Monitoring CO2 in shock states

Abstract

The primary end point when treating acute shock is to restore blood circulation, mainly by reaching macrocirculatory parameters. However, even if global haemodynamic goals can be achieved, microcirculatory perfusion may remain impaired, leading to cellular hypoxia and organ damage. Interestingly, few methods are currently available to measure the adequacy of organ blood flow and tissue oxygenation. The rise in tissue partial pressure of carbon dioxide (CO2) has been observed when tissue perfusion is decreased. In this regard, tissue partial pressure of CO2 has been proposed as an early and reliable marker of tissue hypoxia even if the mechanisms of tissue partial pressure in CO2 rise during hypoperfusion remain unclear. Several technologies allow the estimation of CO2 content from different body sites: vascular, tissular (in hollow organs, mucosal or cutaneous), and airway. These tools remain poorly evaluated, and some are used but are not widely used in clinical practice. The present review clarifies the physiology of increasing tissue CO2 during hypoperfusion and underlines the specificities of the different technologies that allow bedside estimation of tissue CO2 content.

The venous–arterial difference in CO2 should be interpreted with caution in case of respiratory alkalosis in healthy volunteers

“…Venous-arterial difference in CO 2 (DCO 2 ) has been proposed as an index of the adequacy of tissue perfusion in shock states [4,5]. DCO 2 has been beneficially evaluated, associated with other markers, to guide resuscitation in septic shock patients [9,18].…”

“…Several markers are available to its assessment, the venous oxygen saturation and the lactate being the most commonly used but their relations with tissue perfusion or tissue hypoxia are not straightforward and misinterpretation can occur [2,3]. The venous-arterial difference in carbon dioxide tension (DCO 2 ) has been proposed as an index of the adequacy of tissue perfusion in shock states [4,5]. DCO 2 reflects the capacity of venous blood flow to remove CO 2 produced by tissues [6].…”

Clinical use of plasma lactate concentration. Part 2: Prognostic and diagnostic utility and the clinical management of hyperlactatemia

“…Interpreting [LAC] in conjunction with other markers of tissue metabolism may help to unravel the origins of hyperlactatemia in specific patients. For example, in the absence of increased muscle activity, increased [LAC] in conjunction with low venous oxygen content or saturation or high venous carbon dioxide tension suggests inadequate tissue oxygen delivery (via macrocirculatory compromise, microcirculatory compromise, and rarely anemia or hypoxia) . Alternatively, an increased lactate concentration in conjunction with an increased peripheral venous oxygen concentration may suggest reduced oxygen extraction (eg, due to mitochondrial dysfunction with impaired oxygen utilization such as in SIRS) or microcirculatory shunting .…”

“…For example, in the absence of increased muscle activity, increased [LAC] in conjunction with low venous oxygen content or saturation or high venous carbon dioxide tension suggests inadequate tissue oxygen delivery (via macrocirculatory compromise, microcirculatory compromise, and rarely anemia or hypoxia). [147][148][149][150][151][152] Alternatively, an increased lactate concentration in conjunction with an increased peripheral venous oxygen concentration may suggest reduced oxygen extraction (eg, due to mitochondrial dysfunction with impaired oxygen utilization such as in SIRS) or microcirculatory shunting. 153,154 Epinephrine-induced upregulation of Na + -K + -ATPase and extramitochondrial glycolysis may be an under recognized cause of hypokalemia and should be considered when faced with hyperlactatemia with concurrent hypokalemia.…”

Prognostic Utility of Culprit SYNTAX Score in Patients With Cardiogenic Shock Complicating ST-Segment Elevation Myocardial Infarction

“…The importance of TIMI flow and no-reflow for cardiovascular outcome have been well-evaluated. 13,25 The current study used blood carbon dioxide content as a biomarker of tissue hypoxemia instead of arterial lactate because all patients have the information about blood total CO 2 content, which has been used in the shock. 25 In the contemporary era, well-validated, IABP-SHOCK II risk score comprised of six factors: age, stroke, glucose, creatinine, TIMI flow, and arterial lactate.…”