Related Experiment Video
Updated: Jun 2, 2026

Utilizing Percutaneous Ventricular Assist Devices in Acute Myocardial Infarction Complicated by Cardiogenic Shock
Published on: June 12, 2021
Pressure-Volume-Derived Ventricular Energetics Across Mechanical Circulatory Support Strategies in Cardiogenic Shock
Jorge A Ortega-Hernández1,2, Luca Baldetti3, Guglielmo Gallone4,5
1Programa de maestría y doctorado en ciencias médicas y odontológicas de la Salud, Universidad nacional Autónoma de México, Ciudad De México, Mexico.
None:
Bedside pressure-flow variables in cardiogenic shock (CS) incompletely characterize ventricular energetics and coupling. We prospectively derived bedside pressure-volume (PV) loop surrogates from paired pulmonary artery catheter and echocardiographic data in 68 patients (263 paired assessments) with acute myocardial infarction-related CS (AMI-CS) or heart failure-related CS (HF-CS) during microaxial support, intra-aortic balloon pump (IABP) support, or medical therapy. In AMI-CS with microaxial support, arterial elastance decreased (-1.22 mm Hg/ml) with improved coupling (ventriculoarterial coupling [VAC] -1.42), stroke work increased (+140 mm Hg·ml), and pressure-volume area declined (PVA -103 mm Hg·ml), yielding an efficiency rise from ~32% to ~40%, suggesting unloading. In HF-CS, microaxial support reduced elastance modestly (-0.35) with probable efficiency gain (+5%) but heterogeneous PVA changes. In AMI-CS treated with IABP, coupling improved (VAC -0.42) with modest energetic augmentation, whereas HF-CS showed pressure and energy amplification (end-systolic pressure +23.9 mm Hg; PVA +220.6 mm Hg ·ml). Without mechanical support, AMI-CS demonstrated reduced elastance and pressure, while HF-CS exhibited ventricular dilation (end-diastolic volume [EDV]/end-systolic volume ESV increase) with higher energetic demand. Pressure-volume-derived metrics identify device-specific energetic signatures not fully captured by conventional hemodynamic assessment and may provide mechanistic insight into ventricular unloading strategies; validation against conductance catheter-derived PV measurements remains warranted.
Related Concept Videos
Heart Failure II: Pathophysiology
Cardiac Output II: Effect of Stroke Volume on Cardiac Output
Preload
Preload refers to the initial elongation of the cardiac myocytes before contraction and is related to the volume of blood filling the heart at the end of diastole, or end-diastolic volume. The...
Blood Pressure Imbalances and Circulatory Shock
Blood Pressure: Hypertension and Hypotension
Normal blood pressure is 120/80 mm Hg. Elevated blood pressure is 120-129/under 80 mm Hg. Hypertension, warranting treatment at 130/80 mm Hg, is often asymptomatic and can lead to severe cardiovascular events, aneurysms, peripheral arterial disease, chronic renal disease, or cardiac...
Cardiac Output and Stroke Volume
In an average resting adult male, the typical cardiac output averages...
Regulation of Stroke Volume
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...
Physiology of the Heart: The Cardiac Cycle
Diastole: The Relaxation Phase
During diastole, all four heart chambers relax. The atrioventricular (AV) valves open, and the semilunar valves close. This phase sees the lowest chamber pressures, promoting ventricular filling. Venous blood enters the heart through the...