• Blood pressure is derived from the amount of blood leaving the heart times the resistance in the peripheries (blood pressure = cardiac output × peripheral resistance). When either cardiac output or peripheral resistance increases, the blood pressure rises. Drug therapy to reduce hypertension is designed to decrease either cardiac output or peripheral resistance or both. Drug therapy to increase blood pressure increases cardiac output, peripheral resistance, or both. • Hypertension is classifi ed in 3 stages (from prehypertension to stage 2), according to the degree of blood pressure elevation. • In prehypertension, blood pressure is usually managed by lifestyle changes alone. These changes include weight reduction, dietary restriction of saturated fat, moderation of alcohol intake, regular physical activity, reduction of sodium intake, increased intake of potassium- and calcium-rich foods, and smoking cessation. Lifestyle modifi cations continue even if the patient advances to stage 1 or 2 hypertension. • Drug therapy may be initiated in prehypertension if the patient has certain other comorbidities. Drug therapy is always initiated in stage 1 or 2 hypertension Most patients require the use of at least two types of antihypertensives to achieve full therapeutic effect. Patients whose blood pressure is diffi cult to control may be on three or more fi rst-line drugs as well as some second-line drugs. • Drug classes used as fi rst-line therapy include: thiazide diuretics, beta blockers, ACE inhibitors, ARBs, calcium channel blockers (for some patients), and occasionally aldosterone blockers. • Drug classes used as second-line therapy include: vasodilators, alpha-2 stimulants, alpha-1 blockers, peripheral antiadrenergics. • Thiazide diuretics (such as hydrochlorothiazide) are effective and less expensive than other antihypertensives. A thiazide diuretic is usually used as the drug of fi rst choice in monotherapy. Other classes of fi rst-line drugs may be added if necessary. Thiazides are effective in monotherapy in African Americans unlike most of the fi rst-line drugs. The most common adverse effects are related to electrolyte changes and fl uid volume loss (i.e., hypovolemia, low potassium, magnesium, and sodium levels, and elevated uric acid and blood glucose levels). • Beta blockers (such as metoprolol) slow heart rate, speed conduction, and decrease force of contraction and thus decrease cardiac output. This decreases the blood pressure. Although beta blockers (at beta-2 receptor sites) increase peripheral resistance through vasoconstriction, this effect is outweighed by the substantial decrease in cardiac output, thereby lowering blood pressure. Beta blockers also decrease the release of renin from the kidneys so the renin-angiotensin-aldosterone system is not activated, so vasoconstriction does not occur. Beta blockers are used as the initial therapy for patients with certain comorbidities; they are not as effective as monotherapy in African Americans. • Captopril, an ACE inhibitor, inhibits the angiotensinconverting enzyme needed to change the inactive angiotensin I to the active form angiotensin II, thereby preventing sodium and water retention, decreasing peripheral vascular resistance, and lowering blood pressure. A major adverse effect is a chronic cough, which may be so severe that the patient cannot tolerate or continue drug therapy. Firstdose hypotension may occur. As monotherapy it does not achieve the same therapeutic effects in African Americans as in other races. • Aliskaren is a renin inhibitor. Similar to other drugs that alter the renin-angiotensin-aldosterone system, monotherapy with aliskaren produced fewer antihypertensive effects in African Americans, probably because most African Americans are "low-renin hypertensives." • Losartan is an ARB; it does not inhibit ACE. Instead, it blocks the vasoconstricting and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the angiotensin receptors in many tissues, especially in the vascular smooth muscled drenal gland tissues. • Eplerenone is a selective aldosterone receptor blocker. It interferes with the renin-angiotensin-aldosterone system. By blocking the mineralocorticoid aldosterone receptors, it prevents sodium and fl uid reabsorption that leads to hypertension. • Nitroprusside, an agent used in hypertensive crisis, directly relaxes vascular smooth muscle. It is more active on veins than arteries, thereby promoting peripheral pooling of blood. This effect decreases venous return to the heart, reducing left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (preload). The resultant arteriolar dilation reduces systemic resistance and decreases mean arterial pressure (afterload). The result is markedly reduced blood pressure. The ability to decrease the blood pressure is seemingly unlimited. Nitroprusside is rapidly metabolized to cyanide through a reaction with hemoglobin. Cyanide poisoning may occur during its use. If blood pressure remains uncontrolled after 10 minutes at the maximum infusion rate, stop the infusion immediately. The nitroprusside infusion should be controlled by an administration pump, and the blood pressure must be monitored constantly. • Dopamine, a vasopressor, is used to correct the hemodynamic imbalances present in shock. Dopamine is a naturally occurring catecholamine and a precursor to norepinephrine. It stimulates alpha-1 and beta-1 receptors through direct and indirect (releasing the stored epinephrine) methods. It has either no or only a minimal effect on beta-2 receptors. It also has dopaminergic effects. The effects from dopamine are increased renal perfusion, increased cardiac output, increased or decreased peripheral resistance (depending on the dose), and increases in blood pressure. Dopamine is administered by IV continuous infusion. The patient must be monitored closely and continuously while on dopamine infusion.
|Original language||English (US)|
|Title of host publication||Drug Therapy in Nursing|
|Publisher||Wolters Kluwer Health Adis (ESP)|
|Number of pages||140|
|State||Published - Nov 7 2012|
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