CO₂-derived variables for hemodynamic management in critically ill patients

CO₂ measurement carries significant physiologic and clinical information when analyzing hemodynamic status and ventilation of patients. While much focus is on O₂ based data, CO₂ derived parameters can provide a wealth of additional information. This is becoming more readily available as technological advances are making headways in CO₂ measurements.

The classic targets clinicians follow in patients in shock have shortcomings. The central venous oxygen saturation (ScVO₂) was once hailed as the ideal target to guide resuscitation of patients in shock (1). More recent data challenged its role and reduced its value, although it remains a helpful physiologic parameter to follow (2,3). A normal ScVO₂ does not exclude tissue hypoperfusion and could misguide the clinician. Lactic acid is another closely monitored parameter which reflects tissue perfusion. It is also advocated for in multiple guidelines, but also has its own shortcomings: it can be elevated for reasons other than tissue perfusion such as adrenergic stimulation, increased glycolytic activity or reduced clearance from liver dysfunction (4-6). The venous-to-arterial CO₂ partial pressure difference (ΔPCO₂) and tissue CO₂ could help alleviate some of these limitations.

According to the Fick equation, and similar to O₂ metabolism, CO₂ production (VCO₂) is directly proportional to the cardiac output (CO) and the venous-to-arterial CO₂ content difference. The CO₂ content is linearly related to the partial pressure of CO₂ over the general physiological range of CO₂ content (7). Moreover, the mixed venous values correlate with the central venous values (8). Hence the Fick equation can be rewritten as follows: ΔPCO₂ = k × VCO₂/CO, where the k is a pseudo-linear coefficient supposed to be linear in physiological states.

Based on this modified Fick equation, and for patients in a steady state, ΔPCO₂ is inversely proportional to CO. ΔPCO₂ and its relation to the CO has been studied in a number of situations, including patients in shock on vasopressors, and found to be an appropriate target to titrate such agents (9,10).

ΔPCO₂ has similar value in the operating room, where optimizing tissue perfusion and O₂ delivery is essential to reduce post-operative complications. For high risk non cardiac surgical patients, ΔPCO₂ can be used to reflect CO, identify patients that are not adequately resuscitated and along with ΔPCO₂/C(a-v)O₂ ratio predict post-operative complications (11). This might not be true with cardiac surgical patients, who have different macro and micro hemodynamic changes (12).

Tissue hypercarbia is a common observation in patients in circulatory failure. Tissue CO₂ values are a reflection of the adequacy of tissue perfusion, as reduced blood flow leads to blood stagnation and failure of CO₂ washout from the tissues. This stagnant hypercapnia phenomenon reflects tissue hypoperfusion, even earlier than systemic parameters (13). This is especially relevant in sepsis where the impaired microcirculation, arteriovenous shunting and reduction in capillary density culminate in heterogeneous tissue perfusion. Direct optical videoscopy permits to assess these microcirculatory changes, but is yet to reach the bedside for mainstream use. Tissue capnometry, on the other hand, might offer similar data and is becoming more readily available.

Gastric, sublingual, bladder and transcutaneous PCO₂ values have been assessed in critically ill patients. The stomach is easy to access, can be used to detect gastric hypoperfusion and splanchnic ischemia. The gastric PCO₂ correlates with outcomes in the critical care and operating room settings (14). The sublingual vasculature has drawn significant interest as it reflects pathologic changes seen during septic shock. Measuring sublingual CO₂ offers a way to assess the microcirculation in such patients (15). Overall, the tissue CO₂ gap seems to perform better than systemic parameters, paving the way to use it as a resuscitation target for septic shock.

Transcutaneous CO₂ (tcPCO₂) offers another non-invasive method to estimate PaCO₂ with many studies establishing a good correlation between the 2 values (16). Some restrictions persist including the optimal site for tcPCO₂ measurement (earlobe with its high vascularity seems to perform better than other sites), technological delays (time is needed to sensor equilibration) and a gap between PaCO₂ variations and reflection in the tcPCO₂ value. Nonetheless, when the appropriate conditions are met and the skin perfusion is normal, tcPCO₂ reflects PcCO₂. Similar to other tissues, and as was discussed in the prior section, for patients in shock, the transcutaneous CO₂ gap is a good reflection of tissue perfusion and as such can be used for hemodynamic measurements.

Based on the Fick equation as it applies to O₂ and CO₂, the ΔPCO₂/C(a-v)O₂ ratio equals VCO₂/VO₂ and hence the respiratory quotient (RQ). While under aerobic conditions, RQ values ranges between 0.6 to less than 1, RQ changes with anaerobic metabolism. This is due to VCO₂ increases to a larger extent than VO₂ under anaerobic conditions. While this is of paramount importance diagnostically, it was also found to be valuable parameter to target during resuscitation (17,18).

The following review articles summarize the available literature on CO₂ physiology and clinical value, as it pertains to the critical care setting as well as the operating room.

Acknowledgments

None.

References

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