Periop mi final

DIAGNOSIS OF PERI-OPERATIVE MYOCARDIAL INFARCTION

DR.SANDEEP

NMCH, NELLORE

INTRODUCTION

Peri-operative myocardial ischemia (PMI) is the single most cardiac risk factor for an adverse cardiac outcome after non- cardiac surgery.

More than half of postoperative deaths are caused by cardiac events most of which are ischemic.

Identification of vulnerable patients and prevention of a PMI is essential to improve the postoperative outcome.

PERIOPERATIVE MYOCARDIAL ISCHEMIA (PMI)

Traditional Definition of MI includes

1. Patient symptoms2. ECG changes3. Cardiac enzymes

This definition does not hold good under anaesthesia because

1. No symptoms- Deep sedation or Analgesic cover2. Subtle ECG changes3. CK-MB has limited sensitivity (Sk. Muscle injury)

The ACC criteria for PMI includes

1. Typical rise and gradual fall in Cardiac Troponin concentration or

Rapid rise and fall of CK-MB along with typical ischemic symptoms / pathological q waves in ECG / ST segment depression or elevation in ECG / coronary artery intervention.

2. Pathological findings of acute MI

PATHOPHYSIOLOGY

1. Acute Coronary Syndrome {Type I PMI}.

2. Myocardial Oxygen - Supply demand imbalance {Type II PMI}.

Acute Coronary Syndrome {Type I PMI} Plaque rupture can be spontaneous / due to

external stresses. Spont. ACS:-

Intraplaque inflammation Plaque irritability Spont. rupture /fissure / erosion Acute coronary thrombosis / Ischaemia / Infarction.

External stresses:-a) Physiological or emotional stress sympathetic

induced hemodynamic changes, coronary vasospasm, prothrombotic factor release plaque disruption.{increased cathecholamines}

b) Tachycardia and Hypertension:- Shear stress inward (positive)

remodeling or Circumferential Tensile stress outward (negative) remodeling.

c) Increased Peri-op Procoagulant Factors:-

increased- fibrinogen, factor VIII, vWF, ATincreased platelet reactivity

decreased- protein C, AT-III, alpha 2 macroglobulin decreased fibrinolysis post op immobilisation (venous stasis)

OXYGEN SUPPLY DEMAND IMBALANCE

DECREASED OXYGEN DELIVERY

INCREASED OXYGEN REQUIREMENT

Decreased CBF Tachycardia Diastolic hypotension Hypocapnia Coronary artery spasm Decreased oxygen

content Anemia Arterial hypoxemia Shift of ODC to left

Sympathetic nervous system stimulation

Tachycardia Hypertension Increased myocardial

contractility Increased afterload Increased preload

Generally, the diagnosis can be based on:-

1. Electrocardiographic (ECG)

2. Haemodynamic (pulmonary artery capillary wedge and/or left atrial pressure wave)

3. Functional (echocardiogram : Segmental Wall Motion abnormalities, Mitral regurgitation, etc)

4. Metabolic (coronary lactate production)

5. Biochemical (release of creatine kinase-MB isoenzyme and/or troponin) or

6. Reperfusion (scintigram) parameters.

Early recognition of PMI can enable us to prevent morbidity and mortality by employing appropriate pharmacological interventions.

Apart from history and examination, various criteria to establish the diagnosis of PMI include Electrocardiography (ECG), Exercise Stress Testing,

Serum Cardiac Markers, Echocardiography, Nuclear Imaging techniques, Cardiac Computed Tomography (CT), and Magnetic Resonance Imaging (MRI).

PRE-OPERATIVE ASSESSMENT OF PATIENTS

HISTORY:- Elicit the severity, progression, and functional

limitations imposed by IHD.

Focus on determining the presence of major, moderate and minor clinical risk factors in a particular patient.

Symptoms such as angina and dyspnoea may be absent at rest, emphasizing the importance of evaluating the patient's response to various physical activities such as walking or climbing stairs.

Limited exercise tolerance in the absence of significant lung disease is very good evidence of decreased cardiac reserve

Previous Myocardial Infarction

Co-Existing Noncardiac Diseases

Current Medications

ELECTROCARDIOGRAPHY {ECG}

25 to 50% of patients with CAD will have normal resting ECG.

In 25% of patients ECG is not diagnositc (LBBB/WPW).

Still, ECG is the most important preoperative test for patients with IHD.

ELECTROCARDIOGRAPHY {ECG} Ischemic Manifestations:

i) ST SEGMENT CHANGES (most specific)

ii) T wave changes (flattening or inversion in high risk groups)

iii) Dysrhythmias

iv) New conduction abnormalities

v) New atrio-ventricular block

vi) Heart rate changes

ST segment criteria for ischemia Patients with LVH, LBBB, digitalis effect,

ventricular pacing and those not in sinus rhythm are not suitable for ECG-derived diagnosis of MI.

ST Depression: subendocardial ischemia, poor localization1. Horizontal / downsloping depression > 0.1 mV (1

mm) at 60-80 msec after J point2. Upsloping depression > 0.15 mV at 80 msec after

J point

ST Elevation: transmural ischaemia, good localization

> 0.1 mV (>0.2 mV in Men & > 0.15 mV in Women) at 60-80 msec after J point.

Other causes for ST segment elevation are:-

1. Conduction disturbances2. R wave amplitude changes 3. Autonomic Nervous System changes4. Hyperventilation 5. Myocardial contusion

6. Electrolyte changes, hypoglycaemia

7. Neurological (trauma, SAH)

8. Hypothermia

9. Acute pericarditis

10. Body position changes/ retractors

Sensitivity of different ECG lead combinations

No. of leads Combination Sensitivity (%)

1 lead II, V4, V5

336175

2 leads II /V5V4/V5

8090

3 leads V3,V4,V5II,V4,V5

9496

4 leads II, V2-5 100

EXERCISE STRESS TESTING

EXERCISE STRESS TESTING Exercise induced ischemia usually occurs in

coronary arteries that are moderately or severely obstructed (> 75% of the cross sectional area), or in those that develop vasospasm.

Patients with moderate CAD typically exercise to lower stages before termination of the test because of symptoms or heart rate limitation.

During exercise, and in the recovery period, the principal indicator of myocardial ischemia is ST segment deviation.

A criterion of 2 mm deflection has been conventionally accepted.

ST depression of 1-3 mm is associated with 67% probability of one to three vessel disease.

Changes of 2 mm or more, occurring during stage 1 and 2, are associated with 90% probability of one to three vessel disease.

The occurrence of early ST changes is associated with poor prognosis.

Limitation:- Negative tests do not imply lack of disease.

SERUM BIOCHEMICAL MARKERS Serum biomarkers that are indicative of

myocardial damage include

Myoglobin (4 Hrs)

Total Ck(16hrs)

CK-MB Isoenzyme (24 Hrs)

Troponin I And T (24 Hrs)

Lactate Dehydrogenase (76 hrs).

New markers of perioperative cardiac injury include :-

Brain Natriuretic Peptide (BNP)

Soluble CD40 Ligand, And

High Sensitive C-reactive Protein.

ECHOCARDIOGRAPHY Acute MI results in Abnormal Inward Motion and

Thickening of the affected myocardial region.

Regional Wall Motion Abnormalities (RWMA) occur within seconds of inadequate blood flow or oxygen supply.

Abnormalities in Diastolic Function usually precede abnormal changes in systolic function.

Diastolic ventricular function can be assessed by monitoring the Rate Of Filling associated with changes in chamber dimensions.

Regional systolic function can be estimated by

determination of wall thickening and wall motion

during systole in both long and short-axis views of

the ventricle.

The short axis view of the left ventricle at the

papillary muscle level displays myocardium

perfused by three main coronary arteries, and is,

therefore, very useful.

RWMA can be assessed by inward movement of endocardium toward the centre of the cavity during systole.

As the myocardial oxygen supply / demand balance

worsens, RWMAs progress from mild hypokinesia to severe hypokinesia, akinesia, and finally dyskinesia.

Normal contraction is defined as > 30% shortening of the radius from centre to endocardial border.

Mild hypokinesia refers to radial shortening of 10-30%, and severe hypokinesia is defined as < 10% radial shortening

RWMAs are more sensitive than ECG or PA catheter

Limitation of RWMA analysis:-

It does not differentiate stunned or hibernating myocardium from acute ischemia.

It does not differentiate the cause of ischemia between increased oxygen demand and decreased oxygen supply.

TRANSESOPHAGEAL ECHO (TEE)

The most obvious limitation of TEE monitoring is that ischemia cannot be detected during critical periods such as induction, laryngoscopy, intubation, emergence, and extubation.

Dobutamine Stress Echocardiography (DSE) DSE involves the identification of new or worsening

RWMAs using 2D Echo during infusion of intravenous dobutamine.

Advantages of DSE as compared to dipyridamole thallium are: DSE can also assess LV function and valvular abnormalities, Low cost No radiation exposure Shorter duration of study , and Immediate results.

The sensitivity and specificity of DSE for CAD is 89 and 85% respectively.

DIPYRIDAMOLE THALLIUM SCINTIGRAPHY

Dipyridamole works by blocking adenosine receptors and increasing adenosine concentration in the coronary vessels.

Adenosine is a direct coronary vasodilator.

After infusion of the vasodilator, flow is preferentially distributed to area distal to normal coronary arteries, with minimal flow to areas distal to a coronary stenosis.

A radioisotope such as thallium or 99-technetium sestamibi is then injected.

Normal myocardium will show up on initial imaging, while areas of either myocardial necrosis or ischemia distal to a significant coronary stenosis will demonstrate a defect.

After a delay of several hours, or after infusion of second dose of 99-technetium, the myocardium is again imaged.

Those initial defects that remain as defects are consistent with old scars, while those defects that demonstrate normal activity on subsequent imaging are consistent with areas at risk of MI.

Patients at high risk of MI will show increased lung uptake, left ventricular dilatation, increased end-systolic and end-diastolic volumes, stress induced ischemia, and multiple perfusion defects.

Thallium imaging has sensitivity and specificity of around 90% for detection of acute infarct, provides information regarding viability and has prognostic value.

Computed Tomography and Magnetic Resonance Imaging

High-speed CT can visualize coronary artery calcification.

Intravenous administration of radiographic contrast medium enhances the clarity of the images.

MRI provides even greater image clarity and can delineate the proximal portions of the coronary arterial circulation.

However, CT and MRI are more expensive and less mobile than other modalities of cardiac evaluation.

Radionuclide Ventriculography

Radionuclide ventriculography quantitates left and right ventricular systolic and diastolic function.

The EF determined by this method does not provide information that can be used to accurately predict PMI, but an EF of less than 50% does predict an increased risk of postoperative CHF in patients undergoing abdominal aortic surgery.

TREATMENT OF PMI

1. Prevention of myocardial ischaemia:

Attention to prevention of tachycardia (judicious beta blockers) during anaesthesia is extremely important.

Maintenance of adequate depth of anaesthesia Attenuation of pressor responses to laryngoscopy and

endotracheal intubation. If an anaesthetized patient has normal ST segment

and then develops tachycardia followed by ST depression, one should assume tachycardia as the cause of ischaemia, (reduce the heart rate).

If hypovolemic hypotension precedes the onset of ST depression, manage with volume.

2. Treatment of myocardial ischaemia without accompanying haemodynamic disturbances:

In these patients nitroglycerine (sublingual or intranasal) can be useful.

Nitroglycerine decreases preload and wall tension, dilates epicardial coronary arteries increasing the sub-endocardial blood flow

3. Myocardial ischaemia associated with tachycardia and hypertension:

Treat common causes of tachycardia Beta-blockade (aim for HR < 60 bpm) I.V. Esmolol 0.25 - 0.5 mg/kg bolus, 25 - 300

mcg/kg/min infusion Metoprolol 0.5 – 1mg titrated bolus over 15

minutes If beta-blockade is contra-indicated Verapamil 2.5 mg - repeat as needed. Infuse at 1-

10mg/hr [may be first choice if ST segment elevation (coronary spasm)]

Alpha-2 agonists : Clonidine, Dexmedetomidine, Mivazerol

Hypertension

1. Initially treat common causes e.g. light anaesthetic

depth, CO2 retention,

2. GTN – sublingual (0.3-0.9 mg works within 3 min)

3. IV NTG infusion (0.25 - 4 mcg/kg/min titrate to effect)

4. Clonidine (30 mcg every 5 minutes up to 300 mcg)

5. Dexmedetomidine (1mcg/kg load, infuse at 0.2-0.7

mcg/kg/hr)

4. Myocardial ischaemia associated with tachycardia and hypotension:-

Treat cause e.g. hypovolemia (300-500ml of crystalloid)

Reduce anaesthetic depth

Adjust PEEP

Check surgical manipulation (retractors pressing IVC during laparotomy)

Vasopressors are preferred (Metaraminol, Phenylephrine) to increase coronary perfusion pressure

Reduce the heart rate.

5. If ischaemia persists with optimal haemodynamics :-(Persistent MI)

Keep increasing GTN

Combine with vasopressor if there is hypotension

Increase monitoring CVP, PCWP, TEE

Alter surgical plan

6. Severe resistant Myocardial Ischemia:

CONSIDER Acute Coronary Syndrome (unstable angina, myocardial infarct)

Aspirin (Oral / Ryles tube : 325 mg)

Heparin (I.V. 5000 Units bolus, then 1000 U/hr) if surgery

permits

Continue beta-blockade if no signs of CCF

Aspirin & beta-blockade reduce risk of infarct and mortality

Watch for complications- dysrhythmias, CCF, myocardial

infarction

Obtain Cardiology consultation

Intra Aortic Balloon Counterpulsations (IABP )

PTCA

Thrombolysis is generally contraindicated

POSTOPERATIVE MANAGEMENT OF PMI

ICU or CCU postop and/or Cardiology referral

Watch for perioperative Myocardial Infarction

ECG immediately postop and on day 1 and 2

Cardiac troponin at 24 hrs and day 4 (or hosp

discharge) (CK-MB of limited use)

PTCA if needed

LONG TERM risk factor management

Aspirin, Statins, Beta-blockade, ACE inhibitors

TO CONCLUDE:-TREATMENT OF PMI:

100% Oxygen, stop volatile anaesthetics Increase monitoring : Arterial

line,CVP/PCWP/TEE Oral/Ryle’s tube :Aspirin 325 mg NTG Morphine : Analgesia and also effective in

patients with pulmonary vascular congestion complicating ACS.

Hypotension : Volume (300-500ml of crystalloid) Inotropes, vasopressors. Heparin IABP

Thrombolysis :- Should be done within 4 hrs (maximum 12 Hrs) with t-PA

or streptokinase. The major limitation is bleeding so it is contraindicated

in patients with fresh surgical wounds.

Beta blockers : Contraindications are CCF or large anterior wall MI with EF <40%)

Antithrombotics and antiplatelet drugs can be started.

Antiarrhythmic agents, Beta blockers Emergency cath lab & Percutaneous Coronary

Intervention.

References :

1. Miller’s Anesthesia

2. Stoeltings coexisting diseases

3. Perioperative Myocardial Ischemia and

Infarction- a Review. IJA 2007: 51(4) :287-302

4. Internet

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