Should We Be Using Aortic Pulsatility Index Over Cardiac Power Output in Heart Failure Cardiogenic Shock?

Abstract

Cardiac power output (CPO) was first described in 1986 but did not achieve prominence until its identification in 2004 as a strong hemodynamic correlate of mortality in acute myocardial infarction (AMI) complicated by cardiogenic shock. 1 Its use has since gained steam in cardiogenic shock algorithms, regardless of baseline ventricular function-that is, AMI-or heart failure-(HF-) cardiogenic shock.HF-cardiogenic shock has shown to be a separate pathophysiological entity from AMI-cardiogenic shock, and there are conflicting data on the utility of CPO in this population. [2][3]3][4][5][6] We propose that CPO may not be a useful hemodynamic metric in HF-cardiogenic shock.To understand this proposition, let us go back to the underpinnings of cardiac physiologypressure-volume loops.The area within the pressure-volume loop represents the stroke work (SW), which correlates with CPO.In AMI-cardiogenic shock, an acute drop in contractility (Ees) leads to a reduction in stroke volume, and SW, representing CPO, subsequently decreases.In this clinical setting CPO is highly prognostic. 1 However, successive adverse myocardial remodeling activates the renin-angiotensin-aldosterone system leading to volume retention, ventricular dilation, and an increase in end-diastolic volume.This adaptive response in many patients restores a normal, or near-normal, SW, and therefore CPO.However, as the pressure-volume loop shifts to the right, the potential energy (the energy used by the myocardium for basal metabolism, calcium cycling, actin-myosin coupling, and other processes not directly reflected in SW) increases.Therefore, despite normalization of

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