Are there special considerations when treating patients with CHF?
Patients with CHF may be resistant to diuretic therapy. CHF leads to diminished kidney perfusion and consequently to diminished delivery of the diuretic to the kidney. In addition, increased activity of the renin-angiotensin-aldosterone system leads to increased sodium reabsorption at other nephron sites. Finally, in patients treated with an oral loop diuretic, delayed intestinal absorption of the loop diuretic may prevent the threshold rate of diuretic excretion to be reached. Because of these phenomena, addition of a thiazide diuretic may be necessary. Chlorothiazide is the only thiazide diuretic that can be administered intravenously. However, oral hydrochlorothiazide, chlorthalidone, and metolazone are also effective. There are several other special considerations when treating patients with CHF:
• For patients treated with an oral loop diuretic, torsemide or bumetanide may be better choices than furosemide. The bioavailability of oral furosemide averages about 50%, but ranges from 10% to 100%. In addition, the bioavailability may vary greatly over time in an individual patient. The bioavailability of torsemide and bumetanide is more predictable.
• Spironolactone and eplerenone improve survival in patients with heart failure with reduced ejection fraction. This benefit is thought to be independent of the diuretic effect.
• Diuresis may lead to contraction of the vascular compartment, decreased venous return to the heart, decreased cardiac filling pressures, decreased cardiac output, decreased kidney perfusion, and prerenal azotemia. However, patients with elevated central venous pressure have elevated kidney venous pressure. Elevated kidney venous pressure impairs kidney perfusion. In such patients, diuresis may lead to improvement in kidney function.
• Patients with chronic obstructive pulmonary disease may have chronic respiratory acidosis and cor pulmonale. Diuresis can lead to contraction alkalosis. Contraction alkalosis can depress ventilation, thereby exacerbating the hypoxemia and hypercapnia. In this situation, correction of the contraction alkalosis can be achieved by the administration of the carbonic anhydrase inhibitor acetazolamide.