This paper reviews issues related to peri arrest infection. From the abstract:
During the periarrest period, intestinal ischemia may result in barrier dysfunction and bacterial translocation, which has clear mechanistic links to inflammation and cascade stimulation, especially in patients who are treated with therapeutic hypothermia. Despite optimal management, periarrest bacterial translocation may worsen the outcome of cardiac arrest victims.
But the relationship between infection and cardiac arrest is more complex than we might imagine. Emerging evidence is beginning to suggest that antibiotics may be indicated in non-shockable out of hospital cardiac arrest. From the body of the paper:
One of the main goals both during CPR and postresuscitation period is hemodynamic optimization to preserve adequate coronary and cerebral perfusion. However, intestinal ischemia, a neglected consequence of circulatory collapse, and subsequent reperfusion may be extremely detrimental by enhancing bacterial translocation  . This phenomenon is likely more common in patients presenting with asystole or pulseless electrical activity (PEA) rather than ventricular fibrillation or pulseless ventricular tachycardia due to the prolongation of whole-body ischemia in nonshockable cardiac arrest. Asystole has been reported as the most common presenting rhythm in OHCA victims with bacteremia followed by PEA and ventricular fibrillation  , whereas, in a retrospective analysis, shockable rhythms were uncommon among patients with preexisting pneumonia compared with initial arrest rhythms in patients without pneumonia  . Although the initial rhythm in OHCA is rarely recorded and may have evolved to asystole at the time of the recording, we have also reported PEA as the initial cardiac arrest rhythm in severe sepsis and septic shock  .
Research so far has shown that more than one third of OHCA victims are bacteremic upon presentation  ; however, it is difficult to know if sepsis is the reason for cardiac arrest or bacteremia is a downstream effect of intestinal hypoperfusion.
Multiple purported mechanisms are discussed including the use of saline as resuscitation fluid and the use of therapeutic hypothermia.