Introduction: The use of calcium chloride (CaCl2) during CPR remains controversial. CaCl2 may improve the effectiveness of CPR by increasing systemic vascular tone and vital organ perfusion. Alternatively, CaCl2 may cause regional vasoconstriction in the brain and heart, resulting in secondary ischemic injury. We hypothesized that administration of the standard dose of CaCl2 during CPR decreases rCBF. Methods: Under pentobarbital anesthesia, 2-4 week old piglets underwent 6 min of cardiac arrest by ventricular fibrillation, and 30 min of standard CPR. rCBF was measured with microspheres at baseline and after 5, 15 and 30 min of CPR. CaCl2 20 mg/kg (n=5) or saline (n=5) was given after 1 and 19 min of CPR. Data (mean±SE) were analyzed by ANOVA and Student's t-test (* p<05). Results: Ionized (io) Ca decreased from 1.40±.03 at baseline to 1.16±.05* at 15 min and 1.18±.05* at 30 min CPR. After CaCl2, ioCa increased to 2.58±16* at 5 min and 2.04±21* at 30 min, and was not different from baseline at 15 min CPR. Calcium increased aortic pressure (44±2 vs 38±2*) and cerebral perfusion pressure at 5 min CPR. Total CBF was not different between groups at any time point; however, severe regional ischemia (CBF<15 ml/100g/min) was more common after 30 min CPR when CaCl2 was given, particularly in subcortical regions (p<.03). Conclusion: These data show that CaCl2 administration has adverse effects on rCBF during prolonged CPR and may worsen ischemic brain injury. Future studies will determine the effect of CaCl2 on functional and neuropathologic outcome.
|Original language||English (US)|
|Journal||Critical care medicine|
|Issue number||1 SUPPL.|
|State||Published - Dec 1 1999|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine