Do fluctuations of PaCO2 impact on the venous-arterial carbon dioxide gradient?

Abstract

Th e mixed venous–arterial diff erence in carbon dioxide tension (ΔCO 2 ) has been proposed as an index of the adequacy of tissue perfusion in septic shock. Indeed, ΔCO 2 increases with low cardiac output or inadequate microcirculatory perfusion [1,2]. Because carbon dioxide by itself can infl uence vascular tone [3] we hypothesized that, in the same patient, changes in the arterial partial pressure of carbon dioxide (PaCO 2 ) can infl uence ΔCO 2 values. Th e study protocol was approved by the local ethics committee (comite de protection des personnes Sud Est I protocol number 2010-36) and stated that informed consent was not required. We studied 10 patients (age = 66 ± 11 years, Simplifi ed Acute Physiology Score II = 35 ± 6) admitted to the ICU after elective cardiac surgery. Th e patients were all monitored with a pulmonary artery (Swan–Ganz) catheter. Th e tidal volume was set at 8 ml/ kg, and the respiratory rate (RR) was set at 10, 13 or 16 breaths/minute, successively, in a randomized order. After 30 minutes of stabilization in each ventilatory condi tion, arterial and venous blood gases were measured together with the cardiac index and mean arterial pressure. Venous samples were withdrawn from the central venous catheter. Th e three series of measurements for one patient were performed within 2 hours. ΔCO 2 ≤6 mmHg was considered normal [1]. Results are presented as mean ± standard deviation. Data were analyzed by repeated-measures analysis of variance and Scheff e’s post-hoc test or chi-squared test and Bonferroni correction when suitable. PaCO 2 varied consistently with the changes in RR, and we observed a signifi cant increase in ΔCO 2 between RRs of 10 and 16 breaths/minute; this was associated with a signifi cant decrease in the number of patients with a normal ΔCO 2 value (Table 1). Interestingly, central venous saturation also decreased signifi cantly when the RR was increased. In ventilated hemodynamically stable postoperative patients, changes in PaCO 2 variations can infl uence ΔCO 2 . Similarly, in healthy volunteers hyperventilation is associated with an increase of the diff erence between arterial and venous peripheral carbon dioxide [4]. A possible explanation is that hypocapnia induces microvascular constriction, thus increasing stagnation fl ow, and therefore increases the gap. Th is hypothesis could be an explanation for the increment of gut mucosal–arterial PCO 2 gradient observed with acute moderate hypocapnia [5]. In this situation, the decrease in central venous saturation could be interpreted as an increase of tissular oxygen extraction induced by a low oxygen delivery with vasoconstriction [3]. Although the carbon dioxide gap is a valuable index to evaluate perfusion in a shock state, one must be warned of the eff ect of moderate hyperventilation on this gradient. Th e direct eff ect of carbon dioxide on microcirculation needs to be confi rmed by further experiments.