Preventing edema and congestion improves quality of life in heart failure patients and probably their prognosis too. The starting and maximal doses of the common diuretics are shown below (Table): rest, then an afternoon dose, is a useful schedule for higher doses, and does not disrupt sleep. Tell the patient not to take the diuretic at the same time as an angiotensin-converting enzyme (ACE) inhibitor, especially if hypotensive.
Practice guidelines are listed below:
Always start diuretics at their lowest dose in the elderly.
Lying down for 1 hour after dosing increases diuretic efficacy. Take this into consideration when suggesting a specific dosing time, allowing for the patient’s daily activities and the risk of noncompliance to avoid inconvenience or discomfort.
Prescribe on a once-daily or divided dose basis. Once daily is best for an intermediate dose (eg, furosemide 75 mg); a morning dose followed by a
When starting or increasing the dose of ACE inhibitor, avoid excessive diuresis. An increase in azotemia (a side effect of high-dose diuretics), especially if disproportionate to the creatinine level, can usually be corrected by lowering the diuretic dose, and does not necessitate lowering or interrupting the ACE inhibitor.
Hyperkalemia, the major side effect of potassium-losing diuretics, can be decreased by the concomitant use of an ACE inhibitor. It can also occur on treatment with a potassium-sparing diuretic and ACE inhibitor. Remind the patient about checking potassium levels frequently: every 3 days until achieving a stable dose of diuretic and ACE inhibitor, then every 2 to 3 months. Oral potassium supplements have not proved effective in preventing hypokalemia and are rarely able to correct it. Aim to maintain serum potassium levels between 4.5 and 5.0 mEq/L. Consider potassium infusion 20 to 60 mEq/day for more refractory hypokalemia.
If using high-dose diuretics, check the serum magnesium. Consider oral supplementation in the presence of hypomagnesemia (<1.6 mEq/L). Intermediate-to-high doses of diuretic can cause hyperuricemia. Concomitant allopurinol may be useful, even before uric acid levels become abnormal, especially after increasing the dose of diuretic. On symptomatic grounds, increase the dose of diuretic in heart failure outpatients with evidence of congestion. In its initial stages at ieast, ambulatory anticongestion therapy presupposes a well-tried program of daily body weight and electrolyte determination and clinical appraisal. Insufficiently documented patients, principally those with recent-onset congestion requiring assessment in terms of water-electrolyte balance, renal function, net body weight, and correct perfusion/arterial pressure ratio should be hospitalized or at least seen by a specialist. Many patients who respond to an impromptu dose of diuretic are often left with a volume load, at risk of emergency hospitalization. On the other hand, well-documented (eg, recently hospitalized) patients can be treated in an outpatient setting using their usual oral diuretic but at a 50% to 100% higher dose, or else switched to intravenous administration, which secures higher absorption. In diuretic resistance (persistent congestion despite high doses of oral loop diuretics), try diuretic combinations (eg, furosemide + metolazone, or furosemide + amiloride). A thiazide or metolazone taken half an hour beforehand potentiates the effect of the loop diuretic by increasing sodium absorption in the proximal and distal loops. The combination of a loop diuretic + metolazone can cause severe and unpredictable loss of water volume (hence increased renal dysfunction), together with significant hypokalemia and ventricular arrhythmia. Metolazone 2.5 mg is enough to cause a significant increase in diuresis, severe hypotension, and hypokalemia. Reassess the patient clinically and biochemically within 24 hours of the first dose. Again, close follow-up or hospitalization are advisable. Having corrected salt and water retention, lower the diuretic dosage to the bare minimum, within a range that meets the patient’s needs. Remember that diuretics can activate the neurohumoral system. Encourage dosage self-management where feasible, issuing clear instructions based on symptoms and body weight. Long-term metolazone is rarely indicated (due not only to loss of efficacy, but also to significant electrolyte abnormalities). Hospitalize patients with evidence of low-output congestion: pallor, cold extremities, feeble tachy-cardic pulse, hyponatremia, and unstable renal function. Potassium-sparing diuretics can cause significant hypokalemia in patients with diabetic nephropathy, renal dysfunction and insulin resistance who have been treated with an ACE inhibitor combined with a nonsteroidal anti-inflammatory drug: perform frequent laboratory monitoring in such cases. Keywords drug; diuretic therapy; quality of life; edema; thiazide; loop diuretic; potassium-sparing diuretic; side effect; hyperkalemia [gallery ids=""]