Post cardiac arrest syndrome is associated with high morbidity and mortality, which is related not only to a poor neurological outcome but also to respiratory and cardiovascular dysfunctions. The control of gas exchange, and in particular oxygenation and
carbon dioxide levels, is fundamental in mechanically ventilated patients after
resuscitation, as arterial blood
gases derangement might have important effects on the cerebral blood flow and systemic physiology.In particular, the pathophysiological role of
carbon dioxide (CO2) levels is strongly underestimated, as its alterations quickly affect also the changes of intracellular pH, and consequently influence metabolic energy and
oxygen demand. Hypo/
hypercapnia, as well as
mechanical ventilation during and after
resuscitation, can affect CO2 levels and trigger a dangerous pathophysiological vicious circle related to the relationship between pH, cellular demand, and
catecholamine levels. The developing
hypocapnia can nullify the beneficial effects of the
hypothermia. The aim of this review was to describe the pathophysiology and clinical consequences of arterial blood
gases and pH after
cardiac arrest.According to our findings, the optimal
ventilator strategies in post cardiac arrest patients are not fully understood, and
oxygen and
carbon dioxide targets should take in consideration a complex pattern of pathophysiological factors. Further studies are warranted to define the optimal settings of
mechanical ventilation in patients after
cardiac arrest.