The cardiovascular system


Anatomy and physiology

The heart comprises two muscular pumps working in series, covered in a serous sac (pericardium) that allows free movement with each heart beat and respiration ( Fig. 4.1 ). The right heart (right atrium and ventricle) pumps deoxygenated blood returning from the systemic veins into the pulmonary circulation at relatively low pressures. The left heart (left atrium and ventricle) receives blood from the lungs and pumps it round the body to the tissues at higher pressures ( Fig. 4.2 ). Atrioventricular valves (tricuspid on the right side, mitral on the left) separate the atria from the ventricles. The pulmonary valve on the right side of the heart and the aortic valve on the left separate the ventricles from the pulmonary and systemic arterial systems, respectively. Cardiac contraction is coordinated by specialised groups of cells. The cells in the sinoatrial node normally act as the cardiac pacemaker. Subsequent spread of impulses through the heart ensures that atrial contraction is complete before ventricular contraction (systole) begins. At the end of systole the ventricles relax and the atrioventricular valves open, allowing them to refill with blood from the atria (diastole).

Fig. 4.1

The heart chambers and valves.

Fig. 4.2

Normal resting pressures (mmHg) in the heart and great vessels.

dias., diastolic; LA, left atrium; LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle; sys., systolic.

The history

Common presenting symptoms

Cardiovascular disease may present with a number of diverse symptoms; non-cardiac causes must also be considered ( Box 4.1 ).


Common symptoms of heart disease

Symptom Cardiovascular causes Other causes
Chest discomfort Myocardial infarction
Aortic dissection
Oesophageal spasm
Musculoskeletal pain
Breathlessness Heart failure
Valvular disease
Pulmonary embolism
Pulmonary hypertension
Respiratory disease
Palpitation Tachyarrhythmias
Ectopic beats
Syncope/presyncope Arrhythmias
Postural hypotension
Aortic stenosis
Hypertrophic cardiomyopathy
Atrial myxoma
Simple faints
Oedema Heart failure
Constrictive pericarditis
Venous stasis
Nephrotic syndrome
Liver disease

Chest pain

Intermittent chest pain

Chest pain due to intermittent myocardial ischaemia (angina pectoris) is typically a dull discomfort, often described as a tight or pressing ‘band-like’ sensation akin to a heavy weight. It tends to be felt diffusely across the anterior chest and may radiate down one or both arms and into the throat, jaw or teeth. In stable angina (caused by chronic narrowing in one or more coronary arteries), episodes of pain are precipitated by exertion and may occur more readily when walking in cold or windy weather, after a large meal or while carrying a heavy load; the pain is promptly relieved by rest and/or sublingual glyceryl nitrate (GTN) spray, and typically lasts for less than 10 minutes. The degree of physical exertion required to precipitate symptoms is a better guide to disease severity than the intensity of discomfort ( Box 4.2 ). In unstable angina (caused by a sudden severe narrowing in a coronary artery), there is usually an abrupt onset or worsening of chest pain episodes that may occur on minimal exertion or at rest. It may be difficult to distinguish between angina and non-cardiac causes of episodic chest pain, such as oesophageal pain or musculoskeletal problems ( Box 4.3 ). The latter may occur at any site over the chest, often vary with posture or specific movements (such as twisting or turning), and may be associated with tenderness to palpation.


Canadian Cardiovascular Society: functional classification of stable angina

Grade Description
1 Ordinary physical activity, such as walking and climbing stairs, does not cause angina. Angina with strenuous, rapid or prolonged exertion at work or during recreation
2 Slight limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphill, walking or climbing stairs after meals, in cold, in wind, or when under emotional stress, or only during the few hours after awakening
3 Marked limitation of ordinary physical activity. Walking 1–2 blocks on the level and climbing less than one flight in normal conditions
4 Inability to carry on any physical activity without discomfort; angina may be present at rest


Cardiovascular causes of chest pain and their characteristics

Angina Myocardial infarction Aortic dissection Pericardial pain Oesophageal pain
S ite Retrosternal Retrosternal Interscapular/retrosternal Retrosternal or left-sided Retrosternal or epigastric
O nset Progressive increase in intensity over 1–2 minutes Rapid over a few minutes Very sudden Gradual; postural change may suddenly aggravate Over 1–2 minutes; can be sudden (spasm)
C haracter Constricting, heavy Constricting, heavy Tearing or ripping Sharp, ‘stabbing’, pleuritic Gripping, tight or burning
R adiation Sometimes arm(s), neck, epigastrium Often to arm(s), neck, jaw, sometimes epigastrium Back, between shoulders Left shoulder or back Often to back, sometimes to arms
A ssociated features Breathlessness Sweating, nausea, vomiting, breathlessness, feeling of impending death (angor animi) Sweating, syncope, focal neurological signs, signs of limb ischaemia, mesenteric ischaemia Flu-like prodrome, breathlessness, fever Heartburn, acid reflux
T iming Intermittent, with episodes lasting 2–10 minutes Acute presentation; prolonged duration Acute presentation; prolonged duration Acute presentation; variable duration Intermittent, often at night-time; variable duration
E xacerbating/relieving factors Triggered by emotion, exertion, especially if cold, windy
Relieved by rest, nitrates
‘Stress’ and exercise rare triggers, usually spontaneous
Not relieved by rest or nitrates
No manœuvres relieve pain
Sitting up/lying down may affect intensity
NSAIDs help
Lying flat/some foods may trigger
Not relieved by rest; nitrates sometimes relieve
S everity Mild to moderate Usually severe Very severe Can be severe Usually mild but oesophageal spasm can mimic myocardial infarction
Cause Coronary atherosclerosis, aortic stenosis, hypertrophic cardiomyopathy Plaque rupture and coronary artery occlusion Thoracic aortic dissection rupture Pericarditis (usually viral, also post myocardial infarction) Oesophageal spasm, reflux, hiatus hernia

NSAIDs, non-steroidal anti-inflammatory drugs.

Ask about:

  • site, onset, severity and character of the pain, and whether the pain radiates anywhere

  • associated symptoms such as breathlessness

  • aggravating and relieving factors, especially their relationship to exertion

  • frequency and duration of symptoms, and any recent change in pattern

  • degree of limitation caused by symptoms.

Acute chest pain

Myocardial infarction causes symptoms that are similar to, but more severe and prolonged than, those of angina pectoris. Associated features include restlessness, breathlessness and a feeling of impending death ( angor animi ). Autonomic stimulation may result in sweating, pallor, nausea and vomiting.

Pericardial pain is typically a constant anterior central chest pain that may radiate to the shoulders. It tends to be sharp or stabbing in character, exacerbated by inspiration or lying down, and relieved by sitting forwards. It is caused by inflammation of the pericardium secondary to viral infection, connective tissue disease or myocardial infarction, or after surgery, catheter ablation or radiotherapy.

Aortic dissection (a tear in the intima of the aorta) is usually associated with abrupt onset of very severe, tearing chest pain that can radiate to the back (typically the interscapular region) and may be associated with profound autonomic stimulation. If the tear involves the cranial or upper limb arteries, there may be associated syncope, stroke or upper limb pulse asymmetry. Predisposing factors include hypertension and connective tissue disorders, such as Marfan’s syndrome (see Fig. 3.21A–D ).

As with intermittent chest pain, explore the characteristics of the pain, and ask specifically about associated symptoms that may guide you to a likely diagnosis, such as interscapular pain, sweating, nausea, vomiting, syncope or neurological features ( Box 4.3 ).

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.


Some mechanisms and causes of heart failure

Mechanism Cause
Reduced ventricular contractility (systolic dysfunction) Myocardial infarction
Dilated cardiomyopathy, e.g. genetic, idiopathic, alcohol excess, cytotoxic drugs, peripartum cardiomyopathy
Impaired ventricular filling (diastolic dysfunction) Left ventricular hypertrophy
Constrictive pericarditis
Hypertrophic or restrictive cardiomyopathy
Increased metabolic and cardiac demand (rare) Thyrotoxicosis
Arteriovenous fistulae
Paget’s disease
Valvular or congenital lesions Mitral and/or aortic valve disease
Tricuspid and/or pulmonary valve disease (rare)
Ventricular septal defect
Patent ductus arteriosus

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.


New York Heart Association classification of heart failure symptom severity

Class Description
I No limitations. Ordinary physical activity does not cause undue fatigue, dyspnoea or palpitation (asymptomatic left ventricular dysfunction)
II Slight limitation of physical activity. Such patients are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnoea or angina pectoris (symptomatically ‘mild’ heart failure)
III Marked limitation of physical activity. Less than ordinary physical activity will lead to symptoms (symptomatically ‘moderate’ heart failure)
IV Symptoms of congestive heart failure are present, even at rest. With any physical activity, increased discomfort is experienced (symptomatically ‘severe’ heart failure)

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.

Fig. 4.3

Paroxysmal nocturnal dyspnoea.

In acute dyspnoea, ask about:

  • duration of onset

  • background symptoms of exertional dyspnoea and usual exercise tolerance

  • 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:

  • relationship between symptoms and exertion

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

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

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


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 ).


Descriptions of arrhythmias

Extrasystoles Sinus tachycardia Supraventricular tachycardia Atrial fibrillation Ventricular tachycardia
S ite
O nset Sudden Gradual Sudden, with ‘jump’ Sudden Sudden
C haracter ‘Jump’, missed beat or flutter Regular, fast, ‘pounding’ Regular, fast Irregular, usually fast; slower in elderly Regular, fast
R adiation
A ssociated features Nil Anxiety Polyuria, lightheadedness, chest tightness Polyuria, breathlessness
Syncope uncommon
Presyncope, syncope, chest tightness
T iming Brief A few minutes Minutes to hours Variable Variable
E xacerbating/relieving factors Fatigue, caffeine, alcohol may trigger
Often relieved by walking (increases sinus rate)
Exercise or anxiety may trigger Usually at rest, trivial movements, e.g. bending, may trigger
Vagal manœuvres may relieve
Exercise or alcohol may trigger; often spontaneous Exercise may trigger; often spontaneous
S everity Mild (usually) Mild to moderate Moderate to severe Very variable, may be asymptomatic Often severe

Ask about:

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

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

  • precipitants for symptoms or relieving factors

  • associated symptoms: presyncope, syncope or chest pain

  • 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:

  • previous myocardial infarction or cardiac surgery

  • associated syncope or severe chest pain

  • family history of sudden death

  • Wolff–Parkinson–White syndrome

  • 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:

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

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

  • time to recovery of full consciousness and normal cognition

  • current driving status, including occupational driving.

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

  • exact nature of symptoms and associated features such as palpitation

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

  • frequency of episodes and impact on lifestyle

  • possible contributing medications, such as antihypertensive agents ( Box 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.


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).

Fig. 4.4

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.

Past medical history

Obtaining a detailed record of any previous cardiac disease, investigations and interventions is essential ( Box 4.8 ). You may need to consult the patient, family members and electronic case records.


Key elements of the past cardiac history

Ischaemic heart disease Heart failure Valvular disease
Baseline symptoms Exertional angina? If so, ascertain functional limitation (see Box 4.2 )/response to GTN spray Dyspnoea, fatigue, ankle swelling
Record usual functional status (see Box 4.5 )
Often asymptomatic
Exertional dyspnoea (common), chest pain or syncope
Major events Previous myocardial infarction/unstable angina Hospitalisation for decompensated heart failure
Ventricular arrhythmias
Infective endocarditis
Previous rheumatic fever
Investigations Coronary angiography (invasive or computed tomography): presence, extent and severity of coronary artery disease
Exercise electrocardiogram (or other stress test): evidence of inducible ischaemia?
Exercise capacity and symptoms
Echocardiogram (± cardiac magnetic resonance imaging): left ventricular size, wall thickness and systolic function; valvular disease; right ventricular function Echocardiogram (transthoracic ± transoesophageal): nature and severity of valve lesion; ventricular size and function
Procedures Percutaneous coronary intervention (angioplasty and stenting)
Coronary artery bypass graft surgery
Implantable cardioverter–defibrillator
Cardiac resynchronisation therapy
Surgical valve repair or replacement (note whether mechanical or bioprosthetic)
Transcatheter valve procedures

GTN, glyceryl trinitrate.

Also ask about:

  • conditions associated with increased risk of vascular disease such as hypertension, diabetes mellitus and hyperlipidaemia

  • rheumatic fever or heart murmurs during childhood

  • potential causes of bacteraemia in patients with suspected infective endocarditis, such as skin infection, recent dental work, intravenous drug use or penetrating trauma

  • systemic disorders with cardiovascular manifestations such as connective tissue diseases (pericarditis and Raynaud’s phenomenon), Marfan’s syndrome (aortic dissection) and myotonic dystrophy (atrioventricular block).

Drug history

Drugs may cause or aggravate symptoms such as breathlessness, chest pain, oedema, palpitation or syncope (see Box 4.7 ). Ask about ‘over-the-counter’ purchases, such as non-steroidal anti-inflammatory drugs (NSAIDs) and alternative and herbal medicines, as these may have cardiovascular actions.

Family history

Many cardiac disorders such as cardiomyopathies have a genetic component. Ask about premature coronary artery disease in first-degree relatives (< 60 years in a female or < 55 years in a male); sudden unexplained death at a young age may raise the possibility of a cardiomyopathy or inherited arrhythmia. Patients with venous thrombosis may have inherited thrombophilia, such as a factor V Leiden mutation. Familial hypercholesterolaemia is associated with premature arterial disease.

Social history

Smoking is the strongest risk factor for coronary and peripheral arterial disease. Take a detailed smoking history ( p. 14 ). Alcohol can induce atrial fibrillation and, in excess, is associated with obesity, hypertension and dilated cardiomyopathy. Recreational drugs such as cocaine and amphetamines can cause arrhythmias, chest pain, occlusive and aneurysmal peripheral arterial disease and even myocardial infarction. Heart disease may have important consequences for employment. Patients with limiting exertional symptoms may struggle to perform jobs that entail a high degree of physical activity. In addition, some diagnoses such as ischaemic heart disease or cardiac arrhythmia may impact on eligibility for certain occupations that have implications for public safety, such as commercial drivers and pilots.

The physical examination

Tailor the sequence and extent of examination to the patient’s condition. If you suspect that the person may be unstable, deteriorating or critically unwell (breathless, distressed, cyanosed or obtunded, for example), adopt an ABCDE approach initially ( p. 341 ) and defer detailed examination until stabilised. In stable patients, perform a detailed and comprehensive physical examination.

General examination

Look at the patient’s general appearance. Do they look unwell, frightened or distressed? Are there any signs of breathlessness or cyanosis? Is the patient overweight or cachectic? Are there any features of conditions associated with cardiovascular disease such as Marfan’s ( p. 30 ), Down’s ( p. 36 ) or Turner’s syndrome ( p. 36 ), or ankylosing spondylitis ( p. 262 )?

Conclude by examining the entire skin surface for petechiae, checking the temperature ( p. 345 ) and performing urinalysis ( p. 246 ). Fever is a feature of infective endocarditis and pericarditis, and may occur after myocardial infarction. Urinalysis is necessary to check for haematuria (endocarditis, vasculitis), glucosuria (diabetes) and proteinuria (hypertension and renal disease).


Examination sequence

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

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

  • 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 ).

    Fig. 4.5

    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.

  • 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 ).

    Fig. 4.6

    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.

  • Examine the palmar aspect of the hands for:

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

    • 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.


Examination sequence

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

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

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

  • 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.

Arterial pulses

The palpable pulse in an artery reflects the pressure wave generated by the ejection of blood into the circulation from the left ventricle.

When taking a pulse, assess:

  • rate: the number of pulses occurring per minute

  • rhythm: the pattern or regularity of pulses

  • volume: the perceived degree of pulsation

  • character: an impression of the pulse waveform or shape.

The rate and rhythm of the pulse are usually determined at the radial artery; use the larger pulses (brachial, carotid or femoral) to assess the pulse volume and character.

Examination sequence

Radial pulse

  • Place the pads of your index and middle fingers over the right wrist, just lateral to the flexor carpi radialis tendon ( Fig. 4.7A ).

    Fig. 4.7

    The radial, brachial and carotid pulses.

    A Locating and palpating the radial pulse. B Feeling for a collapsing radial pulse. C Assessing the brachial pulse. D Locating the right carotid pulse with the fingers.

  • Assess the rhythm of the pulse and count the number over 15 seconds; multiply by 4 to obtain the rate in beats per minute (bpm).

  • To detect a collapsing pulse: first, check that the patient has no shoulder or arm pain or restriction on movement; next, feel the pulse with the base of your fingers, then raise the patient’s arm vertically above their head ( Fig. 4.7B ).

  • Palpate both radial pulses simultaneously, assessing any delay between the two.

Brachial pulse

  • Use your index and middle fingers to palpate the pulse in the antecubital fossa, just medial to the biceps tendon ( Fig. 4.7C ). Assess the character and volume of the pulse.

Carotid pulse

  • Explain what you are going to do.

  • With the patient semirecumbent, place the tips of your fingers between the larynx and the anterior border of the sternocleidomastoid muscle ( Fig. 4.7D ).

  • Palpate the pulse gently to avoid a vagal reflex, and never assess both carotids simultaneously.

  • Listen for bruits over both carotid arteries, using the diaphragm of your stethoscope in held inspiration.

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 ).


Causes of abnormal pulse rate or rhythm

Abnormality Sinus rhythm Arrhythmia
Fast rate (tachycardia, > 100 bpm) Exercise

  • Sympathomimetics, e.g. salbutamol

  • Vasodilators

Atrial fibrillation
Atrial flutter
Supraventricular tachycardia
Ventricular tachycardia
Slow rate (bradycardia, < 60 bpm) Sleep
Athletic training

  • Beta-blockers

  • Digoxin

  • Verapamil, diltiazem

Carotid sinus hypersensitivity
Sick sinus syndrome
Second-degree heart block
Complete heart block
Irregular pulse Sinus arrhythmia
Atrial extrasystoles
Ventricular extrasystoles
Atrial fibrillation
Atrial flutter with variable response
Second-degree heart block with variable response

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.

Fig. 4.8

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.


Haemodynamic effects of respiration

Inspiration Expiration
Pulse/heart rate Accelerates Slows
Systolic blood pressure Falls (up to 10 mmHg) Rises
Jugular venous pressure Falls Rises
Second heart sound Splits Fuses


Common causes of atrial fibrillation

  • Hypertension

  • Heart failure

  • Myocardial infarction

  • Thyrotoxicosis

  • Alcohol-related heart disease

  • Mitral valve disease

  • Infection, e.g. respiratory, urinary

  • Following surgery, especially cardiothoracic surgery

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 ).


Causes of increased pulse volume


  • Exercise

  • Pregnancy

  • Advanced age

  • Increased environmental temperature


  • Hypertension

  • Fever

  • Thyrotoxicosis

  • Anaemia

  • Aortic regurgitation

  • Paget’s disease of bone

  • Peripheral atrioventricular shunt

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.

Fig. 4.9

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 ).

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.

Fig. 4.11

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.

Blood pressure

Blood pressure (BP) is a measure of the pressure that the circulating blood exerts against the arterial walls. Systolic pressure is the maximal pressure that occurs during ventricular contraction (systole). During ventricular filling (diastole), arterial pressure is maintained at a lower level by the elasticity and compliance of the vessel wall. The lowest value (diastolic pressure) occurs immediately before the next cycle.

BP is usually measured using a sphygmomanometer ( Fig. 4.12 ). In certain situations, such as the intensive care unit, it is measured invasively using an indwelling intra-arterial catheter connected to a pressure sensor.

Dec 29, 2019 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on The cardiovascular system

Full access? Get Clinical Tree

Get Clinical Tree app for offline access