Pearls and Pitfalls in the Use and Abuse of Diuretics for Chronic Congestive Heart Failure

Abstract

The main purpose of using diuretics is usually lost sight of, i.e. it is for the relief of dyspnea by using the least amount of a diuretic. The production of a low output state and hypercoagulation in an attempt to achieve dry weight by lowering blood volume excessively are among the hazards of using more diuretic than is absolutely necessary to achieve the goal of relieving dyspnea. The use of jugular venous pressure measurement and the status of dyspnea should have precedence over body weight in determining diuretic dose adjustment. Often forgotten in using diuretics is that potassium without magnesium will not enter cells and that the almost universal preference for furosemide over thiazides threatens to increase the incidence of osteoporosis. Also, the tendency to ignore loss of the water-soluble vitamins thiamine and ascorbic acid may result in refractory edema and the inability to manage the stresses of congestive heart failure.

Clinical and neurohumoral consequences of diuretic withdrawal in patients with chronic, stabilized heart failure and systolic dysfunction

“…Inclusion criteria were as follows: (1) patients of both genders aged N18 years old; (2) evidence of symptomatic heart failure with past history of NYHA class III or IV; (3) patients had to be stable NYHA class II over the previous 3 months; (4) left ventricular ejection fraction b45% (based on contrast ventriculography, radionuclide scan or echocardiography) within the last 3 months; (5) no symptoms or signs of congestion at the time of inclusion (absence of edema, liver stasis, orthopnea, paroxysmal nocturnal dyspnea, rales, pleural effusion or Kerley B lines on chest X-ray); and (6) in addition, at the time of inclusion, patients were required to be on loop diuretics (maximal dosage 80 mg of furosemide or equivalent) and angiotensin converting inhibitors, digitalis or other vasodilators being optional. Doses should have been unchanged during the last 3 months.…”

Diuretic Medication Therapy Use and Low Thiamin Intake in Homebound Older Adults

“…Even for older individuals who consume an "adequate" intake of thiamin, the assumption cannot be made that thiamin levels are adequate if diuretic therapy is also being received. The main goal of diuretic therapy is to relieve dyspnea and reduce blood pressure by decreasing blood volume through increased urinary excretion (Constant, 1999). As noted above, diuretics increase the excretion of water-soluble vitamins, including thiamin (Brady, Rock, & Horneffer, 1995;Suter, Haller, Hany, & Vetter, 2000); increased urinary loss could potentially produce a greater requirement for those individuals receiving a diuretic therapy regimen.…”

“…Diuretics are one significant example; these agents are frequently prescribed to older persons to treat hypertension, peripheral edema, and dyspnea caused by pulmonary edema in heart failure (Constant, 1999;Nickolls & Sani, 2004). Diuretics act on the kidney to increase excretion of sodium and water, thereby reducing extracellular fluid; the result is decreased blood pressure, and reduced peripheral and pulmonary edema.…”

“…Diuretics act on the kidney to increase excretion of sodium and water, thereby reducing extracellular fluid; the result is decreased blood pressure, and reduced peripheral and pulmonary edema. Health care providers are typically well aware of the risk for reduced serum potassium concentrations with the use of certain types of diuretics and usually monitor potassium status, at least upon initial prescription (Constant, 1999). However, less well monitored is the potential effect of diuretics on thiamin and other water-soluble vitamins; specific concern is that inadequate dietary intake of thiamin can produce clinical thiamin deficiency within three months (Leslie & Gheorghiade, 1996).…”

“…However, less well monitored is the potential effect of diuretics on thiamin and other water-soluble vitamins; specific concern is that inadequate dietary intake of thiamin can produce clinical thiamin deficiency within three months (Leslie & Gheorghiade, 1996). An additional concern with diuretics is that these agents may produce subclinical thiamin deficiency due to the same mechanisms (i.e., increased urinary thiamin excretion or impaired thiamin uptake), at least in the face of a poor dietary intake of thiamin (Constant, 1999;Leslie & Gheorghiade, 1996;Wilcox, 1999).…”