Hypertension : Pathophysiology, Diagnosis And Treatment
is defined by persistent elevation of arterial blood pressure. Patients with diastolic blood pressure (DBP) values less than 90 mm Hg and systolic blood pressure (SBP) values greater than or equal to 140 mm Hg have isolated systolic hypertension
A hypertensive crisis (blood pressure greater than 180/120 mm Hg) may be categorized as either a hypertensive emergency (extreme blood pressure elevation with acute or progressing target organ damage) or a hypertensive urgency (severe blood pressure elevation without acute or progressing target organ injury).
Hypertension is a heterogeneous disorder that may result either from a specific cause (secondary hypertension) or from an underlying pathophysiologic mechanism of unknown etiology (primary or essential hypertension). Secondary hypertension accounts for fewer than 10% of cases, and most of these are caused by chronic kidney disease or renovascular disease. Other conditions causing secondary hypertension include pheochromocytoma, Cushing’s syndrome, hyperthyroidism, hyperparathyroidism, primary aldosteronism, pregnancy, obstructive sleep apnea, and coarctation of the aorta. Some drugs that may increase blood pressure include corticosteroids, estrogens, nonsteroidal anti-inflammatory drugs (NSAIDs), amphetamines, sibutramine, cyclosporine, tacrolimus, erythropoietin, and venlafaxine.
Multiple factors may contribute to the development of primary hypertension, including:
- humoral abnormalities involving the renin-angiotensin-aldosterone system (RAS), natriuretic hormone, or hyperinsulinemia;
- a pathologic disturbance in the central nervous system (CNS), autonomic nerve fibers, adrenergic receptors, or baroreceptors;
- abnormalities in either the renal or tissue autoregulatory processes for sodium excretion, plasma volume, and arteriolar constriction;
- a deficiency in the local synthesis of vasodilating substances in the vascular endothelium, such as prostacyclin, bradykinin, and nitric oxide, or an increase in production of vasoconstricting substances such as angiotensin II and endothelin I;
Diagnosis of Hypertension :
Frequently, the only sign of primary hypertension on physical examination is elevated blood pressure. The diagnosis of hypertension should be based on the average of two or more readings taken at each of two or more clinical encounters.
As hypertension progresses, signs of end-organ damage begin to appear, chiefly related to pathologic changes in the eye, brain, heart, kidneys, and peripheral blood vessels.
Cardiopulmonary examination may reveal an abnormal heart rate or rhythm, left ventricular hypertrophy, precordial heave, third and fourth heart sounds, and rales.
Peripheral vascular examination can detect evidence of atherosclerosis, which may present as aortic or abdominal bruits, distended veins, diminished or absent peripheral pulses, or lower extremity edema.
Patients with Cushing’s syndrome may have the classic physical features of moon face, buffalo hump, hirsutism, and abdominal striae.
Patients with renal artery stenosis may have an abdominal systolic-diastolic bruit.
Treatment of Hypertension :
All patients with prehypertension and hypertension should be prescribed lifestyle modifications, including (1) weight reduction if overweight, (2) adoption of the Dietary Approaches to Stop Hypertension (DASH) eating plan, (3) dietary sodium restriction to less than or equal to 2.4 g/day (6 g/day sodium chloride), (4) regular aerobic physical activity, (5) moderate alcohol consumption (less than or equal to 1 oz ethanol per day), and (6) smoking cessation.
Patients diagnosed with stage 1 or 2 hypertension should be placed on lifestyle modifications and drug therapy concurrently.
Most patients with stage 1 hypertension should be treated initially with a thiazide diuretic. Patients with stage 2 disease should generally be prescribed combination therapy, with one of the agents being a thiazide-type diuretic unless contraindications exist.
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