Key result
Pv-aCO2 inversely correlates with CO and Pv-aCO2/Ca-vO2 with DO2/VO2 in septic shock.
Why the study?
To investigate the link between Pv-aCO2 and cardiac output, and Pv-aCO2/Ca-vO2 and the DO2/VO2 ratio in septic shock patients, including subgroups with and without myocardial dysfunction.
Do Pv-aCO2 and Pv-aCO2/Ca-vO2 correlate with cardiac output and DO2/VO2 in septic shock patients?
Observational (n=597)
No
Do Pv-aCO2 and Pv-aCO2/Ca-vO2 correlate with cardiac output and DO2/VO2 in septic shock patients?
Effect estimate: r=-0.63
p-value: p=<0.01
Pv-aCO2 and Pv-aCO2/Ca-vO2 can serve as simple, non-invasive surrogate markers for cardiac output and oxygen metabolism in septic shock patients, with Pv-aCO2/Ca-vO2 being particularly sensitive in those with myocardial dysfunction.
The study investigates the link between the venous-to-arterial carbon dioxide gap (P v-a CO 2 ) and cardiac output (CO), as well as the venous-to-arterial carbon dioxide gap to arterial-venous oxygen content difference (P v-a CO 2 /C a-v O 2 ) ratio and the oxygen delivery to oxygen consumption (DO 2 /VO 2 ) ratio in septic shock patients, with myocardial dysfunction as a secondary subgroup analysis. A retrospective observational study was conducted in intensive care units (ICUs) from July 1, 2018, to March 31, 2024, focusing on patients with septic shock. Participants were divided into two groups for subgroup analysis: those with myocardial dysfunction and those without, based on ejection fraction (EF). The study collected fundamental data, baseline clinical variables, and prognostic indicators to compare the two groups. The study also examined the correlations between P v-a CO 2 and CO, P v-a CO 2 /C a-v O 2 and DO 2 /VO 2 in the overall cohort and subgroups. The study involved 597 septic shock patients. In the overall cohort, a negative correlation was found between P v-a CO 2 and CO ( r = − 0.63, P < 0.01) and between P v-a CO 2 /C a-v O 2 and DO 2 /VO 2 ( r = − 0.71, P < 0.01). In subgroup analysis, 127 patients had myocardial dysfunction, and 470 did not. No significant differences were noted in basic data, lactate, and other indicators ( P > 0.05). However, significant differences were observed in intubation rate, CO, EF, vasoactive inotropic score (VIS), C-reactive protein (CRP), DO 2 , P v-a CO 2 /C a-v O 2 , sequential organ failure assessment (SOFA) score, acute physiology and chronic health evaluation (APACHE-II) score, and 28-day mortality rate ( P < 0.05) between groups. In myocardial dysfunction subgroup, P v-a CO 2 negatively correlated with CO ( r = − 0.57, P < 0.01), and P v-a CO 2 /C a-v O 2 negatively correlated with DO 2 /VO 2 ( r = − 0.80, P < 0.01). Similarly, in non-myocardial dysfunction subgroup, P v-a CO 2 negatively correlated with CO ( r = − 0.62, P < 0.01), and P v-a CO 2 /C a-v O 2 negatively correlated with DO 2 /VO 2 ( r = − 0.68, P < 0.01). The correlation of P v-a CO 2 /C a-v O 2 with DO 2 /VO 2 was significantly stronger in myocardial dysfunction subgroup ( P = 0.008), while the P v-a CO 2 -CO correlation was similar between subgroups ( P = 0.44). In septic shock patients, P v-a CO 2 and P v-a CO 2 /C a-v O 2 correlate well with CO and DO 2 /VO 2 , indicating they could be surrogate markers for these parameters. As a secondary finding, the correlation of P v-a CO 2 and P v-a CO 2 /C a-v O 2 is stronger in patients with myocardial dysfunction.
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Ye et al. (2026) conducted an observational in Septic shock (n=597). Pv-aCO2 and Pv-aCO2/Ca-vO2 was evaluated on Correlation between Pv-aCO2 and cardiac output (CO) (r=-0.63, p=<0.01). In septic shock patients, Pv-aCO2 negatively correlated with cardiac output (r=-0.63, P<0.01), and Pv-aCO2/Ca-vO2 negatively correlated with the DO2/VO2 ratio (r=-0.71, P<0.01).
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