5.
06 - Hypertension
Hypertension (WHO definition)
 Systolic BP >140mmHg
 Diastolic BP >90 mmHg
 Receiving Medication
for BP
Prevalence/Epidemiology
 29% or 3.6 million over 25
 31% of men, 26% of women
 Prevalence decreased since
1980
 Up to 3x more common in
indigenous Australians
Risk Factors
 Family history
 Overweight
 Physically inactive
 Excess alcohol
 High dietary salt intake
 Low fruit/veg intake
 High saturated fats
 Emotional stress
 Renal disease
Prevention
 Primary – maintain body
weight, reduce salt intake,
regular exercise
 Secondary – early detection
and screening
 Tertiary – meds to lower BP
and decrease risk of end
organ damage
Signs and Symptoms
 Optimal BP <120/80
 HT >140/90, moderate
>160/100, high >180/110
 Palpate kidneys
 Renal artery bruits
 Radio-femoral delay
 Cushingoid signs (endocrine
disease)
 End organ damage – carotic
artery bruits, optic fundi,
neurological signs, lower
limb pulses, heart size
 Signs of CHF
 Arrhythmias – poor effort
tolerance, SOB, dizzy, drop
attacks, palpitations, angina
pain, sudden death, heart
strain, ectopic beats
Aetiology/Pathophysiology
Factors determining blood pressure
 Cardiac Output = volume of blood pumped by heart in a minute
o Blood Volume  fluid retention  Na reabsorption  Aldosterone
o Heart Rate
o Stroke Volume  Contractility + end diastolic volume
 Total Peripheral Resistance
o Systemic  vasoconstrictors + vasodilators  humoral + neuronal
o Local  Pressure + pH + hypoxia
Causes of HT
 Essential (95%) – no underlying cause demonstratable after investigation
o Usually associated with ↑ TRP (may be ↑ CO early in disease)
o Hypotheses – inability of kidney to secrete sodium, overactive RAAS
system, overactive sympathetic NS
 Secondary (5%) – Cause is demonstratable
o Chronic Renal Disease – renovascular hypertension or chronic renal
parenchymal damage (glomerulonephritis, polycystic kidneys) 
alternation of renal perfusion  activates RAAS  ↑ BP
o Endocrine Hypertension - ↑ hormones  ↑ BP
 Adrenal hyperfuncion, phaochromocytoma
o Cardiovascular causes – coarctation of aorta, polyarteritis nodosa
o Others - Alcohol, drugs, contraceptive pill
Endorgan Damage in HT
 Vascular System
o Concentric LV hypertrophy  ↑ demand for blood, ↑ risk MI due to ↓
perfusion through myocytes and loss of reserve  CHF
 Hypertrophied myocytes with large, irregular hyperchromatic
nuclei + may get interstitial fibrosis in heart  VF + ectopics
o RV hypertrophy due to pulmonary vessel disease
o Arteries – ↓ elastin and SM  Atherosclerosis, activation of
endothelium, aneurysms
 Kidneys
o Replacement of smooth muscle with homogenous eosinophilic
hyaline in walls of afferent arterioles  narrowing of lumen,
Tortuosity of vessels, and hypertensive nephrosclerosis
o Ischaemia  loss + damage to nephrons + ↑ RAAS loop
o Nephrosceorsis and renal failure
 Eyes – retinopathy, atriovenous nipping (artery stenoses where vein crosses),
protein exudates on retina
 CNS – increased risk of stroke (cerebral infarction), intracerebral
haemorrhage due to degeneration of arteries, formation and rupture of berry
aneurysms in the circle of Willis  subarachnoid haemorrhage + aneurysms
predispose to stasis and thrombus formation
 Death – congestive cardiac failure, stroke, aortic distension
Investigations/Tests
 Measure BP with mercury sphygmomanometer
 Urinalysis – blood, protein, glucose
 FBC + lipids
 Plasma urea, potassium, glucose, lipids, urate, cardiac enzymes
 CXR – cardiac size, rib notches (coarctation or aorta)
 Electrocardiogram + prolonged ECG monitoring for VF
 Examine retina
 Discretionary tests – renal ultrasound/CT, 24 hours urine protein, Na or creatine
clearance, plasma renin/angiotensin, 24 hr urine catecholamines
(phaeochromatoma), liver enzymes
Management
 Studies have shown both screening and treatment of hypertension is beneficial and ↓ CV risk – stroke by 40%,
CHD by 15%
 Non-pharmacological therapy – diet (salt restriction), weight loss, exercise, stop smoking and alcohol, stress
management, education
 Pharmacological
Drug
Beta adrenoceptor antagonists
– atenolol, metoprolol
Diuretics – thiazides
(combination therapy)
Calcium antagonists
ACE inhibitors – captopril,
enalapril
Angiotensin Receptor
antagonists
Mechanism
↓ BP by reducing HR and CO – also
inhibit renin release
Natriuresis and diuresis, may also have
direct vasodilator effects
Dihydopridines (nifedipine, amlodipine) Tachycardia, flushing, headache (combine
– lower BP by vasodilation
Non-dihydropyridines (verapamil) –
also ↓ AV nodal conduction and
myocardial contractility
Block formation of Angiotensin II
which is a vasoconstrictor
Block AgII receptors on vascular
smooth muscle
Side effects
Tiredness, impotence, exercise limitation,
bradycardia, sleep disturbance, heart block
Hypokalemia, hypercalcemia,
hyperuricemia
with beta blockers)
Contraindicated with beta blockers
Dry cough, ↓ renal function, rash
Less cough – good in patients who cannot
tolerate ACEi

Other Relevant Info.

Screening – systemic application of a test to identify individuals at risk of a specific disorder to benefit from further
investigations or direct preventative action, among persons who are asymptomatic

Short Term Regulation of BP

 Arterial baroreceptor reflex is main mechanism – spray-type nerve endings in walls of carotid sinus and aortic arch
o Signal pressure by responding to change in pressure induced stretch of arterial wall
o Afferent nerve fibres  terminated in nucleus of the solitary tract (NTS) in medulla  vagal and
sympathetic preganglionic neurons  alters activity of nerves innervating heart and blood vessels
o Tonically active at normal levels of arterial BP – signal changes within range of 50~160 mmHg
o Adapt to whatever pressure they are exposed to within 1-2 days  no role in long term regulation
 Arterial chemoreceptors in carotid body and aortic arch – stimulated by ↓ PO2  vasoconstriction
o Afferent fibres fun in glossopharyngeal or vagal nerve  NST
 Receptors in the low pressure part of circulation (partic R atria)  responds to change in blood volume
 ↓ BP  ↑ activity of sympathetic nerves + vasopressin release from hypothalamus  ↑ TPR + ↓ urine production

Long Term Regulation of BP

 Renin-Angiotensin-Aldosterone system (RAAS) – in response to low BP or blood volume renin is released from
the kidney juxtaglomerular cells  converts angiotensinogen to angiotensin I  converted to angiotensin II by
ACE 
o Blood vessels – vasoconstriction
o Kidney - ↑ salt and water reabsorption  overall effect is ↑ BP and ↑ blood volume
o Adrenal cortex  aldosterone release  kidney to ↑ salt and water reabsorption
o Brain  vasopressin (antidiuretic hormone) + ↑ thirst
o Noradrenaline release  stimulates renin release + vasoconstriction
 Renal function curve – shows relationship between arterial pressure and output of salt and water
 Damage to kidney  shifts curve to R – need ↑ arterial pressure to secrete same amount of salt
 ↑ intake of salt and water  move up the curve (↑ pressure) to excrete extra salt
o but salt intake  ↑ BP  ↓ RAAS  ↓ BP back towards normal
 Angiotensin II  effect is to retain salt and water  moves curve to the R  ↑ BP
 Sympathetic nervous system also plays a role in long term BP regulation by affecting the renal function curve:
o Directly – via action of renal vascular resistance
o Indirectly – renin release from kidney or via release of catecholamines
 Renal sympathetic nerve activity could be increased by a chronic resetting of the baroreceptor reflex, Inputs from
other peripheral receptors (chemoreceptors), circulating hormones that act on brain
Ventricular Arrhythmias
 Disturbances of the electrical excitation of the ventricular myocardium which affect the rate and coordination of
contraction, and hence overall pumping efficiency of the heart
 Pumping efficiency determined by ventricular rate and coordination - Rapid rates  shorten diastole  restrict
ventricular filling + ↓ coronary blood flow
 Bradycardias – result of failure of contraction f the normal electrical impulses from the AV node to the ventricles
o His-Purkinje system depolarises spontaneously at 40/min, but may be slower or display no automaticity if
diseased
o Treatment by artificial pacemaker
 Tachycardia – Due to electrical depolarisations arising within the ventricles themselves
o QRS complex is abnormal in shape and of longer duration than normal, + may be ectopic beats –
premature beat (no p wave) with pause after and broader complex
o Commonly arise due to re-entrant tachycardia (depolarisation wave in a circular course) which excites the
ventricles repeatedly
 Refractory period of the myocardium normally prevents this
 Arrhythmias occur when:
 Conduction through myocardium is slowed – scar tissue or ischaemic myocardium
 Ventricles are hypertrophied so longer conduction pathways are possible
o Ventricular fibrillation – totally uncoordinated contraction which occurs when re-entry waves becomes
inconstant or breaks up into multiple uncoordinated re-entry loops
o Treatment –
 Beta adrenergic blockage to modify sympathetic tone
 Anti-arrhythmic drugs which modify conduction time and refractory period
 Defibrillation – interrupts re-entry loops by electrically depolarising al the ventricular
myocardium at once
 Surgical destruction of localised potential re-entry pathways
 LV hypertrophy  larger QRS complex + increased risk of ventricular arrhythmias due to increased space for re-
entry loops, fibrosis, ischaemia, changed AP generation and changed tissue conductance

Obesity Related Hypertension

 Increased fat mass 
o Increased leptin
o OSA  Sympathetic Activation
o ↑ Free fatty acids
o insulin resistance  ↑ insulin
 Sympathetic activation  Vasoconstriction + AgII release via renal sympathetic nerve activity