Resuscitation plus · 2025
Jugular bulb venous to arterial carbon dioxide gradient is associated with treatment-responsive phenotypes of hypoxic-ischemic brain injury.
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Faiver Laura, Gomez Hernando, Coppler Patrick J, Tam Jonathan, Ratay Cecelia R, Drumheller Byron C, Elmer Jonathan, Pittsburgh Post Cardiac Arrest Service Investigators
Аннотация
BACKGROUND: The difference between the jugular bulb venous and arterial carbon dioxide (CO2) tension, the cerebral pCO2 gap, is a marker of global tissue perfusion and can be affected by various mechanisms that underlie hypoxic-ischemic brain injury (HIBI). We hypothesized the CO2 gap and SjvO2 together could identify treatment responsive pathophysiology among those with abnormally elevated SjvO2.
METHODS: In this retrospective study including post-arrest patients, we quantified the relationship between pCO2 gap and SjvO2 using hierarchical regression. Among patients with elevated SjvO2, we assessed whether pCO2 gap predicted response to treatment with hyperosmolar therapy using an interaction between time, treatment, and pCO2 gap. We assessed the association between pCO2 gap and indicators of HIBI using mixed regression models.
RESULTS: Among the 109 patients included, pCO2 gap was lower among patients with normal (β = -4.3; 95 % CI, -5.6 to -3.1) or high SjvO2 (β = -7.8; 95 % CI, -9.1 to -6.6) compared to low SjvO2. In our interaction model, treatment with hyperosmolar therapy was associated with a 14.4 mmHg decrease in SjvO2 (95 % CI, -18.4 to -10.3) among those with a high pCO2 gap, but not those with normal pCO2 gap. pCO2 gap was significantly lower among patients with burst-suppression with identical bursts compared to those without (β = -1.8; 95 % CI, -2.8 to -0.9).
CONCLUSION: When interpreted with SjvO2, the cerebral pCO2 gap may uncover covert cerebral dysfunction, and can identify treatment-responsive causes of elevated SjvO2. Thus, the pCO2 gap may be a useful adjunct for phenotyping HIBI.
METHODS: In this retrospective study including post-arrest patients, we quantified the relationship between pCO2 gap and SjvO2 using hierarchical regression. Among patients with elevated SjvO2, we assessed whether pCO2 gap predicted response to treatment with hyperosmolar therapy using an interaction between time, treatment, and pCO2 gap. We assessed the association between pCO2 gap and indicators of HIBI using mixed regression models.
RESULTS: Among the 109 patients included, pCO2 gap was lower among patients with normal (β = -4.3; 95 % CI, -5.6 to -3.1) or high SjvO2 (β = -7.8; 95 % CI, -9.1 to -6.6) compared to low SjvO2. In our interaction model, treatment with hyperosmolar therapy was associated with a 14.4 mmHg decrease in SjvO2 (95 % CI, -18.4 to -10.3) among those with a high pCO2 gap, but not those with normal pCO2 gap. pCO2 gap was significantly lower among patients with burst-suppression with identical bursts compared to those without (β = -1.8; 95 % CI, -2.8 to -0.9).
CONCLUSION: When interpreted with SjvO2, the cerebral pCO2 gap may uncover covert cerebral dysfunction, and can identify treatment-responsive causes of elevated SjvO2. Thus, the pCO2 gap may be a useful adjunct for phenotyping HIBI.