Haemodynamic effects of etomidate, propofol and electrical shock in patients undergoing implantable cardioverter-defibrillator testing

Background: Anaesthetic drugs and internal electrical shock may alter the haemodynamic status of patients undergoing implantable cardioverter-defibrillator (ICD) testing. Comparative data on the mechanisms of etomidate and propofol-induced changes in haemodynamic parameters are inconsistent. Also the effects of ICD shock on haemodynamics have not been extensively studied. Aim: To compare the haemodynamic effects of etomidate and propofol as well as electrical shock during ICD testing in a prospective, randomised trial. Methods: The study group consisted of 63 consecutive patients (mean age 66 ± 10 years, 51 males) who underwent ICD testing. Haemodynamic parameters were measured using impedance cardiography (Task Force Monitor Systems, CNSystems, Austria) before and after injection of etomidate (n = 30) or propofol (n = 33) as well as immediately after internal defibrillation of ventricular fibrillation (VF). Parameters measured included heart rate, systolic (sBP), diastolic (dBP) and mean (mBP) blood pressure, stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR). Results: Propofol significantly decreased the values of all measured parameters (sBP: 123.4 ± 17.1 vs. 106.3 ± 18 mm Hg, p < 0.0001; dBP: 83.7 ± 12.2 vs. 74.1 ± 13.8 mm Hg, p < 0.0001; mBP: 93.9 ± 13.1 vs. 81.1 ± 16.1 mm Hg, p < 0.0001; SV: 61.1 ± 19.3 vs. 56.4 ± 15.7 mL, p < 0.003; CO: 4.51 ± 1.07 vs. 4.17 ± 0.73 L/min, p < 0.003; and TPR: 1,735.8 ± 532.6 vs. 1,573.9 ± 390.5 dyn×s/cm 5 ), whereas the only significant change following etomidate infusion was a decrease in SV (60.6 ± 11 vs. 56.8 ± 10 mL, p < 0.022). The propofol-induced changes were similar in patients with reduced (< 40%) vs. preserved (≥ 40%) left ventricular ejection fraction (LVEF) and in patients in heart failure NYHA class 0–II vs. class III–IV. Induction of VF and internal electrical shock did not cause major haemodynamic changes apart from significant, albeit very modest, drops in dBP and mBP (77 ± 2 vs. 72.9 ± 18 mm Hg, p < 0.002, and 85.2 ± 17 vs. 81.8 ± 20 mm Hg, p < 0.017, respectively). There were no complications during ICD testing. Conclusions: Propofol significantly decreased BP probably by both reducing CO and causing vasodilatation, whereas etomidate only slightly decreased dBP and mBP without affecting other parameters. Propofol-induced changes were independent of LVEF or NYHA class. Induction of VF and internal defibrillation did not cause clinically significant changes apart from very modest drops in dBP and mBP values.