Matt Harmon

148 Chapter seven study, an observational study focusing on mechanical ventilation practices in patients without ARDS. 8 In addition, a previous study in patients with cardiac arrest found that low V T ventilation was increasingly applied in ICUs in 40 countries over a period of 12 years. 6 Of note, compliance of the respiratory system was low in the majority of patients and PEEP level was set at > 5 cm H 2 0 in more than half of patients. This may suggest that most of the patients may have had a pulmonary complication following cardiac arrest, such as lung contusion following chest compressions, pulmonary edema, atelectasis or aspiration. As a surrogate marker of pulmonary complications, we compared hypoxemic patients to normoxemic patients. In total, 105 patients out of 336 had a P/F ratio below 200, indicating that a relatively large portion of patients may have suffered from pulmonary complications. These patients were ventilated with markedly higher pressure levels. Unfortunately, we did not collect X-rays, so we cannot conclude with certainty about pulmonary conditions of patients. Of note, impaired circulation may also result in hypoxemia. In the loess regression plots, both driving pressure > 20 cmH 2 O as well as plateau pressure > 30 cmH 2 0 show a linear relation with mortality. Thereby, the relationship between ventilation settings and mortality following cardiac arrest appear follow similar trends as in ARDS, although in patients with ARDS the linear relation to proportion of deaths occurs at driving pressures > 10 cmH 2 O and plateau pressures >20 cmH 2 0. 18 Of note, V T was not associated with mortality in this cohort of patients, likely due to the fact that the majority of them was already ventilated at relatively low V T . In multivariate analysis, other ventilation factors were also not independently associated with outcome, as mortality was predominantly associated with non-respiratory factors. In ARDS patients, driving pressure is associated with adverse outcome. 19 The lack of a relationship between driving pressure and 28-day mortality in our cohort may be explained by a low effect size or a limited number of patients with high driving pressure. We are unsure how to explain the association between respiratory rate and 28-day mortality. An explanation may be that neurological damage may have driven the relation between hyperventilation and outcome. Of note, paralysis was not part of standard care. Alternatively, given that respiratory rate was increased in the hypoxemic patients compared to normoxemic patients, increased respiratory rate may have been a consequence of lung injury or altered gas exchange, which may have had a negative interaction with outcome. The clinical relevance of this finding remains to be determined. PaCO 2 levels decreased in both TTM groups, most likely due to sedation. In contrast, etCO 2 levels were lower in the TTM33 group compared to the TTM36 group. This coincided with a significantly higher alveolar dead space fraction in TTM33 compared to the TTM36 group. A possible explanation for this finding