Case-Based Review

Management of Acute Decompensated Heart Failure in Hospitalized Patients


 

References

Case Continued

After 24 hours of medical therapy in the CCU, the patient is no longer clammy and cool but continues to have shortness of breath, and peripheral edema is not improving. She continues to have elevated JVP and S3. Her blood pressure is now 120/79 mm Hg and her heart rate is 110. A Swan-Ganz catheter placed this morning showed a cardiac index of 1.8 L/minute/m2 (reference range, 2.5–4.0 L/min/m2); pulmonary capillary wedge pressure is 28 mm Hg (reference range, 6–12 mm Hg) and systemic vascular resistance is 1932 dyne/second/cm5 (reference range, 800–1200 dynes/sec/cm5). The physician decides to add nitroprusside to lower her filling pressure and systemic vascular resistance.

  • What is the role of vasoactive medications in treatment?

Vasodilators

Nitroglycerin is a venodilating medication with preload reduction properties at low doses and an arterial dilator at high doses [35]. Preload reduction improves left ventricular filling pressures and pulmonary congestion without increasing the oxygen demand in the heart in patients with ADHF. This leads to an improvement of symptoms, including dyspnea, in as early as 5 minutes [36]. For a highly symptomatic patient, nitroglycerin given sublingually can be useful in an acute situation because it is typically immediately available while preparations are made for administration of IV medications. Limitations of nitroglycerin include rapid tachyphylaxis within several hours of continuous exposure at high doses, resistance to the hemodynamic effects of nitroglycerin in up to 20% of patients, and hypotension, which may occur before significant preload reduction effect can be obtained [37]. When symptomatic hypotension becomes a problem, the highest hemodynamically tolerable dose should be given. Another agent with a potent vasodilator effect used in the treatment of heart failure is sodium nitroprusside (SNP). As opposed to nitroglycerin, this drug has an equally potent preload- and afterload-reducing effect [35]. Afterload reduction through its arteriodilator effect has the benefit of increasing cardiac output and decreasing myocardial oxygen demand with improvement of pulmonary congestion [36]. SNP is used in less than 1% of patients hospitalized with heart failure [38], probably due to the potential for causing marked hypotension, its need for invasive hemodynamic monitoring, and the rare risk for thiocyanate toxicity with high doses and/or longer infusions, especially in patients with reduced hepatic perfusion and renal function, as in the case of low-output heart failure [35]. However, data demonstrating safety and efficacy of SNP infusion in patients with ADHF are limited [39].A single-center, retrospective case-control study suggested that the administration of SNP in carefully selected patients with advanced low-output ADHF was safe and may be associated with favorable long-term clinical outcomes [39]. SNP can be attractive in severely congested patients with hypertension or severe mitral regurgitation complicating left ventricular failure, but prospective trials are needed to clarify the safety and efficacy in this patient population.

Nesiritide is a human recombinant form of BNP that has a direct effect on the vascular endothelium by increasing the bioavailability of nitric oxide through stimulation of cyclic guanosine monophosphate. Its primary mechanism of action is to reduce left ventricular filling pressures by a systemic and pulmonary vasodilator effect. It also promotes diuresis and natriuresis [40].The initial efficacy of nesiritide was demonstrated in the VMAC (Vasodilation in the Management of Acute Congestive Heart Failure) study, a randomized trial of IV nesiritide versus IV nitroglycerin or placebo in decompensated heart failure patients. A significant reduction in pulmonary capillary wedge pressure was demonstrated within 15 minutes in the nesiritide group and maintained at 3 hours compared to either nitroglycerin or placebo, with a similar improvement in dyspnea extending out to 24 hours [41].

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