Key result
Higher VA-ECMO flow reduces LVEDP by ~6 mmHg in preclinical cardiogenic shock with aortic stenosis.
Why the study?
The effect of VA-ECMO on left ventricular function in acute cardiogenic shock with severe aortic stenosis or mitral regurgitation was not well understood.
Absolute Event Rate: 19.1% vs 24.9%
p-value: p=<0.01
Higher VA-ECMO flows may protect against LV overload in cardiogenic shock with severe AS; leaves open translation to clinical practice.
Background Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is widely used in the treatment of patients experiencing cardiogenic shock (CS). However, increased VA-ECMO blood flow (EBF) may significantly impair left ventricular (LV) performance. The objective of the present study was to assess the effect of VA-ECMO on LV function in acute CS with concomitant severe aortic stenosis (AS) or mitral regurgitation (MR) in a porcine model. Methods Eight female swine (45kg) underwent VA-ECMO implantation under general anaesthesia and mechanical ventilation. Acute CS was induced by global myocardial hypoxia. Subsequently, severe AS was simulated by obstruction of the aortic valve, while severe MR was induced by mechanical destruction of the mitral valve. Haemodynamic and LV performance variables were measured at different rates of EBF rates (ranging from 1 to 4 L/min), using arterial and venous catheters, a pulmonary artery catheter, and LV pressure-volume catheter. Data are expressed as median (interquartile range). Results Myocardial hypoxia resulted in declines in cardiac output to 2.7 (1.9–3.1) L/min and LV ejection fraction to 15.2% (10.5–19.3%). In severe AS, increasing EBF from 1 to 4 L/min was associated with a significant elevation in mean arterial pressure (MAP), from 33.5 (24.2–34.9) to 56.0 (51.9–73.3) mmHg (P˂0.01). However, LV volumes (end-diastolic, end-systolic, stroke) remained unchanged, and LV end-diastolic pressure (LVEDP) significantly decreased from 24.9 (21.2–40.0) to 19.1 (15.2–29.0) mmHg (P˂0.01). In severe MR, increasing EBF resulted in a significant elevation in MAP from 49.0 (28.0–53.4) to 72.5 (51.4–77.1) mmHg (P˂0.01); LV volumes remained stable and LVEDP increased from 17.1 (13.7–19.1) to 20.8 (16.3–25.6) mmHg (P˂0.01). Conclusion Results of this study indicate that the presence of valvular heart disease may alleviate negative effect of VA-ECMO on LV performance in CS. Severe AS fully protected against LV overload, and partial protection was also detected with severe MR, although at the cost of increased LVEDP and, thus, higher risk for pulmonary oedema.
No takes yet. Share an insight, caveat, or question.
Ošťádal et al. (2022) studied Cardiogenic shock with aortic stenosis or mitral regurgitation (n=8). VA-ECMO blood flow rate escalation vs. 1 L/min was evaluated on Left ventricular end-diastolic pressure (LVEDP) in severe aortic stenosis (p=<0.01). In a porcine model of cardiogenic shock with severe aortic stenosis, increasing VA-ECMO flow from 1 to 4 L/min significantly decreased left ventricular end-diastolic pressure from 24.9 to 19.1 mmHg, indicating protection against left ventricular overload.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: