Pharmacologic Treatment

In addition to determining therapeutic goals, the ACC/AHA staging system delineates specific therapy options based on disease progression.1,11 For patients in stage A, every effort is made to minimize the impact of diseases that can injure the heart. Anti-

hypertensive and lipid-lowering therapies should be utilized when appropriate to decrease the risk for stroke, MI, and HF. ACE inhibitors should be considered in high-risk vascular disease patients. For stage B patients, the goal is to prevent or slow disease progression by interfering with neurohormonal pathways that lead to cardiac damage and mediate pathologic remodeling. The goal is to prevent the onset of HF symptoms. The backbone of therapy in these patients includes ACE inhibitors or ARBs and P-blockers. In stage C patients with symptomatic LV systolic dysfunction (EF less than 40%), the goals focus on alleviating fluid retention, minimizing disability, slowing disease progression, and reducing long-term risk for hospitalizations and death. Treatment entails a strategy that combines diuretics to control intravascular fluid balance with neurohormonal antagonists to minimize the effects of the RAAS and SNS. Additional neurohormonal blockade with aldosterone antagonists or other therapies such as digoxin are often added as cardiac function continues to decline. Patients with advanced stage D disease are offered more modest goals, such as improvement in quality of life. Enhancing quality of life is often achieved at the expense of expected survival. Treatment options include mechanical support, transplantation, and continuous use of IV vasoactive therapies, in addition to maintaining an optimal regimen of chronic oral medications (Fig. 6-1).

Diuretics

Diuretics have been the mainstay for HF symptom management for many years. Diuretics are used for relief of acute symptoms of congestion and maintenance of eu-volemia. These agents interfere with sodium retention by increasing urinary sodium and free water excretion. No prospective data exist on the effects of diuretics on patient outcomes.14 Therefore, the primary rationale for the use of diuretic therapy is to maintain euvolemia in symptomatic or stages C and D HF. Diuretic therapy is recommended for all patients with clinical evidence of fluid overload retention. ,16 In more mild HF, diuretics may be used on an as-needed basis. However, once the development of edema is persistent, regularly scheduled doses will be required.

Two types of diuretics are used for volume management in HF: thiazides and loop diuretics. Thiazide diuretics such as hydrochlorothiazide, chlorthalidone, and metolazone block sodium and chloride reabsorption in the distal convoluted tubule. Thiazides are weaker than loop diuretics in terms of effecting an increase in urine output and therefore are not utilized frequently as monotherapy in HF. They are optimally suited for patients with hypertension who have mild congestion. Additionally, the action of thiazides is limited in patients with renal insufficiency (creatinine clear ance [CrCl] less than 30 mL/min) due to reduced secretion into their site of action. An exception is metolazone, which retains its potent action in patients with renal dysfunction. Metolazone is often used in combination with loop diuretics when patients exhibit diuretic resistance, defined as edema unresponsive to loop diuretics alone.

Loop diuretics are the most widely used diuretics in HF. These agents, including furosemide, bumetanide, and torsemide, exert their action at the thick ascending loop of Henle. Loop diuretics are not filtered through the glomerulus, but instead undergo active transport into the tubular lumen via the organic acid pathway. As a result, drugs that compete for this active transport (e.g., probenecid and organic byproducts of uremia) can lower efficacy of loop diuretics. Loop diuretics increase sodium and water excretion, and induce a prostaglandin-mediated increase in renal blood flow which contributes to their natriuretic effect. Unlike thiazides, they retain their diuretic ability in patients with poor renal function. The various loop diuretics are equally effective when used at equipotent doses, although there are intrinsic differences in pharma-cokinetics and pharmacodynamics (Table 6-6 ).5 The choice of which loop diuretic to use and the route of administration depends on clinical factors, such as presence of intestinal edema and rapidity of desired effect. Oral diuretic efficacy may vary based on differing bioavailability, which is almost complete for torsemide and bumetanide, but averages only 50% for furosemide. Therefore, oral torsemide can be considered an alternative to the IV route of administration for patients who do not respond to oral fur-osemide in the setting of profound edema. The onset of effect is slightly delayed after oral administration but occurs within a few minutes with IV dosing. Consequently, bioequivalent doses of IV furosemide are half the oral dose, whereas bumetanide and torsemide IV doses are generally equivalent to the oral doses.

FIGURE 6-1. Treatment algorithm for chronic HF. Table 6-5 describes staging of heart failure. (ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; EF, ejection fraction; HF, heart failure; LV, left ventricular; MI, myocardial infarction; SOB, shortness of breath.)

Table 6-6 Loop Diuretics Used in HF

Furosemide

Bumetanide

To rse m id e

Usiial daily dose

20-160 mg

0.5—^ mg

10-SO mg

(oral)

Ceiling dose:

Normal renaj

fiO-160 mg

1-2 mg

20-40 mg

function

CrCl 20 50 mL/

160 mg

2 my

40 mg

mln

CrCl than

4i)Q mg

3-1$ mg

100 mg

20 mL/mtn

Bioavailability

10 100%

80-90%

80-100%

(average 50%J

Affected by food

Yes

Yes

No

Half-life

0.3-3.4 hours

0.3-1.5 hours

3-4 hours

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