The episode of PFV occurred during the ascending phase of a PB cycle (Fig 1) leading to a dramatic drop in BP (Fig 1) for 8 to 9 s. This period of asystole was followed by a period of low BP for another 12 s after defibrillation. At the very onset of a cardiac arrest, systemic peripheral blood flow is certainly not instantaneously null, as pressures between the arterial compartment (in which the pressure drops) and the venous system (wherein pressure increases) will slowly equilibrate until the mean filling pressure is reached, creating some peripheral blood flow; however, as soon as the cardiac pump stops, systemic blood flow is expected to reach a level difficult to reconcile with any significant form of gas transport. Therefore, blood flow must have been severely reduced for >20 s after the onset of PFV. Despite the expected reduction in both pulmonary and systemic blood flow, PVF had no visible effect on the periodicity or the amplitude of this or the subsequent PB cycles (Fig 1). Yet, the reduction in blood flow to the carotid chemoreceptors during the period of PVF should have erased the intrabreath oscillations in Paco2-induced CB stimulation.5 In addition, this reduction in systemic blood flow should have also reset any PB pattern, which would have been caused by cerebral blood flow oscillations and/or circulatory delay.3 Upon the slow return to normal circulatory conditions, the blood leaving the pulmonary circulation is expected to have been transiently hypocapnic and hyperoxic, as a result of the persistent ventilatory activity with no (then low) pulmonary blood flow.6 Indeed, as the entire period of PVF occurred during the ascending phase of a PB cycle, the rise in end-tidal Pco2 that occurred typically before the peak of the breathing oscillations was abolished following defibrillation. As shown in Figure 1, this led to a reduction in alveolar Pco2 by 7 mm Hg during the PB cycle, when PVF was triggered, compared with other BP cycles.