Letters To The Editor: Letters & Announcements
To the Editor:
Over the past 10 yr, a number of articles in this and other journals have identified hemodynamic problems during anesthesia in patients treated with angiotensin-converting enzyme (ACE) inhibitors (1–5) and angiotensin type 1 (AT1) receptor antagonists (6,7). The most recent article by Bertrand et al. (8) was well designed to study the differences in blood pressures during induction and early maintenance of anesthesia between patients who had their AT1 receptor antagonists withdrawn before surgery and those who did not. On the basis of their findings related to “severe hypotensive episodes,” the authors fall short of making an explicit recommendation but suggest that “Recommendations to discontinue these drugs on the day before surgery may be justified” (italics mine). Whose recommendations? The recommendations to which they refer in their opening paragraph relate to ACE inhibitors (1–3).
I do not question the authors’ conclusions based on their arterial blood pressure findings (8), although a glance at Figure 1 in their article will reveal that the differences between the two groups, although statistically significant at only three points, are relatively small. This article provides the reader with no data on heart rate, and therein lies the question. Analysis of their previous articles (6,7) reveals that the hypotensive episodes after induction of anesthesia were associated with marked bradycardia of greater severity in patients receiving angiotensin AT1 receptor antagonists (46 ± 5 bpm) than in those receiving β-adrenoceptor or calcium antagonists or ACE inhibitors (7). Such decreases in heart rate may contribute substantially to the degree of arterial hypotension specified in this article. The experimental program for this study required the administration of ephedrine to all patients. Ephedrine exerts a direct β1/β2 adrenoceptor agonist effect that would have increased heart rate in their angiotensin receptor antagonist group but to a much less extent in patients receiving β-adrenoceptor antagonists.
Induction of anesthesia in these patients commenced with a substantial dose of sufentanil (0.4 to 0.5 μg/kg) followed by propofol (1.5 mg/kg). Both these drugs exert central vagotonicity (9,10) and their effects are probably additive (11). It would therefore be more appropriate, especially in an elderly group of patients (mean age between 68 and 71 yr in these studies) to use a prophylactic dose of glycopyrrolate to prevent the bradycardia and ameliorate the arterial hypotension (12).
Before I retired from clinical practice, I anesthetized over many years a number of patients receiving ACE inhibitors, and three patients treated with an AT1 receptor antagonist (Losartan), for the treatment of hypertension and/or congestive cardiac failure. In every case I gave IV glycopyrrolate (x mg) 2 min before induction of anesthesia with fentanyl 5 mg/kg and propofol 0.75–1.0 mg/kg. In no patient did I observe a serious degree of hypotension (SBP <100 mm Hg) or profound bradycardia (HR <60 bpm).
Because these authors have only used one anesthetic induction technique that is highly vagotonic, we cannot judge whether other techniques might produce lesser degrees of hypotension inpatients treated with ACE inhibitors or AT1 receptor antagonists. Before Bertrand and her colleagues recommend withdrawal of these antihypertensive drugs before induction of anesthesia, I would respectfully suggest that they perform a study to test the hypothesis that I have proposed—that prophylactic glycopyrrolate would minimize both bradycardia and arterial hypotension to such an extent that it would not be necessary to withdraw these drugs before anesthesia and surgery.
1. Mirenda JV, Grissom TE. Anesthetic implications of the renin-angiotensin system and angiotensin-converting enzyme inhibitors. Anesth Analg 1991; 72: 667–83.
2. Colson P, Saussine M, Seguin JR, et al. Hemodynamic effects of anesthesia in patients chronically treated with angiotensin-converting enzyme inhibitors. Anesth Analg 1992; 74: 805–8.
3. Coriat P, Richer C, Douraki T, et al. Influence of chronic angiotensin-converting enzyme inhibition on anesthetic induction. Anesthesiology 1994; 81: 299–307.
4. Ryckwaert F, Colson P. Hemodynamic effects of anesthesia in patients with ischemic heart failure chronically treated with angiotensin-converting inhibitors. Anesth Analg 1997; 84: 945–9.
5. Eyraud D, Mouren S, Teugels K, et al. Treating anesthesia-induced hypotension by angiotensin II in patients chronically treated with angiotensin-converting enzyme inhibitors. Anesth Analg 1998; 86: 259–63.
6. Eyraud D, Brabant S, Nathalie D, et al. Treatment of intraoperative refractory hypotension with terlipressin in patients chronically treated with an antagonist of the renin-angiotensin system. Anesth Analg 1999; 88: 980–4.
7. Brabant SM, Bertrand M, Eyraud D, et al. The hemodynamic effects of anesthetic induction in vascular surgical patients chronically treated with angiotensin II receptor antagonists. Anesth Analg 1999; 88: 1388–92.
8. Bertrand M, Godet G, Meersschaert K, et al. Should angiotensin II antagonists be discontinued before surgery? Anesth Analg 2001; 92: 26–30.
9. Cullen PM, Turtle M, Prys-Roberts C, et al. Effect of propofol anesthesia on baroreflex activity in humans. Anesth Analg 1987; 66: 115–20.
10. Reitan JA, Stengert KB, Wymore ML, Martucci RW. Central vagal control of fentanyl-induced bradycardia during halothane anesthesia. Anesth Analg 1978; 57: 31–6.
11. Vuyk J, Mertens MJ, Olofsen E, et al. Propofol anesthesia and rational opioid selection: determination of optimal EC50
propofol-opioid concentrations that assure adequate anesthesia and a rapid return of consciousness. Anesthesiology 1997; 87: 1549–62.
12. Skues M, Richards MJ, Jarvis AP, Prys-Roberts C. Preinduction atropine or glycopyrrolate hemodynamic changes associated with induction and maintenance of anesthesia with propofol and alfentanil. Anesth Analg 1989; 69: 386–90.