Bradycardia after propofol infusion

Thomson, StClair; Yate, P.M.

doi:10.1111/j.1365-2044.1987.tb03994.x

Cited by 41 publications

(24 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The reported effects of propofol on the heart rate have not been uniform: some investigators have described an increase [17,18], whereas others have observed a decrease [19] or minimal or no change [20,21] in heart rate. The reason for these different results is not clear, but may, in part, reflect differences in autonomic tone and the concomitant use of other anesthetic agents [4][5][6][7][8][9]22] Clinically, propofol has been reported to occasionally cause profound sinus bradycardia [4][5][6][7][8], often persisting into the postoperative period [4], and asystolic cardiac arrest [5][6][7][8], especially when used in combination with potent opioid agents [4][5][6][7][8][9]22], Although less frequently, propofol has also been reported to cause significant AV block, resulting in cardiac arrest [9], However, with the exception of published case reports [4][5][6][7][8][9], significant bradyarrhythmias, in general, have not been seen in large number of patients exposed to propofol for a variety of procedures [22,23].…”

Section: Discussionmentioning

confidence: 98%

“…tion and maintenance of sedation/anesthesia during a variety of surgical and nonsurgical procedures [1]. In addition to its cardiac-depressant effects [1][2][3], propofol has been reported to cause profound sinus bradycardia and atrioventricular (AV) block [4][5][6][7][8][9]. However, only lim ited data exist regarding its electrophysiological proper ties [10], Several commonly administered anesthetic agents in fluence cardiac conduction by a variety of mechanisms, including direct electrophysiological effects, neurally me diated changes in autonomic nervous system tone, and indirect electrolyte and acid-base changes that accompa ny spontaneous and controlled ventilation [11], With the advent of catheter ablation procedures to treat cardiac tachyarrhythmias [12], anesthesiologists are often asked to provide sedation and, in selected patients, general anes thesia during such procedures [13], Reliable assessment of changes in the conduction properties of cardiac tissues is important during catheter ablation, and, therefore, ideal ly, the anesthetic agent used during the procedure should have a minimal or no effect on cardiac conduction proper ties.…”

Section: Introductionmentioning

confidence: 99%

“…However, only lim ited data exist regarding its electrophysiological proper ties [10], Several commonly administered anesthetic agents in fluence cardiac conduction by a variety of mechanisms, including direct electrophysiological effects, neurally me diated changes in autonomic nervous system tone, and indirect electrolyte and acid-base changes that accompa ny spontaneous and controlled ventilation [11], With the advent of catheter ablation procedures to treat cardiac tachyarrhythmias [12], anesthesiologists are often asked to provide sedation and, in selected patients, general anes thesia during such procedures [13], Reliable assessment of changes in the conduction properties of cardiac tissues is important during catheter ablation, and, therefore, ideal ly, the anesthetic agent used during the procedure should have a minimal or no effect on cardiac conduction proper ties. Since propofol is reported to cause bradyarrhythmias [4][5][6][7][8][9] and is frequently used in the electrophysiology labo ratory [13], we studied its electrophysiological effects in an attempt to elucidate the mechanism(s) whereby it pro duces bradyarrhythmias.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Electrophysiological Effects of Propofol on the Normal Cardiac Conduction System

et al. 1996

View full text Add to dashboard Cite

To determine the electrophysiological effects of propofol and to explain the potential mechanism(s) whereby it causes bradyarrhythmias, 10 closed-chest pigs weighing 20-25 kg were studied. Each animal was premedicated by intramuscular administration of ketamine hydrochloride, intubated, and mechanically ventilated. Femoral arterial and venous catheters were placed, and a comprehensive electrophysiologic evaluation was performed at baseline and after two doses (1 mg/kg i.v. bolus and 0.1 mg/kg/min infusion and an extra 1-mg/kg i.v. bolus and 0.2 mg/kg/min infusion) of propofol. The electrophysiological effects obtained on low- and high-dose propofol were compared to baseline values. Propofol caused a dose-related decrease in sinus cycle length (baseline 565 ± 36 ms, low-dose propofol 541 ± 28, high-dose propofol 527 ± 26 ms; p < 0.05), a prolongation of the corrected sinus node recovery time (baseline 119 ± 35 ms, low-dose propofol 126 ± 32, high-dose propofol 130 ± 30 ms; p < 0.01), and an increase in the His-ventricular interval (baseline 33 ± 4 ms, low-dose propofol 36 ± 4, high-dose propofol 40 ± 3 ms; p < 0.005). All other electrophysiological parameters remained unchanged, and there were no cases of spontaneous atrioventricular block or sinus pauses. We conclude that propofol causes dose-related depression of sinus node and His-Purkinje system functions, but has no effect on the atrioventricular node function and on the conduction properties of atrial and ventricular tissues in normal pig hearts.

show abstract

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Electrophysiological Effects of Propofol on the Normal Cardiac Conduction System

et al. 1996

View full text Add to dashboard Cite

show abstract

“…The administration of atropine has been shown to mitigate or effectively reverse these events. [1][2][3][4][5][6][7] In our earlier study in dogs, 2~ the total serum concentration of propofol increased from 2.9 • 0.3 to 11.5 • 0.1 /ag.ml -l after graded infusion rates of propofol (6, 9, 12, 15, 18 and 21 mg.kg-khr -l) at 30-min intervals; the peak value of 11.5 l~g.m1-1 is about three times as high as those achieved during maintenance of an adequate level of clinical anesthesia (4 -5 ~ag.ml-1). 21 Therefore, the serum levels of propofol probably reached much higher levels in this study than those in our earlier study, 2~ because of the prolonged perfusion (60 min) and the higher final infusion rate (24 mg.kg-a.hr -1) employed.…”

Section: Discussionmentioning

confidence: 99%

Propofol does not affect the canine cardiac conduction system under autonomic blockade

Ikeno

Akazawa

Shimizu

et al. 1999

Can J Anesth/J Can Anesth

View full text Add to dashboard Cite

Purpose: To determine the effects of propofol on the cardiac conduction system in dogs with pharmacological autonomic blockade. Methods: In eight mongrel dogs receiving 6 mg'kg -l'hr -I propofol and vecuronium under pharmacological autonomic blockade with atropine and propranolol the infusion rates of propofol were increased from 6, (baseline), to 12, 18 and 24 mg'kg -i'hr -l at 60-min intervals. An electrophysiological study assessed sinus rate, sinus node recovery time, corrected sinus node recovery time, intraatrial conduction time, AV nodal effective refractory period, Wenckebach cycle length and AV conduction times. Electrocardiographical variables and arterial pressures were also measured. All measurements were repeated at 30 min after the beginning of each infusion of propofol. Re~uJts: Propofol did not produce direct effects on the electrophysiological or electrocardiographical variables at any infusion rates. Heart rates did not change at higher infusion rates in the presence of decreases in arterial pressures. Conclusion: Propofol did not affect the cardiac conduction system in the presence of autonomic blockade. Thus, the direct cardiac effects of propofol do not play a causative role in the genesis of propofol-associated bradyarrhythmias.Objectif: DEterminer les effets du propofol sur le syst~me de conduction du coeur chez les chiens soumis ~ un blocage nerveux autonome. M&hode : I'&ude a porte sur huit chiens communs qui ont re~ju 6 mg-kg -I-hr t de propofol et du v&uronium sous un blocage pharmacologique nerveux autonome avec de ratropine et du propranolol. La vitesse de peffusion du propofol a augment& passant de 6, au depart, ~ 12, 18 puis 24 mg-kg -~'hr -I ~ des intervalles de 60 min. Un examen Electrophysiologique a permis d'Evaluer le rythme sinusal, le temps de rEcupEration sinusale, le temps de rEcupEration sinusale corrig& le temps de conduction intra-auriculaire, la pEriode rEfractaire effective clu noeud AV, la Iongueur de la p&iode de Wenckebach et les temps de conduction AV. On a aussi mesurE les variables Electrocardiographiques et les pressions artErielles. Toutes les mesures ont EtE reprises 30 min aprEs le debut de chaque perfusion de propofol. l~.~ultats : Le propofol n'a pas eu d'effet direct sur les variables ~lectrophysiologiques ou Electrocardiographiques, r&ultat valable pour route vitesse de perfusion. Les frEquences cardiaques front pas change pendant les perfusions les plus rapides en pr&ence de baisses de pression artErielle. Conclusion: Le propofol n'a pas affect6 la conduction cardiaque en presence d'un blocage nerveux autonome. Par consequent, les effets directs du propofol sur le coeur front pas eu de r61e causal dans I'apparition des bradyarythmies qui lui Etaient associEes.

show abstract

“…This lack of compensation of the HR, the report of bradyarrhythmias 11 , suppression of tachyarrhythmias 5,6 , and conversion of other rhythms into a sinus node rhythm during the use of propofol indicate the possibility of the development of blockade of baroreceptors or depression of CCS caused by this drug 6,15 . Several reports on the development of bradycardia, blockade of CCS, and reversion of tachyarrhythmias into sinus rhythm after the use of propofol have been published in the literature 5,6,11-13 .…”

Section: Pharmacologymentioning

confidence: 97%