Cardiovascular system CVS

Hypertension

definition
‘The level of BP at which the benefits of treatment outweigh the costs and hazards

Aetiology of Hypertension

Primary – 90-95% of cases – also termed “essential” of “idiopathic”Secondary – about 5% of cases -Alcohol ,Obesity, Pregnancy (pre-eclampsia) -Renal disease : Parenchymal renal disease, particularly glomerulonephritis Renal vascular disease • -Endocrine disease : Phaeochromocytoma , Cushing’s syndrome , Primary hyperaldosteronism (Conn’s syndrome) , Acromegaly , Primary hypothyroidism , Thyrotoxicosis , Congenital adrenal hyperplasia • -Drugs : e.g. Oral contraceptives containing oestrogens, anabolic steroids, corticosteroids, NSAIDs, carbenoxolone, ----Coarctation of the aorta

Stages

Identification of hypertensive patients Baseline investigations Initiating therapy Reviewing patients Stepping up therapy Motivation and compliance

Approach to newly diagnosed hypertension

Hypertension is predominantly an asymptomatic condition and the diagnosis is usually made at routine examination or when a complication arises.

The objectives of the initial evaluation of a patient with high BP readings are: • To obtain accurate, representative BP measurements • 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.

History

Family history, lifestyle (exercise, salt intake, smoking habit) and other risk factors should be recorded. A careful history will identify those patients with drug- or alcohol-induced hypertension and may elicit the symptoms of other causes of secondary hypertension, such as phaeochromocytoma (paroxysmal headache, palpitation and sweating, or complications such as coronary artery disease (e.g. angina, breathlessne

Examination

-Left ventricular hypertrophy (apical heave), accentuation of the aortic component of the second heart sound, and a fourth heart sound. ------Radio-femoral delay (coarctation of the aorta; -----Enlarged kidneys (polycystic kidney disease), -----Abdominal bruits (renal artery stenosis) and the ---Characteristic facies and habitus of Cushing’s syndrome secondary hypertension. -Risk factors, such as central obesity and hyperlipidaemia .-Most abnormal signs are due to the complications of hypertension.

Target organ damage

Central nervous system Stroke is a common complication of hypertension and may be due to cerebral haemorrhage or infarction. TIAs are more common in hypertensive patients. Subarachnoid haemorrhage is also associated with hypertension. Hypertensive encephalopathy is a rare condition characterised by high BP and neurological symptom.

Heart

CAD The excess cardiac mortality and morbidity associated with hypertension are largely due to a higher incidence of coronary artery disease. LVH Atrial fibrillation Heart failure

Hypertensive retinopathy

Grade 1 Arteriolar thickening, tortuosity and increased reflectiveness (‘silver wiring’) • Grade 2 Grade 1 plus constriction of veins at arterial crossings (‘arteriovenous nipping’) • Grade 3 Grade 2 plus evidence of retinal ischaemia (flame-shaped or blot haemorrhages and ‘cotton wool’ exudates) • Grade 4 Grade 3 plus papilloedema.

Hypertension: investigation of all patients

-Urinalysis for blood, protein and glucose • ----Blood urea, electrolytes and creatinine •-Blood glucose • -Serum total and HDL cholesterol • -Thyroid function tests • -12-lead ECG (left ventricular hypertrophy, coronary artery disease. Eee

Hypertension: investigation of selected patient

Chest X-ray: to detect cardiomegaly. Ambulatory BP recording• Echocardiogram: • Renal ultrasound: Renal angiography: renal artery stenosis • Urinary catecholamines: to detect possible phaeochromocytoma • Urinary cortisol : Cushing’s syndrome • Plasma renin activity and aldosteron

Management

The sole objective of antihypertensive therapy is to reduce the incidence of adverse cardiovascular events, particularly coronary artery disease, stroke and heart failure.

Threshold for intervention >140/90 Treatment targets <140/90

Antihypertensive drugs
Thiazide and other diuretics ACE inhibitor Angiotensin receptor blockers Calcium channel antagonists. Beta-blockers Other drugs. vasodilators

Non-drug therapy

Correcting obesity, reducing alcohol intake, restricting salt intake, taking regular physical exercise and increasing consumption of fruit and vegetables can all lower BP. Moreover, quitting smoking, eating oily fish and adopting a diet that is low in saturated fat may produce further reductions in cardiovascular risk.

How to measure blood pressure

Use a machine that has been validated, well maintained and properly calibrated • Measure sitting BP routinely, with additional standing BP in elderly and diabetic patients and those with possible postural hypotension • Remove tight clothing from the arm , Support the arm at the level of the heart • Use a cuff of appropriate size (the bladder must encompass more than two-thirds of the arm) • Lower the pressure slowly (2 mmHg per second) • Use phase V (disappearance of sounds) to measure diastolic BP • Take two measurements at each visit

white coat’ hypertension Sphygmomanometry, particularly when performed by a doctor, can cause an unrepresentative surge in BP which has been termed ‘white coat’ hypertension, and as many as 20% of patients with apparent hypertension in the clinic may have a normal BP when it is recorded by automated devices used at home.

Malignant’ or ‘accelerated’ phasehypertension Very high BP and rapidly progressive end organ damage, such as retinopathy (grade 3 or 4), renal dysfunction (especially proteinuria) and/or hypertensive encephalopathy)or Left ventricular failure.

Practical point

Emergency treatment of accelerated phase or malignant hypertension, lowering BP too quickly may compromise tissue perfusion (due to altered autoregulation) and can cause cerebral damage, including occipital blindness, and precipitate coronary or renal insufficiency. Even in the presence of cardiac failure or hypertensive encephalopathy, a controlled reduction to a level of about 150/90 mmHg over a period of 24–48 hours is ideal.


Follow-up