Electrocardiographic and Hemodynamic Changes during Recovery from Bupivacaine Toxicity in Anesthetized Dogs.
10.4097/kjae.2001.40.2.220
- Author:
Hyun Sung CHO
1
;
Soo Joo CHOI
;
Yu Mee LEE
;
Mi Sook GWAK
;
Mi Kyung YANG
;
Duck Hwan CHOI
Author Information
1. Department of Anesthesiology, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Anesthetics, local: bupivacaine;
Monitoring: electrocardiography;
hemodynamics;
Toxicity: bupivacaine
- MeSH:
Acidosis;
Anesthesia, Conduction;
Animals;
Anoxia;
Arrhythmias, Cardiac;
Arterial Pressure;
Bupivacaine*;
Cardiac Output;
Depression;
Dogs*;
Electrocardiography*;
Electrolytes;
Heart Rate;
Hemodynamics*;
Humans;
Hyperkalemia;
Male;
Pentobarbital;
Vascular Resistance
- From:Korean Journal of Anesthesiology
2001;40(2):220-228
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Severe cardiac arrhythmia after accidental intravascular injection of bupivacaine in the practice of regional anesthesia has been reported and is known to be difficult to treat. We evaluated the electrocardiographic and hemodynamic changes during recovery from bupivacaine-induced cardiac toxicity. METHODS: In eight male dogs receiving pentobarbital, after baseline recordings were obtained, 0.5% bupivacaine was infused at a rate of 0.5 mg/kg/min intravenously until cardiac output decreased to 50% or less(1/2 CO), which was defined as the point of cardiac depression in this study. The hemodynamic and electrocardiographic parameters were recorded at 1/2 CO, and 5, 10, 15, 20, 30 and 40 min after 1/2 CO. The following electrocardiographic parameters were measured: duration of QRS complex and T wave, PR interval and the corrected QT interval, all determined on the lead II. RESULTS: Mean arterial pressure was significantly decreased throughout the experimental period after 1/2 CO, and cardiac output and SO2 were significantly decreased until 20 min after 1/2 CO in comparison with those at baseline. All dogs had serious changes on the ECG. Heart rate and ECG changes returned to baseline within 20 min after 1/2 CO, but QRS duration remained increased until 30 min after 1/2 CO. Systemic vascular resistance, pulmonary vascular resistance and serum electrolytes were not changed with time. CONCLUSIONS: In the absence of hypoxia, acidosis, and hyperkalemia, QRS duration returned to control values more slowly than other variables on the EKG after bupivacaine cardiac toxicity. MAP and PCWP recovered the slowest of all hemodynamic variables.
