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Cardiopulmonary resuscitation in a porcine cardiac arrest model produced a paradox of venous acidemia and arterial alkalemia driven by increased venous PCO2 during the initial 8 minutes.
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Demonstrates venous acidemia and arterial alkalemia during porcine cardiac arrest, indicating arterial blood gases fail to reflect systemic tissue acidosis.
In a porcine preparation of cardiac arrest, we demonstrated that there is a marked paradox of venous acidemia and arterial alkalemia. This paradox is related to decreased clearance of CO2 from the lungs when pulmonary blood flow is critically reduced. Accordingly, increased venous PCO2 rather than metabolic acidosis due to lactic acidosis predominates during the initial 8 min of cardiopulmonary resuscitation. Arterial blood gases fail as indicators of systemic acid-base status and therefore as indicators of tissue acidosis.
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GRUNDLER et al. (1986) studied Cardiac arrest. Cardiopulmonary resuscitation was evaluated on Arteriovenous carbon dioxide and pH gradients (venous acidemia and arterial alkalemia). Cardiopulmonary resuscitation in a porcine cardiac arrest model produced a paradox of venous acidemia and arterial alkalemia driven by increased venous PCO2 during the initial 8 minutes.
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