Ventricular Fibrillation Waveform Changes during Controlled Coronary Perfusion Using Extracorporeal Circulation in a Swine Model

• Published in: PloS one 2016-08, Vol.11 (8), p.e0161166-e0161166
• Main Authors: Gazmuri, Raúl J, Kaufman, Christopher L, Baetiong, Alvin, Radhakrishnan, Jeejabai
• Format: Article
• Language: English
• Subjects: Adenosine; Adenosine diphosphate; Analysis; Animals; Artificial blood circulation; Biology and Life Sciences; Blood; Blood circulation; Blood flow; Cardiac arrhythmia; Cardiopulmonary Resuscitation; Chest; Compression; Coronary Circulation - physiology; CPR; Defibrillators; Energy metabolism; Extracorporeal Circulation; Fibrillation; Health aspects; Hemodynamics; Hemodynamics - physiology; Hogs; Ischemia; Lactic acid; Livestock; Male; Medicine and Health Sciences; Metabolism; Myocardium - metabolism; Perfusion; Phosphocreatine; Reduction; Research and Analysis Methods; Resuscitation; Rodents; Swine; Ventricle; Ventricular fibrillation; Ventricular Fibrillation - physiopathology
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0161166

Several characteristics of the ventricular fibrillation (VF) waveform have been found predictive of successful defibrillation and hypothesized to reflect the myocardial energy state. In an open-chest swine model of VF, we modeled "average CPR" using extracorporeal circulation (ECC) and assessed the time course of coronary blood flow, myocardial metabolism, and myocardial structure in relation to the amplitude spectral area (AMSA) of the VF waveform without artifacts related to chest compression. VF was induced and left untreated for 8 minutes in 16 swine. ECC was then started adjusting its flow to maintain a coronary perfusion pressure of 10 mmHg for 10 minutes. AMSA was calculated in the frequency domain and analyzed continuously with a 2.1 s timeframe and a Tukey window that moved ahead every 0.5 s. AMSA progressively declined during untreated VF. With ECC, AMSA increased from 7.0 ± 1.9 mV·Hz (at minute 8) to 12.8 ± 3.3 mV·Hz (at minute 14) (p < 0.05) without subsequent increase and showing a modest correlation with coronary blood flow of borderline statistical significance (r = 0.489, p = 0.0547). Myocardial energy measurements showed marked reduction in phosphocreatine and moderate reduction in ATP with increases in ADP, AMP, and adenosine along with myocardial lactate, all indicative of ischemia. Yet, ischemia did not resolve during ECC despite a coronary blood flow of ~ 30% of baseline. AMSA increased upon return of coronary blood flow during ECC. However, the maximal level was reached after ~ 6 minutes without further change. The significance of the findings for determining the optimal timing for delivering an electrical shock during resuscitation from VF remains to be further explored.