Hemodynamic, respiratory, and perfusion parameters during asphyxia, resuscitation, and post-resuscitation in a pediatric model of cardiac arrest

Abstract

To analyze the evolution of hemodynamic, respiratory, and tissue perfusion parameters in an infant animal model of asphyxial cardiac arrest (CA). This was a secondary analysis of a prospective observational study conducted at a laboratory research department of a university hospital. Seventy-one, 2-month-old piglets were studied. CA was induced by removal of mechanical ventilation. Cardiopulmonary resuscitation (CPR) was performed by means of manual external chest compressions, mechanical ventilation, epinephrine and/or terlipressin intravenous administration. The evolution of hemodynamic (heart rate, blood pressure, cardiac index), respiratory (end-tidal CO(2), blood gas analysis), and tissue perfusion (intramucosal gastric pH, central, cerebral, and renal hemoglobin saturation) parameters was analyzed during three periods: asphyxia, CPR, and after return of spontaneous circulation (ROSC). During asphyxia, a severe arterial and tissue hypoxia with hypercapnia and lactic acidosis quickly developed. Bradycardia, hypotension, and increasing of systemic vascular resistances and pulmonary arterial pressure were also observed. During CPR, arterial, cerebral, and tissue oxygenation were low in spite of ventilation with oxygen 100%. After ROSC a rapid restoration of hemodynamic and respiratory parameters was observed. However, 30min after ROSC, lactic acidosis and low intramucosal gastric pH persisted. Asphyxia leads to sudden hypoxia and hypercapnia with tissue hypoxia and progressive bradycardia. Standard CPR is not able to maintain an adequate tissue oxygenation during CPR in this animal model. When ROSC is achieved, a rapid restoration of the normal values of general hemodynamic and respiratory parameters is observed, although lactic acidosis and splanchnic hypoperfusion persist in time.