Author + information
- Received June 2, 1993
- Revision received January 7, 1994
- Accepted January 12, 1994
- Published online June 1, 1994.
- ↵∗Present address and address for correspondence: Dr. Peng-Sheng Chen, Room 5342, Division of Cardiology, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048.
Objectives. This study was performed to test the hypothesis that sodium channel activity is important in determining ventricular vulnerability to electric shocks.
Background. It is unknown whether sodium channel activity determines the upper limit of vulnerability.
Methods. The ventricles of 10 open chest dogs were paced at 300-, 500-, or 1,000-ms cycle lengths. The shock strength associated with a 50% probability of reaching the upper limit of vulnerability (ULV50) and the shock strength associated with a 50% probability of defibrillation (DFT50) were then determined by means of an up-down algorithm. Lidocaine (9.2-mg/kg body weight loading dose and 285-μg/kg per min maintenance dose) was then given, and the ULV50and the DFT50were redetermined after 1 h of stable infusion.
Results. The mean (±SD) lidocaine concentration was 11.9 ±2.4 μg/ml. At baseline, the ULV50tested with each S1cycle length was not significantly different from the DFT50. During lidocaine infusion, the ULV50determined with cycle lengths of 300 and 500 ms (18.9 ± 11.3 and 16.1 ± 8.9 J, respectively) were significantly (p < 0.05) higher than those simultaneously determined for the DFT50(11.2 ± 4.1 and 10.9 ± 5.6 J, respectively). However, when determined with an S1cycle length of 1,000 ms, the ULV50(10.4 ± 4.1 J) was not found to be significantly different from the DFT50(10.3 ± 5.3 J). Lidocaine infusion increased (p < 0.05) QRS duration and the effective refractory periods for cycle lengths of 300 and 500 ms but not 1,000 ms.
Conclusions. The effect of lidocaine on the upper limit of vulnerability is use dependent. These results are compatible with the hypothesis that sodium enamel activity is important in determining ventricular vulnerability to electrical shocks.
↵1 Dr. Chen was the recipient of an NIH FIRST award (1R29HL50259-01), National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
☆ This work was done during the tenure of a Clinician Scientist Award (88–414) and an Established Investigatorship Award (93002670) to Dr. Chen from the American Heart Association and Wyeth-Ayerst, Dallas, Texas, and was supported in part by grants from the Whitaker Foundation, Mechanicsburg, Pennsylvania; the Department of Veterans Affairs, Washington, D.C.; and an American Heart Association National Center Grant-in-Aid (92009820), Dallas, Texas.
- Received June 2, 1993.
- Revision received January 7, 1994.
- Accepted January 12, 1994.