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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.

BACKGROUND The post cardiac arrest syndrome (PCAS) is responsible for the majority of in-hospital deaths following cardiac arrest (CA). The major elements of PCAS are anoxic brain injury and circulatory failure. OBJECTIVE This study aimed to investigate the clinical characteristics of circulatory failure and inflammatory responses after out-of-hospital cardiac arrest (OHCA) and to identify patterns of circulatory and inflammatory responses, which may predict circulatory deterioration in PCAS. METHODS This study is a single-center cohort study of 50 patients who receive intensive care after OHCA. The patients are followed for 5 days where detailed information from circulatory variables, including measurements by pulmonary artery catheters (PACs), is obtained in high resolution. Blood samples for inflammatory and endothelial biomarkers are taken at inclusion and thereafter daily. Every 10 min, the patients will be assessed and categorized in one of three circulatory categories. These categories are based on mean arterial pressure; heart rate; serum lactate concentrations; superior vena cava oxygen saturation; and need for fluid, vasoactive medications, and other interventions. We will analyze predictors of circulatory failure and their relation to inflammatory biomarkers. RESULTS Patient inclusion started in January 2016. CONCLUSIONS This study will obtain advanced hemodynamic data with high resolution during the acute phase of PCAS and will analyze the details in circulatory state transitions related to circulatory failure. We aim to identify early predictors of circulatory deterioration and favorable outcome after CA. CLINICALTRIAL ClinicalTrials.gov: NCT02648061; https://clinicaltrials.gov/ct2/show/NCT02648061 (Archived by WebCite at http://www.webcitation.org/6wVASuOla)

Hemorrhagic shock is clinically observed as changes in macrocirculatory indices, while its main pathological constituent is cellular asphyxia due to microcirculatory alterations. The coherence between macro‐ and microcirculatory changes in different shock states has been questioned. This also applies to the hemorrhagic shock. Most studies, as well as clinical situations, of hemorrhagic shock include a “second hit” by tissue trauma. It is therefore unclear to what extent the hemorrhage itself contributes to this lack of circulatory coherence. Nine pigs in general anesthesia were exposed to a controlled withdrawal of 50% of their blood volume over 30 min, and then retransfusion over 20 min after 70 min of hypovolemia. We collected macrocirculatory variables, microcirculatory blood flow measurement by the fluorescent microspheres technique, as well as global microcirculatory patency by calculation of Pv‐aCO2, and tissue metabolism measurement by the use of microdialysis. The hemorrhage led to anticipated changes in macrocirculatory variables with a coherent change in microcirculatory and metabolic variables. In the late hemorrhagic phase, the animals' variables generally improved, probably through recruitment of venous blood reservoirs. After retransfusion, all variables were normalized and remained same throughout the study period. We find in our nontraumatic model consistent coherence between changes in macrocirculatory indices, microcirculatory blood flow, and tissue metabolic response during hemorrhagic shock and retransfusion. This indicates that severe, but brief, hemorrhage with minimal tissue injury is in itself not sufficient to cause lack of coherence between macro‐ and microcirculation. ª2017 The Authors.Physiological Reportspublished by Wiley Periodicals, Inc. on behalf ofThe Physiological Society and the American Physiological Society.This is an open access article under the terms of the Creative Commons Attribution License,which permits use, distribution and reproduction in any medium, provided the original work is properly cited.