Related Experiment Video
Updated: Aug 9, 2026
A Rat Model of Ventricular Fibrillation and Resuscitation by Conventional Closed-chest Technique
Published on: April 26, 2015
Effects of sildenafil citrate on defibrillation efficacy
Krekwit Shinlapawittayatorn1, Rattapong Sungnoon, Siriporn Chattipakorn
1Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Insights
High-dose sildenafil citrate significantly increases the defibrillation threshold (DFT) in pigs, requiring stronger shocks to treat ventricular fibrillation (VF). This finding suggests potential implications for managing cardiac arrest in patients with supra-therapeutic sildenafil citrate levels.
Area of Science:
- Cardiology
- Pharmacology
- Critical Care Medicine
Background:
- Sildenafil citrate is associated with fatal arrhythmias, but its impact on defibrillation efficacy is unknown.
- Investigating sildenafil citrate's effect on defibrillation threshold (DFT) during ventricular fibrillation (VF) is crucial.
Purpose of the Study:
- To test if sildenafil citrate increases the shock strength needed for successful defibrillation during VF.
- To evaluate the dose-dependent effect of sildenafil citrate on DFT.
Main Methods:
- 26 pigs underwent defibrillation threshold testing before and after intravenous administration of sildenafil citrate (50 mg or 100 mg) or saline.
- Biphasic shocks were delivered after 10 seconds of VF using a three-reversal up/down protocol.
- Defibrillation threshold (DFT) was determined by voltage and energy required for successful resuscitation.
Main Results:
- A 100-mg sildenafil citrate infusion significantly increased DFT by approximately 19% in voltage and 38% in energy compared to baseline.
- The 50-mg sildenafil citrate dose did not significantly alter the DFT.
- Saline infusion had no significant effect on the DFT.
Conclusions:
- Supra-therapeutic plasma levels of sildenafil citrate significantly elevate the DFT.
- Higher energy or voltage shocks may be necessary for successful defibrillation in patients experiencing VF during high-dose sildenafil citrate treatment.
- These findings highlight potential challenges in managing cardiac arrest in specific patient populations.
Introduction:
Although fatal arrhythmia and sudden death have been reported in patients taking sildenafil citrate, its effect on defibrillation efficacy has not been investigated. The aim of this study was to test the hypothesis that sildenafil citrate increases the shock strength required to successfully defibrillate during ventricular fibrillation (VF).
Methods And Results:
A total of 26 pigs (20-25 kg) were randomly assigned into three groups. In each group, the defibrillation threshold (DFT) was determined at the beginning of the study using a three-reversal up/down protocol. Each shock (RV-SVC, biphasic) was delivered after 10 seconds of VF. Group 1 (n = 10) received 50 mg and group 2 (n = 10) received 100 mg of sildenafil citrate intravenously at a rate of 2 mL/minute for 50 minutes. Group 3 (n = 6) received 100 mL of saline intravenously at the same rate as in group 1. The DFT was determined again after the drug (drug-DFT) and saline (saline-DFT) administration. For 100-mg sildenafil citrate infusion, the DFT (483 +/- 39 V, 18 +/- 3 J) was significantly (P < 0.003 and P < 0.01, respectively) higher than the control-DFT (407 +/- 123 V, 13 +/- 7 J). This sildenafil citrate infusion increased the DFT approximately 19% by voltage, and approximately 38% by total energy. After 50-mg sildenafil citrate infusion, the DFT (454 +/- 28 V, 15 +/- 2 J) was not different than the control DFT (449 +/- 28 V, 15 +/- 2 J). Saline infusion (391 +/- 18 V, 12 +/- 1 J) did not alter the control DFT (399 +/- 22 V, 12 +/- 1 J).
Conclusion:
The 100-mg sildenafil citrate infusion, representing a supra-therapeutic plasma level, significantly increased the DFT. This finding indicates that VF occurring during supra-therapeutic sildenafil citrate treatment would require a stronger shock to successfully defibrillate.
Related Concept Videos
01:23Cardiopulmonary Resuscitation III: AED Use
01:28Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors
Among the PDE5 inhibitors, sildenafil (Revatio) stands out as a competitive and selective inhibitor. It operates by elevating cellular levels of cGMP and augmenting signaling through the cGMP-PKG pathway, promoting vasodilation. Upon oral...
01:25Cardiopulmonary Resuscitation IV: Pharmacological Management
01:25Dysrhythmias VI: Management of Dysrhythmias
01:20Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
01:22Heart Failure Drugs: β-Blockers