Objective: Under conditions of tissue hypoxia total CO2 production (VCO2) should be less reduced than O2 consumption (VO2) since an anaerobic CO2 production should occur. Thus the VCO2/VO2 ratio, and hence the venoarterial CO2 tension difference/arteriovenous O2 content difference ratio (ΔPCO2/C(a-v)O2), should increase. We tested the value of the ΔPCO2/C(a-v)O2 ratio in detecting the presence of global anaerobic metabolism as defined by an increase in arterial lactate level above 2 mmol/l (Lac+). Design and setting: Retrospective study over a 17-month period in medical intensive care unit of a university hospital. Patients: We obtained 148 sets of measurements in 89 critically ill patients monitored by a pulmonary artery catheter. Results: The ΔPCO2/C(a-v)O2 ratio was higher in those with increased (n=73) than in the normolactatemic group (2.0±0.9 vs. 1.1±0.6, p<0.0001). Among all the O2- and CO2-derived parameters the ΔPCO2/C(a-v)O2 ratio had the highest correlation with the arterial lactate level (r=0.57). Moreover, for a threshold value of 1.4 the ΔPCO2/C(a-v)O2 ratio predicted significantly better than the other parameters (receiver operating characteristic curves) the presence of hyperlactatemia (positive and negative predictive values of 86% and 80%, respectively). The overall survival estimate at 1 month was greater when the ΔPCO2/C(a-v)O2 ratio was less than 1.4 on the first set of measurements (38±10% vs. 20±8%, p<0.01). Conclusion: The ΔPCO2/C(a-v)O2 ratio seems a reliable marker of global anaerobic metabolism. Its calculation would be helpful for a better interpretation of pulmonary artery catheter data.

Combination of venoarterial PCO2 difference with arteriovenous O2 content difference to detect anaerobic metabolism in patients.

Septic shock has been associated with microvascular alterations and these in turn with the development of organ dysfunction. Despite advances in video microscopic techniques, evaluation of microcirculation at the bedside is still limited. Venous-to-arterial carbon dioxide difference (Pv-aCO2) may be increased even when venous O2 saturation (SvO2) and cardiac output look normal, which could suggests microvascular derangements. We sought to evaluate whether Pv-aCO2 can reflect the adequacy of microvascular perfusion during the early stages of resuscitation of septic shock. Prospective observational study including 75 patients with septic shock in a 60-bed mixed ICU. Arterial and mixed-venous blood gases and hemodynamic variables were obtained at catheter insertion (T0) and 6 h after (T6). Using a sidestream dark-field device, we simultaneously acquired sublingual microcirculatory images for blinded semiquantitative analysis. Pv-aCO2 was defined as the difference between mixed-venous and arterial CO2 partial pressures. Progressively lower percentages of small perfused vessels (PPV), lower functional capillary density, and higher heterogeneity of microvascular blood flow were observed at higher Pv-aCO2 values at both T0 and T6. Pv-aCO2 was significantly correlated to PPV (T0: coefficient −5.35, 95 % CI −6.41 to −4.29, p < 0.001; T6: coefficient, −3.49, 95 % CI −4.43 to −2.55, p < 0.001) and changes in Pv-aCO2 between T0 and T6 were significantly related to changes in PPV (R
 2 = 0.42, p < 0.001). Absolute values and changes in Pv-aCO2 were not related to global hemodynamic variables. Good agreement between venous-to-arterial CO2 and PPV was maintained even after corrections for the Haldane effect. During early phases of resuscitation of septic shock, Pv-aCO2 could reflect the adequacy of microvascular blood flow.

/pdf/can-venous-to-arterial-carbon-dioxide-differences-reflect-2ozcuijo2o.pdf

Can venous-to-arterial carbon dioxide differences reflect microcirculatory alterations in patients with septic shock?

Recent reports have suggested that increases in venoarterial difference in PCO2 (VAPCO2) and arteriovenous difference in pH (AVpH) represent valuable markers of tissue hypoxia in shock states associated with low cardiac output. We compared the values of VAPCO2 and AVpH with that of blood lactate in their relationship to changes in O2 uptake (VO2) and O2 delivery (DO2) during an acute reduction in blood flow induced by cardiac tamponade. In 13 anesthetized and mechanically ventilated dogs, a catheter was inserted into the pericardium to inject saline and to measure the intrapericardial pressure. VO2 was derived from expired gas analysis. DO2 was calculated by the product of the thermodilution cardiac index and the arterial O2 content. The critical DO2 (DO2crit) was found at 9.9 +/- 1.8 ml/kg.min. VAPCO2 and AVpH, which were 7.1 +/- 4.6 mm Hg and 0.028 +/- 0.025 U, respectively, at baseline, progressively increased to reach 17.5 +/- 6.6 mm Hg and 0.114 +/- 0.054 U, respectively, at DO2crit (both p < 0.01). Below DO2crit they increased more dramatically. These changes were related to both arterial hypocapnia and mixed venous hypercapnia. CO2 excretion decreased from 5.8 +/- 2.0 ml/kg-min at baseline to 3.9 +/- 0.9 ml/kg.min at DO2crit (p < 0.01). End-tidal CO2 tension significantly fell below DO2crit. Lactate levels increased from 2.1 +/- 0.5 to 3.5 +/- 0.5 mmol/L at DO2crit (P < 0.01) and to 6.9 +/- 2.1 mmol/L (p < 0.01) at the end of the study. There was no statistically significant difference between the DO2crit calculated for VAPCO2, AVpH, lactate, or VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriovenous Differences in PCO2 and pH are Good Indicators of Critical Hypoperfusion

Purpose
To evaluate the prognostic value of the Cv-aCO2/Da-vO2 ratio combined with lactate levels during the early phases of resuscitation in septic shock.

/pdf/combination-of-arterial-lactate-levels-and-venous-arterial-2rzqvun8ku.pdf

Combination of arterial lactate levels and venous-arterial CO2 to arterial-venous O2 content difference ratio as markers of resuscitation in patients with septic shock

Splanchnic tonometry: a review of physiology, methodology, and clinical applications.

The authors sought to determine how hypoperfusion influences acid-base balance in arterial and mixed venous blood. In anesthetized, ventilated pigs (n = 12), we determined hemodynamics, O2 uptake, CO2 output, dead-space ventilation, arterial and mixed venous blood acid-base balances, and lactate concentrations during graded reductions in cardiac output by incremental positive end-expiratory pressure (PEEP, 0-20 cm H2O). Cardiac output decreased from 3.2 +/- 0.2 (mean +/- SEM) to 1.2 +/- 0.1 L/min at 20 cm H2O PEEP. Oxygen delivery declined more than O2 uptake did by 60% +/- 2% and 27% +/- 2%, respectively. The decrease in CO2 output (by 21% +/- 2%) was less than that in O2 uptake. Fractional dead-space ventilation increased. At a slight increase in carbon dioxide tension (PCO2) of 4 +/- 1 mm Hg, pH decreased in arterial blood from 7.54 +/- 0.01 to 7.47 +/- 0.02 mmol/L, and standard bicarbonate decreased from 30.3 +/- 0.5 to 27.5 +/- 0.6 mmol/L. The decrease in standard bicarbonate exceeded the increase in blood lactate concentrations. At a similar decrease in standard bicarbonate, the decrease in pH was larger (P less than 0.005) in mixed venous blood than in arterial blood owing to a larger increase in PCO2 (from 40 +/- 2 to 50 +/- 2 mm Hg, P less than 0.005). The changes were reversed after discontinuing PEEP. The authors conclude that ischemia after incremental PEEP results in tissue metabolic acidosis with superimposed respiratory acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial and mixed venous blood acid-base balance during hypoperfusion with incremental positive end-expiratory pressure in the pig.

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Arterial and mixed venous blood acid-base balance during hypoperfusion with incremental positive end-expiratory pressure in the pig.