We determined whether the simultaneous chest compression and ventilation (SCV) technique of car-diopulmonary resuscitation (CPR) enhances cerebral (CBF) and myocardial (MBF) blood flows and cerebral O3 uptake in an infant swine model of CPR as it does in most adult animal CPR models. We also tested whether SCV-CPR sustains CBF and MBF for prolonged periods of CPR when these flows ordinarily deteriorate. CPR was performed in two groups (n = 8) of pentobarbital anesthetized piglets (3.5-5.5 kg) with continuous epinephrine infusion (10 μg/kg/min). Conventional CPR was performed at 100 compressions/min, 60% duty cycle, 1:5 breath to compression ratio and 25-30 mm Hg peak airway pressure. SCV-CPR was performed at 60 compressions/min, 60% duty cycle and 60 mm Hg peak airway pressure applied during each chest compression. Peak right atrial and aortic pressures in excess of $0 mm Hg were generated during CPR in both groups. At 5 min of conventional and SCV-CPR, MBF was 38 ± 7 and 46 ± 7 mL min-1 100 g-1 <±SE), respectively, and CBF was 15 ± 3 and 13 ± 2 mL min1 • 100 g-1, respectively. However, as CPR was prolonged to 50 min, the sternum progressively lost its recoil and the chest became more deformed. Lung inflation at high airway pressure with SCV-CPR did not prevent this chest deformation. Aortic pressure gradually declined, whereas right atrial and intracranial pressure remained constant in both groups. Consequently, MBF and CBF fell less than 10 mL-mhr-1-100 g-1 and cerebral O2 uptake was markedly impaired during prolonged conventional and SCV-CPR. Therefore, SCV-CPR in an infant swine model does not enhance MBF and CBF during early CPR because intrathoracic pressure generation is already high with conventional CPR as reflected by the high right atrial pressure. In addition, SCV-CPR does not prevent the progressive chest deformation and the subsequent decline in CBF and MBF when CPR is prolonged, as is often required in pediatric resuscitation.
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health