Matt Harmon

149 Chapter seven may be that TTM33 resulted in lower pulmonary perfusion due to increased vasoconstriction. This may be in line with the finding of higher lactate levels in TTM33 compared to TTM36.In ARDS, increased dead space in associated with increased mortality 20 , and this finding could have implications for cardiac arrest patients at risk for lung injury. Taken together, although TTM33 does not result in reduced survival compared to TTM36 9 , we feel that decreased pulmonary perfusion with increased dead space fraction are unwanted effects, arguing against maintaining cardiac arrest patients at 33°C. Of note, blood gas was not corrected for temperature in this study. This means that PaCO 2 may have been lower in the TTM33 group, as the solubility of CO 2 increases at lower temperatures, Perhaps, correcting PaCO 2 levels for body temperature may have ultimately allowed for lower ventilation settings in the TTM33 group. There are several limitations to this study. Although the study was predefined, several parameters were retrospectively collected through a post-hoc survey, and results should be considered within the limitations of this study design, including lacking data on cause of death. Also, data could not be obtained from all patients included in the original TTM trial. However, centers in whom patients were missing are both large and small centers, from all countries which contributed to the TTM trial. In comparing patients in this study to those that were left out, there was no difference between most baseline variables, nor in mortality. Also, several variables suffered from missing data, resulting in the necessity to impute data for the logistic regression model. However, running the model with and without imputed data did not alter the outcome, suggesting a stable model. We also lacked information about pulmonary complications. In addition to missing data, another limitation is that paralysis was not applied as per study protocol, which may have allowed for spontaneous breathing efforts, which in turn may have affected respiratory rate and other ventilation data. Conclusions Cardiac arrest patients predominantly receive protective ventilation with low V T and low driving pressures. Higher respiratory rate is associated with increased mortality. TTM33 resulted in decreased etCO 2 with increased alveolar dead space fraction compared to TTM36. Optimization of ventilator parameters and gas- exchange should be considered to improve outcome after cardiac arrest.