Myocardial ischaemia

Ischaemia of the heart results from an imbalance between myocardial oxygen supply and demand, producing pain called angina (Boxes 11.2 and 11.3). Angina is usually a symptom of atherosclerotic coronary artery disease, which impedes myocardial oxygen supply. Other causes of coronary artery disease (Box 11.4) are rare. However, it is important to be vigilant for causes of angina due to increased myocardial oxygen demand, such as aortic stenosis. The history is diagnostic for angina if the location of the pain, its character, its relation to exertion and its duration are typical. 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 and relieved within minutes by rest. The patient’s threshold for angina is typically reduced after eating or in cold weather due to the diversion of blood to the gut and the increased myocardial work consequent upon peripheral vasoconstriction, respectively. Occasionally angina is provoked only by the first significant activity of the day, a phenomenon known as the ‘warm-up effect’ and due to myocardial preconditioning. Less commonly, myocardial ischaemia may manifest as breathlessness, fatigue or symptoms that the patient finds difficult to describe – ‘I just have to stop’ – in which case the clues to the diagnosis are the relation of symptoms to exertion, the presence of risk factors for coronary artery disease and the absence of an alternative explanation for the symptoms, such as heart failure.

Acute coronary syndromes

In these life-threatening cardiac emergencies, the pain is similar in location and character to angina but is usually more severe, more prolonged and unrelieved by rest (Box 11.5).

Pericarditis

This causes 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. Pericarditis is usually idiopathic or caused by Coxsackie B infection. It may also occur as a complication of myocardial infarction, but other causes are seen less commonly (Box 11.6).

Aortic dissection

This produces 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 (Box 11.7).

Pulmonary embolism

Peripheral pulmonary embolism causes 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. Risk factors for pulmonary embolism should be sought in the history (Box 11.8).

Rare cardiovascular causes of chest pain include mitral valve disease associated with massive left atrial dilatation. This causes discomfort in the back, sometimes associated with dysphagia due to oesophageal compression. Aortic aneurysms can also cause pain in the chest owing to local compression.

Anaemia

This may exacerbate angina and heart failure. Pallor of the mucous membranes is a useful but sometimes misleading physical sign, and diagnosis requires laboratory measurement of the haemoglobin concentration.

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 may result when cutaneous vasoconstriction slows the blood flow and increases oxygen extraction in the skin and the lips. It is physiological during cold exposure. It also occurs in heart failure, when reduced cardiac output produces reflex cutaneous vasoconstriction. In mitral stenosis, cyanosis over the malar area produces the characteristic mitral facies or malar flush.

Central cyanosis may result from the 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. Congenital defects associated with central cyanosis include those in which desaturated venous blood bypasses the lungs by (‘reversed’) shunting through septal defects or a patent ductus arteriosus (e.g. Eisenmenger’s syndrome, Fallot’s tetralogy).

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

These are caused by immune complex deposition in the capillary circulation. A vasculitic rash is common, as are splinter haemorrhages in the nail bed, although these are a very non-specific finding. Other ‘classic’ manifestations of endocarditis including Osler’s nodes (tender erythematous nodules in the pulps of the fingers), Janeway lesions (painless erythematous lesions on the palms) and Roth’s spots (erythematous lesions in the optic fundi) are now rarely seen.

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. Pyrexia also occurs for the first 3 days after myocardial infarction.

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. Two mechanisms are responsible:

Salt and water retention expands plasma volume and increases the capillary hydrostatic pressure. Hydrostatic forces driving fluid out of the capillary exceed the osmotic forces reabsorbing it, so that oedema fluid accumulates in the interstitial space. The effect of gravity on capillary hydrostatic pressure ensures that oedema is most prominent around the ankles in the ambulant patient and over the sacrum in the bedridden patient. In advanced heart failure, oedema may involve the legs, genitalia and trunk. Transudation into the peritoneal cavity (ascites), the pleural and pericardial spaces may also occur.

Rate and rhythm

By convention, both are assessed 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, but may also be caused by frequent ectopic beats or self-limiting paroxysmal arrhythmias. In patients with atrial fibrillation, the rate should be measured by auscultation at the cardiac apex, because beats that follow very short diastolic intervals may create a ‘pulse deficit’ by not generating sufficient pressure to be palpable at the radial artery.

Character

This is defined by the volume and waveform of the pulse and should be evaluated at the right carotid artery (i.e. the pulse closest to the heart and least subject to damping and distortion in the arterial tree). Pulse volume provides a crude indication of stroke volume, being small in heart failure and large in aortic regurgitation. The waveform of the pulse is of greater diagnostic importance (Fig. 11.3). Severe aortic stenosis produces a slow-rising carotid pulse; the fixed obstruction restricts the rate at which blood can be ejected from the left ventricle. In aortic regurgitation, in diastole, the left ventricle receives not only its normal pulmonary venous return but also a proportion of the blood ejected into the aorta during the previous systole as it flows back through an incompetent valve. The resultant large stroke volume, vigorously ejected, produces a rapidly rising carotid pulse, which collapses in early diastole owing to backflow through the aortic valve. This collapsing pulse can be exaggerated at the radial artery by lifting the arm. In mixed aortic valve disease, a biphasic pulse with two systolic peaks is occasionally found. Alternating pulse – alternating high and low systolic peaks – occurs in severe left ventricular failure but the mechanism for this is unknown. Paradoxical pulse refers to an inspiratory decline in systolic pressure greater than 10 mmHg (Fig. 11.4). In normal circumstances, inspiration results in an increase in venous return as blood is ‘sucked into’ the thorax by the decline in intrathoracic pressure. This increases right ventricular stroke volume, but left ventricular stroke volume falls slightly (ventricular interdependence). When the heart is constrained in a ‘fixed box’ by a pericardial effusion (cardiac tamponade) or by thickened pericardium (pericardial constriction), the increased inspiratory right ventricular blood volume reduces left ventricular compliance resulting in a more pronounced reduction in left ventricular filling, stroke volume and systolic blood pressure during inspiration. ‘Pulsus paradoxus’ therefore represents an exaggeration of the normal inspiratory decline in systolic pressure and is not truly paradoxical. Pulsus paradoxus in acute severe asthma is thought to be due to negative pleural pressure increasing afterload and thereby impedence to left ventricular emptying.

Figure 11.3 The waveform of the pulse is characterized by the rate of rise of the carotid upstroke. Note that in aortic regurgitation, the upstroke is rapid and followed by abrupt diastolic ‘collapse’. In hypertrophic cardiomyopathy, the upstroke is also rapid and the pulse has a jerky character. In aortic stenosis, the upstroke is slow with a plateau.

Figure 11.4 Paradoxical pulse (radial artery pressure signal). The patient had severe tamponade. Note the exaggerated (>10 mmHg) decline in arterial pressure during inspiration.

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, less commonly by aortic dissection. Coarctation of the aorta causes symmetrical reduction and delay of the femoral pulses compared with the radial pulses (‘radiofemoral delay’), a sign that should be looked for in younger patients with hypertension.

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. Distention of the external jugular vein is a useful clue to an elevated JVP but, strictly speaking, it should not be used because it can be compressed as it passes under the clavicle. 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 (Box 11.12). During inspiration, the pressure within the chest decreases and there is a fall in the JVP. In constrictive pericarditis, and less commonly in 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 (Fig. 11.5).

Figure 11.5 Kussmaul’s sign. Jugular venous pressure recording in a patient with tamponade. The venous pressure is raised and there is a particularly prominent systolic ‘x’ descent, giving the waveform of the JVP an unusually dynamic appearance. Note the inspiratory rise in atrial pressure (Kussmaul’s sign) reflecting the inability of the tamponaded right heart to accommodate the inspiratory increase in venous return.

Waveform of jugular venous pulses

In sinus rhythm, the jugular venous pulse has a double waveform attributable to the ‘a’ and ‘v’ waves separated by the ‘x’ and ‘y’ descents. The ‘a’ wave is produced by atrial systole. It is followed by the ‘x’ descent (marking descent of the tricuspid valve ring), which is interrupted by the diminutive ‘c’ wave caused by tricuspid valve closure. Atrial pressure then rises again, producing the ‘v’ wave as the atrium fills passively during ventricular systole. The decline in atrial pressure as the tricuspid valve opens to allow ventricular filling produces the ‘y’ descent. Important abnormalities of the pattern of deflections are shown in Figure 11.6.

Figure 11.6 Waveform of the jugular venous pulse. (A) The ECG is portrayed at the top of the illustration. Note how electrical events precede mechanical events in the cardiac cycle. Thus the P wave (atrial depolarization) and the QRS complex (ventricular depolarization) precede the ‘a’ and ‘v’ waves, respectively, of the JVP. (B) Normal JVP. The ‘a’ wave produced by atrial systole is the most prominent deflection. It is followed by the ‘x’ descent, interrupted by the small ‘c’ wave marking tricuspid valve closure. Atrial pressure then rises again (‘v’ wave) as the atrium fills passively during ventricular systole. The decline in atrial pressure as the tricuspid valve opens produces the ‘y’ descent. (C) Giant ‘a’ wave. Forceful atrial contraction against a stenosed tricuspid valve or a non-compliant hypertrophied right ventricle produces an unusually prominent ‘a’ wave. (D) 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. (E) Giant ‘v’ wave. This is an important sign of tricuspid regurgitation. The regurgitant jet produces pulsatile systolic waves in the JVP. (F) 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.

In atrial fibrillation, there is no atrial contraction. Consequently, there is no ‘a’ wave and the jugular venous pulse loses its double waveform. It is not always easy to differentiate venous from arterial pulsations in the neck, but several features help to distinguish the jugular venous pulse from the carotid arterial pulse (Box 11.13).

First sound (S1)

This corresponds to mitral and tricuspid valve closure at the onset of systole. It is accentuated in mitral stenosis because prolonged diastolic filling through the narrowed valve ensures that the thickened leaflets are widely separated at the onset of systole. Thus valve closure generates unusually vigorous vibrations. In advanced mitral stenosis, the valve is rigid and immobile and S1 becomes soft again.

Second sound (S2)

This corresponds to aortic and pulmonary valve closure following ventricular ejection. S2 is single during expiration. Inspiration, however, causes physiological splitting into aortic followed by pulmonary components because increased venous return to the right side of the heart delays pulmonary valve closure. Important abnormalities of S2 are illustrated in Figure 11.7.

Figure 11.7 Splitting of the second heart sound. The first sound, representing mitral and tricuspid closure, is usually single, but the aortic and pulmonary components of the second sound normally split during inspiration as increased venous return delays right ventricular emptying. Abnormal splitting of the second heart sound is an important sign of heart disease.

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. Both sounds are best heard with the bell of the stethoscope at the cardiac apex. They are caused by abrupt tensing of the ventricular walls following rapid diastolic filling. Rapid filling occurs early in diastole (S3) following atrioventricular valve opening, and again late in diastole (S4) due to atrial contraction. S3 is physiological in children and young adults but usually disappears after the age of 40. It also occurs in high-output states caused by anaemia, fever, pregnancy and thyrotoxicosis. After the age of 40, S3 is nearly always pathological, usually indicating left ventricular failure or, less commonly, mitral regurgitation or constrictive pericarditis. In the elderly, S4 is sometimes physiological. More commonly, however, it is pathological, and occurs when vigorous atrial contraction late in diastole is required to augment filling of a hypertrophied, non-compliant ventricle (e.g. hypertension, aortic stenosis, hypertrophic cardiomyopathy).

Systolic clicks and opening snaps

Valve opening, unlike valve closure, is normally silent. In aortic stenosis, however, 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. A click later in systole suggests mitral valve prolapse, particularly when followed by a murmur. In 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 (Fig. 11.8). Occasionally the turbulence is caused by increased flow through a normal valve – usually aortic or pulmonary – producing an ‘innocent’ murmur. However, murmurs may also indicate valve disease or abnormal communications between the left and right sides of the heart (e.g. septal defects).

Figure 11.8

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