Alternate deletion and potentiation as the cause of pulsus alternans

We have tested the hypothesis that pulsus alternans could be explained by heterometric autoregulation. Dogs were aseptically prepared one week in advance with ultrasonic flow probes, pressure cannulae, dimension transducers (mutual inductance and sonar methods), and atrial stimulation electrodes. Under light morphine-nembutal anesthesia, rapid pacing usually produced alternation. The aortic back pressure had a consistently high negative correlation with left ventricular stroke volume (LVSV). The correlations of end-diastolic pressure and diameter with LVSV varied widely and were frequently negative. Modeling of the linear effects of ventricular diastolic volume and aortic back pressure on LVSV demonstrated prompt restoration of equilibrium after a transient disturbance rather than a sustained alternation. We agree with early theories of alternate deletion of contraction of some myocardial cells, but present evidence that potentiation is also inherent in pulsus alternans. All cells recover excitability in the interval available, but only a fraction may be restored to normal contractility. This population of cells are then excited but do not contract, allowing the energy from excitation to remain unutilized until the next beat, which will then have twice the amount of energy of excitation, and the alternate beat will be potentiated, similar to the mechanism of paired pulse stimulation.