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Background Mean circulatory filling pressure (Pmcf) provides information on stressed volume and is crucial for maintaining venous return. This study investigated the Pmcf and other determinants of venous return in dysrhythmic and asphyxial circulatory shock and arrest. Methods Twenty Landrace/Large-White piglets were allocated into two groups of 10 animals each. In the dysrhythmic group, ventricular fibrillation was induced with a 9 V cadmium battery, while in the asphyxia group, cardiac arrest was induced by stopping and disconnecting the ventilator and clamping the tracheal tube at the end of exhalation. Mean circulatory filling pressure was calculated using the equilibrium mean right atrial pressure at 5–7.5 s after the onset of cardiac arrest and then every 10 s until 1 min post-arrest. Successful resuscitation was defined as return of spontaneous circulation (ROSC) with a MAP of at least 60 mmHg for a minimum of 5 min. Results After the onset of asphyxia, a ΔPmca increase of 0.004 mmHg, 0.01 mmHg, and 1.26 mmHg was observed for each mmHg decrease in PaO 2 , each mmHg increase in PaCO 2,  and each unit decrease in pH, respectively. Mean Pmcf value in the ventricular fibrillation and asphyxia group was 14.81 ± 0.5 mmHg and 16.04 ± 0.6 mmHg ( p  &lt; 0.001) and decreased by 0.031 mmHg and 0.013 mmHg ( p  &lt; 0.001), respectively, for every additional second passing after the onset of cardiac arrest. With the exception of the 5–7.5 s time interval, post-cardiac arrest right atrial pressure was significantly higher in the asphyxia group. Mean circulatory filling pressure at 5 to 7.5 s after cardiac arrest predicted ROSC in both groups, with a cut-off value of 16 mmHg (AUC = 0.905,  p  &lt; 0.001). Conclusion Mean circulatory filling pressure was higher in hypoxic hypercapnic conditions and decreased at a lower rate after cardiac arrest compared to normoxemic and normocapnic state. A Pmcf cut-off point of 16 mmHg at 5–7.5 s after cardiac arrest can highly predict ROSC.

Determinants of venous return in steady-state physiology and asphyxia-induced circulatory shock and arrest: an experimental study