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Cardiovascular system
baseline. Torsades de pointes may progress to VF. Treatment
is with intravenously administered magnesium sulphate but
the condition is often refractory to this. Antiarrhythmics
may further prolong the QT interval and worsen the condition. Temporary overdrive pacing may be effective.
Ventricular fibrillation
VF is a medical emergency and is the most common arrhythmia in cardiac arrest. Electrical activity in the ventricles becomes completely desynchronized, leading to
mechanical pump failure. Patients should be treated according to the adult advanced life support algorithm for VF/VT
(Fig.27.6).
HINTS AND TIPS
Patients have different interpretations of the word
‘palpitations’. Make sure they are clear with what is
meant. They may mean a fast rate or a sensation of
a single beat, or an awareness of normal heart rate.
Bradycardias
Sinus bradycardia
Sinus bradycardia is defined as a resting pulse rate of less
than 60 per minute. For notes on sinus bradycardia, see
Chapter7.
Fig.27.7 Electrocardiogram of first-degree heart block.
Second-degree heart block—Only some of the atrial impulses are conducted via the AV node. In Wenckebach (Mobitz
type I) heart block, there is progressive widening of the PR interval, culminating in nonconduction through the AV node.
The cycle then repeats (Fig.27.8). Mobitz type II heart block
is intermittent failure of AV conduction (Fig.27.9). This is the
more serious of the two because the block is below the AV
node in the bundle of His, which may lead to third-degree
block. The block occurs in the AV node, and hence escape
rhythms are more stable in Wenckebach block.
Third-degree (complete) heart block—This is complete
dissociation between atrial and ventricular contraction
(Fig.27.10). SA impulses are not propagated to the ventricles.
The ventricular rate assumes a slow ‘escape’ rhythm with a
rate between 30 and 50 bpm. Emergency treatment involves
atropine. If this fails, transcutaneous pacing or isoprenaline,
adrenaline or alternative drugs can be used (see the adult
bradycardia algorithm of the Resuscitation Council). Use of
all negatively chronotropic drugs should be stopped.
Sick sinus syndrome
This is due to irreversible dysfunction of the sinus node, and
can lead to periods of sinus bradycardia with asystole, and
tachycardia. Dual-chamber pacemakers are recommended
by NICE as a treatment option, although they will function
as an atrial pacemaker only if there is no AV conduction
defect.
HINTS AND TIPS
In complete heart block, work out the atrial rate
and the ventricular rate separately by marking them
on a piece of paper. They should both be regular
but have different rates.
Heart block
This refers to aberrant conduction through the heart, and
has three forms: first-, second- and third-degree block. As
the ‘degree of block’ increases, so does the seriousness of
the problem.
First-degree heart block—The ECG shows a prolonged
PR interval (more than 0.2 s) (Fig.27.7). All impulses are
conducted to the ventricles.
Fig.27.6 Electrocardiogram of ventricular fibrillation. Coordinated activity of the ventricles ceases. The electrocardiogram
shows irregular waves of no defined shape. In this trace there are short periods suggestive of ventricular flutter.
Antiarrhythmic drugs
Antiarrhythmics are classified according to the site of their
action (supraventricular, ventricular or both) and their
effects on the action potential (Vaughan Williams classification; Table27.7). Examples of antiarrhythmic drugs are
given next.
178
Arrhythmias
PPPPP
Not conducted to ventricles
P
Absent QRS
PPPP P
PPP(P) PP P
QRS
PR
Fig.27.8 Electrocardiogram of Wenckebach heart block.
Fig.27.9 Electrocardiogram of Mobitz type II heart block showing two P waves for each QRS complex (i.e. 2:1 block).
2727
Fig.27.10 Electrocardiogram of complete heart block. No relationship between atria (P) and ventricles (QRS).
Table27.7 The Vaughan Williams classification of
antiarrhythmic drugs
Class Features
Ia, Ib, Ic Membrane sodium channel blockers
II Antisympathetic nervous system (β-blockers)
III Potassium channel blockers (amiodarone,
IV Calcium channel blockers (excluding
V Other (adenosine, digoxin, magnesium
(e.g. quinidine, lidocaine and flecainide,
respectively)
bretylium, sotalol)
dihydropyridines, e.g. nifedipine)
sulphate)
Supraventricular arrhythmias only
Adenosine—Adenosine is used for terminating SVT. It
is a purine nucleoside which causes transient AV block. It
has a short half-life (<10 s). Side effects include flushing,
arrhythmia, chest pain and bronchospasm. Adenosine is
contraindicated in asthma, decompensated heart failure
and prolonged QT syndromes.
Verapamil—Verapamil is an L-type calcium channel
blocker and an alternative to adenosine. It is negatively
inotropic and interferes with electrical conduction. Side
effects include flushing, headache, dizziness and constipation. Verapamil is contraindicated in bradycardia, severe
left ventricular dysfunction, cardiogenic shock and second
and third-degree heart block. It should not be prescribed
179
Cardiovascular system
with β-blockers, as concurrent use increases the risk of bra-
dycardia and hypotension.
Digoxin—Digoxin is a purified cardiac glycoside (derived from foxgloves) that increases cardiac contractility
(positive inotropic effect) and reduces AV conduction.
Its mechanism of action is not fully understood but is it
thought to work through binding to the Na+/K+-ATPase of
cardiac myocytes, altering Na+ and Ca2+ balance. Its main
role is in treatment of AF, atrial flutter and heart failure. Side
effects include arrhythmias, blurred or yellow vision and
dizziness. It is contraindicated in VT, VF and intermittent
complete and second-degree heart block. Digoxin toxicity
can be dangerous, and the levels should be monitored.
Supraventricular and ventricular arrhythmias
Amiodarone—Amiodarone is effective in both supraventricular and ventricular arrhythmias, with little deleterious effect on haemodynamics. This means it is widely
used in coronary care units in acute settings (e.g. after MI).
Although it is classified as a class III antiarrhythmic, it also
has class Ia, II and IV properties. It has a prolonged halflife of several weeks. It may therefore take some weeks to
achieve steady-state plasma concentration.
It is an iodine-containing compound, and side effects
include hypothyroidism and hyperthyroidism and liver
dysfunction. TFTs and liver function test (LFT) results
should be checked at the baseline and every 6months. It may
cause pulmonary fibrosis, corneal microdeposits (which are
reversible on stopping treatment) and photosensitivity.
β-Blockers—β-Blockers act mainly by attenuating the
effects of the sympathetic nervous system on automaticity
and conductivity within the heart. Sotalol is a β-blocker that
also has class III actions. It is used widely to control paroxysmal AF. β-Blockers are contraindicated in cardiogenic
shock and marked bradycardia. They should be avoided in
patients with asthma.
Flecainide—Flecainide is used to treat a variety of arrhythmias, including AF, SVT and VT. It works by prolonging the action potential. Side effects include arrhythmia,
dizziness and dyspnoea. It is contraindicated in known structural heart disease and left ventricular dysfunction. It should
not be used to control arrhythmias in an acute setting,
Ventricular arrhythmias
Lidocaine—Lidocaine can be used in cardiopulmonary
resuscitation as an alternative to amiodarone if amiodarone
is not available. Side effects include bradycardia, convulsions, hypotension and respiratory depression. It is contraindicated in AV block, severe myocardial depression and SA
disorders.
Magnesium—Magnesium sulphate is indicated as an
emergency treatment for arrhythmias. It is also the treatment of choice for torsades de pointes. In cardiac arrest, it
is indicated in refractory VF in the presence of suspected
hypomagnesaemia or refractory VT in the presence of suspected hypomagnesaemia.
HEART FAILURE
General overview
Heart failure occurs when the heart is unable to maintain
sufficient cardiac output to meet the demands placed on
it by the body. It is a direct consequence of an underlying
disorder such as CVD, valvular dysfunction or cardiomyopathy. The problem is usually one of failure of myocardium,
although excess preload and afterload plus rhythm disturbances and increased demand beyond that of a normal
heart's capacity are possible. Failure can be systolic (impairment of contraction), diastolic (impairment of relaxation)
or both. The incidence rises with age, and over half a million of people in the United Kingdom have heart failure.
Prognosis is poor, with almost 50% 5-year mortality. It is
classified by its severity (Table27.8).
Aetiology
Acute heart failure can occur in patients without known intrinsic cardiac disease. Cardiogenic heart failure is due to
an abnormality of the heart, and can be unmasked when a
heart with reduced reserve is unable to cope with the often
seemingly minor stresses placed on it. These may manifest
themselves at rest, or more commonly on exertion. Causes
include:
• CVD (65% of new UK cases per year);
• hypertension;
• valvular heart disease;
• drugs (e.g. β-blockers, calcium channel blockers);
• toxins: alcohol, chemotherapy, illicit drugs (e.g.
cocaine);
• tachycardia-induced causes (e.g. AF, atrial flutter);
• infection (e.g. viruses, Chagas disease, HIV);
• genetic causes (e.g. HOCM, Duchenne muscular
dystrophy);
• pregnancy;
• nutritional deficiency (e.g. beriberi).
Heart failure can also occur in seemingly normal hearts.
This is a result of cardiac inability to maintain an increased
cardiac output in the face of grossly elevated requirements.
Table27.8 The New York Heart Association
classification of heart failure
Class Features
I No limitation of physical activity
II Slight limitation of physical activity, breathless
climbing two flights of stairs
III Marked limitation of physical activity,
breathless walking 100 m on the flat
IV Inability to perform any physical activity
without discomfort
180
Heart failure
2727
The following conditions cause this form of cardiac
decompensation:
• thyrotoxicosis;
• anaemia;
• fever;
• pregnancy;
• AV shunts;
• Paget disease;
• beriberi.
Clinical features
Left-sided heart failure
In left ventricular failure (LVF) inadequate cardiac output
leads to elevated left atrial pressures. A combination of
these two factors leads to most of the clinical findings.
Symptoms include:
• exertional dyspnoea (most common);
• orthopnoea;
• paroxysmal nocturnal dyspnoea;
• fatigue;
• wheeze (‘cardiac asthma’);
• cough;
• haemoptysis (rare).
Signs include:
• tachypnoea;
• tachycardia;
• cardiomegaly;
• basal crepitations indicating pulmonary oedema;
• pleural effusions;
• pulsus alternans (alternating large- and small-volume
pulse);
• third heart sound (‘S3 gallop’);
• functional mitral regurgitation secondary to dilatation
of the mitral valve annulus;
• peripheral cyanosis and low pulse volume.
Acute LVF is a medical emergency, and typically presents
with severe dyspnoea secondary to pulmonary oedema.
Patients will be sitting up, distressed, pale and sweaty and
may be coughing up pink frothy sputum. Clinical features
will include tachycardia, fine crackles across the lung fields
and a raised jugular venous pressure (JVP).
Right-sided heart failure
This may occur secondary to chronic lung disease, multiple
pulmonary emboli, primary pulmonary hypertension, rightsided heart valve disease, left-to-right shunts or isolated
right ventricular cardiomyopathy. It is commonly associated
with simultaneous ventricular failure, in which case the term
‘congestive cardiac failure’ (see later) is used. Elevated right
atrial pressures lead to peripheral fluid retention.
Symptoms include:
• fatigue;
• swollen ankles;
• breathlessness;
• wasting;
• nausea;
• abdominal discomfort;
• anorexia.
Signs include:
• a raised JVP;
• pitting oedema;
• tachycardia;
• smooth hepatomegaly;
• liver tenderness;
• ascites;
• right ventricular third heart sound;
• functional tricuspid regurgitation.
Congestive cardiac failure
Congestive cardiac failure is failure of both the right ventricle and the left ventricle. As such, the clinical findings are
a combination of those listed above. Bilateral pleural effusions tend to be a common feature.
Investigations
The cause of the heart failure must always be sought because heart failure itself is an inadequate diagnosis. After
the history taking and examination, investigations include
the following.
Blood tests
• FBC: anaemia;
• U&Es: renal dysfunction or electrolyte abnormalities;
• LFTs: liver congestion;
• TFTs;
• B-type natriuretic peptide (BNP) or N-terminal
pro-B-type natriuretic peptide (NT-proBNP) can be
used to rule out the diagnosis of heart failure. NICE
recommends that the following thresholds be used:
BNP level less than 100 ng/L and NT-proBNP level less
than 300 ng/L.
Imaging
• CXR: cardiomegaly, evidence of fluid overload (alveolar
oedema, ‘bat's wings shadowing’, prominent upper lobe
vessels, Kerley B lines, pleural effusions).
• Echocardiography: key test to identify structural
abnormalities and assess ventricular and valvular
function. It is recommended in patients presenting
with suspected new heart failure.
Other
• ECG: CVD, arrhythmias and left ventricular
hypertrophy. Finding a normal ECG has a very strong
negative predictive value against left ventricular systolic
dysfunction.
• Cardiac imaging (as per CVD).
181
Cardiovascular system
Management of acute heart failure
Acute heart failure is a medical emergency. Key treatment
goals include patient stabilization, symptom relief and adequate organ perfusion. Use the ABCDE approach. Ensure:
• The patient is sitting upright.
• Oxygen is administered to hypoxic patients to maintain
oxygen saturations of 94%–98%, unless the patient is at
risk of hypercapnic respiratory failure, where the target
range is usually 88%–92%. Remember that oxygen is
used to treat hypoxaemia and not breathlessness.
• Diuresis is commenced with furosemide. Furosemide
also causes vasodilation.
• There is close fluid balance monitoring.
NICE does not recommend the routine use of nitrates in
people with acute heart failure. If nitrates are used, ensure
that at least level 2 (high-dependency unit) care can be provided. Nitrates are vasodilators and work by reducing preload. NICE does not recommend the routine use of opiates
or sodium nitroprusside in people with acute heart failure.
NICE does not recommend the routine use of respiratory
support with continuous positive airway pressure to improve
oxygenation or noninvasive positive pressure ventilation in
people with acute heart failure and cardiogenic pulmonary
oedema. Consider using such support in patients with severe
dyspnoea and acidaemia. Invasive ventilation should be considered in patients who are deteriorating despite treatment.
Treat other conditions that may compromise cardiac
function (e.g. arrhythmias).
Intravenous inotropic agents may be of value if there is
refractory hypotension. Drugs used include milrinone or
enoximone (phosphodiesterase inhibitors) and dobutamine
(β-agonist). If pulmonary congestion is dominant, dobutamine is preferred. It has vasodilating properties and so may
lower the BP. It can be combined with noradrenaline if needed.
In cases of pulmonary oedema refractory to diuresis,
haemofiltration can be used as a way of fluid removal.
Intraaortic balloon counterpulsation in primary cardiac
failure may be available to support the heart while therapy
is planned.
Management of chronic heart failure
The underlying cause of the heart failure should be sought
and treated appropriately. Exacerbating factors such as anaemia and hypertension should be treated. Patients should be
advised to maintain an optimal weight, avoid excessive salt
intake and alcohol consumption and stop smoking. Annual
vaccinations for influenza and a one-off pneumococcal vaccination should be offered.
Drug treatment
Angiotensin-converting enzyme inhibitors
In patients with heart failure and reduced left ventricular
ejection fraction, treatment with ACE inhibitors should
be started. The renin–angiotensin–aldosterone system
is activated in heart failure, and ACE inhibitors reduce
angiotensin-mediated vasoconstriction, reducing afterload,
and decreasing aldosterone-mediated salt and water retention. This improves cardiac function. In heart failure, ACE
inhibitors reduce both morbidity and mortality.
Side effects include cough, first-dose hypotension, hyperkalaemia and worsening renal function. Contraindications
include bilateral renal artery stenosis and severe renal
impairment. Commonly used drugs include ramipril,
enalapril, perindopril and lisinopril. Angiotensin II receptor antagonists can be used in patients intolerant to ACE
inhibitors.
β-Blockers
For many years it was believed that these were contraindicated in heart failure because the sympathetic nervous
system was compensating for the failing heart and blocking
this was deleterious. This remains true in the acute setting,
where the negatively inotropic and chronotropic effects of
β-blockade can be harmful. However, β-blockers are now
recommended in patients with chronic heart failure and left
ventricular dysfunction.
They reduce morbidity and mortality associated with
heart failure. The β-blockers currently licensed for use in
heart failure are carvedilol, bisoprolol and nebivolol.
Diuretics
Loop diuretics, commonly furosemide and bumetanide,
are very effective at reducing symptoms in patients with
heart failure in both acute and long-term care. They have
beneficial effects on clinical outcomes and reduce mortality. Side effects include hypovolaemia, renal impairment,
electrolyte disturbances (hypokalaemia, hypomagnesaemia,
hyponatraemia, hypocalcaemia) and, rarely, ototoxicity.
Contraindications to their use include severe hypokalaemia
and hyponatraemia.
Aldosterone antagonists
Use of aldosterone antagonists should be started in patients with acute heart failure and reduced left ventricular ejection fraction. Aldosterone may act directly as a
deleterious growth factor on myocytes, in addition to
its salt- and water-retaining effects. In a study using low
(nondiuretic) doses, it reduced morbidity and mortality
(the RALES trial). Side effects include hyperkalaemia and
hyponatraemia.
Hydralazine in combination with a nitrate
This should be considered as second-line treatment in patients with chronic New York Heart Association class III–
IV heart failure, especially if they are of black African or
Caribbean heritage.
Digoxin
NICE recommends digoxin in patients with worsening or
severe heart failure due to left ventricular dysfunction refractory to treatment with first- and second-line drugs.
182
Hypertension
2727
Ivabradine
This is an option in patients with New York Heart
Association class II–IV chronic heart failure who have left
ventricular ejection fraction of 35% or less, are in sinus
rhythm with a heart rate of 75 bpm or more and are already
taking standard therapy (unless contraindicated).
Nondrug therapy
Implantable cardioverter defibrillator and cardiac resynchronization therapy
NICE recommends implantable cardioverter defibrillator
(ICD) insertion for people with previous serious ventricular
arrhythmias without a treatable cause or people who have a familial cardiac condition with a high risk of sudden death (e.g.
hypertrophic cardiomyopathy, long QT syndrome, Brugada
syndrome). In patients with heart failure, ICD placement or
cardiac resynchronization therapy (CRT) is recommended in
patients with left ventricular ejection fraction of 35% or less
and dyssynchrony. CRT, also called ‘biventricular pacing’, refers to devices that apart from standard right atrial and right
ventricular wires also have a left ventricular pacemaker.
Left ventricular assist devices
Left ventricular assist devices are mechanical circulatory devices
that can be used to partially or completely replace the function
of the failing heart. Their most common clinical indication is after cardiac surgery, where the device allows the heart to recover.
Transplantation
Heart transplantation can be performed as a treatment for
chronic heart failure. The extent of the surgery and postoperative immunosuppression means that only a select group
of patients are suitable for transplantation. The current
prognosis for heart transplantation is very good, with 70%
of recipients alive at 5years.
values. When you are diagnosing hypertension, if the reading
is greater than 140/90 mmHg in the clinic, the patient should
be offered ambulatory BP monitoring to confirm the diagnosis. BP persistently of 140/90 mmHg or greater is termed
‘stage 1 hypertension’ and BP persistently of 160/100 mmHg
or greater is termed ‘stage 2 hypertension’. Severe hypertension is defined as systolic BP of 180 mmHg or greater or diastolic BP of 110 mmHg or greater. These are arbitrary cut-off
points that are influenced by age, the presence of end-organ
damage or established CVD, and other cardiovascular risk
factors (e.g. diabetes mellitus). Approximately 95% of all
hypertensive patients have ‘essential’ or ‘primary’ hypertension and have no underlying disease (i.e. no cause can be
found). Clinical notes: mechanisms involved in the development of essential hypertension outlines some mechanisms
that can play a role in the development of essential hypertension. Secondary hypertension can be the result of a range
of different pathological processes (clinical notes: causes of
secondary hypertension).
CLINICAL NOTES
AGE AND HYPERTENSION – FACTORS
ASSOCIATED WITH ADVANCING AGE
• General likelihood of hypertension (>50%).
• Greater damage when hypertensive.
• Diastolic threshold for treatment 90 mmHg.
• As much or more benefit from treatment.
CLINICAL NOTES
MECHANISMS INVOLVED IN THE
DEVELOPMENT OF ESSENTIAL HYPERTENSION
HYPERTENSION
General overview
Hypertension is one of the most important modifiable risk
factors for CVD such as stroke, MI and renal disease and,
as such, premature morbidity and mortality in the world.
Hypertension is defined as systemic BP persistently
above 140/90 mmHg. The prevalence of hypertension differs depending on BP cut-off points, age, sex and race. It
increases with age, and is more common in men and those
of Afro-Caribbean origin. Factors relating to hypertension
associated with advancing age are summarized in clinical
notes: age and hypertension – factors associated with advancing age. Diastolic hypertension is more common in
people younger than 50years. Systolic hypertension is more
prevalent in older people; this results from progressive stiffening and loss of compliance of larger arteries.
The risk of morbidity and mortality rises continuously
with increasing BP, and marginal risk is greater at higher
• Age: prevalence increases with age – around
30% of people aged between 45 and 55years
and 70% of those older than 75years are
thought to have hypertension.
• Obesity: there is a continuous linear relationship
between excess body fat and blood pressure
levels.
• Alcohol: increased alcohol consumption is
related to higher blood pressure.
• Dietary sodium: salt restriction may reduce
systolic blood pressure by 3–5 mmHg in
hypertensives and is most clear-cut in older
people and in those with severer hypertension.
• Genetics: defects in the renin–angiotensin–
aldosterone axis, problems with sodium
handling and increased sympathetic nervous
system activation.
183
Cardiovascular system
CLINICAL NOTES
CAUSES OF SECONDARY HYPERTENSION
A definite underlying cause of hypertension is more
common in younger people, and should be looked
for specifically in those younger than 35years:
• renal: chronic glomerulonephritis, chronic
pyelonephritis, renal artery stenosis, obstructive
uropathy and polycystic kidney disease;
• endocrine: Cushing and Conn syndromes,
hyperparathyroidism, phaeochromocytoma and
acromegaly;
• respiratory: obstructive sleep apnoea;
• pregnancy-induced hypertension and preeclampsia:
associated with oedema and proteinuria;
• congenital: coarctation of the aorta;
• drugs: oestrogen-containing oral contraceptive
pill, NSAIDs, steroids, sympathomimetics,
carbenoxolone and liquorice.
Clinical features
Patients with hypertension are usually asymptomatic.
However, when hypertension is severe or chronic, it can
be associated with complications resulting from end-organ
damage. The following symptoms may occur:
• Headaches.
• Dyspnoea.
• Symptoms of cardiac failure.
• Angina pectoris or MI.
• Transient ischaemic attack or stroke.
• Visual disturbance.
• Hypertensive emergency: hypertensive encephalopathy.
This requires immediate management with
intravenously administered labetalol or calcium
channel blockers and an ACE inhibitor.
The clinical approach to the patient with hypertension is
summarized in Table27.9, and the examination approach is
summarized in Fig.27.11. Complications or an underlying
cause should be sought.
COMMUNICATION
In hypertension, explanation to the patient of
the needs and expectations of treatment is very
important. Patients need to understand that they are
taking treatment to reduce future risks and not to
improve current health. Work together to achieve a
combination of lifestyle changes and drug treatment
that achieves control with minimal side effects.
Table27.9 Clinical evaluation of the patient with
hypertension (look for the five C’s)
Causes of
hypertension
Contributory factors Overweight? Alcohol intake?
Complications Cerebrovascular disease
Contraindications to
drugs
Cardiovascular risk Assessment of other
Drugs causing hypertension?
Paroxysmal features?
(phaeochromocytoma)
Renal disease, history of renal
disease or family history of renal
disease?
General appearance? (Cushing
syndrome)
Radiofemoral delay? (coarctation)
Kidney(s) palpable? (polycystic,
hydronephrosis, neoplasm)
Abdominal or loin bruit? (renal
artery stenosis)
Left ventricular hypertrophy or
cardiac failure
Ischaemic heart disease
Fundal haemorrhages and
exudates (accelerated phase)
Gout, diabetes (thiazides)
Asthma, heart failure, heart block
(β-blockers)
Heart failure, heart block
(verapamil)
cardiovascular risk factors
Investigations
An algorithm for the investigation of the patient with hypertension is given in Fig.27.12. At presentation, all hypertensive patients should undergo the following tests:
• Urine dipstick for blood and protein: parenchymal
disease, urinary tract infection.
• Urine sample for estimation of the albumin/creatinine
ratio.
• Kidney function tests: may indicate renal impairment
or suggest a cause (e.g. Conn syndrome).
• Blood glucose and lipid profile: screen the patient for
modifiable cardiovascular risk factors.
• ECG: significant hypertension may result in left
ventricular hypertrophy.
• Fundoscopy: for presence of hypertensive retinopathy;
indicates end-organ disease.
• Global cardiovascular event risk assessment using a
published risk assessment chart.
Further investigations are warranted in young patients,
where a secondary cause is more likely, in patients
with rapidly rising BP or severe hypertension, in patients with hypertension resistant to treatment and in
patients with deranged urea and electrolyte levels. These
investigations include 24-hour urinary catecholamine and
184
— Measure both arms
Pulse
— Atrial fibrillation
— Radiofemoral delay
Eyes
— Hypertensive retinopathy
Neck
— Carotid bruit
Chest
— Pulmonary oedema
Kidneys
— Palpable kidneys
— Bruit
Hypertension
Brain
— Previous stroke
Heart
— Displaced, heaving
apex beat
— Systolic murmur
(coarctation)
— Fourth heart sound
Blood pressure
2727
Fig.27.11 Examining the patient with hypertension.
metanephrine measurements for phaeochromocytoma
and renal tract ultrasound scan for structural abnormalities; if renovascular disease is suspected, then renal arteriography is indicated.
Further investigations depend on clinical suspicion (e.g.
aortography for coarctation of the aorta).
HINTS AND TIPS
Many patients find visiting their doctor stressful
and will often have a raised blood pressure –
‘white-coat hypertension’. A diagnosis of
hypertension can therefore be made only after
ambulatory blood pressure monitoring.
Extremities
— Peripheral vascular disease
Management
Fig.27.13 summarizes current NICE recommendations
for the clinical management of adult hypertension.
Treatment of the underlying condition may be indicated
in cases of secondary hypertension (e.g. treatment of
an underlying endocrine condition or surgical correction of aortic coarctation). Patients should be educated
about lifestyle modifications which can reduce the risk
of CVD.
The aim is to reduce BP to below 140/90 mmHg in people younger than 80years and below 150/90 mmHg in those
aged 80years or older.
In hypertension, as in many chronic disorders, drugs
are best added ‘stepwise’ until control has been achieved.
Monotherapy controls BP in only 30%–50% of patients, and
most patients need two or more drugs. In uncomplicated
mild hypertension, drugs may be substituted rather than
General
— Cushing syndrome
— Acromegaly
— Neurofibromatosis
— Xanthelasmata
185
Cardiovascular system
Essential
hypertension 95%
No features suggestive
of underlying cause,
end-organ damage or
high cardiovascular risk
No further
investigation
Hypertension
Severe or persistent BP
>160/100 mmHg or >140/90 mmHg
plus high cardiovascular event risk
History
Examination
Urinalysis
Blood glucose/lipids
U&Es
ECG
drug-resistant hypertension
Features suggesting
underlying cause
or
(on 3+ drugs)
Vascular
e.g., coarctation,
renal artery
stenosis
Imaging
angiography
(contrast or MR)
Doppler US
Renal
e.g., nephritides,
polycystic kidney
disease
Renal
investigations
(see Chapter 30)
Endocrine
e.g.,
phaeochromocytoma,
Conn syndrome
Endocrine
investigations
(see Chapter 33)
Obstructive
uropathy
e.g., stones,
prostatism
Urological
investigations
— US
— IVU
— Cytoscopy
— PSA
Fig.27.12 Algorithm for the investigation of the patient with hypertension. BP, Blood pressure; ECG, electrocardiogram;
IVU, intravenous urogram; MR, magnetic resonance; PSA, prostate-specific antigen; U&Es, urea and electrolytes; US,
ultrasonography.
added. NICE recommends antihypertensive drug treatment
for people younger than 80years with stage 1 hypertension
and target organ damage, CVD, kidney disease, diabetes or
a 10-year cardiovascular risk of 20% or more and to anyone
with stage 2 disease.
Angiotensin II receptor blockers
These block the renin–angiotensin system, producing effects similar to ACE inhibitors. They do not affect bradykinin production, and so are useful for people who develop
chronic cough with ACE inhibitors. Angiotensin II receptor
blockers should be considered in preference to ACE inhibi-
Drug treatment
Angiotensin-converting enzyme inhibitors
ACE inhibitors act by inhibiting the renin–angiotensin–aldosterone axis with an increase in the level of vasodilating
bradykinin. They are more effective in patients with higher
renin levels, and so are best used in young white patients
compared with Afro-Caribbean patients. They are highly
effective in heart failure, proteinuric nephropathy and diabetes. They are very potent combined with a diuretic or
calcium channel blocker.
tors in black patients of African or Caribbean family origin.
Calcium channel blockers
These are effective as monotherapy in 50% of patients,
and amlodipine (for which safety has been demonstrated
in heart failure) has become the most common antihypertensive worldwide. Side effects include flushing, headache,
constipation and diuretic-resistant oedema.
Thiazide diuretics
Thiazides mainly lower BP by lowering body sodium stores.
Initially, BP falls because of a decrease in blood volume,
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Valvular heart disease
2727
Aged over 55 years or
Aged under
55 years
Step 1
Step 2
Step 3
Step 4
Consider seeking expert advice
Key
A – ACE inhibitor or angiotensin II receptor blocker (ARB)
C – Calcium-channel blocker (CCB)
D – Thiazide-like diuretic
Fig.27.13 Summary of National Institute for Health and
Care Excellence guidelines for the management of adult
hypertension. ACE, Angiotensin-converting enzyme.
A + C + D
Resistant hypertension
A + C + D consider further
diuretic or α-blocker
or β-blocker
black person of
African or Caribbean
family origin of
any age
CA
A + C
venous return and cardiac output. Gradually, the cardiac
output returns to normal, but the hypotensive effect remains
because the peripheral resistance decreases. Side effects include impaired glucose tolerance and gout. Thiazides are
contraindicated in Addison disease, hypercalcaemia, hyponatraemia and refractory hypokalaemia. Women tolerate
thiazides better than men, and the drug is more effective in
the elderly. Other diuretics, such as spironolactone, can be
considered in treatment of resistant hypertension.
β-Blockers
β-Blockers may be considered in young patients or in
treatment-resistant hypertension. β-Blockers initially
produce a fall in BP by decreasing cardiac output. With continued use, the cardiac output returns to normal but the BP
remains low because the peripheral resistance is ‘reset’ at a
lower level and renin levels are reduced.
α-Adrenergic receptor blockers
α-Blockers such as doxazosin reduce both arteriolar and venous resistance, and maintain a high cardiac output. They
can be considered in resistant hypertension.
Central acting agents
Methyldopa stimulates α2 receptors in the medulla and reduces sympathetic outflow. In 20% of patients it causes a
positive Coombs test result and, rarely, haemolytic anaemia.
Drug-induced hepatitis with fever may also occur.
Vasodilators
Minoxidil is a potent vasodilator and decreases peripheral
resistance. It can be used in the treatment of severe hypertension in addition to a diuretic and a β-blocker. Side effects in-
clude reflex tachycardia, fluid retention and hypertrichosis.
Management of hypertension in pregnancy
Good BP control in pregnancy is important – orally administered methyldopa is safe. β-Blockers are effective and safe
in the third trimester; labetalol is used relatively frequently,
but may cause intrauterine growth retardation when used
earlier in pregnancy. Hydralazine may also be used. Its side
effects include drug-induced lupus.
Malignant (accelerated) hypertension
Malignant hypertension (systolic BP greater than 200 mmHg
or diastolic BP greater than 130 mmHg) with end-organ
damage requires urgent hospital assessment. Treatment is
normally given orally with β-blockers or calcium antagonists to reduce diastolic BP to 100–110 mmHg within the
first 24 hours. Intravenous antihypertensive drugs such as
nitroprusside, GTN or labetalol are used when more rapid
reduction is necessary or when the oral route is unavailable.
Over the next few days, further antihypertensives should be
given to lower BP further.
Very rapid falls in BP should be avoided because the reduction in cerebral perfusion may lead to cerebral infarction,
blindness, worsening renal function and myocardial ischaemia. Sublingually administered nifedipine is best avoided
because of its unpredictable response. Patients with untreated
malignant hypertension have 90% mortality at 1year.
VALVULAR HEART DISEASE
General overview
Valvular heart disease can affect any of the four heart valves.
It is a common condition that may be congenital or acquired.
Clinically, most heart valve abnormalities are asymptomatic
and discovered only by the presence of a heart murmur on
careful auscultation of the praecordium. Heart murmurs are
due to vibration caused by turbulent blood flow within the
heart. The commonest causes are left-sided valvular heart disease and tricuspid regurgitation. Nonvalvular causes include:
• innocent ‘flow’ murmurs, especially in children;
• high cardiac output states (e.g. pregnancy,
thyrotoxicosis and fever);
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