Tissue Post Cardiac Arrest

Hypoperfusion to the gut during cardiac arrest is an important clinical problem. The inability to control pH during metabolic stress, e.g. ischemia, leads to the disruption or halting of processes vital to balancing cellular metabolism. Alterations in cellular pH have been linked to changes in intramucosal permeability, which may result in the leakage of inflammatory mediators or bacteria, or both, into the systemic circulation and contribute to the development of organ failure, shock, or death. A strong relationship exists between energy metabolism and cellular acid-base balance. Acidosis during ischemia is likely due to glycolytic accumulation of CO2, lactic acid, and H. Tissue PCO2 is a recognized clinical marker of perfusion failure, resulting from a variety of conditions (hemorrhagic shock, sepsis, trauma) that arise when tissue O2 requirements can no longer be met and anaerobic metabolism is initiated. The link between gastric mucosal hypercarbia and intracellular pH (pHi) has not been established. The relationship between gut tissue PCO2 and pHi is clinically important since cellular/tissue pHi monitoring technologies are not available at the bedside. To our knowledge, gut pHi under hypoxic conditons has not previously been reported. This study was undertaken, then, to: 1) define baseline pHi of stomach and rectum, two clinically useful monitoring sites; 2) evaluate changes in pHi at these sites during ischemia; 3) identify differences in pHi in the gut layers ; 4) compare pHi to mucosal PCO2; and finally 5) estimate the buffering of pHi in the stomach and rectum and compare these values with arterial bicarbonate (HCO3 ).