Diuretics acute heart failure

The drugs most commonly used in chronic heart failure are diuretics, ACE inhibitors, angiotensin receptor antagonists, and U-blockers (Table 13-1). In acute failure, diuretics and vasodilators play important roles. 

Treatment of acute heart failure targets relief of congestion and optimization of cardiac output utilizing oral or intravenous diuretics, intravenous vasodilators, and when appropriate, inotropes. 

FIGURE 8-2. General treatment algorithm for acute decompensated heart failure (ADHF) based on clinical presentation. IV vasodilators that may be used include nitroglycerin, nesiritide, or nitroprusside. Metolazone or spironolactone may be added if the patient fails to respond to loop diuretics and a second diuretic is required. IV inotropes that may be used include dobutamine or milrinone. (D/C, discontinue HF, heart failure SBP, systolic blood pressure.) (Reprinted and adapted from J Cardiac Fail, Vol 12, pages el-el 22, copyright 2006, with permission from Elsevier.)... 

Starting doses of ACE inhibitors should be low with slow dose titration. Acute hypotension may occur at the onset of ACE inhibitor therapy, especially in patients who are sodium- or volume-depleted, in heart failure exacerbation, very elderly, or on concurrent vasodilators or diuretics. Patients with these risk factors should start with half the normal dose followed by slow dose titration (e.g., 6-week intervals). 

Lithium intoxication can be precipitated by the use of diuretics, particularly thiazides and metola-zone, and ACE inhibitors. NSAIDs can also precipitate lithium toxicity, mainly due to NSAID inhibition of prostaglandin-dependent renal excretion mechanisms. NSAIDs also impair renal function and cause sodium and water retention, effects which can predispose to interactions. Many case reports describe the antagonistic effects of NSAIDs on diuretics and antihypertensive drugs. The combination of triamterene and indomethacin appears particularly hazardous as it may result in acute renal failure. NSAIDs may also interfere with the beneficial effects of diuretics and ACE inhibitors in heart failure. It is not unusual to see patients whose heart failure has deteriorated in spite of increased doses of frusemide who are also concurrently taking an NSAID. 

Furosemide Loop diuretic Decreases NaCI and KCI reabsorption in thick ascending limb of the loop of Henle in the nephron (see Chapter 15) Increased excretion of salt and water reduces cardiac preload and afterload reduces pulmonary and peripheral edema Acute and chronic heart failure severe hypertension edematous conditions Oral and IV duration 2-4 h Toxicity Hypovolemia, hypokalemia, orthostatic hypotension, ototoxicity, sulfonamide allergy... 

Givertz MM et al The effects of KW-3902, an adenosine Al-receptor antagonist, on diuresis and renal function in patients with acute decompensated heart failure and renal impairment or diuretic resistance. 3 Am Coll Cardiol 2007 50(16) 1551. [PMID 17936154]... 

Hill , Yancy CW, Abraham WT Beyond diuretics Management of volume overload in acute heart failure syndromes. Am 3 Med 2006 119 S37. 

Diuretic therapy should be initiated for the acute heart failure. An agent such as furosemide would be appropriate. The aim of the furosemide treatment is to relieve symptoms such as shortness of breath and to make the patient more comfortable. A dose of furosemide 40 mg twice daily (8am and 2pm) would be appropriate as initial therapy. 

In contrast, published case reports and case series have provided more insight into the potential nephrotoxicity associated with COX-2-selective inhibitors. Taken together, these case reports suggest that COX-2 inhibitors, like non-selective NSAIDs, produce similar and consistent renal adverse effects in patients with one or more risk factors that induce prostaglandin-dependent renal function (that is patients with renal and cardiovascular disease and taking a number of culprit medications, such as diuretics and ACE inhibitors). Acute renal insufficiency, disturbances in volume status (edema, heart failure), metabolic acidosis, hyperkalemia, and hyponatremia have been commonly described. The duration of treatment with COX-2 inhibitors before the development of chnically recognized renal impairment ranged from a few days to 3-4 weeks. Withdrawal of COX-2 inhibitors and supportive therapy most often resulted in resolution of renal dysfunction, but in some patients hemodialysis was required (102,108-112). 

Furosemide inhibits the absorption of indometacin (42), while the diuretic and hypotensive effects of most diuretics are blunted by indometacin and probably also other NSAIDs (43). Intravenous furosemide is commonly given to patients with acute heart failure to relieve pulmonary congestion. Symptomatic relief occurs before the onset of diuresis, and the beneficial effect is believed to result from a venodUator action of furosemide, which precedes its diuretic effect. This venodilator response is inhibited by indometacin, suggesting that it occurs through local prostaglandin release. 

A series of 11 spontaneously reported cases in which renal impairment was associated with the use of nimesulide has been described (17). The adverse events were represented by acute renal insufficiency n — 2), acute deterioration of chronic renal insufficiency n — 3), fluid retention n = 4), and oliguria and macro hematuria n = 1 each). The patients had a median age of 57 (range 17-81) years and six had some predisposing condition (chronic renal insufficiency, heart failure, diabetes, use of diuretics) to NSAID-induced functional renal impairment. Apart from one patient, nimesulide was taken for a very short time (less than 8 days). A favorable outcome ensued after withdrawal of therapy in aU patients. The acute deterioration of renal function described in these patients pointed to hemodynamically mediated renal impairment in all cases, with the exception of one man in whom interstitial nephritis was suspected. 

Like all diuretics, the thiazides can cause electrolyte abnormalities, such as hypokalemia and hyponatremia, and dehydration. These complications are uncommon in patients with uncomplicated hypertension, but are more common in patients with heart failure or decompensated hepatic cirrhosis with secondary hyperaldosteronism. Until a patient is accustomed to the effect of a diuretic, dizziness may be experienced. Serum lipid concentrations are slightly raised acutely and hyperglycemia can occur during long-term therapy. Rare effects are thrombocytopenia, rashes, drug fever, cholestatic jaundice, pancreatitis, and precipitation of hepatic... 

Trauma (and other causes of acute blood loss), C third-spacmg of fluid (e.g., burns, pancreatitis, peritonitis), vomiting, diarrhea, diuretics, renal or adrenal (i.e., sodium wasting) disease v Heart failure, hepatic cirrhosis, nephrotic syndrome, iatrogenic (intravenous fluid overload) ... 

Blocker therapy is appropriate to further modify disease in systolic heart failure. In patients on a standard regimen of a diuretic and ACE inhibitor, /3-blockers have been shown to reduce morbidity and mortality.It is of paramount importance that /3-bIockers be dosed appropriately because of the risk of inducing an acute exacerbation of heart failure. They must be started in very low doses, doses much lower than those used to treat hypertension, and titrated slowly to high doses based on tolerability. 

The addition of aldosterone antagonists can rednce morbidity and mortality in systolic heart failure. Spironolactone has been studied in severe heart failure and has shown benefit in addition to diuretic and ACE inhibitor therapy. Eplerenone, the newest aldosterone antagonist, has been smdied in patients with symptomatic systolic heart failure within 3 to 14 days after an acute myocardial infarction in addition to a standard three-drug regimen. Collectively, both these agents should be considered in the specific heart failure population smdied but only in addition to diuretics, ACE/ARBs, and /8-blockers. 

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