Introduction:
There is an inverse relationship between cardiac output and the central venous-arterial difference of partial pressures of carbon dioxide (pCO2 gap), and pCO2 gap has been used to guide early resuscitation of septic shock. It can be hypothesized that pCO2 gap can be used outside the context of sepsis to distinguish type A and type B lactic acidosis and thereby avoid unnecessary fluid resuscitation in patients with high lactate, but without organ hypoperfusion.
Methods:
We performed a structured review of the literature enlightening the physiological background. Next, we retrospectively selected a series of case reports of nonseptic critically ill patients with elevated lactate, in whom both arterial and central venous blood gases were simultaneously measured and the diagnosis of either type A or type B hyperlactataemia was conclusively known. In these cases, we calculated venous-arterial CO2 and O2 content differences and pCO2 gap.
Results:
Based on available physiological data, pCO2 can be considered as an acceptable surrogate of venous-arterial CO2 content difference, and it should better reflect cardiac output than central venous saturation or indices based on venous-arterial O2 content difference. In our case report of nonseptic patients, we observed that if global hypoperfusion was present (i.e., in type A lactic acidosis), pCO2 gap was elevated (>1 kPa), whilst in the absence of it (i.e., in type B lactic acidosis), pCO2 gap was low (<0.5 kPa).
Conclusion:
Physiological rationale and a small case series are consistent with the hypothesis that low pCO2 gap in nonseptic critically ill is suggestive of the absence of tissue hypoperfusion, mandating the search for the cause of type B lactic acidosis rather than administration of fluids or other drugs aimed at increasing cardiac output.