Difference in Acid-Base State between Venous and Arterial Blood during Cardiopulmonary Resuscitation

Abstract

We investigated the acid-base condition of arterial and mixed venous blood during cardiopulmonary resuscitation in 16 critically ill patients who had arterial and pulmonary arterial catheters in place at the time of cardiac arrest. During cardiopulmonary resuscitation, the arterial blood pH averaged 7.41, whereas the average mixed venous blood pH was 7.15 (P less than 0.001). The mean arterial partial pressure of carbon dioxide (PCO2) was 32 mm Hg, whereas the mixed venous PCO2 was 74 mm Hg (P less than 0.001). In a subgroup of 13 patients in whom blood gases were measured before, as well as during, cardiac arrest, arterial pH, PCO2, and bicarbonate were not significantly changed during arrest. However, mixed venous blood demonstrated striking decreases in pH (P less than 0.001) and increases in PCO2 (P less than 0.004). We conclude that mixed venous blood most accurately reflects the acid-base state during cardiopulmonary resuscitation, especially the rapid increase in PCO2. Arterial blood does not reflect the marked reduction in mixed venous (and therefore tissue) pH, and thus arterial blood gases may fail as appropriate guides for acid-base management in this emergency.

Dissociated Oxygen Consumption and Carbon Dioxide Production in the Post–Cardiac Arrest Rat: A Novel Metabolic Phenotype

“…The loss of blood flow caused by CA is widely acknowledged to cause a metabolic pathology, but we struggle to measure the effect of this pathology at the bedside. The cessation of blood flow during CA stops delivery of metabolic substrates and removal of metabolic waste products, rapidly causing a variety of metabolic disorders including loss of ATP, acidemia, hypercarbia, hyperlactemia, loss of the adenosine pool, loss of ion gradients, and loss of water control 5, 6, 7, 8, 9…”

Diferencia veno-arterial de dióxido de carbono como predictor de gasto cardiaco disminuido en modelo pediátrico experimental

“…Se postula que la hipercapnia venosa ocurriría al ser tamponados los hidrogeniones producidos por el metabolismo anaerobio, para mantener el equilibrio ácido-base en células con un potencial redox disminuido. Así como la pCO 2 arterial depende de la ventilación alveolar y del intercambio gaseoso pulmonar, la pCO 2 venosa depende del flujo circulatorio y no necesariamente de la hipoxia hipoxémica, correlacionándose inversamente al GC en falla circulatoria 14,[21][22][23][24][25][26][27][28][29][30] , hallazgo reafirmado en este modelo pediátrico. Concordantemente se ha propuesto un rol de la ΔVACO 2 en guiar la terapia de reanimación, de manera complementaria a la saturación venosa central de oxígeno 13 .…”

Multimodal individualized concept of hemodynamic monitoring

“…As then, several authors have reported increased dCO 2 in different low flow states [40][41][42]. In oxygen debt caused anaerobic metabolism, hydrogen ions are generated through the hydrolysis of ATP to ADP and increased production of lactic acid [43]. These hydrogen ions are buffered by bicarbonate presented in the cells, and this process will generate CO 2 production [44].…”