
• A high nebuliser gas flow is required and the drug solution should be diluted to fill the
nebuliser to capacity.
• Humidification should be discontinued for a few minutes before and throughout
nebulisation. Aerosol deposition from jet nebulisers has been measured in vivo as 1.2–
3.0% in adults.

Fig. 23.5: jet Nebulizer

Ultrasonic nebuliser

• An ultrasonic nebuliser connected to the inspiratory limb of the circuit may also be used.
• The drug solution should be diluted to fill the nebuliser to capacity and humidification
should be discontinued for a few minutes before and throughout nebulisation.
• Aerosol deposition in vivo has been estimated as 1.3% in infants using the Pentasonic.
• In vivo data are lacking in adults.

Fig. 23.6: Ultrasonic nebulizers

Drug treatment

1. Nebulised beta agonists and ipratropium bromide improve lung function in ventilated patients
with acute airflow obstruction and should be used in combination with systemic steroids,
antibiotics, and intravenous bronchodilators.

2. In the management of respiratory syncytial virus (RSV) infection in mechanically ventilated

infants, the small particle aerosol generator (SPAG) should be used for ribavirin until other
equipment has been shown to be as effective or more
Humidification
Humidity is the presence of molecular water in gas .Humidity therapy is the addition of molecular
water to gas that is delivered to patient .When airway is exposed to cold dry air it decreases the mobility
of cilia. Increase airway irritability ,increase mucus production
,thickening of secretions.

A Humidifier is a device that adds molecular water to gas, whereas nebulizer produces aerosol or
suspension of particles in gas .

Clinical Indications for Humidity therapy-

Maintaining normal physiologic conditions-

1. Adequate humidification and heat to inspired gas.
2. Ensure normal operation of the mucociliary transport.
3. Administration of dry medical gases.
4. Delivery of the bypass upper airway

Goals for humidity therapy-

1. Condition gas to approximate normal inspiratory condition at the point that the gas enters
the airway.
2. Proper humidification minimizes the shift of ISB towards the smaller airway.
3. To accomplish this goal , gas delivered to the nose or mouth should be heated and
humidified to room conditions equivalent to 22 degree C at 50% of relative humidity
whereas gas delivered to the trachea through an endotracheal tube or tracheostomy tube
should be 32 degree C at 100% relative humidity.

TYPES OF HUMIDIFIER-

Active Humidifier- add water and some heat to the inspired air. Example- Bubble humidifier.
 Passive Humidifier- uses the heat and moisture that is exhaled by the patient to humidified the
inspired air. Example- Heat moist exchanger.

1) ACTIVE-

Bubble Humidifier- the gas flows in diffused small bubble of gas that pass through heated water
evaporation takes place along the surface area of bubble. It is commonly used unheated with simple
oxygen administration devices for example- nasal cannula, catheters, simple mask, reservoir
rebreathers ,high concentration venture mask.

Passive Humidifier with or without wicks-water vapourises at the interface where the gas contacts
the surface of heated water or saturated absorbent blotter or wick.

Fig. 23.7: Bubble humidifier

Jet Humidifier- in jet type humidifiers gas enters through a restricted orifice jet which is directed
across a capillary tube that creates a pressure differential that draw water from reservoir and shears
the water into aerosol particles .The jet also extends the airflow into the surface of the water
providing direct contact with gas and acting as a baffle for large particles.

Fig. 23.8: Jet humidifier

2) Passive-

Heat moist exchanger- HME is classified as passive humidifier and referred to as artificial nose,
like the nose the HME captures exhaled heat and moisture and uses it to heat and humidity the
next inspiration. The role of HME is to conserve heat of moisture from inspired air and return them
to patient in next inspiration.
HME work in 1 of 3 ways-

1) Condenser Humdifier- The condenser element is usually made up of metallic gauge,

corrugated metal or parallel metal tubes to provide high thermal conductivity .On inspiration
air cools the condenser to room temperature .On exhalation the saturated gas cools as it enters
the condenser and water drains out while the temperature of the condenser is increased
.On the next inspiration the cool dry air is warmed by condenser , by evaporation of water from
the surface.

Fig. 23.9: Condenser humidifier

2) Hydroscopic condenser Humidifier- contains material with low threshold conductivity such
as paper, wool or foam impregnated with hydroscopic chemical such as calcium chloride or
lithium chloride .During exhalation, warm saturated gas precipitates water on the cool
condenser element while the water molecules bind to the salt without transition from vapour
to liquid state. During inspiration the lower water vapour pressure in the inspired gas
3) liberate water molecules from the hydroscopic compound without a decrease in temperature
due to vapouristaion.
4) Hydrophobic condenser Humidifier- it uses the water repellent elements with the large
surface area and low thermal conductivity that means the heat from conduction and latent heat
from condensation is dissipated. During exhalation condenser temperature rises about 35
degree Celsius .On inspiration cool gas and evaporation cool the condenser down to about 10
degree Celsius.
Contraindications and hazards of HME

Contraindications-

1. Presence of thick, copious and bloody secretions.

2. Presence of large leak around endotracheal tube.
3. Body temperature ˂32-degree C.
4. Minute ventilation of˃10l/min.

Hazards

1. Hypothermia.
2. Underhydration.
3. Impaction of pulmonary secretions.
4. Increase in resistive work of breathing through HME.
5. Mucus plugging of the airways.

DOCUMENTATION

✓ Data from respiratory assessment…………….

✓ Oxygen flow rate and method of delivery…………
✓ Amount per oxygen used………………
✓ Time and location of blood gas sampling………………
✓ Location of oximetry probe and range of saturation…………….
✓ Description of sputum expectorated……………….
 ✓ Coughing and deep breathing exercises…………………
✓ Time and evaluation of respiratory treatments…………………
Table 23.1 Recent evidences:

Journal/ Title Methodology Finding

Author/
Impact
Factor
PLOS One/ The effects of 37 healthy male volunteers were The findings showed that
heated enrolled in a double blind, heated humidification to the
Fujita et al., humidification randomized, placebo-controlled nasopharynx could modulate
2019/ IF:2.74 to nasopharynx crossover trial. Participants wore a breathing patterns with
on nasal newly developed heated improvement of subjective
resistance and humidification mask or non-heated- experience and objective nasal
breathing humidification mask (placebo) for resistance.
10-min each. Subjective feelings
pattern
including dry nose, dry throat, nasal
obstruction, ease to breathe,
relaxation, calmness, and good
feeling were asked before and after
wearing each mask. In addition, the
effects of masks on nasal resistance,
breathing pattern, and heart rate
variability were assessed.
Humidification mask improved all
components of subjective feelings
except for ease to breathe.
Journal Of Adding heated The optimal pattern of nebulization The findings of FEV1
Aerosol humidification followed by a randomized double- changes 40 minutes after the
Medicine and to the blind parallel-group trial comparing end of 5 mg salbutamol
Pulmonary nasopharynx salbutamol and placebo aerosols nebulization in patients
Drug delivery/ could delivered during NIV to 43 undergoing NIV, they
modulate intensive care unit patients. observed a slight
Contentin breathing Aerosols were generated by a improvement that was
et al., patterns with vibrating mesh nebulizer positioned statistically significant
2019/ improvement just after the Y-piece. Spirometry compared with the changes
of subjective was performed immediately before observed with an equivalent
IF:2.84
experience and and at several predetermined time saline volume.
objective nasal points after nebulization. Clinical
resistance. and biological safety parameters
were recorded.
 Activity 24

DEMONSTRATION AND PRACTICE OF HEMODYNAMIC

MONITORING IN ICU
INTRODUCTION
Hemodynamic monitoring in the form of invasive arterial, central venous pressure and pulmonary capillary
wedge pressure monitoring may be required in seriously ill Intensive care unit (ICU) patients, in patients
undergoing surgeries involving gross hemodynamic changes and in patients undergoing cardiac surgeries.
These techniques are considered the gold standards of hemodynamic monitoring but are associated with
their inherent risks.
A number of non-invasive techniques based on various physical principles are under investigation at
present.
Critically ill patients demonstrate pathophysiological end organ changes that require closer observation
& scrutiny.
A variety of monitoring techniques exist that allows optimization of flow and organ perfusion

Component of HDM system

• Each fluid-based pressure monitoring system has :

• Intravascular Catheter

• Connecting Tubing & Stopcocks

• Pressure Transducer

• Continuous Flush Device

• Amplifier

• Oscilloscope /Digital Display

• Processor

• Recorder

Units of Measurement

Hemodynamic pressure readings are measured in units of millimeters of mercury (mmHg) in United States
and in Kilopascals (KPa) in other countries using SI units.
From mmHg to KPa – mmHg X 0.13 = KPa {conversion of mmHg to KPa}

From KPa to mmHg – Kpa X 7.501 = mmHg {conversion of KPa to mmHg}

Types of Catheters

Three different catheters are used in invasive hemodynamic monitoring:

1. Arterial catheter used to monitor systemic arterial pressure (SAP).
2. Central venous pressure (CVP) is measured by a catheter in the superior vena cava or right atrium
3. Pulmonary artery catheter i.e., Swan-Ganz catheter is used to measure pulmonary arterial pressure (PAP)
and pulmonary capillary wedge pressure (PCWP).
Arterial Catheter

In hemodynamically unstable patients who are receiving fluid infusion or drugs to improve circulation,
continuous and accurate blood pressure measurements are essential.

Insertion of arterial catheter to measure SAP is usually placed into the radial artery or can be placed in
brachial, femoral or dorsalis pedis artery also. It also gives convenient access to arterial blood gas samples.

Invasive Arterial Pressure

This system consists of

• Arterial line connected by saline filled non-compressible tubing to a pressure transducer.
• This converts the pressure waveform into an electrical signal which is displayed on the bedside monitor
• Pressurized saline for flushing

Fig 24.1 Measuring arterial blood pressure

Sources of error
• Transducer position : pressure displayed is pressure relative to position of transducer
• In order to reflect blood pressure accurately transducer should be at level of heart.
• Over-reading will occur if transducer too low and under-reading if transducer too high.
• Transducer must be zeroed to atmospheric pressure

Damping
• Damping: Important to have appropriate amount of damping in the system.
• Inadequate damping will result in excessive resonance in the system and an overestimate of systolic
pressure and an underestimate of diastolic pressure.
• The opposite occurs with overdamping.
• In both cases the mean arterial pressure is the most accurate.
• An underdamped trace is often characterized by a high initial spike in the waveform.
Arterial catheter waveform
The systolic upstroke reflects the rapid increase in arterial pressure in the blood vessel during the systole.
The downslope or dicrotic limb is caused by the declining pressure that occurs during diastole. Diacrotic
notch is caused by the closure of the semi-lunar valves.

Fig. 24.2 arterial catheter wave form

Normal Arterial Pressure and Mean Arterial Pressure

The normal arterial pressure ranges in 100-140 mmHg systolic and 60-90 mmHg diastolic in the most
adults. From systolic and diastolic pressures mean arterial pressure can be calculated as follows:
{MAP = (P. systolic + 2 X P. diastolic)}
Normal MAP of 60 mmHg is considered the minimum pressure needed to maintain adequate tissue
perfusion.
Arterial pressure is a product of stroke volume and vascular resistance, changes in either of these
parameters can affect arterial pressure

Pulse Pressure
It is the difference between arterial systolic and diastolic pressures. Normal values ranges from 30-40
mmHg.
High pulse pressure may occur in condition where the stroke volume is high, blood vessel compliance is
low, or the heart rate is low. Low pulse pressure may occur in conditions where stroke volume is low, blood
vessel compliance is high, or the heart rate is high.

High pulse pressure – i.e., > 40mmHg can occur with increasing systolic BP or decreasing diastolic BP.
Systolic pressure may increase when the stroke volume is increased or the blood vessel compliance is
decreased. As long as the diastolic pressure does not increase by the same proportion, a high pulse pressure
results. Bradycardia may also lead to a higher pulse pressure because a slow heart rate allows a blood
volume more time for diastolic runoff and causes a lower diastolic pressure.
In elderly patients, a 10 mmHg rise in pulse pressure increases the risk of major cardiovascular
complications and mortality by about 20%
 Conditions leading to high EXAMPLES
pulse pressure
CONDITIONS
1) High stroke volume Hypervolemia
2) Non-complaint blood vessel Arteriosclerosis
3) Abnormal heart beat Bradycardia,
Heart block

Low pulse pressure – i.e., < 30 mmHg. A decreased stroke volume or increased blood vessel compliance
leads to corresponding decrease in systolic pressure. A low pulse is seen when the diastolic pressure does
not decrease by the same proportion. Tachycardia may also lead to low pulse pressure because a high
heart rate provides less time for the diastolic runoff and causes higher diastolic pressure.

Conditions leading to low EXAMPLES

pulse pressure
CONDITIONS
Low stroke volume Congestive heart failure
High compliance blood Septic shock
vessel
Abnormal heart rate Tachycardia

CENTRAL VENOUS CATHETER

It measures the pressure fillings in the right heart. Insertion of the central venous catheter is commonly
inserted into the subclavian vein or internal jugular vein.

Components of central venous pressure waveform

The upstroke in a waveform reflects the right arterial contraction, c wave reflects the closure of tricuspid
valve during the systole, x downslope occurs as the right atrium relaxes, and v is caused by the right
ventricular contraction and the y downslope reflects the ventricular relaxation and rapid filling of the
blood from, right atrium to the right ventricle.

CVP Measurements
CVP is reported as the mean pressure and its normal range in the vena cava is from 0 to 6 mmHg. When
the measurement is taken in the right atrium the normal values range from 2-7 mmHg, slightly higher
than the CVP readings.

Fig. 24.3 Central venous pressure

 CHANGES EXAMPLES
Decrease in CVP Absolute hypovolemia (blood
dehydration)
Relative hypovolemia (shock,
vasodilatation)
Increase in CVP Positive pressure ventilation,
Increased pulmonary vascular
resistance,
Hypervolemia,
Right ventricular failure,
Left ventricular failure (late
change in CVP)

Fig. 24.4 Pulmonary artery catheter

Insertion of pulmonary artery catheter is into the subclavian or internal jugular vein. From there it can
be further advanced to right atrium, right ventricle and into the pulmonary artery eventually to measure
PCWP.

PAP MEASUREMENT
PAP is measured when the catheter inside the pulmonary artery with the balloon deflated. The normal
systolic PAP is about the same as the right ventricular systolic pressure and ranges from 15-25mmHg.
The normal diastolic PAP ranges from 6-12mmHg. Pulmonary hypertension is defined as a systolic PAP
of >35mmHg or Mean PAP of >25mmHg at rest or >30mmHg with exertion.

Conditions that affect the CONDITIONS EXAMPLES

Pulmonary Artery
Pressure PAP
 Increase Mechanical ventilation, PEEP,
Increase in pulmonary Pulmonary embolism,
vascular resistance Hypoxic
vasoconstriction,
Primary pulmonary
Hypotension
,hypervolemia,
Left to right shunt
Left ventricular failure,
Mitral valve disease
Decrease Mechanical ventilation Positive pressure
ventilation,
hypovolemia

Pulmonary capillary wedge pressure

As the balloon inflates, the pulmonary arterial waveform on the monitor will change to wedged pressure
waveform. The balloon is deflated as soon as the reading of PCWP is obtained. This reading is typically
taken at the end of expiration for both spontaneously breathing and mechanically ventilated patients.

PCWP MEASUREMENTS
Normal range is from 8-12mmHg. Positive pressure ventilation or PEEP can affect the reading due to
the over-distension of alveoli. A higher-than-normal wedge pressure may be seen in left ventricular
dysfunction. A PCWP reading of > 18mmHg with normal PAP suggests the presence of left ventricular
dysfunction.
PCWP measurements may be used to distinguish cardiogenic and non-cardiogenic pulmonary edema. In
pulmonary edema that is caused by the left ventricular failure, the PCWP is usually elevated >18mmHg
along with near normal PAP. In pulmonary edema where PCWP is normal, the cause may be acute
pulmonary hypertension or an increase in capillary permeability (e.g., ARDS)

Conditions that affect the CONDITIONS EXAMPLES

pulmonary capillary wedge
pressure PCWP
Increase Increase in pulmonary blood Hypervolemia,
flow, Left ventricular failure,
Left heat pathology, mitral valve disease
Mechanical factor Over wedging of balloon
Decrease Mechanical ventilation PEEP
Decrease in pulmonary hypovolemia
blood flow

Cardiac Output and Cardiac Index

Pulmonary capillary can measure cardiac output by the thermodilution method.

During cardiac output measurement a small amount (10mL) of iced or room temperature fluid (usually
5% dextrose in the water, D5W) is injected into the proximal port of the pulmonary artery catheter.
 The temperature change of the blood flow is recorded as the blood passes by the thermistor at the
catheter tip.

This and other measurements are computed and flow rate through the heart is displayed as cardiac
output.

Normal cardiac output is from 4-8 L/min. It varies from person to person depending on the size of the
individual, it is common to index the value by dividing cardiac output by the body surface area (BSA).
Cardiac index (C.I.) is normally 2.5 to 3.5 L/min/m2 and is calculated as follows.
{C.I. = C.O. / B.S.A.}

Other Hemodynamic Values

From the CVP, PAP, and other measurements following parameters can be calculated:

Stroke Volume and Stroke Volume Index

{S.V. = C.O. / HR}
{S.V.I. = S.V. / B.S.A.}

Oxygen Consumption and Oxygen Consumption Index

{VO2 = QT X C (a-v) O2}
{VO2 index = VO2 / B.S.A.}

Pulmonary Vascular Resistance

{PVR = (PAP - PCWP) X 80 / C.O.}

Systemic Vascular Resistance

{SVR = (MAP - RAP) X 80 / C.O.}

Mixed Venous Oxygen Saturation :

A special version of the pulmonary artery catheter uses fiberoptic technology to monitor the venous
oxygen saturation (SvO2). It measures SvO2 accurately within clinical range (between 50%-80%).

Table 24.1 Conditions that affect SvO2 measurement

SvO2 CONDITIONS EXAMPLES

Decrease Poor oxygen delivery Low cardiac output, anemia,
Excessive oxygen Hypoxic hypoxia
consumption Fever,
Depletion of venous oxygen seizures,
reserve increased metabolic rate,
increased physical activity,
stress,
pain,
severe and prolonged
hypoxia
Increase Technical problem Improperly wedged catheter,
Increase in oxygen delivery increased cardiac output,
Impaired oxygen utilization Increased CaO2,
Decrease in oxygen Sepsis,
consumption cyanide poisoning,
hypothermia,
post anesthesia,
Pharmacological paralysis.

LESS INVASIVE HEMODYNAMIC MONITORING

Pulse Contour Analysis

It uses an arterial catheter and other data to derive the cardiac output. This is done by special algorithms
using the arterial pressure waveform, arterial vascular compliance, and specific patient data to calculate
stroke volume and stroke volume index.

Pulse Contour Parameters Pulse Contour

Cardiac Output PCCO
Arterial Blood AP
Pressure
Heart Rate HR
Stroke Volume ,CO SV
Stroke Volume SVV
Variation
Pulse Pressure PPV
Variation
Systemic Vascular SVR
Resistance
Index of Left dPmx*
Ventricular
Contractility
 Fig 24.5 Oxygen saturation measurement

NON-INVASIVE HEMODYNAMIC MONITORING

Trans-esophageal Echocardiography
It provides diagnosis and monitoring of many structural and functional abnormalities of the heart. It can
also be used to calculate cardiac output from the measurement of blood flow velocity by recording the
Doppler shift of ultrasound.
TEE is a test that uses sound waves to make pictures of your heart’s muscle and chambers, valves and
outer lining (pericardium), as well as the blood vessels that connect to your heart.
Doctors often use TEE when they need more detail than a standard echocardiogram can give them.
The sound waves sent to your heart by the probe in your esophagus are translated into pictures on a
video screen.
After this test, you may have a mild sore throat for a day or two.
Procedure

Specially trained doctors perform TEE. It’s usually done in a hospital or a clinic and lasts 30 to 60
minutes.
A technician sprays your throat with a medicine to numb it and suppress the gag reflex. You’ll lie on
a table.
A nurse puts an IV (intravenous line) in your arm, and gives you a mild sedative (medicine) to help
you stay calm.
The technician then places small metal disks (electrodes) on your chest. He or she attaches the
electrodes by wires to a machine that will record your electrocardiogram (ECG) to track your heartbeat.
The doctor then gently guides a thin, flexible tube (probe) through your mouth and down your throat,
and asks you to swallow as it goes down.
A transducer on the end of the probe sends sound waves to your heart and collects the echoes that
bounce back. These echoes become pictures that show up on a video screen. This part of the test takes
10 to 15 minutes.

When the doctor is finished taking pictures, the probe, IV and electrodes are removed and nurses
watch you until you are fully awake. Then you can usually get up, get dressed and leave the clinic or
hospital.

Findings
The detailed pictures provided by TEE can help doctors see:
The size of your heart and how thick its walls are.

How well your heart is pumping.

If there is abnormal tissue around your heart valves that could indicate bacterial, viral or fungal
infections, or cancer.

If blood is leaking backward through your heart valves (regurgitation) or if your valves are narrowed
or blocked (stenosis).

If blood clots are in the chambers of your heart, in particular the upper chamber, for example after a
stroke.
 Fig. 24.6 Echocardiography

Table 24.2: Title Methodology Finding

Recent
evidences
Journal/
Author/year
Impact Factor
European heart Pulmonary The effect of pulmonary artery The effects of PA
journal, Clephas artery guided HF therapy was monitoring on quality of
et al., 2024, IF: pressure evaluated in the MONITOR- life, clinical events, and PA
37.6 monitoring in HF trial among predefined pressure were consistent in
chronic heart subgroups based on age, sex, the predefined subgroups,
failure: atrial fibrillation, diabetes without any clinically
effects across mellitus, left ventricular relevant heterogeneity
clinically ejection fraction, HF aetiology, within or across all
relevant cardiac resynchronization endpoint categories.
subgroups in therapy, and implantable
the cardioverter defibrillator.
MONITOR- Outcome measures were based
HF trial upon significance in the main
trial and included quality of
life-, clinical-, and PA pressure
endpoints, and were assessed
for each subgroup.
Journal of Safety and Ten patients clinically ready No safety issues or signal
Cardiac Surgery, feasibility of for semi-elective HeartMate 3 interferences were
Veenis et al., hemodynami LVAD surgery were included, observed. The combined
2021, IF: 1.3 c pulmonary all receiving CardioMEMS for endpoint occurred in 60%
artery pre-surgical filling pressure of historical controls, 0% in
pressure optimization. Patients were normal and 83% in elevated
monitoring grouped by mean pulmonary mPAP group. Post‐
using the artery pressure (mPAP): discharge, the hospital‐free
CardioMEM normal (≤25 mmHg, n=4) or survival was significantly
S device in elevated (>25 mmHg, n=6), better, and the QoL
LVAD and compared to a historical improved more in the
management cohort (n=20). Outcomes normal compared to the
assessed included device elevated mPAP group
safety, a composite endpoint
(mortality, kidney injury, renal
therapy, or RV failure),
hospital-free survival, QoL,
and exercise tolerance at one
year.
 ACTIVITY- 25

DEMONSTRATION OF AIRWAY CLEARANCE TECHNIQUE AND

TECHNOLOGIES IN ICU
INTRODUCTION:
Airway clearance may be impaired in patients with disorders that are associated with abnormal cough
mechanics (e.g., muscle weakness), altered mucociliary clearance (e.g., primary ciliary dyskinesia) or
structural defects (e.g. bronchiectasis). A variety of interventions are used to enhance airway clearance
with the goal of improving lung mechanics and gas exchange, and preventing atelectasis and infection.

Active technique consists of:

• Active cycle of breathing technique
• Autogenic drainage

Passive technique consists of:

• Postural drainage
• Manual therapy

ACTIVE CYCLE OF BREATHING TECHNIQUE:

The ACBT is used to mobilize and clear excess pulmonary secretions and to improve lung functions .it
is a flexible method of treatment which can also be used in conjunction with postural drainage
positioning.
It consists of following three phases:
1. Breathing Control
2. Thoracic Expansion Exercise
3. Forced Expiratory Technique

INDICATIONS
Post-surgical /pain (rib fracture)
Chronic increased sputum production e.g. .in chronic bronchitis, cystic fibrosis
Acute increase sputum production.
Poor expansion
Sputum Retention

Cystic fibrosis
Bronchiectasis
Atelectasis
Respiratory muscle weakness
Mechanical ventilation
Asthma
To obtain sputum specimen for diagnostic analysis

CONTRAINDICATIONS:
Patients who are unable to breath spontaneously
Unconscious patients
 Patients unable to follow instructions

EQUIPMENT REQUIRED
Plinth, pillow.

POSITION: ACBT can be performed in sitting, lying, side lying positions.

PROCEDURE:
1. BREATHING CONTROL: The patient is instructed to breath in a relaxed manner using normal tidal
volume. The upper chest and shoulders should remain relaxed, and the lower chest and abdomen should
be active. The breathing control phase should be last as long as it required for the patient to relax and
prepare for the next phases, usually 5 to 10 seconds.
2. THORACIC EXPANSION (3-4 times): The emphasis during the thoracic expansion phase is on
inspiration. The patient is instructed to take in a deep breath to the inspiratory reserve volume; expiration
is passive and relaxed. The caregiver or the patient may place a hand over the area of the thorax being
treated to facilitate increased chest wall movement.
3. FORCED EXPIRATORY TECHNIQUE (2-3 Huffs): This phase consists of huffing interspersed
with breathing control. A huff is a rapid, forced exhalation without maximal effort. This maneuver is
comparable to fogging a pair of eyeglasses with warm breath so they may be cleaned.

Fig. 25.1: Active cycle of breathing technique

PRECAUTIONS
Inadequate pain control of wounds of chest wall/abdomen
Rib fractures
Bronchospasm
Acute unstable head, neck or spinal injury
Increased ICP or known intracranial aneurysm
Inability to control transmission of infection from patients known or suspected

to have to transmission by droplet nuclei e.g. tuberculosis

 Pulmonary enema
Pulmonary embolism

AUTOGENIC DRAINAGE:

AIM: The aim is to maximize airflow within the airways and to improve the clearance of mucus and
ventilation

INTRODUCTION:
Autogenic drainage is also known as self-drainage, it is an anti-dyspnea technique that uses the
expiratory flow to mobilize bronchial secretion. The main principle behind to reach the highest possible
airflow in different generation bronchi by controlled breathing (controlling the desire to cough until
secretion are high up) is put into practice by three phases of breathing exercise.

PHASES OF AUTOGENICDRAINAE:
1. Unsticking Phase: This phase starts with a normal inspiration and is followed by a breath hold to
ensure equal filling of lung segments by collateral filling: then a deep exhalation is made into the
expiratory reserve volume range.
2. Collecting Phase: This phase of tidal volume breathing gradually changing from the expiratory
reserve volume into the inspiratory reserve volume range.
3. Evacuating Phase: It consists of deeper inspiration into the inspiratory reserve volume, with huffing
often used to help in evacuating the mobilized secretions.

Fig. 25.2 Phases of autogenic drainage

INDICATIONS
Secretion retention in patients with unstable or complaint airways
Patient seeking freedom from postural drainage and assistance that prefer the option of upright
posture.
Patient who are older than 8 years who have concentration to learn the techniques.

PASSIVE TECHNIQUE

PROCEDURE:
A rhythmical force is provided

POSTURAL DRAINAGE TECHINQUE

AIM:
The aim of postural drainage is to allow gravity to assist the drainage of the respiratory secretions. There
are different positions which are based on anatomy of the bronchial tree and are aimed at draining lobes
or lung segments. the right lung is divided into three lobes (upper, middle, lower), while left lung is
divide has only two lobes (upper and lower).

INDICATION:
Inability or reluctance of patient to change body position (mechanical ventilator)
Atelectasis
Evidence of difficulty with secretion clearance
Difficulty in clearing secretions with expectorated sputum production greater than 25 -30 ml/day
(adult)
Evidence of retained secretion in the presence of artificial airways.
Presence of atelectasis caused by suspected of being cause by mucus plugging.
Diagnosis of disease e.g. bronchiectasis or COPD.
Patient who are weak or elderly.

EQUIPMENT REQUIRED: Plinth, pillow.

Fig. 25.3: Postural drainage

CONTRAINDICATION

ALL POSITION
• ICP >20mmHg
• Head and neck injury
• Active hemorrhage with hemodynamic instability
• Recent spinal surgery
• Acute spinal injury active hemoptysis

TRENDELENBURG POSITION
ICP>20 mmHg
Patients in with increased ICP e.g. neurosurgery
Uncontrolled hypertension
Distended abdomen
Esophageal surgery

COMPLICATIONS
Hypoxemia
Increased ICP
Pain or injured muscle, ribs or spine.
Acute hypotension
Pulmonary hemorrhage

MANUAL TECHNIQUE

PERCUSSION

AIM:
Loosening retained secretions from the airways so that may remove by suctioning or expectoration by
clapping the therapist cupped hands against the thorax over the affected lung segments, trapping air
between the patient thorax and therapist hand. Frequency: 100-480 times /min.

VIBRATION

AIM:
Removing secretion from the lung’s periphery to the large airways where they may be suctioned or
expectorated

PROCEDURE:
Gentle high frequency force applied on patient’s thorax
Frequency -12-20 Hz

SHAKING
AIM:
Removing the secretions from the lung’s periphery to the large airways where they may be suctioned or
expectorated

PROCEDURE:
An isometric contraction of arm and forearm
Frequency 2 Hz

CONTRAINDICATION
Subcutaneous emphysema
Epidural spinal infusion
Recent skin graft
Open wound
Skin infection of thorax

Recently placed pacemaker

Pulmonary TB
Lung contusion
Bronchospasm
Osteomyelitis of rib
Osteoporosis
Coagulopathy
Complaint of chest wall pain

AIRWAY CLEARANCE DEVICES

Airway clearance devices help in clearing the secretion from the chest, assist in maintaining functional
breathing and maintaining patency of airways /the type of airways clearance device that were developed
to assist in airway clearance.

POSITIVE END EXPIRATORY PRESSURE USED:

OSCILLATORY PEP DEVICES

1. QUAKE
2. FLUTTER
3. ACEPELLA
4. HIGH FREQUENCY CHEST WALL OSCILATION
5. SUCTIONING
6. MANUAL HYPERINFLATION
Fig. 25.4: Quake Fig. 25.5: Acapella Fig. 25.6: Flutter

NON-OSCILLATORY PEP DEVICE

1. Thera PEP

Fig 25.7: Thera PEP device

POSTIVE EXPIRATORY PRESSSURE DEVICES

PEP is the ability to enhance and promote mucus clearance by either preventing Airway collapsed by
stenting the airways or increasing functional residual capacity. One way valve connected to either a
small exit orifice. a disposable or permanent manometer is incorporated into the system between the
one-way valve and the resistor to measure the expiratory pressure. Low pressure pep devices typically
generate a pressure range of 5-20cm of water at mid expiration. High pressure pep ranges from 26- 102
cm water, which is typically achieved by performing a forced expiratory maneuver directly into a pep
mask after maximal inspiration.

INDICATIONS
To aid in mobilization
To prevent reverse atelectasis

CONTRAINDICATIONS
Increase work of breathing
 Increase in intracranial pressure
Hemodynamic instability
Gastric insufflations
Complications associated with –esophageal surgery
Active hemoptysis Untreated tension pneumothorax

PATIENT INSTRUCTION FOR PEP THERAPY

The patient should sit comfortably and upright while loading the mask firmly over the nose and
mouthpiece tightly between the lips.
Adjust the expiratory resistor dial to prescribed the setting
Have the patient breath from the diaphragm, taking in a larger than normal tidal breath, but not the
total lung capacity.
Exhalation time should last approximately 3 times longer than inhalation
Patient should perform 10-20 per breath, and then perform 2-3 forced exhalation or huff.
Repeat steps 3-6 until secretions are cleared, or until the predetermined treatment period has elapsed.

.
HIGH- FREQUENCY CHEST WALL OSCILLATIONS

It is also referred to as high-frequency chest compression, consist of an inflatable vest linked to an air-
pulse generator. It works by differential airflow (i.e., the expiratory flow rate is higher than the
inspiratory flow rate), allowing the mucus to be transported from the periphery to the central airways
for expectoration. It has also been shown to decrease the viscosity of mucus, making it easier to mobilize
the secretion.

TREATMENT WITH HIGH- FREQUENCY CHEST WALL OSCILLATIONS:

The patient should be seated upright in a chair, and tubing should be securely connected to the air
plus generator.
Start the aerosol therapy before turning on HFCWO system.
The pressure control setting should be adjusted according to the patient comfort
The treatment should progress through different frequencies from low (7 to 10 Hz) to medium (10 to
14 Hz) and then to high (14 to 20 Hz), to achieve both higher flow rates and increased lung volume
may be custom made for very large or obese adults.
It can be appropriate for those patients in whom PD positions are contraindicated, and it has also been
used successfully in reclining patients who are unable to tolerate the upright sitting position.
Use of HFCWO may result in time savings at home, as well as in a hospital or long-term care facility,
because nebulized medications may be administered concurrently with the airway clearance treatment
and all lobes of the lungs are treated simultaneously.
 It provides independence for long-term use at home, as well as for acute exacerbations in the hospital.

DISADVANTAGE
Cost of the equipment

Fig 25.8 HFCWO device

INTRAPULMONARY PERCUSSIVE VENTILATION

IPV is an airway clearance method that simultaneously delivers intrathoracic percussion and
aerosolized solution for bronchodilation.
An apparatus known as phasitron is the functional component in the intrapulmonary percussive
ventilator.
The phantom provides high frequency impulses during inspiration, while positive expiratory pressure
is maintained throughout passive exhalation.
The pressure generated is between 10 and 30 cm H2O.
A high output nebulizer provides a dense aerosol to deliver medications and hydrate secretions.
The IPV device made by Percussionaire works in a manner similar to that of the HFCWO except that
a pneumatic device delivers the oscillation internally instead of externally.
A mouthpiece delivers high flow rate mini-bursts of gases into the lungs at rates of 100-240 cycles
per minute. This device provides percussion at 6 to 14 Hz.

Treatment with IPV:

• One IPV model meant for institutional use is the percussionnaire model IPV-1 which is
powered by 50 psi of gas.
• Percussive rates on frequency range from less than 100 to greater than 225 cycles per minute.
• This model has the capability to be used with endotracheal tube and can be installed on a wheel
stand for greater mobility.
• Use of hospital unit must be supervised by respiratory care practitioner.
 • The percussionnaire impulsator is self-contained for home and powered by compressor, but it
may only be used in clinical situation. It generates 40 psi source pressure, which provides for
ancient delivery of impulses and aerosolized medications.
• A new model by percussionaire the HC impulsator, is a portable IPV device that weighs less
than 15 pounds, allowing patients to use it when travelling.

Advantage:
• Delivers of deep penetrating aerosol to the lower airways
• Loosening of thick cohesive and adhesive secretions

• Mobilization and clearance of retained secretions.

• IPV is available for home use and can be continued during hospitalization.
• Homnick reported that three-fourths of the patients using IPV in one study estimated increased
sputum production, and satisfaction was high for comfort and independence

Disadvantage:
A feeling of claustrophobia or chest fullness may be a factor in deciding whether to use IPV.
The availability of IPV in the clinical setting is not as common as other airway clearance devices;
therefore, respiratory care practitioners may not be as familiar or comfortable with its application
The IPV device is more expensive than a PEP device but less costly than a unit for HFCWO

Table 25.1 Recent Title Methodology Finding

evidences:
Journal/
Author/Impact
Factor
BMC Pulmonary Efficacy A randomized controlled trial The 6MWD, end-dyspnea,
Medicine, Xu et and safety included 25 Pre-COPD or mild- and end-fatigue improved
al., 2023, IF: 2.6 of long-term to-very severe COPD patients, significantly in the
use randomized into an intervention intervention group when
of a positive group (n = 13, PEP device, 5 compared with the control
expiratory cmH2O) and a control group (n group. All subjects in the
pressure device = 12, Sham-PEP, 0 cmH2O). intervention group reported
in chronic Using a spring-loaded resistor that 4 h of daily use of the
obstructive face mask, subjects were treated PEP device was well
pulmonary 4 hours daily for 2 months. tolerated and accepted and
disease Outcomes, including the six- there were no adverse
patients, minute walk test, pulmonary events.
a randomized function, Modified British
controlled trial Medical Research Council
score, and end-tidal CO2, were
assessed at baseline and after
two months.
International Effects of This systematic review and From 5439 identified
Journal of High- meta-analysis followed the articles, 13 studies (with 756
Chronic Frequency Preferred Reporting Items for patients) were included in
Obstructive Chest Wall Systematic Review and Meta- this meta-analysis.
Pulmonary Oscillation on analyses (PRISMA) guidelines. Compared to other airway
Disease, Huang et Acute Automated literature database clearance techniques,
al., 2022 Exacerbation searches were conducted from HFCWO significantly
of Chronic the earliest records to March 31, increased expectorated
Obstructive 2022. The methodological sputum volume by 6.18 mL,
Pulmonary quality of the included studies shortened hospital stay by
Disease: A was assessed using the 4.37 days. However, FEV1
Systematic Cochrane Risk of Bias tool (%), PaO2, and PaCO2 did
Review and (RoB 2.0), and meta-analysis not improve significantly.
Meta-Analysis software (RevMan 5.4) was
of Randomized used to analyze the data.
Controlled
Trials

Annals of the The Use of Databases for systematic Eighteen studies with
American Airway reviews and published evidence available data were eligible
Thoracic Society, Clearance were searched. Studies were for this review, totaling 855
Daynes et al., Devices in the included if they were participants. Airway
2021, IF: 6.8 Management randomized and compared an clearance devices
of Chronic airway clearance device to demonstrated significant
Obstructive usual care or control. Studies improvements in sputum
Pulmonary were required to report at least volume. There were
Disease one of the following: significant improvements in
exacerbations, sputum volume, the rate of exacerbation
hospitalizations, and health- frequency at 6 months. No
related quality of life. Data were significant improvement was
extracted and assessed for risk noted for the Saint George’s
of bias, and outcomes were Respiratory Questionnaire in
synthesized using RevMan stable patients. There was an
improvement of 25.73(27.30
to 24.15) for the COPD
Assessment Test and
21.72(22.85 to 20.59) for the
Breathlessness Cough and
Sputum Score.
 ACTIVITY – 26

DEMONSTRATION AND PRACTICE VARIOUS

BREATHING EXERCISE TECHNIQUES IN ICU PATIENTS
Breathing exercise are the fundamental interventions for the prevention for acute and chronic
pulmonary disease patients with high spinal cord lesions and who underwent thoracic and
abdominal surgery and bed ridden patients. Breathing exercise have effect on patient’s rate and
depth of ventilation, so this technique is used to improve the pulmonary status and increase
patients’ overall endurance.

Breathing exercises are designed to retrain the muscles of respiration , improve ventilation , lessen
the work of breathing and improve gaseous exchange and patient’s overall function in daily
activities. Breathing exercises are frequently advised for patients with COPD (chronic bronchitis,
emphysema, asthma) or cystic fibrosis, for patients with a high spinal cord lesion, for patients who
have undergone thoracic or abdominal surgery

Breathing exercises can be of different forms including diaphragmatic breathing, resisted

diaphragmatic breathing , segmental breathing, purse lip breathing, inspiratory resistance training,
incentive spirometry, and breathing techniques for the relief of dyspnoea during exertion.
Breathing exercises or ventilatory training should be used only on the management to improve
pulmonary status and to increase a patient‘s overall endurance and function during daily living
activities. Exercises to improve ventilation often are combined with medication, airway clearance
techniques, the use of respiratory devices, and a graded exercise program are given depending on
the patient‘s underlying pathology .

GOALS OF BREATHING EXERCISES:

• Improve ventilation

• Increase the effectiveness of cough mechanism and promote airway clearance

• To prevent post operative pulmonary complications.

• To improve the strength endurance coordination of the muscle of ventilation.

• Maintain and improve chest and thoracic spine mobility.

• Promote relaxation and relieve stress.

• To teach the patient how to deal with episodes of dyspnea

 • Correct inefficient or abnormal breathing patterns and decrease the work of breathing.

• Improve a patient‘s overall functional capacity for daily living, occupational, and
recreation

PRINCIPLES

• Area of the exercises

• Explanation and Instructions to the patients

• Patients position

• Evaluation of the patient

• Demonstration of exercise

• Patient practice

GUIDELINES FOR TEACHING BREATHING EXERCISES

• Choose a quiet area to get a proper interaction with minimal distraction.

• Explain the patient about the aim and how it works for his impairment.

• Have the patient in relaxed position and loosen the clothes, make him in semi fowler
position with head and trunk elevated approx. -45 degree (total support to the head and
trunk flexing the hip and knees with pillow support) the abdominal muscle become
relaxed. Other positions , such as supine , sitting , or standing , may be used as the patients
progresses during treatment.

• Observe and access the patients spontaneous breathing pattern while at rest and during
activity. Determine whether ventilatory training is indicated. Establish a baseline for
assessing changes, progress, and outcomes of intervention.
• If necessary, teach the patient relaxation techniques, relax the muscles of upper thorax
,neck and shoulder to minimize the use of accessory muscle work

• Special attention on sternocleidomastoids, upper trapezius and levator scapulae.

• Depending on the patient‘s underlying pathology and impairments, determine whether to

emphasize the inspiratory or expiratory phase of ventilation. Demonstrate the desired
breathing pattern to the patient. Have the patient practice the correct breathing pattern in
a variety of positions at rest and with activity

• Have the patient practice the correct technique in variety of positions at the rest and
activity.

PRECAUTIONS

• Never allow the patient to do forced expiration ,it may increase the turbulence in the airway
which leads to bronchospasm and airway resistance.

• Avoid prolonged expiration ,it may cause the patient to gasp with the next inspiration and
the breathing pattern irregular and inefficient.

• Do not allow the patient to initiate inspiration with accessory muscles and upper chest ,
advise him that upper chest should be quiet during breathing.

• Allow the patient to perform deep breathing only for 3-4 times (inspiration and expiration)
to avoid Hyperinflation.
Breathing exercise for Obstructive lung Breathing exercise for restrictive lung disease
disease

• Diaphragmatic breathing • Diaphragmatic breathing

• Pursed lip breathing • Segmental breathing

• Resistive exercise training • Glossopharyngeal breathing

• Breathing exercise synchronized with • Resistive exercise training

activity

• Breathing exercise synchronized with

activity

INDICATIONS

• Cystic fibrosis

• Bronchiectasis

• Atelectasis

• Lung abscess

• Pneumonias

• Acute lung disease

• For patients with a high spinal cord lesion/spinal cord injury, myopathies etc.

• COPD-emphysema, chronic bronchitis

• After surgeries(thoracic or abdominal surgery)

• For patients who must remain in bed for an extended period of time(obstruction due to
retained secretions)

• As relaxation procedures
• CONTRAINDICATION

• Severe pain and discomfort

• Acute medical or surgical emergency

• Patients with reduced conscious level

• Increased ICP

• Unstable head or neck injury

• Active hemorrhage with hemodynamic instability or hemoptysis

• Flail chest

• Uncontrolled hypertension

• Anticoagulation

• Rib or vertebral fractures or osteoporosis

• Acute asthma or tuberculosis

• Patients who have recently experience a heart attack.

• Patients with skin grafts or spinal fusions will have undue stress placed on areas of repair.

• Bony metastases, brittle bones, bronchial hemorrhage , and emphysema are contractions
for undue stress to the thoracic area.

• Recent (within one hour)meal or tube feed.

• Untreated pneumothorax.
TYPES OF BREATHING EXERCISES

• Diaphragmatic breathing

• Glossopharyngeal breathing

• Pursed lip breathing

• Segmental breathing (costal expansion exercise)

a. Apical breathing

b. Lateral costal expansion

c. Posterior basal expansion

DIAPHRAGMATIC BREATHING

• Diaphragm is the primary muscle for breathing(inspiration)

• Diaphragm controls breathing at an involuntary level , a patient with primary pulmonary

disease like COPD can be taught breathing control by optimal use of diaphragm and
relaxation of accessory muscles.

• Diaphragmatic breathing exercise to mobilize lung secretions.

PROCEDURE

• Prepare the patient in relaxed and comfortable position in which the gravity assists the
diaphragm such as semi fowler position. Patient initiates the breathing pattern with the
accessory muscles of inspiration (shoulder and neck musculature), start instruction by
teaching the patient how to relax those muscles (shoulder rolls or shoulder shrugs coupled
with relaxation).

• If you notice any accessory muscle activation ,stop and do relaxation techniques(shoulder
roll or shrugs coupled with relaxation)
• Place your hands over the rectus abdominals just below the anterior coastal margin .Ask
the patient to breath slowly and deeply via nose by keeping the shoulder relaxed and upper
chest quiet allowing the abdominal to rise. Now ask him to slowly let all the air out using
controlled expiration through mouth.

• Have him to practice this for 2-4 times if he finds any difficulty in using diaphragm have
the patient inhale several times in succession through the nose by using sniffing action, this
facilitates the diaphragm.

• For self-monitor have the patient’s hand over the anterior coastal margin and feel the
movement (hand rise and fall) by placing one hand over abdomen, he can also feel the
contraction of abdominal muscles which occurs with controlled expiration or coughing.

• After he understands and able to do the controlled breathing using a diaphragmatic pattern
keep the shoulder relaxed and practice in variety of positions (supine, sitting, standing) and
during activity(walking and climbing stairs).

Fig 26.1 Diaphragmatic breathing

Resisted diaphragmatic breathing

• PT use small weight, such as sand bag to strengthen and improve his/her endurance of the
diaphragm

• Have the patient in a head up position.

• Place a small weight (1.30-2.20 kg or 3-5 lb.) over the epigastric region of his abdomen.

• Tell the patient to breath in deeply while trying to keep the upper chest quiet.

• Gradually increase the time that the patient breaths against the resistance of weight.

• Weight can be increased when he can sustain diaphragmatic breathing pattern without the
use of any accessory muscle of inspiration for 15minutes.

Fig 26.2 Resisted diaphragmatic breathing

Glossopharyngeal breathing

• It is a means of increasing a patient’s inspiratory capacity when there is a severe weakness

of the muscle of inspiration.

• It is taught to patients who have difficulty in deep breathing.

• It is used primarily for ventilatory dependent patients due to absent or incomplete

innervation of diaphragm because of high cervical cord injury or neuromuscular disorders.
 • Glossopharyngeal breathing with inspiratory action of neck muscles can reduce ventilatory
dependence or can be used as an emergency procedure for malfunctioning of ventilator.

Procedure

• Patients take several gulps of air (6 to 10), then by closing the mouth the tongue pushes the
air back and trap it in the pharynx, the air is then forced to lungs when the glottis is opened.

• This increases the depth of inspiration and patient’s inspiratory vital capacity.

Fig 26.3 Glossopharyngeal breathing

Pursed lip breathing

• Pursed lip breathing is a strategy that involves lightly pursing the lips together during
controlled exhalation.

• Teach to patients with COPD to deal with episodes of dyspnea.

• It helps to improve ventilation and releases trapped air in the lungs.

• Keeps the airway open longer and prolonged exhalation slows the breathing rate.

• It moves old air out of the lungs and allow new air to enter the lungs.
 Procedure

• Patient is in a comfortable position and relaxed , explain the patient about the expiration
phase (it should be relaxed and passive).

• Abdominal muscle contraction must be avoided (therapist hand over the patients abdominal
to check for contraction).

• Ask the patient to breathe in slowly and deeply through the nose and then breathe out gently
through lightly pursed lips (blowing on and bending the flame of a candle).

• By providing slightly resistance an increased positive pressure will generate with in the
airway which helps to keep open small bronchioles that otherwise collapse.

• It can be applied as 3-5 minutes” rescue exercise” or an emergency procedure to counteract

acute exacerbations or dyspnea (shortage of air or breathlessness)in COPD and asthma.

Fig 26.4 Pursed lip breathing

Segmental breathing

• It is performed on a segment of lung, or a secretion of chest wall that needs increased

ventilation or movement.
 • Hypoventilation occurs in certain areas of the lungs because of chest wall fibrosis ,pain
after surgery, atelectasis, trauma to chest wall ,pneumonia and post mastectomy scar.

• Therefore, it will be important to emphasize expansion of such areas of the lungs and chest
wall.

Advantages of Segmental breathing

• Prevent accumulation of pleural fluid and secretions.

• Decreases paradoxical breathing

• Decrease panic episode

• Improve chest mobility

Techniques

• Lateral costal expansion

• Posterior basal expansion

• Right middle lobe or lingula expansion

• Apical expansion

Fig 26.5: Apical breathing

Lateral costal expansion

• This is sometimes called lateral basal expansion and may be done unilateral or bilaterally.
• The patient may be sitting or in a hook lying position.

• Place your hand along the lateral aspect of the lower ribs.

• Ask the patient to breathe out, and feel the rib cage move downward and inward.

Fig. 26.6: Lateral costal expansion

• As the patient breathe out, and place firm downward pressure into the ribs with the palms
of your hands.

• Just prior to inspiration, apply a quick downward and inward stretch to the chest. This
places a quick stretch on the external intercostals to facilitate their contraction. These
muscles move the ribs outward and upward during inspiration.

• Apply light manual resistance to the lower ribs to increase sensory awareness as the patient
breaths in deeply and the chest expands.

• When the patient breaths out, assist by gently squeezing the rib cage in a downward and
inward direction.
 • The patient may then teach to perform the maneuver independently, ask him to apply
resistance with his hand or with a towel.

Fig 26.7 Segmental breathing exercises

Posterior basal expansion

• This form of segmental breathing is important for the post-surgical patients who is in bed
in a semi-reclining position for an extended period of time because secretions often
accumulate in the posterior segments of the lower lobes.

• Patient have to sit and lean forward on a pillow, slightly bending the hips.

• Place your hand over the posterior aspect of the lower ribs.

Fig 26.8 Posterior basal expansion

Right middle lobe or lingula expansion

While the patients in sitting, place your hand at either the right or left of the patient’s chest just below
the axilla, and follow the same procedure in lateral costal expansion .

Apical expansion

• Patient in sitting position.

• Apply pressure (usually unilaterally) below the clavicle with the finger tips.

• This pattern is appropriate in appropriate in an apical pneumothorax after a lobectomy.

Fig 26.9 Apical expansion

Incentive spirometry:

Incentive spirometry is a form of ventilatory training that emphasizes sustained maximum

inspirations. The patient inhales as deeply as possible through a small, handheld spirometer that
provides visual or auditory feedback about whether a target maximum inspiration was reached.
Typically, this breathing technique is performed while using a spirometer, but it also may be
performed without the equipment.
The purpose of incentive spirometry is to increase the volume of air inspired. It is used primarily
to prevent alveolar collapse and atelectasis in postoperative patients. Despite the widespread use
of incentive spirometry for patients after surgery, the effectiveness of this technique alone or in
addition to general deep breathing and coughing for the prevention of postoperative pulmonary
complications is not clear.

Fig 26.10: Incentive spirometry

Procedure:

Have the patient assume a comfortable position (semi reclining, if possible) and inhale and exhale
three to four times and then exhale maximally with the fourth breath. Then have the patient place
the spirometer in the mouth, inhale maximally through the mouthpiece to a target setting and hold
the inspiration for several seconds. This sequence is repeated five to ten times several times per
day.
Inspiratory resistance training

Inspiratory resistance training, using pressure- or flow-based devices to provide resistance to

airflow, is designed to improve the strength and endurance of the muscles of inspiration and
decrease the occurrence of inspiratory muscle fatigue. This technique has been studied in patients
with acute and chronic, primary and secondary pulmonary disorders, including COPD, cystic
fibrosis, respiratory failure and ventilator dependence (weaning failure), chronic heart failure,14
and chronic neuromuscular disease. Although reviews of the literature have demonstrated that
outcomes of inspiratory muscle training programs in patients with pathologies are inconsistent,
some positive changes reported after training are increased vital capacity, increased exercise
capacity, and fewer episodes of dyspnea. Inspiratory muscle training also has been studied and
found to be effective (as evidenced by decreased respiratory rate) in patients with cervical-level
spinal cord lesions.

Procedure:

The patient inhales through a resistive training device placed in the mouth. These devices are
narrow tubes of varying diameters or a mouthpiece and adapter with an adjustable aperture that
provide resistance to airflow during inspiration and therefore place resistance on inspiratory
muscles. The smaller the diameter of the aperture and the faster the rate of airflow, the greater is
the resistance. The patient inhales through the device for a specified period of time several times
each day. The time is gradually increased to 20 to 30 minutes at each training session to increase
inspiratory muscle endurance.
 Fig: 26.11: Inspiratory muscle training

Positive expiratory pressure breathing:

Positive expiratory pressure breathing is a technique in which resistance to airflow is applied during
exhalation, similar to what occurs during pursed-lip breathing, except that the patient breathes
through a specially designed mouthpiece or mask that controls resistance to airflow. This breathing
technique is used to hold airways open during exhalation to mobilize accumulated secretions and
improve their clearance. Positive expiratory pressure breathing provides an alternative or adjunct
to postural drainage which a patient can perform independently.
Procedure:
Positive expiratory pressure breathing is performed in an upright position, preferably seated with the
elbows resting on a table. The procedure can be performed against low or high pressure. A low-
pressure technique involves tidal inspiration and active, but not forced, expiration through a
mouthpiece or mask. The patient inhales, holds the inspiration for 2 to 3 seconds, and then exhales,
repeating the sequence for approximately 10 to 15 cycles. The patient removes the mouthpiece or
mask, takes several ―huffs and then coughs to clear the mobilized secretions from the airways. The
breathing sequence typically is repeated four to six times with a total treatment session lasting about
15 minutes
Respiratory resistance training:

The process of improving the strength or endurance of the muscles of ventilation is known as
respiratory resistance training (RRT). Other descriptions used to denote this form of breathing
exercises are ventilatory muscle training, inspiratory (or expiratory) muscle training, inspiratory
resistance training, and flow-controlled endurance training.

These techniques typically focus on training the muscles of inspiration, although expiratory muscle
training also has been described. RRT is advocated to improve ventilation in patients with
pulmonary dysfunction associated with weakness, atrophy, or inefficiency of the muscles of
inspiration or to improve the effectiveness of the cough mechanism in patients with weakness of
the abdominal muscles or other expiratory muscles. the principles of overload and specificity of
training apply to skeletal muscles throughout the body, including the muscles of ventilation. In
humans, it is not feasible to use invasive procedures to evaluate morphological or histochemical
changes in the diaphragm that may occur as the result of strength or endurance training.

Respiratory muscle strength (either inspiratory or expiratory) also is evaluated indirectly with
measurements of inspiratory capacity, forced expiratory volume, inspiratory mouth pressure using
a spirometer, vital capacity, and increased cough effectiveness.
Precautions;
Avoid prolonged periods of any form of resistance training for inspiratory muscles. Unlike muscles
of the extremities, the diaphragm cannot totally rest to recover from a session of resistance
exercises. Use of accessory muscles of inspiration (neck and shoulder muscles) is a sign that the
diaphragm is beginning to fatigue.
Table 26.1 Recent evidences:

Journal/ Title Methodology Finding

Author/
Impact
Factor
Journal of The effect In this study, aim was to assess BP The mean systolic BP (SBP),
clinical of pursed and heart rate effects in HT urgency diastolic BP (DBP), and HR of
hypertension, lip patients practicing pursed-lip the intervention group in the
Mitsungnern breathing breathing and number counting 3rd hour were significantly
et al., 2021, combined (PLB with NC)—a practice that lower than the
IF: 2.7 with promotes mindfulness with baseline values at −28.2 mm
number deep/slow breathing patterns. In a Hg, and −4.9 beats per minute
counting on randomized controlled trial, 110 (bpm), respectively. In the
blood patients were equally allocated to control group, both the mean
pressure intervention and control groups. SBP and DBP were also
and heart The intervention group was trained significantly lower in the 3rd
rate in and encouraged to do PLB with NC hour. However, HR reduction
hypertensiv during their emergency room was inconclusive. When the
e urgency admission, while the control group two groups were compared, a
patients: A received conventional medical care. greater degree of reduction was
randomized found in the intervention group
controlled for SBP, DBP, and HR.
trial.
 ACTIVITY-27
DEMONSTRATION AND PRACTICE OF DEFIBRILLATORS

AND CARDIOPULMONARY RESUSCITATIONS

CARDIOPULMONARY RESUSCITATION:
Is an emergency procedure that combines chest compression often with artificial ventilation in an
effort to manually preserve intact brain function until further measures are taken to restore
spontaneous blood circulation and breathing in a person who is in cardiac arrest.
Or
CPR is an emergency first-aid procedure that is used to maintain respiration and blood circulation
in a person, whose breathing and heartbeats have suddenly stopped, (one or more vital functions
failed).

SIGNS AND SYMPTOMS OF CARDIORESPIRATORY ARREST

• Person becomes unconscious with cold, moist and pale skin.
• Presence of weak or no pulse.
• Blood pressure not recordable.
• Dilatation of pupil due to increased sympathetic discharge.

Cardiac Chain of Survival

To have the best chance of recovering from a cardiac arrest the ARC advises that individuals
should follow the Cardiac Chain of Survival.
The chain starts with early recognition of cardiac arrest and immediately upon recognition
activation of Emergency Medical Services with a rapid response from them.

The second link in the chain is CPR provided by those on scene with the victim immediately at
the time of collapse.

The third link is early defibrillation, when appropriate, by quick use of an AED by bystanders.

The final link is early advanced care as provided by Emergency Medical Services and then a
hospital with the capability of correcting the problem which led to the cardiac arrest.

Time is critical in a cardiac arrest because each minute that someone goes without CPR and use of
an AED their best chance of survival decreases by10%.

Recognition
The signs of cardiac arrest which the ARC teaches people to recognize are unconsciousness and
an absence of breathing. This is a notable difference between the ARC and the AHA who also
teach that any abnormal breathing, such as the gasping breaths that occur shortly before death, are
also signs of cardiac arrest and need to be treated accordingly. Research has shown that bystanders
mistake abnormal but inadequate breathing for acceptable breathing and do not identify the victim
as being in cardiac arrest.

Responding
The ARC uses the mnemonic “Check, Call, Care” for their process of aiding an individual who
has collapsed. The process begins with checking the scene for safety and checking the victim to
see if they are in fact unconscious. The next step is to call for emergency medical services, then to
check for breathing, then check for severe bleeding, then provide care in the form of CPR for
someone who is not breathing.
FIRST AID MEASURES
• Ensure that the airway is clean. To remove mucus or other secretions from the air
passage, a stick with cotton wrapped at one can be used.
• Extend the neck so that the tongue should not fall back and block the airway.
• All tight clothing such as tight collar should be loosened.
• In case of drowning, turn the patient upside down by holding his ankles so as to remove
water; also apply strong pressure on the abdomen

PROCEDURE:
Before starting CPR, check:
• Assess seen and by standers safety
• Is the person conscious or unconscious
• If the person appears unconscious, tap or shake his or her shoulder and ask are you ok
• If the person doesn't respond and two people are available, one should call 911 or the local
emergency number and one should begin CPR.
• If an AED is immediately available, deliver one shock if instructed by the device, then
begin CPR.

Remember to spell C-A-B :

Fig 27.1The American Heart Association uses the acronym of CAB compressions, airway,
breathing to help people remember the order to perform the steps of CPR.
Fig 28.2: (a) Airway (b Breathing (c) Circulation

Compressions: Restore blood circulation

• Put the person on his or her back on a firm surface.
• Kneel next to the person's neck and shoulders.
• Place the heel of one hand over the center of the person's chest, between the nipples. Place
your other hand on top of the first hand. Keep your elbows straight and position your
shoulders directly above your hands.
• Use your upper body weight (not just your arms) as you push straight down on (compress)
the chest at least 2 inches (approximately 5 centimeters). Push hard at a rate of about 100
compressions a minute.
Airway: Clear the airway
• If you're trained in CPR and you've performed 30 chest compressions, open the person's
airway using the head-tilt, chin-lift maneuver. Put your palm on the person's forehead
and gently tilt the head back. Then with the other hand, gently lift the chin forward to
open the airway.
• Check for normal breathing, taking no more than five or 10 seconds. Look for chest
motion, listen for normal breath sounds, and feel for the person's breath on your cheek
and ear. Gasping is not considered to be normal breathing. If the person isn't breathing
normally and you are trained in CPR, begin mouth-to-mouth breathing. If you believe
the person is unconscious from a heart attack and you haven't been trained in emergency
procedures, skip mouth-to-mouth breathing and continue chest compressions.
Breathing: Breathe for the person
• Rescue breathing can be mouth-to-mouth breathing or mouth-to-nose breathing if the
mouth is seriously injured or can't be opened.
• With the airway open (using the head-tilt, chin-lift maneuver), pinch the nostrils shut for
mouth-to-mouth breathing and cover the person's mouth with yours, making a seal.
• Prepare to give two rescue breaths. Give the first rescue breath lasting one second and watch
to see if the chest rises. If it does rise, give the second breath. If the chest doesn't rise, repeat
the head-tilt, chin-lift maneuver and then give the second breath. Thirty chest compressions
followed by two rescue breaths is considered one cycle.
• Resume chest compressions to restore circulation.
• If the person has not begun moving after five cycles (about two minutes) and an automated
external defibrillator (AED) is available, apply it and follow the prompts. Administer one
shock, then resume CPR starting with chest compressions for two more minutes before
administering a second shock. If you're not trained to use an AED, a 911 or other
emergency medical operator may be able to guide you in its use. If an AED isn't available,
go to step 5below.
• Continue CPR until there are signs of movement or emergency medical personnel take
over.

Fig: 27.3: Chest compression

 Fig: 27.4: Defibrillator placement
There are 2 types of AEDs:

➢ Fully Automated
➢ Semi-Automated

• Most AEDs are semi-automated. A semi-automated AED automatically diagnoses heart

rhythms and determines if a shock is necessary. If a shock is advised, the user must then
push a button to administer the shock.
• A fully automated AED automatically diagnoses the heart rhythm and advises the user to
stand back while the shock is automatically given.
Implantable cardioverter-defibrillator (ICD)
• Also known as automatic internal cardiac defibrillator(AICD).
• These devices are implants, similar to pacemakers (and many can also perform the pace
making function).
• They constantly monitor the patient's heart rhythm, and automatically administer shocks
for various life-threatening arrhythmias, according to the device's programming.
• When the life-threatening arrhythmia is ventricular fibrillation, the device is programmed
to proceed immediately to an unsynchronized shock.

Wearable cardiac defibrillator

• A development of the AICD is a portable external defibrillator that is worn like a vest.
• The unit monitors the patient 24 hours a day and will automatically deliver a biphasic shock
if needed.
 • This device is mainly indicated in patients awaiting an implantable defibrillator.

Fig 27.5: Wearable defibrillator.

INTERFACE WITH PERSON:

• The connection between the defibrillator and the patient consists of a pair of
electrodes, each provided with electrically conductive gel in order to ensure a good
connection and to minimize electrical resistance, also called chest impedance
(despite the DC discharge) which would burn the patient.
• Gel may be either wet (similar in consistency to surgical lubricant) or solid (similar
to gummi candy).
• Solid-gel is more convenient, because there is no need to clean the used gel off of
patient's skin after defibrillation (the solid gel is easily lifted off of the patient).
• Paddle electrodes, which were the first type developed, come without gel, and must
have the gel applied in a separate step.
• Self-adhesive electrodes come pre fitted with gel.

Placement:
• Resuscitation electrodes are placed according to one of two schemes.
• The anterior-posterior scheme is the preferred scheme for long-term electrode
placement. One electrode is placed over the left precordium (the lower part of the
chest, in front of the heart).
• The other electrode is placed on the back, behind the heart in the region between the
scapulas. This placement is preferred because it is best for non-invasive pacing.
Table 27.4 Title Methodology Finding
Journal/
Author/
Impact
Factor
BMC The effect A prospective before and after A total of 27,295
Anesthesiolog of audiovisu study was performed to compressions in 30 cardiac
y, Lee et al., al feedback investigate the effect of a real- arrests in the no-feedback
2023, IF: 2.3 of monitor/d time audiovisual feedback period and 27,965
efibrillators system on CPR quality during compressions in 30 arrests
on percenta in-hospital cardiac arrest in in the feedback period
ge intensive care units from were analyzed. The
of appropria November 2018 to February percentage of
te 2022. compressions with both
compression In the feedback period, CPR adequate depth and rate
depth was performed with the aid of was 11.8% in the feedback
and rate the real-time audiovisual period and 16.8% in the
during cardi feedback system. The primary no-feedback period.
opulmonary outcome was the percentage of
resuscitation compressions with both
adequate depth (5.0–6.0 cm)
and rate (100–120/ minute).
Prehospital Verbal A study involved 150 Median compression depth
emergency Motivation vs. laypersons performing 8- did not significantly differ
care, Digital Real- minute CPR on a manikin, between study groups, but
Plata et al.,Time randomized into three groups: post hoc analysis showed
2021, IF: 2.1 Feedback (1) telephone group, receiving greater depth in the
During dispatcher-assisted telephone telephone +motivation
Cardiopulmon CPR; (2) telephone +app group than the telephone
ary group, combining dispatcher- +app group. The telephone
Resuscitation: assisted CPR with a +motivation group had
Comparing smartphone application; and fewer superficial
Bystander (3) telephone +motivation compressions than the
CPR Quality group, receiving dispatcher- telephone +app group.
in a assisted CPR with added Correct-depth
Randomized verbal motivation (“push compressions were more
and Controlled harder, release completely” frequent in the telephone
Manikin Study every 20 seconds after 60 +app group. Median
of Simulated seconds) and a 100-bpm compression rate was
Cardiac Arrest metronome. The study highest in the telephone
compared the effectiveness of +app group compared to
these approaches. other groups.
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