The Effect of Atropine on Hemodynamics during Spinal Anesthesia.
10.4097/kjae.1998.35.5.946
- Author:
Ka Young RHEE
;
Yong Lak KIM
- Publication Type:Original Article
- MeSH:
Anesthesia, Spinal*;
Arterial Pressure;
Atropine*;
Baroreflex;
Blood Pressure;
Bradycardia;
Cardiac Output;
Heart Rate;
Hemodynamics*;
Humans;
Hypotension;
Injections, Intravenous;
Nerve Fibers;
Tachycardia
- From:Korean Journal of Anesthesiology
1998;35(5):946-951
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Background: The major complications of spinal anesthesia are hypotension and bradycardia. In normal condition, hypotension stimulates baroreceptor reflex and compensatory tachycardia is occured. But during spinal anesthesia, there is possibility of a blockade of cardiac sympathetic nerve fibers which would result in increased vagal tone and depress compensatory baroreceptor reflex which is activated during hypotension. Atropine is an anticholinergic agent whose predominant cardiovascular effect was known as increasing heart rate at clinical dose. The purpose of this study was to evaluate hemodynamic effect of atropine during spinal anesthesia. Methods: We compared heart rate, systolic, diastolic and mean arterial pressures and cardiac output in 26 patients of ASA physical status 1, 2 before and after intravenous injection of atropine sulfate 0.01 mg/Kg during spinal anesthesia. Hemodynamic parameters were measured just prior to and 1, 2, 3, 4, 5, 10 minutes after atropine sulfate intravenous injection. The data were analyzed by repeated measures ANOVA. Results: Heart rate, mean blood pressure and diastolic blood pressure after atropine sulfate injection increased with significance. Conclusion: These findings suggest that during spinal anesthesia atropine is effective to produce tachycardia with a dosage of 0.01 mg/Kg in humans. Also hypotension might be improved because atropine makes mean blood pressure and diastolic blood pressure increase.
