Chapter 10: Hypertension

INTRODUCTION

• Hypertension is defined as persistently elevated arterial blood pressure (BP). See Table 10-1 for the classification of BP in adults.

• Isolated systolic hypertension is diastolic blood pressure (DBP) <80 mm Hg and systolic blood pressure (SBP) ≥130 mm Hg.

• Hypertensive crisis (BP >180/120 mm Hg) is categorized as hypertensive emergency (extreme BP elevation with acute or progressing end-organ damage) or hypertensive urgency (extreme BP elevation without acute or progressing end-organ injury).

• This chapter incorporates elements of the 2017 American College of Cardiology/American Heart Association (ACC/AHA) Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults, the most recent evidence-based U.S. guideline for hypertension management.

PATHOPHYSIOLOGY

• Hypertension may result from an unknown etiology (primary or essential hypertension) or from a specific cause (secondary hypertension). Secondary hypertension (<10% of cases) is usually caused by chronic kidney disease (CKD) or renovascular disease. Other conditions are Cushing syndrome, coarctation of the aorta, obstructive sleep apnea, hyperparathyroidism, pheochromocytoma, primary aldosteronism, and hyperthyroidism. Examples of drugs that may increase BP include corticosteroids, estrogens, nonsteroidal anti-inflammatory drugs (NSAIDs), amphetamines, cyclosporine, tacrolimus, erythropoietin, and venlafaxine.

• Factors contributing to development of primary hypertension include:

  • ✔ Humoral abnormalities involving the renin–angiotensin–aldosterone system (RAAS), natriuretic hormone, and hyperinsulinemia;

  • ✔ Disturbances in the CNS, autonomic nerve fibers, adrenergic receptors, or baroreceptors;

  • ✔ Abnormalities in renal or tissue autoregulatory processes for sodium excretion, plasma volume, and arteriolar constriction;

  • ✔ Deficiency in synthesis of vasodilating substances in vascular endothelium (prostacyclin, bradykinin, nitric oxide) or excess vasoconstricting substances (angiotensin II, endothelin I);

  • ✔ High sodium intake or lack of dietary calcium.

• Major causes of death include cerebrovascular events, cardiovascular (CV) events, and renal failure. Probability of premature death correlates with the severity of BP elevation.

CLINICAL PRESENTATION

• Patients with uncomplicated primary hypertension are usually asymptomatic initially.

• Patients with secondary hypertension may have symptoms of the underlying disorder:

  • ✔ Pheochromocytoma—headaches, sweating, tachycardia, palpitations, orthostatic hypotension;

  • ✔ Primary aldosteronism—hypokalemic symptoms of muscle cramps and weakness;

  • ✔ Cushing syndrome—moon face, buffalo hump, hirsutism, weight gain, polyuria, edema, menstrual irregularities, acne, muscle weakness.

DIAGNOSIS

• Elevated BP may be the only sign of primary hypertension on physical examination. Diagnosis should be based on the average of two or more readings taken at each of two or more clinical encounters. Refer to the textbook chapter for the correct procedure for BP measurement.

• Signs of end-organ damage occur primarily in the eyes, brain, heart, kidneys, and peripheral vasculature.

• Funduscopic examination may reveal arteriolar narrowing, focal arteriolar constriction, arteriovenous nicking, retinal ...