Inflammatory Response after Out-of-Hospital Cardiac Arrest: A Potential Therapeutic Target?

Resuscitated Out of Hospital Cardiac Arrest (OHCA) results in a clinical situation called Post Cardiac Arrest Syndrome (PCAS), which in many aspects resamples sepsis. Most if not all biochemical markers of inflammation rises in the hours after the OHCA and the haemodynamic situation is often characterized by vasodilation needing vasopressor treatment and reduced systolic function of the heart. This syndrome is believed to be caused by the brief ischemia as well as reperfusions injury involving the whole body. Routine inflammatory serum markers (CRP, procalcitonin etc) as well as many cytokines (Interleukins, interferon g, tumor necrosis factor-a etc) all increases during the first 24 hours after an OHCA, and the level of most of these inflammatory markers correlates with the severity of the PCAS syndrome as well as with the prognosis and mortality.

Targeted temperature management (TTM) for 24 hours at 33C or 36C is a guideline recommended treatment in comatose survivors after out of hospital cardiac arrest (OHCA. TTM has been assumed to lower inflammation following a cardiac arrest and perhaps to stabilize the circulation – however this may be questioned. Insight from the TTM-trial, which compared 24 hours of TTM at 33C with 36C in resuscitated comatose OHCA patients do not support this. Many serum markers of inflammation were found to be similar in the two groups. New therapies directed directly against the profound inflammation seen after OHCA may prove to be valuable approach that should be tested in randomised controlled clinical trials.