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Background Endotracheal suctioning (ETS) is required in critically ill patients but may lead to adverse physiologic effects. The aim of this study was to investigate risk factors associated with adverse respiratory and circulatory effects of ETS, in post-cardiac arrest patients receiving controlled ventilation. Methods Patients with return of spontaneous circulation after out-of-hospital cardiac arrest were followed the first five days in the intensive care unit (ICU). For each ETS procedure performed, data were extracted from the electronic ICU records 10 min before and until 30 min after the procedure. Adverse events were defined as heart rate > 120 beats/min, systolic blood pressure > 200 or < 80 mmHg or SpO2 < 85%. Multivariate logistic regression was applied with SpO2 < 85% and systolic blood pressure < 80 mmHg as primary outcomes. Results For the 36 patients included in the study, the median number of ETS-procedures per patient was 13 (range 1–33). Oxygen desaturation occurred in 10.3% of procedures and severe hypotension in 6.6% of procedures. In the multivariate analysis, dose of noradrenaline, light sedation and oxygen desaturation prior to suctioning were associated with increased risk of oxygen desaturation. Doses of noradrenaline, suction with manual ventilation, suction in combination with patient repositioning, and first day of treatment in the ICU were significantly associated with severe hypotension. Conclusions The risk of circulatory and respiratory deterioration during ETS in post-cardiac arrest patients is increased the first day of ICU care, and related to sedation, dose of noradrenaline and pre-procedure hypoxemia.

Background Whole body ischemia and reperfusion injury after cardiac arrest leads to the massive inflammation clinically manifested in the post-cardiac arrest syndrome. Previous studies on the inflammatory effect on circulatory failure after cardiac arrest have either investigated a selected patient group or a limited part of the inflammatory mechanisms. We examined the association between cardiac arrest characteristics and inflammatory biomarkers, and between inflammatory biomarkers and circulatory failure after cardiac arrest, in an unselected patient cohort. Methods This was a prospective study of 50 consecutive patients with out-of-hospital cardiac arrest. Circulation was invasively monitored from admission until day five, whereas inflammatory biomarkers, i.e. complement activation, cytokines and endothelial injury, were measured daily. We identified predictors for an increased inflammatory response, and associations between the inflammatory response and circulatory failure. Results We found a marked and broad inflammatory response in patients after cardiac arrest, which was associated with clinical outcome. Long time to return of spontaneous circulation and high lactate level at admission were associated with increased complement activation (TCC and C3bc), pro-inflammatory cytokines (IL-6, IL-8) and endothelial injury (syndecan-1) at admission. These biomarkers were in turn significantly associated with lower mean arterial blood pressure, lower cardiac output and lower systemic vascular resistance, and increased need of circulatory support in the initial phase. High levels of TCC and IL-6 at admission were significantly associated with increased 30-days mortality. Conclusion Inflammatory biomarkers, including complement activation, cytokines and endothelial injury, were associated with increased circulatory failure in the initial period after cardiac arrest.