A 71 year-old man with type 2 diabetes mellitus, chronic kidney disease (baseline creatinine 2.0), paroxysmal atrial fibrillation and ischemic cardiomyopathy (EF 25%) presents for his fourth admission in the last 4 months. He is short of breath with minimal exertion and has no appetite. He has lost nearly 15 pounds in the last year.  

On exam he has a heart rate of 90 bpm that is irregular, a blood pressure of 90/70 mm Hg, and evidence of temporal wasting. His exam is notable for obvious signs of decompensated heart failure.  

Diuresis is begun with intravenous lasix, but the creatinine rises to 2.9. Which of the following is the best next step in his management?

  1. Add nesiritide 0.005 mcg/kg/min
  2. Place a pulmonary artery catheter to guide management
  3. Initiate ultrafiltration
  4. Add low dose dopamine 2 mcg/kg/min
  5. Add sodium nitroprusside

Correct Answer:  B


  1. Yancy C, et al, 2013 ACC/AHA Guideline for the Management of Heart Failure, Circulation. 2013; 128: e240-e327.
  2. Bart B, et al. Ultrafiltration in Decompensated Heart Failure with Cardiorenal Syndrome N Engl J Med 2012; 367:2296-2304
  3. Chen H, et al. Low-dose dopamine or low-dose nesiritide in acute heart failure with renal dysfunction: The ROSE Acute Heart Failure Trial. JAMA 2013; 310(23): 2533-2543.
  4. ESCAPE Investigators and ESCAPE Study Coordinators. Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness: The ESCAPE Trial. JAMA 2005; 294(13): 1625-33.

Rationale:  This patient has recurrent heart failure hospitalizations in the context of advanced heart failure and renal dysfunction. The cachexia, narrow pulse pressure, and worsening renal function with diuresis (despite overt clinical congestion) are all poor prognostic signs and speak to a possible low cardiac output state (Hemodynamic profile C) complicated by cardiorenal syndrome type 1. Patients with low cardiac output and congestion are challenging to manage and frequently require therapy with intravenous vasodilators or inotropes. The selection of appropriate therapy for cardiorenal syndrome is greatly facilitated by knowledge of the cardiac output, filling pressures, and systemic vascular resistance, data which could be provided from a pulmonary artery catheter. Although routine use of a pulmonary artery catheter to guide management acute decompensated heart failure was not shown to be effective in the ESCAPE trial, selective use is still supported by the guidelines in patients where hemodynamics are uncertain there is hypotension or worsening renal function with empiric therapy (as in this case). Use of nesiritide in this circumstance is relatively contraindicated due to the low systolic blood pressure, given the risks of worsening hypotension, and did not improve decongestion over diuretic therapy alone in patients with acute heart failure and renal dysfunction in the ROSE-AHF trial. Ultrafiltration was associated with greater worsening of renal function than intravenous diuretic therapy among patients with acute heart failure enrolled in the CARRESS-HF trial, and would likely not be helpful in this patient with marginal cardiac output. Empiric use of dopamine to provide inotropic support is not unreasonable, but the ‘low-dose’ was ineffective in augmenting diuretic efficacy in the ROSE-AHF trial, and higher doses are likely to be necessary. Sodium nitroprusside may be an effective therapy but would be challenging to use in this patient with marginal renal function (enhanced risk of thiocyanate toxicity) and uncertain systemic vascular resistance; knowledge of the hemodynamics would be an important preliminary step to ensure that the patient has the capacity to tolerate such potent arterial vasodilation.

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