Abstract
Objective: The spleen can rapidly mobilize red blood cells (RBCs) to increase blood O 2 carrying capacity in response to a variety of stressors. However, the contribution of splenic RBC mobilization to blood oxygenation during cardiac arrest (CA) and its impact on resuscitation efforts have not been directly studied. Accordingly, we subjected splenectomized swine to CA to test the hypothesis that splenic RBC mobilization meaningfully affects blood O 2 content during CPR. Methods: Swine (n=18) were randomized to splenectomy (SPLX; n=9) or sham surgery (SHAM; n=9) 1-week before undergoing 8-minutes of electrically-induced VF CA followed by CPR with defibrillation and epinephrine (EPI; 0.015 mg/kg iv). Serial blood sampling was performed to assess hemoglobin, hematocrit, and blood O 2 content before CA, during CPR, and following return of spontaneous circulation (ROSC). Results: Compared to baseline, SHAM animals exhibited a significant 41±5% increase in hemoglobin and hematocrit and 30±4% rise in O 2 carrying capacity during CA that was absent after SPLX ( Figure ). Although this did not significantly affect the rate of ROSC between SPLX (44%) and SHAM (56%) groups, time to ROSC (779±196 vs. 455±37 sec; p=0.02) and EPI needed to achieve ROSC (3.3±1.3 vs. 1.4±0.2 boluses, p=0.04) were significantly higher after SPLX. Among animals that achieved ROSC (n=4/group), between-group differences in hemoglobin, hematocrit, and O 2 carrying capacity persisted for up to 90 min post-ROSC alongside a significant reduction in RBC count in SPLX (6.4±0.1 x 10 6 /μL) vs. SHAM (7.3±0.2 x 10 6 /μL) animals (p=0.01). Conclusion: Splenic RBC mobilization during CA contributes to a significant rise in blood O 2 carrying capacity that is evident during CPR and throughout the early post-ROSC period. The absence of this response is associated with a prolonged time to ROSC and additional hemodynamic support, suggesting that impaired splenic RBC mobilization may adversely affect outcomes after CA.
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