Hypertension: A Comprehensive Overview



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.



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’.



 Randomised controlled trials have

demonstrated that antihypertensive therapy

can reduce the incidence of stroke and, to a

lesser extent, coronary artery disease .



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.



 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.



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.



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.



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

-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.



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.



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 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.



Blackouts can also be caused by non-cardiac

pathology such as epilepsy, cerebrovascular

ischaemia or hypoglycaemia.



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.



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.

:

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

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, 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.



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.



 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.



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.

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

Severe aortic stenosis, hypertrophic

obstructive cardiomyopathy and severe

coronary artery disease can cause

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. Exertional arrhythmias also

occur in these patients.

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

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.

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

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)

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

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.



This stimulates ventricular

mechanoreceptors, producing

parasympathetic (vagal) activation and

sympathetic withdrawal, and causing

bradycardia, vasodilatation or both.



 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.



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 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.



 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.

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

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.



 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 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.



 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.



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 pacing usually prevents

syncope in patients with the more common

cardio-inhibitory response.

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

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.



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.



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.



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.



A provisional

diagnosis can

usually be made

on the basis of a

thorough

history.



 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).



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.



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).



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.



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.



 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.



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).



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.



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.



 Arrhythmias

complicate many types

of heart disease and

can sometimes occur

in the absence of

recognisable structural

abnormalities



 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.



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.



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.



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.



Cardiac arrest may be caused by 

ventricular

fibrillation

, 

pulseless ventricular

tachycardia

, 

asystole

 or 

pulseless

electrical

activity

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

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.



The ECG shows rapid, bizarre and irregular

ventricular complexes.



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.



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.

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

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.



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.

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

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.

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.



 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.



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.



Designated individuals can respond to a

cardiac arrest using basic life support and an

automated external defibrillator.

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

BLS encompasses

manœuvres that aim to

maintain a low level of

circulation until more

definitive treatment

with advanced life

support can be given.



 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.

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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.



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.



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.



 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.



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.



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).



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.



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.



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.



Asystole is treated similarly, with the

additional support of atropine and

sometimes external or transvenous pacing in

an attempt to generate an electrical rhythm.



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.



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.



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.



Clinical evaluation is helpful but an

echocardiogram is often necessary to

confirm the nature of an abnormal heart

sound or murmur.



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.



 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.



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.



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).



Benign murmurs do not occur in diastole and

systolic murmurs that radiate or are associated with

a thrill are almost always pathological.



Timing, intensity,

location, radiation and

quality are all useful

clues to the origin and

nature of a heart

murmur:



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).



 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.



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.

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

These occur in mid-systole and have a

crescendodecrescendo pattern, reflecting the

changing velocity of blood flow.



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.



 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.

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

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.



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).



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.

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

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.