APPROACH TO THE PATIENT

WITH CARDIOVASCULAR
DISEASE

DR DIRESS M.

For pharmacy students

 objective
 At the end of this class students are expected to
 To know the common complaints of cardiac patient
 To do appropriate cardiovascular physical examination
Cardiac Symptoms
Dyspnea
 an abnormally uncomfortable awareness of
breathing that is easily differentiated from
normal, quiet, unnoticed breathing
 heart failure, pulmonary edema, obstructive
airway disease, and pulmonary embolism.

 Onset, precipitating factors, paroxysmal nature

Differential Diagnosis for dyspnea

 COPD(chronic obstructive pulmonary disease)

 Bronchial Asthma
 ILD ( interstitial lung disease)
 PVD( pulmonary vascular disease )
 CPE (cardiogenic pulmonary edema )
 NCPE( noncardiogenic pulmonary edema)
 Anemia
 Deconditioning
 myopathy, kyphoscoliosis
 congestive heart failure
Orthopnea

 Dyspnea that occurs when the patient is lying down

and improves upon sitting.
 Due to increase left atria and pulmonary capillary
pressure on supine position
 It is quantified according to the number of pillows
on which the patient sleeps
 Paroxysmal Nocturnal Dyspnea(PND)
 Describes episodes of sudden dyspnea and orthopnea
that awakens the patient from sleep, usually 1 or 2 hours
after going to bed.
 The patient typically sits up, or goes to a window for air.

 PND may be manifest by coughing or wheezing, possibly

because of increased pressure in the bronchial arteries leading
to airway compression, along with interstitial pulmonary
edema leading to increased airway resistance
Chest pain and discomfort
 Nature of the pain: squeezing, crushing etc.
 Location
 Radiation: to the jaw, left arm, hand etc.
 Exacerbating and Alleviating Factors
 Palpitations
 An unpleasant awareness of the forceful, rapid, or
irregular beating of the heart.
 Patients may at times describe the sensation as a
 rapid fluttering in the chest,
 flip-flopping in the chest, or
 a pounding sensation in the chest or neck.
 It may result from: irregularities, tachycardia, forceful
beat, bradycardia, extra beats.
 Edema

 Accumulation of excessive fluid in the body

 An ascending type of body swelling is characteristic to
cardiac problems.
 Dependant pitting edema with different severity
 Ddx
cardiac,hepatic,renal(crf,ns) ,malnutrition ,hypoprotinimi
a
 CARDIAC SYMPTOMS
 Cardiac Asthma (wheezing secondary to bronchospasm)
 Exertional Fatigue(Exercise intolerance)
 Syncope: loss of postural tone with brief episoide of lose of
consciousness
 Cough
 Hemoptysis
 Intermitant claudication
 Weight lose or gain
 CARDIAC SYMPTOMS
 Cerebral symptoms: such as confusion, disorientation, and
sleep and mood disturbances

 Gastrointestinal symptoms: Anorexia, nausea, and early satiety

associated with abdominal pain and fullness

 Cardiogenic shock

 S udden death
Physical Examination of CVS patient

 General appearance
 Examination of the venous system
 Examination of the arterial system
 Examination of the precordium
 Examination of related findings on other systems
 GENERAL APPEARANCE

 Cardiopulmonary distress
 Pain

 Diaphoresis

 Position assumed by the patient on the

bed( usually 30 to 45 degree bed up)

 Age

 Body build
Examination of the venous
system
 Examination of Jugular Venous pressure or
central venous pressure, cvp

 Examination of peripheral venous system

 CVP, central venous pressure
 Pressure of the right atrium
 Measured in cm of water (CVP= JVP + 5 cm of H2o or
blood)
 Use a column of blood in the jugular veins
 We use blood to estimate this pressure (1.36 cm H2O = 1.0
mm Hg)
 Jugular Venous pressure

 The internal jugular  The external jugular vein is

communicates directly usually more readily visible as
with the right atrium it passes over the
and SVC sternomastoid muscle towards
the mid-clavicle.
 No venous or cardiac  It is easily kinked as it passes
valves intervene through the fascia of the neck
 Act as a manometer of and may give a false
right atrial pressure impression of right atrial
pressure.
JUGULAR VEINS
 Distinguishing the internal
jugularvien from the carotid artery
pulsation
JVP Carotid
 No pulsations palpable  Palpable pulsations
 Pulsations obliterated by
pressure above the clavicle  Pulsations not obliterated by
 Level of pulse wave pressure above the clavicle.
decreased on inspiration;  No effects of respiration on
increased on expiration. pulse.
 Pulsation of the jugular vein 
will vary with position No effect of position
 Usually two pulsations per  One pulsation per systole
systole (x and y descents).  Descents not prominent.
 Prominent descents
 Pulsations sometimes more  No effect of abdominal
prominent with abdominal pressure on pulsations.
pressure.
 Technique of examination for
CVP(JVP)
 Position the patient reclining at an angle of 45°
 Turn the head to the left, Neck should not be sharply flexed
 Observe neck with a light falling obliquely across the neck
 Identify the external jugular veins on each side
 Then find the pulsations of the internal jugular veins
 Observe for a double-complex waveform
 Identify the highest point of pulsation
 With a centimeter ruler measure the vertical distance
between this point and the sternal angle.
 Measurements greater than 3 is abnormal
 JVP cont………
Height of column Increased by
 Deep expiration

 Cough

 Hepatojugular/abdominojugular reflux test: A positive

abdominojugular test is best defined as an increase in JVP(about 3
cm )during 10 s of firm midabdominal compression and sustained
for about 15 minute post compression
 Valsalva manouever

 Supine position

 Kussmaul’s sign: an increase rather than the normal decrease in

the CVP during inspiration
*Constrictive pericarditis
*Right ventricular infarction
 PATHOLOGIC CAUSES OF RAISED JVP

 Heart failure,cor plumonale

 Pericardial effusion ,tamponade

 constrictive pericarditis

 Superior vena cava obstruction

 Pulmonary embolism

 Hypertrophic /restrictive cm

 Iatrogenic fluid overload

Examination of the arterial system
 Pulse
 Blood pressure
 The vessel itself
Arterial Pulses

 The presence and the volume of each pulse should

be compared with the other side

 Detected by gently compressing the vessel against

firm structures, usually bones

 The main peripheral arterial pulses that should be

felt include: radial, brachial, carotid, femoral,
popliteal, posterior tibial and dorsalis pedis.
 Arterial Pulses
 Heart rate: use the radial artery, count for 60 seconds,
if the rhythm is irregular, auscultate
 Rhythm: regular Vs irregular
 If irregular: regularly irregular, irregularly irregular
 Character: form of the wave (speed of upstroke and
downstroke and summit)
Volume (amplitude): rough guide to pulse pressure and
stroke volume
 Delay/symetry: radio-femoral delay in coarctation of the
aorta.
 Character….
 Pulsus paradoxus: A >10 mm Hg fall in systolic pressure with
inspiration is feature of
 Pericardial tamponade
 Severe asthma
 COPD
 constrictive Pericarditis
 Tension pnemothorax
 Hemorrhagic shock
 Massive pulmonary embolism
UNEQUAL OR DELAYED PULSES — may result from:
Obstructive arterial diseases, most commonly
Atherosclerosis
Aortic dissection
Aortic aneurysm
Takayasu disease
Coarctation of the aorta
Supravalvular aortic stenosis in which the right
carotid, brachial, and radial pulses are larger in
amplitude and volume than those on the left side because
of the preferential streaming of the jet toward the
innominate artery
 BLOOD PRESSURE MEASURING APPARATUS

 Mercury sphygmomanometers
 Aneroid sphygmomanometers
 Automated oscillometric BP measuring devices
 Direct Intraarterial measurement
Blood pressure measurement
 Patient should avoid smoking and caffeine for 30
min
 Rest for at least 5 minutes
 The arm should be resting and free of clothing
 Position the hand so that the brachial artery is at the
level of the heart
..BP measurement
 Inflatable bladder over the arm. The lower border of
the cuff should be 2.5cm above the antecubital crease
 Inflate the cuff 30mmHg above the point at which
radial pulse disappears
 Put your stethoscope over the antecubital fossa and
deflate the cuff slowly at a rate of 2-3 mmHg/sec
…BP measurement
 The level at which the Korotkoff are heard is the systolic
pressure
 The disappearance point is the diastolic pressure
 Wait 2 or more minutes and repeat. Average your
readings. ; if readings vary by more than 5 mmHg, take
additional reading until two consecutive readings are
close
 take blood pressure in both arms; if pressures differ, use

the higher arm (normally the measurements should

differ by <10 mm Hg)
 …..BP measurment
 If the arm pressure is elevated, take the pressure in one leg,
particularly in patients under age 30 (Systolic leg pressures
may be as much as 20 mm Hg higher than arm pressures)
 If suspected orthostatic hypotension measure both on supine
and standing (if differ by >20/10 mm Hg)
EXAMINATION OF THE
PRECORDIUM
 INSPECTION
 Activity
 Active

 Quite

 Deformity (e.g. B ulged precordium)

 Apical Impulse

 Pulsations

 Heave (Parasternal Lift)

 PALPATION
1. Apical beat/Apical impulse
2. Point of Maximal Pulsation (PMI)
 The point where maximal pulsation is felt
 Usually located over the apical beat
3. Palpable heart sounds
4. Thrill
 Palpable murmur or bruit
 Use the palm of the hand
 Timing and location
5. Heave/Lift
 Forcefull elevation of the precordium
 Apical/parasternal
 APICAL IMPULSE
 It is the lowest and outer most point of cardiac pulsation
 Evaluation should begin with the patient in the supine
position at 30 degrees
 If the apical impulse is not palpable in this position
 Left latteral (left arm above the head)
 Sitting
 Best appreciated using finger tips
 The normal left ventricular apex impulse is located
 at or medial to the left midclavicular line in the fourth or fifth
intercostal space
 7-9 cm from midline
 CHARACTERIZATION OF THE APICAL IMPULSE
1. Palpable or not
o Causes of abscent apical beat:
 Obesity
 Muscular
 Obscured by ribs
 COPD
 Pericardial effusion
 Weak cardiac muscle contraction
 CHARACTERIZATION OF THE APICAL IMPULSE
2. Localization
o Causes of displaced apical impulse:
 Thoracic cage deformity
 Lung collapse/fibrosis
 Massive pleural effusion/Tension pneumothorax
 Intraabdominal mass/fluid collection
 Left ventricular (LV) cavity enlargement
 LV hypertrophy
 CHARACTERIZATION OF THE APICAL IMPULSE
3. Amplitude
 Tapping
 Thrusting
4. Diameter
 Localized
 Diffuse (> one ICS or > 3 cm in diameter)
5. Direction
6. Duration
 Non-sustained
 Sustained (stayed > 2/3rd of systole)
 PERCUSSION
 Not routinely used: replaced by
 Inspection

 Palpation

 CXR

 May be used if the apical impulse is neither visible

nor palpable
AUSCULTATION
 Quite room
 Stethscope

 Bell: low pitched sound (S3,S4,diastolic murmur at

atrioventricular valves)
 Diaphragm: high pitched sounds (S1,S2,Clicks,opening

snaps,pericardial knocks,atrioventricular valve systolic

murmurs,semilunar valve murmurs)
 STANDARD AUSCULTATORY POSITIONS
1. Supine: all
2. Supine and left latteral
 Apical diastolic murmur
 Apical S3
3. Sitting: all
4. Sitting and leaning forward
 Diastolic murmur at semilunar valves
 Pericardial friction rub
 STANDARD AUSCULTATORY AREAS
1. Aortic area
 Right second intercostal space
2. Pulmonic area
 Left second intercostal space
3. Erbe’s point
 Left third intercostal space
4. Tricuspid area
 Left lower sterna boarder
5. Mitrtal area
 Apex of the heart
 WHAT TO AUSCULTATE?

1. Heart sounds
2. Murmurs
3. Pericardial friction rub
 HEART SOUNDS

1. S1: atrioventricular (AV) valve closure

 Comprises mitral (M1) and tricuspid (T1) valve closure
2. S2: closure of semilunar valves
 Comprises aortic (A2) and pulmonic (P2) valve closure
3. Diastolic sounds
 Third heart sound (S3): or ventricular gallop
 Fourth heart sound (S4) or atrial gallop
 Opening snap (OS)
-A brief, high-pitched, early diastolic sound
4. Systolic sounds
 Ejection sound (Ejection click) Nonejection clicks (Mid-systolic
clicks)
 CARDIAC MURMURS
 Cardiac auscultation is method used for screening of heart
disease.
The production of murmurs is due to 3 main factors:
(1) high blood flow rate through normal or abnormal orifices;
(2) forward flow through a narrowed or irregular orifice into a
dilated vessel or chamber ; or
(3) backward or regurgitant flow through an incompetent valve, septal
defect, or patent ductus arteriosus.

 A heart murmur may have no pathological significance or may be an

important clue to the presence of valvular, congenital, or other
structural abnormalities of the heart .
 Conti…

 Most systolic heart murmurs do not signify cardiac

disease, and many are related to physiological increases
in blood flow velocity
 Diastolic murmurs virtually always represent
pathological conditions and require further cardiac
evaluation,

 Continuous “innocent” murmurs are soft ,systolic and

postional.
 Cont….
 Characterization of a murmur:
1. Intensity (Loudness)

2. Configuration

3. Timing and duration

4. Location

5. Radiation

6. Quality

7. Response to various physiologic maneuvers

.configuration of a murmur may be crescendo, decrescendo,

crescendo-decrescendo (diamond-shaped), or plateau.
Six grades are used to classify the intensity of a murmur:

•Grade I is the faintest murmur that can be heard (with difficulty)

•Grade II is also a faint murmur but can be identified immediately
•Grade III murmur is moderately loud
•Grade IV murmur is loud and is associated with a palpable thrill
•Grade V is very loud but cannot be heard without the
stethoscope(heard after partially raising the stethoscope above the
chest.
•Grade VI is the loudest and can be heard without a
stethoscope(raising the stethoscope above the chest wall)
 Classification of Cardiac Murmurs

1. Systolic murmurs
 Holosystolic (pansystolic) murmurs
 Midsystolic (systolic ejection) murmurs
 Early systolic murmurs
 Mid to late systolic murmurs

2. Diastolic murmurs
 Early high or low-pitched diastolic murmurs
 Middiastolic murmurs
 Presystolic murmurs

3. Continuous murmurs
 Holosystolic (pan systolic) murmurs

 when there is flow between chambers that have

widely different pressures throughout systole, such
as the LV and either the LA or RA ventricle.

 With an abnormal regurgitant orifice, the pressure

gradient and regurgitant jet begin early in contraction
and last until relaxation is almost complete.
 example..MR,TR,VSD,
 Early systolic murmurs
 less common
 begin with S1 and end in midsystole.
 often due to
 TR in the absence of pulm. HTN and in
 acute MR
 VSDs with pulm. HTN and small muscular VSDs,
 Midsystolic (systolic ejection) murmurs

 often crescendo-decrescendo in configuration,

 occur when blood is ejected across the aortic or pulmonic
outflow tracts.
 Starts shortly after S1, when the ventricular pressure rises
sufficiently to open the semilunar valve.
 As ejection increases, the murmur is augmented, and as
ejection declines, it diminishes.
 seen in AS,PS, high out put states as anemia ,pragnancy,
HOCM (hypertrophic obstructive cardiomyopathy)
Late systolic murmurs
 are soft or moderately loud, high pitched murmurs at
the LV apex that start well after ejection and end
before or at S2.

 often due to ischemia or infarction of the mitral

papillary muscles or to their dysfunction due to LV
dilatation.
 TVP,MVP
 Early diastolic murmurs
 begin with or shortly after S2, when the associated ventricular
pressure drops sufficiently below that in the aorta or pulmonary
artery.
 High-pitched murmurs of AR or PR due to pulmonary hypertension.
 The diastolic murmur of PR without is pulmonary hypertension low
to medium pitch
 Middiastolic murmurs

 usually originate from the mitral and tricuspid valves, occur

early during ventricular filling (MS&TS), and

 across the normal mitral valve in patients with VSD or PDA,

and across the normal tricuspid valve in patients with ASD.

 In severe, long-term AR, a low-pitched diastolic murmur

(Austin-Flint murmur) is often present at the LV apex; it may
be either middiastolic or presystolic.
 Continuous murmurs
 arise from high- to low-pressure shunts that persist
through the end of systole and the beginning of diastole.

 Thus, they begin in systole, peak near S2, and continue

into all or part of diastole.
 There are many causes of continuous murmurs, but they
are uncommon in patients with valvular heart disease
 Common examples are PDA,AV fistulas ,AV
malformations
Dynamic Cardiac Auscultation
 is an attentive cardiac auscultation during dynamic
changes in cardiac hemodynamics

 Changes in the intensity of heart murmurs during

various maneuvers
 Interventions Used to Alter the Intensity of Cardiac Murmurs

Respiration
 Right-sided murmurs generally increase with inspiration.

 Left-sided murmurs usually are louder during expiration.

Valsalva maneuver
 Most murmurs decrease in length and intensity.

Two exceptions are

 the systolic murmur of HCM, which usually becomes much louder, &

 that of MVP, which becomes longer and often louder.

 Following release of the Valsalva, right-sided murmurs tend to return

to baseline intensity earlier than left-sided murmurs.
Exercise
•Murmurs caused by blood flow across normal or obstructed
valves (eg, PS, MS) become louder with both isotonic and
submaximal isometric (handgrip) exercise.

•Murmurs of MR, VSD, and AR also increase with handgrip

exercise.

•However, the murmur of HCM often decreases with near-

maximum handgrip exercise.
Positional changes
 With standing, most murmurs diminish,

 2 exceptions being the murmur of HCM, which becomes louder,

and that of MVP, which lengthens and often is intensified.

 With prompt squatting, most murmurs become louder, but those of

HCM and MVP usually soften and may disappear.

 Passive leg raising usually produces the same results as prompt

squatting.
 During the initial relative hypotension following amyl nitrite

inhalation, murmurs of MR, VSD, and AR decrease, while

murmurs of AS increase because of increased stroke volume.
 Thank you!!!