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ECG T-WAVE CHANGES IN THE PACU BAD OR BENIGN

More BAD puns. Shotgun wedding: a case of wife or death.When two egotists meet, it is an I for and I.Every calendar's days are numbered.A chicken crossing the road is poultry in motion.Acupuncture is a jab well done.. OVERVIEW. Discuss perioperative myocardial infarctionDescribe common event in PACUDiscuss possible mechanismsMyocardial ischemia vs infarctionMyocardial stunningMyocardial reperfusionOther causes of anterior wall motion abnormalityDiscuss how to react to T-wave inversion9449

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ECG T-WAVE CHANGES IN THE PACU BAD OR BENIGN

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    1. ECG T-WAVE CHANGES IN THE PACU – BAD OR BENIGN? Raymond C. Roy, Ph.D., M.D. Professor & Chair of Anesthesiology Wake Forest University Baptist Medical Center Winston-Salem, North Carolina 27157-1009 rroy@wfubmc.edu

    3. OVERVIEW Discuss perioperative myocardial infarction Describe common event in PACU Discuss possible mechanisms Myocardial ischemia vs infarction Myocardial stunning Myocardial reperfusion Other causes of anterior wall motion abnormality Discuss how to react to T-wave inversion

    4. WHAT IS THE INCIDENCE AND TIMING OF PERIOPERATIVE MYOCARDIAL INFARCTIONS? “Since the 1970’s the timing and character of perioperative myocardial infarction has shifted from a predominance of Q-wave myocardial infarction peaking between postoperative days 2 and 3 with a high mortality (25-50%) to earlier-occurring non-Q-wave myocardial infarction with a lower mortality” London, Zaugg, Schaub, Spahn. Perioperative ?-adrenergic receptor blockade. Anesthesiology 2004; 100:170.

    5. Timing of Perioperative MI in Non-cardiac Surgery Patients (18/323) Badner. Anesthesiology 1998; 88:561

    6. DIAGNOSING MYOCARDIAL INFARCTION – WHAT IS THE “GOLD STANDARD”? Myocardial infarction redefined – a consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. Eur Heart J 2000; 21:1502. Cardiac troponin I Cardiac troponin T “…absolute specificity of cardiac troponins for myocardial tissue and their high sensitivity for even microscopic zones of myocardial necrosis”

    7. DIAGNOSING MYOCARDIAL INFARCTIONS Decreasing order of sensitivity & specificity 1. Cardiac troponins – new standard 2. CK-MB 3. ECG – old standard

    8. CARDIAC TROPONINS VS CK-MB Cardiac troponins I or T Microinfarctions can produce elevations in cardiac troponins in blood that are not associated with elevations of the CK-MB Silent infarctions Non-ST elevation infarctions Non-Q-wave infarctions MB fraction of creatine kinase (CK-MB) ST elevation infarctions Q-wave infarctions

    9. DEATH BY 42 DAYS (%) VS TROPONIN I RELEASE IN PATIENTS WITHOUT ST ELEVATIONS

    10. WHEN DO PERIOPERATIVE MYOCARDIAL INFARCTIONS OCCUR? Zaugg. Anesthesiology 1999; 91:1674 Atenolol vs no atenolol during major non-cardiac surgery in patient with CAD 9/40 receiving atenolol – elevated troponin I 8/19 not receiving atenolol – elevated troponin I troponin I appeared during surgery # patients affected decreased with atenolol

    11. FREQUENCY OF NEW T-WAVE OBSERVED IN THE PACU Ashton. J Am Geriatr Soc 1991; 39: 575 21% of 206 TURP patients No S/S of myocardial ischemia No elevations of CK-MB IS THIS A SIGN OF A NON-Q-WAVE, NON-ST SEGMENT ELEVATION MYOCARDIAL INFARCTION?

    12. DOES T-WAVE INVERSION MEAN MYOCARDIAL ISCHEMIA? Renkin. Reversal of segmental hypokinesis by coronary angioplasty in patients with unstable angina, persistent T-wave inversions, and left anterior descending coronary artery stenosis. Circulation 1990;82:913. 62 patients with unstable angina 32 – negative T-waves, 30 normal positive T-waves Both groups had LAD lesions PTCA to LAD

    13. MYOCARDIAL INFARCTION VS MYOCARDIAL ISCHEMIA ISCHEMIA OXYEN: DEMAND > SUPPLY – primary mechanism STABLE ATHEROSCLEROTIC PLAQUE ASYMPTOMATIC <-> STABLE ANGINA INFARCTION OCCLUDING THROMBUS – primary mechanism RUPTURE OF UNSTABLE PLAQUE ACUTE CORONARY SYNDROMES

    14. MYOCARDIAL ISCHEMIA Inadequate CBF Short diastole (tachycardia) High LVEDP (hypertension, AS) LVH (subendocardial ischemia) Low CPP (diastolic BP < 60 mmHg) Reduced luminal diameter Atherosclerotic plaque Coronary artery spasm Non-occluding thrombus

    15. DOES PROLONGED MYOCARDIAL ISCHEMIA LEAD TO INFARCTION? Poldermans Elevated cardiac troponin levels have been detected after prolonged myocardial ischemia in patients with coronary artery disease, without angina, and without ECG changes, resulting in a two-fold increase in all-cause mortality Kertal, Bax, Klein, Poldermans. Is there any reason to withhold ?-blockers from high risk patients with coronary artery disease. Anesthesiology 2004;100:4-7.

    16. MYOCARDIAL INFARCTION UNSTABLE CORONARY ARTERY PLAQUE PLAQUE RUPTURE THROMBUS FORMATION CORONARY ARTERY OCCLUSION

    17. UNSTABLE CORONARY ARTERY PLAQUE Thin fibrous cap Vulnerable to rupture Prone to develop fissures (leaks) Lipid core >40% plaque volume Extremely thrombogenic Vasa vasorum (microvessels) Base of plaque

    18. MECHANISM OF UNSTABLE CORONARY ARTERY PLAQUE RUPTURE Loss of integrity of thin fibrous cap Mechanical – sheer forces Vasa vasorum rupture Hemorrhage into plaque Sudden increase in plaque size and intraplaque pressure Exposure of lipid core to blood in coronary artery lumen Thrombus formation

    19. New Diagnostic Test? Ischemic Heart Disease Troponins - current markers for necrosis CD40 ligand - marker for platelet-monocyte aggregation as thrombus is being formed Heeschen. N Engl J Med 2003; 348:1104

    20. SURGERY, ANESTHESIA, & PERIOPERATIVE MYOCARDIAL INFARCTIONS SURGICAL STRESS –> HYPERCOAGUABLE STATE SURGICAL STRESS, SWINGS IN BP & HR INCREASE SHEER FORCES ON PLAQUES INCREASES IN CONTRACTILITY & HR INCREASE ISCHEMIA IN VASA VASORUM AND INCREASE LIKELIHOOD OF RUPTURE PATIENTS EITHER TOO SEDATED OR HAVE SUFFICIENT ANALGESIA TO BE UNAWARE OF CHEST PAIN.

    21. Perioperative Beta-Blockade - Therapeutic Target Auerbach. JAMA 2002; 287:1435 HEART RATE 55 – 65 bpm SYSTOLIC >100 mm Hg Before, during, and after surgery

    22. ??-BLOCKERS – BEST SUBGROUP IS THE ONE IN WHICH PATIENTS ARE TAKING STATINS FEWER PLAQUE RUPTURES ANTI-INFLAMMATORY EFFECT OF STATINS STATINS ACTUALLY HELP DISSOLVE LIPID CORE AND SHRINK PLAQUE SIZE.

    23. T-WAVE INVERSION RELATED TO REPERFUSION? Nakajima. Cardiology 1996;87:91-7 inverted T-waves within 3 days of acute MI in patients in whom myocardial reperfusion was accomplished Deeper T, less hypokinesis lower CK-MB COULD THIS MEAN T-WAVE INVERSION OCCURS BECAUSE OF A NATURAL REPERFUSION (CLOT DISSOLVES OR COLLATERAL FLOW ESTABLISHED)?

    24. T-WAVE INVERSION & REPERFUSION? Hirota. Prominent negative T waves with QT prolongation indicate reperfusion injury and myocardial stunning [after an ischemic episode]. J Cardiol 1992;22:325

    25. T-WAVE INVERSION RELATED TO TRANSIENT CHF? Littman. J Am Col Cardiol 1999;34:1106 Patients without CAD,large T-wave inversions with pulmonary edema Valvular disease (3), dilated cardiomyopathy (2), acute volume overload (1), hypertension (1), CRF (1), eclampsia Lind. Eur J Clin Invest 1995; 25:955 Increased T-wave abnormalities seen with increased heart enlargement on chest X-ray

    26. Another New Diagnostic Test? Congestive Heart Failure A-type natriuretic peptide - secreted by atria in response to chamber dilation B-type natriuretic peptide - secreted by ventricles in response to increased end-diastolic pressure and volume expansion Maisel. N Engl J Med 2002; 347:163

    27. B-type Natriuretic Peptide Plasma Levels Maisel. N Engl J Med 2002; 347:163

    28. FREQUENCY OF NEW T-WAVE OBSERVED IN THE PACU -1 Ashton. J Am Geriatr Soc 1991; 39: 575 21% of 206 TURP patients had new T wave inversion in PACU No S/S of myocardial ischemia No elevations of CK-MB 1/43 had cardiac event within 1 yr [Only perioperative MI occurred in 1 with no ECG changes (but elevated CK-MB)]

    29. Frequency of New T-wave Changes in the PACU - 2 Breslow. Anesthesiology 1986; 64: 398 18% of 394 consecutive patients Young & old, regional & general 46 – flattening; 25 - inversion No S/S of myocardial ischemia

    30. CORONARY ANGIOGRAMS IN PATIENTS WITH DEEP T-WAVE INVERSIONS Sharkey. Chest 1998; 114:98. 22 acutely ill, non-cardiac cause CNS injury (6), acute pulmonary disease (3), sepsis (3), drug OD/metabolic abnormalities (7), post noncardiac surgery (3) ECHOCARDIOGRAM – anterior wall motion abnormal CORONARY ANGIOGRAPM – 1/22 had lesion in LAD

    31. CORONARY ANGIOGRAMS IN PATIENTS WITH DEEP T-WAVE INVERSIONS Okada. J Am Col Cardiol 1994; 24:739 Isolated T-wave changes 63 with chest pain 3 Hypertrophic cardiomyopathy, 63 CAD, 19 normal, 2 pericarditis 23 asymptomatic – 3 HCM, 20 normal Transient causes Hypokalemia, anxiety, fear, food intake, hyperventilation, coronary vasospasm, early HCM

    32. Significance of New T-wave Changes in PACU Most often – benign and transient Occurs in patients without IHD (CAD) Look for Pulmonary edema Congestive heart failure Hypertrophic cardiomyopathy (past ECHO)

    33. Significance of New T-wave Changes in PACU Young – little chance of CAD Observe Elderly – non-textbook signs and symptoms of myocardial ischemia No workup if no other “soft” signs Oriented with no pain Vital signs stable 12 lead ECG – isolated T-wave inversion or no change Lungs clear

    34. Significance of New T-wave Changes in PACU Aggressive workup if any change in rhythm or hemodynamics 12-lead ECG Cardiac enzymes (troponins, CK) Newer diagnostic tests (CD40, B type natriuretic peptide) Surface echocardiogram vs TEE Chest x-ray Cardiology consult - ?reperfusion therapy

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