It is generally believed that
metabolic acidosis prevails during
cardiac arrest. However, recent experimental and clinical studies have demonstrated that
respiratory acidosis in mixed venous blood and
respiratory alkalosis in arterial blood with only minor increases in
lactic acid characterize the early
acid-base changes that follow
cardiac arrest and
cardiopulmonary resuscitation (
CPR). While continued CO2 production with critical reduction in systemic perfusion explains the accumulation of CO2 in the venous side, the reduction of pulmonary blood flow with maintenance of constant minute ventilation explains the decreases in expired CO2 and therefore arterial PCO2. In the heart, marked increases in CO2 tension and
lactic acid are associated with dramatic decreases in myocardial pH with consequent depression of contractile function. Administration of
sodium bicarbonate, however, neither increases resuscitability nor improves long term outcome. Moreover, adverse effects stemming from increases in plasma osmolality, increases in hemoglobin-O2 affinity, induction of alkalemia and generation of CO2 are potentially deleterious for myocardial and cerebral function. Consequently, the American Heart Association has recently discouraged the routine administration of
bicarbonate during the initial 10 minutes of
CPR in which interventions with proven efficacy such as artificial ventilation, precordial compression,
electric defibrillation and
epinephrine administration take place. Alternative experimental
buffer therapy with agents that consume CO2 have also failed to alter the outcome of
cardiac arrest.