Table 3.
Drug or class | Evidence | Indication | Main adverse effects |
---|---|---|---|
Loop diuretics | Never evaluated in large-scale randomized clinical trials | AHFS to relieve congestion | Hypotension, electrolyte abnormalities, and worsening renal function |
Vasodilators | |||
nesiritide | Improves hemodynamics and reduces dyspnea, neutral survival benefit (Abraham et al. 2005) | AHFS to improve symptoms | Hypotension, potential of worsening renal function |
nitrates | High-dose isosorbide dinitrate more effective than furosemide in controlling severe pulmonary edema (Cotter et al. 1998) | First-line therapy for AHFS with adequate blood pressure | Hypotension, headaches, development of nitrate tolerance |
sodium nitroprusside | Favorable hemodynamic effects (Guiha et al. 1974), no data on survival benefit, may increase risk in post-MI patients (Cohn et al. 1982) | Severe AHFS, hypertensive crisis | Hypotension, cyanide toxicity, accumulation in renal insufficiency |
Inotropes | |||
dopamine/dobutamine | Shown to improve symptoms in small scale studies (Liang et al. 1984) | AHFS with hypotension and peripheral hypoperfusion | Tachyarrhythmias, may increase mortality |
milrinone | No effect on duration of hospital stay or mortality (Cuffe et al. 2002) | AHFS refractory to diuretics and vasodilators with preserved blood pressure | Sustained hypotension and tachyarrhythmia |
levosimendan | No mortality benefit, reduces symptoms (Cleland et al. 2007; Mebazaa et al. 2007) | AHFS | Increased rate of atrial fibrillation and ventricular tachycardia |
Ultrafiltration | More weight reduction than loop diuretics (Costanzo et al. 2007) | AHFS resistant to diuretics, or cardiorenal syndrome | Invasive, loss of solutes, procedural complications |
MI, myocardial infarction.