Lidocaine causes a reversible, concentration-dependent increase in defibrillation energy requirements
P Dorian,
ES Fain,
JM Davy,
and
RA Winkle
To investigate the influence of lidocaine on the energy requirements for internal defibrillation, lidocaine (n = 8) or saline solution (n = 12) was administered by intravenous infusion to 20 pentobarbital-anesthetized dogs, and the likelihood of successful defibrillation was examined at various shock energy levels before and after treatment. After lidocaine administration to a mean steady state concentration of 5.6 +/- 2.7 micrograms/ml, the mean energy required to achieve 50 and 90% success in defibrillation (E50 and E90) increased by 61.1 +/- 34.1% (mean +/- SD, p less than 0.005) and 47.1 +/- 28.6% (p less than 0.005), respectively. The steady state log lidocaine concentration correlated positively with the observed increase in E50 (r = 0.887, p less than 0.01) over a concentration range from 1.95 to 9.8 micrograms/ml. In a related experiment, lidocaine infusion was administered to five dogs and then abruptly discontinued. At energy levels achieving a mean 90.0 +/- 10.0% success in defibrillation before treatment, only 43.3 +/- 23.4% success was achieved after 60 minutes of the lidocaine infusion (p less than 0.01) at a mean plasma concentration of 8.4 +/- 2.1 micrograms/ml. The percent of successful defibrillations returned to baseline value (92.0 +/- 18.0%, p less than 0.01) after drug washout at a time when mean lidocaine concentration had declined to 1.8 +/- 0.5 microgram/ml. Lidocaine causes a reversible, concentration-dependent increase in the energy requirements for successful defibrillation; recommendations to administer lidocaine to patients with ventricular fibrillation resistant to defibrillation may need to be reviewed.
This article has been cited by other articles:

|
 |

|
 |
 
J.-q. Zhong, G. Laurent, P. P.-S. So, Xudong Hu, J. K. Hennan, and P. Dorian
Effects of Rotigaptide, a Gap Junction Modifier, on Defibrillation Energy and Resuscitation From Cardiac Arrest in Rabbits
Journal of Cardiovascular Pharmacology and Therapeutics,
March 1, 2007;
12(1):
69 - 77.
[Abstract]
[PDF]
|
 |
|

|
 |

|
 |
 
A. Hamzei, T. Ohara, Y.-H. Kim, M.-H. Lee, O. Voroshilovski, S.-F. Lin, J. N. Weiss, P.-S. Chen, and H. S. Karagueuzian
The Role of Approximate Entropy in Predicting Ventricular Defibrillation Threshold
Journal of Cardiovascular Pharmacology and Therapeutics,
March 1, 2002;
7(1):
45 - 52.
[Abstract]
[PDF]
|
 |
|

|
 |

|
 |
 
L.-P. Lai, J.-L. Lin, W.-P. Lien, Y.-Z. Tseng, and S. K. S. Huang
Intravenous sotalol decreases transthoracic cardioversion energy requirement for chronic atrial fibrillation in humans: assessment of the electrophysiological effects by biatrial basket electrodes
J. Am. Coll. Cardiol.,
May 1, 2000;
35(6):
1434 - 1441.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
G. A. Ewy and J. P. Ornato
Emergency cardiac care: introduction
J. Am. Coll. Cardiol.,
March 15, 2000;
35(4):
825 - 880.
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
A A J Adgey and P W Johnston
Approaches to modern management of cardiac arrest
Heart,
October 1, 1998;
80(4):
397 - 401.
[Full Text]
|
 |
|

|
 |

|
 |
 
D A Chamberlain
Antiarrhythmic drugs in resuscitation
Heart,
October 1, 1998;
80(4):
408 - 411.
[Full Text]
|
 |
|

|
 |

|
 |
 
Advanced Life Support Working Group of the Europea
The 1998 European Resuscitation Council guidelines for adult advanced life support
BMJ,
June 20, 1998;
316(7148):
1863 - 1869.
[Full Text]
|
 |
|

|
 |

|
 |
 
M. R. Ujhelyi, J. J. Sims, and A. W. Miller
High-dose lidocaine does not affect defibrillation efficacy: implications for defibrillation mechanisms
Am J Physiol Heart Circ Physiol,
April 1, 1998;
274(4):
H1113 - H1120.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. R. Ujhelyi, M. Schur, T. Frede, M. Gabel, and M. L. Markel
Differential Effects of Lidocaine on Defibrillation Threshold With Monophasic Versus Biphasic Shock Waveforms
Circulation,
September 15, 1995;
92(6):
1644 - 1650.
[Abstract]
[Full Text]
|
 |
|
|