Hiuretics can cause the depletion of important cations (potassium and magnesium), predisposing to serious cardiac arrhythmias, particularly in the presence of digitalis therapy. The risk is enhanced when two diuretics are used in combination. Electrolyte loss is due to the enhanced delivery of sodium to distal sites in the renal tubules where it exchanges for other cations. This process is potentiated by activation of the renin-angiotensin-aldosterone system.
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Concomitant angiotensin-converting enzyme (ACE) inhibition, alone or in combination with potassium-sparing agents (such as spironolactone), prevents electrolyte depletion in most patients with heart failure.
Diuretics can increase the activation of neurohumoral systems, in particular the renin-angiotensin system, in heart failure. Although higher levels of angiotensin II probably help to maintain blood pressure and renal function during volume depletion, neurohumoral activation may increase the frequency and severity of electrolyte depletion in the short term, and the risk of disease progression in the long term, unless patients receive a neurohumoral antagonist.
Hypotension and azotemia.
Excessive diuretic use can decrease blood pressure and impair renal function, but hypotension and azotemia may also result from worsening heart failure, and thus be exacerbated by a decrease in diuretic dose. In patients without fluid retention, the probable cause of hypotension and azotemia is volume depletion; the diuretic dose should be decreased if the changes in blood pressure and renal function are marked or symptomatic. However, in patients with persistent fluid retention, hypotension and azotemia will be due to worsening heart failure and ineffective peripheral perfusion. Management involves maintaining the dose of diuretic and improving end-organ perfusion with the short-term use of positive inotropics or vasodilators.
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Drug; diuretic; risk; side effect; renal function; electrolyte depletion; neuroendocrine activation; potassium; arrhythmia.