ALTERED TISSUE PERFUSION

Tissue perfusion is the circulation of blood through the vascular bed of tissue, and it is crucial for
organ functions such as the formation of urine, muscle contraction, and exchange of oxygen and carbon
dioxide Tissue perfusion is dependent on blood flow. The three major factors affecting blood flow are the
circulating volume, cardiac pump function, and the vasomotor tone or peripheral vascular resistance.
In conditions where there is decreased tissue perfusion, if temporary, it has minimal consequences to
the health of the patient, if acute, potentially leads to destructive effects on the patient. When diminished
tissue perfusion becomes chronic, it can result in tissue or organ damage or death. Nursing care planning and
management for ineffective tissue perfusion is directed at removing vasoconstricting factors, improving
peripheral blood flow, reducing metabolic demands on the body, patient’s participation, and understanding
the disease process and its treatment, and preventing complications.
Cardiovascular Physical Assessment
Physical exam and history taking are essential to evaluate patients with suspected or known heart disease,
and to detect early symptoms of worsening heart failure. A focused assessment of the cardiac system
includes the following.
 Subjective Data
 Chest pain- assess location, when it occurs, intensity, type, duration, with or without exertion,
radiation, associated symptoms (shortness of breath, sweating, nausea, palpitations, anxiety), and
alleviating factors.
 Palpitations-assess for sensation of skipping, racing, fluttering, pounding, or stopping of the heart.
 Shortness of breath or dyspnea-assess whether it occurs: with lying down and is relieved by sitting up
(orthopnea); upon awakening 1 to 2 hours after going to sleep and is relieved by sitting up or standing
(paroxysmal nocturnal dyspnea); with bending over or occurs with the presence of cough.
 Assess for edema, ask if whether it is worse in morning or evening, and whether it improves with
elevation.
 Include risk factors such as: family or personal history of heart disease including hypertension,
smoking status, diet (BMI-obesity, lipids, salt intake), alcohol and illicit drug use, physical activity,
and type 2 diabetes

 Objective Data
 Patient’s vital signs, if abnormal value, repeat the measurement to ensure its accuracy. Systolic blood
pressure increases with age due to increased rigidity of the blood vessel walls, temperature decreases
with age, and respiratory rate often increases with age or underlying pathology. The difference
between the apical pulse and radial pulse is called the pulse deficit. This is an indirect measurement
of the ability of each cardiac contraction to eject sufficient blood into the peripheral circulation.
 Height and weight. These are important for evaluating nutritional status and assessing fluid loss or
gain. Weight loss over months or years can be a clue to advancing CVD and be a sign of muscle
wasting and poor nutrition. An abrupt weight gain may be an indication of worsening heart failure,
whereas abrupt weight loss may be an indication of over diuresis. Weight should be measured first
 thing in the morning, after urination but before dressing or eating. Note: weight can vary depending
on the time of day it is measured, the scale used, and the amount of clothing being worn.
 Inspection
 General appearance: thin, obese, level of alertness, skin color, turgor, texture, temperature, and
diaphoresis.
 Observe mucous membranes for pallor and extremities for clubbing of fingers or cyanosis.
 While the patient is sitting or lying flat, observe pulsations, retractions, heaves. Locate the point of
maximal impulse normally found in the left fifth intercostal space, medial to the left midclavicular
line, Displacement to the left can indicate an enlarged heart.
 Examine extremities to assess arterial or venous disorders and symmetry, noting skin color,
hemosiderin staining, edema, weeping, lesions, scars, or clubbing, and pattern and distribution of
body hair
 Examine the blood vessels in the neck. The carotid artery should have a local, brisk pulsation that
does not decrease when the patient is upright or inhales, or during palpation. Note for jugular veins
distension, this indicates blood volume and pressure in the right side of the heart.
 Palpation
 Palpate over the precordium to find the apical impulse. Also note any thrills, heaves, or fine
vibrations, carotid, brachial, radial, femoral, popliteal, posterior tibial, and dorsalis pedis pulses using
the pads of the index and middle fingers. All pulses should be regular in rhythm and equal in
strength.
 Palpate the patient's legs and arms to assess skin temperature, texture, turgor, and edema.
 Percussion
Percussion is not as useful as other methods of assessment in evaluating the cardiovascular system, but it
may help locate the cardiac borders.
 Auscultation
 Listening for heart sounds. S1and S2 are normal heart sound. A third heart sound, S3, is commonly
heard in patients with a high cardiac output and in children. It is called a ventricular gallop when it
occurs in adults. S3 may be a cardinal sign of heart failure. S3 is best heard at the apex when the
patient is lying on his left side. S4 is considered an adventitious sound and is called an atrial gallop
(or presystolic gallop). It is heard best over the tricuspid or mitral areas with the patient on his left
side. It may be heard in patients who are elderly, those with hypertension, aortic stenosis, or a history
of myocardial infarction.
 Listening for Murmurs. Murmurs occur when there is turbulent blood flow caused by structural
defects in the heart’s chambers or valves. Note the characteristics of the assessed murmurs have
various characteristics, low, medium, and high pitched.
Cardiovascular Common Diagnostic Assessment
Cardiovascular diagnostic and screening tests can provide information about the electrical activity of the
heart, how well blood is pumping through the heart’s chambers and valves, how easily blood is flowing
through the coronary arteries and determine abnormalities in the structure of the cardiovascular system.
1. Non-invasive Cardiovascular Diagnostic Assessment
a. Electrocardiogram (ECG)
b. Echocardiography
 Electrocardiogram (ECG)
The electrocardiogram (ECG) is a graphical record of the heart’s electrical activity. Electrodes are
applied to the body surface to obtain a graphical representation of cardiac electrical activity.
The 12-lead ECG is used to diagnose dysrhythmias, conduction abnormalities, and chamber
enlargement, as well as myocardial ischemia, injury, or infarction. It can also suggest cardiac effects of
electrolyte disturbances (high or low calcium and potassium levels) and the effects of antiarrhythmic
medications. A 15-lead ECG adds three additional chest leads across the right precordium and is used for
early diagnosis of right ventricular and left posterior (ventricular) infarction. The 18-lead ECG adds three
posterior leads to the 15-lead ECG and is useful for early detection of myocardial ischemia.
To assess the cardiac rhythm accurately, a prolonged recording from one lead is used to provide a
rhythm strip. Lead II, which usually gives a good view of the P wave, is most commonly used to record the
rhythm strip.

 Normal sinus rhythm Criteria

1. Rhythm: regular
2. Heart rate: 60 – 100 / minute
3. QRS: less than 0.10 seconds
4. P wave: only one precedes each QRS, all have same size, shape and deflection
5. PR interval: 0.12 - 0.20 seconds

 Steps in ECG Interpretation

1. Calculate the heart rate
o Use P waves to determine the atrial rate and R waves for the ventricular rate. Several approaches
can be used to determine the heart rate.
o Count the number of complexes in a 6-second rhythm strip and multiply by 10. This provides an
estimate of the rate and is particularly valuable if rhythms are irregular.
o Count the number of large boxes between two consecutive complexes and divide 300 (the
number of large boxes in 1 minute) by this number. For example, there are 6 large boxes between
two R waves; 300 divided by 6 equals a ventricular rate of 50 bpm.
o Count the number of small boxes between two consecutive complexes and divide 1500 (the
number of small boxes in 1 minute) by this number. For example, there are 19 small boxes
between two R waves; 1500 divided by 19 equals a ventricular rate of 79 bpm. This is the most
precise measurement of heart rate.
o Determine if the patient's heart rate is bradycardic (less than 60 beats per minute); within a
normal range (60-100 bpm); tachycardic (100-150 bpm) or a potentially dangerous rhythm above
 150 bpm such as supraventricular tachycardia or ventricular tachycardia with a pulse and
administer the appropriate intervention if needed.
2. Is the ECG rhythm regular or irregular?
Using a six second strip, measure the R to R intervals between QRS segments and determine if the
rhythm is regular or irregular. s. Place one point of a caliper on the peak of the P wave (for atrial rhythm)
or the R wave (for ventricular rhythm). Adjust the other point to the peak of the next wave, P to P or R to
R, Evaluate intervals between consecutive waves. The rhythm is regular if all caliper points fall on
succeeding wave peaks. Alternately, use a strip of blank paper on top of the ECG strip, marking the
peaks of two or three consecutive waves. Then move the paper along the strip to consecutive waves.
Wave peaks that vary by more than one to three small boxes (depending on the rate) are irregular.
Irregular rhythms may be irregularly irregular (if the intervals have no pattern) or regularly irregular (if a
consistent pattern to the irregularity can be identified)
If abnormality or irregularity are assessed in any of the subsequent findings on the ECG, ask the
patient if this is normal for them and look for any associated symptoms such as— chest pain,
hypotension, altered mental status, poor perfusion, or shortness of breath (C.H.A.P.S.).
3. Assess P wave. The presence or absence of P waves helps determine the origin of the rhythm. All the
P waves should be alike in size and shape (morphology). If P waves are not seen or they differ in
shape, the rhythm may not originate in the sinoatrial node. The P wave represents the depolarization
of the atria, the two upper chambers of the heart, which receive blood from the vena cava and
pulmonary veins. P waves are upright in Lead II on the cardiac monitor and are followed by a QRS
segment If the criteria are present, it is likely the electrical impulse began in the sinoatrial (SA) node,
the normal pacemaker of the heart.
4. Assess P to QRS relationship. Determine the relationship between P waves and QRS complexes.
There should be one and only one P wave for every QRS complex, because the normal stimulus for
ventricular contraction originates in the sinoatrial node.
5. Measure the PR interval The PR interval is the time interval between the P wave (atrial
depolarization) to the beginning of the QRS segment (ventricular depolarization). The normal PR
interval is 0.12-0.20 seconds, or 3-5 small boxes on the ECG graph paper. A prolonged PR interval
suggests a delay in getting through the atrioventricular (AV) node, the electrical relay system
between the upper and lower chambers of the heart.
6. Measure the QRS segment. The normal QRS segment has three graphical deflections — the first
negative wave (Q wave); the positive wave above the isoelectric line (R wave) and the negative wave
after the positive wave (S wave) — and the normal time duration is 0.04-0.10 seconds. If QRS
segment is prolonged, it might be due to a bundle branch block which could be relatively benign or a
sign of underlying heart disease.
7. Measure the QT interval. Normally QT interval is 0.32 to 0.44 second. It varies inversely with the
heart rate: the faster the heart rate, the shorter the QT interval. A prolonged QT interval indicates a
prolonged relative refractory period of the heart.
8. Observe the T wave. The T wave represents repolarization (recovery) of the ventricles and should be
upright in Lead II and appear after the QRS segment. Any variations in the T waves are important to
note. Inverted T waves could be due to a lack of oxygen to the heart; too much potassium
(hyperkalemia) could cause peaked T waves; flat T waves may be due to too little potassium and a
raised ST segment which is the end of the QRS segment to the beginning of the T wave, might be
due to a heart attack.
9. Note any ectopic beats. An ectopic beat is a change in a heart rhythm caused by beats arising from
fibers outside the SA node, the normal impulse-generating system of the heart. If you notice ectopic
beats, determine if they are premature atrial contractions (PACs); premature junctional contractions
(PJCs) or premature ventricular contractions (PVCs). Also, note how many ectopic beats are present
in the ECG, the interval at which they are appearing, their shape, and if they arise singularly or in
groups.
  Related Nursing Care
 Make sure that all electrical equipment and outlets are grounded to avoid electric shock
 Clean patient skin and clip hair where electrodes will be place.
 Instruct client to relax and breathe normally
 Tell patient to avoid tightening of muscles, grasping bedrails and talking during ECG tracing
 Tell the client that ECG will not cause any pain or discomfort
 Echocardiography
Ultrasound test use to identify abnormal heart structure, size, function, and valvular disease. The
techniques most commonly used in echocardiography are M-mode (motion mode), for recording the motion
and dimensions of intracardiac structures, and two-dimensional (cross-sectional), for recording lateral
motion and providing the correct spatial relationship between structures. transducer directs ultrahigh-
frequency sound waves toward cardiac structure, which reflect these waves. The echoes are converted to
images that are displayed on a monitor and recorded.
 Related Nursing Care
 Explanation of the procedure to the patient
 No food and fluid restrictions
 Position client to his left or right or supine position
 Offer wipes to clean the water-soluble gel
2. Invasive Cardiovascular Diagnostic Assessment
a. Cardiac Catheterization
b. Central Venous Pressure (CVP)
c. Pulmonary Artery Pressure (PAP)
d. Intra-arterial Blood Pressure Monitoring (IABP)
e. Left-arterial Pressure Monitoring

 Cardiac Catheterization
Cardiac catheterization may be performed to identify CAD or cardiac valvular disease, to determine
pulmonary artery or heart chamber pressures, to obtain a myocardial biopsy, to evaluate artificial valves, or
to perform angioplasty or stent an area of CAD. The test is performed by inserting a long catheter into a vein
or artery (depending on whether the right side or the left side of the heart is being examined) in the arm or
leg using fluoroscopy, the catheter is then threaded to the heart chambers or coronary arteries, or both.
Contrast dye is injected, and heart structures are visualized, and heart activity is filmed.
 Central Venous Pressure (CVP) Monitoring
CVP is the venous pressure in right auricle of the heart. The determination of the central venous pressure
(CVP) provides a direct measurement of the changes in the pressure of blood returning to the heart. CVP is
useful hemodynamic parameter to observe when managing an unstable patient’s fluid volume status. It is
acquired by threading a central venous catheter (subclavian double lumen central line shown) into any of
several large veins. It is threaded so that the tip of the catheter rests in the lower third of the superior vena
cava. The pressure monitoring assembly is attached to the distal port of a multi-lumen central vein catheter.
 Pulmonary Artery Pressure (PAP)
This one of the most commonly measured parameters during a cardiac catheterization case. Mean PAP,
systolic PAP and diastolic PAP are often derived by visually marking the waveform output by a fluid-filled
transducer.
Pulmonary artery pressure monitoring is used in critical care for assessing left ventricular function,
diagnosing the etiology of shock, and evaluating the patient’s response to medical interventions (e.g., fluid
administration, vasoactive medications). A pulmonary artery catheter and a pressure monitoring system are
used. Once the catheter is in position, the following are measured: right atrial, pulmonary artery systolic,
pulmonary artery diastolic, mean pulmonary artery, and pulmonary artery wedge pressures.
 Left-Atrial Pressure Monitoring
Left atrial pressure indicates the left ventricular filling pressure in patients who have systolic or diastolic
left ventricular dysfunction or valvular heart disease. Left atrial pressure is difficult to measure directly.
However, a special catheter designed for this purpose, called a pulmonary artery balloon occlusion catheter
or Swan-Ganz catheter, is clinically used for indirect pressure measurements. This catheter is inserted into a
large vein (usually the internal jugular vein in the neck or the femoral vein in the groin) and passed through
the right heart into a pulmonary artery. The catheter tip is equipped with a small soft balloon that, when
inflated, lodges in a segmental pulmonary artery and temporarily blocks flow to the segment. After a short
period of equilibration, because there is no blood flow passing the catheter tip, the pressure measured at the
tip of the catheter reflects the pressure “downstream” in the pulmonary veins and left atrium.
Conditions with Altered Tissue Perfusion
A. Acute Ischemic Heart Disease (ACS)
ACS refers to an imbalance between myocardial oxygen supply and demand secondary to an acute
plaque disruption or erosion; a dynamic state in which coronary blood flow is acutely reduced, but not fully
occluded. The spectrum of ACS includes unstable angina ST-segment elevation myocardial infarction
(STEMI) and Non-ST segment elevation myocardial infarction or heart attack (NSTEMI) Most people
affected by ACS have significant stenosis of one or more coronary arteries.
Unstable angina occurs at rest and do not respond to nitroglycerin and rest, no detectable release of
cardiac enzymes and biomarkers. NSTEMI is defined by clinical presentation of chest pain with an elevation
in cardiac biomarkers and electrocardiograph (ECG) changes that may include T-wave inversion or ST-
segment depression but no ST-segment elevation. STEMI is based on elevated cardiac biomarkers plus ST-
segment elevation on ECG signifying ischemia. Of the three, STEMI is the most serious and life threatening.
Time is essential in diagnosing and treating patients with ACS. Patients presenting with a STEMI are high
priority for intervention. An ECG is the primary assessment tool that guides the type of intervention.
 Etiology
ACS is a manifestation of CHD (coronary heart disease) and usually a result of plaque disruption in
coronary arteries (atherosclerosis). The common risk factors for the disease are smoking, hypertension,
diabetes, hyperlipidemia, male sex, physical inactivity, family obesity, and poor nutritional practices.
Cocaine abuse can also lead to vasospasm. A family history of early myocardial infarction (55 years of age)
is also a high-risk factor.
 Pathophysiology
The underlying pathophysiology in ACS is decreased blood flow to part of heart musculature which is
usually secondary to plaque rupture and formation of thrombus. Sometimes ACS can be secondary to
vasospasm with or without underlying atherosclerosis. The result is decreased blood flow to a part of heart
musculature resulting first in ischemia and then infarction of that part of the heart.
 Manifestations
The cardinal manifestation of ACS is chest pain, usually substernal or epigastric. The pain often radiates
to the neck, left shoulder and/or left arm. The pain may occur at rest and typically lasts longer than 10 to 20
minutes. Dyspnea, diaphoresis, pallor and cool skin may be present. Tachycardia and hypotension may
occur. The person may be nauseated or will feel light headedness.

 Diagnosis
 Acute coronary syndrome requires emergency medical care at a hospital. Tests are done to check the
heart and determine the cause. Some tests may be done while your health care team asks you questions
about your symptoms or medical history. Tests for acute coronary syndrome may include:
Electrocardiogram (ECG or EKG). This quick test measures the heart's electrical activity. Sensors
called electrodes are attached to the chest and sometimes to the arms or legs. Changes in the
heartbeat may mean the heart is not working properly. Certain patterns in electrical signals may show
the general location of a blockage. The test may be repeated several times.
 Blood tests. Certain heart proteins slowly leak into the blood after heart damage from a heart attack.
Blood tests can be done to check for these proteins.
 Medical and Surgical Management
Initial therapy focuses on stabilizing patient’s condition, relieve chest pain and provide medications to
reduce myocardial ischemia and to reduce the risk of blood clotting.
 Pharmacologic Management
 Thrombolytic drugs. These drugs break down the fibrin in blood clots restoring blood flow to
ischemic cardiac muscle and can prevent permanent damage.
 Nitrates and beta-blockers. Used to restore blood flow to the ischemic myocardium reducing
the workload of the heart. Glyceryl trinitrate is given by sublingual tablet or buccal spray. If chest
pain is unrelieved after three doses 5 minutes apart, an intravenous glyceryl trinitrate infusion is
initiated. The infusion may be continued until the chest pain is relieved or for 12 to 24 hours.
Topical or oral nitrates are then initiated. Beta-adrenergic blockers are initially given
intravenously, followed by oral beta-blockers.
 Aspirin, clopidogrel and other antiplatelet drugs and heparin are given to clients who do not have
an excessive bleeding risk. These drugs inhibit blood clotting and reduce the risk of thrombus
formation, suppress platelet aggregation, interrupting the process of forming a stable blood clot.
 Non -Surgical Revascularization Procedures
Several procedures may be used to restore blood flow and oxygen to ischemic tissue. Non-surgical
techniques include transluminal coronary angioplasty, laser angioplasty, coronary atherectomy and
intracoronary stents.
 Percutaneous transluminal coronary revascularization (PTCA). PTCA procedures are
similar to the procedure used for coronary angiography. A catheter is introduced into the arterial
circulation and is guided into the opening of the narrowed coronary artery using local
anesthesia. Complications following PTCA procedures include hematoma at the catheter
insertion site, pseudoaneurysm, embolism, hypersensitivity to contrast dye, arrhythmias,
bleeding and vessel perforation. Other complications include restenosis or reclusion of the
treated vessel.
 Intracoronary stents are metallic scaffolds used to maintain an open arterial lumen. The stent
is placed over a balloon catheter, guided into position and expanded as the balloon is inflated. It
then remains in the artery as after the balloon is removed. Endothelial cells will completely line
the inner wall of the stent to produce a smooth inner lining. Antiplatelet medications are given
following stent insertion to reduce the risk of thrombus formation at the site.
 Atherectomy procedures is different form stenting. In contrast to stent procedures, which
enlarge the artery by displacing plaque, atherectomy remove plaque from the identified lesion.
The directional atherectomy catheter shaves the plaque off vessel walls using a rotary cutting
head, retaining the fragments in its housing and removing them from the vessel. Rotational
atherectomy catheters pulverize plaque into particles small enough to pass through the coronary
microcirculation. Laser atherectomy devices use laser energy to remove plaque.
  Surgical Revascularization Procedures
 Coronary artery bypass grafting (CABG)
This surgery involves a section of a vein or artery to create a connection for bypass between the aorta
and the coronary artery beyond the obstruction. This allows blood to perfuse the ischemic portion of the
heart. The vessels most commonly blood vessels used for CABG are the internal mammary artery in the
chest and the saphenous vein from the leg Bypass grafts are safe and effective. Angina is totally relieved or
significantly reduced in 90% of people who undergo complete revascularization. While anginal pain may
recur within 3 years, it rarely is as severe as before surgery.
 Nursing Responsibilities
Preoperative care
1. Provide routine preoperative care and teaching
2. Verify presence of laboratory and diagnostic test results in the chart, including CBC, coagulation
profile, urinalysis, chest x-ray and coronary angiogram. These baseline data are important for
comparison of postoperative results and values.
3. Type and crossmatch four or more units of blood as ordered. Blood is made available for use during
and after surgery as needed.
4. Provide the person and their family with specific teaching related to procedure and postoperative
care. such as tubes, drains, monitoring equipment, including cardiac and hemodynamic monitoring
systems. endotracheal tube, incisions and dressings and pain management. Preoperative teaching
reduces anxiety and prepares the person and family for the postoperative environment and expected
sensations.
Postoperative care
1. Provide routine postoperative care having major surgery
2. Assess for signs and symptoms of decreased cardiac output. Pallor, mottling or cyanosis, cool and
clammy skin, and diminished pulse amplitude are indicators of decreased cardiac output. Cardiac
output may be compromised postoperatively due to bleeding and fluid loss; depression of myocardial
function by drugs, hypothermia, and surgical manipulation; arrhythmias; increased vascular
resistance; and a potential complication, cardiac tamponade, compression of the heart due to
collected blood or fluid in the pericardium.
3. Assess for signs of cardiac tamponade: increased heart rate, decreased BP, decreased urine output,
increased central venous pressure, a sudden decrease in chest tube output, muffled/distant heart
sounds and diminished peripheral pulses. Notify the doctor immediately. Cardiac tamponade is a
life-threatening complication that may develop postoperatively. It interferes with ventricular filling
and contraction, decreasing cardiac output. If untreated, cardiogenic shock and possible cardiac
arrest ensue.
4. Monitor vital signs, oxygen saturation and hemodynamic parameters every 15 minutes. Report
significant changes to the doctor. Initial hypothermia and bradycardia are expected; the heart rate
should return to the normal range with rewarming. The blood pressure may fall during rewarming as
peripheral vasodilation occurs. Hypotension and tachycardia, however, may indicate low cardiac
output. Pulmonary artery pressure (PAP), pulmonary artery wedge pressure (PAWP), cardiac output
and oxygen saturation are often monitored to evaluate fluid volume, cardiac function and gas
exchange.
5. Auscultate heart and breath sounds on admission and at least every 4 hours. A ventricular gallop, or
S3, is an early sign of heart failure; an S4 may indicate decreased ventricular compliance. Muffled
heart sounds may be an early indication of cardiac tamponade. Adventitious breath sounds may be a
bhp n manifestation of heart failure or respiratory compromise.
6. Assess skin color and temperature, peripheral pulses and level of consciousness with vital signs.
Changes indicates decrease cardiac output
7. Continuously monitor and document cardiac rhythm. Arrhythmias are common and may interfere
with cardiac filling and contractility, decreasing the cardiac output.
 8. Measure intake and output hourly. Report urine output less than 30 mL/h for 2 consecutive hours.
Intake and output measurements help evaluate fluid volume status. Decrease urine output may be an
early indicator of decreased cardiac output.
9. Record chest tube output hourly. Chest tube drainage greater than 70 mL/h or that is warm, bright
red and free flowing indicates hemorrhage and may necessitate a return to surgery. A sudden drop in
chest tube output may indicate impending cardiac tamponade. Monitoring for the presence of pulsus
paradoxus and pulsus alternans should occur.
10. Monitor hemoglobin, hematocrit, and serum electrolytes. Low hemoglobin and hematocrit may
indicate hemorrhage. Electrolyte imbalances ln potassium, calcium and magnesium affect cardiac
rhythm and contractility.
11. Administer intravenous fluids, fluid boluses and blood transfusions as ordered. Fluid and blood
replacement helps ensure adequate blood volume and oxygen-carrying capacity.
12. Administer medications as ordered. Medications ordered. Early postoperative period drugs
administered to maintain the cardiac output are inotropic drugs (e.g., dopamine, dobutamine) in order
to increase the force of myocardial contractions, vasodilators (e.g. nitroprusside or glyceryl trinitrate)
to decrease vascular resistance and afterload; and antiarrhythmic agents to correct arrhythmias that
affect cardiac output.
13. Keep a temporary pacemaker at the bedside; initiate pacing as indicated. Temporary pacing may be
needed to maintain the cardiac output with bradyarrhythmia’s, such as high-level AV blocks.

 Nursing Management For ACS

 Acute intervention
o Pain (nitroglycerin, morphine, oxygen)
 Continuous monitoring
o ECG, vs, pulse oximetry
o Heart and lung sounds
 Rest and comfort
o Balance rest and activity
o Begin cardiac rehabilitation

B. Heart Failure
Heart failure is recognized as a clinical syndrome characterized by signs and symptoms of fluid
overload or inadequate tissue perfusion caused by conditions that impair the ejection of oxygen- and
nutrient-rich blood from the ventricles. It is a clinical syndrome resulting from structural or functional
cardiac disorders that impair the ability of the ventricles to fill or eject blood It is often a long-term effect of
coronary heart disease (CHD) and myocardial infarction (MI) when left ventricular damage is extensive
enough to impair cardiac output.
In the past, HF was often referred to as congestive heart failure (CHF), because many patients
experience pulmonary or peripheral congestion with edema. The term heart failure indicates myocardial
disease in which impaired contraction of the heart (systolic dysfunction) or filling of the heart (diastolic
dysfunction) may cause pulmonary or systemic congestion. Some cases of HF are reversible, depending on
the cause. Most often, HF is a chronic, progressive condition that is managed with lifestyle changes and
medications to prevent episodes of decompensated heart failure.
 Figure 4. Classification of Heart Failure
 Etiology
Atherosclerosis of the coronary arteries is a primary cause of HF Several conditions causing heart failure
are coronary artery disease, hypertension, cardiomyopathy, valvular disorders, and renal dysfunction with
volume overload.

Figure 5. Pathophysiology of Heart Failure

 Pathophysiology
Heart failure (HF) is a complex clinical syndrome that centers on the heart’s impaired ability to support
physiologic circulation. A wide range of etiologies can be responsible for HF, including but not limited to
ischemic heart disease, valvular heart disease, infiltrative disease, restrictive physiology, genetic conditions,
and idiopathic cardiomyopathy. The cardinal manifestations are dyspnea and fatigue.
The syndrome of HF is a continuum of interrelated stages, starting from an asymptomatic with risk
factors for HF or evidence of structural changes in the heart to debilitating functional limitations related to
dyspnea and a high risk of sudden cardiac death. Guideline-directed medical therapy has most successfully
improved morbidity and mortality in patients with reduced left ventricular ejection fraction, while therapy
for patients with preserved ejection fraction largely focuses on symptomatic management.
For patients with advanced HF who are refractory to conventional therapy, including oral agents,
implantable electronic cardiac devices, and comprehensive care interventions, options may include inotropic
therapy, mechanical circulatory support, cardiac transplantation, or transition to comfort-focused care.
Figure 6. Types of Heart Failure

In compensated heart failure, symptoms are stable, and many overt features of fluid retention and
pulmonary oedema are absent. Decompensated heart failure refers to a deterioration, which may present
either as an acute episode of pulmonary edema or as lethargy and malaise, a reduction in exercise tolerance,
and increasing breathlessness on exertion.
Left-sided heart failure is when the left ventricle of the heart no longer pumps enough blood around
the body resulting to blood build up in the pulmonary veins This causes shortness of breath especially during
physical activity. There are two types of left-sided heart failure systolic failure and diastolic heart failure. In
systolic heart failure, there is alteration in ventricular contraction while in diastolic heart failure there is
difficulty for the ventricle to fill. In right-sided heart failure, the right ventricle of the heart is too weak to
pump enough blood to the lungs. This causes blood to build up in the veins leading to a buildup of fluid in
the legs, or less commonly in the genital area, organs or the abdomen. In biventricular or bilateral heart
failure is when both sides of the heart are affected causing the same symptoms of both left-sided and right-
sided heart failure.
High and low output heart failures are fewer common forms of heart failure. In high output cardiac
failure, cardiac function is normal but there is decreased systemic vascular resistance, either secondary to
diffuse arteriolar dilation or possible bypass of the arterioles and capillary beds, leading to activation of
neurohormones. Low-output heart failure is a clinical syndrome characterized by decreased cardiac output
accompanied by end-organ hypoperfusion.
Acute heart failure, in most cases, occurs very suddenly and should be considered a medical
emergency requiring immediate intervention. Chronic heart failure is generally a condition that develops
gradually over time.
Manifestations
These signs and symptoms are related to congestion and poor perfusion. The signs and symptoms of
HF can also be related to the ventricle that is most affected. Left-sided heart failure (left ventricular failure)
causes different manifestations than right-sided heart failure (right ventricular failure). In chronic HF,
patients may have signs and symptoms of both left and right ventricular failure. The clinical manifestation of
left sided heart failure is pulmonary congestion such as dyspnea, cough, pulmonary crackles, and low
oxygen saturation levels. An extra heart sound, the S3, or “ventricular gallop,” maybe detected on
auscultation. It is caused by abnormal ventricular filling.
However right sided heart failure has systemic clinical manifestations including edema of the lower
extremities (dependent edema), hepatomegaly (enlargement of the liver), ascites (accumulation of fluid in
the peritoneal cavity), and weight gain due to retention of fluid.

Figure 7. Manifestation of Left and Right Heart Failure

 Diagnostic Tests
HF may go undetected until the patient presents with signs and symptoms of pulmonary and
peripheral edema. Assessment of ventricular function is an essential part of the initial diagnostic workup. An
echocardiogram is usually performed to determine the ejection fraction, identify anatomic features such as
structural abnormalities and valve malfunction, and confirm the diagnosis of HF. This information may also
be obtained noninvasively by radionuclide ventriculography or invasively by ventriculography as part of a
cardiac catheterization procedure. A chest x-ray and a 12-lead electrocardiogram (ECG) are obtained to
assist in the diagnosis. Laboratory studies usually performed during the initial workup include serum
electrolytes, blood urea nitrogen (BUN), creatinine, liver function tests, thyroid-stimulating hormone,
complete blood count (CBC), B - type natriuretic peptide (BNP) and routine urinalysis. The BNP level is a
key diagnostic indicator of HF; high levels are a sign of high cardiac filling pressure and can aid in both the
diagnosis and management of HF. The results of these laboratory studies assist in determining the
underlying cause and can also be used to establish a baseline to assess effects of treatment. Cardiac stress
testing or cardiac catheterization may be performed to determine whether coronary artery disease and
cardiac ischemia are causing the HF.
 Medical and Surgical Management
The goals of management of HF are to relieve patient symptoms, to improve functional status and
quality of life, and to extend survival. The prognosis for HF patients has improved with the use of evidence-
based protocols for patient management. Specific interventions are based on the stage of HF. The objectives
of guideline-directed patient management include the following: Improvement of cardiac function with
optimal pharmacologic management Reduction of symptoms and improvement of functional status
Stabilization of patient condition and lowering of the risk of hospitalization Delay of the progression of HF
and extension of life expectancy Promotion of a lifestyle conducive to cardiac health Treatment options vary
according to the severity of the patient’s condition and may include oral and intravenous (IV) medications,
major lifestyle changes, supplemental oxygen, and surgical interventions including implantation of cardiac
devices and cardiac transplantation.
Figure 8. Pharmacologic Management for Heart Failure

 Medications for Heart Failure

Several medications are routinely prescribed for HF, including ACE inhibitors, beta-blockers, and
diuretics These medications, improve symptoms and extend survival. Others, such as diuretics, improve
symptoms but may not affect survival. Anticoagulants may be prescribed, especially if the patient has a
history of atrial fibrillation or a thromboembolic event. Antiarrhythmic drugs such as amiodarone
(Cordarone) may be prescribed for patients with dysrhythmias, along with evaluation for device therapy
with an implantable cardioverter defibrillator (ICD). Medications that manage hyperlipidemia (e.g., statins)
are also routinely prescribed. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Motrin)
should be avoided because they decrease renal perfusion, especially in older adults.
  Nutritional Therapy
Usually recommended diet is following a low-sodium (no more than 2 g/day) diet and avoiding
excessive fluid intake. Although studies differ regarding the effectiveness of sodium restriction Decreasing
dietary sodium reduces fluid retention to decrease the amount of circulating blood volume thereby
decreasing myocardial work. Low sodium diet also reduces the symptoms of peripheral and pulmonary
congestion. Any change in diet should consider good nutrition as well as the patient’s likes, dislikes, and
cultural food patterns. Patient adherence is important because dietary indiscretions may result in severe
exacerbations of HF requiring hospitalization.
 Additional Therapy
Oxygen therapy may become necessary as HF progresses. The need is based on the degree of
pulmonary congestion and resulting hypoxia. Some patients require supplemental oxygen only during
periods of activity.
 Surgical and Non- surgical Intervention
A number of procedures and surgical approaches may benefit patients with HF. If the patient has
underlying coronary artery disease, coronary artery revascularization with PCI or coronary artery bypass
surgery may be considered. Patients with HF are at high risk for dysrhythmias, and sudden cardiac death is
common among patients with advanced HF. In patients with severe left ventricular dysfunction and the
possibility of life-threatening dysrhythmias, placement of an ICD can prevent sudden cardiac death and
extend survival.
Patients with HF who do not improve with standard therapy may benefit from cardiac
resynchronization therapy (CRT). CRT involves the use of a biventricular pacemaker to treat electrical
conduction defects. The use of a pacing device with leads placed in the right atrium, right ventricle, and left
ventricular cardiac vein can synchronize the contractions. This intervention improves cardiac output,
optimizes myocardial energy consumption, reduces mitral regurgitation, and slows the ventricular
remodeling process.
Ultrafiltration is an alternative intervention for patients with severe fluid overload. It is reserved for
patients with advanced HF who are resistant to diuretic therapy. A dual-lumen central IV catheter is placed,
and the patient’s blood is circulated through a small bedside filtration machine. Liters of excess fluid and
plasma are removed slowly from the patient’s intravascular circulating volume over a number of hours. The
patient’s output of filtration fluid, blood pressure, and hemoglobin are monitored as indicators of volume
status.
 Heart transplant
Heart transplant is the transfer of a heart from one person to another. This is the treatment of
choice for patients with refractory end stage heart failure, cardiomyopathy and inoperable CAD. Donor
and recipient matching is based on body heart size and ABO compatibility. The recipient is prepared for
surgery and cardiopulmonary bypass is used. The usual procedure involves the removal of the patient’s
heart except the posterior right and left atrial walls and their venous connections and the donor heart will
be transplanted.
 Post -Transplant Issues
 Bleeding is a major concern in the early postoperative period. Chest tube drainage is frequently
monitored (initially every 15 minutes), as are the cardiac output, pulmonary artery pressures and
CVP.
 Cardiac tamponade (compression of the heart). This can develop either a sudden event or a
gradual process. Chest tubes are gently milked as needed to maintain patency.
 Atrial arrhythmias. These are relatively common following cardiac transplant. Temporary pacing
wires are placed during surgery as the conduction system may be disrupted by surgical
manipulation or postoperative swelling.
 Hypothermia. Hypothermia is induced during surgery; postoperatively, the person is gradually
rewarmed over a 1- to 2-hour period. Prevention of rapid rewarming and shivering are important to
maintain hemodynamic stability and reduce oxygen consumption. Cardiac function is impaired in
up to 50% of transplanted hearts during the early postoperative period. Inotropic agents such as
low-dose dopamine or dobutamine may be required to support cardiac function and circulation.
 Rejection. Rejection is one of the major cause of mortality rate post heart transplantation. This may
develop immediately after transplant or within weeks to months or even years after the transplant.
Acute rejection usually presents within weeks of the transplant, developing when the transplanted
organ is recognized by the immune system as foreign. Lymphocytes infiltrate the organ and
myocardial cell necrosis can be detected on biopsy. Acute rejection often can be treated using
immunosuppressive drugs. Although immunosuppressive medications help prevent organ
rejection, they impair the person’s defenses against infection.
 Early postoperative infections. This is also one of the major causes of mortality post heart
transplantation. Infection are commonly cause by bacterial or fungal (Candida). Multiple invasive
lines, prolonged ventilator support and immunosuppressive therapy contribute to the transplant
recipient’s risk of infection. Nursing care directed at prevention of infection is vital and includes
strict aseptic technique, early extubation to reduce the risk of ventilator associated infections.
 Palliative Care for End Stage Heart Failure
Palliative care is initiated when patients are diagnosed with any serious or advanced chronic illness.
As illness progresses, the ratio of palliative care to life prolonging care gradually increases. Palliative care
improves outcomes, including patient and family satisfaction with care and symptom management
Ultimately, life prolonging care is discontinued according to patient’s wishes or when the harm of treatment
outweighs its benefit. At this point, the transition to hospice care is made. After death, palliative care
services continue and help family members with bereavement.
 Nursing Diagnosis
Heart failure impacts on quality of life and interferes with activities of daily living (ADLs). Reducing
myocardial oxygen demand is a major nursing care goal for the individual in acute heart failure. This
includes providing rest and undertaking the prescribed interventions to reduce cardiac work, improve
contractility and manage symptoms. Based on the assessment data, major nursing diagnoses may include the
following:
 Activity intolerance related to decreased cardiac output
 Excess fluid volume related to the HF syndrome
 Anxiety related to clinical manifestations of HF
 Powerlessness related to chronic illness and hospitalizations
 Ineffective family health management
 Nursing Interventions
 Promoting physical activities.
 Reducing fatigue.
 Relieving fluid overload symptoms.
 Decreasing anxiety.
 Increasing the patient’s ability to manage anxiety.
 Encouraging the patient to verbalize his or her ability to make decisions and influence outcome.
 Teaching the patient about self-care program.
 Other Nursing Diagnoses with Interventions
 Decreased cardiac output related to pump failure AEB decreased upstroke volume and tissue perfusion.
A. Monitor vital signs and oxygen saturation. Decreased cardiac output stimulates the SNS to
increase the heart rate in an attempt to restore CO. Tachycardia at rest is common. Diastolic
blood pressure may initially be elevated because of vasoconstriction; in late stages,
compensatory mechanisms fail, and the person’s BP will fall. Oxygen saturation levels provide
a measure of gas exchange and tissue perfusion.
 B. Report manifestations of decreased cardiac output and tissue perfusion including changes in
mentation, decreased urine output, cool, clammy skin, diminished pulses, pallor or cyanosis,
and arrhythmias. Early detection prevents complication and early interventions.
C. Administer supplemental oxygen as needed. This improves oxygenation of the blood,
decreasing the effects of hypoxia and ischemia.
D. Administer prescribed medications as ordered. Drugs are used to decrease the cardiac workload
and increase contractility.
E. Encourage rest, explaining the rationale. Elevate the head of the bed to reduce the work of
breathing. Provide a bedside commode and assist with ADLs. Instruct the person to avoid the
Valsalva maneuver and encourage the use of stool softeners to reduce strain. These measures
reduce cardiac workload.
F. Encourage the person to rest and teach methods to decrease anxiety. Maintain a quiet
environment and encourage expression of fears and feelings. Explain care measures and their
purpose. Reducing anxiety diminishes the sympathetic nervous system effects, resulting in an
improved balance between oxygen demand and supply.
 Excess Fluid Volume related to impaired cardiac pump and salt and water retention manifested by
crackles and pitting edema.
A. Assess respiratory status and auscultate lung sounds at least every 4 hours. Notify the doctor of
significant changes in condition. Declining respiratory status indicates worsening left heart
failure. Immediately notify the doctor if the person develops dyspnea, tachypnoea, severe
orthopnea, a cough productive of large amounts of pink, frothy sputum, or an overwhelming
sense of impending doom or panic. Acute pulmonary edema is a medical emergency and can
develop rapidly. Immediate intervention is required to preserve life.
B. Monitor intake and output. Notify the doctor if urine output is less than 30 mL/h. Careful
monitoring of fluid volume is important during treatment of heart failure. Diuretics may reduce
circulating volume, producing hypovolemia despite persistent peripheral edema. A fall in urine
output may indicate significantly reduced cardiac output and renal ischemia.
C. Weight daily is an objective measure of fluid status: 1 L of fluid is equal to 1 kg of weight.
Weight changes may indicate worsening of the condition.

C. Coronary Arterial Disease (CAD)

Coronary heart disease or coronary artery disease (CAD) is narrowing, or blockage of the coronary
arteries usually caused by the accumulation of atherosclerotic plaque in the coronary arteries. Coronary heart
disease may be asymptomatic or may lead to angina pectoris, acute coronary syndrome, myocardial
infarction (MI), arrhythmias, heart failure and even sudden death.
 Etiology
Coronary atherosclerosis is the most common cause of reduced coronary blood flow. The two main
coronary arteries, the left and the right, supply blood, oxygen and nutrients to the myocardium. They
originate in the root of the aorta, just outside the aortic valve Overweight, physical inactivity, unhealthy
eating, and smoking tobacco are risk factors for CAD. A family history of heart disease also increases your
risk for CAD, especially a family history of having heart disease at an early age (50 or younger).
 Pathophysiology
The inflammatory response involved with the development of atherosclerosis begins with injury to the
vascular endothelium and progresses over many years. The endothelium undergoes changes and stops
producing the normal antithrombotic and vasodilating agents. The presence of inflammation attracts
inflammatory cells, such as monocytes (macrophages). The macrophages ingest lipids, becoming “foam
cells” that transport the lipids into the arterial wall forming fatty streaks. The activated macrophages also
release biochemical substances that can further damage the endothelium by contributing to the oxidation of
low-density lipoprotein (LDL). The oxidized LDL is toxic to the endothelial cells and fuels progression of
the atherosclerotic process. These deposits, called atheromas, or plaques, protrude into the lumen of the
vessel, narrowing it and obstructing blood flow. At this point, the lipid core may grow, causing the fibrous
plaque to rupture. A ruptured plaque attracts platelets and causes thrombus formation. A thrombus may then
obstruct blood flow, leading to acute coronary syndrome (ACS), which may result in an acute myocardial
infarction (MI). When an MI occurs, a portion of the heart muscle no longer receives blood flow and
becomes necrotic. Although heart disease is most often caused by atherosclerosis of the coronary arteries,
other phenomena may also decrease blood flow to the heart.
Figure 9. Coronary Artery Disease Pathogenesis

 Manifestations
The signs and symptoms of coronary arterial disease include the following: chest pain or pressure, jaw
pain, shortness of breath, fatigue, dizziness, palpitation, irregular heart rhythm heart murmurs.

Figure 10. Clinical Manifestation of CAD

 Diagnostic Tests
Laboratory testing is used to assess for risk factors such as an abnormal blood lipid profile (elevated
triglyceride and LDL levels and decreased HDL levels). Total serum cholesterol is elevated in
hyperlipidemia. Lipid profile includes triglyceride (TG), HDL and LDL levels. The ratio should be at least
1:5, with 1:3 being the ideal ratio. Lipoprotein C-reactive protein may also be measured. These are serum
protein associated with inflammatory processes. Recent evidence suggests that elevated blood levels of this
protein may be predictive of CHD.
An inexpensive, non-invasive test for peripheral vascular disease that may be predictive of CAD may
also be perform. This is the ankle–brachial blood pressure index (ABI). The systolic blood pressure in the
brachial, posterior tibial and dorsalis pedis arteries is measured by Doppler. An ABI of < 0.9 in either leg
indicates the presence of peripheral arterial disease and a significant risk of CHD. Exercise ECG testing may
be performed. ECGs are used to assess the response to increased cardiac workload induced by exercise. The
test is considered ‘positive’ for CHD if myocardial ischemia is detected on the ECG (depression of the ST
segment by greater than 3 mm), the person develops chest pain or the test is stopped due to excess fatigue,
arrhythmias or other symptoms before the predicted maximal heart rate is achieved. Another test is Electron
Beam Computed Tomography (EBCT), it creates a three-dimensional image of the heart and coronary
arteries that can reveal plaque and other abnormalities. This non-invasive test requires no special preparation
and can identify individuals at risk of developing myocardial ischemia.
Myocardial perfusion imaging (scintigraphy) may also be used to evaluate myocardial blood flow and
perfusion, both at rest and during stress testing. Perfusion imaging studies are costly and therefore are not
recommended for routine CHD risk assessment.
 Medical and Surgical Management
The treatment goals are to relieve symptoms and prevent future cardiac events. It’s important to reduce
or control risk factors and seek treatment to lower the chance of a heart attack and stroke, Treatment also
depends on your current health condition, risk factors, and overall wellbeing.
 Lifestyle changes
To reduce m risk of heart disease and stroke. Quit smoking tobacco, reduce or stop your consumption
of alcohol, regular exercise, lose weight to a healthy level eat low in trans-fat, low in sodium and low sugar
diet , and stress management.
 Medications
 Anti-platelet medication (eg. Aspirin, clopidogrel) to prevent platelet aggregation
 Statins (eg. atorvastatin, Simvastatin) inhibit the enzyme HMG-CoA reductase in the liver,
lowering LDL synthesis and serum levels. The statins are first-line treatment for elevated LDL,
used in conjunction with diet and lifestyle changes.
 Fibric acid derivatives. The fibrates (fenofibrate, gemfibrozil) are used to lower serum triglyceride
levels; they have only a slight to modest effect on LDL. They affect lipid regulation by blocking
triglyceride synthesis. They are used to treat very high triglyceride levels and may be used in
combination with statins.
 Beta blockers (eg. Atenolol, metoprolol) to reduce myocardial oxygen consumption by blocking
the beta-adrenergic stimulation of the heart.
 Calcium channel blockers (eg. amlodipine, diltiazem) to induce negative inotropic effects
 Non-nitrate anti -anginal (eg. Ranolazine) it can inhibit the cardiac late sodium 205 current (INa),
which may affect the electrolyte balance in the myocardium, relieving angina symptoms. Also
inhibits fatty acid oxidation. This enhances glucose oxidation, reduces the production of lactic
acid, and improves heart function.
 Nitrates (eg. Nitroglycerin) to reduce myocardial oxygen consumption through selective
vasodilation
 ACE inhibitors (eg. Captopril, Enalapril) produce vasodilation by inhibiting the formation of
angiotensin II to improve the amount of blood the heart pumps and to lower blood pressure
 Angiotensin II receptor blockers (ARBs) (eg. Losartan, valsartan) blocks receptors that the
hormone acts on, specifically AT1 receptors, which are found in the heart, blood vessels and
kidneys. Blocking the action of angiotensin II helps to lower blood pressure and prevent damage to
the heart and kidneys.
 Repatha (Evolocumab), a human monoclonal antibody that inhibits proprotein convertase
subtilisin/ kexin type 9 (PCSK9). Repatha binds to PCSK9 and inhibits circulating PCSK9 from
binding to the low-density lipoprotein (LDL) receptor (LDLR), preventing PCSK9-mediated
LDLR degradation and permitting LDLR to recycle back to the liver cell surface. By inhibiting the
binding of PCSK9 to LDLR, Repatha increases the number of LDLRs available to clear LDL from
the blood, thereby lowering LDL-C levels.1
 Anticoagulants (e.g., heparin, enoxaparin) to prevent thrombus formation
 Surgical Interventions
If condition does not improve with medication and lifestyle changes, surgical interventions are
recommended to increase blood flow to the heart.
 Coronary artery bypass graft surgery: to restore blood flow to the heart in open chest surgery
 Balloon angioplasty: to widen blocked arteries and smoosh down the plaque buildup, usually
performed with insertion of a stent to help keep the lumen open after the procedure coronary artery
bypass graft surgery.
 Enhanced external counter pulsation: to stimulate the formation of new small blood vessels to
naturally bypass clogged arteries in a noninvasive procedure
 Other Treatment Modalities
 Angiogenesis. Stem cells and other genetic material are introduced through the vein or directly into
the damaged heart tissue. It helps new blood vessels grow.
 Other approach which is an outpatient procedure is the enhanced external counter pulsation
(EECP) Cuffs are applied on the legs, inflating and deflating the cuffs to boost blood supply to the
coronary arteries.
 Nursing Diagnoses and Interventions
 Acute Pain (Angina) related to decreased oxygen supply to the myocardium
A. Assess location, character, and severity of the pain. Record severity on a subjective 0 (no pain)
to 10 (worst pain) scale. --- This assessment monitors degree, character, precipitator, and trend
of pain for the initial check and subsequent comparisons.
B. Assess HR and BP during episodes of chest pain. Be alert to and report significant findings. ---
Increases in HR and changes in systolic blood pressure (SBP) greater than 20 mm Hg from
baseline signal increased myocardial O2 demands and necessitate prompt medical intervention.
C. Administer O2 as prescribed. --- Hypoxia is common because of the decreased perfusion and
adds stress to the compromised myocardium.
D. Administer sublingual NTG at the onset of pain (if not on an IV NTG drip) and explain to the
patient that it is to be administered as soon as angina begins, repeating q5min ×3 if necessary.
--- NTG increases microcirculation, perfusion to the myocardium, and venous dilation. Venous
dilation causes pooling in the periphery so that less blood comes back to the right side of the
heart, which in turn lowers O2 demand.
E. Notify the health care provider of unrelieved pain. --- If pain is unrelieved or returns very
quickly, emergency medical treatment is advised.
F. As prescribed, administer morphine sulfate and monitor HR, RR, and BP. --- for adequate pain
relief, but also decreases heart rate, BP, RR,
G. Monitor and Obtain ECG as prescribed. --- ECG patterns may reveal ischemia, as evidenced by
dynamic ST- or T-wave changes, evidence of new Q waves, or left bundle branch block.
H. Stay with the patient and provide reassurance during periods of angina. --- These measures
reduce anxiety, which might otherwise worsen the angina.
 I. Instruct the patient to avoid activities and factors known to cause stress. --- Stress may
precipitate angina.
J. Discuss the value of relaxation techniques, including tapes, soothing music, biofeedback,
meditation, or yoga. --- Relaxation helps reduce stress and anxiety, which otherwise may
precipitate angina.
K. Administer beta-blockers (e.g., metoprolol, atenolol, carvedilol) as prescribed. --- These
medications block beta stimulation to the sinoatrial (SA) node and myocardium. HR, BP, and
contractility are decreased, subsequently reducing workload of the heart and myocardial oxygen
demand.
L. Administer long-acting nitrates (isosorbide preparations) and/or topical nitrates as prescribed.
--- Nitrates are given for anginal prophylaxis via vasodilation, lowering of BP, and decreasing
O2 demand.
M. Administer angiotensin-converting enzyme (ACE) inhibitor (e.g., enalapril, captopril, quinapril,
ramipril) as prescribed. --- ACE inhibitors reduce BP, down-regulate the renin-angiotensin
aldosterone system (RAAS)
N. Administer calcium channel blockers (e.g., nifedipine, diltiazem) as prescribed. --- Calcium
channel blockers decrease coronary artery vasospasm, a potential cause of ischemia and
subsequent angina. They also cause the vessels to dilate, increasing blood flow to the heart.
O. Administer aspirin as prescribed. --- Aspirin reduces platelet aggregation, which helps prevent
obstruction of the coronary arteries.
P. Administer antihyperlipidemic agents (e.g., atorvastatin, rosuvastatin) as prescribed. --- These
agents, also known as “statin” drugs, are used to reduce hyperlipidemia and can stabilize
plaque.
Q. Administer stool softeners as prescribed. --- Straining at stool or constipation can increase
myocardial work.
 Activity Intolerance related to generalized weakness and imbalance between oxygen supply and demand
occurring with tissue ischemia secondary to MI.
A. Assess the frequency of angina, noting alleviating and precipitating factors. Observe whether
angina occurs at rest and is relieved or unrelieved by NTG. Document accordingly. --- This
assessment detects evidence of imbalance between oxygen supply and demand and hence
potential activity intolerance.
B. Assess the patient’s response to activity and report significant findings. --- Chest pain, increase
in HR (greater than 20 bpm), change in SBP (20 mm Hg over or under resting BP), excessive
fatigue, and shortness of breath are signs of activity intolerance that should be reported
promptly for timely intervention.
C. Help the patient recognize and limit activities that increase O2 demands, such as exercise and
anxiety. --- This information helps patients recognize and attempt to control factors that
increase ischemia.
D. Administer O2 as prescribed for angina episodes. --- This measure increases oxygen supply to
the myocardium.
E. Have the patient perform range-of-motion (ROM) exercises, depending on tolerance and
prescribed activity limitations. --- Cardiac intolerance to activity can be further aggravated by
prolonged bedrest.
F. Consult the health care provider about in-bed exercises and activities that can be performed by
the patient as the condition improves. --- This intervention enables progressive pacing toward
the patient’s optimal activity potential. In addition, the cardiac rehabilitation department should
be consulted for early and progressive activity.
 Additional Nursing Diagnoses/Problems:
 Psychosocial Support
 Psychosocial Support for the Patient’s Family and Significant Others
 Pulmonary Embolus
 Risk for Bleeding related to anticoagulation therapy
 Cardiac Surgery
  Dysrhythmias and Conduction Disturbance

D. Hypertensive Crisis
Hypertensive crisis is a severe increase in blood pressure that can lead to a stroke. Extremely high
blood pressure having systolic pressure of 180 mm Hg or higher and a diastolic pressure of 120 mm Hg or
higher which can damage blood vessels.
Hypertensive crisis is present if the elevated blood pressure (BP) is complicated by progressive target
organ dysfunction, Acute end-organ damage in the setting of a hypertensive emergency may include the
following.
 Neurologic: hypertensive encephalopathy, cerebral vascular accident/cerebral infarction,
subarachnoid hemorrhage, intracranial hemorrhage.
 Cardiovascular: myocardial ischemia/infarction, acute left ventricular dysfunction, acute pulmonary
edema, aortic dissection, unstable angina pectoris.
 Other cases are acute renal failure/insufficiency, retinopathy, eclampsia, microangiopathic hemolytic
anemia.
Two classes of hypertensive crisis that require immediate intervention include hypertensive emergency
and hypertensive urgency. Hypertensive emergencies and urgencies may occur in patients whose
hypertension has been poorly controlled, whose hypertension has been undiagnosed, or in those who have
abruptly discontinued their medications.
A hypertensive emergency is a situation in which blood pressures are extremely elevated and must be
lowered quickly (not necessarily to less than 140/90 mm Hg) to halt or prevent damage to the target organs
(Monnet & Marik, 2015).
Hypertensive urgency describes a situation in which blood pressure is very elevated but there is no
evidence of impending or progressive target organ damage (Bisognano, 2015). Elevated blood pressures
associated with severe headaches, nosebleeds, or anxiety are classified as urgencies. In these situations, oral
agents can be given with the goal of normalizing blood pressure within 24 to 48 hours (Monnet & Marik,
2015)
 Etiology
The most common cause for a hypertensive crisis is chronic hypertension with an acute exacerbation. A
variety of secondary causes of HTN can lead to a hypertensive crisis including, renal parenchymal disease,
renovascular disease, renal infarction, pregnancy (preeclampsia and eclampsia), central nervous system
disorders.
Poorly controlled hypertension in a patient requiring emergency surgery is also a hypertensive crisis
because of the increased cardiovascular risk that accompanies inadequate pre-operative BP control and the
accompanying perioperative increase in catecholamine levels and increased vascular resistance.
Severe hypertensive crisis can also occur in patients with extensive burn injury or children receiving
high-dose cyclosporine for allogenic bone marrow transplantation. In quadriplegic patients, hypertensive
crisis may develop due to autonomic hyperreflexia from stimulation of nerves below the level of spinal cord
injury. Hypertensive crises may also complicate acute rejection or transplant renal artery stenosis in patients
with renal allograft.
 Risk factors
Risk factors leading to hypertensive crisis are systemic illnesses with renal involvement, such as:
systemic lupus erythematosus, scleroderma, microangiopathic hemolytic anemia , endocrine disorders such
as Cushing disease, primary aldosteronism, or a pheochromocytoma, and autonomic hyperactivity in spinal
cord/head injuries, or cerebrovascular accident infarction/ hemorrhage Severe postoperative hypertension is
another risk factor for hypertensive crisis requiring immediate BP control because it can cause hypertensive
encephalopathy or intracranial hemorrhage, or jeopardize the integrity of vascular suture and lead to
postoperative hemorrhage.
 Pathophysiology
Blood pressure is the product of cardiac output multiplied by peripheral resistance. Cardiac output is the
product of the heart rate multiplied by the stroke volume. Each time the heart contracts, pressure is
transferred from the contraction of the heart muscle to the blood and then pressure is exerted by the blood as
it flows through the blood vessels. Hypertension can result from increases in cardiac output, increases in
peripheral resistance (constriction of the blood vessels), or both. Increases in cardiac output are often related
to an expansion in vascular volume. Although no precise cause can be identified for most cases of
hypertension, it is understood that hypertension is a multifactorial condition. For hypertension to occur there
must be a change in one or more factors affecting peripheral resistance or cardiac output. In addition, there
must also be a problem with the body’s control systems that monitor or regulate pressure
The pathophysiology resulting in end-organ dysfunction in hypertensive emergencies is not fully
understood. However, the mechanical stress on vascular walls likely leads to endothelial damage and a pro-
inflammatory response. These results increased vascular permeability, platelet, and coagulation cascade
activation, and fibrin clot deposition leads to hypoperfusion at the level of the target organ tissue.
Another pathologic process is the dilatation of cerebral arteries following a breakthrough of the normal
autoregulation of cerebral blood flow. Under normal conditions, cerebral blood flow is kept constant by
cerebral vasoconstriction in response to increases in BP. In patients without hypertension, flow is kept
constant over a mean pressure of 60-120 mm Hg. In patients with hypertension, flow is constant over a mean
pressure of 110-180 mm Hg because of arteriolar thickening. When BP is raised above the upper limit of
autoregulation, arterioles dilate. This results in hyperperfusion and cerebral edema, which cause the clinical
manifestations of hypertensive encephalopathy.
 Manifestations
The most common non-specific symptoms are chest pain, headache, blurred vision, weight loss and less
common presenting symptoms include dizziness, nausea, dyspnea, fatigue, malaise, epigastric pain,
polyuria, gross hematuria.
The specific symptoms related to end organ damage include chest pain (myocardial ischemia or MI),
back pain (aortic dissection), dyspnea (pulmonary edema or congestive heart failure) neurologic symptoms
seizures altered consciousness (hypertensive encephalopathy).
 Diagnosis
In patients presenting with severe hypertension, a thorough clinical assessment is of utmost importance
to differentiate a hypertensive crisis from severe uncomplicated hypertension and guide appropriate therapy.
Determination of type of hypertensive crisis through history taking. A detailed history about the onset,
duration, and severity of hypertension, a history drug and alcohol use, a list of antihypertensive
medications , and compliance with the antihypertensive regimen.
Physical examination, directed toward the cardiovascular and neurological systems. BP must be
measured in both arms to detect any significant differences. Other tests include peripheral pulse exploration
for absence or delay (which would suggest aortic dissection), cardiac and lung auscultation (S3, rales),
assessment of volume status and mental status, and examination for focal or lateralizing neurologic signs
that are infrequent in hypertensive encephalopathy and usually suggest some other cerebrovascular disease
(hemorrhage, embolism, or atherosclerotic thrombosis).
Examination of the ocular fundus. This is of great importance in the assessment of hypertensive crisis to
diagnose malignant hypertension. The appearance of striate, and hemorrhage and exudates spots with or
without papilledema. Striate hemorrhage and exudate spots result from high intravascular pressure and
ischemic infarction of nerve fiber bundles in retina, respectively and most commonly occur within three-disc
diameter of the optic disc. In contrast, dot hemorrhage and hard exudates as a result of benign hypertensive
retinal arteriosclerosis, usually occur in the periphery of the fundus.
Basic laboratory tests, including serum electrolytes, blood urea nitrogen, creatinine, complete blood
count, electrocardiogram, chest X-ray, and urinalysis should be obtained to evaluate for potential secondary
causes of hypertension and to define the extent of target organ damage. Malignant hypertension can cause
nephrotic range proteinuria and gross or microhematuria. In contrast significant proteinuria and hematuria
are rare in other types of hypertensive crisis. However, the level of protein excretion is of little value in the
differentiation of primary malignant hypertension from malignant hypertension due to secondary causes.
 Medical Management
 Typical management with ICU level-care
 Arterial line for close bp management
 At about 24 hours, switch to oral bp medications as wean IV meds.
Initial therapeutic goal is for blood pressure reduction. The medications used for treating hypertension
decrease peripheral resistance, blood volume, or the strength and rate of myocardial contraction. There is a
theoretical risk of cerebral hypoperfusion from impaired autoregulation during rapid reduction of BP.
However, the proven benefit of acute reduction of BP in hypertensive crisis clearly outweighs the theoretic
risk of cerebral ischemia. In general, an initial BP reduction to 160 to 170 mm Hg systolic, and 100 to 110
mm Hg diastolic or to a mean arterial pressure of 120 to 130 mm Hg over 2-4 hours can be safely
accomplished.
Alternatively, the initial antihypertensive therapy can be individualized and reduction of mean arterial
BP by 20% should be the initial goal for first 1-2 hours. This goal should be achieved using the parenteral
antihypertensives. The use of potent parenteral agents with rapid onset and short duration of action has
obvious advantages. If overshoot hypotension or neurologic sequelae develop, they can be quickly reversed
by allowing the BP to stabilize at a higher level. During the reduction of BP with parenteral
antihypertensives, the patient should be monitored closely for evidence of cerebral or myocardial
hypoperfusion (yawning, nausea, hyperventilation or chest pain).
Some patients, particularly those with normal kidney function, may have some element of volume
depletion because of the preceding pressure natriuresis that occurred in the setting of very high BPs. Thus, in
the absence of clinical signs of volume overload, some volume expansion with intravenous saline solution
will help to suppress renin secretion and to prevent significant hypotension with initiation of vasodilator
therapy.
Oral doses of fast-acting agents such as beta-adrenergic blockers (i.e., labetalol [Trandate]), ACE
inhibitors (i.e., captopril [Capoten]), or alpha2-agonists (i.e., clonidine [Catapres]) are recommended for the
treatment of hypertensive urgencies
 Sodium nitroprusside is a potent intravenous hypotensive agent with an immediate onset (seconds
to 2 minutes) and brief duration of action (1 to 3 minutes). It causes vasodilation of both arteriolar
and venous vessels resulting in decrease of both systemic vascular resistance (SVR) and venous
return. The combined decrease in preload and afterload reduces left ventricular wall tension and
myocardial oxygen demand.
 Fenoldopam is a selective dopamine receptor (DA1) agonist and decreases SVR. It also increases
renal blood flow and causes natriuresis and aquauresis. It is six times more potent than dopamine in
causing renal vasodilatation. Its dosage adjustment is not required in renal and hepatic insufficiency.
This agent has a rapid onset of action (within 10 minutes) and ease of BP titration. Fenoldopam is
contraindicated in the setting of glaucoma. Side effects include headache, flushing, dizziness,
tachycardia or bradycardia, hypokalemia, and local phlebitis. It should be avoided in patient with
sulfa allergy.
 Labetalol has selective α1- and nonselective β-blocking properties resulting in decrease in systemic
vascular resistance without an appreciable change in cardiac output Labetalol is contraindicated for
 heart failure, heart block, and chronic obstructive pulmonary disease and for hypertensive crisis
following coronary artery bypass graft surgery.
 Esmolol is an ultra-short-acting cardioselective β-blocker. It decreases arterial pressure by
decreasing heart rate and myocardial contractility, and thus cardiac output Esmolol is contraindicated
in patient with chronic obstructive pulmonary disease, heart failure, bradycardia and patients already
on β-blocker therapy.
 Nicardipine is a second-generation, dihydropyridine derivative calcium-channel antagonist with
high vascular selectivity, and strong cerebral and coronary vasodilator activity. of 15 mg/hour until
the desired blood pressure control is achieved. Since, nicardipine increases both stroke volume and
coronary blood flow with a favorable effect on myocardial oxygen balance, it is particularly useful in
patients with coronary artery disease and systolic heart failure.
 Clevidipine is a new short-acting intravenous third-generation dihydropyridine calcium-channel
blocker, which is a selective arterial vasodilator with very little or no effect on the myocardial
contractility or chronotropy and venous capacitance. The action of clevidipine is independent of
renal or hepatic functional status. Clevidipine is contraindicated in patients with allergies to
soybeans, soy products, eggs, or egg products, and patients with defective lipid metabolism.
 Nitroglycerine is a potent venodilator and only at high dose affects arterial tone. It reduces blood
pressure by reducing preload and cardiac output. Intravenous nitroglycerin. It is generally not
considered as a first line therapy for hypertensive crisis because of its low efficacy. Low dose
administration (~60 mg/minute) may, however, be used as an adjunct to other intravenous
antihypertensives in emergencies associated with acute coronary syndrome or pulmonary edema.
 Phentolamine is a nonselective α-adrenergic blocking agent and is useful in the management of
pheochromocytoma in conjunction with concomitant β-adrenergic blocker.
 Enalaprilat is an intravenous angiotensin converting enzyme inhibitor and because of its slow onset
and long duration of action, is a poor choice for use in a hypertensive crisis. In addition, it has
potential to cause renal failure, and hyperkalemia in circulatory decompensated states.
 Nifedipine, Clonidine, is immediate release formulations and oral clonidine loading must be
abandoned as a treatment option in the management of hypertensive crisis because of erratic effect
on BP. Figure 11. Parenteral Drugs Use for Hypertensive Crisis
 Nursing Diagnosis
 Ineffective tissue perfusion related to compromised blood flow secondary to severe hypertension
resulting in end-organ damage.
A. Monitor arterial BP continuously and note sudden increases or decrease in readings. --- A
precipitous drop in BP can cause reflex ischemia to the heart, brain, kidneys, and/or GI tract.
Note trends in mean arterial pressure and the patient’s response to therapy.
B. Monitor hourly urine output and note any presence of blood in the urine. --- To determine any
kidney injury
C. Continuously monitor the ECG. --- To detect dysrhythmias, injury and ischemia
D. Review BUN and creatinine. --- To evaluate the effect of BP on kidneys. BUN>20 mg/dL and
creatinine - >1.5 mg/dL suggest renal impairment.
E. Review serial chest radiography. --- To identify pulmonary congestion
F. Provide oxygen at 2 to 4 liters/min. --- To maintain or improve oxygenation.
G. Maintaining the patient at bed rest. --- Minimize oxygen demand
H. Help the patient decrease anxiety --- Minimize oxygen demand
I. Administer nitrates as ordered. --- To reduce preload and afterload.
J. Prepare the patient and family for surgical intervention to correct the underlying cause, if this is
indicated. --- Awareness reduces anxiety resulting to reduce oxygen demand
 Deficient Knowledge related to unfamiliarity with the need for frequent blood pressure (BP)
checks, adherence to antihypertensive therapy, and lifestyle changes
A. Assess the patient’s health care literacy (language, reading, comprehension) --- This assessment
helps ensure that information is selected and presented in a manner that is appropriate.
B. Teach the importance of assessing BP at frequent intervals and adhering to the prescribed
medication therapy. --- Frequent assessment provides feedback on response to therapy and may
help improve adherence to therapy
C. Provide teaching guidelines on the importance of exercise, stress reduction, weight loss (if
appropriate), decreased alcohol intake, and a less than 2 g/day sodium diet. Review how to read
food labels and choose low sodium foods. Refer to a nutritionist and exercise program, if
appropriate. --- Primary treatment for this disease includes promotion of lifestyle modification,
which can lower BP significantly when adhered to.
D. Teach medication actions, administration times, side effects, adverse effects, and the
importance of taking as prescribed. Include drug-drug, food-drug, and herb-drug interactions.
 Other Nursing Diagnoses
 Fatigue related to effects of hypertension and stresses of daily life.
 Imbalanced nutrition: more than body requirements related to excessive food intake. Ineffective
health maintenance related to inability to modify lifestyle.

E. Cardiomyopathy
Cardiomyopathies are disorders that affect the heart muscle affecting both systolic and diastolic
functions. Cardiomyopathies may be either primary or secondary in origin. Primary cardiomyopathies are
idiopathic; their cause is unknown. Secondary cardiomyopathies occur as a result of other processes, such as
ischemia, infectious disease, exposure to toxins, connective tissue disorders, metabolic disorders or
nutritional deficiencies. In many cases, the cause of cardiomyopathy is unknown.
 Figure 12. Cardiomyopathy

 Pharmacological Management
 Dilated cardiomyopathy
Treatment for dilated cardiomyopathy is essentially the same with the treatment of chronic heart
failure. Drug classes include angiotensin – converting enzymes inhibitors, Angiotensin II receptor
blockers, ,beta blockers, cardiac glycosides, diuretics, vasodilators, anti- arrhythmic, inotropic agents and
anti-coagulants for some patients.
 Hypertrophic Cardiomyopathy
The purpose is to reduce the pressure gradient across the left ventricle outflow, reducing the inotropic
state thus improving its compliance and reduce diastolic dysfunction. Amiodarone (Cordarone) has shown to
reduce the incidence of arrhythmogenic sudden cardiac death. Drug classes include beta-adrenergic
blockers, anti- arrhythmic, calcium channel blockers, anticoagulants.
Treatment is symptomatic relief. The goals are to reduce systemic and pulmonary congestion, lowering
ventricular filling pressure, augmenting systolic function pump’s function and reducing the risk for
embolism. Drug classes include diuretics, nitrates, beta blockers, calcium channel blockers, vasodilators,
anticoagulants, and inotropic.
 Non-Pharmacologic Interventions
Sodium diet restriction to 2 gms/day, Fluid restriction, cardiac rehabilitation program and aerobic
exercises.
 Surgical Management
Surgery without definitive treatment, individuals with cardiomyopathy develop end-stage heart failure.
Cardiac transplant is the definitive treatment for dilated cardiomyopathy. Ventricular assist devices may be
used to support cardiac output until a donor heart is available. Transplantation is not a viable option for
restrictive cardiomyopathy because transplantation does not eliminate the underlying process causing
infiltration or fibrosis and eventually the transplanted organ is affected as well. An implantable cardioverter-
defibrillator (ICD) often is inserted to treat potentially lethal arrhythmias. A dual-chamber pacemaker also
may be used to treat hypertrophic cardiomyopathy.
 Nursing Care
Nursing assessment and care for individuals with dilated and restrictive cardiomyopathies are similar to
those for individuals with heart failure. Teaching about the disease process and its management is vital.
Some degree of activity restriction is often necessary; assist to conserve energy while encouraging selfcare.
Support coping skills and adaptation to required lifestyle changes. Provide information and support for
decision making about cardiac transplantation if that is an option. Discuss the toxic and vasodilator effects
of alcohol and encourage abstinence. The person with hypertrophic cardiomyopathy requires care similar to
that provided for myocardial ischemia; If surgery is performed, nursing care is similar to that for any person
undergoing open heart surgery. Discuss the genetic transmission of hypertrophic cardiomyopathy and
suggest screening of close relatives (parents and siblings). Provide pre- and postoperative care and teaching
as appropriate for individuals undergoing invasive procedures or surgery for cardiomyopathy.
Community-based care Cardiomyopathies are chronic, progressive disorders generally managed in home
and community care settings unless surgery or transplant is planned, or end-stage heart failure develops.
When teaching the person and family for home care, teach about activity restrictions and dietary changes to
reduce manifestations and prevent complications, compliance to the prescribed drug regimen, its rationale,
intended and possible adverse effects. Discuss about the disease process, its expected ultimate outcome and
treatment options like cardiac transplantation, including the procedure, the need for lifetime
immunosuppression to prevent transplant rejection and the risks of postoperative infection and long term
immunosuppression and report what symptoms require immediate care. Refer the person and their family for
home and social services and counselling as indicated. Provide community resources such as support groups.
 Nursing Diagnosis
 Risk of decreased cardiac output related to impaired left ventricular filling, contractility, or outflow
obstruction.
 Risk of fatigue related to decreased cardiac output.
 Risk of ineffective breathing pattern related to heart failure.
 Risk of fear related to risk of sudden cardiac death.
 Risk of ineffective role performance related to decreasing cardiac function and activity restrictions.
 Risk of anticipatory grieving related to poor prognosis.

F. Arrythmia
Dysrhythmias are abnormal rhythms of the heart caused by conditions that alter the formation or
conduction (or both) of the electrical impulse within the heart. Dysrhythmias originate in different areas of
the conduction system, such as the sinus node, atrium, atrioventricular node, His Purkinje system, bundle
branches, and ventricular tissue. These disorders can cause disturbances of the heart rate, the heart rhythm,
or both. Dysrhythmias are named according to the site of origin of the electrical impulse and the mechanism
of formation or conduction involved.
 Figure 13. Electrical Conduction Flow

 Normal Electrical Conduction

The heart rhythm is orchestrated by the cardiac conduction system. This system has a complex network
of pathways that regulate the heartbeat. The conduction system of the heart consists of the Sinoatrial Node
(SA Node), which is the normal pacemaker of the heart situated at the right atrium. The electrical impulses
in the heart are initiated from here.
After this, these electrical impulses go through the atrioventricular node (VA Node), which slows down
the electrical impulses acting as a gatekeeper. The electrical impulses now travel through the Bundle of HIS
and Purkinje Fibres which transmit them rapidly ensuring the synergy of contractions in the heart chamber.
Through this complete process, the blood flow remains seamless in the body, and all the tissues receive an
adequate amount of oxygen and nutrients.
 Etiology
Many conditions and diseases may cause dysrhythmias; the most common are coronary artery disease
(CAD) and myocardial infarction (MI). Other causes include fluid and electrolyte imbalance, hormonal
imbalance, changes in oxygenation, medications, and drug toxicity
 Pathophysiology
Arrhythmias result from abnormalities of impulse initiation or impulse conduction or a combination of
both. Abnormal impulse initiation results from either automaticity or triggered activity. Automaticity can
further be subdivided into (1) automaticity caused by the normal automatic mechanism (a normal property
of cardiac cells in the sinus node, in some parts of the atria, in the atrioventricular junctional region, and in
the His-Purkinje system) and (2) automaticity caused by an abnormal mechanism (resulting from a decrease
in membrane potential of cardiac fibers, which normally have a high level of membrane potential).
Triggered activity is caused by afterdepolarizations, which are second depolarizations that occur either
during repolarization (referred to as early afterdepolarizations) or after repolarization is complete or nearly
complete (referred to as delayed afterdepolarizations). Abnormal impulse conduction results in reentrant
excitation. Usually, a combination of slowed conduction and unidirectional conduction block provides the
conditions necessary for reentry to occur. Slow conduction and block may result from a decrease in the
resting potential and velocity of depolarization of the action potential or may be a consequence of the
anisotropic structure of cardiac muscle, in which case resting potential and action potential upstroke velocity
may be normal.
Figure 14. Pathophysiology of Cardiac Arrhytmia

Disruption In the Normal Rhythm Of The Heart

Disruption in the normal rhythm of the heart is caused when its conduction system is disturbed because of
various factors. This disturbance is characterized by cardiac arrhythmias which are responsible for
irregularities in heart rhythm. Let’s discuss the causes of this disruption in the normal rhythm of the heart
below:
 Dysfunction of the Sinus Node:
The most common form of arrhythmias takes place when the sinoatrial node, i.e. the natural pacemaker of
the heart, is dysfunctional. This dysfunction occurs due to multiple factors ranging from genetics to
underlying heart conditions.
 Atrial Arrhythmias:
Arrhythmias arising in the atrium of the heart are common factors for disruption of normal heart rhythm.
Atrial Fibrillation and atrial flutter are some of the most common arrhythmias disrupting the heart rhythm
through chaotic atrial contractions which lead to an irregular response to the ventricles and disturb the
overall heart rhythm.
 Atrioventricular Block:
If the connection through the AV node is not proper, then it can lead to first-degree, second-degree, or
complete heart block. Due to this, the heart rate gets slowed abruptly causing an arrhythmia called
bradycardia.
 Ventricular Arrhythmias:
Arrhythmias originating in the ventricles of the heart can cause the heart rate to exceed its normal range and
go too fast. This type of arrhythmia can potentially lead to various heart abnormalities.
 Imbalances of the Electrolytes:
Due to imbalances of the electrolytes, such as magnesium, potassium, and calcium, the normal heart rhythm
gets disrupted as they normally lead to various arrhythmias.
 Supraventricular Arrhythmias:
The Wolf-Parkinson-White Syndrome is a type of arrhythmia belonging to supraventricular arrhythmias that
can cause heart abnormalities through rapid heartbeats.
 Ischemic Heart Disease:
Ischemic heart disease leads to conditions where the blood flow to the heart through the coronary arteries is
reduced. This causes abnormalities in the heart rhythm and leads to myocardial infarction (heart attack), scar
tissue formation, and different arrhythmias.
 Cardiomyopathies:
Structural abnormalities arise in the heart’s muscles at various times propelling different types of
arrhythmias.
 Manifestation
Signs and symptoms vary from absence of symptoms to complete cardiopulmonary collapse. General
indicators include alterations in level of consciousness (LOC), vertigo, syncope, seizures, weakness, fatigue,
activity intolerance, shortness of breath, dyspnea on exertion, chest pain, palpitations, sensation of “skipped
beats,” anxiety, and restlessness.
 Physical assessment: Increases or decreases in heart rate, blood pressure, and respiration rate;
changes in heart rhythm; dusky color or pallor; crackles (rales); cool skin; decreased urine output;
weakened and paradoxical pulse; and abnormal heart sounds.
 Diagnostic Tests
To diagnose a heart arrhythmia, gather medical history and conduct physical examination. Once signs
and symptoms are established, diagnostic tests are performed. Diagnostic tests for arrhythmias include the
electrocardiogram, cardiac monitoring and electrophysiology studies. Laboratory tests such as serum
electrolytes, drug levels and ABGs may be done to help identify the cause of the arrhythmia.
 12-lead ECG: To detect dysrhythmias and identify possible origin.
 Serum electrolyte levels: To identify electrolyte abnormalities that can precipitate dysrhythmias. The
most common are potassium and magnesium abnormalities.
 Drug levels: To identify toxicities (e.g., of digoxin, quinidine, procainamide, aminophylline) that can
precipitate dysrhythmias, or to determine substance abuse that can affect heart rate and rhythm, such
as cocaine.
 Ambulatory monitoring (e.g., Holter monitor or cardiac event recorder): To identify subtle
dysrhythmias, associate abnormal rhythms by means of patient’s symptoms, and assess response to
exercise.
 Electrophysiology study: Invasive test in which two to three catheters are placed into the heart,
giving it a pacing stimulus at varying sites and of varying voltages. The test determines origin of
dysrhythmia, inducibility, and effectiveness of drug therapy in dysrhythmia suppression.
  Exercise stress testing: Used in conjunction with Holter monitoring to detect advanced grades of
PVCs (those caused by ischemia) and to guide therapy. During the test, ECG and BP readings are
taken while the patient walks on a treadmill or pedals a stationary bicycle; response to a constant or
increasing workload is observed. The test continues until the patient reaches target heart rate or
symptoms such as chest pain, severe fatigue, dysrhythmias, or abnormal BP occur. Oximetry or ABG
values: To document trend of hypotension.
 SINUS NODE ARRHYTHMIAS
Sinus node arrhythmias may occur as a normal compensatory response (e.g. to exercise) or because of
altered automaticity. In these rhythms, as in NSR, the initiating impulse is from the sinus node. They differ
from NSR in the rate or regularity of the rhythm. Sinus arrhythmias include sinus arrhythmia, sinus
tachycardia and sinus bradycardia
 Sinus arrhythmia. Sinus arrhythmia is a sinus rhythm in which the rate varies with respirations,
causing an irregular rhythm. The rate increases during inspiration and decreases with expiration.
Sinus arrhythmia is common in the very young and the very old. It can be caused by an increase in
vagal tone, by digoxin toxicity or by morphine administration.
 Sinus tachycardia. Sinus tachycardia has all of the characteristics of NSR, except that the rate is
greater than 100 bpm. Tachycardia arises from enhanced automaticity in response to changes in the
internal environment. Sympathetic nervous system stimulation or blocked vagal (parasympathetic)
activity increases the heart rate. Tachycardia is a normal response to any condition or event that
increases the body’s demand for oxygen and nutrients, such as exercise or hypoxia. If the person on
bed rest or someone who has done little to increase oxygen demand has tachycardia, this is an
ominous sign. Sinus tachycardia may be an early sign of cardiac dysfunction, such as heart failure.
Tachycardia is detrimental in the person with cardiac disease because it increases oxygen demand
and decreases oxygen supply (because of decreased diastole reducing coronary artery filling
time).Common causes of sinus tachycardia include exercise, excitement, anxiety, pain, fever,
hypoxia, hypovolemia, anemia, hyperthyroidism, myocardial infarction, heart failure, cardiogenic
shock, pulmonary embolism, caffeine intake and certain drugs, such as atropine, adrenaline or
isoprenaline. Manifestations include a rapid pulse rate. The person may complain of feeling that the
heart is ‘racing’, shortness of breath and dizziness. In the presence of heart disease, sinus tachycardia
may precipitate chest pain.
 Sinus bradycardia. Sinus bradycardia has all of the characteristics of NSR, but the rate is less than
60 bpm. Sinus bradycardia may result from increased vagal (parasympathetic) activity or from
depressed automaticity due to injury or ischemia to the sinus node. Sinus bradycardia may be normal
(e.g. in the person with athletic heart syndrome). The heart rate also normally slows during sleep
because the parasympathetic nervous system is dominant at this time. Other causes of sinus
bradycardia include pain, increased intracranial pressure, sinus node disease, AMI (especially with
inferior wall damage), hypothermia, acidosis and certain drugs. Sinus bradycardia may be
asymptomatic; it is important to assess the person before treating the rhythm. Manifestations of
decreased cardiac output, such as decreased level of consciousness, syncope (faintness) or
hypotension, indicate a need for intervention.
 SUPRAVENTRICULAR ARRHYTHMIAS
Supraventricular arrythmias are arrythmias when an action potential originates in atrial tissue outside
the sinus node. In these arrhythmias, an ectopic pacemaker takes over or overrides the SA node. They may
also occur when the SA node fails; an escape rhythm develops as a fail-safe mechanism to maintain the heart
rate. The most common supraventricular arrhythmias are premature atrial contractions, paroxysmal
supraventricular tachycardia, atrial flutter and atrial fibrillation. These rhythms may be paroxysmal; that is,
occur in bursts with an abrupt beginning and end.
 Premature atrial contractions. A premature atrial contraction (PAC) is an ectopic atrial beat that
occurs earlier than the next expected sinus beat. PACs can arise anywhere in the atria. They are
usually asymptomatic and benign, but they may initiate paroxysmal supraventricular tachycardia in
susceptible individuals. PACs are common in older adults, often occurring without an obvious cause.
 Strong emotions, excessive alcohol intake, tobacco and stimulants such as caffeine can precipitate
PACs. They also may be associated with myocardial infarction, heart failure and other cardiac
disorders, hypoxemia, pulmonary embolism, digoxin toxicity and electrolyte or acid–base
imbalances. In people with underlying heart disease, PACs may precede a more serious arrhythmia.
The ectopic impulse of the PAC is usually conducted normally, leading to depolarisation of cardiac
muscle and a normal QRS complex. Because the impulse arises above the ventricles, it follows
normal conduction pathways through the ventricles. The shape of the P wave of a PAC differs from
normal P waves because its impulse arises outside the sinus node. A non-compensatory pause
usually follows, as the PAC resets the SA node rhythm. If frequent, they may cause palpitations or a
fluttering sensation in the chest. Early beats may be noted on auscultating or palpating the pulse.
 Paroxysmal supraventricular tachycardia. Paroxysmal supraventricular tachycardia (PSVT) is
tachycardia of sudden onset and termination. PSVT is usually initiated by a re-entry loop in or
around the AV node; that is, an impulse re-enter the same section of tissue over and over, causing
repeated depolarizations and occurs more frequently in women. Sympathetic nervous system
stimulation and stressors such as fever, sepsis and hyperthyroidism may precipitate PSVT. It also
may be associated with heart diseases such as CHD, myocardial infarction, rheumatic heart disease,
myocarditis or acute pericarditis.
 Atrial flutter. Atrial flutter is a rapid and regular atrial rhythm thought to result from an intra-atrial
re-entry mechanism. Causes include sympathetic nervous system stimulation due to anxiety or
caffeine and alcohol intake; thyrotoxicosis; coronary heart disease or myocardial infarction;
pulmonary embolism; and abnormal conduction syndromes, such as WPW syndrome. Older people
with rheumatic heart disease and/or valvular disease is especially vulnerable. People with atrial
flutter may complain of palpitations or a fluttering sensation in the chest or throat. If the ventricular
rate is rapid, manifestations of decreased cardiac output, such as decreased level of consciousness,
hypotension, decreased urinary output and cool, clammy skin, may be noted.
 Atrial fibrillation. Atrial fibrillation is a common arrhythmia characterized by disorganized atrial
activity without discrete atrial contractions. Multiple small reentry circuits develop in the atria. Atrial
cells cannot repolarize in time to respond to the next stimulus. Manifestations of atrial fibrillation
are dependent on the ventricular rate. With rapid ventricular response rates, manifestations of
decreased cardiac output such as hypotension, dyspnea, fatigue and angina may develop. People with
extensive heart disease may develop syncope or heart failure. Peripheral pulses are irregular and of
variable amplitude (strength).
 VENTRICULAR ARRHYTHMIAS
Ventricular arrhythmias originate in the ventricles. Because the ventricles pump blood into the
pulmonary and systemic vasculature, any disruption of their rhythm can affect cardiac output and tissue
perfusion. A wide and bizarre QRS complex (greater than 0.12 sec) is a characteristic feature of ventricular
arrhythmias. This occurs because ventricular ectopic impulses begin and travel outside normal conduction
pathways. Other characteristics include no relationship of the QRS complex to a P wave, increased
amplitude of the QRS complex, an abnormal ST segment and a T wave deflected in the opposite direction
from the QRS complex.
 Premature Ventricular Contractions (PVCs) are ectopic ventricular beats that occur before the
next expected beat of the underlying rhythm. They usually do not reset the atrial rhythm and are
followed by a full compensatory pause. PVCs often have no significance in people without heart
disease. Frequent, recurrent or multifocal PVCs may be associated with an increased risk of lethal
arrhythmias. PVCs result from either enhanced automaticity or a re-entry phenomenon. They may be
triggered by anxiety or stress; tobacco, alcohol or caffeine use; hypoxia, acidosis and electrolyte
imbalances; sympathomimetic drugs; coronary heart disease; heart failure; mechanical stimulation of
the heart (e.g. the insertion of a cardiac catheter); or reperfusion after thrombolytic therapy.
 Ventricular Tachycardia (VT, V tach) is a rapid ventricular rhythm defined as three or more
consecutive PVCs. Ventricular tachycardia may occur in short bursts or ‘runs’, or may persist for
more than 30 seconds (sustained ventricular tachycardia). The rate is greater than 100 bpm and the
rhythm is usually regular. Re-entry is the usual electrophysiological mechanism responsible for VT.
 Myocardial ischemia and infarction are the most common predisposing factors for VT. It also is
associated with cardiac structural disorders such as valvular disease, rheumatic heart disease or
cardiomyopathy. It may occur in the absence of heart disease and with anorexia nervosa, metabolic
disorders and drug toxicity. Non-sustained VT may occur paroxysmal and convert back to an
effective rhythm spontaneously. The person may experience a fluttering sensation in the chest or
complain of palpitations and brief shortness of breath.
 Ventricular Fibrillation (VF, V fib) is extremely rapid, chaotic ventricular depolarization causing
the ventricles to quiver and cease contracting; the heart does not pump. This is known as cardiac
arrest; it is a medical emergency requiring immediate intervention with cardiopulmonary
resuscitation (CPR). VF is the most common initial rhythm and is found in 60–80% of all cardiac
arrests. Survival rates are poor; however, strong predictors of a favorable outcome are the return of
spontaneous circulation within 20 minutes and being less than 60 years of age. Ventricular
fibrillation is usually triggered by severe myocardial ischemia or infarction.
 ATRIOVENTRICULAR ARRHYTHMIAS
Atrioventricular conduction blocks are conditions where there is conduction defects that delay or block
transmission of the sinus impulse through the AV node. Impaired conduction may result from tissue
injury or disease, increased vagal (parasympathetic) tone, drug effects or a congenital defect. AV
conduction blocks vary in severity from benign to severe.
 First-Degree AV Block, is a benign conduction delay that generally poses no threat, has no
symptoms and requires no treatment. Impulse conduction through the AV node is slowed, but all
atrial impulses are conducted to the ventricles. It may result from injury or infarct of the AV node,
other cardiac diseases or drug effects. The ECG shows all characteristics of NSR, except the PR
interval is greater than 0.20 second.
 Second-Degree AV Block is characterized by failure to conduct one or more impulses from the atria
to the ventricles. Two patterns of second-degree AV block are seen, identified as type I and type II.
o Second-degree AV block—type I Type I second-degree AV block (Mobitz type I or
Wenckebach phenomenon) is characterized by a repeating pattern of increasing AV
conduction delays until an impulse fails to conduct to the ventricles. On the ECG, PR
intervals progressively lengthen until one QRS complex is not conducted or dropped. The
ventricular rate remains adequate to maintain cardiac output and the person usually is
asymptomatic. Mobitz type I AV block usually is transient, associated with acute MI or drug
intoxication (e.g. digoxin, beta-blockers or calcium channel blockers). It rarely progresses to
complete heart block.
o Second-degree AV block—type II Type II second-degree AV block (Mobitz type II) involves
intermittent failure of the AV node to conduct an impulse to the ventricles without preceding
delays in conduction. The PR interval remains constant, but not all P waves are followed by
QRS complexes (e.g. there may be two P waves for every QRS). Conduction through the
His–Purkinje system usually is delayed as well, causing a widened QRS complex. Mobitz
type II block is frequently associated with acute anterior wall MI and a high rate of mortality
(Grossman & Mattson, 2013). Manifestations of Mobitz type II block depend on the
ventricular rate. Pacemaker therapy may be required to maintain the cardiac output.
 Third-Degree AV Block (complete heart block) occurs when atrial impulses are completely
blocked at the AV node and fail to reach the ventricles. As a result, the atria and ventricles are
controlled by different and independent pacemakers, with separate rates and rhythms. The
ventricular impulse arises from either junctional fibres (with a rate of 40 to 60 bpm) or a ventricular
pacemaker at a rate of less than 40 bpm. Third-degree block is frequently associated with an inferior
or anteroseptal myocardial infarction. Other causes include congenital conditions, acute or
degenerative cardiac disease or damage, drug effects and electrolyte imbalances. The slow escape
rhythm significantly affects cardiac output, causing manifestations such as syncope (known as a
Stokes–Adams attack), dizziness, fatigue, exercise intolerance and heart failure. Third-degree AV
block is life threatening and requires immediate intervention to maintain adequate cardiac output.
 Medical and Surgical Management
 Medications
The goal of drug therapy is to suppress arrhythmia formation. Antiarrhythmic drugs are primarily
used for acute treatment of arrhythmias, although they may also be used to manage chronic conditions. The
overall goal of therapy is to maintain an effective cardiac output by stabilizing cardiac rhythm. Most
antiarrhythmic drugs are classified by their effects on the cardiac action potential.
 Class I drugs: Sodium channel blockers Class IA Class IA drugs decrease the flow of sodium into
the cell and prolong the action potential. These decreases automaticity, slows the rate of impulse
conduction and prolongs refractoriness. They are used to treat both supraventricular and ventricular
tachycardias. Class IB Class IB, or lignocaine-like, drugs decrease the refractory period but have
little effect on automaticity. Drugs in this class are used primarily to treat ventricular arrhythmias,
including PVCs and ventricular tachycardia. Class IC Class IC drugs slow impulse conduction
velocity but have little effect on refractoriness. They are used to reduce or eliminate
tachyarrhythmias associated with re-entry. Their significant proarrhythmic effects limit their
usefulness, but they may be used to treat supraventricular tachycardia.
 Class II drugs: Beta-blockers Class II drugs are beta-blockers that decrease automaticity and
conduction through the AV node. They also reduce the heart rate and myocardial contractility. They
are used to treat supraventricular tachycardia and to slow the ventricular response rate to atrial
fibrillation. These drugs may cause bronchospasm and are contraindicated for people with asthma,
chronic obstructive pulmonary disease (COPD) or other restrictive or obstructive lung diseases.
 Class III drugs: Potassium channel blockers Class III drugs block potassium channels, prolonging
repolarization and the refractory period. Drugs in this class are used primarily to treat ventricular
tachycardia and ventricular fibrillation. Amiodarone may also be used for supraventricular
tachycardias.
 Class IV drugs: Calcium channel blockers Calcium channel blockers decrease automaticity and AV
nodal conduction. They are used to manage supraventricular tachycardias. Like the beta-blockers,
calcium channel blockers reduce myocardial contractility. Other drugs Adenosine and digoxin
decrease conduction through the AV node and are used to treat supraventricular
 Nursing responsibilities
1. Obtain baseline data, including vital signs, cardiac rhythm (including rate, PR, and QT intervals, and QRS
duration) and physical assessment (especially cardiac, neurological, and respiratory status).
2. Assess medication regimen to identify drugs that may interfere with antiarrhythmic therapy.
3. Monitor ECG to evaluate the effectiveness of therapy and to assess for possible arrhythmias precipitated
by treatment.
4. Immediately report manifestations of drug toxicity:
a. Procainamide—signs of heart failure; conduction delays or ventricular arrhythmias; skin rash,
myalgias or arthralgias, flu-like symptoms
b. Lignocaine—changes in neurological status, such as agitation, confusion, dizziness, nervousness.
c. Amiodarone—pulmonary fibrosis (increasing dyspnea, cough, hepatic dysfunction—changes in
liver function tests, jaundice); vision changes, photosensitivity.
d. Digoxin—anorexia, nausea, vomiting; blurred or double vision; yellow–green halos; new-onset
arrhythmias.
5. Use an infusion pump to administer intravenous infusions. Monitor the dose and assess its appropriateness
(in mg/min or μg/kg/min).
6. Health education for the person and family
7. Take the drug exactly as prescribed. Do not skip or double doses. Check with the medical officer
regarding instructions for a missed dose.
8. Pulse rates should be taken and recorded daily before rising. The record should be brought to all
appointments with healthcare professionals.
9. Report irregular pulse rates or rhythms, dizziness, eye pain, changes in vision, skin rashes or color
changes, wheezing or other respiratory problems, or changes
 Countershock
Countershock is used to interrupt cardiac rhythms that compromise cardiac output and the person’s
welfare. Delivery of a direct current charge depolarizes all cardiac cells at the same time. This simultaneous
depolarization may stop a tachyarrhythmia and allow the sinus node to recover control of impulse formation.
There are two types of countershock: synchronized cardioversion and defibrillation.

Figure 15. Countershock

 Synchronized Cardioversion
Synchronized cardioversion delivers direct electrical current synchronized with the person’s heart
rhythm, delivering of the shock with the QRS complex. This will prevent ventricular fibrillation by avoiding
current delivery during the vulnerable period of repolarization. Cardioversion is usually done as an elective
procedure to treat supraventricular tachycardia, atrial fibrillation, atrial flutter or hemodynamically stable
ventricular tachycardia. The nurse assists with cardioversion by preparing the individual before the
procedure; obtaining any laboratory tests ordered; obtaining and documenting ECG strips prior to, during
and after treatment; setting up the equipment; and monitoring the person’s response. Patient in atrial
fibrillation are at high risk of thromboembolism following cardioversion. Loss of atrial contractions with
atrial fibrillation leads to blood pooling in the atria, increasing the risk of clot formation. When the atria
begin to contract following successful cardioversion, clots may be dislodged, embolizing to the pulmonary
or systemic circulation. If possible, anticoagulants are given for several weeks before cardioversion is
attempted.
 Defibrillation
 Defibrillation is an emergency procedure that delivers direct current without regard to the cardiac
cycle. Ventricular fibrillation is immediately treated as soon as the arrhythmia is recognized. Early
defibrillation has been shown to improve survival in people experiencing VF. Defibrillation can be delivered
by external or internal paddles or pads. Conductive gel pads or paste is applied and external paddles or pads
are placed on the chest wall at the apex and base of the heart. Internal paddles are applied directly on the
heart and may be used in surgery, the emergency department or critical care. Internal defibrillation is done
only by a doctor; external defibrillation may be performed by any healthcare provider who has been trained
in the procedure. Automatic external defibrillators (AEDs) are available on most hospital units to allow early
defibrillation for cardiac arrest.
Figure 16. Defib Paddle /Pad Position

Figure 17. Pacemaker

 Pacemaker Therapy
A pacemaker is a pulse generator used to provide an electrical stimulus to the heart when the heart fails
to generate or conduct its own at a rate that maintains the cardiac output. The pulse generator is connected to
leads (insulated wires) passed intravenously into the heart or sutured directly to the epicardium. The leads
sense intrinsic electrical activity of the heart and provide an electrical stimulus to the heart when necessary
(pacing). Pacemakers are used to treat both acute and chronic conduction defects such as third-degree AV
block. They also may be used to treat bradyarrhythmia’s and tachyarrhythmias.
  Temporary pacemakers use an external pulse generator attached to a lead threaded intravenously into
the right ventricle, to temporary pacing wires implanted during cardiac surgery or to external
conductive pads placed on the chest wall for emergency pacing.
 Permanent pacemakers use an internal pulse generator placed in a subcutaneous pocket in the
subclavian space or abdominal wall. The generator connects to leads sewn directly onto the heart
(epicardial) or passed transvenous into the heart (endocardial). Epicardial pacemakers require
surgical exposure of the heart. Leads may be placed during cardiac surgery or using a small
subxiphoid incision to expose the heart. Transvenous pacemaker leads are positioned in the right
heart via the cephalic, subclavian or jugular vein. Local anesthesia can be used for permanent
pacemaker insertion. Pacemakers are programmed to stimulate the atria or the ventricles (single-
chamber pacing) or both (dual-chamber pacing).
The most commonly used pacemakers either: (1) sense activity in and pace the ventricles only; or (2)
sense activity in and pace both the atria and the ventricles. Dual-chamber or atrioventricular sequential
pacing stimulates both chambers of the heart in sequence. AV pacing imitates the normal sequence of atrial
contraction followed by ventricular contraction, improving cardiac output. Pacing is detected on the ECG
strip by the presence of pacing artefact. A sharp spike is noted before the P wave with atrial pacing and
before the QRS complex with ventricular pacing.
 Potential Complications from Insertion of a Pacemaker
1. Local infection at the entry site of the leads for temporary pacing, or at the subcutaneous site for
permanent generator placement. Prophylactic antibiotic and antibiotic irrigation of the subcutaneous pocket
prior to generator placement has decreased the rate of infection.
2. Pneumothorax; the use of sheaths marketed as “safe” reduces this risk. Bleeding and hematoma at the lead
entry sites for temporary pacing, or at the subcutaneous site for permanent generator placement. This can be
managed with cold compresses and discontinuation of antiplatelet and antithrombotic medications.
3. Hemothorax from puncture of the subclavian vein or internal mammary artery.
4. Ventricular ectopy and tachycardia from irritation of the ventricular wall by the endocardial electrode.
5. Movement or dislocation of the lead placed transvenous (perforation of the myocardium).
6. Phrenic nerve, diaphragmatic (hiccupping may be a sign), or skeletal muscle stimulation if the lead is
dislocated or if the delivered energy(mA) is set high. The occurrence of this complication is avoided by
testing during device implantation
7. Cardiac perforation resulting in pericardial effusion and, rarely, cardiac tamponade, which may occur at
the time of implantation or months later. This condition can be recognized by the change in QRS complex
morphology, diaphragmatic stimulation, or hemodynamic instability.
8. Twiddler syndrome may occur when the patient manipulates the generator, causing lead dislodgement or
fracture of the lead.
9. Pacemaker syndrome (hemodynamic instability caused by ventricular pacing and the loss of AV
synchrony).
 Cardioverter Defibrillator
The implantable cardioverter defibrillator (ICD) detects life-threatening changes in the cardiac rhythm
and automatically delivers an electric shock to convert the arrhythmia back into a normal rhythm. ICDs are
used for sudden death survivors, people with recurrent ventricular tachycardia and individuals with
demonstrated risk factors for sudden death. ICDs can deliver a shock as needed, provide pacing on demand
and can store ECG records of tachycardic episodes. A pulse generator connected to lead electrodes for
rhythm detection and current delivery is implanted in the left pectoral region. The lead is threaded
transvenously to the apex of the right ventricle. The ICD is programmed to sense a change in heart rate or
rhythm. When it detects a potentially lethal rhythm, it shocks the heart to convert the rhythm. The device
can be programmed or reprogrammed at the bedside as necessary. The ICD may be tested prior to discharge.
Local or general anesthesia is used and the individual may be discharged within 24 hours. The lithium-
powered battery must be surgically replaced every 5 years. Complications and nursing care are similar to
that for an individual having a permanent pacemaker implant. The person may briefly lose consciousness
before the device discharges, typically regaining consciousness quickly after the episode. Some people
report significant discomfort with ICD discharge (like a ‘blow to the chest’). A person in direct contact with
the individual when the device discharges may experience a tingling sensation.
 Cardiac Mapping and Catheter Ablation
Cardiac mapping and catheter ablation are used to locate and destroy an ectopic focus. These diagnostic
and therapeutic measures use electrophysiology techniques and can be performed in the cardiac
catheterization laboratory. Cardiac mapping is used to identify the site of earliest impulse formation in the
atria or the ventricles. Intracardiac and extracardiac catheter electrodes and computer technology are used to
pinpoint the ectopic site on a map of the heart. These same catheters can be used to deliver the ablative
intervention. Ablation destroys, removes or isolates an ectopic focus. In most instances, radio-frequency
energy produced by high frequency alternating current is used to create heat as it passes through tissue.
Catheter ablation is used to treat supraventricular tachycardias, atrial fibrillation and flutter, and, in
some cases, paroxysmal ventricular tachycardia. Anticoagulant therapy may be started after catheter ablation
to reduce the risk of clot formation at the ablation site
 Other Therapies
In addition to medications and interventional techniques, other measures may be used to treat selected
arrhythmias. Vagal maneuvers that stimulate the parasympathetic nervous system may be used to slow the
heart rate in supraventricular tachycardias. These maneuvers include carotid sinus massage and the Valsalva
maneuver. Carotid sinus massage is performed only by a medical officer during continuous cardiac
monitoring. Excessive slowing of the heart rate may result. The Valsalva maneuver is performed by forced
exhalation against a closed glottis (e.g. bearing down) this increases the intrathoracic pressure and vagal
tone, slowing the pulse rate
 Complementary and Alternative Therapies (CAM)
The practice of complementary and alternative medicines is very common in many countries of the
world, including where modern biomedical healthcare is predominant and readily available (Shaikh et al.,
2008). The apparent reversal of trend from modern to traditional medicine is partly attributed to the
multifaceted factors including the fact that synthetic drugs have always shown adverse reactions and other
undesirable side effects (Erasto & Majinda, 2011).In addition, the high cost of administering modern drugs,
which is beyond the reach of many people in the low income group and of those living in the rural areas is
also responsible for this trend.
The National Center for Complementary and Alternative Medicine (NCCAM) defines complementary
and alternative medicine (CAM) as “a group of diverse medical and health care systems, practices, and
products that are not generally considered part of conventional medicine. Complementary medicine is used
along with conventional medicine, whereas alternative medicine is used in place of conventional medicine.
The Philippine Institute of Traditional and Alternative Health Care (PITAHC) advocates for the
development and use of traditional and alternative healthcare in the country. PITAHC was created with the
objective of improving the quality and delivery of health care services to Filipinos by integrating traditional
and alternative health care into the national health care delivery system.
CAM Effects on the Cardiovascular System and CVD Risk Factors
 Biologically Based Therapies
The biologically based therapies include aromatherapy, chelation therapy, diet based therapies, folk
medicine, iridology, megavitamin therapy, neural therapy, and phytotherapy/herbal medicine . A number of
these therapies have purported cardiovascular effects, but most research on these products is either
inconclusive, conflicting, or shows no benefit for their use. It is equally important for the advancement of
the legitimate and rigorous study of CAM to report negative as well as positive results, and it illustrates the
need for studies of higher quality in this area.
 Marine-derived omega-3 polyunsaturated fatty acids (fish oil) are often promoted as being
preventative of major cardiovascular adverse outcomes by the postulated mechanisms of lowering
triglyceride levels (for which they are approved by the United States Food and Drug Administration
(FDA)), preventing arrhythmias, decreasing platelet aggregation, or lowering blood pressure. And
while experts agree that fish rich in omega-3 fatty acids should be included in a heart-healthy diet,
there is no evidence that omega-3 fatty acids in supplement form protect against heart disease
 Garlic is used most frequently as a dietary supplement for treatment of hyperlipidemia, heart disease,
and hypertension. A well-conducted, randomized trial demonstrated that there was no significant
difference in LDL cholesterol, HDL-cholesterol, triglycerides, or total cholesterol-HDL ratio after
six months of treatment with three preparations of garlic versus placebo . There is evidence that
garlic is associated with blood pressure reductions in patients with elevated systolic blood pressures
(10–12 mm Hg systolic, 6–9 mm Hg diastolic), but not in normotensive patients . However, there is
insufficient evidence to determine whether garlic provides a therapeutic advantage versus placebo in
terms of reducing the risk of cardiovascular morbidity and mortality.
 Ginseng use, there is some evidence that ginseng has a plethora of cardiovascular benefits, including
cardio protection, antihypertensive effects, and attenuation of myocardial hypertrophy and heart
failure. However, a randomized, double-blind, placebo-controlled study demonstrated that Korean
red ginseng had no significant effect on blood pressure, lipid profile, oxidized low density
lipoprotein, fasting blood glucose, or arterial stiffness in subjects with metabolic syndrome
 Ginkgo biloba is purported to have cardioprotective effects by several studies through its antioxidant,
antiplatelet, antithrombotic, vasodilatory, and antihypertensive properties A double-blind, placebo-
controlled, randomized clinical trial determined, however, that the herb does not reduce blood
pressure or the incidence of hypertension in elderly men and women. The trial also noted that there
was no evidence that ginkgo biloba reduced total or CVD mortality or CVD events; there were,
however, more peripheral vascular disease events in the placebo arm, suggesting that the herb may
reduce the risk of developing peripheral arterial disease.
 Hawthorn leaf and flower extracts are advocated as an oral treatment option for patients with chronic
heart failure; in fact, the German Commission E approved the use of hawthorn extracts in patients
with heart failure graded stage II . The results of a Cochrane review suggest that there is a significant
benefit in symptom control and physiologic outcomes from hawthorn extract as a treatment adjunct
for chronic heart failure. Hawthorn extract increased exercise tolerance, beneficially decreased
cardiac oxygen consumption, and improved symptoms such as shortness of breath and fatigue as
compared with placebo . However, no data on relevant mortality and morbidity were reported .
Finally, the study suggested that treatment with hawthorn may reduce sudden cardiac deaths
specifically in patients with left ventricular ejection fractions between 25% and 35%.
 Nursing Responsibilities
Assisting with External Defibrillation or Cardioversion
1. Multifunction conductor pads or paddles are used, with a conducting medium between the paddles and the
skin in the proper locations. The conducting medium is available as a sheet, gel, or paste. Gels or pastes with
poor electrical conductivity (e.g., ultrasound gel) should not be used.
2. Paddles or pads should be placed so that they do not touch the patient’s clothing or bed linen and are not
near medication patches or in the direct flow of oxygen
3. Women with large breasts should have the left pad or paddle placed underneath or lateral to the left
breast.
4. During cardioversion, the monitor leads must be attached to the patient in order to set the defibrillator to
the synchronized mode (“in sync”). If defibrillating, the defibrillator must not be in the synchronized mode
(most machines default to the “not-sync” mode).
5. When using paddles, 20–25 lb of pressure must be used in order to ensure good skin contact.
6. When using a manual discharge device, it must not be charged until it is ready to shock; then thumbs and
fingers must be kept off the discharge buttons until paddles or pads are on the chest and ready to deliver the
electrical charge.
7. When it is time to defibrillate, whomever is delivering the charge should announce, “charging to (number
of joules)” prior to discharging. “Clear!” must be called three times before discharging: As “Clear” is called
the first time, the discharger must visually check that he or she is not touching the patient, bed, or
equipment; as “Clear” is called the second time, the discharger must visually check that no one else is
touching the bed, the patient, or equipment, including the endotracheal tube or adjuncts; and as “Clear” is
called the third time, the discharger must perform a final visual check to ensure that everyone is clear of the
patient and anything touching the patient.
8. The delivered energy and resulting rhythm are recorded. Cardiopulmonary resuscitation (CPR) is
immediately resumed after the defibrillation charge is delivered, if appropriate, starting with chest
compressions.
9. If CPR is warranted, after five cycles (about 2 minutes) of CPR, the cardiac rhythm is checked again, and
another shock is delivered. A vasoactive or antiarrhythmic medication is given as soon as possible after the
rhythm check to facilitate a positive response to defibrillation.
10.After the event is complete, the skin under the pads or paddles is inspected for burns; if any are detected,
the primary provider or a wound care nurse is consulted about appropriate treatment.
11.The defibrillator is plugged back into an outlet, and supplies are restocked as needed