In the field of anesthesiology, there is wide debate on discontinuing angiotensin-converting enzyme inhibitor (ACEI) and angiotensin receptor blocker (ARB) therapy the day of noncardiac surgery. Although there have been many studies attributing perioperative hypotension to same-day ACEI and ARB use, there are many additional variables that play a role in perioperative hypotension. Additionally, restoring blood pressure in these patients presents a unique challenge to anesthesiologists. A case report is presented in which a patient took her ACEI the day of surgery and developed refractory hypotension during surgery. The evidence of ACEI use on the day of surgery and development of hypotension is reviewed, and additional variables that contributed to this hypotensive episode are discussed. Lastly, current challenges in restoring blood pressure are presented, and a basic model on treatment approaches for refractory hypotension in the setting of perioperative ACEI use is proposed. 1. Introduction Approximately 65 million Americans actively receive antihypertensive agents for elevated blood pressure [1]. During surgery, beta-adrenergic blockers and alpha 2 agonists are routinely continued perioperatively because of their role in protecting the myocardium [2–5]. Additionally, calcium channel blockers are used in the perioperative period because of their reduction in myocardial ischemia, infarction, arrhythmias, and overall mortality [6, 7]. Since angiotensin-converting enzyme inhibitor (ACEI) attenuates the adrenergic response to stressful stimuli in cardiac, vascular, and cerebrovascular patients, ACEI is strongly recommended prior to and during these specific surgeries [8–11]. However, the use of ACEI and angiotensin receptor blocker (ARB) therapy in the preoperative period in noncardiac patients has been controversial because of its potential role in causing hemodynamic instability. Patients on chronic ACEI or ARB therapy have a dampened sympathetic response [8]. Additionally, surgical patients can be volume depleted because of preoperative fasting, and this condition can cause additional stress during surgery. These combining factors result in reduced vascular capacitance and venous return, leading to decreased cardiac output and subsequent hypotension. To compensate for this hypotension, angiotensin II (ANG2) plays an important role in maintaining blood pressure through vasoconstriction. This vasoconstriction shunts blood away from the kidneys, bowels, and spleen [12, 13]. ANG2’s short-term effect is to maintain blood pressure through vasoconstriction
References
[1]
J. D. Wright, J. P. Hughes, Y. Ostchega, S. S. Yoon, and T. Nwankwo, “Mean systolic and diastolic blood pressure in adults aged 18 and over in the United States, 2001–2008,” National Health Statistics Reports, no. 35, pp. 1–22, 2011.
[2]
D. T. Mangano, E. L. Layug, A. Wallace, and I. Tateo, “Effect of atenolol on mortality and cardiovascular morbidity after noncardiac surgery. Multicenter Study of Perioperative Ischemia Research Group,” New England Journal of Medicine, vol. 335, no. 23, pp. 1713–1720, 1996.
[3]
A. Wallace and D. T. Mangano, “Use of β-blockade to prevent death after noncardiac surgery,” Western Journal of Medicine, vol. 166, no. 3, pp. 203–204, 1997.
[4]
A. Wallace, B. Layug, I. Tateo et al., “Prophylactic atenolol reduces postoperative myocardial ischemia. McSPI Research Group,” Anesthesiology, vol. 88, no. 1, pp. 2–17, 1998.
[5]
R. D. Stevens, H. Burri, and M. R. Tramer, “Pharmacologic myocardial protection in patients undergoing noncardiac surgery: a quan-titative systematic review,” Anesthesia & Analgesia, vol. 97, no. 3, pp. 623–633, 2003.
[6]
D. N. Wijeysundera and W. S. Beattie, “Calcium channel blockers for reducing cardiac morbidity after noncardiac surgery: a meta-analysis,” Anesthesia & Analgesia, vol. 97, no. 3, pp. 634–641, 2003.
[7]
J. Butterworth and C. D. Furberg, “Improving cardiac outcomes after noncardiac surgery,” Anesthesia & Analgesia, vol. 97, no. 3, pp. 613–615, 2003.
[8]
M. Licker, P. Neidhart, S. Lustenberger et al., “Long-term angiotensin-converting enzyme inhibitor treatment attenuates adrenergic responsiveness without altering hemodynamic control in patients undergoing cardiac surgery,” Anesthesiology, vol. 84, no. 4, pp. 789–800, 1996.
[9]
M. Licker, M. Bednarkiewicz, P. Neidhart et al., “Preoperative inhibition of angiotensin-converting enzyme improves systemic and renal haemodynamic changes during aortic abdominal surgery,” British Journal of Anaesthesia, vol. 76, no. 5, pp. 632–639, 1996.
[10]
H. Tohmo, M. Karanko, M. Scheinin, O. Viinamaki, M. Salonen, and V. Nieminen, “Enalapril premedication attenuates the blood pressure response to tracheal intubation and stabilizes postoperative blood pressure after controlled hypotension with sodium nitroprusside in neurovascular patients,” Journal of Neurosurgical Anesthesiology, vol. 5, no. 1, pp. 13–21, 1993.
[11]
F. Ryckwaert and P. Colson, “Hemodynamic effects of anesthesia in patients with ischemic heart failure chronically treated with angiotensin-converting enzyme inhibitors,” Anesthesia & Analgesia, vol. 84, no. 5, pp. 945–949, 1997.
[12]
R. Behnia, A. Molteni, and R. Igi？, “Angiotensin-converting enzyme inhibitors: mechanisms of action and implications in anesthesia practice,” Current Pharmaceutical Design, vol. 9, no. 9, pp. 763–776, 2003.
[13]
J. A. Herd, “Cardiovascular response to stress,” Physiological Reviews, vol. 71, no. 1, pp. 305–330, 1991.
[14]
E. D. Miller, D. E. Longnecker, and M. J. Peach, “The regulatory function of the renin-angiotensin system during general anesthesia,” Anesthesiology, vol. 48, no. 6, pp. 399–403, 1978.
[15]
P. Coriat, C. Richer, T. Douraki et al., “Influence of chronic angiotensin-converting enzyme inhibition on anesthetic induction,” Anesthesiology, vol. 81, no. 2, pp. 299–307, 1994.
[16]
T. Comfere, J. Sprung, M. M. Kumar et al., “Angiotensin system inhibitors in a general surgical population,” Anesthesia & Analgesia, vol. 100, no. 3, pp. 636–644, 2005.
[17]
D. J. Rosenman, F. S. McDonald, J. O. Ebbert, P. J. Erwin, M. LaBella, and V. M. Montori, “Clinical consequences of withholding versus administering renin-angiotensin-aldosterone system antagonists in the preoperative period,” Journal of Hospital Medicine, vol. 3, no. 4, pp. 319–325, 2008.
[18]
V. V. Da Costa, A. C. Caldas, L. G. Nunes, P. S. Beraldo, and R. A. Saraiva, “Influence of angiotensin-converting enzyme inhibitors on hypotension after anesthetic induction: is the preoperative discontinuation of this drug necessary?” Revista Brasileira de Anestesiologia, vol. 59, no. 6, pp. 704–715, 2009.
[19]
S. Kheterpal, O. Khodaparast, A. Shanks, M. O'Reilly, and K. K. Tremper, “Chronic angiotensin-converting enzyme inhibitor or angiotensin receptor blocker therapy combined with diuretic therapy is associated with increased episodes of hypotension in noncardiac surgery,” Journal of Cardiothoracic and Vascular Anesthesia, vol. 22, no. 2, pp. 180–186, 2008.
[20]
T. J. Ebert, D. D. Kanitz, and J. P. Kampine, “Inhibition of sympathetic neural outflow during thiopental anesthesia in humans,” Anesthesia & Analgesia, vol. 71, no. 4, pp. 319–326, 1990.
[21]
M. Weisenberg, D. I. Sessler, M. Tavdi et al., “Dose-dependent hemodynamic effects of propofol induction following brotizolam premedication in hypertensive patients taking angiotensin-converting enzyme inhibitors,” Journal of Clinical Anesthesia, vol. 22, no. 3, pp. 190–195, 2010.
[22]
A. D. Wheeler, J. Turchiano, and J. D. Tobias, “A case of refractory intraoperative hypotension treated with vasopressin infusion,” Journal of Clinical Anesthesia, vol. 20, no. 2, pp. 139–142, 2008.
[23]
D. Godínez-Hernández, I. A. Gallardo-Ortíz, P. López-Sánchez, and R. Villalobos-Molina, “Captopril therapy decreases both expression and function of alpha-adrenoceptors in pre-hypertensive rat aorta,” Autonomic and Autacoid Pharmacology, vol. 26, no. 1, pp. 21–29, 2006.
[24]
B. Mets, “Management of hypotension associated with Angiotensin-axis blockade and general anesthesia administration,” Journal of Cardiothoracic and Vascular Anesthesia, vol. 27, no. 1, pp. 156–167, 2013.
