Chest pain

Dyspnoea (breathlessness)

Heart failure is the most common cardiovascular cause of both acute and chronic dyspnoea ( Box 4.4 ). Other cardiovascular causes of acute breathlessness include pulmonary embolism and arrhythmias. Patients with acute heart failure and pulmonary oedema (accumulation of fluid in the alveoli) usually prefer to be upright, while patients with massive pulmonary embolism are often more comfortable lying flat and may faint (syncope) if made to sit upright.

Exertional dyspnoea is the symptomatic hallmark of chronic heart failure. The New York Heart Association grading system is used to assess the degree of symptomatic limitation caused by the exertional breathlessness of heart failure ( Box 4.5 ). Dyspnoea caused by myocardial ischaemia is known as ‘angina equivalent’. It may occur instead of, or with, chest discomfort, especially in patients who are elderly or who have diabetes. It has identical precipitants to angina and may be relieved by GTN.

Orthopnoea, dyspnoea on lying flat, may occur in patients with heart failure, where it signifies advanced disease or incipient decompensation. Lying flat increases venous return and in patients with left ventricular impairment may precipitate pulmonary oedema. The severity can be graded by the number of pillows used at night: ‘three-pillow orthopnoea’, for example. Paroxysmal nocturnal dyspnoea is caused by the same mechanism, resulting in sudden breathlessness that wakes the patient from sleep ( Fig. 4.3 ). Patients may choke or gasp for air, sit on the edge of the bed and open windows in an attempt to relieve their distress. It may be confused with asthma, which can also cause night-time dyspnoea, chest tightness, cough and wheeze, but patients with heart failure may also produce frothy white or blood-stained sputum.

Paroxysmal nocturnal dyspnoea.

In acute dyspnoea, ask about:

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  duration of onset

  
  
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  background symptoms of exertional dyspnoea and usual exercise tolerance

  
  
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  associated symptoms: chest pain, syncope, palpitation or respiratory symptoms (such as cough, sputum, wheeze or haemoptysis; p. 79 ).

In patients with chronic symptoms, ask about:

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  relationship between symptoms and exertion

  
  
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  degree of limitation caused by symptoms and their impact on everyday activities

  
  
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  effect of posture on symptoms and/or episodes of nocturnal breathlessness

  
  
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  associated symptoms: ankle swelling, cough, wheeze or sputum.

Palpitation

Palpitation is an unexpected or unpleasant awareness of the heart beating in the chest. Detailed history taking can help to distinguish the different types of palpitation ( Box 4.6 ).

Ask about:

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  nature of the palpitation: is the heart beat rapid, forceful or irregular? Can the patient tap it out?

  
  
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  timing of symptoms: speed of onset and offset; frequency and duration of episodes

  
  
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  precipitants for symptoms or relieving factors

  
  
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  associated symptoms: presyncope, syncope or chest pain

  
  
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  history of underlying cardiac disease.

Healthy people are occasionally aware of their heart beating with normal (sinus) rhythm, especially after exercise or in stressful situations such as when waiting for an interview or examination. The sensation is often more common in bed at night and slim people may notice it when lying on their left side.

Ectopic beats (extrasystoles) are a benign cause of palpitation at rest and are abolished by exercise. The premature ectopic beat produces a small stroke volume and an impalpable impulse due to incomplete left ventricular filling. The subsequent compensatory pause leads to ventricular overfilling and a forceful contraction with the next beat. Accordingly, patients often describe ‘missed beats’, sometimes followed by a particularly strong heart beat (‘jolt’ or ‘thump’).

Supraventricular tachycardia produces sudden paroxysms of rapid, regular palpitation that can sometimes be terminated with vagal stimulation using Valsalva breathing manœuvres or carotid sinus pressure. It often affects young patients with no other underlying cardiac disease. Ventricular tachycardia can produce similar symptoms but is more commonly associated with presyncope or syncope, and tends to affect patients with cardiomyopathy or previous myocardial infarction.

High-risk features that increase the likelihood of a life-threatening arrhythmia such as ventricular tachycardia include:

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  previous myocardial infarction or cardiac surgery

  
  
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  associated syncope or severe chest pain

  
  
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  family history of sudden death

  
  
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  Wolff–Parkinson–White syndrome

  
  
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  significant structural heart disease such as hypertrophic cardiomyopathy or aortic stenosis.

Syncope and presyncope

Syncope is a transient loss of consciousness due to transient cerebral hypoperfusion. Causes include postural hypotension, neurocardiogenic syncope, arrhythmias and mechanical obstruction to cardiac output. The same mechanisms may lead to a sensation of lightheadedness and impending loss of consciousness without progressing to actual loss of consciousness (presyncope). The main differential diagnosis of syncope is seizure ( p. 122 ), while lightheadedness and presyncope must be distinguished from dizziness or vertigo due to non-cardiovascular causes ( p. 123 ).

In patients who present with syncope, ask about:

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  circumstances of the event and any preceding symptoms: palpitation, chest pain, lightheadedness, nausea, tinnitus, sweating or visual disturbance

  
  
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  duration of loss of consciousness, appearance of the patient while unconscious and any injuries sustained (a detailed witness history is extremely helpful)

  
  
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  time to recovery of full consciousness and normal cognition

  
  
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  current driving status, including occupational driving.

In patients with presyncopal symptoms of lightheadedness or dizziness, ask about:

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  exact nature of symptoms and associated features such as palpitation

  
  
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  precipitants for symptoms, such as postural change, prolonged standing, intense emotion or exertion

  
  
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  frequency of episodes and impact on lifestyle

  
  
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  possible contributing medications, such as antihypertensive agents ( Box 4.7 ).

  
  
  
  

  4.7

  
  

  Symptoms related to medication

  
  

  
  

  
  

  
  

  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  

  Symptom	Medication
  Angina	Aggravated by thyroxine or drug-induced anaemia, e.g. aspirin or NSAIDs
  Dyspnoea	Beta-blockers in patients with asthma Exacerbation of heart failure by beta-blockers, some calcium channel antagonists (verapamil, diltiazem), NSAIDs
  Palpitation	Tachycardia and/or arrhythmia from thyroxine, β 2 stimulants, e.g. salbutamol, digoxin toxicity, hypokalaemia from diuretics, tricyclic antidepressants
  Syncope/presyncope	Vasodilators, e.g. nitrates, alpha-blockers, ACE inhibitors and angiotensin II receptor antagonists Bradycardia from rate-limiting agents, e.g. beta-blockers, some calcium channel antagonists (verapamil, diltiazem), digoxin, amiodarone
  Oedema	Glucocorticoids, NSAIDs, some calcium channel antagonists, e.g. nifedipine, amlodipine

   

  
  

  
  

  ACE, angiotensin-converting enzyme; NSAIDs, non-steroidal anti-inflammatory drugs.

  
  

Postural hypotension, a fall of more than 20 mmHg in systolic blood pressure on standing, may lead to syncope or presyncope. It can be caused by hypovolaemia, drugs ( Box 4.7 ) or autonomic neuropathy and is common in the elderly, affecting up to one-third of individuals over 65 years.

In simple faint and other forms of reflex syncope or presyncope, abnormal autonomic reflexes produce a sudden slow heart rate (bradycardia) and/or vasodilatation. These may be triggered in healthy people forced to stand for a long time in a warm environment or subject to painful or emotional stimuli, such as the sight of blood. There is typically a prodrome of lightheadedness, tinnitus, nausea, sweating and facial pallor, and a darkening of vision from the periphery as the retinal blood supply (the most oxygen-sensitive part of the nervous system) is reduced. The person then slides to the floor, losing consciousness. When laid flat to aid cerebral circulation the individual wakes up, often flushing from vasodilatation and nauseated or even vomiting due to vagal overactivity. If the person is held upright by misguided bystanders, continued cerebral hypoperfusion delays recovery and may lead to a seizure and a mistaken diagnosis of epilepsy. In patients with hypersensitive carotid sinus syndrome, pressure over the carotid sinus may lead to reflex bradycardia and syncope.

Arrhythmias can cause syncope or presyncope. The most common cause is bradyarrhythmia caused by sinoatrial disease or atrioventricular block: Stokes–Adams attacks. Rate-limiting drugs are a common cause of bradyarrhythmia. Supraventricular tachyarrhythmias, like atrial fibrillation, rarely cause syncope whereas ventricular tachycardia often causes syncope or presyncope, especially in patients with impaired left ventricular function.

Mechanical obstruction to left ventricular outflow, including severe aortic stenosis and hypertrophic cardiomyopathy, can cause syncope or presyncope, especially on exertion, when cardiac output cannot meet the increased metabolic demand. Massive pulmonary embolism can lead to syncope by obstructing outflow from the right ventricle; associated features are usually apparent and include acute dyspnoea, chest pain and hypoxia. Cardiac tumours, such as atrial myxoma, and thrombosis or failure of prosthetic heart valves are rare causes of syncope.

Oedema

Excess fluid in the interstitial space causes oedema (tissue swelling). It is usually gravity-dependent and so is seen especially around the ankles, or over the sacrum in patients lying in bed. Unilateral lower limb oedema may occur in deep vein thrombosis ( p. 70 ). Heart failure is a common cause of bilateral lower limb oedema but other causes include chronic venous disease, vasodilating calcium channel antagonists (such as amlodipine) and hypoalbuminaemia. An elevated jugular venous pressure strongly suggests a cardiogenic cause of oedema. Enquire about other symptoms of fluid overload, including dyspnoea, orthopnoea and abdominal distension.

Other symptoms of cardiac disease

Infective endocarditis, microbial infection of a heart valve, frequently presents with non-specific symptoms, including weight loss, tiredness, fever and night sweats.

Embolisation of intracardiac thrombus, tumour (such as atrial myxoma) or infective ‘vegetations’ ( Fig. 4.4 ) may produce symptoms of stroke ( p. 123 ), acute limb ischaemia (p. 65) or acute mesenteric ischaemia (p. 66).

Cardiac sources of systemic embolism: echocardiographic images.

A A large apical thrombus in the left ventricle (arrow) . B An atrial myxoma attached to the interatrial septum (arrow) . C A vegetation on the mitral valve (arrow) in infective endocarditis. Because all of these lesions are located within the left side of the heart, emboli would flow to the systemic (or coronary) circulation. Conversely, emboli from the right side of the heart would flow to the pulmonary circulation.

Advanced heart failure may result in either abdominal distension due to ascites, or weight loss and muscle wasting (‘cardiac cachexia’) due to a prolonged catabolic state.

Hands

Examination sequence

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  Feel the temperature of the hands and measure capillary refill time ( p. 343 ).

  
  
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  Examine the hands for tobacco staining (see Fig. 5.8 ), skin crease pallor (anaemia) or peripheral cyanosis.

  
  
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  Look at the nails for finger clubbing ( p. 24 ) and for splinter haemorrhages: linear, reddish-brown marks along the axis of the fingernails and toenails ( Fig. 4.5B ).

  
  

  
  

  
  

  

  
  

  
  

  Peripheral signs that may be present in infective endocarditis.

  
  

  A Janeway lesions on the hypothenar eminence (arrows) . B Splinter haemorrhages. C Osler’s nodes. D Roth’s spot on fundoscopy. E Petechial haemorrhages on the conjunctiva.

  
  

  (B and E) From Walker BR, Colledge NR, Ralston SR, Penman ID, eds. Davidson’s Principles and Practice of Medicine. 22nd edn. Edinburgh: Churchill Livingstone; 2014. (D) From Forbes CD, Jackson WF. Color Atlas of Clinical Medicine. 3rd edn. Edinburgh: Mosby; 2003.

  
  
  
  
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  Examine the extensor surface of the hands for tendon xanthomata: hard, slightly yellowish masses over the extensor tendons of the hand from lipid deposits ( Fig. 4.6B ).

  
  

  
  

  
  

  

  
  

  
  

  Features of hyperlipidaemia.

  
  

  A Xanthelasmata. B Tendon xanthomata. C Corneal arcus.

  
  

  (B) From Swartz M. Textbook of Physical Diagnosis. 6th edn. Philadelphia: Saunders; 2009. (C) From Kanski J. Clinical Diagnosis in Ophthalmology. London: Mosby; 2006.

  
  
  
  
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  Examine the palmar aspect of the hands for:

  
  
  
  
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    Janeway lesions: painless, blanching red macules on the thenar/hypothenar eminences ( Fig. 4.5A )

    
    
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    Osler’s nodes: painful raised erythematous lesions, typically on the pads of the fingers ( Fig. 4.5C ).

  
  

The hands usually feel dry and warm at ambient temperature. Normal capillary refill time is 2 seconds or less. Cool extremities and prolonged capillary refill time signify impaired peripheral perfusion, which may occur in shock ( p. 343 ) or chronic conditions associated with a low cardiac output state (as in severe aortic stenosis, mitral stenosis or pulmonary hypertension).

One or two isolated splinter haemorrhages from trauma are common in healthy individuals, especially in manual workers. Splinter haemorrhages ( Fig. 4.5B ) are found in infective endocarditis and some vasculitic disorders. A petechial rash (caused by vasculitis), most often present on the legs and conjunctivae ( Fig. 4.5E ), is a transient finding in endocarditis and can be confused with the rash of meningococcal disease. Janeway lesions and Osler’s nodes ( Fig. 4.5A and C ) are features of endocarditis but are rare in the modern era.

Tendon xanthomata ( Fig. 4.6 ) are a sign of familial hypercholesterolaemia, a genetic disorder associated with severe elevations in serum cholesterol and premature coronary artery disease.

Face

Examination sequence

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  Look in the mouth for central cyanosis: a purplish blue discoloration of the lips and underside of the tongue (see Fig. 5.11 ).

  
  
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  Examine the eyelids for xanthelasmata: soft, yellowish plaques found periorbitally and on the medial aspect of the eyelids ( Fig. 4.6A ).

  
  
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  Look at the iris for corneal arcus: a creamy yellow discoloration at the boundary of the iris and cornea ( Fig. 4.6C ).

  
  
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  Examine the fundi ( p. 164 ) for features of hypertension ( p. 165 ), diabetes ( p. 165 ) or Roth’s spots (flame-shaped retinal haemorrhages with a ‘cotton-wool’ centre; Fig. 4.5D ).

Cardiac causes of central cyanosis include heart failure sufficient to cause pulmonary congestion and oedema impairing gas exchange, or, rarely, congenital heart disease, in which case it is associated with right-to-left shunting and finger clubbing ( p. 24 ).

Xanthelasmata and corneal arcus ( Fig. 4.6A and C ) are associated with hyperlipidaemia but also occur frequently in normolipidaemic patients. The presence of xanthelasma is an independent risk factor for coronary heart disease and myocardial infarction but corneal arcus has no independent prognostic value.

Rate and rhythm

Resting heart rate is normally 50–95 bpm but should be considered in the clinical context. A pulse rate of 40 bpm can be normal in a fit young adult, whereas a pulse rate of 65 bpm may be abnormally low in acute heart failure. Bradycardia is defined as a pulse rate of < 60 bpm; tachycardia is a rate of > 100 bpm. The most common causes of bradycardia are medication, athletic conditioning and sinoatrial or atrioventricular node dysfunction. The most common cause of tachycardia is sinus tachycardia ( Box 4.9 ).

The pulse may be regular or irregular ( Box 4.9 ). Sinus rhythm is regular ( Fig. 4.8A ) but heart rate varies with the respiratory cycle, particularly in children, young adults or athletes (sinus arrhythmia). During inspiration, parasympathetic tone falls and the heart rate increases; on expiration, the heart rate decreases ( Box 4.10 ). With intermittent extrasystoles ( Fig. 4.8B ) or second-degree atrioventricular block, there may be an underlying regularity to the pulse, interspersed with periods of irregularity (sometimes referred to as ‘regularly irregular’). In atrial fibrillation the pulse has no appreciable pattern and is often described as ‘irregularly irregular’ ( Fig. 4.8C and Box 4.11 ). The rate in atrial fibrillation depends on the number of beats conducted by the atrioventricular node. Untreated, the ventricular rate may be very fast (up to 200 bpm). The variability of the pulse rate (and therefore ventricular filling) explains why the pulse volume varies and there may be a pulse deficit, with some cycles not felt at the radial artery. The pulse deficit can be calculated by counting the radial pulse rate and subtracting this from the apical heart rate, assessed by auscultation.

Electrocardiogram rhythm strips.

A Sinus rhythm. B Ventricular ectopic beat. C Atrial fibrillation with ‘controlled’ ventricular response. D Atrial flutter: note the regular ‘saw-toothed’ atrial flutter waves at about 300/min. E Ventricular tachycardia, with a ventricular rate of about 200/min.

Volume and character

The ventricles fill during diastole. Longer diastolic intervals are associated with increased stroke volume, which is reflected by increased pulse volume on examination. Abnormalities of pulse volume and character are highly subjective, however, and tend to have poor interobserver agreement.

A large pulse volume is a reflection of a large pulse pressure, which can be physiological or pathological ( Box 4.12 ).

Low pulse volume may result from severe heart failure and conditions associated with inadequate ventricular filling such as hypovolaemia, cardiac tamponade and mitral stenosis. Asymmetric pulses may represent occlusive peripheral arterial disease or stenosis and, rarely, aortic dissection. Coarctation is a congenital narrowing of the aorta, usually distal to the left subclavian artery ( Fig. 4.9 ); it may produce reduced-volume lower limb pulses, which are also delayed relative to the upper limb pulses (radiofemoral delay). In adults, coarctation usually presents with hypertension and heart failure.

Coarctation of the aorta.

Magnetic resonance image showing the typical site of aortic coarctation, just distal to the origin of the left subclavian artery (arrow) . This explains why there is synchrony of the radial pulses but radiofemoral delay.

A slow-rising pulse has a gradual upstroke with a reduced peak occurring late in systole, and is a feature of severe aortic stenosis ( Fig. 4.10 ).

Pulse waveforms.

A collapsing pulse may occur with severe aortic regurgitation. The peak of the pulse wave arrives early and is followed by a rapid fall in pressure ( Fig. 4.10 ) as blood flows back into the left ventricle, resulting in a wide pulse pressure (systolic − diastolic blood pressure > 80 mmHg). This rapid fall imparts the ‘collapsing’ sensation, and is exaggerated by raising the patient’s arm above the level of the heart (see Fig. 4.7B ).

Pulsus bisferiens, an increased pulse with a double systolic peak separated by a distinct mid-systolic dip, is classically produced by concomitant aortic stenosis and regurgitation. Pulsus alternans, beat-to-beat variation in pulse volume with a normal rhythm, may occur in advanced heart failure. Both of these signs are rare, however, and of limited relevance in contemporary practice.

Pulsus paradoxus is an exaggeration of the normal variability of pulse volume with breathing. Pulse volume normally increases in expiration and decreases during inspiration due to intrathoracic pressure changes affecting venous return to the heart. This variability is exaggerated when ventricular diastolic filling is impeded by elevated intrapericardial pressure. This is usually due to accumulation of pericardial fluid (cardiac tamponade; Fig. 4.11 ) but can occur to a lesser extent with pericardial constriction and in acute severe asthma. If suspected, pulsus paradoxus can be confirmed using a blood pressure cuff (see later and Fig. 4.12 ); a fall of > 10 mmHg between the cuff pressure at which Korotkoff sounds appear in expiration only and the cuff pressure at which Korotkoff sounds persist throughout the respiratory cycle is diagnostic.

Clinical and echocardiographic features of cardiac tamponade.

A and B Echocardiographic images taken from the subcostal position at the onset of systole (A) and in early diastole (B). The right ventricle (arrows) is collapsed in the early phase of diastole due to the elevated intrapericardial pressure; this is an important echo finding in tamponade. In both images there is a large pericardial effusion adjacent to the right ventricle. C Clinical features.

JVP, jugular venous pressure.