pCO2 gap

Reviewed and revised 7 January 2016

OVERVIEW

• pCO2 gap is a surrogate for cardiac output
• pCO2 gap = PcvCO2 – PaCO2
• pCO2 gap >6 mmHg suggests a persistent shock state that may be amenable to fluid resuscitation +/- intrope support
• a “ScvO2-cvaCO2gap-guided protocol” has been proposed by Vallet et al (2013) to guide the management of septic shock

RATIONALE

From Vallet et al (2013):

• CO2 is the end product of aerobic metabolism
• PCO2 in the venous blood reflects the global tissue blood flow relative to metabolic demand
• CO2 is about 20 times more soluble than O2 so it more reliably diffuses out of ischemic tissues into the venous effluent making it a sensitive marker of hypoperfusion
• in situations where an O2 diffusion barrier exists (e.g. non-functional and obliterated capillaries), “masking” poor O2 extraction (O2ER) and increased tissue O2 debt, CO2 still diffuses to the venous effluent, “unmasking” the low perfusion state for the clinician when venous-to-arterial CO2 difference is evaluated
• the gap is a marker of adequacy of venous blood flow to remove CO2 produced rather than a marker of tissue hypoxia or dysoxia

PCO2 GAP IN DIFFERENT SHOCK STATES

From Vallet et al (2013):

Shock type	Lactate	O2ER	ScvO2	cvaCO2gap
Cardiogenic or hypovolemic	HIGH	HIGH	LOW	HIGH
Anemic or hypoxemic	HIGH	HIGH	LOW	LOW
Distributive	HIGH	LOW	HIGH	HIGH
Cytopathic	HIGH	LOW	HIGH	LOW

EVIDENCE

• early days, mostly small proof of concept studies in humans so far

Severe sepsis and septic shock

• some authors suggest targeting a PCO2 gap <6mmHg as an index of adequate tissue perfusion
• supported by observational data suggesting a role in identifying patients with ScvO2 >70% who are still inadequately resuscitated (Vallee et al, 2008) and predicts lactate clearance (Mesquida et al, 2015 and Mallat et al, 2014)
• this approach is not widely used in current Australasian practice

References and Links

Journal articles

• Mallat J, Pepy F, Lemyze M. Central venous-to-arterial carbon dioxide partial pressure difference in early resuscitation from septic shock: a prospective observational study. European journal of anaesthesiology. 31(7):371-80. 2014. [pubmed]
• Mesquida J, Saludes P, Gruartmoner G. Central venous-to-arterial carbon dioxide difference combined with arterial-to-venous oxygen content difference is associated with lactate evolution in the hemodynamic resuscitation process in early septic shock. Critical care. 19:126. 2015. [pubmed]
• Vallée F, Vallet B, Mathe O. Central venous-to-arterial carbon dioxide difference: an additional target for goal-directed therapy in septic shock? Intensive care medicine. 34(12):2218-25. 2008. [pubmed]
• Vallet B, Pinsky MR, Cecconi M. Resuscitation of patients with septic shock: please “mind the gap”! Intensive Care Med. 2013 Sep;39(9):1653-5. PMC3732761.
• Vallet B, Teboul JL, Cain S, Curtis S. Venoarterial CO2 difference during regional ischemic or hypoxic hypoxia. J Appl Physiol. 2000;89:1317–1321. PMID: 11007564