-Myocardial Infar

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    Presentation onPresentation on

    myocardial infarctionmyocardial infarction

    ByBy-- Dr.Vinay VatsayanDr.Vinay Vatsayan

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    Presenting Symptoms of Acute

    MI Pain-

    *typical-crushing substernal chest pain

    *atypical - jaw, neck, shoulder, back pain,

    indigestion*painless - silent

    Dyspnea-

    systolic and/or diastolic dysfunction

    Dizziness-hypotension, arrhythmia

    Nausea, vomiting

    Elderly patients: Failure to thrive

    Anxiety, restlessness, sense of impending doom

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    Presenting Signs in Acute MI

    Appearance: Pallor, diaphoretic, anxious

    Vital Signs: Normal or abnormal BP and P

    Hypertension and tachycardia: SNS

    Hypotension and tachycardia:

    Cardiogenic shock

    Myocardial rupture

    Tachyarrhythmia

    Hypotension and bradycardia

    vagal stimulation

    Bradyarhythmia

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    Presenting Signs in Acute MI

    (Cont.)

    Lungs: Rales - CHF

    Heart: Displaced LV impulse

    S3

    S4

    Murmur of mitral regurgitation

    Murmur of ventricular septal

    rupture

    Pericardial rub

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    Evolution of ECG changes in acute MI

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    Cardiac enzymes

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    Natural History of Acute

    Myocardial Infarction Death-

    Arrhythmia: VT/VF

    Asystole Myocardial rupture

    Cardiogenic shock

    ChronicHeart Disease -

    LV dysfunction - remodeling

    Papillary muscle dysfunction: MR

    RV dysfunction

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    Natural History of Acute

    Myocardial Infarction, (Cont.)

    Stabilizationpcompensated LV

    dysfunction Post-infarction angina/ischemia

    (spontaneous or induced)

    Recurrent MI Post-infarction ventricular

    tachycardia

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    Treatment of Acute Myocardial

    Infarction: Acute Phase Prevent/resuscitate from sudden

    death: monitor, admit to CCU

    Re-establish coronary flow

    Thrombolytic therapy

    Primary infarct angioplasty/stent

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    Major Contraindications To the Use of

    Thrombolytic Therapy

    Any previous history of hemorrhagic stroke

    History of stroke, dementia, or central nervous system

    damage within 1 year

    Head trauma or brain surgery within 6 months Known intracranial neoplasm

    Suspected aortic dissection

    Internal bleeding within 6 weeks

    Active bleeding or known bleeding disorder

    Major surgery, trauma, or bleeding within 6 weeks

    Traumatic cardiopulmonary resuscitation within 3

    weeks

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    Treatment of acute MI:

    acute phase (cont.) Decrease myocardial oxygen demand

    Pain relief/anxiolytics (Morphine sulfate)

    SlowH

    R, control BP (beta blockers) Increase myocardial oxygen supply

    Oxygen

    Prevent platelet aggregation/coronarythrombus (aspirin, IIbIIIa inhibitors,

    clopidigrel/heparin) Prevent spasm (nitrates)

    Augment collateral flow (nitrates)

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    Treatment of Acute Myocardial

    Infarction: Acute Phase (C

    ont.)

    Stabilize plaques, restore endothelialfunction

    ?HMGCoA reductase inhibitors (statins)

    Prevent ventricular remodeling

    ACE inhibitors

    Prevent mural thrombus/embolization

    Heparin

    Coumadin for patients at high risk forthrombus (anterior wall akinesis).

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    Treatment of Acute Myocardial

    Infarction - Intermediate Phase Monitor/treat arrhythmias

    Monitor/treat heart failure: systolic,

    diastolic, MR

    Monitor/treat recurrent ischemia/infarction

    Watch for pericarditis, Dresslers Syndrome

    Monitor for myocardial rupture (free wall,VSD, MR)

    Monitor for stroke

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    Determinants or Prognosis

    after Acute MI

    LV function (ejection fraction)

    Inducible ischemia/coronary anatomy Arrhythmia potential

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    Tests for LV function

    Echocardiogram

    Radionuclide ventriculogram(MUGA)

    Contrast left ventriculogram (cath)

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    Echocardiogram in Acute

    Myocardial Infarction

    Wall motion abnormalities

    Ejection fraction

    Thrombus

    Right ventricular MI

    Papillary muscle dysfunction- mitral

    regurgitation

    Free wall rupture/ventricular septal

    defect/papillary muscle rupture

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    Test for Inducible ischemia:

    Stress Test 1. Positive: Ischemic ST segment

    depression - u1mm horizontal or

    downsloping ST depression

    2. Negative: Patient reaches 85%

    maximum predicted heart rate (MPHR)

    without #1

    3. Nondiagnostic: No ischemia but patient

    fails to reach 85% MPHR

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    Test to Define Coronary

    Anatomy: Coronary

    Angiogram

    Controversy: Should all patients

    undergo coronary angiogram after anMI?

    Definite indications for coronary

    angiogram after MI:

    Recurrent chest pain

    Positive stress test

    High risk features: CHF, low EF, prior MI

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    Risks ofCoronary

    Angiography: (all are rare)

    Stroke

    Myocardial infarction Arrhythmia

    Renal failure

    Allergic reaction to contrast agent

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    Tests to Determine Arrhythmia

    Risk:

    Monitoring throughout

    hospitalization Stress test

    Electrophysiologic testing

    Controversy: Who should undergo EPstudy after MI?

    Sustained VT

    Nonsustained VT with depressed ejection

    fraction

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    Treatment of Acute Myocardial Infarction

    Late Phase (Post-Hospital)

    Risk factor reduction:

    Smoking

    Hypertension

    Diabetes

    Dyslipidemia

    Obesity/sedentary life style

    Hyperhomocysteinemia

    Stress/depression

    Monitor for recurrent ischemia

    Monitor for LV remodeling/CHF

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    ABCs of Treatment and

    Secondary Prevention of AMI Aspirin-prophylactic Rx for recurrent ischemic events;

    give for at least 3 mo. after AMI, probably indefinitely

    Beta blockers-prophylactic, for reduction of cardiac

    mortality; Rx for 2 yr-indefinitely

    Converting enzyme inhibitors-all pts with LV

    dysfunction to reduce risk of progressive heart failure

    and death.

    Diet and lipid lowering Rx-statins have been shown

    to reduce risk of subsequent MI, need for

    revascularization and mortality (4S, Care)

    Exercise and rehabilitation-essential in restoration of

    confidence and improvement in quality of life

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    Creatine Phosphokinase (CK)

    Rises within 4-8 hours, rapidly cleared by 24-24 hours

    Other Sources:

    Skeletal

    Hypothyroidism Renal failure

    Stroke

    Isoenzymes

    MM skeletal muscle

    BB brain

    MB cardiac

    CKMBu 4% suggests acute myocardial infarction+++

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    Cardiac Specific Troponins

    (cTnT, cTnI)

    Rise within 4-8 hours, remain elevated7-14 days (T>I)

    30% of patients with UAP show o

    levels cTnT or I, indicating increased

    risk of adverse outcome

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    Relative Contraindications To the Use of

    Thrombolytic Therapy

    Oral anticoagulant therapy

    Acute pancreatitis

    Pregnancy or within 1 week postpartum

    Active peptic ulceration

    Transient ischemic attack within 6 months

    Dementia

    Infective endocarditis

    Active cavitating pulmonary tuberculosis

    Advanced liver disease

    Intracardiac thrombi

    Uncontrolled hypertension (systolic blood Pressure >180 mm Hg, diastolic blood

    pressure > 110 mm Hg

    Puncture of noncompressible blood vessel within 2 weeks

    Previous streptokinase therapy