Hemodynamic collapse, geometry, and the rapidly paced upper limit of ventricular vulnerability to fibrillation by T-wave stimulation.

There is an upper limit to the vulnerability (ULV) of the ventricles to fibrillation (VF) induced by T-wave stimuli. Across species, disease states, and pharmacological treatments, the ULV is correlated to the defibrillation threshold (DF50). However, one factor known to increase the ULV far above the DF50 is rapid pacing. In this article we test the hypothesis that this increase is owing to an accompanying hemodynamic collapse or geometric change. In 18 dogs, T-wave stimuli were delivered from transvenous defibrillating electrodes. The T-wave shock strength that induced VF 50% of the time (the ULV50) was measured using a 10-step Bayesian up-down protocol. T-wave stimuli were delivered after 15 paced beats at one of several rates: normal (80% of the R-R interval), rapid (the interval just fast enough to cause hemodynamic collapse), or 10 milliseconds greater than rapid (which did not cause hypotension). We measured the geometry of the left ventricle at the moment of T-wave stimulation using linear ultrasound. Rapid pacing significantly increased the ULV50 above the normal rate ULV (507 +/- 62.9 vs 379 +/- 70.6 V, P < .005, n = 18), even in the subset without hemodynamic collapse (505 +/- 84.4 vs 394 +/- 66.5 V, P < .005, n = 6). No significant geometric changes were noted between rapid (19.8 mm) and normal (20.6 mm, n = 6, P < NS) pacing, but QT interval reduction appears to correlate with the ULV50 (QT vs ULV50, r > 0, P < .01). Rapid pacing can dramatically increase the measured ULV50. The most likely cause is a concurrent change in the electrophysiology, eg, QT or APD, of the myocardium. As the only known factor to consistently alter the relationship between ULV and the DF50, rapid pacing offers a unique opportunity for the study of the link between defibrillation and ULV testing.