Successful Cardiopulmonary Resuscitation After Cardiac Arrest as a “Sepsis-Like” Syndrome

Abstract

Background-We investigated the immunoinflammatory profile of patients successfully resuscitated after cardiac arrest, representing a model of whole-body ischemia/reperfusion syndrome. Methods and Results-Plasma cytokine, endotoxin, and ex vivo cytokine production in whole-blood assays was assessed in 61, 35, and 11 patients, respectively. On admission, high levels of plasma interleukin (IL)-6, IL-8, IL-10, and soluble tumor necrosis factor (TNF) receptor type II could discriminate between survivors and nonsurvivors. Among nonsurvivors, the initial need for a vasopressor agent was associated with higher levels of IL-1 receptor antagonist, IL-10, and IL-6 on day 1. Plasma endotoxin was detected in 46% of the analyzed patients within the 2 first days. Endotoxin-induced TNF and IL-6 productions were dramatically impaired in these patients compared with healthy control subjects, whereas an unaltered production was observed with heat-killed Staphylococcus aureus. In contrast, IL-1 receptor antagonist productions were enhanced in these patients compared with healthy control subjects. The productions of T-cell-derived IL-10 and interferon-␥ were also impaired in these patients. Finally, using in vitro plasma exchange between healthy control subjects and patients, we demonstrated that the endotoxin-dependent hyporeactivity was an intrinsic property of patients' leukocytes and that an immunosuppressive activity was also present in their plasma. Conclusions-Altogether, the high levels of circulating cytokines, the presence of endotoxin in plasma, and the dysregulated production of cytokines found in these patients recall the immunological profile found in patients with sepsis. (Circulation. 2002;106:562-568.)

Persistently elevated extracellular HSP70 (HSPA1A) level as an independent prognostic marker in post-cardiac-arrest patients

“…However, we did not find significant correlations between HSP70 and APACHE II or SAPS II scores, i.e., two correlates of clinical severity. In agreement with previous observations (Adrie et al 2002), we also found higher CRP, and S100B levels in nonsurvivors than in survivors, indicating that the severity of cellular damage and/or host response to this damage is detrimental, as regards survival. Considering these associations between the biomarkers and mortality, we performed Cox regression analysis to investigate the potential influence of the covariates.…”

Metformin Improves Neurologic Outcome Via AMP‐Activated Protein Kinase–Mediated Autophagy Activation in a Rat Model of Cardiac Arrest and Resuscitation

“…CA results in a rapid and complete loss of oxygen and severe energy deficit, which leads to interruption of cellular function, membrane and pump dysfunction, and increased free radical generation to induce neuronal injury 5, 47, 48. The resultant energy deficiency will elevate the AMP/ATP ratio to activate AMPK in the brain 21.…”

From Door to Recovery: A Collaborative Approach to the Development of a Post–Cardiac Arrest Center

“…The post-cardiac arrest syndrome has pathophysiologic characteristics similar to those seen in sepsis. [18][19][20] Figure 1 Post-cardiac arrest syndrome. If return of spontaneous circulation is achieved rapidly after the onset of cardiac arrest, post-cardiac arrest syndrome will not occur.…”

“…Proinflammatory cytokines are produced in the presence of free oxygen radicals. 18,19 Injured neurons may recover, die as a result of lysis causing regional damage in surrounding tissues, or die via apoptosis. Capillary beds may also restore perfusion or remain occluded.…”

“…Similar to sepsis syndrome, the period immediately after cardiac arrest is characterized by elevated serologic markers of global inflammation, endothelial dysfunction, and microcirculatory hypoperfusion. 18 Global myocardial hypokinesis or stunning results from lack of coronary blood flow during cardiac arrest and a shift to anaerobic metabolism that affects calcium and sodium exchange and cellular energy production. A myocardial infarction may be responsible for regional hypokinesis or akinesis.…”