Central Venous-To-Arterial CO2-Gap May Increase in Severe Isovolemic Anemia

Abstract

Despite blood transfusions are administered to restore adequate tissue oxygenation, transfusion guidelines consider only hemoglobin as trigger value, which gives little information about the balance between oxygen delivery and consumption. Central venous oxygen saturation is an alternative, however its changes reflect systemic metabolism and fail to detect regional hypoxia. A complementary parameter to ScvO2 may be central venous-to-arterial carbon dioxide difference (CO2-gap). Our aim was to investigate the change of alternative transfusion trigger values in experimental isovolemic anemia. After splenectomy, anesthetized Vietnamese mini pigs (n = 13, weight range: 18–30 kg) underwent controlled bleeding in five stages (T1–T5). During each stage approximately 10% of the estimated starting total blood volume was removed and immediately replaced with an equal volume of colloid. Hemodynamic measurements and blood gas analysis were then performed. Each stage of bleeding resulted in a significant fall in hemoglobin, the O2-extraction increased significantly from T3 and ScvO2 showed a similar pattern and dropped below the physiological threshold of 70% at T4. By T4 CO2-gap increased significantly and well correlated with VO2/DO2 and ScvO2. To our knowledge, this is the first study to show that anemia caused altered oxygen extraction may have an effect on CO2-gap.

Effects of red blood cell transfusion on global oxygenation in anemic critically ill patients

“…The Pv-aCO 2 could be used as a marker of global oxygen saturation and reflect the adequacy of cardiac output if VO 2 remains constant. 11,19 In our study, Pv-aCO 2 was significantly more elevated in patients with initial S(c) vO 2 less than 70% but, in contrast to S(c)vO 2 , did not change after transfusion, limiting the utility of this marker in decisions to transfuse. Although the partial pressure of carbon dioxide (PCO 2 ) gap could potentially be used in association with other markers in the management of resuscitation, it is a marker that changes late in the development of anemia.…”

“…The Pv‐aCO 2 could be used as a marker of global oxygen saturation and reflect the adequacy of cardiac output if VO 2 remains constant 11,19 . In our study, Pv‐aCO 2 was significantly more elevated in patients with initial S(c)vO 2 less than 70% but, in contrast to S(c)vO 2 , did not change after transfusion, limiting the utility of this marker in decisions to transfuse.…”

“…We therefore studied the effects of RBC transfusion on systemic oxygenation parameters, including mixed (central) venous oxygen saturation (S(c)vO 2 ), lactate concentrations as a marker of cellular metabolism dysfunction, 10 the venous-to-arterial carbon dioxide difference (Pv-aCO 2 ) 11,12 and the cardiac index (CI)/EO 2 with use of invasive hemodynamic monitoring. 13,14 We investigated the usefulness of these parameters compared to Hb concentrations in transfusion decisions.…”

Perfusion indices revisited

“…In addition to its value in septic shock patients, P (v-a) CO 2 is also negatively correlated with cardiac output in cardiogenic shock patients [ 27 ] and patients with severe isovolemic anemia [ 28 ].…”

RBC Transfusion Triggers: Is There Anything New?

“…However, there are also other clinical situations, and by that other mechanisms that can compensate for an increase in oxygen demand (e.g., an increase in CO) leaving SvO 2 unchanged despite increased tissue oxygen demand. If DO 2 is decreased by normovolemic anemia, there is usually a certain time point when SvO 2 decreases [42]. This time point is often referred to as a potential transfusion threshold as it could indicate that other compensatory mechanisms fail to maintain sufficient oxygen delivery [43].…”