Cardiac responses to premature monophasic and biphasic field stimuli. Results from cell and tissue modeling studies.
Experimental and clinical observations confirm that certain biphasic (BP) defibrillation shocks are significantly more efficacious than equivalent monophasic (MP) shocks, yet the mechanisms underlying these improvements are still not well understood. The authors used two separate, but related, computer models to investigate in detail the excitation responses of active cardiac cells and tissue to idealized premature extracellular MP and BP field stimuli. The results revealed a large disparity in MP and BP excitation responses to low-strength, but not high-strength, fields. In particular, at these low-strength levels, the polarity reversal within BP shocks effectively extends excitability to earlier cellular refractory states than can be achieved with simple MP shocks. Moreover, whereas low-strength MP shocks induce a distinct all-or-none excitatory response to varying shock prematurities, the excitatory response to equivalent BP shocks remains highly graded. In tissue simulations where such field stimuli intersected propagating wave fronts, the all-or-none excitatory response elicited by low-strength MP shocks created a postshock discontinuity in the spatial transmembrane voltage profile, which initiated a new propagation wave front. In contrast, the graded excitatory response elicited by BP waveforms effectively prevented the formation of postshock wave fronts. High-strength MP and BP stimuli prevented renewed propagation equally well. In conclusion, these results suggest a new mechanisms for BP defibrillation superiority over MP waveforms: that the graded excitatory response to BP stimuli at low-field strengths effectively prevents the formation of large spatial transmembrane voltage gradients, which can lead to renewal of propagated wave fronts.
Fishler
M G
MG
Johns Hopkins University School of Medicine, Department of Biomedical Engineering, Baltimore, Maryland, USA.
Sobie
E A
EA
Tung
L
L
Thakor
N V
NV
D000200:Action Potentials; D005117:Cardiac Complexes, Premature / Q000503:physiopathology; D003198:Computer Simulation; D004554:Electric Countershock; D004558:Electric Stimulation; D004562:Electrocardiography; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D008564:Membrane Potentials / Q000502:physiology; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology; D012032:Refractory Period, Electrophysiological