Cardiovascular disease gives rise to a relatively limited
range of symptoms. Differential diagnosis depends on
careful analysis of the factors that provoke symptoms,
the subtle differences in how they are described by the
patient, the clinical findings and appropriate investigations.
A close relationship between symptoms and exercise
is the hallmark of heart disease. The New York
Heart Association (NYHA) functional classification is
used to grade disability
Chest pain is a common presentation of cardiac disease
but can also be a manifestation of anxiety or disease
of the respiratory, musculoskeletal or gastrointestinal
systems (see Box below). Some patients deny
‘pain’ in favour of ‘discomfort’ but the significance
remains the same.
Characteristics of cardiac pain
Several key characteristics help to distinguish cardiac
pain from that of other causes (Fig. ). Diagnosis
Typical ischaemic cardiac pain. Characteristic hand
gestures used to describe cardiac pain. Typical radiation of pain is shown
in the schematic.
may be difficult and it is helpful to classify pain as
typical, atypical or non-cardiac chest pain, based on the
balance of evidence (Fig. ).
• Site. Cardiac pain is typically located in the centre
of the chest because of the derivation of the nerve
supply to the heart and mediastinum.
Identifying ischaemic cardiac pain: the ‘balance’ of evidence.
• Radiation. Ischaemic cardiac pain may radiate to
the neck, jaw, and upper or even lower arms.
Occasionally, cardiac pain may be experienced
only at the sites of radiation or in the back. Pain
situated over the left anterior chest and radiating
laterally is unlikely to be due to cardiac ischaemia
and may have many causes, including pleural or
lung disorders, musculoskeletal problems and
• Character. Cardiac pain is typically dull, constricting,
choking or ‘heavy’, and is usually described as
squeezing, crushing, burning or aching but not
sharp, stabbing, pricking or knife-like. The sensation
can be described as breathlessness. Patients often
emphasise that it is a discomfort rather than a pain.
They typically use characteristic hand gestures (e.g.
open hand or clenched fist) when describing
ischaemic pain (see Fig.).
• Provocation. Anginal pain occurs during (not
after) exertion and is promptly relieved (in less
than 5 minutes) by rest. The pain may also be
precipitated or exacerbated by emotion but tends
to occur more readily during exertion, after a large
meal or in a cold wind. In crescendo or unstable
angina, similar pain may be precipitated by
minimal exertion or at rest. The increase in venous
return or preload induced by lying down may also
be sufficient to provoke pain in vulnerable patients
(decubitus angina). The pain of MI may be
preceded by a period of stable or unstable angina
but often occurs de novo. In contrast, pleural or
pericardial pain is usually described as a ‘sharp’ or
‘catching’ sensation that is exacerbated by
breathing, coughing or movement. Pain associated
with a specific movement (bending, stretching,
turning) is likely to be musculoskeletal in origin.
• Onset. The pain of MI typically takes several
minutes or even longer to develop; similarly, angina
builds up gradually in proportion to the intensity of
exertion. Pain that occurs after rather than during
exertion is usually musculoskeletal or psychological
in origin. The pain of aortic dissection, massive
pulmonary embolism or pneumothorax is usually
very sudden or instantaneous in onset.
• Associated features. The pain of MI, massive
pulmonary embolism or aortic dissection is often
accompanied by autonomic disturbance, including
sweating, nausea and vomiting. Breathlessness, due
to pulmonary congestion arising from transient
ischaemic left ventricular dysfunction, is often a
prominent and occasionally the dominant feature of
MI or angina (angina equivalent). Breathlessness
may also accompany any of the respiratory causes
of chest pain and can be associated with cough,
wheeze or other respiratory symptoms.
Gastrointestinal disorders, such as gastrooesophageal
reflux, peptic ulceration or biliary colic,
may present with chest pain but effort-related
‘indigestion’ is usually due to heart disease.
Differential diagnosis of chest pain
Common causes of chest pain are listed in Box.
Psychological aspects of chest pain
Emotional distress is a common cause of atypical or noncardiac
chest pain. This diagnosis should be considered
if there are features of anxiety and the pain lacks a
predictable relationship with exercise. However, the
prospect of heart disease is a frightening experience,
particularly when it has been responsible for the death
of a close friend or relative; psychological and organic
features therefore often coexist. Anxiety may amplify
the effects of organic disease and can create a very confusing
picture. Patients who believe they are suffering
from heart disease are sometimes afraid to take exercise
and this may make it difficult to establish their true
effort tolerance; assessment may also be complicated by
the impact of physical deconditioning.
Myocarditis and pericarditis
Pain is characteristically felt retrosternally, to the left of
the sternum, or in the left or right shoulder, and typically
varies in intensity with movement and the phase of respiration.
The pain is described as ‘sharp’ and may ‘catch’
the patient during inspiration, coughing or lying flat;
there may be a history of a prodromal viral illness.
Mitral valve prolapse
Sharp left-sided chest pain that is suggestive of a
problem may be a feature of mitral
valve prolapse .
This pain is severe, sharp and tearing, is often felt in or
penetrating through to the back, and is typically very
abrupt in onset . The pain follows the path of the
This can mimic the pain of angina very closely, is sometimes
precipitated by exercise and may be relieved by
nitrates. However, it is usually possible to elicit a history
relating chest pain to supine posture or eating, drinking
or oesophageal reflux. It often radiates to the interscapular
region and dysphagia may be present.
Patients with reversible airways obstruction, such as
asthma, may describe exertional chest tightness that is
relieved by rest. This may be difficult to distinguish from
ischaemic chest tightness. Bronchospasm may be associated
with wheeze, atopy and cough .
Musculoskeletal chest pain
This is a common problem that is very variable in site
and intensity but does not usually fall into any of the
patterns described above. The pain may vary with
posture or movement of the upper body and is sometimes
accompanied by local tenderness over a rib or
costal cartilage. There are numerous causes, including
arthritis, costochondritis, intercostal muscle injury and
Coxsackie viral infection (epidemic myalgia or Bornholm
disease). Many minor soft tissue injuries are related
to everyday activities, such as driving, manual work and
sport. The differential diagnosis of peripheral or pleural
chest pain .
Initial evaluation of suspected cardiac pain
A careful history is crucial in determining whether pain
is cardiac or not. Although the physical findings and
subsequent investigations may help to confirm the
diagnosis, they are of more value in determining the
nature and extent of any underlying heart disease,
the risk of a serious adverse event, and the best course
Effort-related chest pain is the hallmark of angina pectoris
or ‘choking in the chest’ (Fig. ). The reproducibility,
predictability and relationship to physical
exertion (and occasionally emotion) of the chest pain are
Pathophysiology, clinical features and risk assessment of patients with stable or unstable coronary heart disease.
the most important features. The duration of symptoms
should be noted because patients with recent-onset
angina are at greater risk than those with long-standing
and unchanged symptoms.
Physical examination is often normal but may reveal
evidence of risk factors (e.g. xanthoma indicating hyperlipidaemia),
left ventricular dysfunction (e.g. dyskinetic
apex beat, gallop rhythm), other manifestations of arterial
disease (e.g. bruits, signs of peripheral vascular
disease) and unrelated conditions that may exacerbate
angina (e.g. anaemia, thyroid disease). Stable angina is
usually a symptom of coronary artery disease but may
be a manifestation of other forms of heart disease, particularly
aortic valve disease and hypertrophic cardiomyopathy.
In patients with angina in whom a murmur
is found, echocardiography should be performed.
A full blood count, fasting blood glucose, lipids,
thyroid function tests and a 12-lead ECG are the most
important baseline investigations. Exercise testing may
confirm the diagnosis and also identify high-risk patients
who require further investigation and treatment .
CT coronary angiography is very useful to exclude the
presence of coronary artery disease where doubt exists.
Acute coronary syndromes
Prolonged, severe cardiac chest pain may be due to
unstable angina (which comprises recent-onset limiting
angina, rapidly worsening or crescendo angina, and
angina at rest) or acute MI; these are known collectively
as the acute coronary syndromes. Although there may
be a history of antecedent chronic stable angina, an
episode of chest pain at rest is often the first presentation
of coronary artery disease. Diagnosis depends on analysis
of the character of the pain and its associated features.
Physical examination may reveal signs of important
comorbidity, such as peripheral or cerebrovascular
disease, autonomic disturbance (pallor or sweating) and
complications (arrhythmia or heart failure).
Patients presenting with symptoms consistent with
an acute coronary syndrome require urgent evaluation
because there is a high risk of avoidable complications,
such as sudden death and MI. Signs of haemodynamic
compromise (hypotension, pulmonary oedema), ECG
changes (ST segment elevation or depression) and biochemical
markers of cardiac damage, such as elevated
troponin I or T, are powerful indicators of short-term
risk. A 12-lead ECG is mandatory and is the most useful
method of initial triage (Fig. ). The release of
Summary of treatment for acute coronary syndrome (ACS). *Not required following PCI. Amended from SIGN 93.(ACE = angiotensin-converting enzyme; GP = glycoprotein; LMW = low molecular weight; PCI = percutaneous coronary intervention).
markers such as creatine kinase, troponin and myoglobin
is relatively slow but can help guide immediate
management and treatment.
If the diagnosis is unclear, patients with a suspected
acute coronary syndrome should be observed in hospital.
Repeated ECG recordings are valuable, particularly
if obtained during an episode of pain. Plasma troponin
concentrations should be measured at presentation
and, if normal, repeated 6–12 hours after the onset of
symptoms or hospital admission. New ECG changes or
an elevated plasma troponin concentration confirm the
diagnosis of an acute coronary syndrome.
If the pain has not recurred, troponin concentrations
are not elevated and there are no new ECG changes, the
patient may be discharged from hospital. At this stage,
an exercise test or CT coronary angiogram may help
diagnose underlying coronary artery disease.
Dyspnoea of cardiac origin may vary in severity from an
uncomfortable awareness of breathing to a frightening
sensation of ‘fighting for breath’. The sensation of dyspnoea
originates in the cerebral cortex .
There are several causes of cardiac dyspnoea: acute
left heart failure, chronic heart failure, arrhythmia and
angina equivalent (Box ).
Acute left heart failure
Acute left heart failure may be triggered by a major
event, such as MI, in a previously healthy heart, or by a
relatively minor event, such as the onset of atrial
fibrillation, in a diseased heart. An increase in the left
ventricular diastolic pressure causes the pressure in the
LA, pulmonary veins and pulmonary capillaries to rise.
When the hydrostatic pressure of the pulmonary capillaries
exceeds the oncotic pressure of plasma (about
25–30 mmHg), fluid moves from the capillaries into
alveoli. This stimulates respiration through a series of
autonomic reflexes, producing rapid shallow respiration.
Congestion of the bronchial mucosa may cause
wheeze (cardiac asthma).
Acute pulmonary oedema is a terrifying experience
because of the sensation of ‘fighting for breath’. Sitting
upright or standing may provide some relief by helping
to reduce congestion at the apices of the lungs. The
patient may be unable to speak and is typically distressed,
agitated, sweaty and pale. Respiration is rapid,
with recruitment of accessory muscles, coughing and
wheezing. Sputum may be profuse, frothy and bloodstreaked
or pink. Extensive crepitations and rhonchi are
usually audible in the chest and there may also be signs
of right heart failure.
Chronic heart failure
Chronic heart failure is the most common cardiac cause
of chronic dyspnoea. Symptoms may first present on
moderate exertion, such as walking up a steep hill, and
may be described as a difficulty in ‘catching my breath’.
As heart failure progresses, the dyspnoea is provoked
by less exertion and, ultimately, the patient may be
breathless walking from room to room, washing, dressing
or trying to hold a conversation. Other symptoms
• Orthopnoea. Lying down increases the venous return
to the heart and provokes breathlessness. Patients
may prop themselves up with pillows to prevent this.
• Paroxysmal nocturnal dyspnoea. In patients with
severe heart failure, fluid shifts from the interstitial
tissues of the peripheries into the circulation within
1–2 hours of lying down. Pulmonary oedema
supervenes, causing the patient to wake and sit
upright, profoundly breathless.
• Cheyne–Stokes respiration. This cyclical pattern of
respiration is due to impaired responsiveness of the
respiratory centre to carbon dioxide and occurs in
severe left ventricular failure. The pattern of slowly
diminishing respiration, leading to apnoea,
followed by progressively increasing respiration
and hyperventilation, may be accompanied by a
sensation of breathlessness and panic during the
period of hyperventilation. The Cheyne–Stokes
cycle length is a function of the circulation time.
The condition can also occur in diffuse cerebral
atherosclerosis, stroke or head injury, and may be
exaggerated by sleep, barbiturates and opiates.
Any arrhythmia may cause breathlessness but usually
only does so if the heart is structurally abnormal, such
as with the onset of atrial fibrillation in a patient with
Breathlessness is a common feature of angina. Patients
will sometimes describe chest tightness as ‘breathlessness’.
However, myocardial ischaemia may also
induce true breathlessness by provoking transient left
ventricular dysfunction or heart failure. When breathlessness
is the dominant or sole feature of myocardial
ischaemia, it is known as ‘angina equivalent’. A
history of chest tightness, the close correlation with
exercise, and objective evidence of myocardial ischaemia
from stress testing may all help to establish the
Acute circulatory failure (cardiogenic shock)
‘Shock’ is used to describe the clinical syndrome that
develops when there is critical impairment of tissue perfusion
due to some form of acute circulatory failure.
There are numerous causes of shock. The important
Some common causes of cardiogenic shock.
features and causes (Fig.) of acute heart failure or cardiogenic shock are
The downward spiral of cardiogenic shock.
Shock in acute MI is due to left ventricular dysfunction
in more than 70% of cases. However, it may also be due
to infarction of the RV and a variety of mechanical complications,
including tamponade (due to infarction and
rupture of the free wall), an acquired ventricular septal
defect (due to infarction and rupture of the septum) and
acute mitral regurgitation (due to infarction or rupture
of the papillary muscles).
Severe myocardial systolic dysfunction causes a fall
in cardiac output, BP and coronary perfusion pressure.
Diastolic dysfunction causes a rise in left ventricular
end-diastolic pressure, pulmonary congestion and
oedema, leading to hypoxaemia that worsens myocardial
ischaemia. This is further exacerbated by peripheral
vasoconstriction. These factors combine to create the
‘downward spiral’ of cardiogenic shock (Fig. ).
Hypotension, oliguria, confusion and cold, clammy
peripheries are the manifestations of a low cardiac
output, whereas breathlessness, hypoxaemia, cyanosis
and inspiratory crackles at the lung bases are typical
features of pulmonary oedema. A chest X-ray (see
Fig. ) may reveal signs of pulmonary congestion
Radiological features of heart failure. A Chest X-ray of
a patient with pulmonary oedema. B Enlargement of lung base showing
septal or ‘Kerley B’ lines (arrow).
when clinical examination is normal. If necessary, a
Swan–Ganz catheter can be used to measure the pulmonary
artery wedge pressure and to guide fluid replacement.
The findings can be used to categorise patients
with acute MI into four haemodynamic subsets (Box).
Those with cardiogenic shock should be considered
for immediate coronary revascularisation.
The viable myocardium surrounding a fresh infarct
may contract poorly for a few days and then recover.
This phenomenon is known as myocardial stunning
and means that acute heart failure should be treated
intensively because overall cardiac function may
Acute massive pulmonary embolism
This may complicate leg or pelvic vein thrombosis and
usually presents with sudden collapse. Bedside
echocardiography may demonstrate a small, underfilled,
vigorous LV with a dilated RV; it is sometimes
possible to see thrombus in the right ventricular outflow
tract or main pulmonary artery. CT pulmonary angiography
usually provides a definitive diagnosis.
This is due to a collection of fluid or blood in the pericardial
sac, compressing the heart; the effusion may be
small and is very occasionally less than 100 mL. Sudden
deterioration (Box) may be due to bleeding into the
pericardial space. Tamponade may complicate any form
of pericarditis but can be caused by malignant disease.
Other causes include trauma and rupture of the free wall
of the myocardium following MI.
An ECG may show features of the underlying disease,
such as pericarditis or acute MI. When there is a large
pericardial effusion, the ECG complexes are small and
there may be electrical alternans: a changing axis with
alternate beats caused by the heart swinging from side
to side in the pericardial fluid. A chest X-ray shows
an enlarged globular heart but can look normal. Echocardiography
is the best way of confirming the diagnosis
and helps to identify the optimum site for aspiration
of the fluid. Prompt recognition of tamponade is
important because the patient usually responds dramatically
to percutaneous pericardiocentesis or
Valvular heart disease
Acute left ventricular failure and shock may be due to
the sudden onset of aortic regurgitation, mitral regurgitation
or prosthetic valve dysfunction (Box ).
The clinical diagnosis of acute valvular dysfunction
is sometimes difficult. Murmurs are often unimpressive
because there is usually a tachycardia and a low cardiac
output. Transthoracic echocardiography will establish
the diagnosis in most cases; however, transoesophageal
echocardiography is sometimes required, especially in
patients with prosthetic mitral valves.
Patients with acute valve failure usually require
cardiac surgery and should be referred for urgent assessment
in a cardiac centre.
Aortic dissection may lead to shock by causing aortic
regurgitation, coronary dissection, tamponade or blood
Heart failure describes the clinical syndrome that develops
when the heart cannot maintain adequate output, or
can do so only at the expense of elevated ventricular
filling pressure. In mild to moderate forms of heart
failure, cardiac output is normal at rest and only becomes
impaired when the metabolic demand increases during
exercise or some other form of stress. In practice, heart
failure may be diagnosed when a patient with significant
heart disease develops the signs or symptoms of a
low cardiac output, pulmonary congestion or systemic
Almost all forms of heart disease can lead to heart
failure. An accurate aetiological diagnosis (Box) is
important because treatment of the underlying cause
may reverse heart failure or prevent its progression.
Heart failure is most common in the elderly. The
prevalence of heart failure rises from 1% in those aged
50–59 years to over 10% in those aged 80–89 years. In
the UK, most patients admitted to hospital with heart
failure are more than 70 years old; they remain hospitalised
for a week or more and may be left with chronic
disability. The most common aetiology is coronary
artery disease and myocardial infarction.
Although the outlook depends, to some extent, on the
underlying cause of the problem, untreated heart failure
carries a poor prognosis; approximately 50% of patients
with severe heart failure due to left ventricular dysfunction
will die within 2 years, because of either pump
failure or malignant ventricular arrhythmias.
Cardiac output is determined by preload (the volume
and pressure of blood in the ventricles at the end of
diastole), afterload (the volume and pressure of blood in
the ventricles during systole) and myocardial contractility;
this is the basis of Starling’s Law (Fig.).
Starling’s Law. Normal (A), mild (B), moderate (C) and
severe (D) heart failure. Ventricular performance is related to the degree of
myocardial stretching. An increase in preload (end-diastolic volume,
end-diastolic pressure, filling pressure or atrial pressure) will therefore
enhance function; however, overstretching causes marked deterioration. In
heart failure, the curve moves to the right and becomes flatter. An increase
in myocardial contractility or a reduction in afterload will shift the curve
upwards and to the left (green arrow).
In patients without valvular disease, the primary
abnormality is impairment of ventricular myocardial
function, leading to a fall in cardiac output. This can
occur because of impaired systolic contraction, impaired
diastolic relaxation, or both. This activates counterregulatory
neurohumoral mechanisms that, in normal
physiological circumstances, would support cardiac
function but, in the setting of impaired ventricular function,
can lead to a deleterious increase in both afterload
and preload (Fig.). A vicious circle may be established
because any additional fall in cardiac output will
cause further neurohumoral activation and increasing
peripheral vascular resistance.
Stimulation of the renin–angiotensin–aldosterone
system leads to vasoconstriction, sodium and water
retention, and sympathetic nervous system activation.
This is mediated by angiotensin II, a potent constrictor
of arterioles, in both the kidney and the systemic circulation
(see Fig. ). Activation of the sympathetic
Neurohumoral activation and compensatory mechanisms in heart failure. There is a vicious circle in progressive heart failure.
nervous system may initially sustain cardiac output
through increased myocardial contractility (inotropy)
and heart rate (chronotropy). Prolonged sympathetic
stimulation also causes negative effects, including
cardiac myocyte apoptosis, hypertrophy and focal myocardial
necrosis. Sympathetic stimulation also causes
peripheral vasoconstriction and arrhythmias. Sodium
and water retention is promoted by the release of aldosterone,
endothelin-1 (a potent vasoconstrictor peptide
with marked effects on the renal vasculature) and, in
severe heart failure, antidiuretic hormone (ADH). Natriuretic
peptides are released from the atria in response to
atrial stretch, and act as physiological antagonists
to the fluid-conserving effect of aldosterone.
After MI, cardiac contractility is impaired and neurohumoral
activation causes hypertrophy of non-infarcted
segments, with thinning, dilatation and expansion of the
Infarct expansion and ventricular remodelling.
Full-thickness Ml causes thinning and stretching of the infarcted segment
(infarct expansion), which leads to increased wall stress with progressive
dilatation and hypertrophy of the remaining ventricle (ventricular
infarcted segment (remodelling; see Fig. ).
This leads to further deterioration in ventricular function
and worsening heart failure.
Pulmonary and peripheral oedema occurs because of
high left and right atrial pressures, respectively; this
is compounded by sodium and water retention, caused
by impairment of renal perfusion and by secondary
Types of heart failure
Left, right and biventricular heart failure
The left side of the heart comprises the functional unit
of the LA and LV, together with the mitral and aortic
valves; the right heart comprises the RA, RV, and tricuspid
and pulmonary valves.
• Left-sided heart failure. There is a reduction in left
ventricular output and an increase in left atrial and
pulmonary venous pressure. An acute increase in
left atrial pressure causes pulmonary congestion or
pulmonary oedema; a more gradual increase in left
atrial pressure, as occurs with mitral stenosis, leads
to reflex pulmonary vasoconstriction, which
protects the patient from pulmonary oedema. This
increases pulmonary vascular resistance and causes
pulmonary hypertension, which can, in turn, impair
right ventricular function.
• Right-sided heart failure. There is a reduction in right
ventricular output and an increase in right atrial
and systemic venous pressure. Causes of isolated
right heart failure include chronic lung disease (cor
pulmonale), pulmonary embolism and pulmonary
• Biventricular heart failure. Failure of the left and right
heart may develop because the disease process,
such as dilated cardiomyopathy or ischaemic heart
disease, affects both ventricles or because disease of
the left heart leads to chronic elevation of the left
atrial pressure, pulmonary hypertension and right
Diastolic and systolic dysfunction
Heart failure may develop as a result of impaired myocardial
contraction (systolic dysfunction) but can also be
due to poor ventricular filling and high filling pressures
stemming from abnormal ventricular relaxation (diastolic
dysfunction). The latter is caused by a stiff, noncompliant
ventricle and is commonly found in patients
with left ventricular hypertrophy. Systolic and diastolic
dysfunction often coexist, particularly in patients with
coronary artery disease.
A large arteriovenous shunt, beri-beri ), severe
anaemia or thyrotoxicosis can occasionally cause heart
failure due to an excessively high cardiac output.
Acute and chronic heart failure
Heart failure may develop suddenly, as in MI, or gradually,
as in progressive valvular heart disease. When
there is gradual impairment of cardiac function, several
compensatory changes may take place.
The term ‘compensated heart failure’ is sometimes
used to describe the condition of those with impaired
cardiac function, in whom adaptive changes have prevented
the development of overt heart failure. A minor
event, such as an intercurrent infection or development
of atrial fibrillation, may precipitate overt or acute heart
failure (Box ). Acute left heart failure occurs, either
de novo or as an acute decompensated episode, on a
background of chronic heart failure: so-called acute-onchronic
Acute left heart failure
Acute de novo left ventricular failure presents with
a sudden onset of dyspnoea at rest that rapidly
progresses to acute respiratory distress, orthopnoea and
prostration. The precipitant, such as acute MI, is often
apparent from the history.
The patient appears agitated, pale and clammy. The
peripheries are cool to the touch and the pulse is rapid.
Inappropriate bradycardia or excessive tachycardia
should be identified promptly, as this may be the precipitant
for the acute episode of heart failure. The BP is
usually high because of sympathetic nervous system
activation, but may be normal or low if the patient is in
The jugular venous pressure (JVP) is usually elevated,
particularly with associated fluid overload or right heart
failure. In acute de novo heart failure, there has been no
time for ventricular dilatation and the apex is not displaced.
A ‘gallop’ rhythm, with a third heart sound,
is heard quite early in the development of acute leftsided
heart failure. A new systolic murmur may
signify acute mitral regurgitation or ventricular septal
rupture. Auscultatory findings in pulmonary oedema
are crepitations at the lung bases, or throughout the
lungs if pulmonary oedema is severe. Expiratory wheeze
often accompanies this.
Acute-on-chronic heart failure will have additional
features of long-standing heart failure (see below).
Potential precipitants, such as an upper respiratory tract
infection or inappropriate cessation of diuretic medication,
should be identified.
Chronic heart failure
Patients with chronic heart failure commonly follow a
relapsing and remitting course, with periods of stability
and episodes of decompensation, leading to worsening
symptoms that may necessitate hospitalisation. The
clinical picture depends on the nature of the underlying
heart disease, the type of heart failure that it has evoked,
and the neurohumoral changes that have developed (see
Clinical features of left and right heart failure.
(JVP = jugular venous pressure)
Low cardiac output causes fatigue, listlessness and a
poor effort tolerance; the peripheries are cold and the BP
is low. To maintain perfusion of vital organs, blood flow
is diverted away from skeletal muscle and this may contribute
to fatigue and weakness. Poor renal perfusion
leads to oliguria and uraemia.
Pulmonary oedema due to left heart failure presents
as above and with inspiratory crepitations over the lung
bases. In contrast, right heart failure produces a high JVP
with hepatic congestion and dependent peripheral
oedema. In ambulant patients, the oedema affects the
ankles, whereas, in bed-bound patients, it collects
around the thighs and sacrum. Ascites or pleural effusion
may occur (see Fig. ). Heart failure is not the
only cause of oedema (Box ).
Chronic heart failure is sometimes associated with
marked weight loss (cardiac cachexia), caused by a combination
of anorexia and impaired absorption due to
gastrointestinal congestion, poor tissue perfusion due to
a low cardiac output, and skeletal muscle atrophy due
In advanced heart failure, the following may occur:
• Renal failure is caused by poor renal perfusion due
to low cardiac output and may be exacerbated by
diuretic therapy, angiotensin-converting enzyme
(ACE) inhibitors and angiotensin receptor blockers.
• Hypokalaemia may be the result of treatment with
potassium-losing diuretics or hyperaldosteronism
caused by activation of the renin–angiotensin
system and impaired aldosterone metabolism
due to hepatic congestion. Most of the body’s
potassium is intracellular and there may be
substantial depletion of potassium stores, even
when the plasma concentration is in the reference
• Hyperkalaemia may be due to the effects of drugs
which promote renal resorption of potassium,
in particular the combination of ACE inhibitors
(or angiotensin receptor blockers) and
mineralocorticoid receptor antagonists. These effects
are amplified if there is renal dysfunction due to
low cardiac output or atherosclerotic renal vascular
• Hyponatraemia is a feature of severe heart failure
and is a poor prognostic sign. It may be caused by
diuretic therapy, inappropriate water retention due
to high ADH secretion, or failure of the cell
membrane ion pump.
• Impaired liver function is caused by hepatic venous
congestion and poor arterial perfusion, which
frequently cause mild jaundice and abnormal liver
function tests; reduced synthesis of clotting factors
can make anticoagulant control difficult.
• Thromboembolism. Deep vein thrombosis and
pulmonary embolism may occur due to the effects
of a low cardiac output and enforced immobility.
Systemic emboli occur in patients with atrial
fibrillation or flutter, or with intracardiac thrombus
complicating conditions such as mitral stenosis, MI
or left ventricular aneurysm.
• Atrial and ventricular arrhythmias are very common
and may be related to electrolyte changes (e.g.
hypokalaemia, hypomagnesaemia), the underlying
cardiac disease, and the pro-arrhythmic effects of
sympathetic activation. Atrial fibrillation occurs in
approximately 20% of patients with heart failure
and causes further impairment of cardiac function.
Sudden death occurs in up to 50% of patients with
heart failure and is often due to a ventricular
arrhythmia. Frequent ventricular ectopic beats and
runs of non-sustained ventricular tachycardia are
common findings in patients with heart failure and
are associated with an adverse prognosis.
Serum urea, creatinine and electrolytes, haemoglobin,
thyroid function, ECG and chest X-ray may help to
establish the nature and severity of the underlying heart
disease and detect any complications. Brain natriuretic
peptide (BNP) is elevated in heart failure and is a marker
of risk; it is useful in the investigation of patients with
breathlessness or peripheral oedema.
Echocardiography is very useful and should be considered
in all patients with heart failure in order to:
• determine the aetiology
• detect hitherto unsuspected valvular heart
disease, such as occult mitral stenosis, and other
conditions that may be amenable to specific
• identify patients who will benefit from long-term
drug therapy, e.g. ACE inhibitors (see below).
(continuous positive airways pressure (CPAP) of
5–10 mmHg) by a tight-fitting facemask results in a
more rapid clinical improvement.
• Administer nitrates, such as IV glyceryl trinitrate
(10–200 μg/min or buccal glyceryl trinitrate 2–5 mg,
titrated upwards every 10 minutes), until clinical
improvement occurs or systolic BP falls to less than
• Administer a loop diuretic, such as furosemide
(50–100 mg IV).
The patient should initially be kept rested, with continuous
monitoring of cardiac rhythm, BP and pulse
oximetry. Intravenous opiates must be used sparingly in
distressed patients, as they may cause respiratory
depression and exacerbation of hypoxaemia and
If these measures prove ineffective, inotropic agents
may be required to augment cardiac output, particularly
in hypotensive patients. Insertion of an intra-aortic
balloon pump may be beneficial in patients with acute
cardiogenic pulmonary oedema and shock.
Syncope and presyncope
The term ‘syncope’ refers to sudden loss of consciousness
due to reduced cerebral perfusion. ‘Presyncope’
refers to lightheadedness in which the individual thinks
he or she may black out. Syncope affects around 20% of
the population at some time and accounts for more than
5% of hospital admissions. Dizziness and presyncope
are very common in old age . Symptoms are disabling,
undermine confidence and independence, and
can affect an individual’s ability to work or to drive.
There are three principal mechanisms that underlie
recurrent presyncope or syncope:
• cardiac syncope due to mechanical cardiac
dysfunction or arrhythmia
• neurocardiogenic syncope, in which an abnormal
autonomic reflex causes bradycardia and/or
• postural hypotension, in which physiological
peripheral vasoconstriction on standing is impaired,
lead to hypotension.
Loss of consciousness can also be caused by non-cardiac
pathology, such as epilepsy, cerebrovascular ischaemia
or hypoglycaemia (Fig.).
The differential diagnosis of syncope and presyncope.
History-taking, from the patient or a witness, is the
key to establishing a diagnosis. Attention should be
paid to potential triggers (e.g. medication, exertion,
posture), the victim’s appearance (e.g. colour, seizure
activity), the duration of the episode and the speed
of recovery (Box ). Cardiac syncope is usually
sudden but can be associated with premonitory lightheadedness,
palpitation or chest discomfort. The blackout
is usually brief and recovery rapid. Neurocardiogenic
syncope will often be associated with a situational
trigger, and the patient may experience flushing,
nausea and malaise for several minutes afterwards.
Patients with seizures do not exhibit pallor, may have
abnormal movements, usually take more than 5 minutes
to recover and are often confused. A history of rotational
vertigo is suggestive of a labyrinthine or vestibular
disorder . The pattern and description of
the patient’s symptoms should indicate the probable
mechanism and help to determine subsequent investigations
(Fig. 18.30). Postural hypotension is normally
obvious from the history, with presyncope or, less commonly,
syncope, occurring within a few seconds of
A simple guide to the investigation and diagnosis of recurrent presyncope and syncope.
Lightheadedness may occur with many arrhythmias,
but blackouts (Stokes–Adams attacks) are usually
due to profound bradycardia or malignant ventricular
tachyarrhythmias. The 12-lead ECG may show evidence
of conducting system disease (e.g. sinus bradycardia,
atrioventricular block, bundle branch block or axis deviation),
which would predispose a patient to bradycardia,
but the key to establishing a diagnosis is to obtain an
ECG recording while symptoms are present. Since minor
rhythm disturbances are common, especially in old age,
symptoms must occur at the same time as a recorded
arrhythmia before a diagnosis can be made. Ambulatory
ECG recordings are helpful only if symptoms occur
several times per week. Patient-activated ECG recorders
are useful for examining the rhythm in patients with
recurrent dizziness but are not useful in assessing
sudden blackouts. When these investigations fail to
establish a cause in patients with presyncope or syncope,
an implantable ECG recorder can be sited subcutaneously
over the upper left chest. This device continuously
records the cardiac rhythm and will activate automatically
if extreme bradycardia or tachycardia occurs. The
ECG memory can also be tagged by the patient, using
a hand-held activator. Stored ECGs can be accessed by
the implanting centre, using a telemetry device in a
clinic, or using a home monitoring system via an
Structural heart disease
Severe aortic stenosis and hypertrophic obstructive cardiomyopathy
can lead to lightheadedness or syncope on
exertion. This is caused by profound hypotension due to
a fall in cardiac output, or failure to increase output
during exertion, coupled with exercise-induced peripheral
vasodilatation. Severe coronary artery disease can
produce the same symptoms because of ischaemic left
ventricular dysfunction. Exertional arrhythmias also
occur in these patients.
This encompasses a family of syndromes in which
bradycardia and/or hypotension occur because of a
series of abnormal autonomic reflexes. The two main
conditions are hypersensitive carotid sinus syndrome
and malignant vasovagal syncope.
This is the collective name given to some variants of
neurocardiogenic syncope that occur in the presence of
identifiable triggers (e.g. cough syncope, micturition
This is normally triggered by a reduction in venous
return due to prolonged standing, excessive heat or a
large meal. It is mediated by the Bezold–Jarisch reflex,
in which a combination of sympathetic activation, and
reduced venous return due to an impaired vasoconstrictor
response to standing, leads to vigorous contraction
of relatively under-filled ventricles. This stimulates ventricular
mechanoreceptors, producing parasympathetic
(vagal) activation and sympathetic withdrawal, causing
bradycardia, vasodilatation or both. Head-up tilt-table
testing is a provocation test used to establish the diagnosis,
and involves positioning the patient supine on a
padded table that is then tilted to an angle of 60–70° for
up to 45 minutes, while the ECG and BP responses are
monitored. A positive test is characterised by bradycardia
(cardio-inhibitory response) and/or hypotension
(vasodepressor response) associated with typical symptoms.
Initial management involves lifestyle modification
(salt supplementation and avoiding prolonged standing,
dehydration or missing meals). In resistant cases, drug
therapy can be tried, although efficacy is inconsistent in
clinical trials. Fludrocortisone (causes sodium and water
retention and expands plasma volume), disopyramide
(a vagolytic agent) or midodrine (a vasoconstrictor
α-adrenoceptor agonist) may be helpful. Beta-blockers
(inhibit the initial sympathetic activation) are seldom
effective and are rarely used. In patients with resistant
vasovagal syncope in which bradycardia is the predominant
response, a dual-chamber pacemaker can be useful.
Patients with a urinary sodium excretion of less than
170 mmol/day may respond to salt loading.
Hypersensitive carotid sinus syndrome
Hypersensitive carotid sinus syndrome (HCSS) causes
presyncope or syncope because of reflex bradycardia
and vasodilatation. Carotid baroreceptors are involved
in BP regulation and are activated by increased BP,
resulting in a vagal discharge that causes a compensatory
drop in BP. In HCSS, the baroreceptor is sensitive
to external pressure (e.g. during neck movement or if a
tight collar is worn), so that pressure over the carotid
artery causes an inappropriate and intense vagal discharge.
The diagnosis can be established by monitoring
the ECG and BP during carotid sinus pressure. This
manoeuvre should not be attempted in patients with a
carotid bruit or with a history of cerebrovascular disease
because of the risk of embolic stroke. A positive cardioinhibitory
response is defined as a sinus pause of
3 seconds or more; a positive vasodepressor response is
defined as a fall in systolic BP of more than 50 mmHg.
Carotid sinus pressure will produce positive findings in
about 10% of elderly individuals but less than 25% of
these experience spontaneous syncope. Symptoms
should not therefore be attributed to HCSS unless they
are reproduced by carotid sinus pressure. Dual-chamber
pacemaker implantation usually prevents syncope in
patients with the more common cardio-inhibitory
This is caused by a failure of normal postural compensatory
mechanisms. Relative hypovolaemia (often due to
excessive diuretic therapy), sympathetic degeneration
(diabetes mellitus, Parkinson’s disease, ageing) and drug
therapy (vasodilators, antidepressants) can all cause or
aggravate the problem. Treatment is often ineffective;
however, withdrawing unnecessary medication and
advising the patient to wear graduated elastic stockings
and to get up slowly may be helpful. Fludrocortisone,
which can expand blood volume through sodium and
water retention, may be of value.