Heart Failure in the Emergency Department

Pharmacological Therapy

Pharmacological management is the mainstay for treating HF. No other acute therapy (eg, NIV) has demonstrated a morality benefit (See Table 4 for specific dose and administration strategies).⁵⁵ The time to initiate pharmacological therapy and whether an aggressive approach is indicated must be based on the severity of the clinical symptoms and objective risk stratification measures (eg, NP, troponin levels).

Table 4.

Furosemide. Except for hypertensive HF—in which case BP lowering is the most important goal—diuretics are a mainstay of AHF treatment, and consensus guidelines provide a class I recommendation for their use^.3 The DOSE (Diuretic Strategies in Patients with ADHF) trial⁵⁶ prospectively evaluated diuretics in 308 hospitalized AHF patients and found no outcome differences in administration route (bolus or continuous infusion) or dose (high vs low dose). This study reported trends toward greater improvement with higher furosemide dosing, as well as greater diuresis, but at a cost of transient worsening of renal function.

In general, diuretics should be administered in an intravenous (IV) dose equal to 1 to 2.5 times the patient’s usual daily oral dose. For patients who are diuretic-naïve, a dose of 40 mg IV furosemide or 1 mg IV bumetanide, with subsequent dosing titrated to urine output, is recommended.

Vasodilators. In patients with both AHF and even mildly elevated BP, vasodilators can be extremely effective in achieving symptom improvement. The choice of vasodilator, and how aggressive to increase dosing, depends upon symptom severity. The purpose of vasodilators is to lower BP and therefore, should not be used in the setting of hypotension or signs of hypoperfusion. Flow-limiting, preload-dependent CV states (eg, right ventricular infarction) increase the risk of hypotension, and are relative contraindications to the use of vasodilators. For patients who are severely dyspneic and with critical presentations, the emergency physician (EP) should preclude a detailed history and examination to initiate immediate therapy with short-acting agents that can be terminated rapidly in the case of an adverse event (eg, unexpected hypotension) are preferred.

Nitroglycerin. Nitroglycerin is the vasodilation agent of choice for hypertensive AHF. It is a short-acting, rapid-onset, venous and arterial dilator that decreases BP by preload reduction, and by afterload reduction in higher doses. Nitroglycerin has coronary vasodilatory effects associated with decreased ischemia, but should be avoided in patients taking phosphodiesterase inhibitors.⁵⁵ Its most common side effect is headache, and hypotension occurs in about 3.5% of patients.⁵⁷

Commonly given as a continuous infusion at IV doses up to 400 mcg/min, nitroglycerin may be associated with higher costs and longer LOS.⁵⁸ Some authors suggest that bolus nitroglycerin therapy may be superior: In a retrospective study of 395 patients, an IV bolus of nitroglycerin 0.5 mg was superior to both an infusion, or a combination of bolus and infusion, as demonstrated by lower rates of ICU admission (48% vs 67% and 79%, respectively, P = 0.006) and shorter hospital stays (4.4 vs 6.3 and 7.3 days, respectively, P = 0.01). In all cohorts, adverse event rates were similar for hypotension, troponin elevation, and creatinine increase over 48 hours.⁵⁹ Nitroprusside. Nitroprusside is a potent arterial and venous dilator that causes rapid decrease in BP and LV-filling pressures. It is usually considered more effective than nitroglycerin, despite a small study showing similar hemodynamic responses.⁶⁰

Initial dosing of nitroprusside starts at 0.3 µg/kg/min IV, and is increased every 5 minutes to a maximum of 10 mcg/kg/min, based on BP and clinical response. The most common acute complication of nitroprusside infusions is hypotension. Cyanide toxicity may occur with prolonged use, high doses, or in patients with renal failure.⁵⁵

Nesiritide. Exogenously administered, the B-type NP nesiritide is effective in lowering BP and improving dyspnea in AHF,⁵⁵ although large prospective studies showed it had little long-term advantage over standard care.⁶¹ In a small, randomized, controlled trial, nesiritide reduced 30-day revisit LOS when given in an OU.⁶² The 22-minute half-life of nesiritide is longer than that of the nitrates, and its side effect is predominately hypotension, which occurs at rates similar to those of other vasodilators.⁵⁵

Angiotensin Converting Enzyme Inhibitors. Because angiotensin converting enzyme inhibitors (ACEIs) have chronic mortality reduction benefits, their use in the acute setting is theoretically attractive, however, this has been poorly proven in AHF ED patients. In a retrospective review of 103 patients with elevated NTproBNP levels receiving bolus IV enalaprilat within 3 hours of presentation, the mean SBP decreased by 30 mm Hg, with only 2% of patients developing hypotension.⁶³ However, with the longer half-life of ACEIs, if hypotension occurs, the potential for a prolonged BP-lowering effect exists.

Calcium Channel Blockers. Clevidipine and nicardipine are rapidly acting IV calcium channel blockers that lower BP by selective arteriolar vasodilation and increased cardiac output as vascular resistance declines.⁵⁵ Because these agents have no negative inotropic or chronotropic effects, they may be beneficial in hypertensive AHF. In an open-label trial of 104 hypertensive AHF patients, clevidipine was more effective than standard care for the rapid control of BP and relief of dyspnea.⁶⁴

Morphine. Large registry analyses have demonstrated potential harm with the routine use of morphine,⁶⁵ as do recent propensity score matched analyses.⁶⁶ Until there are studies demonstrating benefit, the use of morphine at present should be reserved for palliative care.