Acidosis during cardiac arrest

Acidosis occurs during cardiac arrest because of decreased blood flow and inadequate ventilation. Chest compressions generate only about 20% to 30% of normal cardiac output, leading to inadequate organ perfusion, tissue hypoxia, and metabolic acidosis. Furthermore, the lack of ventilation causes retention of carbon dioxide, leading to respiratory acidosis. The combined acidosis reduces myocardial contractility and may cause arrhythmias because of a lower fibrillation threshold. 

NADH, which enters the Krebs cycle. However, during cerebral ischaemia, metabolism becomes anaerobic, which results in a precipitous decrease in tissue pH to below 6.2 (Smith etal., 1986 Vonhanweh etal., 1986). Tissue acidosis can now promote iron-catalysed free-radical reactions via the decompartmentalization of protein-bound iron (Rehncrona etal., 1989). Superoxide anion radical also has the ability to increase the low molecular weight iron pool by releasing iron from ferritin reductively (Thomas etal., 1985). Low molecular weight iron species have been detected in the brain in response to cardiac arrest. The increase in iron coincided with an increase in malondialdehyde (MDA) and conjugated dienes during the recirculation period (Krause et al., 1985 Nayini et al., 1985). 

At one time it was suggested to administer bicarbonate during cardiopulmonary resuscitation following cardiac arrest however, recent evidence suggests that little benefit is provided and its use may be detrimental. For treatment of acidosis in this clinical situation, concentrate efforts on restoring ventilation and blood flow. According to the American Heart Association guidelines, use as a last resort after other standard measures have been utilized. 

Studies by Hossmann et al. have shown that prolonged global ischemia may result in secondary deterioration during the reperfusion phase followed by depletion of energy metabolites, acidosis and a dramatic increase in lactate content (Hossmann et al. 1994). However, in some animals recovery can be observed that is dependent on successful reperfusion. This pathologic condition that imitates cardiac arrest in man, results in a rapid (< 10 min) and marked (68% of control) decrease in the ADC when measured by repeated MR diffusion imaging (Hossmann et al. 1994) (Fig. 4.6). 

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