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

More BAD puns

Shotgun wedding: a case of wife or death. When two egotists meet, it is an I for and I. Every calendars days are numbered. A chicken crossing the road is poultry in motion. Acupuncture is a jab well done.

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

WHAT IS THE INCIDENCE AND TIMING OF PERIOPERATIVE MYOCARDIAL INFARCTIONS?

Since the 1970s 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 (2550%) to earlier-occurring non-Q-wave myocardial infarction with a lower mortality London, Zaugg, Schaub, Spahn. Perioperative adrenergic receptor blockade. Anesthesiology 2004; 100:170.

Timing of Perioperative MI in Noncardiac Surgery Patients (18/323)

Badner. Anesthesiology 1998; 88:561
8 7 6 5 4 3 2 1 0

Myocardial Infarction

Day of Surgery

Postop Day 2

Postop Day 4

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

DIAGNOSING MYOCARDIAL INFARCTIONS

Decreasing order of sensitivity & specificity
1. Cardiac troponins new standard 2. CK-MB 3. ECG old standard

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

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

8 7 6 5 4 3 2 1 0 0-<0.4 0.4<1.0 1.0<2.0 2.0<5.0 5.0<9.0 >9.0 Cardiac Troponin I

WHEN DO PERIOPERATIVE MYOCARDIAL INFARCTIONS OCCUR? Zaugg. Anesthesiology 1999; 91:1674

Atenolol vs no atenolol during major noncardiac 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

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?

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

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

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

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.

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

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

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

New Diagnostic Test?

Ischemic Heart Disease
Troponins - current markers for necrosis

CD40 ligand - marker for plateletmonocyte aggregation as thrombus is being formed

Heeschen. N Engl J Med 2003; 348:1104

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.

Perioperative Beta-Blockade - Therapeutic Target

Auerbach. JAMA 2002; 287:1435
HEART RATE 55 65 bpm SYSTOLIC >100 mm Hg Before, during, and after surgery

-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.

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)?

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

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

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 enddiastolic pressure and volume expansion
Maisel. N Engl J Med 2002; 347:163

B-type Natriuretic Peptide Plasma Levels

Maisel. N Engl J Med 2002; 347:163
700 600 500 400 300 200 100 0 Normal SOB, nl Diastole cardiac Dysfn CHF B-type Natriuretic Peptide Plasma Levels pg/ml

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)]

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

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

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

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)

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

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