Predictors of hemodynamic compromise with propofol during defibrillator implantation: a single center experience
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Intra-operative hypotension has been reported in cardiac resynchronization therapy defibrillator (CRT-D) clinical trials but this phenomenon is not well characterized. The purpose of this study was to understand the frequency and determinants of intra-operative hypotension in patients undergoing defibrillator implantations.
We retrospectively reviewed clinical data of all CRT-D implantations over a 21-month period. We compared a randomly selected contemporaneous group undergoing implantable cardiac defibrillator (ICD) implantations as a reference group. Procedure protocol involved intra-arterial blood pressure monitoring throughout the case. Lidocaine (1%) was routinely used along with propofol for sedation in all patients. Procedure time was defined as the time from initial administration of lidocaine for arterial line access, to completion of defibrillator pocket closure. Cumulative dose of propofol was calculated in each patient. Hypotension was defined as a fall in the systolic blood pressure of ≥30% from baseline or a systolic blood pressure of ≤80 mm Hg for >3 min. CRT-D and ICD patients were divided into hypotensive and non-hypotensive subsets.
The incidence of hypotension in the CRT-D group (N = 100) was 56%, as compared to 40% in the ICD group (N = 97). The mean duration of procedure in the CRT-D group was 114 ± 95 min in the hypotensive subset versus 69 ± 31.9 min in the non-hypotensive subset (p = 0.0015). The mean NYHA class in the hypotensive subset of the CRT-D group was 2.85 ± 1.2 vs 2.2 ± 1.5 in the non-hypotensive subset (p = 0.0179). Cumulative dose of propofol in the hypotensive subset of the CRT-D group was 386 ± 22 mg, while that in the non hypotensive subset was 238.3 ± 17 mg (p < 0.0001). Creatinine clearance in the hypotensive subset of the CRT-D group was 63.8 ± 12.8 ml/min, while that in the non-hypotensive subset was 78.7 ± 23.5 ml/min (p = 0.003). Patients in the CRT-D group who developed hypotension had a lower left ventricular ejection fraction of 21.1 ± 10.2% versus 29 ± 14.8% in the non-hypotensive subset (p = 0.0035).
Hypotension is a common occurrence during defibrillator implantation under conscious sedation. Risk factors for significant hypotension include: higher NYHA class, lower left ventricular ejection fraction, lower creatinine clearance, higher doses of propofol and longer procedure times.
- León, A. R., Abraham, W. T., Curtis, A. B., Daubert, J. P., Fisher, W. G., Gurley, J., et al. (2005). Safety of transvenous cardiac resynchronization system implantation in patients with chronic Heart failure. Journal of the American College of Cardiology, 46, 2348–2356. CrossRef
- Abraham, W. T., Fisher, W. G., Smith, A. L., Delurgio, D. B., Leon, A. R., Loh, E., et al. (2002). for the MIRACLE study group. Cardiac resynchronization in chronic heart failure. The New England Journal of Medicine, 346, 1845–1853. CrossRef
- Young, J. B., Abraham, W. T., Smith, A. L., Leon, A. R., Lieberman, R., Wilkoff, B., et al. (2003). For the Multicenter InSync ICD randomized clinical evaluation (MIRACLE ICD) trial investigators. Combined cardiac resynchronization and implantable cardioversion defibrillation in advanced heart failure. The MIRACLE ICD trial. Journal of the American Medical Association, 289, 2685–2694. CrossRef
- León, A. R., Abraham, W. T., Brozena, S., Daubert, J. P., Fisher, W. G., Gurley, J. C., et al. (2005). Cardiac resynchronization with sequential biventricular pacing for the treatment of moderate-to-severe heart failure. Journal of the American College of Cardiology, 46, 2298–2304. CrossRef
- Lippmann, M., & Kakazu, C. (2006). Hemodynamics with propofol: is propofol dangerous in classes III-V patients? Anesthesia and Analgesia, 103(1), 260. CrossRef
- Punnam, S. R., Holliday, J., Janes, R., Touma, R., Li, H., Patel, M., et al. (2007). Hemodynamic collapse during left ventricular lead implantation. Pacing and Clinical Electrophysiology, 30(9), 1112–1115. CrossRef
- Lai, R. W., & Volosin, K. J. (2004). Asystole following left ventricular pacing. Pacing and Clinical Electrophysiology, 27, 815–817. CrossRef
- Zhou, W., Fontenot, H. J., Wang, S. N., & Kennedy, R. H. (1999). Propofol-induced alterations in myocardial [beta]-adreno receptor binding and responsiveness. Anesthesia and Analgesia, 89, 604–608. CrossRef
- Marik, P. E. (2004). Propofol: therapeutic indications and side effects. Current Pharmaceutical Design, 10(29), 3639–3649. CrossRef
- Gan, T. J. (2006). Pharmacokinetic and Pharmacodynamic characteristics of medications used for moderate sedation. Clinical Pharmacokinetics, 45(9), 855–869. CrossRef
- Jacobi, J., Fraser, G. L., Coursin, D. B., Riker, R. R., Fontaine, D., Wittbrodt, E. T., et al. (2002). Clinical Practice Guidelines for the Sustained Use of Sedatives and Analgesics in the Critically Ill Adult. Critical Care Medicine, 30(1), 119–141. CrossRef
- Gross, J. B., Bailey, P. L., Connis, R. T., Cotes, C. J., Davis, F. G., & Epstein, B. S. (2002). Practice Guidelines for Sedation and Analgesia by Non-Anesthesiologists. An Updated Report by the American Society of Anesthesiologist Task Force on Sedation and Analgesia by Non-anesthesiologists. Anesthesiology, 96, 1004. CrossRef
- Langley, M. S., & Heel, R. C. (1988). Propofol: A Review of its Pharmacodynamic and Pharmacokinetic Properties and Use as an Intravenous Anesthetic. Drugs, 35, 334. CrossRef
- Rau, R. H., Li, Y. C., Cheng, J. K., Chen, C. C., Ko, Y. P., & Huang, C. J. (2004). Predicting blood pressure change caused by rapid injection of propofol during anesthesia induction with a logistic regression model. Acta Anaesthesiol Taiwan, 42(2), 81–86.
- Ebert, T. J. (2005). Sympathetic and hemodynamic effects of moderate and deep sedation with propofol in humans. Anesthesiology, 103(1), 20–24. CrossRef
- Reich, D. L., Hossain, S., Krol, M., Baez, P., Patel, P., Bernstein, A., et al. (2005). Predictors of hypotension after induction of general anesthesia. Anesthesia and Analgesia, 101(3), 622–628. CrossRef
- Warden, J. C., & Pickford, D. R. (1995). Fatal cardiovascular collapse following propofol induction in high-risk patients and dilemmas in the selection of a short-acting induction agent. Anaesthesia and Intensive Care, 23(4), 485–487.
- Reich, D. L., Hossain, S., Krol, M., Baez, P., Patel, P., Bernstein, A., & Bodian, C. A. (2005). Predictors of hypotension after induction of general anesthesia. Anesthesia and Analgesia, 101(3), 622–628. CrossRef
- Wysowski, D. K., & Pollock, M. L. (2006). Reports of death with use of propofol (Diprivan) for nonprocedural sedation and literature review. Anesthesiology, 105(5), 1047–1051. CrossRef
- Brussel, T., Theissen, J. L., Vigfusson, G., Lunkenheimer, P. P., Van Aken, H., & Lawin, P. (1989). Hemodynamic and cardiodynamic effects of propofol and etomidate: Negative inotropic properties of propofol. Anesthesia and Analgesia, 69, 35–40.
- Schenkman, K. A., & Yan, S. (2000). Propofol impairment of mitochondrial respiration in isolated perfused guinea pig hearts determined by reflectance spectroscopy. Critical Care Medicine, 28, 172–177. CrossRef
- Favetta, P., Degoute, C. S., Perdrix, J. P., Drfresne, C., Boulieu, R., & Guitton, J. (2002). Propofol metabolites in man following propofol induction and maintenance. British Journal of Anaesthesia, 88(5), 653–658. CrossRef
- Predictors of hemodynamic compromise with propofol during defibrillator implantation: a single center experience
Journal of Interventional Cardiac Electrophysiology
Volume 25, Issue 2 , pp 145-151
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- 1. Thoracic and Cardiovascular Institute, Sparrow Health System, Michigan State University, 405 West Greenlawn, Suite 400, Lansing, MI, 48910, USA
- 2. Department of Epidemiology and Biostatistics, Michigan State University, Lansing, MI, USA