Echocardiographic assessment of the haemodynamic effects of propofol: a comparison with etomidate and thiopentone

Abstract

SummaryThe haemodynamic eflects of propofol (2 mglkg), etomidate (0.2 mglkg) and thiopentone ( 4 mglkg) were studied in 30 ASA 1 and 2 patients in whom anaesthesia had been induced with midazolam 0.1 mglkg, fentanyl5 pglkg, vecuronium 0.1 mglkg and atropine 10 pglkg, and maintained with nitrous oxide in oxygen. Arterial pressure was measured directly and left ventricular diameters were determined by transoesophageal echocardiography. Systolic blood pressure after propofol and thiopentone and the end-systolic quotient (systolic pressurelend-systolic diameter), a measure of inotropy, decreased. Fractional shortening ( end-diastolic -end-systolic diameterlend-diastolic diameter) decreased only in the thiopentone group, Diastolic blood pressure and end-diastolic diameter ( a measure of preload) did not change in any of the groups, and the etomidate group showed no changes in the haemodynamic variables measured. Propofol shows simultaneous negative inotropy and afterload reduction, while thiopentone is exclusively negatively inotropic. Key wordsAnaesthetics, intravenous; propofol, thiopentone, etomidate. Measurement techniques; transoesophageal echocardiography, electroencephalography.Many studies have reported a reduction in arterial blood pressure after injection of the intravenous anaesthetic agent propofol. Reductions in blood pressure were more marked, and hypotensive reactions more frequent after propofol in comparison with etomidate' and thio~entone?~ but there is still no consensus in the literature why these reductions occur, be they negative inotropy, afterload reduction or both.Almost all the patient studies to date, which were based on load-dependent variables, have differentiated poorly between the inotropic effects of propofol and its influence on myocardial loading factors.The aim of our study was to demonstrate whether the decrease in arterial blood pressure after propofol is from negative inotropy and (or) changes in myocardial loading (prelafterload), using a method considered to be relatively insensitive to load factors: namely inotropy measurements by transoesophageal echocardiography (TEE). In addition, we compared the haemodynamic effects of propofol with those of thiopentone and etomidate. MethodsThirty normotensive surgical or orthopaedic patients in ASA groups 1 and 2 were placed at random into either a propofol (n = lo), thiopentone (n = 10) or etomidate (n = 10) group. None of the patients was receiving any concomitant cardiovascular medication, and all gave written informed consent to the study; the study itself was approved by the Ethics committee of the University of Ulm.Each patient received orally 20 mg clorazepam as premedication one hour before the study. We injected atropine 10 pg/kg intravenously 5 minutes before induction, which was with midazolam 0.1 mg/kg and fentanyl 5 pg/kg. Vecuronium 0.1 mg/kg was given to facilitate tracheal intubation. Anaesthesia was continued after tracheal intubation, with controlled ventilation with N,O:O, (no, = 0.3) to normocapnia (PE'co, = 4.6-6.0 k...

Variation in rapid sequence induction techniques: current practice in Wales

“…Anaesthetists viewed bowel obstruction as an indication for etomidate, with few choosing propofol. Etomidate offers the advantage of haemodynamic stability [13] but even a single dose has been shown to cause adrenocortical suppression [14][15][16] with an unknown affect on mortality [17,18]. Our interpretation of these results is that anaesthetists regard propofol as an acceptable induction agent in patients with reasonable cardiovascular reserve, but are less likely to use it for potentially unstable patients.…”

Prevention of hypotension during induction of anesthesia with propofol and fentanyl: Comparison of preloading with crystalloid and intravenous ephedrine.

“…The cause of this hypotension has been found to be a reduced systemic vascular resistance and a depression of myocardial contractility [13] . Fentanyl was used to supplement induction of anesthesia with propofol.…”

Electrophysiological Effects of Propofol on the Normal Cardiac Conduction System

“…Using standard techniques [14], the electrophysiological parameters were deter mined at baseline (isoflurane-ketaminc anesthesia) and after two dif ferent doses of propofol (1 mg/kg bolus followed by a continuous infusion of 0.1 mg/kg/min and an extra 1-mg/kg bolus followed by an infusion of 0.2 mg/kg/min, given immediately after completion of the study on low-dose propofol). For purposes of clarity, the propofol doses are labeled low and high; however, these dosages reflect com monly used concentrations in clinical practice [1][2][3] …”

“…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.…”