Abstract 78: Potassium Chloride Improves the Outcome of Cardiopulmonary Resuscitation and Reduces the Cerebral Injury in a Rat Cardiac Arrest Model
Introduction: It is well known that potassium chloride (KCL) has protective effects on the myocardial ischemia reperfusion injury (IRI) in an isolated cardiac model. However, it is unclear whether this phenomenon occurs in cerebrum as well.
Hypothesis: We hypothesized that KCL also has protective effects on the whole cerebral IRI following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR).
Methods: We established different rat CA models and then compared the outcomes of CPR and the changes of neurogenic injury after restoration of spontaneous circulation (ROSC). Forty five healthy male SD rats were randomized into 5 groups: sham group (n=5 without CA/CPR), 5 min KCL group (n=10), 5 min pacing group (n=10), 8 min KCL group (n=10) and 8 min pacing group (n=10). CA was induced by intravenous injection of KCL (40ug/g) or by transesophageal cardiac pacing and then CPR was started at 5 min or 8 min of CA.
Results: The rates of ROSC and 72 hours survival were 10/10, 7/10, 10/10, 5/10 and 10/10, 5/10, 8/10, 0/10 respectively in 5 min KCL group, 5 min pacing group, 8 min KCL group and 8 min pacing group. The rates of ROSC in KCL groups were higher than those in pacing groups in the setting of the same duration of CA, especially in 8 min CA group (P<0.05). The rates of 72 hours survival in 5 min and 8 min KCL group were significantly higher than those in 5 min and 8 min pacing group (P<0.05 and P<0.01 respectively). Blood pressure in KCL groups was relatively stable but that in pacing groups dropped gradually after ROSC within 1 hour. The neurological deficit score in 5 min KCL group was better than that in 5 min pacing group (P<0.05), and the cerebral pathological injury in 5 min KCL group was less severe than that in 5 min pacing group.
Conclusions: KCL improves the outcome of CPR and alleviates the cerebral IRI in the rat CA model induced by KCL compared with that induced by transesophageal cardiac pacing in the setting of the same duration of CA.
- © 2010 by American Heart Association, Inc.