Cardiac physical examination

• A cardiac examination is a fixed sequence: general look and hands, pulses and blood pressure, the neck veins, then the chest wall (look, feel, listen), then the signs of congestion in the lungs, liver and legs.
• The jugular venous pressure (JVP) is the bedside estimate of right atrial pressure. Raised, it points to congestion; its waveform can name arrhythmias and valve or pericardial disease.
• Heart sounds and murmurs are timed against the cycle (systole or diastole), then described by shape, position, radiation and what changes them.
• Diastolic and continuous murmurs are always abnormal; systolic murmurs may be harmless flow murmurs.
• Breathing, Valsalva, squatting, standing and handgrip change murmurs in predictable ways, and that is how you tell look-alikes apart (for example hypertrophic cardiomyopathy from aortic stenosis).

By the end of this page you should be able to:

1. Perform the cardiac examination in order and say what each step is looking for.
2. Measure and interpret the JVP, including its waveform, Kussmaul sign and hepatojugular reflux.
3. Place the stethoscope on the auscultation areas and explain why they differ from the true valve positions.
4. Identify S1, S2 (and its splitting), S3, S4, clicks and the opening snap.
5. Describe the main systolic and diastolic murmurs and predict how respiration and manoeuvres change them.
6. Recognise the abnormal pulse forms and the causes of pulsus paradoxus.
7. Recognise the peripheral signs of endocarditis and the meaning of clubbing, and tell pulmonary from peripheral oedema.
8. Measure blood pressure with the correct cuff.

This page teaches the cardiac examination as a set of questions the body can answer. Each sign comes from a mechanism: pressure, flow or timing. If you know the mechanism you do not need to memorise the sign. Examination does not replace the ECG or echocardiography, but it tells you which to order and how urgently, and in many settings it is the only test available.

Examine the heart in anyone with breathlessness, chest pain, palpitations, syncope, oedema, a fever with no clear source, a new murmur, a stroke or limb ischaemia, hypertension, or before surgery. A collapse in a young person with an unremarkable examination still needs an ECG, because pre-excitation (see Wolff-Parkinson-White syndrome) and many other causes give no murmur at all.

• A stethoscope with both a diaphragm (best for high-pitched sounds) and a bell (best for low-pitched sounds such as S3, S4 and the mitral stenosis rumble). Press the bell lightly: heavy pressure stretches the skin into a diaphragm and filters out low frequencies.^[2]
• A quiet room, warm hands, privacy and a chaperone as appropriate; the patient exposed to the waist (women appropriately covered).
• A bed that can be raised to about 45 degrees. For the precordium, the usual position is 30 to 45 degrees, with the examiner on the patient's right.^[1]
• A sphygmomanometer with cuffs of several sizes, a watch with a second hand, and a light for the neck veins.

The order below moves from the periphery inwards. Do the same order every time so that nothing is missed.

Count the respiratory rate, look for breathlessness at rest, cyanosis, jaundice, pallor, and cachexia. Then the hands.

• Clubbing is enlargement of the ends of the fingers with loss of the angle at the nail base. Prolonged infective endocarditis can cause it.^[4] Clubbing is most often linked to respiratory disease, and also to cardiovascular disease (including cyanotic congenital heart disease), inflammatory bowel disease, Graves disease and chronic liver disease. The mechanism is not fully settled: chronic cyanosis is thought to trigger a reflex that opens digital arteriovenous shunts and raises blood flow, with prostaglandins, ferritin and vascular endothelial growth factor implicated.^[13]
• Splinter haemorrhages are small linear haemorrhages under the nail, running along its length.^[4] They occur in endocarditis but also with trauma, so a single one means little; several, in a feverish patient with a murmur, mean a great deal.
• Osler nodes are painful red nodules on or near the pulps of the fingers and toes.^[4]
• Janeway lesions are painless, flat or slightly raised haemorrhagic marks on the palms or soles.^[4]
• Roth spots (round or oval retinal haemorrhages with a pale centre) are seen with an ophthalmoscope.^[4]

These signs of endocarditis come from emboli of infected material and from the body's immune response. In the modified Duke criteria, Janeway lesions are a vascular phenomenon, and Osler nodes and Roth spots are immunologic phenomena; splinter haemorrhages and clubbing are supporting signs, not Duke criteria.^[4] The painful-or-painless split is the quickest way to tell Osler from Janeway.

Feel the radial pulse for rate and rhythm, then the carotid for the shape of the pulse wave (the carotid is closer to the aorta, so the waveform is not distorted on its way out to the wrist). Check both arms: a difference of 15 mmHg or less is normal, and a larger one suggests aortic or arterial disease such as a dissection.^[1] See abnormal pulses below.

Measuring blood pressure. Seat the patient for more than 5 minutes, back supported, feet on the floor, arm supported at heart level, no clothing under the cuff, and no exercise, caffeine or tobacco for at least 30 minutes.^[1] The cuff matters: the bladder should encircle about 80% of the limb and be about 40% as wide as it is long round.^[1] For one device with four cuff sizes, the fit was by mid-arm circumference (small 17 to under 22 cm, medium 22 to under 32 cm, large 32 to under 42 cm, extra-large 42 to 57 cm). A cuff one size too small can overestimate systolic pressure (by about 5 mmHg in one study) and one a size too large can underestimate it (by about 4 mmHg).^[11] Systolic pressure is the first sound heard as the column falls; diastolic is where the sound disappears (phase V).^[1] Measure the legs too when coarctation or peripheral arterial disease is possible: leg pressure normally runs 15 to 20 mmHg above arm pressure.^[1]

The right internal jugular vein runs almost straight down to the right atrium with no reliable valve between them (a valve near its lower end is variably competent), so the height of its blood column is a gauge of right atrial pressure. The JVP can differ from the true right atrial pressure, and when it does it is always the lower one.^[12]

Method.

1. Lie the patient at about 45 degrees (adjust the angle until the top of the column is visible), with the head turned slightly away from the side you are examining and the neck muscles relaxed.^[12]
2. Look along the right side of the neck, with tangential light, for the double flicker of the venous pulse behind the sternocleidomastoid. It does not rise on palpation, it disappears when you press on the vein at the base of the neck, and it changes with position and with breathing. The carotid pulse is the opposite: single, forceful, palpable, unaffected by pressure at the base.
3. Find the top of the pulsating column. Measure the vertical height above the sternal angle (the bony ridge where the manubrium meets the body of the sternum), using a ruler held vertically and a straight edge held horizontally from the column.
4. If the column is not visible, lower the head of the bed until it appears (very high pressure) or sit the patient up (low pressure).

Normal and raised. Measured above the sternal angle at about 45 degrees, the upper limit of normal is usually given as 3 to 4 cm (about 3 cm in the Cleveland Clinic review; many teaching texts use 4 cm), and more than that is jugular venous distension.^[12] The MSD Manual gives 4 cm above the sternal notch instead.^[1] Older teaching quotes about 8 cm because it measures from the right atrium (3 cm plus an assumed 5 cm; the angle-to-atrium distance measured in patients is 8 to 10 cm).^[12] Always check which convention a paper or colleague is using, and write your own measurement as "X cm above the sternal angle at 45 degrees". It is raised in right heart failure, volume overload, tamponade, constrictive pericarditis, tricuspid disease, superior vena cava obstruction and reduced right ventricular compliance, and low in hypovolaemia.^[1]

The waveform. Each component corresponds to an event in the right atrium.^[1]

To distinguish the waves, feel the carotid pulse while watching the neck: the a wave precedes the carotid pulse, and the v wave is a systolic wave.

Kussmaul sign. The JVP normally falls on inspiration, as the chest pressure drops and the right heart takes in the extra blood. In Kussmaul sign it rises, because inspiration increases the pressure gradient from abdomen to thorax and drives venous return into a right ventricle that cannot accept more volume. Causes are constrictive pericarditis (in only a minority of cases), restrictive cardiomyopathy, massive pulmonary embolism, right ventricular infarction, tricuspid stenosis and severe right heart failure. It does not occur in pure cardiac tamponade, which helps to separate tamponade from constriction.^[12]

Hepatojugular reflux (also called the abdominojugular test). Ask the patient to breathe normally, because straining or breath-holding raises the venous pressure on its own. Press firmly and steadily over the abdomen (traditionally the right upper quadrant) and watch the JVP. In healthy people it rises a little and returns to baseline within a few seconds even while the pressure is kept on; a rise that persists beyond 10 seconds and falls abruptly when the hand is lifted is abnormal.^[12] The MSD Manual counts a sustained rise of more than 3 cm as positive.^[1] A positive test means much the same as a raised resting JVP: a right heart that cannot take more volume, most often from heart failure, but it is not specific.^[12]

Look for scars (sternotomy, thoracotomy), a pacemaker, deformity (pectus), and visible pulsation.

• Apex beat. Normally in the 4th to 5th intercostal space just medial to the midclavicular line, under 2 to 3 cm across.^[1] A displaced, diffuse apex means a dilated ventricle; a sustained, heaving thrust means left ventricular hypertrophy.^[1]
• Parasternal heave. A lift to the left of the sternum suggests right ventricular hypertrophy or dilation.^[1]
• Thrills are palpable murmurs. A thrill at the right 2nd space in systole suggests aortic stenosis, at the apex mitral regurgitation, at the left 2nd space pulmonary stenosis, and at the left 4th space a small muscular ventricular septal defect.^[1]

Listening is covered in detail in its own sections below. The sequence is: start at the apex with the patient lying on the left side, then lie supine and move from the lower left sternal edge up through each space to the upper right sternal edge, and finally listen in the left axilla and over the carotids. Sit the patient forward to hear the early diastolic murmur of aortic regurgitation, and listen to the back for the signs of pulmonary congestion.^[2]

Feel the liver for pulsation (tricuspid regurgitation),^[15] check the abdomen for ascites, look at the sacrum and legs for oedema, feel the femoral and foot pulses, and take a lying and standing blood pressure if indicated (a fall of more than 20 mmHg systolic or more than 10 mmHg diastolic within 3 minutes is orthostatic hypotension).^[1]

The listening sites are conventional positions where each valve's sound is best heard, and they differ from the valves' surface markings.

The table is drawn from an anatomy teaching resource.^[8] Sounds are not heard only at "their" valve: aortic stenosis is often loudest at the right upper sternal border but is heard at the apex and over the carotids too, and the louder the murmur, the wider it spreads. Listen in all four areas, in the axilla and over the carotids.

S1 is the closure of the mitral valve, with a tricuspid component. It is loud in mitral stenosis, and soft or absent in first-degree AV block and in mitral regurgitation from rigid, scarred leaflets (but often well heard when the cause is myxomatous degeneration).^[2]

S2 has two components, aortic (A2) then pulmonary (P2).^[2] Inspiration lowers chest pressure, brings more blood into the right heart, and delays P2, so the split opens on inspiration and closes on expiration. That is physiological splitting. The abnormal patterns are:^[2]

• Widely split, but still varying with breathing: delayed P2, as in right bundle branch block or pulmonary stenosis.
• Fixed split (does not vary with breathing): typical of a secundum atrial septal defect.
• Paradoxical (reversed) split: split on expiration, single on inspiration, because A2 is late. Typical of left bundle branch block and aortic stenosis.
• Single S2: severe aortic stenosis or regurgitation, among others.

An early systolic click is typical of congenital aortic or pulmonary stenosis; a mid-to-late systolic click means mitral or tricuspid valve prolapse.^[2] Standing or the strain of a Valsalva manoeuvre moves a prolapse click earlier, nearer S1, and lying flat moves it nearer S2. Clicks can come and go between examinations.^[2]

The opening snap is a short high-pitched early diastolic sound, typical of mitral stenosis: the stiff leaflets snap open under pressure. The more severe the stenosis, the earlier it follows S2. It is loudest when the leaflets are still mobile and disappears as the valve calcifies.^[2] See atrial myxoma for a tumour that can mimic mitral valve disease.

Both are low-pitched, heard best with the bell, and are called gallops because the heart then sounds like a three-beat canter.

• S3 comes early in diastole, when blood rushes into a dilated, non-compliant ventricle. In adults it usually signals significant systolic dysfunction (see heart failure), though it may be normal in children, in pregnancy and up to about age 40.^[2][6] A left-sided S3 is best heard in expiration, in the left lateral position, and a right-sided one is louder on inspiration.^[2]
• S4 comes in late diastole, when the atrium contracts against a stiff ventricle. It is therefore absent in atrial fibrillation. It is heard in hypertension, aortic stenosis, hypertrophy and acute ischaemia.^[2]

The MSD Manual states that an S4 is always abnormal, although some teaching texts disagree.^[2] The two sounds fuse into a single loud summation gallop in tachycardia.

A murmur is a noise from turbulent flow. Name it by timing, shape (how loudness changes), position, radiation, loudness, pitch and quality.

Grading loudness (systolic murmurs). Grade 1 is barely audible, 2 soft but easily heard, 3 loud without a thrill, 4 loud with a thrill, 5 loud with minimal stethoscope contact, 6 audible with the stethoscope off the chest. Diastolic murmurs are graded 1 to 4.^[2]

Timing rules. Systolic murmurs may be normal or abnormal. Diastolic and continuous murmurs are always abnormal.^[2] A soft, short systolic murmur with a normal second sound, no symptoms and no other signs is most likely a flow murmur (faster flow across normal valves, as in pregnancy, anaemia or hyperthyroidism) and echocardiography settles any doubt.^[2]

Respiration. Right-sided murmurs (tricuspid regurgitation, pulmonary stenosis) get louder on inspiration; left-sided murmurs are quieter then, or louder on expiration.^[3] In a study of 50 patients, inspiration increased right-sided murmurs with a sensitivity of 100% and a specificity of 88%.^[9]

The manoeuvres change preload (venous return), afterload (resistance the left ventricle works against) or ventricular volume, and each murmur responds in its own way.^[3]

In the patient study summarised in the University of Washington evidence table, the HCM murmur increased with Valsalva (sensitivity 65%, specificity 96%) and with the move from squatting to standing (sensitivity 95%, specificity 84%); raising the legs reduced it (sensitivity 85%, specificity 91%). Handgrip increased the murmur of mitral regurgitation and ventricular septal defect (sensitivity 68%, specificity 92%).^[9]

For mitral valve prolapse, handgrip and squatting make the murmur softer, and Valsalva makes it louder.^[3] Standing moves the click earlier, so timing, not just loudness, should be recorded.^[2]

Oedema is excess fluid in the tissues, and the site tells you the side of the heart.

• Pulmonary oedema comes from raised left atrial and pulmonary venous pressure, as in left ventricular failure or mitral stenosis. It produces breathlessness, orthopnoea and basal crackles that do not clear on coughing.^[6]
• Peripheral oedema comes from raised right atrial pressure, so right or biventricular failure; the JVP is raised.^[1][6] Press for 5 seconds over the shin, ankle or (in bed-bound patients) the sacrum, and note the extent, symmetry, warmth, tenderness and pitting.^[1] Pitting is graded 1 to 4, but the grades have no agreed definition.^[1] One swollen, tender, warm leg suggests cellulitis or venous thrombosis, not heart failure; non-pitting swelling suggests a lymphatic or vascular cause.^[1]
• Non-cardiac causes of peripheral oedema include low plasma albumin (as in nephrotic syndrome or liver disease), lymphatic obstruction, venous disease and drugs such as calcium channel blockers (dihydropyridines such as amlodipine are common culprits).^[1][16] A normal JVP makes right heart failure an unlikely cause.^[12]

Feel the pulse for rate, rhythm, volume and shape, and then compare sides. Normally the arm pulses are equal and a difference above 15 mmHg in blood pressure between arms suggests arterial disease.^[1]

Coarctation. Pulses in the legs are diminished or delayed compared with the arms, the left arm pulse and pressure may be diminished, and blood pressure should be measured in all four limbs. An ejection-type systolic murmur may be heard over the upper left sternal border, the left axilla or between the shoulder blades on the left and a click from a bicuspid aortic valve may be present; Turner syndrome accompanies 10 to 20% of cases.^[5]

Definition. Systolic pressure normally falls by up to 10 mmHg on inspiration. A fall of more than 10 mmHg is pulsus paradoxus.^[1][10]

Mechanism. Inspiration increases venous return to the right ventricle, so the septum bows into the left ventricle, which then fills less and ejects less. When the heart is squeezed by fluid in a stiff pericardium, or when breathing creates large pressure swings, the effect is exaggerated.^[10]

Causes. Cardiac tamponade (the classic), constrictive pericarditis, restrictive cardiomyopathy, severe asthma, chronic obstructive pulmonary disease (COPD), and severe pulmonary embolism.^[1][10] In acute asthma it is used to judge severity and response to treatment.

Measuring. Inflate the cuff above systolic pressure, then deflate no faster than 2 mmHg per heartbeat. Note the pressure at which sounds are first heard (only on expiration) and the pressure at which they are heard with every beat. The difference is the pulsus paradoxus.^[1] Sometimes it is felt in the pulse as a weaker beat with each breath.

• JVP. Reading the carotid pulse as the venous pulse. Letting the patient strain or hold their breath during hepatojugular reflux, which raises the JVP by itself.
• Cuff size. The commonest cause of a wrong blood pressure in clinic; use the mid-arm circumference.^[11]
• Murmurs. A loud murmur in a well person can be a flow murmur, and a quiet one can be a severe lesion (a very low-flow aortic stenosis is quiet). Never decide on the murmur alone.
• Atrial fibrillation removes the a wave and the S4, and a presystolic accentuation in mitral stenosis.^[2]
• Pulses. Palpate the radial and femoral together, not one after the other.

Children. A soft mid-systolic murmur and an S3 are common and harmless in healthy children, but a fixed split S2 or a diastolic murmur is abnormal at any age.^[2]

Pregnancy. Flow murmurs and an S3 are common and normal.^[2]

Refer urgently when there is a diastolic or loud systolic murmur with symptoms, a new murmur with fever (endocarditis), syncope with a murmur, a raised JVP with low blood pressure (tamponade), or a pulsus paradoxus with breathlessness. Any murmur found in a symptomless adult with a normal examination can usually be assessed electively.