EXAMINATION OF CVS

Vineetha K
Lecturer, DM WIMS Nursing College
 HISTORY

• Chest Pain- CAD & Myocardial infarction, pericarditis, Aortic dissection, Pulmonary
embolism, MVP,AS, HCM,Tachyarrhythmias.
• Dyspnea- Exertional dyspnea, Orthopnea, Paroxysmal nocturnal dyspnea.
• Fatigue- Exertional fatigue
• Palpitation- Tachyarrhythmias.
• Dizziness & Syncope- Postural hypotension, vasovagal syncope, carotid sinus
hypersensitivity, valvular obstruction, Stokes-Adams attacks.
 CHEST PAIN

• Acute, severe chest pain: Myocardial ischaemia, pericarditis, aortic dissection and
pulmonary embolism.
• Chronic, recurrent chest pain : angina, oesophageal reflux or musculoskeletal pain.

• Acute Coronary Syndrome: Chest pain and shortness of breath. Pain usually prolonged
and often described as ‘heaviness’ or ‘tightness’, with radiation into arms, neck or jaw.
Alternative descriptions include ‘congestion’ or ‘burning’, which may be confused with
indigestion
 CHEST PAIN

• Pericarditis : Central chest pain, which is sharp in character and aggravated by deep
inspiration, cough or postural changes. Characteristically, the pain is exacerbated by lying
recumbent and reduced by sitting forward.
• Aortic dissection : Severe tearing pain in either the front or the back of the chest. The onset
is abrupt, unlike the crescendo quality of ischaemic cardiac pain.
• Pulmonary embolism: Sudden onset sharp, pleuritic chest pain, breathlessness and
haemoptysis. Major, central pulmonary embolism presents with breathlessness, chest pain
that can be indistinguishable from ischaemic chest pains and syncope.
 DYSPNOEA

• Exertional dyspnoea: Exercise causes a sharp increase in left atrial pressure and this
contributes to the pathogenesis of dyspnoea by causing pulmonary congestion.

• Orthopnoea: In patients with heart failure, lying flat causes a steep rise in left atrial and
pulmonary capillary pressure, resulting in pulmonary congestion and severe dyspnoea.

• Paroxysmal nocturnal dyspnoea: Frank pulmonary oedema on lying flat wakes the patient
from sleep with distressing dyspnoea and fear of imminent death. The symptoms are corrected by
standing upright, which allows gravitational pooling of blood to lower the left atrial and pulmonary
capillary pressure, the patient often feeling the need to obtain air at an open window.
 FATIGUE

• Towards the end of day

• Inadequate oxygen delivery to exercising muscle, reflecting impaired cardiac output.
• Partly by deconditioning and muscular atrophy.
 DIZZINESS & SYNCOPE

• Transient hypotension, resulting in abrupt cerebral hypoperfusion.

• Postural hypotension: Syncope on standing upright reflects inadequate baroreceptor-

mediated vasoconstriction.
• Vasovagal syncope: This is caused by autonomic overactivity, usually provoked by
emotional or painful stimuli, less commonly by coughing or micturition.
• Carotid sinus hypersensitivity: Exaggerated vagal discharge following external
stimulation of the carotid sinus causes reflex vasodilatation and slowing of the pulse.
 DIZZINESS & SYNCOPE

• Valvular obstruction: Fixed valvular obstruction in aortic stenosis may prevent a

normal rise in cardiac output during exertion, such that the physiological vasodilatation
that occurs in exercising muscle produces an abrupt reduction in blood pressure and
cerebral perfusion, resulting in syncope.
 DIZZINESS & SYNCOPE

• Stokes-Adams attacks: These are caused by self-limiting episodes of asystole or rapid

tachyarrhythmias (including ventricular fibrillation). The loss of cardiac output causes
syncope and striking pallor. Following restoration of normal rhythm, recovery is rapid and
associated with flushing of the skin as flow through the dilated cutaneous bed is re-
established.
 Structure Of Cardiac History
• Presenting complaint (PC): The symptom that prompts the patient to seek medical
attention – commonly chest pain, breathlessness (dyspnoea), palpitation, dizziness or
blackouts (syncope)
• History of presenting complaint (HPC): This should define the nature of the symptoms,
initially through open questioning. Closed questions are used to elicit the presence or
absence of features which help to differentiate between diagnoses:
• – Chest pain: site, radiation, character, duration, provoking and relieving factors,
associated symptoms?
• – Breathlessness: orthopnoea, paroxysmal nocturnal dyspnoea, ankle swelling, cough,
wheeze, haemoptysis?
• – Palpitation: sudden onset and offset, ‘thumps’ or ‘pauses’, presyncope or syncope?
• – Dizziness/syncope: provoking factors, warning, duration, recovery?
 Structure Of Cardiac History
• Risk factors for cardiovascular disease: Smoking, hypertension,
hypercholesterolaemia, diabetes, family history of premature vascular disease
• Past medical history (PMH): Stroke or transient ischaemic attack (TIA), renal
impairment, rheumatic fever, peripheral vascular disease, other. Operations,
hospital clinic attendances
• Family history: Cardiac disease, sudden death
• Drug history: Include quantification of alcohol intake
 CVS Examination Routine
1. Wash hands 10. Inspect the face, eyes and mucous
membranes for xanthelasma, corneal arcus
2. Introduce yourself to patient
and anaemia, and cyanosis, respectively
3. Recline patient at 45°
11. Inspect the chest for scars and pulsations
4. Observe general appearance – comfortable,
breathless, pale? 12. Assess the position and character of the
apex beat
5. Inspect the hands for clubbing, splinter
13. Palpate the precordium for heaves and
haemorrhages, nicotine staining
thrills
6. Examine the radial pulse(s) for symmetry,
14. Auscultate the heart
rate, rhythm, character (collapsing?)
7. Measure the blood pressure 15. Auscultate the lungs
16. Examine the ankles and sacrum for oedema
8. Assess the height and waveform of the JVP.
17. Examine the peripheral pulses
9. Examine the carotid pulse character (slow
rising?) and volume (Corrigan’s sign?)
 Inspection of the patient
• Shape of chest
• Apex beat
• Visible pulsations: Large ventricular or aortic aneurysms, 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.
• Chest wall deformities:
• Pectus excavatum: These may compress the heart and displace the apex, giving a spurious impression of
cardiac enlargement. The presence of a median sternotomy scar usually
• Median sternotomy scar usually indicates previous coronary artery bypass graft (CABG) and/or cardiac
valve surgery. The long saphenous vein is the standard conduit for vein grafts so patients with prior CABG
often also have a scar along the medial aspect of one or both legs.
• A lateral thoracotomy scar : previous mitral valvotomy.
 Inspection of the patient
• PICCLE
• Anemia
• Cyanosis: This is a blue discoloration of the skin and mucous membranes caused by increased concentration
of reduced haemoglobin in the superficial blood vessels.
• Peripheral cyanosis : Cutaneous vasoconstriction slows the blood flow and increases oxygen extraction in
the skin and the lips, physiological during cold exposure, also occurs in heart failure.
• Central cyanosis
• Reduced arterial oxygen saturation caused by cardiac or pulmonary disease.
• It affects not only the skin and the lips but also the mucous membranes of the mouth.
• Cardiac causes include pulmonary oedema (which prevents adequate oxygenation of the blood) and
• Congenital heart disease: CCHD- Fallot’s tetralogy, Eisenmenger’s syndrome).
 Inspection of the patient
• Clubbing of the fingers and toes
• In congenital cyanotic heart disease, clubbing is not present at birth but develops during infancy and may
become very marked.
• Infective endocarditis is the only other cardiac cause of clubbing.

• Other cutaneous and ocular signs of infective endocarditis

• A vasculitic rash is common,
• Splinter haemorrhages in the nail bed, although
• Osler’s nodes (tender erythematous nodules in the pulps of the fingers)
• Janeway lesions (painless erythematous lesions on the palms)
• Roth’s spots (erythematous lesions in the optic fundi)
 Inspection of the patient
• Coldness of the extremities
• In patients hospitalized with severe heart failure, this is an important sign of reduced cardiac output. It is caused by
reflex vasoconstriction of the cutaneous bed.
• Pyrexia
• Infective endocarditis is invariably associated with pyrexia, which may be low grade or ‘swinging’ in nature if
paravalvular abscess develops.
• 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) to provide effective
compression. Oedema is caused by salt and water retention by the kidney.
 Arterial Pulse

• Rate and rhythm

• By palpating the right radial pulse.

• Rate, expressed in beats per minute (bpm), is measured by counting the number of beats in a timed period
of 15 seconds and multiplying by four.

• Normal sinus rhythm is regular, but in young patients may show phasic variation in rate during respiration
(sinus arrhythmia).

• An irregular rhythm usually indicates atrial fibrillation, frequent ectopic beats or self-limiting paroxysmal
arrhythmias.
 Arterial Pulse

• Character

• By examining the Carotid Pulse.

• Slow rising carotid pulse: Aortic Stenosis.

• Collapsing pulse: AR

• Biphasic pulse: Mixed aortic valve disease

• Alternating pulse: Severe left ventricular failure.

• Pulsus paradoxus: Cardiac tamponade, acute severe asthma.

 Arterial Pulse

• Symmetry

• Symmetry of the radial, brachial, carotid, femoral, popliteal and pedal pulses should be confirmed.

• A reduced or absent pulse indicates an obstruction more proximally in the arterial tree, caused usually by
atherosclerosis or thromboembolism or aortic dissection.

• Radiofemoral delay: Coarctation of the aorta causes symmetrical reduction and delay of the femoral pulses compared
with the radial pulse.
 Blood Pressure

• Patients should be sitting or lying at ease as significant changes in arterial pressure occur with exertion,
anxiety and changes in posture.

• The manometer should be at the same level of the cuff on the patient’s arm and the observer’s eye.

• For most adult patients, a standard cuff (12 cm width) is appropriate, but obese subjects require use of a wider
(thigh) cuff of 15 cm or the blood pressure will be overestimated.

• For children, various sized cuffs are available; select the one which covers most of the upper arm leaving a
gap of 1 cm or so below the axilla and above the antecubital fossa.
 Blood Pressure
• Palpate the radial pulse as the cuff is inflated to a pressure of 20 mmHg above the level at which radial
pulsation can no longer be felt.
• Place the stethoscope lightly over the brachial artery and reduce the pressure in the cuff at a rate of 2-3
mmHg/second until the first sounds are heard.
• Korotkoff sounds:
1. Begin to appear. This is the systolic BP
2. Sounds Louder sounds, sometimes with a murmur like tail
3. Higher intensity tapping sounds
4. Muffling
5. Total disappearance of sounds. This is the diastolic BP

Earlier phase 4 used to be taken as diastolic BP, now phase 5 is taken at all ages. However in situations like AR,
phase 4 is taken
 Blood Pressure

• Supine and erect blood pressure measurements provide an assessment of baroreceptor function, a postural

drop being defined by a fall in systolic blood pressure on standing.

 Jugular Venous Pulse

• Fluctuations in right atrial pressure during the cardiac cycle generate a pulse that is transmitted backwards
into the jugular veins.

• It is best examined in good light while the patient reclines at 45°.

• If the right atrial pressure is very low, however, visualization of the jugular venous pulse may require a
smaller reclining angle.

• Hepatojugular reflux: Manual pressure over the upper right side of the abdomen may be used to produce a
transient increase in venous return to the heart which elevates the jugular venous pulse.
 Jugular Venous Pressure
• The jugular venous pressure (JVP) should be assessed from the waveform of the internal jugular vein which
lies adjacent to the medial border of the sternocleidomastoid muscle.
• The JVP is measured in centimetres vertically from the sternal angle to the top of the venous waveform.
• The normal upper limit is 4 cm.
• This is about 9 cm above the right atrium and corresponds to a pressure of 6 mmHg.
• Elevation of the JVP indicates a raised right atrial pressure unless the superior vena cava is obstructed,
producing engorgement of the neck veins.
• During inspiration, the pressure within the chest decreases and there is a fall in the JVP.
• Kussumaul’s sign: In constrictive pericarditis and tamponade, inspiration produces a paradoxical rise in the
JVP (Kussmaul’s sign) because the increased venous return that occurs during inspiration cannot be
accommodated within the constrained right side of the heart.
Jugular Venous Pressure
Jugular Venous Pressure
• Normal JVP.

• ‘a’ wave: Atrial systole, most prominent wave.

• ‘x’ descent: Descent of the tricuspid valve ring

• ‘c’ wave: tricuspid valve closure.

• ‘v’ wave: Atrial pressure then rises again (‘v’ wave)

as the atrium fills passively during ventricular
systole.

• ‘y’ descent: The decline in atrial pressure as the

tricuspid valve opens produces the ‘y’ descent
• Giant ‘a’ wave: Forceful atrial contraction against a stenosed
tricuspid valve or a non-compliant hypertrophied right ventricle
produces an unusually prominent ‘a’ wave.
• Cannon ‘a’ wave. This is caused by atrial systole against a
closed tricuspid valve. It occurs when atrial and ventricular rhythms
are dissociated (complete heart block, ventricular tachycardia) and
marks coincident atrial and ventricular systole.

• Giant ‘v’ wave. This is an important sign of tricuspid

regurgitation. The regurgitant jet produces pulsatile systolic waves
in the JVP.

• Prominent ‘x’ and ‘y’ descents. These occur in constrictive

pericarditis and give the JVP an unusually dynamic appearance. In
tamponade, only the ‘x’ descent is usually exaggerated.
 Palpation of the chest wall
• Apex beat

• Lowest and most lateral point at which the cardiac impulse can be palpated.

• 5th intercostal space in the MCL.

• Cardiomegaly- inferior and laterally displaced apex beat- Chronic volume overload- MR, AR

• Double thrust apex beat- Palpable 3rd and 4th heart sounds.

• Left parasternal heave: Right ventricular enlargement produces a systolic thrust (heave) in the left parasternal
area.

• Other pulsations: Left ventricular aneurysms: Palpable medial to the cardiac apex.

• Thrills: The turbulent flow responsible for murmurs may produce palpable vibrations (thrills) on the chest wall,
particularly in aortic stenosis, ventricular septal defect and patent ductus arteriosus.
 Auscultation of the heart

• Apex- Mitral area

• Lower left sternal edge- Tricuspid area

• Upper left sternal edge- Pulmonary area

• Upper right sternal edge- Aortic area

• These areas should be auscultated in turn and loosely identify sites at which sounds and
murmurs arising from the four valves are best heard
 ERB’S POINT

• Erb’s point: Erb’s Point is found in the third intercostal space on the left

side of the sternum. It is one intercostal space below where the pulmonic valve

is auscultated. Hear both the S1 and S2 sounds.

 First Sound (S1)
• Mitral and tricuspid valve closure at the onset of systole.
• Accentuated S1:Mitral stenosis- thickened leaflets of the valve closure generates unusually
vigorous vibrations.
• Soft S1: Advanced mitral stenosis, the valve is rigid and immobile.
 Second Sound (S2)

• Aortic and pulmonary valve closure following ventricular ejection.

• 2 components- A2P2

• S2 is single during expiration.

• Physiological splitting of S2: During inspiration increased venous return to the right side

of the heart delays pulmonary valve closure. A2à P2

Abnormalities Of
S2
 Third and Fourth sounds (S3, S4)
• These low-frequency sounds occur early and late in diastole, respectively. When present, they give a
characteristic ‘gallop’ to the cardiac rhythm.

• Best heard with the bell of the stethoscope at the cardiac apex.

• Caused by abrupt tensing of the ventricular walls following rapid diastolic filling.

• S3:

• Rapid filling in early diastole following AV valve opening.

• Physiologic in children and young adults, disappear after 40 years of age.

• High output states- anaemia, fever, pregnancy, thyrotoxicosis.

• Abnormal after 40 years of age- LV failure, MR, constrictive pericarditis.

 Third and Fourth sounds (S3, S4)

• S4:

• Rapid filling in late diastole due to atrial contraction.

• Sometimes physiological in elderly.

• Most commonly pathological- vigorous atrial contraction late in diastole to augment filling of a hypertrophied, non

compliant ventricle- Hypertension, aortic stenosis, HCM

 Systolic clicks and Opening snaps
• Valve opening, unlike valve closure, is normally silent.
• Systolic clicks:
• Ejection Clicks:
• Aortic stenosis.
• Valve opening produces a click in early systole which precedes the ejection murmur.
• The click is only audible if the valve cusps are pliant and non-calcified, and is particularly prominent in
the congenitally bicuspid valve.
• Mid systolic click: MVP (Followed by a murmur)
• Opening snap:
• Mitral stenosis, elevated left atrial pressure causes forceful opening of the thickened valve leaflets. This
generates a snap early in diastole that precedes the mid-diastolic murmur.
 Heart Murmurs

• These are caused by turbulent flow within the heart and great vessels.

• Innocent Murmurs: Occasionally the turbulence is caused by increased flow through a normal valve –

usually aortic or pulmonary.

• However, murmurs may also indicate valve disease or abnormal communications between the left and right

sides of the heart (e.g. septal defects).

 Heart Murmurs

• Heart murmurs are defined by four characteristics:

• Loudness
• Quality
• Location & radiation
• Timing
 Heart Murmurs
• Loudness:
• The loudness of a murmur reflects the degree of turbulence. This relates to the volume and velocity of flow and not the
severity of the cardiac lesion.
• Grading of Murmur:
I. Barely audible
II. Medium intensity
III. Loud, but no thrill
IV. Loud with a thrill
V. Very loud, but still require positioning of stethoscope at least partly on the chest.
VI. Audible even without application of the stethoscope to the chest wall
 Heart Murmurs
• Quality: Relates to its frequency and is best described as low, medium or high-pitched.
• Location: Depends on its site of origin and has led to the description of four valve areas.
• Radiation of murmurs: Some murmurs radiate, depending on the velocity and direction of blood flow.
• AS: Directed towards the neck
• MR: Axilla
• AR: Left sternal edge
• Timing:
• Timed according to the phase of systole or diastole during which they are audible.
• Systolic murmurs: are either mid-systolic, pansystolic or late systolic;
• Diastolic murmurs are either early diastolic, mid-diastolic or presystolic in timing.
• Continuous murmurs are audible in both phases of the cardiac cycle.
 Heart Murmurs
• Mid-systolic (‘ejection’) murmur:
• Turbulence in the left or right ventricular outflow tract during ejection.
• It starts following opening of the aortic or pulmonary valve, reaches a crescendo in mid-systole and
disappears before the second heart sound.
• The murmur is loudest in the aortic area (with radiation to the neck) when it arises from the left ventricular
outflow tract, and in the pulmonary area when it arises from the right ventricular outflow tract.
• It is best heard with the diaphragm of the stethoscope while the patient sits forward.
• Aortic ejection murmurs : Aortic stenosis and hypertrophic cardiomyopathy, also in AR due to increased
stroke volume and velocity of ejection.
• Pulmonary ejection murmurs: Pulmonary stenosis, infundibular stenosis (Fallot’s tetralogy), also in ASD
due to increased blood flow across pulmonary valve.
• Innocent murmurs:
 Heart Murmurs
• Mid-systolic murmur:
• Innocent murmurs:
• Unrelated to heart disease are always mid-systolic in timing.
• Caused by turbulent flow in the left (sometimes right) ventricular outflow tract.
• In most cases, there is no clear cause, but they may reflect a hyperkinetic circulation in conditions such as
anaemia, pregnancy, thyrotoxicosis or fever.
• They are rarely louder than grade 3,
• Often vary with posture,
• May disappear on exertion and are
• Not associated with other signs of heart disease.
 Heart Murmurs

• Pansystolic murmurs: MR, TR, VSD, MVP

• Audible throughout systole from the first to the second heart sounds.

• Caused by regurgitation through incompetent atrioventricular valves and by ventricular septal defects.

• MR: Murmur is loudest at the cardiac apex and radiates into the left axilla. It is best heard using the
diaphragm of the stethoscope with the patient lying on the left side.

• TR & VSD: Loudest at the lower left sternal edge. Inspiration accentuates the murmur of TR because the
increased venous return to the right side of the heart increases the regurgitant volume.

• MVP: Sometimes produce PSM, ,more commonly, prolapse occurs in mid-systole, producing a click
followed by a late systolic murmur.
 Heart Murmurs

• Early diastolic murmurs: AR, Pulmonary regurgitation

• High-pitched and start immediately after the second heart sound, fading away in mid-diastole.

• Caused by regurgitation through incompetent aortic and pulmonary valves and are best heard using the

diaphragm of the stethoscope while the patient leans forward.

• AR: Murmur radiates from the aortic area to the left sternal edge, where it is usually easier to hear, in

maintained expiration with the patient leaning forward.

• Pulmonary regurgitation is loudest at the pulmonary area.

 Heart Murmurs

• Mid-diastolic murmurs: Mitral stenosis

• Caused by turbulent flow through the atrioventricular valves.
• They start after valve opening, relatively late after the second sound, and continue for a variable period during mid-
diastole.
• Mitral stenosis: Principal cause of a mid-diastolic murmur which is best heard at the cardiac apex using the bell of the
stethoscope while the patient lies on the left side.
• VSD, MR: Increased flow across a non-stenotic mitral valve occurs in ventricular septal defect and mitral regurgitation
and may produce a mid-diastolic murmur.
• Austin Flint Murmur: In severe aortic regurgitation, pre-closure of the anterior leaflet of the mitral valve by the
regurgitant jet may produce mitral turbulence associated with a mid-diastolic murmur (Austin Flint murmur).
• Tricuspid stenosis, ASD, TR: A mid-diastolic murmur at the lower left sternal edge, accentuated by inspiration, is
caused by tricuspid stenosis and also by conditions that increase tricuspid flow (e.g. atrial septal defect, tricuspid
regurgitation)
 Heart Murmurs

• Pre-Systolic Murmur: MS, Tricuspid stenosis

• In MS and TS, atrial systole produces a presystolic murmur immediately before the first heart sound.

• Accentuation of the mid-diastolic murmur associated with these conditions.

• Because presystolic murmurs are generated by atrial systole, they do not occur in patients with atrial

fibrillation.
 Heart Murmurs

• Continuous Murmurs: PDA

• Heard during systole and diastole, and are uninterrupted by valve closure.

• The commonest cardiac cause is patent ductus arteriosus, in which flow from the high-pressure aorta to the

low-pressure pulmonary artery continues throughout the cardiac cycle, producing a murmur over the base

of the heart which, though continuously audible, is loudest at end systole and diminishes during diastole.

• Ruptured sinus of Valsalva aneurysm also produces a continuous murmur.

 Friction rubs and venous hums

• Friction Rub:

• Seen in Pericarditis

• It is best heard in maintained expiration with the patient leaning forward as a high-pitched scratching noise
audible during any part of the cardiac cycle and over any part of the left precordium.

• Continuous venous hum:

• At the base of the heart reflects hyperkinetic jugular venous flow.

• It is particularly common in infants and usually disappears on lying flat.

 THANK YOU

Vineetha K
Lecturer, DM WIMS Nursing College

Thank you..