Acute respiratory failure and inflammatory response after out-of-hospital cardiac arrest: results of the Post-Cardiac Arrest Syndrome (PCAS) pilot study

Abstract

Background: Although the lungs are potentially highly susceptible to post-cardiac arrest syndrome injury, the issue of acute respiratory failure after out-of-hospital cardiac arrest has not been investigated. The objectives of this analysis were to determine the prevalence of acute respiratory failure after out-of-hospital cardiac arrest, its association with post-cardiac arrest syndrome inflammatory response and to clarify its importance for early mortality. Methods: The Post-Cardiac Arrest Syndrome (PCAS) pilot study was a prospective, observational, six-centre project (Poland 2, Denmark 1, Spain 1, Italy 1, UK 1), studying patients resuscitated after out-of-hospital cardiac arrest of cardiac origin. Primary outcomes were: (a) the profile of organ failure within the first 72 hours after out-of-hospital cardiac arrest; (b) in-hospital and short-term mortality, up to 30 days of follow-up. Respiratory failure was defined using a modified version of the Berlin acute respiratory distress syndrome definition. Inflammatory response was defined using leukocytes (white blood cells), platelet count and C-reactive protein concentration. All parameters were assessed every 24 hours, from admission until 72 hours of stay. Results: Overall, 148 patients (age 62.9±15.27 years; 27.7% women) were included. Acute respiratory failure was noted in between 50 (33.8%) and 75 (50.7%) patients over the first 72 hours. In-hospital and short-term mortality was 68 (46.9%) and 72 (48.6%), respectively. Inflammation was significantly associated with the risk of acute respiratory failure, with the highest cumulative odds ratio of 748 at 72 hours (C-reactive protein 1.035 (1.001–1.070); 0.043, white blood cells 1.086 (1.039–1.136); 0.001, platelets 1.004 (1.001–1.007); <0.005). Early acute respiratory failure was related to in-hospital mortality (3.172, 95% confidence interval 1.496–6.725; 0.002) and to short-term mortality (3.335 (1.815–6.129); 0.0001). Conclusions: An inflammatory response is significantly associated with acute respiratory failure early after out-of-hospital cardiac arrest. Acute respiratory failure is associated with a worse early prognosis after out-of-hospital cardiac arrest.

Monocyte subsets predict mortality after cardiac arrest

“…31,32 This might further explain our findings of prognostic abilities of monocyte subsets only after 72 h. Several observations confirm our findings of a strong inflammatory activation in patients after CA, with 1 study analyzing monocyte behavior. [21][22][23] The authors of the latter finding suggested changes in monocyte pattern recognition receptor signaling pathways and inflammasome activation may play a role in PCAS. 23 Monocyte subsets were implicated in the pathophysiology of acute myocardial infarction and correlated with outcome and left ventricular function in those patients.…”

“…However, inflammatory mechanisms have been implicated in myocardial reperfusion injury and thus might play an important role in whole body reperfusion injury. 21,22 As innate immune effector cells, monocytes may play an important role in the pathophysiology of PCAS. 23 According to their surface expression pattern of CD14 and CD16, monocytes can be distin-guished into at least three subtypes, namely CM (CD14 ++ CD16 + ), IM (CD14 ++ CD16 + CCR2 + ), and NCM (CD14 + CD16 ++ CCR2).…”

“…As myocardial failure and brain injury are thought to represent the main causes of death, therapeutic interventions and prognostication efforts mainly focus on those areas. However, inflammatory mechanisms have been implicated in myocardial reperfusion injury and thus might play an important role in whole body reperfusion injury 21,22 …”

High Platelet-Lymphocyte Ratio is a Risk Factor for 30-day Mortality In In-Hospital Cardiac Arrest Patients: A Case-Control Study

“…Prolonged hypoxia can lead to activation of endothelial cells, and comprehensive activation of multiple in ammatory pathways can lead to systemic in ammatory response syndrome, which can eventually lead to multiple organ failure and even death of patients [10]. Therefore, strengthening the monitoring of early in ammatory markers and administering targeted treatment and intervention probably improve the organ function and prognosis of patients [11][12][13].…”

The hospitalised out-of-hospital cardiac arrest patient: We need more research

“…5 Furthermore, Czerwinska-Jelonkiewicz et al illustrated that the respiratory failure often seen after OHCA is related to the inflammatory response in these patients. 6 Finally, Wiberg et al demonstrated in muscle biopsies from OHCA patients that mitochondrial dysfunction may be a significant part of the PCAS. 7 Although the latter may not be directly related to inflammation, these studies clearly indicate that the inflammatory response after OHCA is important and, therefore, represents a logical target for future randomised trials.…”