Professor of Anesthesiology

Professor of Anesthesiology
Anesthesia for patients with coronary artery disease undergoing non-cardiac surgery Gamal Fouad S Zaki, MD Professor of Anesthesiology Ain Shams University During 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.

In Non-Cardiac Surgery:
Stress associated with surgery is extreme & persistent 4-5% of patients with or at risk of heart disease suffer cardiac complications perioperatively Perioperative MI carries a 15-25% hospital mortality Shah 1990, Badner 1998, Kumar 2001 Cardiac arrest has a hospital mortality of 65% and is an independent predictor of death during the following 5 yrs

Epidemiology 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 procedures Number of non-cardiac surgical procedures in older persons will increase Prevalence of CAD increases with age More likely to get patient with CAD in OR

Historical Background
1952 1977 1986 1982+ 1985-6 1990 1995+ 1996 Late90s Perioperative MI identified as a problem Goldman Cardiac Risk Index Detsky: Modified Cardiac Risk Index Specialized tests for risk stratification Intraoperative risk factors identified Postop Ischemia main outcome predictor β-Blockers fight ischemia ACC/AHA Guidelines From Risk Stratification to Risk Modification 1950s: adoption of ECG in intraoperative monitoring

Myocardial Oxygen Balance
Supply Demand Slow, empty, well perfused The 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 flow CPP=AoDP-LVEDP Arterial O2 Content Inotropic state Systolic wall tension Heart Rate

Myocardial Oxygen Imbalance
Supply Demand Supply ischemia: hemodynamically silent Tachycardia / hypotension Increase LVEDP Coronary stenosis Coronary A (graft) spasm Plaque erosion/rupture/triggers Myocardial 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 atherosclerosis Tachycardia Increase Contractility Hypertension

Pathology of Atheroma Triggers of Plaque Rupture: Smoking
Foam Cells T-Lymphocytes Triggers of Plaque Rupture: Smoking Hypercholesterolemia Inflammatory Response Shear Stress Macrophages 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.

Pathophysiology 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 process Perioperative factors: systemic inflammatory response, sympathetic hyperactivity, and hypercoagulability (platelet hyperaggregability)

Preoperative assessment
Goals: Identify high risk patients who may benefit from pharmacologic optimization and/or revascularization Plan for intraoperative management Plan for postoperative management Produce a risk assessment useful for patient and surgeon

Preoperative Preparation
Components: History / Examination Non-Invasive Testing Preoperative Optimization: Control medical conditions: HTN, BA Employ pharmacologic protection Minimal role for preoperative revascularization CABG, Angioplasty

Lee 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

Preoperative Evaluation: not “Clearance”
Update 2002 Based on “Clinical Predictors” functional capacity, underlying medical conditions, surgicalrisk Intervention rarely necessary to reduce surgical risk unless indicated w/o surgery Preoperative Evaluation: not “Clearance” Produce risk profile useful for making treatment decisions by: patient, surgeon, anesthesiologist Testing: only when likely to influence treatment Modified Cardiac Risk Index: Detsky These 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.

History: 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 pts Questioned about number of blocks they could walk, or flights of stairs they could climb Poor 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 complications If assessment not possible (knee): further testing The 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.

Cardiac 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) outcome Difference may be in the etio-pathology: plaque rupture vs. supply/demand imbalance Stress 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.

Dobutamine Stress Echocardiography
Commonly chosen, good predictive value New or worsened RWMA: positive Represent areas at risk of ischemia Dynamic assessment of LV function Patients with RWMA in 1-4 segments benefit from beta blockers >5 segments do not benefit, need intervention. Boersma et al. JAMA 2001 Dobutamine 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

Trigger a cascade of riskier interventions
Low predictive value of positive non-invasive tests, preop revascularization not beneficial Trigger a cascade of riskier interventions Increased cost, delayed surgery β-blockers and may be statins shown to reduce perioperative ischemia Need to shift emphasis from risk stratification to risk modification: drugs Many 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.

Grayburn 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.

Preoperative Revascularization
prior CABG confers protection against perioperative cardiac events Paul SD, Eagle KA. Med Clin N Amer 1995 Not 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

Pharmacologic Optimization
β-adrenergic blockers α2-adrenergic agonists Nitroglycerine: IV, Transdermal?? Calcium channel blockers Antiplatelet drugs Statins (HMG-CoA Reductase Inhibitors) ACE Inhibitors LMWH

Design: 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

Intervention: 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) NS 30 deaths during 2 years follow-up including 21 deaths in placebo and 9 in atenolol.

Overall Survival in 2 Years after Noncardiac Surgery among 192 Patients in Atenolol and Placebo Groups Who Survived to Hospital Discharge.

Event-free Survival in 2 Years after Noncardiac Surgery in 192 patients in Atenolol and Placebo Groups who Survived to Hospital Discharge

Design: RCT 112 patients Inclusion: abdominal aortic or infrainguinal arterial reconstruction with: Age>70, angina, prior MI, CHF, ventricular arrhythmias, diabetes, class III symptoms AND Dobutamine echo → stress induced wall motion abnormalities AND Not 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 postoperatively Stopped for HR<50 or SBP<100. Endpoints: Death from cardiac causes or nonfatal MI

Patient homogeneity. Higher risk patients
Results Mortality: 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=6 Combined endpoint 34% in placebo arm suffered cardiac death or nonfatal MI vs 3.4% in the bisoprolol group ARR 31%; NNT=3 Advantages over Mangano’s study: Patient homogeneity. Higher risk patients Exclusion of prior beta blocker use. Use of oral β-blocker

Kaplan-Meier estimates of cumulative percentage of patients who died of cardiac causes or had a non-fatal MI during perioperative period.

Retrospective 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.

Intraoperative Management Monitoring:
ECG Non-Invasive BP Temperature Invasive Blood Pressure: Arterial line CVP TEE PA Catheter ?

Intraoperative Management Monitoring: ECG
V5 most sensitive London et al. Anesthesiol 1988 V4 most sensitive Landesberg et al. Anesthesiol 2002 Two or 3 precordial leads will detect >90% of ischemia from 12 leads OR monitors: only one precordial lead Automated ST-segment analysis of at least 2 leads considered standard.

Intraoperative Myocardial Ischemia: Localization by continuous 12-lead electrocardiography. London M et al. Anesthesiology 1988 More 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

Landesberg 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 MI Early 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.

Landesberg 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.

Automated ST-segment Analysis
I-point J-point J+60mS Some software versions allow you to move the J+60msec point because 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

Intraoperative Management Monitoring: TEE
Regional function is evaluated in terms of: Wall Motion (endocardial excursion) & / or Wall Thickening TEE 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 thickening Or wall motion & wall thickening

A10 Inferior 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.

Intraoperative Management: Regional or General Anesthesia
Long lasting debate No scientific evidence supporting either More important: sound physiologic goals: Hemodynamic stability, normothermia, avoidance of anemia Although 50% of ECG ischemia is hemodynamically silent, there is association between Tachycardia and both intraoperative and postoperative ischemia The 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.

Opioid based gives hemodynamic stability but may require postoperative ventilation Often GA + epidural block Volatile Agents: possess Cardioprotective properties, “Anesthetic Preconditioning”: reduce infarct size, attenuate endothelial dysfunction: open mitochondrial ATP sensitive K channel: mito KATP Only Epidural Anesthesia/Analgesia with local anesthetics+opioids capable of attenuating neuroendocrine stress response 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. Volatile agents modulate the mito ATP sensitive K channel

Cardiac Troponin I in the SEVO and Propofol Groups

Volatile agents and opioids induce preconditioning
Inhalation anesthetics and opioids induce preconditioning

Anesthetic 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.

LAD Ligation in Anesthetized dogs
Infarct Size Myocardial Edema Post con is as effective as precon in reducing infarct size, may be applicable to situations where reperfusion injury is an issue.

Rodgers A. Reduction of postoperative mortality and morbidity with epidural or spinal anaesthesia: results from overview of randomised trials. BMJ 2000; 321(7275): 1493 Meta-analysis of 141 trials, 9559 patients Mortality reduced by 1/3 with neuraxial blockade 103/4871 vs. 144/4688 patients Decreased 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.

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 surgery Randomized: Epidural + General A with postop epidural analgesia (72 hrs) vs. General A 30 day Mortality: 23/447 Epidural vs. 19/441 control No difference in mortality and major morbidity Significant reduction in Respiratory failure & Pain Scores with Epidural INTERPRETATION: 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 analgesia This 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.

Singh N et al. The effects of the type of anesthesia on outcomes of lower extremity infrainguinal bypass. J Vasc Surg 44: , November 2006 Prospectively 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 bypass 99% Males, Mean Age: 65.8 yrs Another 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.

Singh N et al. The effects of the type of anesthesia on outcomes of lower extremity infrainguinal bypass J Vasc Surg 44: , November 2006 Type of anesthesia affected graft failure Compared to SA and EA, GETA associated with: More graft failure at 30 days More cardiac events (MI, C Arrest), More postoperative pneumonia No difference between SA and EA regarding graft failure and cardiac events GETA is not the best strategy Another 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.

My Preference: BOTH Epidural 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 fentanyl Postop: Ropivacaine 0.2% + Fentanyl 2μg/ml Major abdominal surgery: EA+GA I avoid Pancuronium. Volatile: MAC HR will be stable No need for intra or postop IV opioids Early recovery, Easy extubation SEVO

Postoperative Management:
First 3 postoperative days: Period of greatest risk of cardiac complications Hypercoagulability, Increased adrenergic stress Management focused on factors increasing risk of cardiac complications: Tachycardia Anemia Hypothermia, shivering Hypertension Hypoxemia Inadequate analgesia First three days associated with highest incidence of complications

Most postoperative ischemia is silent: Most MIs preceded by prolonged ST depression Early detection and aggressive management MAY prevent progression to MI Detective strategy:(Silent) ST-segment Monitoring: automated, continuous 12 Lead ECG q. 8 hrs in day1, then daily for day 2, 3 Serial Enzymes: Cardiac Troponins (TnT, TnI)

Cardiac Troponins (TnT, TnI) More specific than CK-MB More prognostic value, Suggest treatment strategy Unstable Angina: some have small rise TnT<0.1 ng/ml, increased M&M, respond to LMWH, Gp IIb-IIIa blockers Time to rise Peak rise Normalized CK-MB 3-5 hrs 10-18 hrs 2-3 days Gold standard Not Prognostic low specificity TnT 3.8 hrs 18 hrs, 3ds 5-14 days High sensetivity & specificity, Prognostic TnI 3-12 hrs 24 hrs 5-10 days not affected by CRF, slow rise TnT affected by renal failure

Postoperative Management: Cardiac complications
Treatment based on extrapolation from non-operative setting, AHA/ACC guidelines: Transmural Q-wave MI Non Q-wave MI (NQWMI) Unstable Angina

Postoperative Management: Transmural Q-wave MI
Goal: quickly reopen occluded vessel Aspirin: early Thrombolytics contraindicated post surgery?? If Lytics CI: consider Cath/Stent β-Blockers: aggressive block NTG: only for ongoing ischemia ACE Inhibitors: improve LV remodelling Heparin: when lytics CI Magnesium: good, Statins: evolving evidence LMWH, Gp IIb/IIIa blockers: no evidence

Postoperative Management: Non Q-wave MI (NQWMI)
Majority of perioperative MI Higher Morbidity, equal Mortality to QWMI Cardiac status closer to Unstable Angina Diagnosis: Cardiac Enzymes β-Blockers & Aspirin for all NQWMI NTG: only for ongoing ischemia Heparin: 48 hours, improves outcome LMWH: used instead, caution, no reversal Gp IIb/IIIa blockers ?? Used in non-operative

Postoperative Management: Unstable Angina
Goal: prevent progression to MI, death β-Blockers & Aspirin: dec MI, Mortality NTG: only for ongoing ischemia, nitrate tolerance develops in hrs continuous administration Heparin: 48 hours, improves outcome Angio / stent?? Troponin Positive Unstable Angina (Minor Myocardial Injury): LMWH & Gp IIb/IIIa blockers: Abciximab, Agrastat TnT affected by renal failure

Epilogue: CAD patients are high risk patients
Optimum strategy is multimodal: Improved preoperative assessment Sympatholytic pharmacologic optimization Intraoperative management based on physiologic goals & scientific evidence Postoperative Monitoring: “detective” Postoperative MI, U Angina: inc M & M: β-Blockers & Aspirin, selective use of invasive procedures

Detectives Detectives

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