Cardiovascular and nervous system

• Look for finger clubbing, characterised by fluctuant nail beds, loss of angle between the nail plate and posterior nail fold, and increased nail curvature. Cardiac causes include cyanotic heart disease and infective endocarditis.

• Look for cyanosis due to right-to-left cardiac shunts.

• Look for palmar or tendon xanthomata.

• Look for peripheral stigmata of infective endocarditis (Table 3.1).

Table 3.1

Peripheral signs of infective endocarditis

Sign	Appearance
Splinter haemorrhages	Multiple linear reddish-brown marks on the linear axis of nails (one or two may occur in healthy people)
Osler’s nodes	Small painful, purplish nodules at the finger pulps representing digital microinfarction
Janeway lesions	Pink palmar macules
Roth’s spots	Flame-shaped retinal haemorrhages with a cotton wool centre

Face and neck

• Look for central cyanosis at the tongue.

• Note any pallor or abnormal skin markings, specifically a malar flush. A malar flush may be a sign of pulmonary hypertension and you should especially consider mitral stenosis as a cause.

• Look for corneal arcus, a creamy yellow discoloration at the boundary of the iris and cornea caused by cholesterol deposition; it can be normal. Look for xanthelasmata.

Jugular venous pulse (JVP)

There are no valves between the right atrium and internal jugular vein, such that the degree of rise and distension of the JVP is dictated by right atrial pressure. The external jugular vein is superficial, prone to kinking in the fascial layers and thus not a guide to right atrial pressure. The right internal jugular vein is used in preference to the left. It runs a relatively straight course medial and deep to the sternomastoid, from between the sternal and clavicular heads to the angle of the jaw. It differs from the arterial pulse (Table 3.2) in numerous ways.

Table 3.2

Differences between jugular and carotid pulse

	Jugular	Carotid
Number of waveforms	Two: ‘a’ and ‘v’	One
Upper level	Definite	Not defined
Shape of movement	Rapid inward	Rapid outward
Palpability	Impalpable	Palpable
Effect of respiration	Falls during inspiration (venous return increased by suction effect of lungs)	No effect
Effect of position	Varies	No effect
Effect of abdominal pressure	Rises	No effect

The JVP has a characteristic waveform (Table 3.3, Fig. 3.1).

Table 3.3

Normal waveform of the jugular venous pressure

Waveform	When it occurs	What it represents
‘a’	Presystolic	Venous distension due to right atrial contraction – blood, as well as entering the right ventricle, passes back through the open channel between the right atrium entrance and the jugular vein
‘c’ (a flicker in the x descent)	Ventricular systole	Closure of tricuspid valve whose leaflets bulge back towards the right atrium during ventricular systole
‘x’	Synchronous with carotid pulse	Tricuspid valve drawing away from the right atrium as the right ventricle empties in systole (atrial relaxation also contributes to ‘x’)
‘v’	Not synchronous with ventricular systole	Venous return to right atrium whilst tricuspid valve still closed
‘y’	Precedes atrial contraction	Opening of tricuspid valve and blood rushing from the right atrium into the right ventricle just prior to ‘kick’ of atrial contraction

Figure 3.1 Normal waveforms of the jugular venous pulse.

Note that in relation to the electrocardiogram (ECG) the ‘a’ wave thus corresponds to a P wave and the ‘x’ descent to the QRS complex.

• Examine the JVP by positioning the patient at 45° and estimate the vertical height in centimetres between the top of the venous pulsation and the sternal angle to give the venous pressure in cm (Fig. 3.2). Normal is up to 3–4 cm.

Figure 3.2 Measuring the jugular venous pulse.

Abnormal waveforms of the JVP are outlined in Table 3.4.

Table 3.4

Abnormal waveforms of the jugular venous pulse (JVP)

Chest wall

• Look for a median sternotomy scar consistent with coronary artery bypass grafting, open mitral valvotomy or valve replacement, aortic valve surgery or mediastinal surgery.

• Look for a left lateral / inframammary thoracotomy scar consistent with closed mitral valvotomy.

• Look for the scar of (and palpable) a permanent pacemaker or implantable cardiac defibrillator.

Palpation

Arterial pulse

• Note the heart rate and rhythm.

• Palpate the radial or carotid pulse. Important abnormalities in arterial pulse character are shown in Table 3.5.

Table 3.5

Abnormalities in arterial pulse character

Pulse character	Causes	Description / what it represents
Normal		The percussion wave is the dominant wave transmitted along elastic arterial walls The dicrotic notch (difficult to detect) is a normal blip on the downstroke of the percussion wave representing aortic valve closure
Slow rising, plateau pulse (‘anacrotic’ pulse)	Aortic stenosis	Slow rising with delayed percussion wave and sometimes a palpable judder on the upstroke Characteristically associated with narrow pulse pressure (narrow difference between systolic and diastolic pressure) if severe
Collapsing pulse	Aortic regurgitation Arteriovenous fistula Patent ductus A large-volume, hyperkinetic pulse may occur in any cause of high cardiac output, e.g. thyrotoxicosis, Paget’s disease, severe anaemia; a small-volume collapsing pulse (quickly rising but small percussion wave) is associated with ventricular run-off states, e.g. mitral regurgitation, ventricular septal defect	Very brisk upstroke followed by ‘collapse’ occurs when there is ‘run-off’ from the aorta Characteristically associated with wide pulse pressure (wide difference between systolic and diastolic blood pressure) if severe May be visible at brachials or carotids and best felt by raising the patient’s arm, feeling the radial pulse ‘slap’ against your fingertips or palm
Pulsus alternans	Aortic stenosis Left ventricular failure	Alternating large and small beats A sign of poor left ventricular function
Pulsus paradoxus	Cardiac tamponade Pericardial constriction Acute severe asthma compromising venous return	Excessive fall in pulse pressure (> 10 mmHg) during inspiration Not, in fact, a paradox, but an exaggeration of normal physiology Difficult to detect
Jerky pulse	Hypertrophic cardiomyopathy	Ventricular ejection in ‘stops and starts’

Blood pressure

• Take (or ask for) the blood pressure. Ensure you have the correct cuff size. Obese patients need a large cuff; a standard cuff will exert greater pressure to compress the artery and give falsely elevated readings. The point at which you hear the first Korotkoff sound is the systolic pressure and the point at which the sound disappears (fifth Korotkoff sound) is the diastolic pressure. The fourth Korotkoff sound (muffling) is acceptable in patients in whom sound does not disappear.

Be alert to a wide pulse pressure (aortic regurgitation) and a narrow pulse pressure (aortic stenosis). Be aware of the significance of differences in blood pressure between arms (leaking thoracic aneurysm) and greater than 15–20 mmHg between arms and legs, always palpating for radio-femoral delay otherwise silent aortic coarctation is missed.

Apex

• Aim to locate the apex beat with your middle finger, normally palpable in the fifth intercostal space at the mid-clavicular line, and determine if it is displaced (Fig. 3.3). An absent apex beat may be a sign of obesity, emphysema, pericardial effusion or dextrocardia, but it may be best palpable in the left lateral position. Many terms have been used to describe abnormalities in apex beat character (Box 3.1).

Box 3.1 Apex beat abnormalities

• A double impulse may be a sign of hypertrophic cardiomyopathy.

• A tapping apex is the palpable equivalent of a loud first heart sound and should alert you to mitral stenosis.

• A hyperdynamic or thrusting apex should alert you to aortic regurgitation.

• A sustained apex beat should alert you to aortic stenosis.

• A heaving apex is a sign of left ventricular hypertrophy.

Apex beat abnormalities can be difficult. As a rule of thumb, try to determine whether the apex beat is displaced or undisplaced, and whether or not it is forceful.

Undisplaced apex

This is normal or implies pressure overload, as in aortic stenosis (raised left ventricular pressure with hypertrophy) and mitral stenosis (raised left atrial pressure with hypertrophy / dilatation).

Displaced apex

This implies volume overload, as in aortic regurgitation (left ventricular dilatation) and mitral regurgitation (left atrial and left ventricular dilatation).

Figure 3.3 Determining the position of the apex beat (A) and palpating for a right ventricular heave (B).

Table 3.6

Predicting valve abormalities before auscultation

Percussion

Percussion of the cardiac border or cardiac dullness adds little to clinical assessment. Omit unless other signs suggest the presence of a pericardial effusion.

Auscultation

Auscultation sites

• Start at the apex with the diaphragm followed by the bell of your stethoscope, then move through the areas shown in Figure 3.4 with the diaphragm. The bell is a resonating chamber that amplifies low-pitched sounds, such as the diastolic murmur of mitral stenosis or a third or fourth heart sound. If not applied lightly it becomes a diaphragm.

Figure 3.4 Auscultatory sites and surface markings of the heart valves: 1, right atrium; 2, right atrial appendage; 3, left atrial appendage; 4, atrioventricular groove; 5, right ventricle; 6, left ventricle; 7, apex of the heart; 8, anterior interventricular groove. Note: areas refer to where sound best heard, not anatomical location of the valve.

• Next listen at the apex with the patient in the left lateral position and at the aortic and pulmonary areas with the patient sitting forward. Which you do first depends upon where you think the pathology lies, but be seen to do both. In both positions listen in expiration (‘breathe in, and out, and hold your breath…and breathe again’) and in inspiration if you suspect a right-sided (pulmonary or tricuspid) murmur. Inspiration increases the loudness of right-sided murmurs and expiration the loudness of left-sided murmurs.

Heart sounds

Heart sounds are vibrations caused by closure of heart valves combined with rapid changes in blood flow and tensing within cardiac structures.

• Listen for the first and second heart sounds, and any extra third or fourth heart sound.

First heart sound (S1).

S1 (‘lub’) represents mitral (and to a lesser extend tricuspid) valve closure at the onset of ventricular systole. Only one sound is audible. The intensity of S1 may be altered (Table 3.7) by the position of the mitral valve leaflets at the onset of systole, the rate of rise of the left ventricular pressure pulse, the amount of tissue, fluid or air between valve and stethoscope, and mitral valve disease.

Table 3.7

Abnormalities of S1 intensity

Loud S1	Soft S1	Variable S1
Tachycardia (shortened diastolic filling time, and faster valve closure)	Bradycardia (prolonged diastolic filling time)	Atrial fibrillation Ventricular ectopic beats
Short PR interval (atrial contraction precedes ventricular contraction in an unusually short time, again with faster valve closure)	Long PR interval (first-degree heart block)	Complete heart block
Mitral stenosis with pliable valve (high left atrial pressure forces leaflets further apart during atrial systole so that they are very far apart by the end of ventricular diastole and come together again more forcefully) Tricuspid stenosis	Mitral stenosis with non-pliable valve (anterior leaflet immobile owing to rigid calcification) Mitral regurgitation and left ventricular failure (imperfect closure or coaptation of leaflets)
Increased atrioventricular flow in high cardiac output states	Poor chest wall conduction

Second heart sound (S2).

S2 (‘dub’) comprises aortic valve closure (A2) followed by pulmonary valve closure (P2) at the onset of diastole. Diastole is normally longer than systole. S2 is of slightly lower intensity than S1. Normally A2–P2 is slightly split (< 0.05 seconds apart) and A2 comes first – think of the efficient left ventricle contracting swiftly, offloading its stroke volume compared with the lower pressure within the right side of the heart.

There are four types of S2 splitting (Table 3.8).

Table 3.8

Types of S2 splitting

The intensity of S2 may be altered by disease (Table 3.9).

Table 3.9

Abnormalities of S2 intensity

Third heart sound (S3).

This is described in Box 3.2.

Box 3.2 Extra heart sounds

Third heart sound (S3)

S3 is a low-pitched sound just after S2 (causing a gallop rhythm – ‘Tennessee’ or ‘lub-dub-d’ or ‘d-d-d’). It is due to rapid ventricular filling in early diastole from a very full or engorged left atrium such that blood crashes into the left ventricle with a ‘boing’. A left-sided S3 is best heard with the bell at the apex in the left lateral position in expiration. A right-sided S3 is best heard at the left sternal edge in inspiration. S3 occurs normally in healthy children, young adults, athletes, pregnancy, fever and other hyperdynamic states, but usually signifies a heart under strain as in heart failure or mitral regurgitation. Some physicians describe a ‘tictac’ rhythm in which S1 and S2 appear to be in a hurry (‘lub-dub’-‘lub-dub’-‘lub-dub’ becomes ‘dd’-‘dd’-‘dd’ ’) just before a true gallop arises (the heart anticipating S3!) or coexisting with gallops.

Fourth heart sound (S4)

S4 is a low-pitched, presystolic sound occurring before S1 as a result of vigorous atrial contraction filling a stiff (less compliant) ventricle (‘d-lub-dub’). As the mitral valve opens, the left atrium is ‘looking down into a half full ventricle’. S4 peaks in intensity at the left ventricular apex and is heard best with the bell in the left lateral position. There may be palpable or even visible presystolic distension of the left ventricle. S4 may be accentuated by isotonic and isometric exercise. It may occur in systemic hypertension, aortic stenosis, left ventricular hypertrophy, ischaemic heart disease and restrictive cardiomyopathies. Most typically, it occurs in heart failure and simply represents a ‘tired heart’; it is also common in acute myocardial infarction. It is always pathological. It cannot occur in atrial fibrillation.

S3 and S4 are often never detected by doctors but become easier to detect if you are expecting them, in heart failure for example. If S1and S2 appear in a hurry (tictac rhythm or ‘dd’), then S3 or S4 may become apparent (‘dd’-‘d’-‘dd’-‘d’-‘dd’-‘d’, where ‘d’ is S3 if detected just after ‘dd’ or S4 if detected just before ‘dd’). If the heart rate is very fast, S3 and S4 may be superimposed as one audible sound. It does not necessarily imply a heart under stress unless one or both sounds persist when the heart is slowed. If both S3 and S4 are present the situation is a quadruple rhythm, a sign of severe ventricular dysfunction.

Fourth heart sound (S4).

This is described in Box 3.2.

Added sounds

• Listen for added sounds (Box 3.3).

Box 3.3 Added sounds

Opening snap (OS)

This is a brief, high-pitched, early diastolic sound occurring as the mitral valve is forced open by high left atrial pressure in mitral stenosis. The S2–OS interval is shorter the higher the left atrial pressure.

Ejection click or sound

This is a sharp, high-pitched sound in early systole soon after S1. It may occur in non-calcified aortic stenosis or pulmonary stenosis with a pliable valve, the mechanism similar to an opening snap and the sound preceding the typical ejection systolic murmur.

Mid-systolic (non-ejection) click

This may occur in mitral valve prolapse as one or both leaflets prolapse into the left atrium. There may be an accompanying late systolic murmur of mitral regurgitation.

Metallic prosthetic sounds

These may be audible without auscultation.

Pericardial knock

This is a third-heart-sound equivalent heard in diastole in constrictive pericarditis.

Pericardial friction rub

This is a scratching presystolic, systolic or early diastolic sound heard best with the diaphragm. It is due to pericarditis.

Murmurs

Heart murmurs result from vibrations in the bloodstream and surrounding heart and great vessels as a result of turbulent flow.

• Try to determine the character, location and radiation of any murmur you hear (Box 3.4).

Box 3.4 Character, location and radiation of murmurs

Specific murmurs are described in more detail in individual cases. The location and radiation helps diagnostically. For example, aortic stenosis murmurs are usually loudest in the right second intercostal space and may radiate to the carotids; mitral regurgitation murmurs are often loudest at the apex and may radiate to the axilla (especially if the anterior leaflet is mostly affected) or the left sternal border and base of the heart (especially if the posterior leaflet is mostly affected). As a general rule, aortic murmurs tend to radiate more than mitral murmurs. However, the character or quality of a murmur is invariably more helpful than its location. You are the same person wherever you go – murmurs are no different.

• Try to grade the intensity or loudness of any murmur you hear (Table 3.10).

Table 3.10

Intensity of murmurs

Grade	Description
1	Very soft, heard only by experts
2	Heard by non-expert in optimum conditions
3	Easily heard but no thrill
4	Loud with thrill
5	Very loud with easily palpable thrill
6	Extremely loud and heard without stethoscope

• Try to determine the timing (with the carotid pulse) and duration of any murmur you hear (Table 3.11). Whilst this is expected by examiners and straightforward in theory, many candidates find timing difficult; what sounded like the typical whispering decrescendo murmur of aortic regurgitation suddenly becomes mitral regurgitation on the basis of dubious timing when all the evidence is with the former and against the latter. Keep in mind that the character of a murmur is more compellingly helpful than anything else when you might otherwise ‘hedge your bets.’

Table 3.11

Timing of murmurs

ASD, atrial septal defect; HCM, hypertrophic cardiomyopathy; VSD, ventricular septal defect.

Murmurs and physiological manoeuvres

Murmurs and respiration.

Right-sided heart murmurs are louder in inspiration because in inspiration blood flow increases through the right side of the heart. Left-sided heart murmurs are louder in expiration because in expiration blood flow increases through the left side of the heart.

Murmurs and dynamic auscultation.

Subtle murmurs may be enhanced by certain manoeuvres (Table 3.12). Tell the examiners that you would consider them but never ask a patient to perform these unless directed to do so by examiners.

Table 3.12

Effect of dynamic auscultation on murmurs

Additional examination

Complete cardiovascular system examination includes assessment of lower limb pulses and examining for pulmonary, sacral and lower limb oedema.

Summary

A summary of the cardiovascular examination sequence is in the Summary box.

Summary box – cardiovascular system examination sequence

Look at the hands and arms for clubbing, peripheral cyanosis, xanthomata or peripheral signs of endocarditis.

Look at the face for central cyanosis, pallor, a malar flush, corneal arcus or xanthelasmata.

Determine the height of the jugular venous pulse and any abnormal waveform.

Determine pulse rate, rhythm and character.

Ask for the blood pressure.

Determine the position of the apex and any abnormalities in apex beat character.

Feel for a right ventricular heave.

Feel for thrills.

Ask yourself if pulse character, blood pressure and apex position predict any valve abnormality.

Listen for S1 and S2; note any abnormal intensity of S1 and any abnormal splitting of S2.

Listen for any S3 or S4.

Listen for added sounds.

Listen for murmurs.

Consider the character, location, radiation, intensity and timing of murmurs (but give greatest attention to character).

Remember to listen in the left lateral position and with the patient sitting forward.

Cases

Case 3.1 Mitral stenosis

Instruction

This 65-year-old woman is thought to have a heart murmur. She is short of breath on exercise. Please examine her pulse, and palpate and auscultate her heart. Tell the examiners the signs you elicit, and discuss your proposed management.

Recognition

Signs of mitral stenosis are shown in Figure 3.5.

Figure 3.5 Mitral stenosis. JVP, jugular venous pulse.

Interpretation

Confirm the diagnosis

Listen in the left lateral position and in expiration to accentuate the murmur. The differential diagnosis includes:

• Tricuspid stenosis (rare, louder in inspiration)

• Atrial myxoma (rare, fever, constitutional symptoms, raised inflammatory markers)

• Carey Coombs murmur (acute rheumatic fever)

• Austin Flint murmur (see Case 3.4).

Encountering a ‘full-house’ of signs is improbable and even when present they are difficult to elicit. Many physicians say they have never heard an opening snap. Atrial fibrillation renders a murmur difficult to time. But the rumbling murmur is characteristic, not unlike heavy rain on a tin roof, the rumble of a subway train or a buffalo stampede!

What to do next – consider causes

Tell the examiners that causes of mitral stenosis include:

• Rheumatic heart disease (the most common cause worldwide, but dramatically decreased over last 50 years in developed countries; in Australia, for example, where streptococcal infection is highly prevalent within the Aboriginal population, rheumatic heart disease is a major health burden)

• Congenital

• Left atrial myxoma

• Connective tissue disease.

Two-thirds of patients are female.

Consider severity / decompensation / complications

Signs of severe mitral stenosis are listed in Box 3.5.

Box 3.5 Signs of severe mitral stenosis

• Signs of pulmonary hypertension (Case 1.18)

• Short interval between S2 and opening snap (the shorter the interval the higher the left atrial pressure)

• Long diastolic murmur

Tell the examiners that:

• Pulmonary hypertension may be irreversible.

• Thromboembolic disease, especially stroke, may result from systemic emboli originating in the left atrium

• Infective endocarditis may lead to valve decompensation.

• Ortner’s phenomenon is rare and refers to hoarseness resulting from an enlarged left atrium exerting pressure on the left recurrent laryngeal nerve supplying the vocal cord.

• Any situation that increases heart rate, such as exercise, pregnancy or sepsis, further increases the trans-mitral pressure gradient and can provoke increased pulmonary pressure and pulmonary oedema.

Consider function

Tell the examiners you would establish the limitations provoked by exertional dyspnoea and consider fitness for surgery.

Discussion

What happens to the valve pathologically?

The mitral valve is funnel shaped, dipping into the left ventricle. In mitral stenosis the valve leaflets and chordae tendinae are diffusely thickened by fibrosis and calcification resulting in their fusion, thickening and reduced mobility. These narrow the apex of the funnel. The orifice reduces from its normal 4 cm² to 1 cm² or less, and blood can only be propelled into the ventricle by an abnormally elevated left atrial pressure.

What is the most common presenting symptom of mitral stenosis?

Exertional dyspnoea.

Why should patients experience exertional dyspnoea?

As blood flow increases with exercise across the mitral valve, the increased left atrial pressure needed to propel blood across the valve raises pulmonary venous and capillary pressures, which reduce pulmonary compliance, and pulmonary artery pressure increases.

Tachycardia also diminishes diastole disproportionately more than systole and thus the time for flow across the stenosed valve is reduced. Therefore at any given level of cardiac output, tachycardia increases the transvalvular gradient and further elevates left atrial pressure.

When the valve orifice is reduced to 1 cm², a left atrial pressure of 25 mmHg is needed to maintain normal cardiac output. Pulmonary oedema may occur if there is a sudden surge of flow across a tight valve.

Eventually there is decreased cardiac output on exertion and at rest. The ability of the left atrium to generate sufficient pressure to maintain transvalvular flow is overcome.

What other symptoms may occur in mitral stenosis?

Symptoms may be the result of atrial arrhythmias, including premature atrial contractions, paroxysmal atrial tachycardia, atrial flutter and atrial fibrillation. Haemoptysis, due to the rupture of pulmonary–bronchial venous connections in pulmonary venous hypertension, is unusual but occurs in patients with raised left atrial pressure but without significantly increased pulmonary vascular resistance.

How does pulmonary hypertension arise?

Passive transmission backwards of raised left atrial pressure leads to raised pulmonary venous and capillary pressure, pulmonary arteriolar constriction triggered by pulmonary venous hypertension (reactive pulmonary hypertension), interstitial oedema and pressure damage to and fibrosis or obliteration of the pulmonary vascular bed.

What are the diagnostic criteria for rheumatic fever?

Rheumatic fever (Box 3.6) and rheumatic heart disease remain common in the developing world, the latter a common usher for infective endocarditis. In the developed world the legacy of rheumatic fever remains, most commonly as mitral stenosis and sometimes as other valvular heart disease (VHD), but VHD in developed countries is now most commonly degenerative. Two major criteria or one major and two minor criteria plus evidence of antecedent group A streptococcal infection are required for a diagnosis of rheumatic fever.

Box 3.6 Diagnostic criteria (Jones) for rheumatic fever

Major criteria