2Professor of Anesthesiology Anesthesia for patients with coronary artery disease undergoing non-cardiac surgeryGamal Fouad S Zaki, MDProfessor of AnesthesiologyAin Shams UniversityDuring the last 50 years, noncardiac surgery has made substantial advances in treating diseases (cancer) and improving quality of life (arthroplasty).The number of non-cardiac surgical procedures has increased. However such surgery is associated with significant cardiac morbidity and mortality, and cost (cardiac death, acute MI, unstable angina, non-fatal cardiac arrest).The literature is abundant as regards this subject, with more opinion than science.In the next half hour or so, I will try to high light the magnitude of the problem, the pathophysiology, the methods of risk stratification, risk modification, anesthetic techniques and management of postop complications.
3In Non-Cardiac Surgery: Stress associated with surgery is extreme & persistent4-5% of patients with or at risk of heart disease suffer cardiac complications perioperativelyPerioperative MI carries a 15-25% hospital mortality Shah 1990, Badner 1998, Kumar 2001Cardiac arrest has a hospital mortality of 65% and is an independent predictor of death during the following 5 yrs
4Epidemiology Incidence of CAD on the rise Aging population: age group >65 years:will increase by 25% in next 30 years (USA)Largest number of surgical proceduresNumber of non-cardiac surgical procedures in older persons will increasePrevalence of CAD increases with ageMore likely to get patient with CAD in OR
5Historical Background 1952197719861982+1985-619901995+1996Late90sPerioperative MI identified as a problemGoldman Cardiac Risk IndexDetsky: Modified Cardiac Risk IndexSpecialized tests for risk stratificationIntraoperative risk factors identifiedPostop Ischemia main outcome predictorβ-Blockers fight ischemiaACC/AHA GuidelinesFrom Risk Stratification to Risk Modification1950s: adoption of ECG in intraoperative monitoring
6Myocardial Oxygen Balance SupplyDemandSlow, empty, well perfusedThe physiology of myocardial oxygen balance was classically described in terms of supply & demand.So we can talk about supply side ischemia, and demand side ischemia.The ischemic myocardium is happy (balance maintained) when it is slow, empty, and well perfused.Coronary blood flowCPP=AoDP-LVEDPArterial O2 ContentInotropic stateSystolic wall tensionHeart Rate
7Myocardial Oxygen Imbalance SupplyDemandSupply ischemia: hemodynamically silentTachycardia / hypotensionIncrease LVEDPCoronary stenosisCoronary A (graft) spasmPlaque erosion/rupture/triggersMyocardial ischemia was classically described as a disturbance of myocardial oxygen balance caused by either increased demand, and / or reduced supply. Intraoperatively, increased demand may be caused by tachycardia, hypertension, or increased contractility. A decreased supply may be due to tachycardia, hypotension (especially with an increased wedge pressure), coronary artery spasm, and coronary atheromatous plaque rupture. The concept was that maintaining demand at low levels by strict hemodynamic control, would prevent ischemia. However, it was observed that most episodes of intraoperative ischemia occur without preceding hemodynamic disturbance. This means that most intraoperative ischemia is supply-side ischemia. Coronary atheromas are not simple, static lesions, but are rather dynamic inflammatory lesions, with infection proposed as a possible etiology. Plaque rupture triggers, and prevention of plaque rupture will be the area of future progress. Lipid lowering schemes may help reduce acute MI without concomitant reduction in severity of atherosclerosisTachycardiaIncrease ContractilityHypertension
8Pathology of Atheroma Triggers of Plaque Rupture: Smoking Foam CellsT-LymphocytesTriggers of Plaque Rupture:SmokingHypercholesterolemiaInflammatory ResponseShear StressMacrophages infiltrate the intima and consume the cholesterol delivered by the lipoproteins, becoming enlarged foam cells prone to rupture, forming, together with T-lymphocytes, the lipid core of the atheroma. Endothelial dysfunction and necrosis results in platelet aggregation, and formation of the fibrous cap. Progressive Thinning of the fibrous cap, continuing underlying infiltration by inflammatory cells, and distension of the lipid core, results in plaque rupture.
9Pathophysiology of Perioperative MI Unknown:Myocardial O2 supply/demand imbalance (perioperative stress)Rupture of Atheromatous plaques:Dawood MM, Gutpa DK, et al. Pathology of fatal perioperative myocardial infarction: implications regarding pathophysiology and prevention. Int J Cardiol 1996;57:37-44.Triggers of plaque rupture: hemodynamic sheer stress, coronary spasm, plaque ischemia and inflammatory processPerioperative factors: systemic inflammatory response, sympathetic hyperactivity, and hypercoagulability (platelet hyperaggregability)
11Preoperative assessment Goals:Identify high risk patients who may benefit from pharmacologic optimization and/or revascularizationPlan for intraoperative managementPlan for postoperative managementProduce a risk assessment useful for patient and surgeon
12Preoperative Preparation Components:History / ExaminationNon-Invasive TestingPreoperative Optimization:Control medical conditions: HTN, BAEmploy pharmacologic protectionMinimal role for preoperative revascularization CABG, Angioplasty
13Lee Revised Cardiac Risk Index High risk surgical procedure• History of ischemic heart disease• History of congestive heart failure• History of TIA or stroke• Preoperative insulin therapy• Preoperative serum creatinine >2.0 mg/dL
14Preoperative Evaluation: not “Clearance” Update 2002Based on “Clinical Predictors” functional capacity, underlying medical conditions, surgicalriskIntervention rarely necessary to reduce surgical risk unless indicated w/o surgeryPreoperative Evaluation: not “Clearance”Produce risk profile useful for making treatment decisions by: patient, surgeon, anesthesiologistTesting: only when likely to influence treatmentModified Cardiac Risk Index: DetskyThese guidelines present an organized approach to the surgical patient with known or suspected cardiac disease, based on the presence of “clinical predictors” (history, underlying medical conditions), functional capacity, and surgical risk. The interaction of these factors determines the need for noninvasive testing.
15History: Exercise Tolerance Reilly et al. Self-reported exercise tolerance and the risk of serious perioperative complications. Arch Intern Med. 1999;159:600 non-cardiac surgery ptsQuestioned about number of blocks they could walk, or flights of stairs they could climbPoor exercise tolerance: < 4 blocks or 2 flights, (< 6 METs: metabolic equivalents)more periop complications (20.4% vs. 10.4%), more myocardial ischemia, cardiovascular and neurologic complicationsIf assessment not possible (knee): further testingThe most important aspect of the guidelines is the evaluation of the patient’s exercise tolerance. Unless there are very high risk features, a patient able to perform at least 6 metabolic equivalents (6 METS: e.g. carry groceries up a flight of stairs) should be able to undergo most surgical procedures at an acceptable risk. Patients in whom exercise tolerance could not be assessed (e.g. knee problems), and patients who have high risk features should undergo further non-invasive cardiac testing.
16Cardiac stress testing Why does inducible ischaemia on stress testing not predict perioperative events satisfactorily?Stress testing predicts intermediate and long term prognosis of CAD patients.(Lee, Boucher. N Engl J Med 2001;344:1840)The culprit is extrapolating this to short term perioperative (96 hrs) outcomeDifference may be in the etio-pathology: plaque rupture vs. supply/demand imbalanceStress tests are capable of predicting intermediate and long term prognosis of patients with CAD,Extrapolating this to predicting short term perioperative outcome is the culprit.
17Dobutamine Stress Echocardiography Commonly chosen, good predictive valueNew or worsened RWMA: positiveRepresent areas at risk of ischemiaDynamic assessment of LV functionPatients with RWMA in 1-4 segments benefit from beta blockers>5 segments do not benefit, need intervention. Boersma et al. JAMA 2001Dobutamine stress echocardiography is frequently the choice of preoperative test. The appearance of new or worsened regional wall motion abnormalities is considered a positive test. These represent areas at-risk for myocardial ischemia. The advantage of this test is that it is a dynamic assessment of ventricular function. Dobutamine echocardiography has also been studied and found to be among the best positive and negative predictive tests. Importantly, the results of dobutamine stress echocardiography should be quantitated, with those who develop wall motion abnormalities at low heart rates at greatest risk. Boersma et al. demonstrated that patients with regional wall motion abnormalities in 1-4 segments benefit significantly from perioperative beta-blockade while those with > 5 segments demonstrating no significant benefit, suggesting the need for other interventions.18
18Trigger a cascade of riskier interventions Low predictive value of positive non-invasive tests, preop revascularization not beneficialTrigger a cascade of riskier interventionsIncreased cost, delayed surgeryβ-blockers and may be statins shown to reduce perioperative ischemiaNeed to shift emphasis from risk stratification to risk modification: drugsMany patients undergo non-invasive testing for the detection of coronary artery disease before non-cardiac surgery. This is despite the low predictive value of positive tests in this population and the lack of any evidence of benefit of coronary revascularisation before non-cardiac surgical procedures. Further, this strategy often triggers a clinical cascade exposing the patient to progressively riskier testing and intervention and results in increased costs and unnecessary delays. On the other hand, administration of b blockers, and more recently statins, has been shown to reduce the occurrence of perioperative ischaemic events. Therefore, there is a need for a shift in emphasis from risk stratification by non-invasive testing to risk modification by the application of interventions, which prevent perioperative ischaemia—principally, perioperative b adrenergic blockade and perhaps treatment with statins. Clinical risk stratification tools reliably identify patients at high risk of perioperative ischaemic events and can guide in the appropriate use of perioperative medical treatment.
19Grayburn et al. Cardiac events in patients undergoing noncardiac surgery: shifting the paradigm from noninvasive risk stratification to therapy. Ann Intern Med 2003;138:506“The paradigm is shifting from predicting which patient is at high risk for having a perioperative cardiac event to minimizing the likelihood of such an event with specific perioperative pharmacologic therapy”Estimating this risk in an individual patient is difficult and complex. Although noninvasive imaging tests are often used for this purpose, a review of the literature reveals that the positive predictive value of noninvasive imaging tests is uniformly low and that they do not provide information beyond that obtained by assessing simple clinical risk variables. Moreover, no evidence exists that noninvasive imaging tests lead to a therapeutic strategy that reduces the risk for perioperative myocardial infarction or cardiac death. Since the publication of guidelines for preoperative risk stratification by the American College of Cardiology/American Heart Association in 1996 and the American College of Physicians in 1997, three clinical trials have shown that beta-blocker therapy reduces the risk for perioperative cardiac events. This paper focuses on the relationship between risk stratification and subsequent therapy to minimize or eliminate risk. In short, the paradigm is shifting from predicting which patient is at high risk for having a perioperative cardiac event to minimizing the likelihood of such an event with specific perioperative pharmacologic therapy.
20Preoperative Revascularization prior CABG confers protection against perioperative cardiac events Paul SD, Eagle KA. Med Clin N Amer 1995Not recommended for all high risk patients for non-cardiac surgery. Combined risks of CABG followed by non-cardiac surgery is greater than surgery alone.Angioplasty: not recommended before non-cardiac surgery, angioplasty within one month of non-cardiac surgery associated with increased complications and death. Kaluza et al. Catastrophic outcomes of noncardiac surgery soon after coronary stenting. J Am Coll Cardiol 2000;35:ACC/AHA Guidelines recommended waiting a minimum of 2-4 weeks after Angioplasty
22Design: RCT; 200 Veterans for non-cardiac surgery Inclusion: Known CAD or 2 or more CAD risk factors.Exclusion: CHF, 3rd degree AVB, Bronchospam, HR<55 or SBP<100
23Intervention:Perioperative: Atenolol 5mg given IV on call to OR. Repeated 5 minutes later.Postoperative: Same regimen repeated immediately post-op. Starting on POD#1 Atenolol mg PO qd (or placebo) was given.Outcome:Primary: All cause of mortality at D/C and at 2 years.Secondary: Survival free from MI, unstable angina, CHF, need for revascularization.Results:6 in-hospital deaths, including 3 from PMI (2 in placebo group and 1 in atenolol) NS30 deaths during 2 years follow-up including 21 deaths in placebo and 9 in atenolol.
24Overall Survival in 2 Years after Noncardiac Surgery among 192 Patients in Atenolol and Placebo Groups Who Survived to Hospital Discharge.
25Event-free Survival in 2 Years after Noncardiac Surgery in 192 patients in Atenolol and Placebo Groups who Survived to Hospital Discharge
26Design: RCT 112 patientsInclusion: abdominal aortic or infrainguinal arterial reconstruction with:Age>70, angina, prior MI, CHF, ventricular arrhythmias, diabetes, class III symptoms ANDDobutamine echo → stress induced wall motion abnormalities ANDNot on a beta blocker already, no extensive resting wall motion abnormalities, no evident LM or 3VD.Intervention:Bisoprolol 5mg qd (or placebo) started at least 1 week prior to surgery; increased to 10mg if HR>60, continued postoperativelyStopped for HR<50 or SBP<100.Endpoints:Death from cardiac causes or nonfatal MI
27Patient homogeneity. Higher risk patients ResultsMortality: 9 (17%) cardiac deaths in placebo arm vs 2 (3.4%) in bisoprolol arm p=.002 ARR 13.5%; NNT=7.Nonfatal MI: 9 (17%) nonfatal MIs in placebo group and 0 in bisoprolol group ARR 17%; NNT=6Combined endpoint 34% in placebo arm suffered cardiac death or nonfatal MI vs 3.4% in the bisoprolol group ARR 31%; NNT=3Advantages over Mangano’s study:Patient homogeneity. Higher risk patientsExclusion of prior beta blocker use. Use of oral β-blocker
28Kaplan-Meier estimates of cumulative percentage of patients who died of cardiac causes or had a non-fatal MI during perioperative period.
29Retrospective study of 800,000 major noncardiac surgery pts, of whom 18% received BB in the first 2 hospital days.Perioperative BB associated with a reduced risk of in-hospital death among high-risk (RCRI), but not low-risk, patients. Patient safety may be enhanced by increasing the use of beta-blockers in high-risk patients.Retrospective study of 800,000 major noncardiac surgery patients, of whom 18% received BB in the first 2 hospital days.Perioperative beta-blocker therapy is associated with a reduced risk of in-hospital death among high-risk, but not low-risk, patients undergoing major noncardiac surgery. Patient safety may be enhanced by increasing the use of beta-blockers in high-risk patients.Revised cardiac risk inex RCRI.
31Intraoperative Management Monitoring: ECG V5 most sensitive London et al. Anesthesiol 1988V4 most sensitive Landesberg et al. Anesthesiol 2002Two or 3 precordial leads will detect >90% of ischemia from 12 leadsOR monitors: only one precordial leadAutomated ST-segment analysis of at least 2 leads considered standard.
32Intraoperative Myocardial Ischemia: Localization by continuous 12-lead electrocardiography. London M et al. Anesthesiology 1988More recent work by Dr Martin London & his associates gives us a better perspective.The sensitivity of single leads detect ST changes pathognomonic of ischemia compared to standard paper recorded ECG.Leads I, AVL, & AVR practically see no ischemia
33Landesberg et al. Anesthesiol 2002 Histogram showing the incidence in which prolonged ischemia was first noted by each lead at the onset of ischemia in all 38 longest ischemic events and in the 12 ischemic events that progressed to MIEarly detection and treatment of silent ischemia in patients at high risk for coronary artery disease may improve outcome. Unfortunately, current monitoring technology is not optimized to detect ischemia. Many monitoring areas are primarily focused on arrhythmia detection and treatment. In fact, optimal lead placement for arrhythmia detection is not the same location for optimal ischemia detection. In addition, older ischemia detection software analyzes absolute changes from the isoelectric baseline rather than relative changes from preoperative ST-segment analysis. This fact is important with respect to the large percentage of at risk patients who preoperatively have abnormalities on their ECGs. To achieve the highest sensitivity in ischemia detection, 2 precordial leads, chosen from V3 to V5 , with baseline ST segments closest to the isoelectric baseline, should be selected. The authors demonstrated the superiority of V4 , over the conventional V5 , when a single lead is used for ischemia detection. The full economic and mortality impact of routine perioperative ischemia monitoring is not known.
34Landesberg et al. Anesthesiol Histogram showing the incidence of all leads demonstrating greater than 1 mm relative ST deviation during peak ischemia and the lead with maximal ST deviation in the 12 patients with myocardial infarction.
35Automated ST-segment Analysis I-pointJ-pointJ+60mSSome software versions allow you to move the J+60msec pointbecause of the possibility of early takeoff of the T wave after CPB, then the vertical tick will fall on the T rather than the ST
36Intraoperative Management Monitoring: TEE Regional function is evaluated in terms of:Wall Motion (endocardial excursion)& / orWall ThickeningTEE Reserved for situations where a diagnosis or treatment question will be answered by the additional information.Tee is capable of identifying isch myocardium through detection of abnormalities of regional myoc function:In terms of :Endocardial excursion &Myocardial thickeningOr wall motion & wall thickening
37A10Inferior Akinesis (RT)||On the left is a cardiac cycle captured prior to cardiopulmonary bypass. Mild lateral wall (from 1 o'clock to 3 o'clock) hypokinesis is seen. On the right is a cardiac cycle captured early after cardiopulmonary bypass. Inferior wall akinesis is noted. Left ventricular filling is somewhat reduced due to the use of nitroglycerin. However, nitroglycerin did not resolve this new segmental wall-motion abnormality.$Dopamine was also administered to this patient, but the inferior wall abnormality persisted and ultimately cardiopulmonary bypass was reestablished and an additional graft placed in this inferior wall. Following that intervention, the function of this wall improved markedly.
38Intraoperative Management: Regional or General Anesthesia Long lasting debateNo scientific evidence supporting eitherMore important: sound physiologic goals: Hemodynamic stability, normothermia, avoidance of anemiaAlthough 50% of ECG ischemia is hemodynamically silent, there is association between Tachycardia and both intraoperative and postoperative ischemiaThe debate of perioperative outcome related to type of anesthesia, general or regional, continues.No evidence.I will try to outline for u the evidence available from studies comparing various techniques and what we know about each technique.
39Intraoperative Management: Regional or General Anesthesia Opioid based gives hemodynamic stability but may require postoperative ventilationOften GA + epidural blockVolatile Agents: possess Cardioprotective properties, “Anesthetic Preconditioning”: reduce infarct size, attenuate endothelial dysfunction: open mitochondrial ATP sensitive K channel: mito KATPOnly Epidural Anesthesia/Analgesia with local anesthetics+opioids capable of attenuating neuroendocrine stress responseThe debate of perioperative outcome related to type of anesthesia, general or regional, continues. This article is a systematic review of randomized trials--the problem is that there is often a publication bias toward positive results. Nevertheless, this work supports the concept that neuraxial blockade reduces postoperative morbidity and mortality.Volatile agents modulate the mito ATP sensitive K channel
40Cardiac Troponin I in the SEVO and Propofol Groups
41Volatile agents and opioids induce preconditioning Inhalation anesthetics and opioids induce preconditioning
42Anesthetic Postconditioning Anesthetic preconditioning (APC) refers to the phenomenon whereby exposure of the heart to a volatile anesthetic before myocardial ischemia results in protection against the deleterious effects of myocardial ischemia and reperfusion. Compared with control conditions, this protection manifests as an improvement at the level of different variables such as infarct size and contractile function, but also coronary flow and free radical release at reperfusion. This type of protection strongly resembles ischemic preconditioning (IPC), which is a powerful endogenous protective mechanism that is present at different organ levels and occurs in various species. IPC refers to the phenomenon whereby a brief period of ischemia is able to protect the myocardium (ie, precondition) against the reversible and irreversible consequences of a subsequent longer period of ischemia, such as stunning, infarction, and the occurrence of arrhythmias. The mechanisms underlying IPC involve a complex system of intracellular signalling pathways, many of which are shared by APC. In addition, recent experimental data have indicated that APC is able to confer additional cardioprotection after IPC .Anesth Postconditioning: administration after reperfusion from ischemia, reuces reoxygenation injury.
43LAD Ligation in Anesthetized dogs Infarct SizeMyocardial EdemaPost con is as effective as precon in reducing infarct size, may be applicable to situations where reperfusion injury is an issue.
45Intraoperative Management: Regional or General Anesthesia Rodgers A. Reduction of postoperative mortality and morbidity with epidural or spinal anaesthesia: results from overview of randomised trials.BMJ 2000; 321(7275): 1493Meta-analysis of 141 trials, 9559 patientsMortality reduced by 1/3 with neuraxial blockade 103/4871 vs. 144/4688 patientsDecreased odds of DVT(44%), PE (55%), transfusion (50%), pneumonia (39%), and respiratory depression (59%) (all p<0.001)The debate of perioperative outcome related to type of anesthesia, general or regional, continues. This article is a systematic review of randomized trials--the problem is that there is often a publication bias toward positive results. Nevertheless, this work supports the concept that neuraxial blockade reduces postoperative morbidity and mortality.
46Intraoperative Management: Regional or General Anesthesia Rigg JR. Epidural anaesthesia and analgesia and outcome of major surgery: a randomised trial. Lancet 2002; 359(9314):Prospective trial, with1 of 9 comorbid states, 915 patients, major abdominal surgeryRandomized: Epidural + General A with postop epidural analgesia (72 hrs) vs. General A30 day Mortality: 23/447 Epidural vs. 19/441 controlNo difference in mortality and major morbiditySignificant reduction in Respiratory failure & Pain Scores with EpiduralINTERPRETATION: Most adverse morbid outcomes in high-risk patients undergoing major abdominal surgery are not reduced by use of combined epidural and general anaesthesia and postoperative epidural analgesia. However, the improvement in analgesia, reduction in respiratory failure, and the low risk of serious adverse consequences suggest that many high-risk patients undergoing major intra-abdominal surgery will receive substantial benefit from combined general and epidural anaesthesia intraoperatively with continuing postoperative epidural analgesiaThis is an important study—randomized trials such as this are very difficult to do and the authors are to be congratulated. They failed to show that many adverse outcomes in high-risk patients undergoing major abdominal surgery are reduced by use of epidural anesthesia and analgesia. Nevertheless, the lower pain scores in the postoperative epidural group are salutatory and mean that these patients do indeed receive benefit from epidural analgesia.
47Intraoperative Management: Regional or General Anesthesia Singh N et al. The effects of the type of anesthesia on outcomes of lower extremity infrainguinal bypass.J Vasc Surg 44: , November 2006Prospectively collected database of National Surgical Quality Improvement Program (NSQIP)The NSQIP database identified 14,788 patients (GETA, 9757 pts; SA, 2848 pts; EA, 2183 pts) underwent infrainguinal arterial bypass99% Males, Mean Age: 65.8 yrsAnother trial at answering the same question in a vascular surgery population who are known to have a 50% incidence of CAD.This study is an analysis of a prospectively collected database by the National Surgical Quality Improvement Program (NSQIP) of the Veterans Affairs Medical Centers.The NSQIP database identified 14,788 patients (GETA, 9757 patients; SA, 2848 patients; EA, 2183 patients) who underwent a lower extremity infrainguinal arterial bypass during the study period. Almost all patients (99%) were men, and the mean age was 65.8 years. The type of anesthesia significantly affected graft failure at 30 days. Compared with SA, the odds of graft failure were higher for GETA (odds ratio, 1.43; 95% confidence interval [CI], ; P = .001). There was no statistically significant difference in 30-day graft failure between EA and SA. Regarding cardiac events, defined as postoperative myocardial infarction or cardiac arrest, patients with normal functional status (activities of daily living independence) and no history of congestive heart failure or stroke did worse with GETA than with SA (odds ratio, 1.8; 95% CI, ; P < .0001). There was no statistically significant difference between EA and SA in the incidence of cardiac events. GETA, when compared with SA and EA, was associated with more cases of postoperative pneumonia (odds ratio: 2.2 [95% CI, ; P = .034]. There was no significant difference between EA and SA with regard to postoperative pneumonia. Compared with SA, GETA was associated with an increased odds of returning to the operating room (odds ratio, 1.40; 95% CI, ; P < .001), as was EA (odds ratio, 1.17; 95% CI, ; P = .005). GETA was associated with a longer surgical length of stay on univariate analysis, but not after controlling for confounders. There was no significant difference in 30-day mortality among the three groups with univariate or multivariate analyses.Conclusions Although GETA is the most common type of anesthesia used in infrainguinal bypasses, our results suggest that it is not the best strategy, because it is associated with significantly worse morbidity than regional techniques.
48Intraoperative Management: Regional or General Anesthesia Singh N et al. The effects of the type of anesthesia on outcomes of lower extremity infrainguinal bypass J Vasc Surg 44: , November 2006Type of anesthesia affected graft failureCompared to SA and EA, GETA associated with:More graft failure at 30 daysMore cardiac events (MI, C Arrest),More postoperative pneumoniaNo difference between SA and EA regarding graft failure and cardiac eventsGETA is not the best strategyAnother trial at answering the same question in a vascular surgery population who are known to have a 50% incidence of CAD.This study is an analysis of a prospectively collected database by the National Surgical Quality Improvement Program (NSQIP) of the Veterans Affairs Medical Centers.The NSQIP database identified 14,788 patients (GETA, 9757 patients; SA, 2848 patients; EA, 2183 patients) who underwent a lower extremity infrainguinal arterial bypass during the study period. Almost all patients (99%) were men, and the mean age was 65.8 years. The type of anesthesia significantly affected graft failure at 30 days. Compared with SA, the odds of graft failure were higher for GETA (odds ratio, 1.43; 95% confidence interval [CI], ; P = .001). There was no statistically significant difference in 30-day graft failure between EA and SA. Regarding cardiac events, defined as postoperative myocardial infarction or cardiac arrest, patients with normal functional status (activities of daily living independence) and no history of congestive heart failure or stroke did worse with GETA than with SA (odds ratio, 1.8; 95% CI, ; P < .0001). There was no statistically significant difference between EA and SA in the incidence of cardiac events. GETA, when compared with SA and EA, was associated with more cases of postoperative pneumonia (odds ratio: 2.2 [95% CI, ; P = .034]. There was no significant difference between EA and SA with regard to postoperative pneumonia. Compared with SA, GETA was associated with an increased odds of returning to the operating room (odds ratio, 1.40; 95% CI, ; P < .001), as was EA (odds ratio, 1.17; 95% CI, ; P = .005). GETA was associated with a longer surgical length of stay on univariate analysis, but not after controlling for confounders. There was no significant difference in 30-day mortality among the three groups with univariate or multivariate analyses.Conclusions Although GETA is the most common type of anesthesia used in infrainguinal bypasses, our results suggest that it is not the best strategy, because it is associated with significantly worse morbidity than regional techniques.
49Intraoperative Management: Regional or General Anesthesia My Preference: BOTHEpidural Catheter inserted after fluid preloading, test dose, then 8 ml of your favorite LA, wait for sure signs of onset of block, then induce:General Anesthesia: Fentanyl 2μg/kg, wait for at least 3min, Thiopentone 2-4 mg/kg, your favorite non-depolarizer, ETT, Isoflurane %, or Sevo 1-2%, normocarbia. Maintain Epidural block (LA + Opioid), Little or no IV fentanylPostop: Ropivacaine 0.2% + Fentanyl 2μg/mlMajor abdominal surgery: EA+GAI avoid Pancuronium. Volatile: MACHR will be stableNo need for intra or postop IV opioidsEarly recovery, Easy extubationSEVO
50Postoperative Management: First 3 postoperative days: Period of greatest risk of cardiac complicationsHypercoagulability, Increased adrenergic stressManagement focused on factors increasing risk of cardiac complications:TachycardiaAnemiaHypothermia, shiveringHypertensionHypoxemiaInadequate analgesiaFirst three days associated with highest incidence of complications
51Postoperative Management: Most postoperative ischemia is silent:Most MIs preceded by prolonged ST depressionEarly detection and aggressive management MAY prevent progression to MIDetective strategy:(Silent)ST-segment Monitoring: automated, continuous12 Lead ECG q. 8 hrs in day1, then daily for day 2, 3Serial Enzymes: Cardiac Troponins (TnT, TnI)
52Postoperative Management: Cardiac Troponins (TnT, TnI)More specific than CK-MBMore prognostic value, Suggest treatment strategyUnstable Angina: some have small rise TnT<0.1 ng/ml, increased M&M, respond to LMWH, Gp IIb-IIIa blockersTime to risePeak riseNormalizedCK-MB3-5 hrs10-18 hrs2-3 daysGold standard Not Prognostic low specificityTnT3.8 hrs18 hrs, 3ds5-14 daysHigh sensetivity & specificity, PrognosticTnI3-12 hrs24 hrs5-10 daysnot affected by CRF, slow riseTnT affected by renal failure
53Postoperative Management: Cardiac complications Treatment based on extrapolation from non-operative setting, AHA/ACC guidelines:Transmural Q-wave MINon Q-wave MI (NQWMI)Unstable Angina
54Postoperative Management: Transmural Q-wave MI Goal: quickly reopen occluded vesselAspirin: earlyThrombolytics contraindicated post surgery??If Lytics CI: consider Cath/Stentβ-Blockers: aggressive blockNTG: only for ongoing ischemiaACE Inhibitors: improve LV remodellingHeparin: when lytics CIMagnesium: good, Statins: evolving evidenceLMWH, Gp IIb/IIIa blockers: no evidence
55Postoperative Management: Non Q-wave MI (NQWMI) Majority of perioperative MIHigher Morbidity, equal Mortality to QWMICardiac status closer to Unstable AnginaDiagnosis: Cardiac Enzymesβ-Blockers & Aspirin for all NQWMINTG: only for ongoing ischemiaHeparin: 48 hours, improves outcomeLMWH: used instead, caution, no reversalGp IIb/IIIa blockers ?? Used in non-operative
56Postoperative Management: Unstable Angina Goal: prevent progression to MI, deathβ-Blockers & Aspirin: dec MI, MortalityNTG: only for ongoing ischemia, nitrate tolerance develops in hrs continuous administrationHeparin: 48 hours, improves outcomeAngio / stent??Troponin Positive Unstable Angina(Minor Myocardial Injury):LMWH & Gp IIb/IIIa blockers: Abciximab, AgrastatTnT affected by renal failure
57Epilogue: CAD patients are high risk patients Optimum strategy is multimodal:Improved preoperative assessmentSympatholytic pharmacologic optimizationIntraoperative management based on physiologic goals & scientific evidencePostoperative Monitoring: “detective”Postoperative MI, U Angina: inc M & M:β-Blockers & Aspirin, selective use of invasive procedures