Need for Active Left-Ventricular Decompression during Percutaneous Cardiopulmonary Support in Cardiac Arrest

Abstract

During ventricular fibrillation, myocardial hemodynamic and metabolic effects of percutaneous cardiopulmonary support (PCPS) were analyzed in 11 adult sheep (body weight 77-112 kg). During supported fibrillation, an abrupt increase in left-ventricular pressures with alignment to aortic pressures was observed in 2 animals, which was probably due to spontaneous aortic regurgitation, and resulted in deterioration of coronary perfusion. In 9 animals, left-ventricular pressures rose from 22.9 ± 4.9 to 31.2 ± 7.9 mm Hg elevating left ventricular wall stress from 16,750 ± 8,745 to 28,835 ± 8,892 dyn/cm² after 10 min of PCPS-supported fibrillation (mean flow rate 4.5 ± 0.7 liters/min). Simultaneously, myocardial perfusion pressures decreased from an average of 32.4 ± 11.7 to 22.3 ± 9.4 mm Hg and myocardial lactate release was observed. Additional transapical LV venting using a 9-Fr catheter led to a decrease in both LV pressure (to 25.7 ± 5.3 mm Hg) and wall stress (to 20,612 ± 7,499 dyn/cm²). Left-ventricular decompression decreased myocardial oxygen consumption (from 5.3 ± 1.4 to 4.8 ± 0.9 ml/min· 100 g), and reduced myocardial lactate release, which indicates myocardial protection. Protective effects were most pronounced using 12-Fr-, and 21-Fr-venting cannulas (with 21 Fr: decrease in myocardial oxygen consumption to 2.7 ± 0.6 ml/min· 100 g, and reversal of myocardial lactate release to lactate uptake during fibrillation).Conclusions.Hemodynamic and metabolic data clearly demonstrate the deleterious effects of PCPS to the unvented left ventricle during cardiac arrest. The results emphasize the need for active left-ventricular decompression during PCPS in ventricular fibrillation.

Transfromation of Percutaneous Extracorporeal Life Support to Paracorporeal Ventricular Assist Device: A Case Report

“…However, due to its inability to directly drain the left heart, its effectiveness in assisting the heart is limited [1]. Additionally, several factors including severely reduced LV function, blood from native pulmonary and bronchial circulation, and increased afterload due to retrograde perfusion from the arterial cannula may lead to LV distension.…”

“…The effect of P-ECLS on LV distension was investigated previously by some authors [1,3]. In an animal model of acute heart failure, Kawashima et al [2] reported that the resolution of ventricular fibrillation was related to LV unloading and reduction in myocardial oxygen consumption.…”

Reperfusionstherapie und mechanische Kreislauf-unterstützung bei Patienten mit kardiogenem Schock

“…Artificial pulmonary valve insufficiency (arrow at bottom), which was induced by a special spreading catheter 10 minutes after the start of fibrillation, led to a marked decrease in pulmonary artery pressure (Ppulm) followed by a decrease in left vent¡ pressure (PLV) anda small increase in total myocardial blood flow (MBF) (Scholz et al [69]). stieg auch im kleinen Kreislauf, was offenbar auf eine gleichzeitige Mitralinsuffizienz zurª252 ist [68]. Wir haben experimentell w~ihrend kardiopulmonalen Bypasses bei K a m m e r f l i m m e r n die Auswirkungen einer artifiziell induzierten Pulmonalktappeninsuffizienz (Spreizung der Pulmonalklappe mit Hilfe eines speziellen Katheters) anatysiert.…”

Stepwise use of circulatory support devices in a patient refractory to cardiopulmonary resuscitation

“…Recent data [1] have suggested that veno-arterial extracorporeal membrane oxygenation (VA-ECMO) may be useful in this setting and is termed: extracorporeal cardiopulmonary resuscitation (eCPR) [2]. However, the use of VA-ECMO in the context of eCPR may not be sufficient to achieve haemodynamic stability and can lead to high left ventricular and pulmonary pressures [3,4]. In this setting, some reports have indicated the use of a percutaneous left ventricle assist device (LVAD) for left ventricular unloading [5][6][7].…”