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  • 2020–2021 BCSC Basic and Clinical Science Course™

    Go to Academy Store Learn more and Purchase.

    1 Update on General Medicine

    Chapter 3: Hypertension

    Treatment of Hypertension

    Pharmacologic Treatment

    Several classes of drugs effectively lower BP and reduce the complications resulting from hypertension. The most commonly prescribed antihypertensive drugs include diuretics, β-blockers, ACE inhibitors, ARBs, and CCBs. Table 3-5 lists these and other types of oral antihypertensive drugs. Figure 3-2 provides an algorithm for the treatment of hypertension.

    The 2017 ACC/AHA guidelines focus on the pharmacologic treatment of hypertension. The JNC 7 guidelines recommended thiazide-type diuretics as the initial drug therapy unless compelling reasons dictated otherwise. In the 2017 ACC/AHA guidelines, thiazides are not necessarily the first-line therapy; CCBs, ACE inhibitors, ARBs, and β-blockers are alternatives. The initial drug choice for nonblack patients may be selected from 4 drug classes, based on clinical setting and comorbidities: thiazide-type diuretics, CCBs, ACE inhibitors, and ARBs. For black patients, the initial drug choice may be selected from 2 drug classes: thiazide-type diuretics and CCBs.

    Table 3-4 2017 Recommended Nonpharmacologic Interventions for Prevention and Treatment of Hypertensiona

    Table 3-5 Oral Antihypertensive Drugs

    Antihypertensive Drugs

    Diuretics Diuretics are categorized by their site of action in the kidney and are divided into thiazide, loop, and potassium-sparing types.

    Thiazide-type diuretics send more of a sodium load to the kidney’s distal tubules, initially decreasing plasma volume and cardiac output through natriuresis. As the renin-angiotensin-aldosterone system compensates for the diminished plasma volume, cardiac output returns to normal and peripheral vascular resistance is lowered. Chlorthalidone, 12.5–25 mg, can be used in patients with a glomerular filtration rate (GFR) of less than 30 mL/min and has a strong safety and cardio-protective profile.

    Loop diuretics act on the ascending loop of Henle and block sodium resorption, increasing free water loss, resulting in an initial decrease in plasma volume. As with thiazide-type diuretics, BP is eventually lowered because of decreased peripheral vascular resistance. Loop diuretics are used primarily in treating patients with moderate renal insufficiency.

    Figure 3-2 Blood pressure (BP) thresholds and recommendations for treatment and follow-up.

    (Modified with permission from Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the prevention, detection, evaluation and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018; 71[6]:e74.)

    Potassium-sparing diuretics may block the actions of aldosterone to prevent potassium loss from the distal tubule, or they may act directly on the distal tubule to inhibit aldosterone-induced sodium resorption in exchange for potassium. They are often used as adjuncts to the thiazide-type or loop diuretics to counteract potassium depletion, but in patients with suspected hyperaldosterone states they may be used alone.

    Side effects of diuretics vary according to class. Thiazide-type diuretics can cause weakness, muscle cramps, impotence, hypokalemia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, hypomagnesemia, hyponatremia, azotemia, and pancreatitis. Thiazide-type diuretics may also unmask type 2 diabetes and aggravate lipid disorders. On a positive note, they may also slow the demineralization that occurs with osteoporosis. Loop diuretics can cause ototoxicity, as well as electrolyte abnormalities such as hypokalemia, hypocalcemia, and hypomagnesemia. Potassium-sparing diuretics can cause hyperkalemia, renal calculi, renal tubular damage, and gynecomastia. Diuretics are particularly effective in individuals with salt-sensitive hypertension such as older persons and in black persons.

    Angiotensin-converting enzyme inhibitors Angiotensin-converting enzyme (ACE) catalyzes the conversion of angiotensin I to angiotensin II. Angiotensin II, a potent vasoconstrictor, is the primary vasoactive hormone of the renin-angiotensin-aldosterone system, and it plays a major role in the pathophysiology of hypertension. ACE inhibitors block the conversion of angiotensin I to angiotensin II, resulting in vasodilation with decreased peripheral vascular resistance and natriuresis. They also decrease aldosterone production and increase levels of vasodilating bradykinins. Some ACE inhibitors stimulate production of vasodilatory prostaglandins. The efficacy of ACE inhibitors is enhanced when they are used in combination with diuretics, reducing hypokalemia, hypercholesterolemia, hyperglycemia, and hyperuricemia caused by diuretic therapy. ACE inhibitors are beneficial in patients with left ventricular dysfunction and with proteinuria, especially in patients with diabetes. ACE inhibitors may also help improve insulin sensitivity.

    Adverse effects of ACE inhibitors include a dry cough (5%–20% of patients), angioneurotic edema, hypotension, hyperkalemia, abnormal taste, leukopenia, and proteinuria; in addition, patients may have a reduced GFR (30% of patients). Preexisting renal artery stenosis should be considered in this clinical situation. In patients with volume-reduced states, ACE inhibitors should be suspended and reassessed later. ACE inhibitors should be avoided in patients with a history of angioedema or known renal artery stenosis (RAS). They are contraindicated during pregnancy and in patients trying to become pregnant because of the adverse effects on fetal renal function and risk of fetal death.

    Angiotensin II receptor blockers Angiotensin II receptor blockers (ARBs) inhibit the vasoconstrictive and aldosterone-secreting effects of angiotensin II by selectively blocking the angiotensin II receptors that are found in such tissues as vascular smooth muscle and the adrenal gland, resulting in decreased peripheral vascular resistance. ARBs are effective in managing hypertension in a variety of situations, including in patients with heart failure who are unable to tolerate ACE inhibitors. ARBs also have been associated with a reduced incidence of new-onset diabetes mellitus and, like ACE inhibitors, improve insulin sensitivity.

    The adverse effects of ARBs are similar to those occurring with ACE inhibitors, though they occur less commonly with ARBs. The dry cough caused by ACE inhibitors generally does not occur with use of ARBs, and angioedema is rare. Like ACE inhibitors, ARBs are contraindicated in pregnancy unless there is profound proteinuria, and then use is very closely monitored. ACE inhibitors should not be combined with ARBs.

    Calcium channel blockers Calcium channel blockers (CCBs) block the entry of calcium into vascular smooth muscle cells, resulting in reduced myocardial contractility and decreased systemic vascular resistance. CCBs are divided into 2 types: dihydropyridine and nondihydropyridine. Dihydropyridine (DHP) CCBs tend to be more potent vasodilators, whereas the nondihydropyridine CCBs have more marked negative inotropic effects.

    Adverse effects of CCBs vary according to the agent but include constipation, headache, fatigue, dizziness, nausea, palpitations, flushing, edema, gingival hyperplasia, arrhythmias, and cardiac ischemia. Because of their negative inotropic effects, nondihydropyridine CCBs should generally be avoided in patients with cardiac conduction abnormalities such as atrial fibrillation or heart failure associated with left ventricular dysfunction and in patients with acute MI. Dihydropyridine CCBs may be helpful in patients with Raynaud syndrome and in some arrhythmias.

    β-Blockers There are 2 types of β-adrenergic receptor sites: β1 is present in vascular and cardiac tissue, and β2 is found in the bronchial system. Circulating or locally released catecholamines stimulate β sites, resulting in vasoconstriction, bronchodilation, tachycardia, and increased myocardial contractility. β-Blockers inhibit these effects. They also decrease plasma renin, reset baroreceptors to facilitate lower BP, induce the release of vasodilatory prostaglandins, and decrease plasma volume, and they may have a central nervous system–mediated antihypertensive effect.

    β-Blockers are divided into those that are nonselective (β1 and β2), those that are cardioselective (primarily β1), and those that have intrinsic sympathomimetic activity (ISA). The cardioselective agents may be prescribed with caution in patients with pulmonary disease, diabetes mellitus, or peripheral arterial disease, but at higher doses they lose their β1 selectivity and can cause adverse effects in these patients. Those agents with ISA minimize the bradycardia caused by other β-blockers. β-Blockers with α-blocking properties, such as carvedilol or labetalol, have additional vasodilatory effects caused by selective α1-receptor blockade. In patients with heart failure due to systolic dysfunction, the use of certain β-blockers—particularly carvedilol, metoprolol succinate, and bisoprolol—reduces hospitalizations for heart failure and improves survival rates. Nebivolol has nitric oxide–potentiating vasodilatory effects. β-Blockers are beneficial in the treatment of atrial fibrillation and tachyarrhythmias, migraine, thyrotoxicosis, and essential tremor.

    Adverse effects of β-blockers include bronchospasm, bradycardia, masking of insulin-induced hypoglycemia, insomnia, fatigue, depression, impotence, impaired peripheral circulation, impaired exercise tolerance, nasal congestion, and hypertriglyceridemia (except for β-blockers with ISA). Angina pectoris and increased BP can be precipitated by abrupt cessation of β-blocker therapy. β-Blockers should generally be avoided in patients with asthma, reactive airway disease, or second-degree or third-degree heart block.

    Ophthalmic Considerations β-Blockers are used in the treatment of glaucoma and are effective in lowering intraocular pressure; they have a long duration of action. Systemic adverse effects resulting from the use of these topical agents may occur; these can be minimized by nasolacrimal occlusion for 3 minutes after drop installation.

    α1-Blockers α1-Adrenergic antagonists block postsynaptic α-receptors, resulting in arterial and venous vasodilation. Selective α1-blockers have replaced older nonselective agents in the treatment of hypertension. Although these agents are not as effective as diuretics, CCBs, and ACE inhibitors, they may be prescribed as adjunct therapy in selected cases, not as a primary agent.

    Adverse effects include the “first-dose effect,” in which BP is decreased more with the initial dose than with subsequent doses; orthostatic hypotension; headache; dizziness; and drowsiness.

    Combined α-adrenergic and β-adrenergic antagonists Combined α-adrenergic and β-adrenergic antagonists block the action of catecholamines at both α-adrenergic and β-adrenergic receptor sites. Adverse effects are similar to those of other α-adrenergic and β-adrenergic antagonists.

    Centrally acting adrenergic drugs Centrally acting adrenergic drugs are potent antihypertensive agents that stimulate presynaptic α2-adrenergic receptors in the central nervous system (CNS), causing reductions in the tone and contractility of smooth muscle, cardiac output, and peripheral vascular resistance.

    Adverse effects include fluid retention, dry mouth, drowsiness, dizziness, orthostatic hypotension, rash, impotence, and hepatitis; positive results on the direct antiglobulin (Coombs) test and the antinuclear antibody (ANA) test; and heart failure in patients with decreased left ventricular dysfunction. There may also be severe rebound hypertension if the drug is abruptly discontinued.

    Methyldopa continues to be widely used in pregnancy because of its proven safety. Older centrally acting sympatholytic agents (eg, reserpine) have significant adverse effects and are seldom used.

    Direct vasodilators Direct-acting vasodilators such as minoxidil and hydralazine decrease peripheral vascular resistance by direct arterial vasodilation. They are generally reserved for special situations, such as pregnancy or intractable hypertension. They should be avoided or used with caution in patients with ischemic heart disease.

    Adverse effects include headache, tachycardia, edema, nausea, vomiting, a lupuslike syndrome, and hypertrichosis. Because of the sympathetic hyperactivity and the sodium and fluid retention caused by direct vasodilators, they are often used in conjunction with diuretics or β-blockers.

    Combination therapy Combination therapy usually includes small doses of a diuretic, which potentiates the effects of other drugs such as ACE inhibitors, ARBs, and β-blockers. This therapy may improve patient adherence and reduce BP to target levels more quickly than other classes of drugs. Another advantage of combination therapy is that low-dose therapy with 2 antihypertensive drugs is associated with fewer adverse effects than is higher-dose therapy with a single agent.

    Direct renin inhibitors Aliskiren is the first orally active renin inhibitor launched to treat hypertension. It has a high specificity for renin and has a long half-life (approximately 24 hours), which makes it ideal for once-daily treatment of hypertension. Direct renin inhibitors (DRIs) are more likely to be effective in younger white patients, who, in general, have a more active renin system, and in any patients receiving diuretics or CCBs, in whom the renin system has been activated. The main adverse effect of DRIs is possible diarrhea at higher doses.

    Parenteral antihypertensive drugs Parenteral antihypertensive therapy is indicated for immediate reduction of BP in hypertensive emergencies.

    Sodium nitroprusside, a direct arterial and venous vasodilator, is the drug of choice for most hypertensive emergencies. Nitroglycerin may be preferable in patients with severe coronary insufficiency or advanced kidney or liver disease. Labetalol is also effective and is the drug of choice in hypertensive emergencies that occur in pregnancy. Esmolol is a cardioselective β-adrenergic antagonist that can be used in hypertensive emergencies when β-blocker intolerance is a concern; it is also useful in treating aortic dissection. Phentolamine is effective in managing hypertension with acute drug intoxication or withdrawal. Nicardipine is a CCB that can be administered intravenously for postoperative hypertension. Intravenous enalapril is an ACE inhibitor that can be effective in the treatment of postoperative hypertension, although unpredictable results have been reported with its use. Diazoxide and hydralazine are used infrequently now, but hydralazine does have a long-established safety profile and may be useful in pregnancy-related hypertensive emergencies.

    Excerpted from BCSC 2020-2021 series: Section 1 - Update on General Medicine. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.

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© American Academy of Ophthalmology 2021