SYSTEMIC HYPERTENSION

Hypertension is one of the leading causes of the global burden of disease. Hypertension doubles the risk of cardiovascular diseases, including coronary heart disease (CHD), congestive heart failure (CHF), ischemic and hemorrhagic stroke, renal failure, and peripheral arterial disease. Although antihypertensive therapy clearly reduces the risks of cardiovascular and renal disease, large segments of the hypertensive population are either untreated or inadequately treated.

Definition Hypertension currently is defined as a usual BP of 140/90 mm Hg or higher, for which the benefits of drug treatment have been definitively established

Staging of Office Blood Pressure BP STAGE SYSTOLIC BP (mm Hg) DIASTOLIC BP (mm Hg) Normal <120 <80 Prehypertension 120-139 80-89 Stage 1 hypertension 140-159 90-99 Stage 2 hypertension ≥160 ≥100

Aetiology Primary (Essential) hypertension The majority (90–95%) of patients with hypertension have primary elevation of blood pressure, i.e. essential hypertension of unknown cause. Secondary hypertension (5-10%).

Many factors may contribute to development of essential HT Neural Mechanisms Baroreflex control of sinus node function is abnormal Obesity-Related Hypertension Obstructive Sleep Apnea Renal Mechanisms acquired or inherited defect in the kidneys' ability to excrete the excessive sodium load Low Birth Weight Genetic Contributions

Vascular Mechanisms Hormonal Mechanisms Endothelial Cell Dysfunction Vascular Remodeling: An increase in the medial thickness relative to lumen diameter (increased media-to-lumen ratio) is the hallmark of hypertensive remodeling in small and large arteries. Hormonal Mechanisms Activation of the renin-angiotensin-aldosterone system (RAAS) is one of the most important mechanisms contributing to endothelial cell dysfunction, vascular remodeling, and hypertension

Secondary hypertension Renal diseases These account for over 80% of the cases of secondary hypertension. The common causes are: ■ diabetic nephropathy ■ chronic glomerulonephritis ■ adult polycystic disease ■ chronic tubulointerstitial nephritis ■ renovascular disease.

Congenital cardiovascular causes Endocrine causes These include: Conn’s syndrome Congenital adrenal hyperplasia phaeochromocytoma Cushing’s syndrome acromegaly. Hyperparathyroidism Primary hypothyroidism Thyrotoxicosis Congenital cardiovascular causes The major cause is coarctation of the aorta

Drugs: NSAIDs, oral contraceptives, steroids, carbenoxolone, liquorice, sympathomimetics and vasopressin. Pregnancy (pre-eclampsia) Alcohol Obesity

All adults should have blood pressure measured routinely at least every 5 years until the age of 80 years. Seated blood pressure when measured after 5 minutes’ resting with appropriate cuff size and arm supported is usually sufficient, but standing blood pressure should be measured in diabetic and elderly subjects to exclude orthostatic hypotension. The cuff should be deflated at 2 mm/s and the blood pressure measured to the nearest 2 mmHg. Two consistent blood pressure measurements are needed to estimate blood pressure, and more are recommended if there is variation in the pressure. When assessing the cardiovascular risk, the average blood pressure at separate visits is more accurate than measurements taken at a single visit.

Assessment History Family history, lifestyle (exercise, salt intake, smoking habit) and other risk factors should be recorded. The patient with mild hypertension is usually asymptomatic. Higher levels of blood pressure may be associated with headaches, epistaxis or nocturia. Attacks of sweating, headaches and palpitations point towards the diagnosis of phaeochromocytoma. Breathlessness may be present owing to left ventricular hypertrophy or cardiac failure, symptoms of peripheral arterial vascular disease suggest the diagnosis of atheromatous renal artery stenosis.

Examination Findings related to hypertension Loud A2 S4 Forceful sustained apical impulse (heaving)

Examination Secondary causes: 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 are all examples of physical signs that may help to identify causes of secondary hypertension. Risk factors: Examination may also reveal features of important risk factors such as central obesity and hyperlipidaemia (tendon xanthomas etc.). Complications: The optic fundi are often abnormal and there may be evidence of generalised atheroma or specific complications such as aortic aneurysm or peripheral vascular disease.

investigation of all patients Investigations investigation of all patients Urinalysis for blood, protein and glucose Blood urea, electrolytes and creatinine N.B. Hypokalaemic alkalosis may indicate primary hyperaldosteronism but is usually due to diuretic therapy Blood glucose Serum total and HDL cholesterol 12-lead ECG (left ventricular hypertrophy, coronary artery disease)

investigation of selected patients Chest X-ray: to detect cardiomegaly, heart failure, coarctation of the aorta Ambulatory BP recording: to assess borderline or 'white coat' hypertension Echocardiogram: to detect or quantify left ventricular hypertrophy & for the diagnosis ofcoactation of aorta Renal ultrasound: to detect possible renal disease Renal angiography: to detect or confirm presence of renal artery stenosis Urinary catecholamines: to detect possible phaeochromocytoma Urinary cortisol and dexamethasone suppression test: to detect possible Cushing's syndrome Plasma renin activity and aldosterone: to detect possible primary aldosteronism

Ambulatory blood pressure monitoring Indirect automatic blood pressure measurements can be made over a 24-hour period using a measuring device worn by the patient. they are used to confirm the diagnosis in those patients with ‘white-coat’ hypertension, i.e. blood pressure is completely normal at all stages except during a clinical consultation These devices may also be used to monitor the response of patients to drug treatment and, in particular, can be used to determine the adequacy of 24-hour control with once-daily medication

Ambulatory blood pressure recordings seem to be better predictors of cardiovascular risk than clinic measurements. Analysis of the diurnal variation in blood pressure suggests that those hypertensives with loss of the usual nocturnal fall in blood pressure (‘non-dippers’) have a worse prognosis than those who retain this pattern.

Complications

Central nervous system Blood vessels In larger arteries (> 1 mm in diameter), the internal elastic lamina is thickened, smooth muscle is hypertrophied and fibrous tissue is deposited. In smaller arteries (< 1 mm), hyaline arteriosclerosis aortic aneurysm and aortic dissection Central nervous system Stroke (due to cerebral haemorrhage or infarction). Carotid atheroma and transient ischaemic attacks 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 symptoms, including transient disturbances of speech or vision, paraesthesiae, disorientation, fits and loss of consciousness. Papilloedema is common. Retina central retinal vein thrombosis Hypertensive retinopathy Grade I 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 papilloedema

'Malignant' or 'accelerated' phase hypertension (Diastole>130 mmgh) Heart coronary artery disease. left ventricular hypertrophy Atrial fibrillation Diastolic dysfunction LV failure. Kidneys Long-standing hypertension may cause proteinuria and progressive renal failure by damaging the renal vasculature. 'Malignant' or 'accelerated' phase hypertension (Diastole>130 mmgh) This rare condition may complicate hypertension of any aetiology and is characterised by accelerated microvascular damage and by intravascular thrombosis. The diagnosis is based on evidence of high BP and rapidly progressive end organ damage, such as retinopathy (grade 3 or 4), renal dysfunction (especially proteinuria) and/or hypertensive encephalopathy . Left ventricular failure may occur and, if this is untreated, death occurs within months.