Effects of chronic angiotensin II receptor antagonist and angiotensin-converting enzyme inhibitor treatments on neurohormonal levels and haemodynamics during cardiopulmonary bypass †

Oh, Young Jun; Lee, J.H.; Nam, Seok Woo; Shim, Jæ Kwang; Song, Joon Ho; Kwak, Young Lan

doi:10.1093/bja/ael268

Cited by 34 publications

(22 citation statements)

References 28 publications

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“…Unfortunately, perioperative use of ACEI has been plagued with controversy, primarily because of historical reports linking it to protracted vasoplegia before, during, and after CPB. [21][22][23] Consequently, in the setting of surgery, its pattern of practice, both in the United States and internationally, is uncertain, and cessation of ACEI therapy may be as detrimental as statin and ␤-blocker withdrawal. 24,25 Therefore, the International Multicenter Study on Perioperative Ischemia (McSPI)-Epidemiology II (EPI-II) Research Group sought to prospectively characterize the pattern of perioperative ACEI use in patients having CABG surgery with CPB, to describe related hemodynamic effects, and to determine the association between the timing of ACEI renewal and in-hospital fatal and nonfatal vascular events.…”

mentioning

confidence: 99%

Patterns of Use of Perioperative Angiotensin-Converting Enzyme Inhibitors in Coronary Artery Bypass Graft Surgery With Cardiopulmonary Bypass

Drenger¹,

Fontes²,

Miao³

et al. 2012

Circulation

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mentioning

confidence: 99%

Patterns of Use of Perioperative Angiotensin-Converting Enzyme Inhibitors in Coronary Artery Bypass Graft Surgery With Cardiopulmonary Bypass

Drenger¹,

Fontes²,

Miao³

et al. 2012

Circulation

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“…In a recent case report, NE was shown to be effective when PE administration was not. 52 Nevertheless, therapy with arginine vasopressin is recommended in patients receiving angiotensin receptor blockade, 53 or where arginine vasopressin deficiency has been described as found in patients with septic shock, 54 liver failure, 55 or with vasodilatory shock after cardiac surgery 54 (Fig. 1).…”

Section: Comparison Of Norepinephrine and Phenylephrine To Manage Hypmentioning

confidence: 99%

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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“…Patients taking agents that antagonize this system are thus left without a key compensatory mechanism. Catecholamine resistance in patients taking ACE inhibitors and angiotensin II receptor blockers has been reported in the literature [8][9][10]. Eyraud et al [8] reported that 10 of 51 patients taking these agents had hypotension refractory to three doses of a catecholamine, and that these patients responded to the vasopressin agonist, terlipressin.…”

Section: Discussionmentioning

confidence: 99%

“…Eyraud et al [8] reported that 10 of 51 patients taking these agents had hypotension refractory to three doses of a catecholamine, and that these patients responded to the vasopressin agonist, terlipressin. In a cohort of adult patients undergoing cardiac surgery and cardiopulmonary bypass, Oh et al [9] reported that patients taking angiotensin II receptor blockers (candesartan, losartan, irbesartan, or valsartan) required higher doses of phenylepherine to maintain BP.…”

Section: Discussionmentioning

confidence: 99%

A case of refractory intraoperative hypotension treated with vasopressin infusion

Wheeler

Turchiano

Tobias

2008

Journal of Clinical Anesthesia

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Effects of chronic angiotensin II receptor antagonist and angiotensin-converting enzyme inhibitor treatments on neurohormonal levels and haemodynamics during cardiopulmonary bypass †

Abstract: Chronic ARA treatment resulted in more profound hypotension than ACEI treatment during CPB, and this may be associated with the blockade of angiotensin II receptors by ARA.

Cited by 34 publications

References 28 publications

Patterns of Use of Perioperative Angiotensin-Converting Enzyme Inhibitors in Coronary Artery Bypass Graft Surgery With Cardiopulmonary Bypass

Patterns of Use of Perioperative Angiotensin-Converting Enzyme Inhibitors in Coronary Artery Bypass Graft Surgery With Cardiopulmonary Bypass

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

A case of refractory intraoperative hypotension treated with vasopressin infusion

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