Does the aetiology of ventricular fibrillation affect its dominant frequency over time in a greyhound model?
The dominant frequency of ventricular fibrillation varies significantly depending on its aetiology, which may explain poor responses to DC countershock in conditions like hyperkalaemia or cardiac glycoside toxicity.
Fast Fourier Transform analysis was used to study ventricular fibrillation induced by several different methods in 43 greyhounds anaesthetized with sodium pentobarbitone. The dominant frequency at the body surface of ventricular fibrillation induced electrically in non-ischaemic hearts was initially 9.9 +/- 0.7 Hz, remained above 9 Hz for 70 s and then rapidly fell to 5 Hz. The dominant frequency of ventricular fibrillation induced by acute occlusion (initially 12.3 +/- 0.2 Hz), or by reperfusion (12.2 +/- 0.4 Hz) of the anterior descending branch of the left coronary artery, showed a similar time-course. However, ventricular fibrillation induced by administration of potassium (4.8 +/- 0.8 Hz) or ouabain (7.1 +/- 1.1 Hz) was significantly slower. Fibrillation recorded from the endocardium of the heart initially showed a similar dominant frequency to that recorded at the body surface, but there was no significant fall in frequency over 3.3 mins. There was little difference in the time-course of fibrillation in the non-ischaemic heart recorded directly from the epicardium or from a surface lead. These findings may be of relevance to the poor response to DC countershock after prolonged ventricular fibrillation, hyperkalaemia or cardiac glycosides.
CARLISLE et al. (Thu,) studied this question.