Reply to “Central Venous-Arterial CO2 Difference in Cardiac Surgery Patients—A Parameter in Relationship to Cardiac Output and Altered Microcirculatory Blood Flow”

Abstract

Reply: Dr Zante Bjoern and Dr Stefan Kluge, Thanks for your letter entitled “Central venous-arterial CO2 difference in cardiac surgery patients—A parameter in relationship to cardiac output and altered microcirculatory blood flow.” The comments that Dr Zante Bjoern and Dr Stefan Kluge raised were very important and valuable. They commented “alterations in microcirculatory blood flow may further affect P(v-a)CO2. These alterations appear characterized by increased heterogeneity of perfused and non-perfused capillaries, which may result in increased P(v-a)CO2 even when cardiac output is sufficient.” We totally agreed with their comments. In the previous study, the P(v-a)CO2 values ranging between 2 mm Hg and 6 mm Hg may reflect un-normal conditions (1). Experimental studies in which blood flow was progressively reduced, an elevation in P(v-a)CO2 following the reduction in oxygen delivery (DO2) was reported, while a constant oxygen consumption (VO2) was measured. When DO2 was more diminished under its critical value, a drop in VO2 was noticed, insinuating O2 supply dependency and occurrence of anaerobic metabolism. The progressively increasing value of P(v-a) CO2 observed before DO2 achieving the critical point, was amplified by an acute rise in P(v-a)CO2, then DO2 declined below that point (2). From the analysis of the data of these experimental studies, it can be reasonably supposed that an abrupt increase in P(v-a)CO2 should not be easily attributed to the outset of hypoxia but rather to an additional decrease in cardiac output (3). Since the association between P(v-a)CO2 and cardiac output is curvilinear (Fick equation), an enormous rise in P(v-a)CO2 must be noticed for a reduction in cardiac output in its lowest scale. In our study (4), we focused on the association between P(v-a)CO2 and poor outcomes after cardiac surgery, and demonstrated that there is a negative correlation between P(v-a)CO2 and cardiac index. It was entirely consistent with the Fick equation. It is also similar to a recent study (5), while another study (6) that reported P(v-a)CO2 and outcome were unrelated defined more complications. The best cutoff of the P(v-a)CO2 was 7.12 mm Hg in our study which had exceeded the cutoff of “un-normal condition” (1). Therefore, the P(v-a)CO2 may provide an alternative to predict poor outcomes of patients with postoperative cardiogenic shock. However, a cutoff of 7.12 mm Hg might misinterpret pathophysiological alterations in extracorporeal circulation (ECC)-treated patients. It may be caused by the poor outcomes which were widely identified. The poor outcomes in our study were identified as sudden death, cardiac arrest, use of extracorporeal membrane oxygenation, and high vasoactive inotropic agents score. The cut-off values might be changed in different postoperative situations. As Dr Zante Bjoern and Dr Stefan Kluge mentioned “P(v-a)CO2 may be altered in cardiac surgery patients especially after ECC use due to impaired microcirculation and/or a discrepancy of blood flow and/or altered metabolic conditions,” the cut-off value of P(v-a)CO2 might be increased or decreased in patients with using ECC postoperatively. Our study was conducted at a single institution as a retrospective observational study. We regret that we could not investigate P(v-a)CO2 value for every single postoperative complication. Thus, we recommend further high-quality trials to answer questions about the best cutoff of P(v-a)CO2 or P(v-a)CO2 combined with lactate in different situations after cardiac surgery, especially in ECC-treated patients.