Presenting symptoms (Table 4.1)

Ankle swelling

Some patients present with bilateral ankle swelling due to oedema from cardiac failure. Patients with the recent onset of oedema and who take a serious interest in their weight may have noticed a gain in weight of 3 kg or more. Ankle oedema of cardiac origin is usually symmetrical and worst in the evenings, with improvement during the night. It may be a symptom of biventricular failure or right ventricular failure secondary to a number of possible underlying aetiologies. As failure progresses, oedema ascends to involve the legs, thighs, genitalia and abdomen. There are usually other symptoms or signs of heart disease.

It is important to find out whether the patient is taking a vasodilating drug (e.g. a calcium channel blocker), which can cause peripheral oedema. There are other (more) common causes of ankle oedema than heart failure that also need to be considered (page 71). Oedema that affects the face is more likely to be related to nephrotic syndrome (page 213).

Risk factors for coronary artery disease

An essential part of the cardiac history involves obtaining detailed information about a patient’s risk factors—the patient’s cardiovascular risk factor profile (Questions box 4.4).

Previous ischaemic heart disease is the most important risk factor for further ischaemia. The patient may know of previous infarcts or have had a diagnosis of angina in the past.

Hypercholesterolaemia is the next most important risk factor for ischaemic heart disease. Many patients now know their serum cholesterol levels because widespread testing has become fashionable. The total serum cholesterol is a useful screening test, and levels above 5.2 mmol/L are considered undesirable. Cholesterol measurements (unlike triglyceride measurements) are accurate even when a patient has not been fasting. Patients with established coronary artery disease benefit from lowering of total cholesterol to below 4 mmol/L. An elevated total cholesterol level is even more significant if the high-density lipoprotein (HDL) level is low (less than 1.0 mmol/L). Significant elevation of the triglyceride level is a coronary risk factor in its own right and also adds further to the risk if the total cholesterol is high. If a patient already has coronary disease, hyperlipidaemia is even more important. Control of risk factors for these patients is called ‘secondary prevention’. Patients who have multiple risk factors for ischaemic heart disease (e.g. diabetes and hypertension) should have their cholesterol controlled aggressively. If the patient’s cholesterol is known to be high, it is worth obtaining a dietary history. This can be very trying. It is important to remember that not only foods containing cholesterol but those containing saturated fats contribute to the serum cholesterol level. High alcohol consumption and obesity are associated with hypertriglyceridaemia.

Smoking is probably the next most important risk factor for cardiovascular disease and peripheral vascular disease. Some patients describe themselves as non-smokers even though they stopped smoking only a few hours before. The number of years the patient has smoked and the number of cigarettes smoked per day are both very important (and are recorded as packet-years, page 6). The significance of a history of smoking for a patient who has not smoked for many years is controversial. The risk of symptomatic ischaemic heart disease falls gradually over the years after smoking has been stopped. After about 2 years the risk of myocardial infarction falls to the same level as for those who have never smoked. After 10 years the risk of developing angina falls close to that of non-smokers.

Hypertension is another important risk factor for coronary artery disease. Find out when hypertension was first diagnosed and what treatment, if any, has been instituted. The treatment of hypertension probably does reduce the risk of ischaemic heart disease, and certainly reduces the risk of hypertensive heart disease, cardiac failure and cerebrovascular disease. Treatment of hypertension has also been shown to reverse left ventricular hypertrophy.

A family history of coronary artery disease increases a patient’s risk, particularly if it has been present in first-degree relatives (parents or siblings) and if it has affected these people below the age of 60. Not all heart disease, however, is ischaemic; a patient whose relatives suffered from rheumatic heart disease is at no greater risk of ischaemic heart disease than anybody else.

A history of diabetes mellitus increases the risk of ischaemic heart disease very substantially. A diabetic without a history of ischaemic heart disease has the same risk of myocardial infarction as a non-diabetic who has had an infarct. It is important to find out how long a patient has been diabetic and whether insulin treatment has been required. Good control of the blood sugar level of diabetics reduces this risk. An attempt should therefore be made to find out how well a patient’s diabetes has been controlled.

Chronic kidney disease is associated with a very high risk of vascular disease. This is possibly related to high calcium-times-phosphate product and may be reduced by dietary intervention, ‘phosphate binders’, efficient dialysis, in renal transplant. Ischaemic heart disease is the most common cause of death in renal failure patients on dialysis.

The presence of multiple risk factors makes control of each one more important. Aggressive control of risk factors is often indicated in these patients.

It is interesting to note that in the diagnosis of angina the patient’s description of typical symptoms is more discriminating than is the presence of risk factors which only marginally increase the likelihood that chest pain is ischaemic. Previous ischaemic heart disease is an exception. Certainly a patient who has had angina before and says he or she has it again, is usually right.

Treatment

The medications a patient is taking often give a good clue to the diagnosis. Find out about any ill-effects from current or previous medications. The surgical history must also be elicited. The patient may have had a previous angioplasty or coronary artery bypass grafting, and may know how many arteries were dilated or bypassed. If the patient is unable to provide a history, a midline sternotomy scar and scars consistent with previous saphenous vein harvesting support this diagnosis.

Past history

Patients with a history of definite previous angina or myocardial infarction remain at high risk for further ischaemic events. It is very useful at this stage to find out how a diagnosis of ischaemic heart disease was made and in particular what investigations were undertaken. The patient may well remember exercise testing or a coronary angiogram, and some patients can even remember how many coronary arteries were narrowed, how many coronary bypasses were performed (having more than three grafts often leads to a certain amount of boasting). The angioplasty patient may know how many arteries were dilated and whether stents (often called coronary stunts by patients and cardiac surgeons) were inserted. Acute coronary syndromes are now usually treated with early coronary angioplasty.

Patients may recall a diagnosis of rheumatic fever in their childhood, but many were labelled as having ‘growing pains’.¹¹ A patient who was put to bed for a long period as a child may well have had rheumatic fever. A history of rheumatic fever places patients at risk of rheumatic valvular disease.

Hypertension may be caused or exacerbated by aspects of the patient’s activities and diet (Questions box 4.5). A high salt intake, moderate or greater alcohol use, lack of exercise, obesity and kidney disease may all be factors contributing to high blood pressure. Non-steroidal anti-inflammatory drugs cause salt and fluid retention and may also worsen blood pressure. Ask about these, about previous advice to modify these factors, and about any drug treatment of hypertension when interviewing any patient with high blood pressure.

Social history

Both ischaemic heart disease and rheumatic heart disease are chronic conditions that may affect a patient’s ability to function normally. It is therefore important to find out whether the patient’s condition has prevented him or her from working and over what period. Patients with severe cardiac failure, for example, may need to make adjustments to their living arrangements so that they are not required to walk up and down stairs at home.

Most hospitals run cardiac rehabilitation programmes for patients with ischaemic heart disease or chronic heart failure. They provide exercise classes that help patients regain their confidence and physical fitness, along with information classes about diet and drug treatment, and can help with psychological problems. Find out if the patient has been enrolled in one of these and whether it has been helpful. Is this service used as a point of contact for the patient if he or she has concerns about new symptoms or the management of medications?

The return of confidence and self-esteem are very important issues for patients and for their families after a life-threatening illness.

Positioning the patient

It is important to have the patient lying in bed with enough pillows to support him or her at 45 degrees (Figure 4.7). This is the usual position in which the jugular venous pressure (JVP) is assessed. Even a ‘targeted’ cardiovascular examination in an outpatients’ clinic or surgery can only be performed adequately if the patient is lying down and an examination couch should be available. During auscultation, optimal examination requires further positioning of the patient, as discussed later.

Figure 4.7 Cardiovascular examination: positioning the patient

General appearance

Look at the general state of health. Does the patient appear to be ill? If he or she looks ill, try to decide why you have formed that impression. Note whether the patient at rest has rapid and laboured respiration, suggesting dyspnoea (see Table 5.6, page 110).

The patient may look cachectic: that is, there may be severe loss of weight and muscle wasting. This is commonly caused by malignant disease, but severe cardiac failure may also have this effect (cardiac cachexia). It probably results from a combination of anorexia (due to congestive enlargement of the liver), impaired intestinal absorption (due to congested intestinal veins) and increased levels of inflammatory cytokines such as TNF-α.

There are also some syndromes that are associated with specific cardiac disease. Marfan’s syndrome^f (Figure 4.8, page 50), Down syndrome^g (page 314) and Turner’s syndrome^h (page 314) are important examples.

Figure 4.8 Marfan’s syndrome

Tall stature, thoracic kyphosis, pectus excavatum, arachnodactyly (spider fingers), long limbs, aortic regurgitation and a high, arched palate

The hands

Pick up the right hand. Look first at the nails. Now is the time for a decision as to the presence or absence of clubbing. Clubbing is an increase in the soft tissue of the distal part of the fingers or toes. The causes of clubbing are surprisingly varied (Table 4.9). The mechanism is unknown but there are, of course, several theories. One current theory is that platelet-derived growth factor (PDGF), released from megakaryocyte and platelet emboli in the nail beds, causes fibrovascular proliferation. Megakaryocytes and clumps of platelets do not normally reach the arterial circulation. Their large size (up to 50 μm) prevents their passing through the pulmonary capillaries when they are released from the bone marrow. In conditions where platelets may clump in the arterial circulation (infected cardiac valve) or bypass the pulmonary capillaries (right to left shunt associated with congenital heart disease), they can reach the systemic circulation and become trapped in the terminal capillaries of the fingers and toes. Damage to pulmonary capillaries from various lung disorders can have the same effect.

TABLE 4.9 Causes of clubbing

Proper examination for clubbing involves inspecting the fingernails (and toenails) from the side to determine if there is loss of the angle between the nail bed and the finger—the hyponychial angle (Figure 4.9). One accepted measurement is the interphalangeal depth ratio. The anteroposterior (AP) dimension of the finger is measured at the distal interphalangeal joint and compared with the AP diameter at the level of the point where the skin joins the nail. A ratio of more than 1 means clubbing.^12,i Eventually, the distal phalanx becomes enlarged, due to soft-tissue swelling. This angle can be measured with a shadowgraph, which projects the silhouette of the finger so that it can be measured with a protractor. It is not in common use. If the angle is greater than 190°, clubbing is generally agreed to be present. Patients hardly ever notice that they have clubbing, even when it is severe. They often express surprise at their doctor’s interest in such an unlikely part of their anatomy.

Figure 4.9 Finger clubbing: (a) appearance; (b) phalangeal depth ratio

Before leaving the nails, look for splinter haemorrhages in the nail beds (Figure 4.10). These are linear haemorrhages lying parallel to the long axis of the nail. They are most often due to trauma, particularly in manual workers. However, an important cause is infective endocarditis (page 79), which is a bacterial or other infection of the heart valves or part of the endocardium. In this disease splinter haemorrhages are probably the result of a vasculitis in the nail bed, but this is controversial. Other rare causes of splinter haemorrhages include vasculitis, as in rheumatoid arthritis, polyarteritis nodosa or the antiphospholipid syndrome, sepsis elsewhere in the body, haematological malignancy or profound anaemia.

Figure 4.10 Splinter haemorrhages in the fingernails of a patient with staphylococcal aortic valve endocarditis

From Baker T, Nikolić G, O’Connor S, Practical Cardiology, 2nd edn. Sydney: Churchill Livingstone, 2008, with permission.

Osler’s nodes^j are a rare manifestation of infective endocarditis. These are red, raised, tender palpable nodules on the pulps of the fingers (or toes), or on the thenar or hypothenar eminences. They are reported to have occurred in 50% of patients before antibiotic treatment of endocarditis became available. Currently they are seen in fewer than 5% of patients. Janeway lesions^k (Figure 4.11) are non-tender erythematous maculopapular lesions containing bacteria, which occur very rarely on the palms or pulps of the fingers in patients with infective endocarditis.^l

Figure 4.11 Janeway lesion

Tendon xanthomata are yellow or orange deposits of lipid in the tendons that occur in type II hyperlipidaemia. These can be seen over the tendons of the hand and arm. Palmar xanthomata, and tuboeruptive xanthomata over the elbows and knees, are characteristic of type III hyperlipidaemia (Figure 4.12).

Figure 4.12 Tuboeruptive xanthomata of the knee

The arterial pulse

The accomplished clinician is able, while inspecting the hands, to palpate the radial artery at the wrist. Patients expect to have the pulse taken as part of a proper medical examination. The clinician can feel the pulse while talking to the patient and while looking for other signs. When this traditional part of the examination is performed with some ceremony, it may help to establish rapport between patient and doctor.

Although the radial pulse is distant from the central arteries, certain useful information may be gained from examining it. The pulse is usually felt just medial to the radius, using the forefinger and middle finger pulps of the examining hand (Figure 4.13). The following observations should be made: (i) rate of pulse, (ii) rhythm and (iii) presence or absence of delay of the femoral pulse compared with the radial pulse (radiofemoral delay). The character and volume of the pulse are better assessed from palpation of the brachial or carotid arteries.

Figure 4.13 Taking the radial pulse

Measuring the blood pressure with the sphygmomanometer

The usual blood pressure cuff width is 12.5 cm. This is suitable for a normal-sized adult forearm. However, in obese patients with large arms (up to 30% of the adult population) the normal-sized cuff will overestimate the blood pressure and therefore a large cuff must be used. A range of smaller sizes are available for children. Use of a cuff that is too large results in only a small underestimate of blood pressure.

The cuff is wrapped around the upper arm with the bladder centred over the brachial artery (Figure 4.16). This is found in the antecubital fossa, one-third of the way over from the medial epicondyle. For an approximate estimation of the systolic blood pressure, the cuff is fully inflated and then deflated slowly (3–4 mmHg per second) until the radial pulse returns. Then, for a more accurate estimation of the blood pressure, this manoeuvre is repeated with the diaphragm of the stethoscope placed over the brachial artery, slipped underneath the distal end of the cuff’s bladder.

Figure 4.16 Measuring the blood pressure, with the patient lying at 45 degrees

The patient’s brachial artery should be at about the level of the heart which is at the level of the fourth intercostal space at the sternum. If the arm is too high, e.g. at the level of the supraclavicular notch, the blood pressure reading will be about 5 mmHg lower; and if the arm is too low the reading will be higher than is accurate.

Five different sounds will be heard as the cuff is slowly released (Figure 4.17). These are called the Korotkoff^o sounds. The pressure at which a sound is first heard over the artery is the systolic blood pressure (Korotkoff I). As deflation of the cuff continues, the sound increases in intensity (KII), then decreases (KIII), becomes muffled (KIV) and then disappears (KV). Different observers have used KIV and KV to indicate the level of the diastolic pressure. KV is probably the best measure. However, this provides a slight underestimate of the arterial diastolic blood pressure. Although diastolic pressure usually corresponds most closely to KV, in severe aortic regurgitation KIV is a more accurate indication. KV is absent in some normal people and KIV must then be used.

Figure 4.17 Korotkoff sounds

Systolic pressure is determined by the appearance of the first audible sound, and diastolic pressure is determined by its disappearance.

Occasionally, there will be an auscultatory gap (the sounds disappear just below the systolic pressure and reappear before the diastolic pressure) in healthy people. This can lead to an underestimate of the systolic blood pressure if the cuff is not pumped up high enough.

The systolic blood pressure may normally vary between the arms by up to 10 mmHg; in the legs the blood pressure is normally up to 20 mmHg higher than in the arms, unless the patient has coarctation of the aorta. Measurement of the blood pressure in the legs is more difficult than in the arms. It requires a large cuff that is placed over the mid-thigh. The patient lies prone and the stethoscope is placed in the popliteal fossa, behind the knee.

During inspiration, the systolic and diastolic blood pressures normally decrease (because intrathoracic pressure becomes more negative, blood pools in the pulmonary vessels, so left-heart filling is reduced). When this normal reduction in blood pressure with inspiration is exaggerated, it is termed pulsus paradoxus. Kussmaul meant by this that there was a fall in blood pressure and a paradoxical rise in pulse rate. A fall in arterial pulse pressure on inspiration of more than 10 mmHg is abnormal and may occur with constrictive pericarditis, pericardial effusion, or severe asthma. To detect this: lower the cuff pressure slowly until KI sounds are heard intermittently (expiration) and then until KI is audible with every beat. The difference between the two readings represents the level of the pulsus paradoxus.

Variations in blood pressure

When blood pressure is measured with an intra-arterial catheter it becomes clear that blood pressure varies from minute to minute in normal people. Short-term changes of 4 mmHg in the systolic and 3 mmHg in the diastolic readings are common. Hour-to-hour and day-to-day variations are even greater. The standard deviation between visits is up to 12 mmHg for systolic pressure and 8 mmHg for diastolic. This means that when there is concern about an abnormal reading, repeat measurements are necessary.

When the heart is very irregular (most often because of atrial fibrillation), the cuff should be deflated slowly, and the point at which most of the cardiac contractions are audible (KI) taken as the systolic pressure and the point at which most have disappeared (KV) taken as diastole.

High blood pressure

This is difficult to define.¹³ The most helpful definitions of hypertension are based on an estimation of the level associated with an increased risk of vascular disease. There have been many classifications of blood pressure, as what is considered normal or abnormal changes as more information comes to hand. Table 4.11 gives a useful guide to current definitions. If recordings above 140/90 mmHg are considered abnormal, high blood pressure may occur in up to 20% of the adult population.^p Blood pressure measured by the patient at home, or by a 24-hour monitor, should be up to 10/5 mmHg less than that measured in the surgery.

TABLE 4.11 A classification of blood pressure readings^*

^* Khan NA, Rahim SA, Avand SS et al. Does the clinical examination predict lower extremity peripheral arterial disease? JAMA 2006 Feb 1; 295(5):536–546.

Postural blood pressure

The blood pressure should routinely be taken with the patient both lying down and standing (Figure 4.18).¹⁵ A fall of more than 15 mmHg in systolic blood pressure or 10 mmHg in diastolic blood pressure on standing is abnormal and is called postural hypotension (Table 4.12). It may cause dizziness or not be associated with symptoms. The most common cause is the use of antihypertensive drugs, α-adrenergic antagonists in particular.

Figure 4.18 Measuring the blood pressure, with patient standing

TABLE 4.12 Causes of postural hypotension (HANDI)

^* Thomas Addison (1793–1860), London physician.

Carotid arteries

The carotids are not only easily accessible, medial to the sternomastoid muscles (Figure 4.21), but provide a great deal of information about the wave form of the aortic pulse, which is affected by many cardiac abnormalities. Never palpate both carotid arteries simultaneously as they provide much of the blood supply to the brain (a vital organ).

Figure 4.21 Palpating the carotid pulse

Evaluation of the pulse wave form (the amplitude, shape and volume) is important in the diagnosis of various underlying cardiac diseases and in assessing their severity. It takes considerable practice to distinguish the different important types of carotid wave forms (Table 4.13). Auscultation of the carotids may be performed now or in association with auscultation of the praecordium.

TABLE 4.13 Arterial pulse character

Jugular venous pressure (JVP)—pulsation

Just as the carotid pulse tells us about the aorta and left ventricular function, the jugular venous pressure (JVP) (Figure 4.5, page 47) tells us about right atrial and right ventricular function.¹⁶ The positioning of the patient and lighting are important for this examination to be done properly. The patient must be lying down at 45 degrees to the horizontal with his or her head on pillows and in good lighting conditions. This is a difficult examination and there is considerable inter- (and intra-)observer variation in the findings.

When the patient is lying at 45 degrees, the sternal angle is also roughly in line with the base of the neck (Figure 4.5c). This provides a convenient zero point from which to measure the vertical height of the column of blood in the jugular vein. The jugular venous pulsation (movement) can be distinguished from the arterial pulse because: (i) it is visible but not palpable and has a more prominent inward movement than the artery; (ii) it has a complex wave form, usually seen to flicker twice with each cardiac cycle (if the patient is in sinus rhythm); (iii) it moves on respiration—normally the JVP decreases on inspiration; and (iv) it is at first obliterated and then filled from above when light pressure is applied at the base of the neck.

The JVP must be assessed for height and character. When the JVP is more than 3 cm above the zero point, the right-heart filling pressure is raised (a normal reading is less than 8 cm of water: 5 cm + 3 cm). This is a sign of right ventricular failure, volume overload or of some types of pericardial disease.

The assessment of the character of JVP is difficult even for experienced clinicians. There are two positive waves in the normal JVP.^r The first is called the a wave and coincides with right atrial systole.^s It is due to atrial contraction. The a wave also coincides with the first heart sound and precedes the carotid pulsation. The second impulse is called the v wave and is due to atrial filling, in the period when the tricuspid valve remains closed during ventricular systole. Between the a and v waves there is a trough caused by atrial relaxation. This is called the x descent. It is interrupted by the c point, which is due to transmitted carotid pulsation and coincides with tricuspid valve closure; it is not usually visible. Following the v wave, the tricuspid valve opens and rapid ventricular filling occurs; this results in the y descent (Figure 4.22).

Figure 4.22 The jugular venous pressure, and its relationship to the first (S1) and second (S2) heart sounds

In Table 4.14, characteristic changes in the JVP are described. Any condition in which right ventricular filling is limited (e.g. constrictive pericarditis, cardiac tamponade or right ventricular infarction) can cause elevation of the venous pressure, which is more marked on inspiration when venous return to the heart increases. This rise in the JVP on inspiration, called Kussmaul’s^t sign, is the opposite of what normally happens. This sign is best elicited with the patient sitting up at 90 degrees and breathing quietly through the mouth.

TABLE 4.14 Jugular venous pressure (pulse)

The abdominojugular reflux test (hepatojugular reflux) is a way of testing for right or left ventricular failure or reduced right ventricular compliance.¹⁷ Pressure exerted over the middle of the abdomen for 10 seconds will increase venous return to the right atrium. The JVP normally rises transiently following this manoeuvre.^u If there is right ventricular failure or left atrial pressures are elevated (left ventricular failure), it may remain elevated (>4cm) for the duration of the compression—a positive hepatojugular reflux. The sudden fall in the JVP (>4 cm) as the pressure is released may be easier to see than the initial rise. It is not necessary to compress the liver and so the older name, hepatojugular reflux, is not so appropriate. It is important that the patient be relaxed, breathe through the mouth and not perform a Valsalva manoeuvre. The examiner should press firmly with the palm over the middle of the abdomen. It is not necessary to apply pressure for more than 10 seconds.

Cannon a waves occur when the right atrium contracts against the closed tricuspid valve. This occurs intermittently in complete heart block where the two chambers beat independently.

Giant a waves are large but not explosive a waves with each beat. They occur when right atrial pressures are raised because of elevated pressures in the pulmonary circulation or obstruction to outflow (tricuspid stenosis).

The large v waves of tricuspid regurgitation should never be missed. They are a reliable sign of tricuspid regurgitation and are visible welling up into the neck during each ventricular systole.

Inspection

Inspect first for scars. Previous cardiac operations will have left scars on the chest wall. The position of the scar can be a clue to the valve lesion that has been operated on. Most valve surgery requires cardiopulmonary bypass and for this a median sternotomy (a cut down the middle of the sternum) is very commonly used. This type of scar is occasionally hidden under a forest of chest hair. It is not specifically helpful, as it may also be a result of previous coronary artery bypass grafting. Alternatively, left- or even right-sided lateral thoracotomy scars, which may be hidden under a pendulous breast, may indicate a previous closed mitral valvotomy. In this operation a stenosed mitral valve is opened through an incision made in the left atrial appendage; cardiopulmonary bypass is not required. Coronary artery bypass grafting and even valve surgery are now sometimes performed using small lateral ‘port’ incisions for video-assisted instruments.

Skeletal abnormalities such as pectus excavatum (funnel chest, page 121) or kyphoscoliosis (Greek kyphos ‘hunchbacked’, skolios ‘curved’), a curvature of the vertebral column (page 121), may be present. Skeletal abnormalities such as these, which may be part of Marfan’s syndrome, can cause distortion of the position of the heart and great vessels in the chest and thus alter the position of the apex beat. Severe deformity can interfere with pulmonary function and cause pulmonary hypertension (page 81).

Another surgical ‘abnormality’ that must not be missed, if only to avoid embarrassment, is a pacemaker or cardioverter-defibrillator box. These are usually under the right or left pectoral muscle just below the clavicle, are usually easily palpable and obviously metallic. The pacemaker leads may be palpable under the skin, leading from the top of the box. The box is normally mobile under the skin. Fixation of the skin to the box or stretching of the skin over the box may be an indication for repositioning. Erosion of the box through the skin is a serious complication because of the inevitable infection that will occur around this foreign body. Rarely, a loose lead connection will lead to twitching of the muscles of the chest wall around the box. Penetration of the right ventricular lead into or through the right ventricular wall may lead to disconcerting paced diaphragmatic contractions (hiccups) at whatever rate the pacemaker is set. Defibrillator boxes are larger than pacemakers. They are currently about 10 × 5 cm and a little less than 1 cm thick.

Look for the apex beat. Its normal position is in the fifth left intercostal space, 1 cm medial to the midclavicular line (Figure 4.23). It is due primarily to recoil of the heart as blood is expelled in systole. There may be other visible pulsations—for example, over the pulmonary artery in cases of severe pulmonary hypertension.

Figure 4.23 The apex beat

Coin is over the apex. Intercostal spaces are numbered. Vertical lines show right and left midclavicular and left anterior axillary lines. Care must be taken in identifying the midclavicular line; the inter-observer variability can be as much as 10 cm!

Palpation

The apex beat must be palpated (Figures 4.23 and 4.24).¹⁸ It is important to count down the number of interspaces. The first palpable interspace is the second. It lies just below the manubriosternal angle. The position of the apex beat is defined as the most lateral and inferior point at which the palpating fingers are raised with each systole. The normal apex is felt over an area the size of a 20 cent (50 p) coin (Figure 4.23). Use firm pressure with the tips of the fingers into the rib interspaces. The heel of the examiner’s hand is lifted off the patient’s sternum. Note that the apex beat is palpable in only about 50% of adults.

Figure 4.24 Feeling for the apex beat

It is worth noting that the palpable apex beat is not the anatomical apex of the heart but a point above it. At the time the apex beat is palpable,^v the heart is assuming a more spherical shape and the apex is twisting away from the chest wall. The area above the apex, however, is moving closer to the chest and is palpable. If the apex beat is displaced laterally or inferiorly, or both, this usually indicates enlargement,¹⁸ but may sometimes be due to chest wall deformity, or pleural or pulmonary disease (page 121).

The character of the apex beat may provide the examiner with vital diagnostic clues. The normal apex beat gently lifts the palpating fingers. There are a number of types of abnormal apex beats. The pressure loaded (heaving, hyperdynamic or systolic overloaded) apex beat is a forceful and sustained impulse. This occurs with aortic stenosis or hypertension. The volume loaded (thrusting) apex beat is a displaced, diffuse, non-sustained impulse. This occurs most commonly in advanced mitral regurgitation or dilated cardiomyopathy. The dyskinetic apex beat is an uncoordinated impulse felt over a larger area than normal in the praecordium and is usually due to left ventricular dysfunction (e.g. in anterior myocardial infarction). The double impulse apex beat, where two distinct impulses are felt with each systole, is characteristic of hypertrophic cardiomyopathy (page 91). The tapping apex beat will be felt when the first heart sound is actually palpable (heart sounds are not palpable in health) and indicates mitral or very rarely tricuspid stenosis. The character, but not the position, of the apex beat may be more easily assessed when the patient lies on the left side.

In many patients the apex beat may not be palpable. This is most often due to a thick chest wall, emphysema, pericardial effusion, shock (or death) and rarely to dextrocardia (where there is inversion of the heart and great vessels). The apex beat will be palpable to the right of the sternum in many cases of dextrocardia.

Other praecordial impulses may be palpable in patients with heart disease. A parasternal impulse may be felt when the heel of the hand is rested just to the left of the sternum with the fingers lifted slightly off the chest (Figure 4.25). Normally no impulse or a slight inward impulse is felt. In cases of right ventricular enlargement or severe left atrial enlargement, where the right ventricle is pushed anteriorly, the heel of the hand is lifted off the chest wall with each systole. Palpation with the fingers over the pulmonary area may reveal the palpable tap of pulmonary valve closure (palpable P2) in cases of pulmonary hypertension (Figure 4.26).

Figure 4.25 Feeling for the parasternal impulse

Figure 4.26 Palpating the base of the heart

Turbulent blood flow, which causes cardiac murmurs on auscultation, may sometimes be palpable. These palpable murmurs are called thrills. The praecordium should be systematically palpated for thrills with the flat of the hand, first over the apex and left sternal edge, and then over the base of the heart (this is the upper part of the chest and includes the aortic and pulmonary areas) (Figure 4.26).

Apical thrills can be more easily felt with the patient rolled over to the left side (the left lateral position) as this brings the apex closer to the chest wall. Thrills may also be palpable over the base of the heart. These may be maximal over the pulmonary or aortic areas, depending on the underlying cause, and are best felt with the patient sitting up, leaning forwards and in full expiration. In this position the base of the heart is moved closer to the chest wall. A thrill that coincides in time with the apex beat is called a systolic thrill; one that does not coincide with the apex beat is called a diastolic thrill.

The presence of a thrill usually indicates an organic lesion. Careful palpation for thrills is a useful, but often neglected, part of the cardiovascular examination.

Percussion

It is possible to define the cardiac outline by means of percussion^w but this is not routine (page 124).¹⁹ Percussion is most accurate when performed in the fifth intercostal space. The patient should lie supine and the examiner percusses from the anterior axillary line towards the sternum. The point at which the percussion note becomes dull represents the left heart border. A distance of more than 10.5 cm between the border of the heart and the middle of the sternum indicates cardiomegaly. The sign is not useful in the presence of lung disease.

Auscultation

Now at last the stethoscope is required.²⁰ However, in some cases the diagnosis should already be fairly clear. In the viva voce examination, the examiners will occasionally stop a candidate before auscultation and ask for an opinion.

Auscultation of the heart begins in the mitral area with the bell of the stethoscope (Figures 4.1, page 45, and 4.27). The bell is designed as a resonating chamber and is particularly efficient in amplifying low-pitched sounds, such as the diastolic murmur of mitral stenosis or a third heart sound. It must be applied to the chest wall lightly, because forceful application will stretch the skin under the bell so that it forms a diaphragm. Some modern stethoscopes do not have a separate bell; the effect of a bell is produced when the diaphragm is placed lightly on the chest, and of a diaphragm when it is pushed more firmly.

Figure 4.27 Auscultation in the mitral area with the bell of the stethoscope

Listening for mitral stenosis in the left lateral position.

Next, listen in the mitral area with the diaphragm of the stethoscope (Figure 4.28), which best reproduces higher-pitched sounds, such as the systolic murmur of mitral regurgitation or a fourth heart sound. Then place the stethoscope in the tricuspid area (fifth left intercostal space) and listen. Next inch up the left sternal edge to the pulmonary (second left intercostal space) and aortic (second right intercostal space) areas (Figures 4.29 and 4.30), listening carefully in each position with the diaphragm.

Figure 4.28 Auscultation at the apex with the diaphragm of the stethoscope

Figure 4.29 Auscultation at the base of the heart (pulmonary area)

Figure 4.30 Auscultation at the base of the heart (aortic area)

For accurate auscultation, experience with what is normal is important. This can be obtained only through constant practice. Auscultation of the normal heart reveals two sounds called, not surprisingly, the first and second heart sounds. The explanation for the origin of these noises changes from year to year; the sounds are probably related to vibrations caused by the closing of the heart valves in combination with rapid changes in blood flow and tensing within cardiac structures that occur as the valves close.

The first heart sound (S1) has two components: mitral and tricuspid valve closure. Mitral closure occurs slightly before tricuspid, but usually only one sound is audible. The first heart sound indicates the beginning of ventricular systole.

The second heart sound (S2), which is softer, shorter and at a slightly higher pitch than the first and marks the end of systole, is made up of sounds arising from aortic and pulmonary valve closures. In normal cases, although left and right ventricular systole end at the same time, the lower pressure in the pulmonary circulation compared with the aorta means that flow continues into the pulmonary artery after the end of right ventricular systole. As a result, closure of the pulmonary valve occurs later than that of the aortic valve. These components are usually (in 70% of normal adults) sufficiently separated in time so that splitting of the second heart sound is audible. Because the pulmonary component of the second heart sound (P2) may not be audible throughout the praecordium, splitting of the second heart sound may best be appreciated in the pulmonary area and along the left sternal edge. Pulmonary valve closure is further delayed (by 20 or 30 milliseconds) with inspiration because of increased venous return to the right ventricle; thus, splitting of the second heart sound is wider on inspiration. The second heart sound marks the beginning of diastole, which is usually longer than systole.

It can be difficult to decide which heart sound is which. Palpation of the carotid pulse will indicate the timing of systole and enable the heart sounds to be more easily distinguished. It is obviously crucial to define systole and diastole during auscultation so that cardiac murmurs and abnormal sounds can be placed in the correct part of the cardiac cycle. Students are often asked to time a cardiac murmur; this is not a request to measure its length, but rather to say in which part of the cardiac cycle it occurs. Even the experts can mistake a murmur if they do not time it. It is important, during auscultation, to concentrate separately on the components of the cardiac cycle. The clinician should attempt to identify each and listen for abnormalities. There can be more than 12 components to identify in patients with heart disease. An understanding of the cardiac cycle is helpful when interpreting the auscultatory findings (Figure 4.31).

Figure 4.31 The cardiac cycle

Normally the onset of left ventricular systole precedes the onset of pressure rise in the right ventricle. The mitral valve, therefore, closes before the tricuspid valve. Because the pulmonary artery diastolic pressure is lower than aortic diastolic pressure, the pulmonary valve opens before the aortic valve. Therefore, pulmonary ejection sounds occur closer to the first heart sound than do aortic ejection sounds. During systole the pressure in the ventricles slightly exceeds the pressure in the corresponding great arteries. Towards the end of systole, the ventricular pressure falls below the pressure in the great arteries, and when diastolic pressure is reached the semilunar valves close. Normally, aortic valve closure precedes pulmonary valve closure. The mitral and tricuspid valves begin to open at the point at which the ventricular pressures fall below the corresponding atrial pressures.

Adapted from Swash M, ed. Hutchison’s clinical methods, 20th edn. Philadelphia: Baillière Tindall, 1995, with permission.

Abnormalities of the heart sounds

Murmurs of the heart

In deciding the origin of a cardiac murmur, a number of different features must be considered. These are: timing, the area of greatest intensity, the loudness and pitch, associated features (peripheral signs), and the effect of dynamic manoeuvres, including respiration and the Valsalva manoeuvre (Figure 4.32). The presence of a characteristic murmur is very reliable for the diagnosis of certain valvular abnormalities, but for others less so.

Figure 4.32 Sites of maximum intensity and radiation of murmurs and heart sounds

(a) Systolic murmurs:

AS = aortic stenosis;

MR = mitral regurgitation;

HCM = hypertrophic cardiomyopathy;

PS = pulmonary stenosis;

VSD = ventricular septal defect;

I = innocent.

(b) Diastolic murmurs and sounds:

AR = aortic regurgitation;

MS = mitral stenosis;

S3 = third heart sound;

PR = pulmonary regurgitation;

PDA = patent ductus arteriosus (continuous murmur).

Dynamic manoeuvres (GOOD SIGNS GUIDE 4.2)

All patients with a newly diagnosed murmur should undergo dynamic manoeuvre testing (Table 4.16).²⁸

Respiration. Murmurs that arise on the right side of the heart become louder during inspiration as this increases venous return and therefore blood flow to the right side of the heart. Left-sided murmurs are either unchanged or become softer. Expiration has the opposite effect. This can be a sensitive and specific way of differentiating right- and left-sided murmurs.

Deep expiration. A routine part of the examination of the heart (Figure 4.33) includes leaning a patient forward in full expiration and listening to the base of the heart for aortic regurgitation, which may otherwise be missed. In this case the manoeuvre brings the base of the heart closer to the chest wall. The scraping sound of a pericardial friction rub is also best heard in this position.

The Valsalva manoeuvre.^z This is a forceful expiration against a closed glottis. One should ask the patient to hold his or her nose with the fingers, close the mouth, breathe out hard and completely so as to pop the eardrums, and hold this for as long as possible. Listen over the left sternal edge during this manoeuvre for changes in the systolic murmur of hypertrophic cardiomyopathy, and over the apex for changes when mitral valve prolapse is suspected.

GOOD SIGNS GUIDE 4.2 Dynamic auscultation

Sign	Positive LR	Negative LR
Louder on inspiration—right-sided murmur	7.8	0.2
Louder with Valsalva strain—hypertrophic cardiomyopathy	14.0	0.3
Louder squatting to standing—hypertrophic cardiomyopathy	6.0	0.1
Softer with isometric handgrip—hypertrophic cardiomyopathy	3.6	0.1
Louder with isometric handgrip—mitral regurgitation	5.8	0.3

From McGee S, Evidence-based physical diagnosis, 2nd edn. St Louis: Saunders, 2007.

TABLE 4.16 Dynamic manoeuvres and systolic cardiac murmurs

Figure 4.33 Dynamic auscultation for aortic regurgitation or a pericardial friction rub; patient in deep expiration

The Valsalva manoeuvre has four phases. In phase 1 (beginning the manoeuvre), a rise in intrathoracic pressure and a transient increase in left ventricular output and blood pressure occurs. In phase 2 (the straining phase), systemic venous return falls, filling of the right and then the left side of the heart is reduced, and stroke volume and blood pressure fall while the heart rate increases. As stroke volume and arterial blood pressure fall, most cardiac murmurs become softer; however, because the left ventricular volume is reduced, the systolic murmur of hypertrophic cardiomyopathy becomes louder and the systolic click and murmur of mitral valve prolapse begins earlier. In phase 3 (the release of the manoeuvre), first right-sided and then left-sided cardiac murmurs become louder briefly before returning to normal. Blood pressure falls further because of pooling of blood in the pulmonary veins. In phase 4, the blood pressure overshoots as a result of increased sympathetic activity as a response to the previous hypotension. Changes in heart rate are opposite to the blood pressure changes.

The blood pressure responses can be measured by inflating a cuff to 15 mmHg over the systolic pressure before the manoeuvre. Korotkoff sounds will then appear in phases 1 and 4 in a normal patient. Absence of the phase 4 overshoot is a sign of cardiac failure. The left ventricle is unable to increase cardiac output despite increased sympathetic activity.

Standing to squatting. When the patient squats rapidly from the standing position, venous return and systemic arterial resistance increase simultaneously, causing a rise in stroke volume and arterial pressure. This makes most murmurs louder. However, left ventricular size is increased, which reduces the obstruction to outflow and therefore reduces the intensity of the systolic murmur of hypertrophic cardiomyopathy, while the midsystolic click and murmur of mitral valve prolapse are delayed.

Squatting to standing. When the patient stands up quickly after squatting, the opposite changes in the loudness of these murmurs occurs.

Isometric exercise. Sustained hand grip or repeated sit-ups for 20 for 30 seconds increases systemic arterial resistance, blood pressure and heart size. The systolic murmur of aortic stenosis may become softer because of a reduction in the pressure difference across the valve but often remains unchanged. Most other murmurs become louder, except the systolic murmur of hypertrophic cardiomyopathy, which is softer, and the mitral valve prolapse murmur, which is delayed because of an increased ventricular volume.

Auscultation of the neck

This is often performed as a part of dynamic auscultation for valvular heart disease, but certain aspects of the examination may be considered here. Abnormal sounds heard over the arteries are called bruits. These sounds are low-pitched and may be more easily heard with the bell of the stethoscope. Carotid artery bruits are most easily heard over the anterior part of the sternomastoid muscle above the medial end of the clavicle. Ask the patient to stop breathing for a brief period to remove the competing noise of breath sounds. It may be prudent to ask the patient not to speak. The amplified voice is often painfully loud when heard through the stethoscope.

A systolic bruit may be a conducted sound from the heart. The murmur of aortic stenosis is always audible in the neck and a soft carotid bruit is sometimes audible in patients with severe mitral regurgitation or pulmonary stenosis. A bruit due to carotid stenosis will not be audible over the base of the heart. Move the stethoscope from point to point onto the chest wall; if the bruit disappears, it is likely the sound arises from the carotid. It is not possible to exclude a carotid bruit in a patient with a murmur of aortic stenosis that radiates to the neck. Carotid artery stenosis is an important cause of a carotid bruit. More severe stenosis is associated with a noise that is longer and of increased pitch. Total obstruction of the vessel leads to disappearance of the bruit. It is not possible to make a diagnosis of significant (>60% obstruction) carotid stenosis clinically. The bottom line is that a carotid bruit poorly predicts significant carotid stenosis or stroke risk.Thyrotoxicosis can result in a systolic bruit (page 303) due to the increased vascularity of the gland.

A continuous noise is sometimes audible at the base of the neck. This is usually a venous hum, a result of audible venous flow. It disappears if light pressure is applied to the neck just above the stethoscope. Occasionally a loud machinery murmur (page 93) or severe aortic regurgitation (page 86) may cause a similar sound. Haemodialysis patients frequently have an audible bruit transmitted from their arterio-venous fistula.