hj

3.  High BP is a trait as opposed to a specific
disease and represents a quantitative rather
than a qualitative deviation from the norm.
 Any definition of hypertension is therefore
arbitrary.

4.  Systemic BP rises with age, and the
incidence of cardiovascular disease
(particularly stroke and coronary artery
disease) is closely related to average BP at
all ages, even when BP readings are within
the so-called ‘normal range’.

5.  Randomised controlled trials have
demonstrated that antihypertensive therapy
can reduce the incidence of stroke and, to a
lesser extent, coronary artery disease .

6.  The cardiovascular risks associated with a
given BP are dependent upon the
combination of risk factors in an individual,
such as age, gender, weight, physical
activity, smoking, family history, serum
cholesterol, diabetes mellitus and pre-
existing vascular disease.

7.  Effective management of hypertension
requires a holistic approach, based on the
identification of those at highest
cardiovascular risk and the use of
multifactorial interventions, targeting not
only BP but all modifiable cardiovascular
risk factors.

8.  Thus a practical definition of hypertension is
‘the level of BP at which the benefits of
treatment outweigh the costs and hazards’.
 The British Hypertension Society
classification of hypertension is consistent
with those defined by the European Society
of Hypertension and the World Health
Organization–International Society of
Hypertension.

9.  Hypertension is predominantly an
asymptomatic condition and the diagnosis is
usually made at routine examination or
when a complication arises.
 A BP check is advisable every 5 years in
adults.

10.  The objectives of the initial evaluation of a
patient with high BP readings are:
-to obtain accurate and representative
measurements of BP
-to identify contributory factors and any
underlying cause (secondary hypertension)
- to assess other risk factors and quantify
cardiovascular risk

11. -to detect any complications (target organ
damage) that are already present
-to identify comorbidity that may influence the
choice of antihypertensive therapy.
 These goals are attained by a careful history,
clinical examination and some simple
investigations.

13.  The term ‘syncope’ refers to sudden loss of
consciousness due to reduced cerebral
perfusion.
 ‘Presyncope’ refers to lightheadedness
where the individual thinks he or she may
black out.

14.  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.

15.  There are several 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 hypotension.

17.  Blackouts can also be caused by non-cardiac
pathology such as epilepsy, cerebrovascular
ischaemia or hypoglycaemia.

19.  History-taking, from the patient or a
witness, is the key to establishing a
diagnosis.
 Attention should be given 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.

20.  Cardiac syncope is usually sudden but can
be associated with premonitory
lightheadedness, palpitation or chest
discomfort.
 The blackout is usually brief and recovery
rapid.

21.  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.

22.  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.

24. :Arrhythmia
 Lightheadedness may occur with many
arrhythmias, but blackouts (Stokes–Adams
attacks) are usually due to profound
bradycardia or malignant ventricular
tachyarrhythmias.

25.  The 12-lead ECG may show evidence of
conducting system disease (e.g. sinus
bradycardia, AV 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 during symptoms.

26.  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.

27.  Patient activated ECG recorders are useful
for examining the rhythm in patients with
recurrent dizziness, but are not useful in
assessing sudden blackouts.

28.  In patients with presyncope or syncope in
whom these investigations fail to establish a
cause, an implantable ‘loop recorder’ can be
placed subcutaneously in the upper chest.
 This device continuously records the
cardiac rhythm and will activate
automatically if extreme bradycardia or
tachycardia occurs.

29.  The ECG memory can also be frozen by the
patient using a hand-held activator. Stored
ECGs can be accessed by the implanting
centre, using a telemetry device.

30. Structural heart disease:
 Severe aortic stenosis, hypertrophic
obstructive cardiomyopathy and severe
coronary artery disease can cause
lightheadedness or syncope on exertion.

31.  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. Exertional arrhythmias also
occur in these patients.

32. Neurocardiogenic syncope:
 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 (HCSS) and
malignant vasovagal syncope.

33. Situational 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 syncope)

34. Vasovagal syncope:
 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 there is an initial sympathetic
activation that leads to vigorous contraction
of the relatively underfilled ventricles.

35.  This stimulates ventricular
mechanoreceptors, producing
parasympathetic (vagal) activation and
sympathetic withdrawal, and causing
bradycardia, vasodilatation or both.

36.  Head-up tilt-table testing is a provocation
test used to establish the diagnosis, and
involves asking the patient to lie on a table
that is then tilted to an angle of 60–70° for
up to 45 minutes, while the ECG and BP are
monitored.

37.  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).

38.  In resistant cases, drug therapy can be used;
fludrocortisone, which causes sodium and
water retention and expands plasma volume,
β-blockers, which inhibit the initial
sympathetic activation, disopyramide (a
vagolytic agent) or midodrine (a
vasoconstrictor α-adrenoceptor agonist) may
be helpful.

39.  A dual-chamber pacemaker can be useful if
symptoms are predominantly due to
bradycardia. Patients with a urinary sodium
excretion of less than 170 mmol/day may
respond to salt loading.

40. Carotid sinus hypersensitivity:
 This 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.

41.  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.

42.  The diagnosis can be established by
monitoring the ECG and BP during carotid
sinus massage for 6 seconds.
 This manœuvre should not be attempted in
patients with a carotid bruit or with a history
of cerebrovascular disease because of the
risk of embolic stroke.

43.  A positive cardio-inhibitory 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.

44.  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.

45.  Dual chamber pacing usually prevents
syncope in patients with the more common
cardio-inhibitory response.

46. Postural hypotension:
 This is caused by a failure of the normal
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.

47.  Treatment is often ineffective; however,
withdrawing unnecessary medication and
advising the patient to wear graduated
elastic stockings and get up slowly may be
helpful.
 Fludrocortisone, which can expand blood
volume through sodium and water retention,
may be of value.

49.  Palpitation is a very common and sometimes
frightening symptom. Patients use the term
to describe a wide variety of sensations
including an unusually erratic, fast, slow or
forceful heart beat, or even chest pain or
breathlessness.

50.  Initial evaluation should concentrate on
determining its likely mechanism, and
whether or not there is significant
underlying heart disease.
 A detailed description of the sensation is
essential and patients should be asked to tap
out the heart beat they experience, on their
chest or a table.

51.  A provisional
diagnosis can
usually be made
on the basis of a
thorough
history.

53.  It helps to obtain an ECG recording during
an episode using an ambulatory monitor or a
patient-activated ECG recorder.
 Recurrent but short-lived bouts of an
irregular heart beat are usually due to atrial
or ventricular extrasystoles (ectopic beats).

54.  Some patients will describe the experience
as a ‘flip’ or a ‘jolt’ in the chest, while others
report dropped or missed beats.
Extrasystoles are often more frequent during
periods of stress or debility; they can be
triggered by alcohol or nicotine.

55.  Episodes of a pounding, forceful and
relatively fast (90–120/min) heart beat are a
common manifestation of anxiety.
 They may also reflect a hyperdynamic
circulation, such as anaemia, pregnancy and
thyrotoxicosis, and can occur in some forms
of valve disease (e.g. aortic regurgitation).

56.  Discrete bouts of a very rapid (> 120/min)
heart beat are more likely to be due to a
paroxysmal tachyarrhythmia.
 Supraventricular and ventricular
tachycardias may all present in this way.
 In contrast, episodes of atrial fibrillation
typically present with irregular and usually
rapid palpitation.

57.  Palpitation is usually benign and, even if the
patient’s symptoms are due to an
arrhythmia, the outlook is good if there is no
underlying structural heart disease.

58.  Most cases are due to an awareness of the
normal heart beat, a sinus tachycardia or
benign extrasystoles, in which case an
explanation and reassurance may be all that
is required.
 Palpitation associated with presyncope or
syncope may reflect more serious structural
or electrical disease and should be
investigated promptly.

60.  Cardiac arrest describes the sudden and
complete loss of cardiac output due to
asystole, ventricular tachycardia or
ventricular fibrillation, or loss of mechanical
cardiac contraction (pulseless electrical
activity).

61.  The clinical diagnosis is based on the victim
being unconscious and pulseless; breathing
may take some time to stop completely after
cardiac arrest.
 Death is virtually inevitable unless effective
treatment is given promptly.

62.  Sudden cardiac death is usually caused by a
catastrophic arrhythmia and accounts for
25–30% of deaths from cardiovascular
disease, claiming an estimated 70000–90000
lives each year in the UK.
 Many of these deaths are potentially
preventable.

63.  Arrhythmias
complicate many types
of heart disease and
can sometimes occur
in the absence of
recognisable structural
abnormalities

64.  Sudden death less often occurs because of
an acute mechanical catastrophe such as
cardiac rupture or aortic dissection.
 Coronary artery disease, especially acute
MI, is the most common condition leading
to cardiac arrest.

65.  Ventricular fibrillation or ventricular
tachycardia is common in the first few hours
of MI and many victims die before medical
help is sought.
 Up to one-third of people developing MI
die before reaching hospital, emphasising
the importance of educating the public to
recognise symptoms and to seek medical
help quickly.

66.  Acute myocardial ischaemia (in the absence
of infarction) can also cause these
arrhythmias, although less commonly.
 Patients with a history of MI may be at risk
of sudden arrhythmic death, especially if left
ventricular function is impaired or there is
ongoing myocardial ischaemia.

67.  In these patients, the risk is reduced by the
appropriate treatment of heart failure with β-
blockers and ACE inhibitors, and by
coronary revascularisation, and many
require implantation of a cardiac
defibrillator.

68.  Cardiac arrest may be caused by ventricular
fibrillation, pulseless ventricular
tachycardia, asystole or pulseless electrical
activity.

69. Ventricular fibrillation and pulseless ventricular
tachycardia:
 These are the most common and most easily
treatable cardiac arrest rhythms. Ventricular
fibrillation produces rapid ineffective
uncoordinated movement of the ventricles,
which therefore produce no pulse.

70.  The ECG shows rapid, bizarre and irregular
ventricular complexes.

71.  Ventricular tachycardia can cause cardiac
arrest if the ventricular rate is so rapid that
effective mechanical contraction and
relaxation cannot occur, especially if it
occurs in the presence of severe left
ventricular impairment.

72.  It may degenerate into ventricular
fibrillation.
 Defibrillation will restore cardiac output in
more than 80% of patients if delivered
immediately.
 However, the chances of survival fall by at
least 10% with each minute’s delay, and by
more if basic life support is not given; thus
provision of these is the key to survival.

73. Asystole:
 This occurs when there is no electrical
activity within the ventricles and is usually
due to failure of the conducting tissue or
massive ventricular damage complicating
MI.

74.  A precordial thump, external cardiac
massage, or administration of intravenous
atropine or adrenaline (epinephrine) may
restore cardiac activity.
 When due to conducting tissue failure,
permanent pacemaker implantation will be
required if the individual survives.

75. Pulseless electrical activity:
 This occurs when there is no effective
cardiac output despite the presence of
organised electrical activity.
 It may be caused by reversible conditions,
such as hypovolaemia, cardiac tamponade or
tension pneumothorax , but is often due to a
catastrophic event such as cardiac rupture or
massive pulmonary embolism, and therefore
carries an extremely poor prognosis.

76. The Chain of Survival:
 This term refers to the sequence of events that are
necessary to maximise the chances of a cardiac
arrest victim surviving.

77.  Survival is most likely if all links in the
chain are strong, i.e. if the arrest is
witnessed, help is called immediately, basic
life support is administered by a trained
individual, the emergency medical services
respond promptly, and defibrillation is
achieved within a few minutes.

78.  Good training in both basic and advanced
life support is essential and should be
maintained by regular refresher courses.
 In recent years, public access defibrillation
has been introduced in places of high
population density, particularly where traffic
congestion may impede the response of
emergency services, e.g. railway stations,
airports and sports stadia.

79.  Designated individuals can respond to a
cardiac arrest using basic life support and an
automated external defibrillator.

80. Basic life support (BLS):
 BLS encompasses
manœuvres that aim to
maintain a low level of
circulation until more
definitive treatment
with advanced life
support can be given.

81.  Management of the collapsed patient
requires prompt assessment and restoration
of the airway, maintenance of breathing
using rescue breathing (‘mouth-to-mouth’
breathing) and maintenance of the
circulation using chest compressions.

82. Advanced life support (ALS):
 ALS aims to restore normal cardiac rhythm
by defibrillation when the cause of cardiac
arrest is due to a tachyarrhythmia, or to
restore cardiac output by correcting other
reversible causes of cardiac arrest.

83.  ALS can also involve administration of
intravenous drugs to support the circulation,
and endotracheal intubation to ventilate the
lungs.
 If cardiac arrest is witnessed, a precordial
thump may sometimes convert ventricular
fibrillation or tachycardia to normal rhythm,
but this is futile if cardiac arrest has lasted
longer than a few seconds.

84.  The priority is to assess the patient’s cardiac
rhythm by attaching a defibrillator/monitor.
 Ventricular fibrillation or pulseless
ventricular tachycardia is treated with
immediate defibrillation.

85.  Defibrillation is more likely to be effective
if a biphasic shock defibrillator is used,
where the polarity of the shock is reversed
midway through its delivery.

86.  Defibrillation is usually administered using
a 150 Joule biphasic shock, and CPR
resumed immediately for 2 minutes without
attempting to confirm restoration of a pulse,
because restoration of mechanical cardiac
output rarely occurs immediately after
successful defibrillation.

87.  If after 2 minutes a pulse is not restored, a
further biphasic shock of 150–200 joules is
given.
 Thereafter, additional biphasic shocks of
150–200 joules are given every 2 minutes
after each cycle of cardiopulmonary
resuscitation (CPR).

88.  During resuscitation, adrenaline
(epinephrine, 1 mg i.v.) should be given
every 3–5 minutes and consideration given
to the use of intravenous amiodarone,
especially if ventricular fibrillation or
ventricular tachycardia reinitiates after
successful defibrillation.

89.  Ventricular fibrillation of low amplitude, or
‘fine VF’, may mimic asystole.
 If asystole cannot be confidently diagnosed,
the patient should be regarded as having
‘fine VF’ and defibrillated.
 If an electrical rhythm is present that would
be expected to produce a cardiac output,
‘pulseless electrical activity’ is present.

90.  There are several potentially reversible
causes that can be easily remembered as a
list of four Hs and four Ts.
 Pulseless electrical activity is treated by
continuing CPR and adrenaline
(epinephrine) administration whilst seeking
such causes.

91.  Asystole is treated similarly, with the
additional support of atropine and
sometimes external or transvenous pacing in
an attempt to generate an electrical rhythm.

93.  Patients who survive a cardiac arrest caused
by acute MI need no specific treatment
beyond that given to those recovering from
an uncomplicated infarct, since their
prognosis is similar.
 Those with reversible causes, such as
exercise-induced ischaemia or aortic
stenosis, should have the underlying cause
treated if possible.

94.  Survivors of ventricular tachycardia or
ventricular fibrillation arrest in whom no
reversible cause can be identified may be at
risk of another episode, and should be
considered for an implantable cardiac
defibrillator and anti-arrhythmic drug
therapy.

96.  The first clinical manifestation of heart
disease may be the discovery of an abnormal
sound on auscultation.
 This may be incidental—for example,
during a routine childhood examination—or
may be prompted by symptoms of heart
disease.

97.  Clinical evaluation is helpful but an
echocardiogram is often necessary to
confirm the nature of an abnormal heart
sound or murmur.

99.  Additional heart sounds and murmurs
demonstrate a consistent relationship to a
specific part of the cardiac cycle but
extracardiac sounds (e.g. pleural rub or
venous hum) do not.

100.  Pericardial friction produces a characteristic
scratching or crunching noise, which often
has two components corresponding to atrial
and ventricular systole, and may vary with
posture and respiration.

101.  Pathological sounds and murmurs are the
product of turbulent blood flow or rapid
ventricular filling due to abnormal loading
conditions.
 Some added sounds are physiological but
may also occur in pathological conditions;
for example, a third sound is common in
young people and in pregnancy but is also a
feature of heart failure.

102.  Similarly, a systolic murmur due to
turbulence across the right ventricular
outflow tract may occur in hyperdynamic
states (e.g. anaemia, pregnancy) but may
also be due to pulmonary stenosis or an
intracardiac shunt leading to volume
overload of the RV (e.g. atrial septal defect).

103.  Benign murmurs do not occur in diastole and
systolic murmurs that radiate or are associated with
a thrill are almost always pathological.

104.  Timing, intensity,
location, radiation and
quality are all useful
clues to the origin and
nature of a heart
murmur:

105.  Radiation of a murmur is determined by the
direction of turbulent blood flow and is only
detectable when there is a high-velocity jet,
such as in mitral regurgitation (radiation
from apex to axilla) or aortic stenosis
(radiation from base to neck).

106.  Similarly, the pitch and quality of the sound
can help to distinguish the murmur, such as
the ‘blowing’ murmur of mitral regurgitation
or the ‘rasping’ murmur of aortic stenosis.

107.  The position of a murmur in relation to the
cardiac cycle is crucial and should be
assessed by timing it with the heart sounds,
carotid pulse and apex beat.

109. Systolic murmurs associated with ventricular
:outflow tract obstruction
 These occur in mid-systole and have a
crescendodecrescendo pattern, reflecting the
changing velocity of blood flow.

110.  Pansystolic murmurs maintain a constant
intensity and extend from the first heart
sound throughout systole (up to and beyond
the second heart sound).
 They occur when blood leaks from a
ventricle into a low-pressure chamber at an
even or constant velocity.

111.  Mitral regurgitation, tricuspid regurgitation
and ventricular septal defect are the only
causes of a pansystolic murmur.
 Late systolic murmurs are unusual but may
occur in mitral valve prolapse, if the mitral
regurgitation is confined to late systole,
hypertrophic obstructive cardiomyopathy if
dynamic obstruction occurs late in systole.

112. Mid-diastolic murmurs:
 These are due to accelerated or turbulent
flow across the mitral or tricuspid valves.
 They are low-pitched noises that are often
difficult to hear and should be evaluated
with the bell of the stethoscope.

113.  A mid-diastolic murmur may be due to
mitral stenosis (located at the apex and
axilla), tricuspid stenosis (located at the left
sternal edge), increased flow across the
mitral valve (e.g. the to-and-fro murmur of
severe mitral regurgitation) or increased
flow across the tricuspid valve (e.g. left-to-
right shunt through a large atrial septal
defect).

114.  Early diastolic murmurs have a soft,
blowing quality with a decrescendo pattern
and should be evaluated with the diaphragm
of the stethoscope.
 They are due to regurgitation across the
aortic or pulmonary valves and are best
heard at the left sternal edge with the patient
sitting forwards in held expiration.

115. Continuous murmurs:
 These result from a combination of systolic
and diastolic flow (e.g. persistent ductus
arteriosus), and must be distinguished from
extracardiac noises such as bruits from
arterial shunts, venous hums (high rates of
venous flow in children) and pericardial
friction rubs.