Wikis > General Medicine > Cardiology > Hypertension


Most common cardiovascular problem  major epidemiological health problem. Could be present in up to 20% of middle aged population (affects 50% of those >60yrs; severe in 5% of adult population). Most is undiagnosed.

Major modifiable risk factor for coronary heart disease, myocardial infarction, kidney disease, blindness and stroke. Those in higher fifth of blood pressure levels have a 16 fold increased risk for stroke relative to lowest fifth. Improvement in blood pressure  decreased risk.

Two types:
1) Primary/Essential/Idiopathic hypertension (70-95%) – no overt underlying disease process; chronic progressive disorder  pressure gradually rises over time
2) Secondary hypertension (5-30%) – underlying disease process (eg Cushing’s disease- 0.1%; renal vascular disease – 4%; polycystic kidney disease; Pheochromocytoma – 0.1%; oral contraceptive related – 1%; hyperalderosteronism; acromegaly; thyrotoxicosis)

Aetiology of primary hypertension:
Main factors are:
• High salt intake (relationship between salt intake and blood pressure levels demonstrated in epidemiological studies and intervention studies; gene defects that cause hypertension are related to the kidneys ability to excrete sodium)
• Low potassium intake (high potassium intake protects against the effects of high salt intake on blood pressure)
• Obesity (weight loss  reduction in blood pressure; associated with other metabolic disorders)
• Alcohol consumption
• Physical inactivity
• Family history (inheritance accounts for about 25% of the variability in blood pressure)
• Stress (no evidences for stress)

Blood pressure distribution follows a bell shaped curve  no clear line with normotensive and hypertensive. Pressure should be measured both seated and standing.
Usually asymptomatic, unless malignant hypertension.
General guidelines:
1) Systolic pressure (SBP) values:
• high normal – 130-139mmHg
• mild – 140-159mmHg (Stage 1)
• moderate – 160-179mmHg (Stage 2)
• severe – 180-209mmHg (Stage 3)
• very severe – > 210mmHg
2) Diastolic pressure (DBP) values
• high normal – 85-89mmHg
• mild – 90-99mmHg (Stage 1)
• moderate – 100-109mmHg (Stage 2)
• severe – 110-119mmHg (Stage 3)
• very severe – > 120mmHg

Diagnosis is based on a number of readings over several weeks – not a single reading.
In epidemiologic studies, systolic pressure is more predictive of cardiovascular risk than diastolic.

Complications/consequences (end organ damage):
• large arteries  internal elastic lamina becomes thickened; smooth muscle is hypertrophied; fibrous tissue deposited  atherosclerosis (endothelial function is also affected by hypertension)
• smaller arteries  hyaline arteriosclerosis, lumen narrows, aneurysms may develop (Charcot Bouchard aneurysms in intracerebral arteries)
• atheroma (if combined with other risk factors (eg smoking, hyperlipidaemia)  increased risk for coronary and cerebrovascular events/disease
• CNS  stroke, hypertensive encephalopathy
• Eye  hypertensive retinopathy
• Heart – increased load on heart  left ventricular hypertrophy (LVH)  fourth heart sound; atrial fibrillation; if hypertension severe  left ventricular failure; LVH increase risk for ischamic heart disease by 4 fold and stroke by 12 fold.
• Kidneys  hypertensive damage to renal vessels can lead to renal failure

Malignant hypertension:
Severe form; systolic >200mmHg and diastolic >130mmHg; may directly damage small arterioles; usually have retinal exudates and haemorrhages, papilloedema, visual disturbances, renal failure and headaches (may be due to hypertensive encephalopathy); needs urgent treatment and is reversible in early stages; later renal failure may need dialysis and/or transplant.

Risk stratification (? Australian guidelines)

Generally, cure is not possible  lifelong management ( potential for compliance problems)
1) Nonpharmacologic:
• risk factor modification (RFM)  have greater benefits than just on blood pressure
• aerobic exercise (30-45 mins, most days); salt/sodium restriction; increase potassium intake (fruit and vegetables) & adequate calcium and magnesium intake; stop smoking; limit alcohol and caffeine intake; weight loss; reduce dietary saturated fat and cholesterol
2) Pharmacologic:
a) Diuretics
• mainstay of management – reduce blood pressure on own and enhance effects of other hypotensives; inexpensive
• thiazide diuretics (most common; reduce blood volume; reduce arterial resistance; but produce hypokalaemia; act by inhibiting tubular sodium resorption); high-ceiling/loop diuretics (stronger and shorter acting than thiazides; reduce blood volumes; promote vasodilation; but, produce hypokalaemia, dehydration, hyperglycaemia and hyperuricaemia; act by inhibiting sodium resorption in the ascending loop of Henle); potassium sparing diuretics (weakly diuretic; act on distal tubule to reduce excretion of potassium and increase sodium excretion)
b) Sympatholytics
• suppress effects of sympathetic nervous system; widely used
• beta-adrenergic blockers (most common hypertensive; exact mechanism unclear; decrease heart rate and contraction force, suppress reflex tachycardia due to vasodilators, reduces kidney release of renin, reduce peripheral vascular resistance; but, can cause bradycardia, decreased AV conduction, bronchoconstriction); alpha1-adrenergic blockers (lowers peripheral resistance by blocking postsynaptic alpha1-adrenergic smooth muscle receptors; useful in those with insulin resistance syndrome (hypertension, obesity, type 2 diabetes, dyslipidaemia); but potential for hypotension is high); centrally acting alppha2 agonists (act in brainstem  suppresses sympathetic outflow  vasodilation and reduced cardiac output); adrenergic neuron blockers (work via inhibit release of norepinephrine in postganglionic sympathetic neurons or depletion of norepinephrine)
c) Angiotension-converting enzyme (ACE) inhibitors
• eg Captopril, Cilazapril, Enalapril
• decrease peripheral resistance and enhance vasodilation – blocks conversion of angiotensin I to angiotensin II  prevents angiotensin II induced vasoconstriction
• slows progressive kidney damage
d) Angiotension II receptor blockers
• block effects of angiotensin II
e) Calcium channel blockers
• lowers calcium concentration in vascular smooth muscle  increase vasodilation and decrease in peripheral resistance
• can produce reflex tachycardia
f) Direct acting vasodilators
• eg minoxidil, hydralazine
• act directly on arterioles  dilation (minimal effect on venous vessels  low risk for hypotension)
• serious side effect of hydralazine is systemic lupus erythematosus

Implications for Podiatric Management:
May suspect an undetected case
Check control if concerned
Use of diuretics  ?nocturnal leg cramps; lower limb weakness; fatigue
changes to macro- and micro-vasculature
implications for surgical intervention (eg if hypertension poorly controlled  not suitable for day surgery)

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