Management of Hypotension Associated With Angiotensin-Axis Blockade and General Anesthesia Administration

Mets, Berend

doi:10.1053/j.jvca.2012.06.014

Cited by 31 publications

(22 citation statements)

References 109 publications

(85 reference statements)

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“…Patients presenting for surgery with angiotensin axis blockade (AAB) from therapy with either angiotensin‐converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) experience an increased incidence of perioperative hypotension . Debate continues as to whether this hypotension results in any significant clinical sequelae.…”

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“…Patients presenting for surgery with angiotensin axis blockade (AAB) from therapy with either angiotensinconverting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) experience an increased incidence of perioperative hypotension. [1][2][3][4] Debate continues as to whether this hypotension results in any significant clinical sequelae. Some authors found that the use of an ACEI decreased the incidence of acute kidney injury (AKI), 5 mortality, and septicemia in cardiac and vascular surgical patients.…”

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Angiotensin axis blockade, hypotension, and acute kidney injury in elective major orthopedic surgery

Nielson

Hennrikus

Lehman

et al. 2014

Journal of Hospital Medicine

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BACKGROUND:Patients presenting for surgery with angiotensin axis blockade (AAB) from therapy with either angiotensin-converting enzyme inhibitors or angiotensin receptor blockers experience an increased incidence of perioperative hypotension. Acute kidney injury (AKI) in patients receiving preoperative AAB has been demonstrated after lung, vascular, and cardiac surgery. However, there is little literature evaluating the hypotensive and renal effects of preoperative AAB and major orthopedic surgery.

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Angiotensin axis blockade, hypotension, and acute kidney injury in elective major orthopedic surgery

Nielson

Hennrikus

Lehman

et al. 2014

Journal of Hospital Medicine

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“…2,3 Yet, the associated hypotension is commonly treated with phenylephrine (PE), a synthetic vasoconstrictor. 4,5 Theoretically, NE might better combat this general anesthesia-induced hypotension by restoring decreased circulating concentrations of this catecholamine and maintaining cardiac output (CO). However, NE is rarely used in these circumstances.…”

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Should Norepinephrine, Rather than Phenylephrine, Be Considered the Primary Vasopressor in Anesthetic Practice?

Mets

2016

Anesthesia &Amp; Analgesia

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T he induction of general anesthesia is associated with sympatholysis 1 and a decrease in circulating norepinephrine (NE) and epinephrine (E) concentrations. 2,3 Yet, the associated hypotension is commonly treated with phenylephrine (PE), a synthetic vasoconstrictor. 4,5 Theoretically, NE might better combat this general anesthesia-induced hypotension by restoring decreased circulating concentrations of this catecholamine and maintaining cardiac output (CO). However, NE is rarely used in these circumstances. In this article, I will propose that patients might be better served by using NE rather than PE as the primary vasopressor to combat hypotension during general anesthesia. PHARMACOLOGYThe pharmacology of PE and NE is well known and is summarized in Table 1. 6-8 PE is now readily accepted as a first-line agent to combat hypotension from both general and spinal anesthesia. 4,9 In contrast, NE has been viewed with some trepidation. This is reflected in the moniker, "leav-em-dead" when referring to its common trade name, Levophed. 10 Thus, NE use has been largely confined to "sicker patients" and restricted to cardiac anesthesia and the management of sepsis. 11,12 PE, because of α 1 selectivity, has purely vasoconstrictor effects on vascular beds. 6,13 Arteriolar vasoconstriction results in an increase in arterial blood pressure, which in turn results in a baroreceptor-triggered, vagally mediated, decrease in heart rate and CO. In venous capacitance vessels, such vasoconstriction may increase vascular return and so potentially improve CO. However, this effect on CO may be impaired with PE because of an increase in venous resistance, limiting venous return to the heart. 13,14 An increase in venous resistance is not found with NE, which has both α 1 and β 1 effects as well as some β 2 effects, 7 resulting in a β-induced venous vascular relaxing effect on venous resistance. Hence, NE better enhances venous return to the heart and so CO. 14,15 The β 1 effects also result in a positive inotropic effect on the myocardium with little to no chronotropic effect when compared with E. 6 Thus, NE increases arterial blood pressure through arteriolar vasoconstriction and an increase (or maintenance) of heart rate, stroke volume, and CO. [16][17][18][19] NE is the neurotransmitter of the sympathetic nervous system. 20 Plasma levels are reported as being 264 ± 162 pg/mL (mean ± SD; n = 27) before induction of anesthesia with thiopental and 127 ± 78 pg/mL afterward, during isoflurane and sufentanil anesthesia. 2 Only 2% of circulating NE is attributed to release from the adrenal medulla. 20,21 Plasma NE concentrations are dependent on the net amount of "spillover" from sympathetic nerve terminals and NE clearance by organ tissue. 20 The net NE spillover into surrounding venous beds is a function of immediate neuronal reuptake. Spillover may be increased by disease (hypothyroidism, depression, renal failure) and drugs (chlorthalidone) or decreased by them (hyperthyroidism, clonidine, desipramine, and PE). 20 Plasma clearance by th...

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“… Figure 2 explains the physiology behind the treatment model for refractory hypotension. The most recent suggested treatment protocol for hypotension in patients on chronic ACEI or ARB therapy is shown in Figure 3 [24]. Thus, there are multiple factors that contribute to the development of refractory hypotension in this patient including age, use of ACEI on the day of surgery, chronic use of ACEI and diuretic therapy as antihypertensives, and the dose of propofol administered at the time of induction.…”

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Multifactorial Model and Treatment Approaches of Refractory Hypotension in a Patient Who Took an ACE Inhibitor the Day of Surgery

Srivastava

Sacher

Nelson

et al. 2013

Case Reports in Anesthesiology

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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.

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Management of Hypotension Associated With Angiotensin-Axis Blockade and General Anesthesia Administration

Cited by 31 publications

References 109 publications

Angiotensin axis blockade, hypotension, and acute kidney injury in elective major orthopedic surgery

Angiotensin axis blockade, hypotension, and acute kidney injury in elective major orthopedic surgery

Should Norepinephrine, Rather than Phenylephrine, Be Considered the Primary Vasopressor in Anesthetic Practice?

Multifactorial Model and Treatment Approaches of Refractory Hypotension in a Patient Who Took an ACE Inhibitor the Day of Surgery

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