Anaerobic Metabolism and Metabolic Acidosis During Cardiopulmonary Bypass

Aim – determine a forms of metabolic acidosis (MetAc) after cardiac surgery with cardiopulmonary bypass (CPB). Estimate signiﬁcance of MetAc in an early postoperative period.Material and methods. We included the 129 adult cardiac surgery patients. We studied the indicators of acid-base blood status, markers of systemic inﬂammation, an oxygen delivery and consumption, the hemodynamic parameters, the clinical course of the postoperative period.Results. The acid-base disorders were found in 73.6 % of cases. The metabolic acidosis was in 51.2 % of cases: the lactate acidosis was in 92.4 % and the hyperchloremic acidosis was in 7.6 %. The metabolic lactate acidosis was represented by two forms: 1. the acid-base disorders due to a low cardiac output syndrome with a decrease in oxygen delivery and contractility (14.7 %); 2. the lactate acidosis due to a systemic inﬂammatory response syndrome (49.2 % of cases). It is associated with a high delivery and a low oxygen extraction, increased cardiac output and a vasoplegia. Patients with these disorders had a higher level of leukocytosis after 24 hours of the end the operation, had a longer duration of respiratory support and a long ICU stay and hospital stay.Conclusion. The lactate acidosis is represented by two forms: the lactate acidosis associated with the low cardiac output syndrome and lactate acidosis associated with the systemic inﬂammatory response. The lactate acidosis is a predictor of adverse outcome after cardiac surgery with CPB and associated with a postoperative complications and a mortality.

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Oxygen consumption, carbon dioxide production and lactic acid during normothermic cardiopulmonary bypass

Perfusion ◽

10.1177/026765910001500506 ◽

2000 ◽

Vol 15 (5) ◽

pp. 441-446 ◽

Cited By ~ 2

Author(s):

Milo Engoren ◽

Michael Evans

Keyword(s):

Oxygen Consumption ◽

Lactic Acid ◽

Cardiopulmonary Bypass ◽

Anaerobic Metabolism ◽

Tertiary Care ◽

Carbon Dioxide Production ◽

Care Community ◽

Tissue Ischemia ◽

Measure Oxygen Consumption ◽

A Prospective Study

The objective of this study was to measure oxygen consumption, carbondioxide production and lactic acid levels during normothermic cardiopulmonary bypass. A prospective study was undertaken in a tertiary care community hospital, involving 20 adults undergoing cardiopulmonary bypass with prolonged (>65 min) crossclamping of the aorta. O2 consumption, CO2 production, hemoglobin and lactic acid levels were measured 5, 35 and 65 min after crossclamping of the aorta. O2 consumption was 79.7 ± 14.5, 78.8 ± 15.4 and 81.5 ± 14.1 ml/min/m2 at 5, 35 and 65 min after crossclamping the aorta. CO2 production was 61.8 ± 42.9, 60.6 ± 26.3 and 62.2 ± 35.9 ml/min/m2 at the same times. Lactic acid levels were 1.6 ± 0.5 mM/dl at all three times and did not correlate with O2 consumption or CO2 production. In conclusion, although oxygen consumption was low, there was no evidence of abnormal lactate or anaerobic metabolism to suggest tissue ischemia.

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Ratio of venous-to-arterial PCO2 to arteriovenous oxygen content difference during regional ischemic or hypoxic hypoxia

Scientific Reports ◽

10.1038/s41598-021-89703-5 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Jihad Mallat ◽

Benoit Vallet

Keyword(s):

Metabolic Acidosis ◽

Oxygen Content ◽

Anaerobic Metabolism ◽

Experimental Models ◽

Tissue Hypoxia ◽

Hypoxic Hypoxia ◽

Arterial Pco2 ◽

Mechanically Ventilated ◽

Content Difference ◽

The Difference

AbstractThe purpose of the study was to evaluate the behavior of the venous-to-arterial CO2 tension difference (ΔPCO2) over the arterial-to-venous oxygen content difference (ΔO2) ratio (ΔPCO2/ΔO2) and the difference between venous-to-arterial CO2 content calculated with the Douglas’ equation (ΔCCO2D) over ΔO2 ratio (ΔCCO2D/ΔO2) and their abilities to reflect the occurrence of anaerobic metabolism in two experimental models of tissue hypoxia: ischemic hypoxia (IH) and hypoxic hypoxia (HH). We also aimed to assess the influence of metabolic acidosis and Haldane effects on the PCO2/CO2 content relationship. In a vascularly isolated, innervated dog hindlimb perfused with a pump-membrane oxygenator system, the oxygen delivery (DO2) was lowered in a stepwise manner to decrease it beyond critical DO2 (DO2crit) by lowering either arterial PO2 (HH-model) or flow (IH-model). Twelve anesthetized and mechanically ventilated dogs were studied, 6 in each model. Limb DO2, oxygen consumption ($${\dot{\text{V}}\text{O}}_{2}$$ V ˙ O 2 ), ΔPCO2/ΔO2, and ΔCCO2D/ΔO2 were obtained every 15 min. Beyond DO2crit, $${\dot{\text{V}}\text{O}}_{2}$$ V ˙ O 2 decreased, indicating dysoxia. ΔPCO2/ΔO2, and ΔCCO2D/ΔO2 increased significantly only after reaching DO2crit in both models. At DO2crit, ΔPCO2/ΔO2 was significantly higher in the HH-model than in the IH-model (1.82 ± 0.09 vs. 1.39 ± 0.06, p = 0.002). At DO2crit, ΔCCO2D/ΔO2 was not significantly different between the two groups (0.87 ± 0.05 for IH vs. 1.01 ± 0.06 for HH, p = 0.09). Below DO2crit, we observed a discrepancy between the behavior of the two indices. In both models, ΔPCO2/ΔO2 continued to increase significantly (higher in the HH-model), whereas ΔCCO2D/ΔO2 tended to decrease to become not significantly different from its baseline in the IH-model. Metabolic acidosis significantly influenced the PCO2/CO2 content relationship, but not the Haldane effect. ΔPCO2/ΔO2 was able to depict the occurrence of anaerobic metabolism in both tissue hypoxia models. However, at very low DO2 values, ΔPCO2/ΔO2 did not only reflect the ongoing anaerobic metabolism; it was confounded by the effects of metabolic acidosis on the CO2–hemoglobin dissociation curve, and then it should be interpreted with caution.

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