Atrioventricular Mobitz I Block during Propofol Anesthesia for Laparoscopic Tubal Ligation

Ganansia, M. F.; Francois, T.; Ormezzano, X.; Pinaud, M∘; Lepage, Jean-Yves

doi:10.1213/00000539-198910000-00019

Cited by 24 publications

(11 citation statements)

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“…In clinical anaesthesia, propofol has been associated with conversion of supraventricular tachycardia into normal sinus rhythm (Hermann & Vettermann, 1992). Transient AV conduction block has also been found in patients who had received propofol as an anaesthetic (James et al , 1989; Ganansia et al , 1989). The direct suppressive effects of propofol on AV node, as demonstrated by this study, may be responsible for these phenomena.…”

Section: Discussionmentioning

confidence: 60%

Comparative direct electrophysiological effects of propofol on the conduction system and ionic channels of rabbit hearts

Sun

1997

British J Pharmacology

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1 Propofol, an intravenous anaesthetic agent, can a ect cardiac conduction but the ionic mechanisms have not been well de®ned. 2 This study measured the direct e ects of propofol on the cardiac conduction system by using intracardiac recording/stimulation in Langendor -perfused rabbit hearts. The underlying ionic mechanism was elucidated by using the whole-cell voltage clamp on rabbit isolated atrial and ventricular myocytes. 3 Propofol prolonged signi®cantly the AV conduction (AH) interval at a clinically relevant concentration (3 mM). This AH interval prolongation was dose-dependent (3 to 100 mM). At higher concentrations, the AV nodal Wenckebach cycle length and its refractory period were also prolonged (10 to 100 mM). In addition, the conduction through the His-Purkinje system (HV interval) and the atrial tissue (SA interval), as well as the spontaneous cycle length, were lengthened dose-dependently (30 to 100 mM). 4 In isolated ventricular myocytes, Na current was decreased dose-dependently by propofol. In part this was due to a negative-shift of the steady-state voltage-dependent inactivation and a slowed rate of recovery from inactivation. The I Na suppression by propofol was frequency-dependent. Propofol also blocked the I Ca . The ED 50 for peak current inhibition was 6.9+0.9 (n=6) and 8.3+1.5 mM (n=7) for I Na and I Ca , respectively. 5 The transient outward potassium current (I to ) of atrial myocytes was suppressed with an ED 50 of 5.7+0.8 mM (n=11), which was only partly caused by a left-shift of the steady-state inactivation. The inward recti®er K current (I K1 ) of the ventricular cells was reduced somewhat by propofol. 6 In summary, propofol can cause direct dromotropic and chronotropic e ects on the cardiac conduction system, especially the atrioventricular node. These changes can be attributed, at least in part, to its direct dose-dependent suppression of the cardiac I Ca , I Na and I to . Special concerns in the use of propofol anaesthesia for cardiac patients and the therapeutic antiarrythmic potential of propofol-like compounds are addressed.

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Section: Discussionmentioning

confidence: 60%

Comparative direct electrophysiological effects of propofol on the conduction system and ionic channels of rabbit hearts

Sun

1997

British J Pharmacology

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“…This seems contradictory to previously published studies (18–20), although many variables could influence direct comparison (21). Several reports (16,22–25) on propofol‐associated bradycardia and suppression of atrial dysrhythmias have illustrated such a circumstance. Droperidol has been reported to alter the antegrade and retrograde refractory periods of accessory pathways (26), and has been recommended for use in anaesthetics for WPW syndrome to prevent SVT.…”

Section: Discussionmentioning

confidence: 99%

An assessment of desflurane for use during cardiac electrophysiological study and radiofrequency ablation of supraventricular dysrhythmias in children

Schaffer

Snyder

Morrison

2000

Pediatric Anesthesia

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Desflurane has several properties making it a desirable agent for use in electrophysiological studies (EPS) for diagnosis and treatment of cardiac dysrhythmias. We studied 47 children, mean age 12.8+/-4.6 years, mean weight 52.9+/-24.0 kg, with clinical history of supra- ventricular tachycardia (SVT) during EPS using desflurane in a crossover comparison with fentanyl. The patients served as their own controls. All received oral premedication with lorazepam, and intravenous induction with thiopentone, rocuronium, and oxygen. Group 1 (n=24) were administered fentanyl 10 microg.kg-1 bolus i.v. with an infusion of 3 microg.kg-1.h-1 during initial EPS. Fentanyl was discontinued and desflurane, 6% endtidal, was administered and the EPS repeated. Group 2 (n=23) were initially administered 6% desflurane after induction, and following EPS the desflurane was discontinued and the patients administered fentanyl 3 microg.kg-1 bolus and EPS repeated (explanations of EPS abbreviations are provided). Desflurane reduced the mean arterial pressure (MAP) in all patients. In Group 1, desflurane shortened the sinus cycle length (SCL), i.e. increasing the heart rate, and atrial effective refractory period (AERP) while Group 2 demonstrated no such effect on AERP. There were no other significant differences between fentanyl or desflurane techniques in terms of EPS measurements. SVT was inducible with both agents in both groups. Desflurane seems an acceptable agent for use during EPS procedures.

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“…Previous studies have demonstrated that propofol concomitantly blocks other ionic currents, especially L type Ca 2+ current (I Ca,L ) in ventricular myocytes (Yang et al, 1996), which results in minimal or no effect on ventricular action potential duration and QTc interval in experimental and clinical settings (Kojima et al, 2015;Puttick and Terrar, 1992;Staikou et al, 2014). It should also be added that propofol administration depresses cardiac contractility and induces bradyarrhythmias, such as sinus bradycardia and atrioventricular conduction block, especially when used at higher concentrations (Ganansia et al, 1989;Sebel and Lowdon, 1989;Tramèr et al, 1997). These suppressive effects of propofol on cardiac functions may be mediated at least partly by its inhibitory effects on various ion channels, including hyperpolarizationactivated inward current (I f ) and I Ca,L (Kojima et al, 2015;Yang et al, 1996).…”

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confidence: 99%

Interaction of propofol with voltage-gated human Kv1.5 channel through specific amino acids within the pore region

Kojima

Ito

Ding

et al. 2015

European Journal of Pharmacology

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Atrioventricular Mobitz I Block during Propofol Anesthesia for Laparoscopic Tubal Ligation

Cited by 24 publications

References 0 publications

Comparative direct electrophysiological effects of propofol on the conduction system and ionic channels of rabbit hearts

Comparative direct electrophysiological effects of propofol on the conduction system and ionic channels of rabbit hearts

An assessment of desflurane for use during cardiac electrophysiological study and radiofrequency ablation of supraventricular dysrhythmias in children

Interaction of propofol with voltage-gated human Kv1.5 channel through specific amino acids within the pore region

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