Anesthesia & Analgesia Volume Issue 2001 [Doi 10.1097%2F00000539-200101000-00006] Bertrand, Mich__le; Godet, Gilles; Meersschaert, Karolin; Brun, -- Should the Angiotensin II Antagonists Be Discontinu

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Angiotensin II Antagonists be Discontinued Before Surgery
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   Should the Angiotensin II Antagonists be DiscontinuedBefore Surgery? Michèle Bertrand,  MD , Gilles Godet,  MD , Karolin Meersschaert,  MD , Luc Brun,  MD ,Eduardo Salcedo,  MD , and Pierre Coriat,  MDDepartment of Anesthesiology, Pitié-Salpêtrière Hospital, Paris, FranceAngiotensinIIantagonists(AIIA)arepartofanewratio-nal treatment of hypertension. Because adverse circula-toryeffectsduringanesthesiacanoccurinpatientschron-ically treated with angiotensin-converting enzymeinhibitors, some clinicians discontinue them at least 24 h before operation. No data are available concerning AIIAadministrationinpatientsscheduledforvascularsurgeryperformedundergeneralanesthesia.Theaimofthispro-spectiverandomizedstudywastocomparehemodynam-ics during induction of anesthesia in patients chronicallytreatedwithAIIAandthoseofpatientsnotreceivingthisdrug on the morning before operation. Thirty-seven pa-tients chronically treated with AIIA for hypertensionwere randomly assigned to two groups: Group I: AIIAdiscontinuedonthedaybeforesurgery( n  18);GroupII:AIIA given 1 h before anesthesia ( n    19). Patients re-ceived sufentanil 0.4   g/kg, propofol 1.5 mg/kg, andatracurium 0.5 mg/kg. During the procedure, the anes-thesiologistwasrequiredtomaintainsystolicbloodpres-sure and heart rate within 30% of baseline values usingintravascular fluid administration and vasoconstric-tors (e.g., ephedrine, phenylephrine, or terlipressin).Hemodynamic variables were recorded each 1 min. He-modynamicstudyendedatincision.Thenumberanddu-ration of hemodynamic events were collected, and totaldosesofvasoactivedrugswerenotedineachgroup.Sys-tolic arterial pressure was significantly decreased inGroupIIat5,15and23minafterinductionofanesthesia(* P  0.05). In this group, the decrease in systolic arterialpressure was associated with more frequent episodes of hypotension(AIIAwithdrawn:1  1;AIIAgiven:2  1; P  0.01), with a larger number of patients developing atleast1episodeofhypotension(AIIAwithdrawn:12;AIIAgiven:19; P  0.01),andalongerdurationofanepisodeof hypotension(AIIAwithdrawn:3  4min;AIIAgiven:8  7 min;  P  0.01), and an increased need for vasoactivedrugs. In conclusion, blockade of the renin-angiotensinsystemincreasesthepotentialhypotensiveeffectofanes-theticinduction.Aseverehypotensiveepisode,requiringvasoconstrictor treatment, occurs after induction of gen-eral anesthesia in patients chronically treated with AIIA.RecommendationstodiscontinueAIIAdrugsontheday beforethesurgerymaybejustified.(AnesthAnalg2001;92:26–30)  A  ngiotensin II antagonists (AIIA) are part of a newrational treatment of hypertension (HT) (1). AIIAinterfere with the renin-angiotensin system byinhibiting angiotensin II from binding to its receptor,resulting in increased angiotensin II and normal bra-dykinin plasma levels. Adverse circulatory effectsduring anesthesia are well known in patients chroni-cally treated with angiotensin-converting enzyme in-hibitors (ACEI), leading to the recommendation todiscontinue them at least 24 hrs before anesthesia andsurgery (2–4). Similarly, a case of refractory hypoten-sion was reported after induction of anesthesia in apatient chronically treated with AIIA (5). Brabant et al.(6) found a more frequent incidence of hypotensionduring induction of anesthesia in patients chronicallytreated with AIIA, in comparison with matched pa-tients receiving   -adrenergic blocking drugs, calcium-channel blockers, or ACEI. In these studies, in contrastwith other drugs, ACEI were discontinued by theanesthesiologist on the day before the operation.Moreover, an important result of this study was toclarify that the hypotension observed in the patientstreated with AIIA was less responsive to conventionalvasopressors such as ephedrine or phenylephrine.There are no data concerning AIIA administrationin patients scheduled for vascular surgery performedunder general anesthesia. The aim of this prospectiverandomized study was to compare hemodynamicsduring induction of anesthesia in patients chronicallytreated with AIIA versus those of patients not receiv-ing this drug on the morning before operation. Ourhypothesis is that the incidence and the severity of hypotension during induction of anesthesia are less Accepted for publication September 26, 2000.Correspondence and reprint requests should be addressed toGilles Godet, MD, Département d’Anesthésie-Réanimation, HôpitalPitié-Salpêtrière, 47-83 Bd de l’Hôpital, 75013, Paris. ©2001 by the International Anesthesia Research Society 26  Anesth Analg 2001;92:26–30 0003-2999/01  when AIIA are discontinued on the day before theanesthesia. Methods Patients chronically treated with AIIA for HT duringthe previous 3 months and scheduled for elective ma- jor vascular surgery were included. Thirty-seven pa-tients were enrolled in this prospective randomizedstudy and gave informed consent after approval of thestudy by the Ethic Committee for Human Research of our Institution. Patients were randomly assigned toone of the study groups by a computer-generated listcompiled before the start of the study.Patients were randomized in 2 groups as follows:Group I, AIIA discontinued on the day before surgery( n    18); and Group II, AIIA given 1 h before anes-thesia ( n  19).Exclusion criteria were the following: severe heartfailure (stages III-IV of the New York Heart Associa-tion), severe renal insufficiency (creatinine plasmalevel more than 200   mol/L), and patients chronicallytreated with ACEI.In all patients, premedication consisted of PO mi-dazolam 5 mg. Patients received their cardiovascularmedication on the morning before the operation. Aradial catheter was inserted before induction and pa-tients were monitored with continuous ST-T analysis(Marquette, Milwaukee).After a 10 mL/kg crystalloid infusion and breathinga 100% oxygen, patients received sufentanil 0.4  g/kg,propofol 1.5 mg/kg, and atracurium 0.5 mg/kg IV.Mechanical ventilation was performed using a mix-ture of 50% N 2 O in oxygen. Maintenance of anesthesiaconsisted of isoflurane administration. Boluses of sufentanil were administered intraoperatively asneeded.Hemodynamic variables were recorded each 1 min,from 10 min before the induction of anesthesia, andduring at least the next 30 min. Hemodynamic studyended at incision.During the procedure, systolic blood pressure andheart rate were maintained within 30% of baselinevalues (defined as the average of three repeated mea-sures on the day before surgery), using IV fluid ad-ministration and vasoconstrictors (e.g., ephedrine,phenylephrine, or terlipressin).Hemodynamic events were defined as follows: ã  Hypotension: systolic blood pressure value lessthan 80 mm Hg lasting more than 1 min, ã  Hypertension: systolic blood pressure value morethan 160 mm Hg lasting more than 1 min, Table 1.  Clinical Characteristics of the PatientsGroup I(AIIA withdrawn)Group II(AIIA given)  P  ValueSex ratio (male/female) 15/3 15/4 NSAge (yr) (mean  sd ) 68  11 68  13 NSHypertension 18 19 NSCoronary diseaseAngina 1 1 NSHistory of myocardial infarction 5 1 NSPrevious coronary revascularization 3 1 NSCongestive heart failure 1 0 NSChronic pulmonary disease 6 7 NSChronic renal disease a 4 3 NSDiabetes mellitus 6 4 NSASA physical statusII 12 16 NSIII 6 3 NSCardiovascular treatmentCalcium blockers 12 3   0.01Nitrates 7 1   0.02Diuretics 4 4 NS  -blockers 7 2 NSCEI 0 0 NSOther vasoactive 0 0 NSPreoperative arterial pressure (mm Hg) (mean  sd )Systolic 145  12 145  22 NSDiastolic 78  11 77  13 NSMean 101  9 100  13 NS AIIA  angiotensin II antagonists; NS  not significant; CEI  converting enzyme inhibitors. a Creatinine plasma level between 120 and 200   mol/L.ANESTH ANALG CARDIOVASCULAR ANESTHESIA BERTRAND ET AL.  27 2001;92:26–30 ANGIOTENSIN II ANTAGONISTS AND ANESTHETIC INDUCTION  ã  Tachycardia: heart rate (HR) value more than90 bpm lasting more than 1 min, ã  Bradycardia: HR value less than 40 bpm lastingmore than 1 min. ã  Refractory hypotension: SBP that did not remainmore than 100 mm Hg after the administration of either 6 mg of ephedrine until 24 mg (if HR lessthan 60 bpm) and/or 100   g of phenylephrineuntil 300   g (if HR more than 60 bpm). Previ-ously, treatment of refractory hypotension wasangiotensin that is no longer commercially avail-able (7,8). As previously described (9), terlipres-sin, an agonist of the vasopressin system, is effec-tive in rapidly restoring arterial blood pressure inpatients chronically treated with ACEI or AIIAwho presented with refractory hypotension afterthe induction of anesthesia, without a detrimentaleffect in left ventricular function. A bolus of 1 mgof terlipressin is repeated once or twice asnecessary.The number and duration of hemodynamic eventswere collected, and total doses of vasoactive drugswere noted in each group.After surgery, patients were transferred to our re-covery room. Treatments for HT were orally contin-ued in the postoperative period. Hemodynamic eventssuch as HT (more than 130% of control value) weretreated with a bolus of nicardipine 1 mg or titratedesmolol when associated with increased HR (morethan 85 bpm) or clonidine. Postoperative myocardialischemia, defined as a ST depression  1 mm at 60 msafter the J point, was treated with diltiazem, or nitratesin case of poor left ventricular function. Postoperativeanalgesia included paracetamol administration andmorphine administered by patient-controlled analge-sia. Postoperative period ended at discharge. Postop-erative cardiac complications were defined as follows:congestive heart failure, pulmonary edema, cardiacdeath, supraventricular arrhythmia, ventricular ar-rhythmia, new Q-wave or ST-T depression longer than48 h on twice-daily 12-lead electrocardiogram, associ-ated or not with clinical findings such as circulatoryfailure with the need for catecholamines, or a decreasein global or regional function on echography, or anincrease of cardiac troponin I (cTnI). cTnI was meas-ured at recovery and on the first, second, and thirdpostoperative days, using an immunoenzymofluoro-metric assay on a Stratus autoanalyzer™ (Dade-Behring, Deerfield, IL). Normal values are 0–0.5ng/mL.Statistical analysis was performed by using NCSS6.0™ software (Statistical Solutions, Cork, Ireland). He-modynamic variables were analyzed using analysis of variance and paired- t -test; clinical characteristics of thepatients, hemodynamic events, and use of vasoactivedrugs were analyzed using paired- t  or K2 tests whenappropriate, and normality of the variables werechecked by using the Kolmogorov-Smirnov test. Results The two groups were comparable in age, sex ratio, andmain preoperative characteristics (Table 1). There wasan increased incidence of treatment with calciumchannel blockers and nitrates in the group in whichAIIA were withdrawn. Arterial blood pressure wasidentical between both groups before the start of thestudy. Type of surgery and doses of anesthetics usedduring the induction of anesthesia were identical be-tween both groups (Tables 2,3).Systolic arterial pressure was significantly less inGroup II at 5, 15, and 23 min after the induction (Fig.1) (* P    0.05). In this group, the decrease in systolicarterial pressure was associated with more frequentepisodes of hypotension (AIIA withdrawn: 1    1;AIIA given: 2    1;  P    0.01), in more patients (AIIA Figure 1.  * P  0.05 Table 2.  Surgical Characteristics Group I(AIIA withdrawn)Group II(AIIA given)Type of surgeryCarotid endarterectomy 9 10Abdominal aortic repair 6 7Infrainguinal revascularization 3 2 P  not significant. Table 3.  Induction Characteristics Group I(AIIA withdrawn)Group II(AIIA given)Dose of propofol (mg) 110  40 120  40Dose of sufentanil (  g) 33  9 32  10Intravascular fluid volumeexpansion (mL)980  220 840  260 P  not significant. 28  CARDIOVASCULAR ANESTHESIA BERTRAND ET AL. ANESTH ANALGANGIOTENSIN II ANTAGONISTS AND ANESTHETIC INDUCTION 2001;92:26–30  withdrawn: 12; AIIA given: 19;  P  0.01), and a longerduration of episodes of hypotension (AIIA with-drawn: 3  4 min; AIIA given: 8  7 min.;  P  0.01),and an increased need for vasoactive drugs ( P  0.02)(Table 4).During recovery, 8 of 18 patients with AIIA with-drawn developed HT, as opposed to 5 of 19 patientswhen AIIA were given. Terlipressin was administeredin only 2 of these last 5 patients.Only one patient in each group developed a post-operative complication: one patient in Group I devel-oped it during the postoperative period, a transientnew chest pain with ST-T abnormalities on electrocar-diogram, but without increased cTnI, necessitating acircumflex angioplasty on postoperative day 3. Onepatient in Group II developed transient ST-T abnor-malities without pain nor increased cTnI on postoper-ative day 1. Discussion ThisstudyconfirmsthatpatientstreatedwithAIIAuntilthe morning of surgery developed severe and more fre-quent hypotensive episodes during the induction of an-esthesia in comparison with those in whom the AIIAwas delayed on the previous day. Patients treated withAIIA until the morning of surgery have developed se-vere hypotensive episodes after the induction of generalanesthesia and required vasoconstrictor treatment.Moreover, in these patients, hypotension refractory torepeatedepinephrineorphenylephrineoccurred,requir-ing the use of an agonist of the vasopressin system. Nostudy patient developed a severe postoperative compli-cation such as stroke, myocardial infarction, respiratory,orrenalfailure,orneedforreoperation.Theincidenceof HT during recovery was identical in both groups.Adverse circulatory effects during anesthesia arewell known in patients chronically treated with ACEI,leading to the recommendation to discontinue them atleast 24 hours before the induction of anesthesia. Sim-ilarly, a case of refractory hypotension was reportedafter the induction of anesthesia in a patient chroni-cally treated with AIIA (5,6).AIIA acts by binding to specific membrane-boundreceptors that are coupled to one of several signaltransduction pathways. The AT 1 receptor mediatesthe major cardiovascular action of the renin angioten-sin system. Losartan, the leader in this field, is a se-lective AT1 receptor antagonist that was demon-strated to be an effective antagonist of manyangiotensin II-induced actions and an effective anti-hypertensive drug in many animal models of HT (10).Clinical studies have confirmed the AIIA action of losartan and suggest that it is as effective in the treat-ment of essential HT, and congestive heart failure, asACEI. The key advantage AIIA provide over ACEI isthat they may avoid unwanted side effects that arerelated to bradykinin potentiation with the latterdrugs (10–13).Blockade of the renin-angiotensin system increasesthe blood-pressure decreasing effect of anesthetic in-duction. A severe hypotensive episode, requiring va-soconstrictor treatment, occurs after the induction of general anesthesia in patients chronically treated withAIIA. Recommendations to discontinue these drugson the day before the surgery may be justified. Conclusion We conclude that significant adverse effects oc-curred during the induction of anesthesia in patientschronically treated with AIIA when the drug was Table 4.  Hemodynamic EventsGroup I(AIIA withdrawn)Group II(AIIA given) P valueSystolic blood pressurePreinduction 159  24 151  26 NSPostinduction 126  33 109  24 NSIntubation 136  34 121  33 NSLowesr value 159  24 151  26 NSEpisodes of hypotension (No.) 1  1 2  1   0.01Patients with at least 1 episode (No.) 12 19   0.01Duration of episodes (min) 3  4 8  7   0.01Patients receiving ephedrine (No.) 12 17 NSDose of ephedrine (mg) 10  10 15  9 NSPatients receiving neosynephrine 0 5   0.02Dose of neosynephrine (  g) 0  0 47  86   0.05Patients receiving terlipressine 0 6   0.01Dose of terlipressine (mg) 0  0 0.3  0.5   0.01Patients with HT during recovery 8 5 NS Values expressed as mean  sd .HT  hypertension.ANESTH ANALG CARDIOVASCULAR ANESTHESIA BERTRAND ET AL.  29 2001;92:26–30 ANGIOTENSIN II ANTAGONISTS AND ANESTHETIC INDUCTION
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