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 fib rillation (VF) induced by T-wave stimuli. Across species, disease states, a nd pharmacological treatments, the ULV is correlated to the defibrillation threshold (DF50). However, one factor known to increase the ULV far above t he DF50 is rapid pacing. In this article we test the hypothesis that this i ncrease is owing to an accompanying hemodynamic collapse or geometric chang e. In 18 dogs, T-wave stimuli were delivered from transvenous defibrillatin g electrodes. The T-wave shock strength that induced VF 50% of the time (th e ULV50) was measured using a 10-step Bayesian up-down protocol. T-wave sti muli were delivered after 15 paced beats at one of several rates: normal (8 0% of the R-R interval), rapid (the interval just fast enough to cause hemo dynamic collapse), or 10 milliseconds greater than rapid (which did not cau se hypotension). We measured the geometry of the left ventricle at the mome nt of T-wave stimulation using linear ultrasound. Rapid pacing significantl y 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 (5 05 +/- 84.4 vs 394 +/- 66.5 V, P < .005, n = 6). No significant geometric c hanges were noted between rapid (19.8 mm) and normal (20.6 mm, n = 6, P < N S) pacing, but QT interval reduction appears to correlate with the ULV50 (Q T vs ULV50, r > O, P < .01). Rapid pacing can dramatically increase the mea sured ULV50. The most likely cause is a concurrent change in the electrophy siology, eg, QT or APD, of the myocardium. As the only known factor to cons istently alter the relationship between ULV and the DF50, rapid pacing offe rs a unique opportunity for the study of the link between defibrillation an d ULV testing.