The following is a case presentation courtesy of Dr. Lau:
56 yo M h/o DM, HTN, previous cocaine abuse, CHF (EF 15-20%) presents with mild shortness of breath and chest pain. Initially, vitals BP 105/62, 85, 20, 98%. Patient not in distress but was walking about ED and complaining multiple times that he was not seen yet. After initial assessment, Lasix 40mg IVP given. Approximately 15-20 minutes later, patient developed respiratiory distress and was transferred to CCT (where I saw patient). On presentation to CCT, patient was altered, tachypneic, BP 101/59, lung exam with diffuse rhonchi. On review, CXR was clear with possible mild pulmonary edema. Repeat CXR was essentially the same.
Can you explain why this patient decompensated?
Continue reading below for a discussion. . .
Although the patient could have decompensated spontaneously, it is likely that interventions in the ED caused this acute episode of distress in a patient with a chronic process. Giving furosemide IVP in a patient with a borderline blood pressure with advanced CHF is the likely culprit. There is a known entity called “lasix allergy,” which is not an allergy at all, but respiratory distress caused by sudden increase in serum angiotensin II by furosemide that worsens hemodynamics in the pulmonary bed. Decrease in preload in a preload-dependent advanced CHF patient probably contributes to this as well.
There is plenty of literature showing that furosemide does not improve survival of acutely decompensated heart failure but symptomatic improvement is often cited for the reason to give furosemide in the ED. Here is a randomized controlled trial showing that subjective perception of dyspnea is not improved by giving furosemide: Holzer-Richling N, Holzer M, Herkner H, et al. Randomized placebo controlled trial of furosemide on subjective perception of dyspnoea in patients with pulmonary oedema because of hypertensive crisis. Eur J Clin Invest 2011;41:627-34.
Conclusion:
Giving furosemide in the ED for decompensated CHF is rarely (or never) indicated. For patients with low EF and borderline blood pressure it can actually cause harm.
References:
- von Dossow V, Spies C, Schenk H, Schlesinger S, von Heymann C. Secondary pulmonary hypertension: haemodynamic effects of torasemide versus furosemide. Clin Drug Investig 2008;28:17-26.
- Young JB, Cheng M, Mills RM. Hemodynamics, diuretics, and nesiritide: a retrospective VMAC analysis. Clin Cardiol 2009;32:530-6.
Thanks Dr. Lau for today’s Morning Report! Leave any comments below.
Jay Khadpe MD
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