Structure and function

The adult heart (Fig. 6.1) consists of two pumps working in series. The ‘right heart’, comprising the right atrium, tricuspid valve, right ventricle, pulmonary valve and pulmonary artery, is a low pressure pump receiving blood from the systemic veins and pumping it to the lungs. The left heart, comprising the left atrium, mitral valve, left ventricle, aortic valve and aorta, is a high pressure pump receiving blood from the lungs and pumping it round the body. In the early embryo, the heart forms as a simple tube down the midline of the body. As the embryo grows, the tube elongates more rapidly than the tissues around it and thus develops a loop and a twist. It also becomes divided into left and right chambers by the growth of a partition or septum down the middle.

Fig. 6.1 Arrangement of the heart chambers as a flow diagram (above) and in their approximate anatomical positions (below).

In the ninth week of gestation, the fetal heart rotates in a clockwise direction until the right ventricle comes to rest anteriorly behind the sternum. Most of the left ventricle comes to lie posteriorly, apart from a small portion of left ventricular muscle which forms the left heart border when seen from the front and the extreme tip or apex of the heart (Fig. 6.2). The way the heart is situated within the chest cavity is also well demonstrated on the computerised tomographic scan of the chest shown in Figure 6.3. Note that the heart lies obliquely in the chest and that its long axis, the planes of the interatrial and interventricular septum, and the planes of the various valves, are not aligned with any of the conventional anatomical planes. The chambers of the heart can be examined after death by injecting wax or plastic and dissolving away the muscle (Fig. 6.4). They can also be examined during life by injecting radio-opaque contrast medium through catheters placed in the various chambers of the heart and taking cine radiographs. By tilting the x-ray tube and image detector appropriately, it is possible to obtain detailed pictures of the full extent of the ventricular cavities (Fig. 6.5).

Fig. 6.2 Most of the anterior surface of the heart is formed by the right ventricle and pulmonary artery. The tip of the left ventricle and the left atrial appendage also appear on the left border of the heart.

Fig. 6.3 Computerised tomography scan of the heart showing the position of the heart within the chest cavity. Viewed from below.

Fig. 6.4 A ‘corrosion cast’ of the chambers of the heart, made by filling the chambers with wax or plastic and dissolving away the muscle.

Fig. 6.5 Left ventricular cine-angiogram made by injecting radio-opaque contrast medium into the heart through a catheter passed via the femoral artery and aorta. The x-ray tube and image intensifier are tilted into the ‘right anterior oblique’ position to outline the full extent of the left ventricle.

HEART MUSCLE

Ventricles

Heart muscle or myocardium is a special type of muscle that is extremely resistant to fatigue. As a result of the higher pressures that it normally generates, the wall of the left ventricle is much thicker than the wall of the right ventricle. In a section taken through both ventricles, left ventricular myocardium, including the intraventricular septum, has a roughly circular outline with the right ventricle appearing to be wrapped around one side of it (Fig. 6.6). The muscle fibres of the heart are arranged in a complicated spiral arrangement so that when they contract (systole) not only is blood forced out of the ventricles but the heart also elongates and rotates on the fixed base provided by the attachment of the major blood vessels. It is this movement that is felt as the beating of the heart by a hand placed on the chest. The heart normally lies in its own serous cavity, the pericardium, which allows it to move without friction. Apart from moving with each heart beat, the position of the pericardium and the heart can be altered by the phase of respiration or by rolling from one side to the other.

Fig. 6.6 ‘Short axis’ view of the heart. In the short axis or transverse section, the thinner (low pressure) right ventricle is ‘wrapped around’ the left ventricle.

Atria

The atria of the heart are also muscular but are much thinner walled than the ventricles (Fig. 6.7). They contract a fraction of a second before the ventricles and, in doing so, they assist in the filling of the ventricles, particularly when there is a need for increased cardiac output. The atrial component of cardiac filling can contribute up to 30% of cardiac output. Patients in whom, as a result of disease, the atria are paralysed or are beating out of synchrony with the ventricles are usually comfortable at rest but may become short of breath on exercise.

Fig. 6.7 Relative thickness of muscle in different parts of the heart.

CARDIAC HYPERTROPHY AND DILATATION

Like any muscle, cardiac muscle responds to an increased workload by growth. The heart responds in different ways to pressure load and volume load. Pressure load is caused by an increased resistance to ejection of blood from the heart. The response to pressure load is cardiac hypertrophy, initially without dilatation of the chamber involved. For example, in aortic stenosis, the left ventricular wall becomes excessively thickened but the left ventricular cavity remains of normal size. Eventually, when the pressure load is extreme or growth of the heart muscle has outstripped its blood supply, failure of the muscle occurs and the cavity begins to enlarge.

The heart responds to a volume load, for example, a leaking mitral or aortic valve, an arteriovenous fistula or left-to-right shunt, by both hypertrophy of the myocardium and dilatation of the chamber involved. This is to accompany the increased stroke volume that is required to deal with the volume load. The chest radiograph shows cardiac enlargement (Fig. 6.8) and this is also found on echocardiography. Ventricular hypertrophy produces characteristic electrocardiographic changes and it is possible to identify the cardiac chamber involved from the electrocardiographic appearances.

Fig. 6.8 Chest radiograph showing cardiac enlargement in response to a volume load chronic mitral regurgitation (compare with Fig. 6.2).

HEART VALVES

There are four heart valves. They fall anatomically and functionally into two groups: the inflow or atrioventricular valves and the outflow or ‘semilunar’ valves. The tricuspid and mitral valves separate right atrium and right ventricle and left atrium and left ventricle, respectively. Both develop from the endocardial cushions of the embryonic heart and are composed of thin flexible leaflets that are prevented from prolapsing back into the atrium when the ventricle contracts by being attached by chordae tendineae to specialised portions of ventricular muscle, the papillary muscles (Fig. 6.9). The hydrodynamic efficiency of the mitral and tricuspid valves is very high. Their pliable edges smooth out eddies and turbulence in blood flow and allow the rapid transfer of blood from atrium to ventricle with a very small pressure differential. The aortic and pulmonary valves develop from two spiral ridges that divide the single great vessel leaving the embryonic heart into aortic and pulmonary trunks. Each normally has three cusps whose arrangement reflects their embryonic origin (Fig. 6.10). As each cusp is shaped like a half moon, they are sometimes called the semilunar valves.

Fig. 6.9 Postmortem specimen showing attachment of valve cusps to papillary muscles by chordae tendineae.

Fig. 6.10 The common ‘great vessel’ of the fetal heart is divided into aorta and pulmonary artery by the growth of the spiral ridges.

HEART SOUNDS

Closure of the heart valves at different stages of the cardiac cycle gives rise to sounds that are readily audible through a stethoscope. The sounds are normally described as ‘lub-dup’. The first heart sound (‘lub’) is caused by the closure of the mitral and tricuspid valves, and the second heart sound, the rather higher pitched (‘dup’), is caused by the closure of aortic and pulmonary valves. The relationship between the heart sound, the electrocardiogram and the arterial pulse wave is shown in Figure 6.11. In children or in young adults, the second heart sound splits into two components during inspiration (‘lub da-dup’) and comes together again in expiration. This physiological splitting of the second heart sound is the result of minor changes in the stroke volume of left and right ventricles during the normal respiratory cycle.

Fig. 6.11 Relationship between heart sounds, electrocardiogram and arterial pulse.

During inspiration, venous return to the right side of the heart is increased, thus increasing right ventricular stroke volume and delaying pulmonary valve closure. At the same time, pooling of blood in the pulmonary veins reduces filling of the left ventricle and makes aortic valve closure slightly earlier than in expiration. The split may be widened by other factors that delay right ventricular contraction, such as right bundle branch block or pulmonary valve stenosis. Conversely, anything that delays left ventricular contraction, such as left bundle branch block, hypertrophic obstructive cardiomyopathy or severe aortic stenosis, may so delay the aortic component of the second heart sound that the normal relationship is reversed and there is increasing splitting of the second heart sound on expiration with the sounds coming together on inspiration. This is known as paradoxical splitting of the second heart sound. Finally, in an atrial septal defect, there is a characteristically fixed splitting of the second heart sound because the hole in the intra-atrial septum means that left and right atrial pressure remains equal throughout the respiratory cycle (Fig. 6.12).

Fig. 6.12 Beat to beat variations in left and right ventricular stroke volume cause splitting of the second heart sound in phase with breathing. Splitting of the second sound with inspiration is normal. Other patterns may indicate cardiac abnormalities.

Electrical activity of the heart

The signal for contraction of each heart muscle cell is the electrical depolarisation of its membrane. The electrical signal is transmitted from cell to cell in an orderly way so that under normal circumstances the heart contracts in an orderly fashion. The physiological cardiac pacemaker comprises a small group of cells in the sinoatrial node situated close to where the right atrium joins the superior vena cava. Normally, these cells undergo cyclical repolarisation and depolarisation at a faster rate than cells in other parts of the heart. The electrical impulse spreads out from the sinoatrial node (Fig. 6.13) through the cardiac muscle of the atria. The atria and the ventricles are separated by a fibrous ring of tissue to which the tricuspid and mitral valves are attached and which does not support conduction of the cardiac impulse. The only electrical pathway through this ring is through the atrioventricular node, a localised area of specialised conducting tissue lying between the tricuspid valve and the aorta. There is a delay of 0.12–0.20s while the impulse passes through the atrioventricular node, ensuring the correct delay between atrial and ventricular contraction. Once through the atrioventricular node, the electrical impulse is rapidly conducted to ventricular tissue through specialised conducting fibres which form the bundle of His and its branches.

Fig. 6.13 Paths of the spread of electrical impulses in the heart (note that there are no specific electrical pathways in the atria).

ELECTROCARDIOGRAM

The electrocardiogram (ECG) is an electrical and structural map of the heart and is an invaluable aid to studying normal heart rhythm and its disturbances. It works by sensing and amplifying the very small electrical potential changes between different points on the surface of the body caused by the cyclical depolarisation and repolarisation of the heart cells. Electrical potentials are picked up by electrodes that are attached to the skin. The points at which the electrodes are attached and the conventional ways in which they are connected enable the ECG to ‘look at’ the heart from a sequence of different directions (Fig. 6.14). The cycle of electrical changes during a single heart beat is termed an ECG complex. Different parts of the ECG complex reflect the activation of different parts of the heart. The P wave signals atrial activity and the QRS complex indicates ventricular activity (Fig. 6.15).

Fig. 6.14 How the ECG ‘looks at’ the heart from different directions (a concept due to Goldberger and Wilson).

Fig. 6.15 Different parts of an ECG ‘complex’.

In patients suspected of intermittent arrhythmias, the ECG may be displayed as a continuous monitor trace (Fig. 6.16). In patients outside hospital, the ECG can be recorded continuously digitally for periods of 24–48 h and then played back to analyse any rhythm disturbances. This process is called ‘ambulatory ECG’ or ‘Holter monitoring’. The ECG can be used to detect hypertrophy of the different chambers of the heart (Fig. 6.17), abnormal rhythms and cardiac damage.

Fig. 6.16 ECG trace displayed on a monitor at the nursing station or bedside.

Fig. 6.17 Electrocardiographic changes can be used to identify hypertrophy of the cardiac chambers.

Cardiac arrhythmias

Abnormalities of heart rhythm can be divided into those in which the heart goes too slowly (bradycardia) and those in which the rate is abnormally rapid (tachycardia). Physiologically, heart rate can vary in a normal young adult from 40 beats/min during sleep to 180 beats/minute or more during vigorous exercise. The physiological control of heart rate is due to a balance between sympathetic nervous activity, which speeds the heart rate, and vagal activity, which slows it down.

There are two principal mechanisms of arrhythmia generation: automaticity and re-entry phenomena. The latter comprises 90% of arrhythmias. Automaticity implies normal conduction tissue or abnormal conduction (ectopic) tissue that is repetitively firing faster than usual. Re-entry phenomenon is described under tachycardia below.

BRADYCARDIA

Bradycardia may be caused by drugs, particularly β-adrenoceptor blocking drugs (‘beta-blockers’); it may also be a physiological finding in fit young athletes with a high vagal tone. Extreme bradycardia may be caused by heart block with failure of conduction of the electrical impulse, most often as it passes through the atrioventricular node or bundle of His (Fig. 6.18).

Fig. 6.18 Heart block is one cause of bradycardia; there is failure of conduction of the electrical impulses from atrium to ventricle.

TACHYCARDIA

Ectopic beats

As all heart muscle and not only the sinoatrial node exhibits the capacity for spontaneous depolarisation, it is not uncommon to find an ‘ectopic focus’ of electrical activity which can initiate extra beats out of time with the normal cardiac cycle. These extra beats or extrasystoles may be generated in the atrium or ventricle. In otherwise healthy people, extrasystoles are usually benign and harmless. Following myocardial infarction or during a viral infection of the heart, they may act as markers for metabolic damage and, consequently, excessive irritability of the heart muscle (Fig. 6.19).

Fig. 6.19 Extrasystoles are caused by an ectopic focus of electrical activity.

Sustained tachycardia

A persistent tachycardia may be caused by several ectopic beats occurring in sequence (e.g. as the manifestation of a particularly irritable ectopic focus). This is called a ‘focal tachycardia’.

A more common mechanism for sustained tachycardia is, however, the phenomenon of re-entry (Fig. 6.20). The basic principle of a re-entry tachycardia is that there are two alternative pathways for the conduction of the electrical impulse; these pathways differ both in their speed of conduction and their refractory period. Under normal conditions, the cardiac impulse will be conducted by both pathways but an exceptionally early beat may find one pathway still refractory to conduction and therefore the impulse will be conducted down the other one alone. However, by the time it reaches the end of this pathway, the other pathway will have recovered and be able to conduct the impulse in the reverse direction. This sets up the possibility of a ‘circus movement’ or oscillation and the re-entry circuit can act as a focus for generating a tachycardia. This tachycardia may continue until one of the pathways fatigues and cannot conduct fast enough to maintain the circuit or until the process is interrupted by an electrical stimulus which breaks the circuit and re-establishes normal conduction (Fig. 6.21).

Fig. 6.20 Mechanism of a re-entry tachycardia, based on the ‘paradigm’ of the Wolff–Parkinson–White syndrome. The left hand diagram shows the ECG pattern produced when conduction is all along the bypass pathway, when it is all along the normal pathway and when it is along both simultaneously.

Fig. 6.21 A critically timed extra stimulus can terminate a re-entry tachycardia by making both pathways refractory.

Fibrillation

The most extreme form of arrhythmia occurs when the coordinated conduction of impulses between cells completely breaks down and individual cells contract haphazardly. This process is termed fibrillation. Atrial fibrillation is common but not particularly hazardous because the atrioventricular node acts as a ‘filter’, preventing the ventricles from being stimulated at too rapid a rate. Ventricular fibrillation is, however, rapidly lethal because the rapidly contracting ventricles are ineffective and unable to pump any blood into the circulation. The only treatment for ventricular fibrillation is to pass an artificial competing electric current through the heart. This technique is referred to as defibrillation and causes momentary extinction of all electrical activity, allowing the whole system to reset (Fig. 6.22).

Fig. 6.22 A defibrillator (a). An electrical charge is built up within the machine and discharged through paddles applied to the patient’s chest (b).

Blood supply to the heart

Heart muscle needs a supply of blood to support both its basal metabolic needs and the increased oxygen requirements of exercise. The blood supply must be capable of increasing to meet the heart’s demands during exercise because heart muscle, unlike skeletal muscle, can only work aerobically. The arterial blood supply to the heart is provided by the right and left coronary arteries. The right coronary artery supplies mainly the right ventricle and the inferior surface of the left ventricle. It divides at the end of its course into the posterolateral branch and the posterior descending branch, which supplies the posterior and lateral parts of the left ventricle The left coronary has a common trunk (the left main stem) which divides soon after its origin into the left anterior descending coronary artery, which supplies the interventricular septum, the anterior surface and the apex of the left ventricle, and the circumflex coronary artery, which supplies the lateral part of the left ventricle (Fig. 6.23).

Fig. 6.23 Cine-angiograms to show (left and middle) the left coronary artery and (right) the right coronary artery (RCA).

(Cx, left circumflex artery; LAD, left anterior descending artery; LMCA, left main coronary artery)

In common with other arteries in the body, coronary arteries are prone to atheroma which predisposes to thrombosis and coronary artery occlusion. The clinical features of coronary thrombosis and the myocardial infarction are described later.

INTRACARDIAC SHUNTING

In the fetus, the placenta, rather than the lungs, participates in respiratory gas exchange and the unexpanded lungs offer a high resistance to blood flow. Both sides of the fetal heart work to pump a mixture of deoxygenated blood from the systemic veins and oxygenated blood from the placenta into the aorta and thus to the rest of the body. Blood entering in the right atrium may pass either through the tricuspid valve into the right ventricle or through a hole in the intra-atrial septum, the foramen ovale. Blood entering the right ventricle is pumped into the pulmonary artery, with only a small proportion of it entering the lungs. The remainder passes via the ductus arteriosus into the aorta (Fig. 6.24).

Fig. 6.24 In the fetal circulation, oxygenated blood from the umbilical vein bypasses the liver through the ductus venosus; a portion is shunted from the right to left atrium through the foramen ovale and a further portion passes through the arterial duct.

After birth, as the lungs inflate with air, intrapulmonary vascular resistance of the lungs rapidly falls. The subsequent fall in right atrial pressure and rise in left atrial pressure creates a pressure change which forces the valve-like foramen ovale to close and seals the interatrial septum. At the same time, the ductus arteriosus constricts and closes (Fig. 6.25). This separates the work of the right and left sides of the heart and causes them to work in series rather than in parallel. However, abnormalities in the process of transition from fetal to adult circulation, or anatomical defects in the partitions or ‘septa’ dividing the right and left sides of the heart, may lead to short-circuits or ‘shunts’.

Fig. 6.25 Changes that occur in the fetal circulation at birth. The ductus arteriosus constricts and the fall in right arterial pressure as the lungs expand closes the foramen ovale.

Left to right shunt

A congenital or acquired defect in the interatrial septum, interventricular septum or failure of closure of the ductus arteriosus will produce a left to right shunt. Blood follows the path of least resistance from the high pressure left-sided chamber to the lower pressure right-sided chamber. The result is that, instead of matching left and the right sided cardiac outputs, the right side of the heart has to cope with the extra load of blood shunted from the left. A two-to-one shunt means that the output at the right side of the heart is twice that of the left side of the heart and the increased workload on the right side of the heart may lead to heart failure. Alternatively, the excessively high blood flow through the lungs may lead to irreversible damage to the pulmonary vasculature and the development of pulmonary hypertension. Examples of left to right shunts are shown in Figure 6.26.

Fig. 6.26 (a) Left to right shunt atrial septal defect. Blood passes from the left to right atrium. The overall result is an increase in pulmonary blood flow. (b) Left to right shunt: ventricular septal defect. Blood passes from the high pressure left ventricle to the lower pressure right ventricle. (c) Left to right shunt: persistent ductus arteriosus. Blood passes from the high pressure aorta to the lower pressure pulmonary artery.

Right to left shunt

If a septal defect or persistent ductus arteriosus is combined with a further lesion that raises the pressure on the right side of the heart then, instead of blood flowing from the left-sided chamber to the right-sided chamber, it will flow in the opposite direction, from the right side of the heart to the left. The most common example of congenital heart disease causing a right to left shunt is Fallot’s tetralogy (Fig. 6.27) which is physiologically equivalent to a ventricular septal defect plus pulmonary valve stenosis. A right to left shunt can occur when pulmonary vascular damage occurs in a patient with a severe left to right shunt. The resistance of the pulmonary arteries rises, resulting in increased pressure on the right side of the heart and a reversal of the shunt. This is called Eisenmenger’s syndrome (Fig. 6.28).

Fig. 6.27 Fallot’s tetralogy is the most common ‘congenital’ cause of a right to left shunt. (The ‘tetralogy’ comprises pulmonary stenosis, ventricular septal defect, over-riding aorta and right ventricular hypertrophy.) (Note that cyanosis sometimes develops several weeks after birth because dynamic hypertrophy of muscle in the right ventricular outflow tract worsens the obstruction.)

Fig. 6.28 Eisenmenger’s syndrome is caused by a secondary rise in pulmonary vascular resistance as a consequence of pulmonary damage from increased blood flow initially due to a left to right shunt. (In some children, the pulmonary vasculature may never develop normally in the presence of such a shunt.)

The striking clinical feature about patients with right to left shunts is central cyanosis due to the admixture of desaturated venous blood with saturated blood coming from the pulmonary vein. It differs from cyanosis caused by lung disease or pulmonary oedema as it is not corrected by administering supplemental oxygen.

In patients with right to left shunts clinical signs of long-term adaptation to chronic reduction in systemic arterial oxygen saturation include finger clubbing (Fig. 6.29), polycythaemia and acne (particularly in adolescent children).

Fig. 6.29 Cyanosis and finger clubbing in a girl with Eisenmenger’s syndrome.

The arterial system

The arterial system distributes oxygenated blood from the heart to the tissues and organs of the body. At the points where arteries pass close to the body surface or can be compressed against the bony skeleton, they can be felt as ‘pulses’ (Fig. 6.30). During each cardiac cycle, the left ventricle ejects blood into the aorta and initiates a pulse wave that is transmitted to the periphery. It is important to remember that the pulse wave travels to the periphery much more rapidly than the actual flow of blood. An intra-arterial recording of pressure against time indicates the shape of the pulse wave, which approximates to that which would be felt by a finger placed on the arterial wall (Fig. 6.31). The shape of the arterial pulse wave depends on many factors (see ‘differential diagnosis’ box).

Fig. 6.30 Some of the points at which arterial pulsation can be felt. (Note the similarity to first-aiders’ ‘pressure points’.)

Fig. 6.31 Relationship between the pulse and the arterial waveform.

The venous system

The most important mechanism allowing individual organs to adjust their blood supply according to metabolic need is by decreasing or increasing the arteriolar resistance to inflow (i.e. very small arteries 200–300 mm in diameter). Thus, food ingestion considerably reduces gut vascular resistance and increases gut blood flow. Similarly, exercising skeletal muscle strikingly reduces its vascular resistance, thereby increasing local blood flow. Alteration of blood flow to the skin is one of the important mechanisms controlling heat loss or conservation. The arteriolar resistance in the skin and the gut is under autonomic sympathetic nervous system control; sympathetic nervous system stimulation causes arteriolar constriction resulting in a rise in blood pressure. The most important blood vessels contributing to control of peripheral vascular resistance are the small muscular arteries and arterioles; larger blood vessels such as the femoral, carotid or radial arteries are conduits and play little or no role in the control of blood pressure.

The major veins of the body are shown in Figure 6.32. Systemic veins collect blood from the tissues and return it to the right atrium of the heart. The venous return from the gut is specialised because it flows into the hepatic portal vein and first enters the liver before flowing out through the hepatic veins into the inferior vena cava. The venous system operates at a much lower pressure than the arterial system. Veins draining the chest and abdomen drain passively into the vena cava, either directly or via the azygos vein. In the upright position, venous drainage from the head and neck is assisted by gravity. Passive venous drainage alone is inadequate for the limbs and, in particular, the lower limbs. Here, the venous system is divided into superficial and deep veins (Fig. 6.33) separated by one-way valves. Contraction of the arm and leg muscles during normal activities massage the deep veins and this pumping action actively propels blood back towards the heart. The one-way valve system between the deep and superficial venous systems of the lower limb ensures unidirectional blood flow.

Fig. 6.32 Principal veins of the body.

Fig. 6.33 Veins in the leg form a ‘muscle pump’ in conjunction with the calf muscles. Muscle contraction forces blood from superficial to deep veins, and from periphery to centre.

Clinical history

A carefully taken history sets the scene for the subsequent physical examination. Particular symptoms that need to be enquired of in the cardiovascular history include breathlessness, chest pain, palpitation, syncope and claudication. The presence or absence of these symptoms provides clues to the likely findings anticipated on physical examination.

BREATHLESSNESS

Patients with heart disease characteristically experience breathlessness during physical exertion (exertional dyspnoea) and sometimes when lying flat (known as positional dyspnoea or orthopnoea). There is evidence that orthopnoea is caused by stimulation of fine nerve endings in the lungs as a result of increased pulmonary capillary pressure, caused by redistribution of fluid between peripheral tissues and the lungs when the patient lies flat. Sometimes, the patient wakes extremely breathless from sleep and has to sit up gasping for breath, a symptom known as paroxysmal nocturnal dyspnoea. In extreme forms, this may be accompanied by a cough productive of white frothy sputum indicative of pulmonary oedema.

The mechanism of exercise-associated dyspnoea is controversial. It may be partly due to the same mechanism as orthopnoea, with increased venous return from exercising muscles raising left atrial pressure. However, in exercising patients, the sensation of breathlessness does not always correlate well with directly measured left atrial pressure. Other factors such as reduced arterial blood oxygen saturation and alteration of muscle function in chronic heart failure have also been invoked as mechanisms contributing to the sensation of breathlessness.

A commonly used classification of exercise tolerance in heart failure is that proposed by the New York Heart Association (NYHA). This is commonly used in clinical trials and has been shown to correlate with prognosis. For practical purposes, when taking the history, it is helpful to record the symptoms verbatim. Reflecting the patient’s description of symptoms over time can be particularly useful in assessing progress. Left ventricular failure may present with associated wheezing. However, cardiac asthma should always be distinguished from obstructive airways disease; both history and examination should be helpful in distinguishing heart failure from asthma.

Symptoms and signs

New York Heart Association classification of heart failure

Grade I	No symptoms at rest, dyspnoea only on vigorous exertion
Grade II	No symptoms at rest, dyspnoea on moderate exertion
Grade III	May be mild symptoms at rest, dyspnoea on mild exertion, severe dyspnoea on moderate exertion
Grade IV	Significant dyspnoea at rest, severe dyspnoea even on very mild exertion. Patient often bed bound

It can sometimes be difficult to decide whether dyspnoea is caused by heart disease or lung disease. Paroxysmal nocturnal dyspnoea or orthopnoea points more to left ventricular failure, whereas wheezing or productive cough accompanying dyspnoea and risk features for lung disease would favour a pulmonary cause.

Differential diagnosis

Dyspnoea

• Heart failure

• Ischaemic heart disease (atypical or ‘silent’ angina)

• Pulmonary embolism

• Lung disease

• Severe anaemia

Anxiety should always be considered in the differential diagnosis of breathlessness. The pattern described by the patient is different; they might describe the sensation of suddenly feeling the need to take a deep breath unrelated to physical exertion, excessive sighing or a feeling of air hunger.

CHEST PAIN

PALPITATION

Palpitation is defined as abnormal awareness of the heart beat. This may be perceived with exercise, when it is quite normal, or when there is an irregularity of the heart beat. It may be helpful to ask the patient to tap out the heart rhythm on the table. Ask about the duration of the palpitations and whether they end abruptly. In patients with extrasystoles, it is often not the extra beat itself that the patient perceives, but rather the following beat, which is characterised by a longer than usual pause and an excessively forceful beat. The patient may describe a jumping sensation or the feeling that the heart is about to stop. Ask about precipitating factors such as exercise, emotion or foods, in particular tea, coffee, alcohol and chocolates. You should also ask carefully about any medication, particularly over-the-counter decongestants and ‘cold cures’ which often contain sympathomimetic drugs.

Ectopic beats are often more apparent when the background heart rate is slow (e.g. when the patient lies down to rest). Paroxysmal tachycardias are often precipitated by exercise or by particular movements such as stooping down to open a drawer or reaching to remove an item from a high shelf.

Differential diagnosis

Palpitation

• Extrasystoles

• Paroxysmal atrial fibrillation

• Paroxysmal supraventricular tachycardia

• Thyrotoxicosis

• Perimenopausal

The need to treat an arrhythmia is usually dictated by its haemodynamic effects. Enquire whether the arrhythmia is simply a transient inconvenience or whether the patient has to stop their activity and perhaps even lie down. Cardiac arrhythmias may cause loss of consciousness (cardiac syncope).

Many patients with paroxysmal tachycardia learn to use a modified Valsalva manoeuvre to terminate an attack. This might be achieved by forcibly exhaling with the nose and the mouth held shut or even by head immersion in cold water. Some patients with tachycardia describe a period of excessive urination following the palpitation. This is due to the release of atrial natriuretic hormone (ANP) during the tachycardia.

SYNCOPE (FAINTING, BLACKOUTS)

Syncope is defined as loss of consciousness resulting from a transient failure of blood supply to the brain. The presentation is readily confused with certain forms of epilepsy. Key features in the history that distinguish cardiogenic syncope from epilepsy includes lack of warning or aura, colour change (patients look pale during the event and flushed upon recovery due to hyperaemia) and rapid recovery. Remember that generalised convulsions can also occur following cerebral anoxia if the blood supply to the brain is interrupted for long enough. Common causes of syncope include simple fainting (vasovagal syncope), its variants such as micturition and cough syncope, postural hypotension, vertebrobasilar insufficiency and cardiac arrhythmias, particularly intermittent heart block.

Simple fainting is caused by a vagally mediated bradycardia combined with sudden reflex vasodilatation. It is usually caused by a combination of diminished venous return (e.g. standing still on a hot parade ground), coupled with increased sympathic drive caused by excitement, fear or disgust. Malignant vasovagal syncope is a rare disorder characterised by an exaggerated tendency to faint, resulting in recurrent episodes of unexpected syncope. Micturition syncope characteristically occurs at night in middle-aged or elderly men with a degree of prostatic obstruction, in whom the fall in venous return is caused by straining to empty the bladder accompanied by the sympathic stimulation of the consequences of not doing so. Cough syncope is an exaggerated vagal response to violent coughing and, uncommonly, is a cause of syncope in patients with chronic lung disease.

The Stokes–Adams attack is a term used by some physicians to describe cardiogenic syncope. It was originally defined as syncope due to cortical hypoperfusion caused by transient asystole or a ventricular tachyarrhythmia.

Differential diagnosis

Stokes–Adams versus epilepsy

Stokes–Adams	Epilepsy
No aura or warning Transient loss of consciousness	Aura often present Prolonged loss of consciousness
Pale during attack Rapid recovery Hot flush on recovery	Tonic/clonic phases Prolonged recovery/drowsy No hot flush on recovery