1. HISTORY & PHYSICAL
EXAMINATION OF CVS
Presented by:
Mandeep Duarah
(CRI)

2. HISTORY TAKING IN CVS
Should record the details of:
 PRESENTING SYMPTOMS – chest pain, fatigue
& dyspnoea, palpitations, and presyncope or
syncope.
 PREVIOUS ILLNESS
 HABITS – smoking, alcohol abuse
 FAMILY HISTORY
 DRUG HISTORY

3. PRESENTING SYMPTOMS
CHEST PAIN
1. Myocardial ischaemia
 Ischaemia of the heart results from an
imbalance between myocardial oxygen
supply & demand, producing pain called
angina.
 The patient describes retrosternal pain
which may radiate into the arms, the throat
or the jaw.
 It has a constricting character, is provoked
by exertion & relieved rapidly by rest.

4. 2. Pericarditis
 Also causes central chest pain, which is sharp in
character & aggravated by deep inspiration,
cough or postural changes.
 Usually idiopathic or caused by coxsackie B
infection.

5. 3. Aortic dissection
 Severe tearing pain in either the front or the back
of the chest.
 Onset is abrupt, unlike the crescendo quality of
ischaemic cardiac pain.

6. DYSPNOEA
 A major symptom of many cardiac disorders,
particularly left heart failure.
1. Exertional Dyspnoea
 Most troublesome symptom in heart failure.
 Exercise causes a sharp increase in left atrial
pressure & this contributes to the pathogenesis of
dyspnoea by causing pulmonary congestion.

7. 2. Orthopnoea
 In patients with heart failure lying flat causes a
steep rise in left atrial pressure, resulting in
pulmonary congestion & severe dyspnoea.
3. Paroxysmal Nocturnal Dyspnoea
 Caused by congestion (excessive or abnormal
accumulation of blood) in the lungs, along with
accumulation of excess fluid in the lungs
(pulmonary edema), which occurs as a result of
left sided heart failure.

8. FATIGUE
 Important symptom of heart failure.
 Caused partly by deconditioning & muscular
atrophy but also by inadequate oxygen delivery to
exercising muscle, reflecting impaired cardiac
output.

9. PALPITATION
 Description of the rate & rhythm of the palpitation
is essential.
 Rapid irregular palpitation is typical of atrial
fibrillation
 Rapid regular palpitation of abrupt onset occurs in
atrial, junctional & ventricular tachyarrhythmias.

10. DIZZINESS & SYNCOPE
 Cardiovascular disorders produces dizziness &
syncope by transient hypotension, resulting in
abrupt cerebral hypoperfusion.
 Recovery is usually rapid.

11. PHYSICAL EXAMINATION OF CVS
 INSPECTION OF THE PATIENT
 EXAMINATION OF THE RADIAL PULSE
 MEASUREMENT OF HEART RATE & BLOOD
PRESSURE
 JUGULAR VENOUS PULSE
 PALPATION OF THE ANTERIOR CHEST WALL
 AUSCULTATION OF THE HEART

12. INSPECTION OF THE PATIENT
 Chest wall deformities such as pectus
excavatum (hollowed chest) should be
noticed.
 Most common congenital deformity of
anterior chest wall
 Sunken appearance of sternum, may
compress the heart & displace the apex
 Hypothesized that there is impairment
of CVS function.

13.  Large ventricular or aortic aneurysms
may cause visible pulsations.
 Superior vena caval obstruction is
associated with prominent venous
collaterals on the chest wall.
 Prominent venous collaterals around
the shoulder occur in axillary or
subclavian vein obstruction.

14. ANAEMIA
 May exacerbate angina & heart failure.
 Pallor of the mucous membranes is a useful
physical sign but for confirmed diagnosis lab
measurements of haemoglobin concentration is
required.
CYANOSIS
 Bluish discoloration of the skin & mucous
membranes caused by increased concentration
of reduced haemoglobin in the superficial blood
vessels.

15. a. Central cyanosis
 Caused by reduced arterial oxygen sauration
caused by cardiac or pulmonary disease.
 Affects not only the skin & lips but also the
mucous membrane of the mouth.
 Causes include pulmonary oedema (which
prevents adequate oxygenation of the blood) &
congenital heart disease (tetralogy of fallot,
eisenmenger’s syndrome).

16. b. Peripheral cyanosis
 Cutaneous vasoconstriction slows the blood flow
& increases oxygen extraction in the skin & lips.
 Can be seen in fingers, underneath fingernails,
other extremities.
 Occurs in heart failure and mitral stenosis.

17. CLUBBING
 Congenital cyanotic heart disease &
infective endocarditis.
OTHER CUTANEOUS AND OCULAR
SIGNS OF INFECTIVE
ENDOCARDITIS
 Splinter haemorrhages in nail bed
 Oslers nodes (tender erythematous
nodules in the pulp of the fingers)
 Janeway lesions (painless
erythematous lesions on the palm)

18. COLDNESS OF THE EXTREMITIES
 Important sign of reduced cardiac output in
severe heart failure.
 Caused by reflex vasoconstriction of the
cutaneous bed.
PYREXIA
 Infective endocarditis is associated with pyrexia
 Can also occur for the first 3 days after
myocardial infarction.

19. OEDEMA
 Subcutaneous oedema that pits on digital
pressure is a cardinal feature of congestive heart
failure.
 Pressure should be applied over a bony
prominence (tibia,lateral malleoli,sacrum)
 In advanced heart failure oedema may involve
the legs, genitalia & trunk.

20. ARTERIAL PULSE
Should be palpated for evaluation of:
1. RATE & RHYTHM
 Rate, expressed in beats per minute (bpm), is
measured by counting over a timed period of 15
seconds.
 An irregular rhythm usually indicates atrial
fibrillation.

21. 2. CHARACTER
 Defined by the volume & waveform and should be
evaluated at the right carotid artery (pulse
closest to the heart & least subject to damping &
distortion)
 Pulse volume is small in heart failure & large in
aortic regurgitation.
 Pulsus alternans – relatively high amplitude or
normal amplitude pulse followed by a pulse of
lower amplitude, occurs in severe left ventricular
disease.

22.  Pulsus paradoxus – occurs when the pulse
prssure falls by >10mm hg with each inspiration,
found in constructive pericarditis & cardiac
tamponade.
 Bisferiens pulse (biphasic pulse) – with 2 systolic
peaks is usually attributed to a combination of
aortic stenosis & aortic regurgitation.

23. 3. SYMMETRY
 Symmetry of the radial, branchial, carotid,
femoral, popliteal & pedal pulses should be
confirmed.
 Coarctation of the aorta causes symmetrical
reduction & delay of the femoral pulses compared
with the radial pulses.

24. MEASUREMENT OF BLOOD
PRESSURE
 Measured using sphygmomanometer
 Patient is placed at supine position
 A cuff of atleast 40% the arm circumference in
width is attached to a mercury manometer &
inflated around the extended arm
 Auscultation over the brachial artery reveals 5
phases of korotkoff sounds as the cuff is deflated:

25.  Phase 1: the first appearance of the sounds
marking systolic pressure
 Phase 2 & 3: increasingly loud sounds
 Phase 4: abrupt muffling of the sounds
 Phase 5: disappearance of the sounds.
Conditions where korotkoff sounds remain audible
despite complete deflation of the cuff (aortic
regurgitation, arteriovenous fistula) phase 4 must
be used for the diastolic measurement.

26. JUGULAR VENOUS PULSE
 Best examined while the patient reclines at 45 degrees
with patients head partially rotated to one side.
 Sternal angle is reference point for JVP
 Differentiate from carotid
- multiple wave forms
- can be abolished by gental digital pressure
where as carotid pulsation is always palpable & cannot
be abolished by gentle digital pressure.

27. JUGULAR VENOUS PRESSURE
• Position the patient so that the upper level of JV pulse is
visible
• Place ruler at sternal angle which is 5cm above the RA
• Hold another ruler horizontally at the top of JV pulse
• Note how many cms this is above the sternal angle , add
5cms to this number & total is JV pressure
• Normal pressure is less than or equal to 9cm.

28. CAUSES OF ELEVATED JUGULAR
VENOUS PRESSURE
 Congestive heart failure
 Cor pulmonale
 Pulmonary embolism
 Right ventricular infarction
 Tricuspid valve disease
 Tamponade
 Constrictive pericarditis
 Superior vena cava obstruction

29. PALPATION OF CHEST WALL
 Used for detection of parasternal heaves &
apex beat
 Parasternal heave is discerned with the heel or
flat of the right hand against the left
parasternal region, right ventricular
hypertrophy causes a left parasternal heave.
 Apex beat is defined as the lowest & most
lateral point at which the cardiac impulse can
be palpated.
 The apex beat is normally located in the fifth
left intercostal space in the mid-clavicular line.
 Apex beat is displaced in left ventricular
dilation.

30. AUSCULTATION OF THE HEART
 Use the diaphragm for high pitched
sounds & murmers
 Use the bell for low pitched sounds &
murmers
 Sequence of auscultation
- Upper right sternal border (URSB) with
diaphragm(aortic area)
- Upper left sternal border (ULSB) with diaphragm
(pulmonary area)
- Lower left sternal border (LLSB) with diaphragm
(tricuspid)
- Apex ( mitral area)

31.  After the age of 40 S3 is nearly always
pathological, usually indicating left ventricular
failure, mitral regurgitation
 S4 is also pathological and heard in aortic
stenosis, hypertrophic cardiomyopathy.

32. systolic clicks & opening snaps
 Valve opening is normally silent
 In aortic stenosis valve opening produces a click,
the click is only audible if the valve cusps are
pliant & non-calcified, and is prominent in
bicuspid valve.
 In mitral stenosis, elevated left atrial pressure
causes forceful opening of the thickened valve
leaflets, this generates a snap.

33. Heart murmurs
 Caused by turbulent flow within the heart &
greater vessels.
 Turbulence is caused by increased flow through a
normal valve usually aortic and pulmonary.
 Murmurs may also indicate valve disease or
abnormal communications between the left &
right sides of the heart (septal defects).

34. According to the phase of systole or diastole during
which it is heard murmurs are classified as:
1. Systolic murmurs
 Midsystolic murmur – caused by turbulence in the
left or right ventricular outflow
 Pansystolic murmur – mitral regurgitation, tricuspid
regurgitation, ventricular septal defect
 Late systolic murmur – mitral valve prolapse,
tricuspid valve prolapse.

35. 2. Diastolic murmurs
 Early diastolic murmurs – caused by regurgitation
through aortic and pulmonary valves
 Mid diastolic murmurs – caused by turbulent flow
through the atrioventricular valves (mitral stenosis)
 Presystolic murmur – mitral & tricuspid stenosis.
3. Continuous murmurs
 Heard during systole & diastole
 Patent ductus arteriosus

36. THANK YOU