KMID : 0385920230340060498
|
|
Journal of the Korean Society of Emergency Medicine 2023 Volume.34 No. 6 p.498 ~ p.504
|
|
Association between pralidoxime administration during cardiopulmonary resuscitation and brain tissue oxygen tension in a swine model of cardiac arrest
|
|
Ko Sang-Won
Min Young-Il Jeung Kyung-Woon Lee Hyoung-Youn Jung Yong-Hun Lee Byung-Kook Lee Dong-Hun Heo Tag
|
|
Abstract
|
|
|
Objective: Previous studies have suggested that epinephrine reduces brain tissue O2 tension (PbtO2) after the return of spontaneous circulation (ROSC) via ¥á1-adrenoceptor stimulation and that pralidoxime had ¥á1-adrenoceptor inhibitory action together with non-adrenergic vasopressor action. We sought to investigate the effects of pralidoxime administered during cardiopulmonary resuscitation (CPR) as a sole vasopressor on PbtO2 after ROSC. We hypothesized that pralidoxime administration would lead to a comparable ROSC rate and a higher PbtO2 after ROSC when compared to epinephrine administration.
Methods: After 7 minutes of ventricular fibrillation, 24 pigs randomly received either pralidoxime or epinephrine during CPR. Cerebral measurements, including PbtO2, were measured from the parietal cortices during the 60-minute post- ROSC period.
Results: Coronary perfusion pressure (CPP) during CPR was significantly higher in the epinephrine group than in the pralidoxime group (P=0.012). All the animals in the epinephrine group achieved ROSC, while seven (58.3%) did so in the pralidoxime group (P=0.037). The area under the curves for PbtO2 during the post-ROSC period did not differ between the two groups.
Conclusion: Pralidoxime alone was significantly inferior to epinephrine in increasing CPP and achieving ROSC. In addition, pralidoxime administration did not improve PbtO2 during the post-resuscitation period as compared with epinephrine.
|
|
KEYWORD
|
|
Pralidoxime, Epinephrine, Cardiopulmonary resuscitation
|
|
FullTexts / Linksout information
|
|
|
|
Listed journal information
|
|
|