Jo Kramer-Johansen, Theresa M. Olasveengen
Early observations during treatment of patients in cardiac arrest suggested that the appearance of ventricular fibrillation (VF) was related to outcome, and from the mid-eighties there have been several attempts to quantify the important features of the VF and to elucidate the underlying biological processes in the myocardium.
In this issue of Resuscitation, Bonnes et al. write a new chapter in this story with an analysis of VF characteristics in patients undergoing electrically induced VF in the setting of the electrophysiology laboratory. In 186 patients undergoing implantation of an ICD, analysis of the VF-signal recorded with the intracardiac electrodes showed different patterns in patients with previous myocardial infarction, but apparently no relationship between VF-characteristics and shock success.
The physiological basis for different electrical features of VF is probably related to the fact that even if VF looks chaotic and irregular, the underlying electrical activity is organized in depolarization waves and local re-entry circuits. The surface ECG that we observe both in normal rhythm and in arrhythmias, is the spatially and temporally summation of electrical signals from the heart. The deflections of the ECG-signal are organized (by convention) so that net depolarization is an upward deflection and the height of the deflection is related to the magnitude of the signal. The magnitude of the signal is dependent of the number of cells changing their membrane potential at the same time. A simplification of VF is that when it starts there are areas of the ventricle that depolarize autonomously and in separate re-entry circles or rotors, resulting in coarse VF with large amplitude signals (many cells are still synchronous) and low frequency (larger circles means longer time for the electrical signal to make its way around). As the metabolic substrate of the myocardium is expended and the local homeostasis disrupted, more and more cells cannot maintain their electrical activity and instead act as isolators. This means that the number of rotors or re-entry circles increases and the mean size of each is reduced, resulting in lower amplitudes – i.e. fine VF.
Predictions could be made from this simplistic model, which makes it possible to employ hypotheses testing in a scientific manner rarely (!) seen in resuscitation science. VF characteristics will be expected to change with elapsed time, as has been shown in animal and human studies., Therapy that restores metabolic substrate to cardiomyocytes such as chest compressions and reperfusion would be expected to reverse the changes. Retrospective analyses of VF before and after intervals with chest compressions have shown improvement in VF characteristics. However, in a recent clinical randomized study only half of the patients with fine VF randomized to 2?min of CPR before shock actually improved their VF-score. It is also obvious from this theory that other factors may influence the appearance and development of VF: Pre-existing intra-ventricular conduction abnormalities caused by for instance cardiomyopathies or chronic ischemic disease could modify the starting state and development of the arrhythmia. Acute myocardial ischemia would result in some areas of the myocardium with poor metabolic status at the start of the arrhythmia and also areas distal to an acute thrombus could be less responsive to therapy such as chest compressions. Studies have indeed confirmed that chronic and acute myocardial infarction changes VF characteristics in pigs and humans., , Medications that change the conduction velocity and excitability in the myocardium such as beta-blockers and amiodarone might also change the temporal development and appearance of VF, and this response could be different when provided chronically or during the resuscitation.
Bonnes et al. study does not study the effect of time delay, because, understandably, very short time was allowed for the VF to develop in this cohort of elective ICD-implantation. They found interesting differences between patients with pre-existing myocardial infarction and with and without antiarrhythmic medications. They found no difference in shock success in relation to the frequency related VF characteristics studied (fundamental frequency, median frequency, and organization index). The lack of signals from surface electrodes precluded analysis of amplitude related and combined measures of VF signals, and this is an area open for a follow-up study. The lack of predictive power in the current study could be due to the fact that in this therapeutic setting the first shock success rate was very high (84%) indicating that almost all exceeded a hypothetic threshold, or reflect the fact that electrical conversion is only the first necessary step in the conversion from VF to return of spontaneous circulation (ROSC). Electrical termination of VF is fairly easy to achieve, but not enough to bring patients back. After even a short time of untreated cardiac arrest high quality CPR is needed to empty the dilated right ventricle, restore coronary blood flow and mechanical cardiac activity.
The authors declare that they have no conflict of interest.