Myocardial Infarction

Dr. Abdur Rehan

Dr. Muhammad Aamir Iqbal

West Medical Ward

Definition

• Know as heart attack

• An MI occurs when there is a diminished blood supply to the heart which leads to myocardial cell damage and ischemia.

• Contractile function stops in the necrotic areas of the heart.

• Ischemia usually occurs due to blockage of the coronary vessels.

Definition cont.• This blockage is often the result of

thrombus that is superimposed on an ulcerated or unstable atherosclerotic plaque formation in the coronary artery.

• MI’s are described by the area of occurrence.

• Anterior, Inferior, Lateral or Posterior.

Coronary Artery Anatomy

Coronary artery events

• Ischemia – Outer most area, source of arrhythmias, viable if no further infarction.

• Injury – Viable tissue found between ischemic and infarcted areas.

• Infarction/necrosis – Center area, dead not viable tissue that turn into scar.

MI Classifications

• MI’s can be subcategorized by anatomy and clinical diagnostic information.

Anatomic

• Transmural and Subendocardial

Diagnostic

• ST elevations (STEMI) and non ST elevations (NSTEMI).

Risk Factors

• The presence of any risk factor is associated with doubling the risk of an MI.

Non Modifiable

• Age

• Gender

• Family history

Risk Factors

Modifiable

• Smoking

• Diabetes Control

• Hypertension

• Hyperlipidemia

• Obesity

• Physical Inactivity

Smoking

• Tobacco use increases the risk of coronary artery disease two to six times more than non smokers.

• Nicotine increases platelet thrombus adhesion and vessel

inflammation.

Diabetes & Hypertension

• Diabetes not only increases the rate of atherosclerotic formation in vascular vessels but also at an earlier age.

• The constant stress of high blood pressure has been associated with the increased rate of plaque formation.

• Shearing Stress and inflammation of endothelial lining begins the process.

Hyperlipidemia

• Elevated levels of cholesterol, LDL’s or triglycerides are associated with the increased risk of coronary plaque formation and MI.

Obesity and Physical Inactivity

• Mortality rate from CAD is higher in those who are obese.

• Some evidence shows that those who carry their weight in their abdomen have a higher incidence of CAD

• Physically inactive people have lower HDL levels with higher LDL levels and an increase in clot formation.

Pathophysiology• Ischemia develops when there is an

increased demand for oxygen or a decreased supply of oxygen.

• Ischemia can develop within 10 seconds and if it lasts longer than 20 minutes, irreversible cell and tissue death occurs.

• Myocardial cell death begins at the endocardium. The area most distal to the arterial blood supply.

Pathophysiology

• As vessel occlusion continues cell death spreads to the myocardium and eventually to the epicardium.

• Severity of the MI depends on three factors.– Level of occlusion– Length of time of occlusion– Presence or absence of collateral circulation

Signs and Symptoms

• Signs and symptoms are unique to each individual patient.

• Ranging from no symptoms to sudden cardiac arrest.

Clinical Presentation• Retrosternal pain, more severe and lasts

longer i.e. > 30 min, present at rest, heavy, squeezing & crushing, stabbing or burning radiating to arms, back, lower jaw, neck & epigastrium.

• Associated with nausea, vomiting, anxiety & palpitation.

• Painless STEMIs in diabetics in older age group

• Sudden onset of breathlessness

• Sudden loss of consciousness & confusion state

Diagnostics

• Typical chest pain

• ECG

• Serum cardiac enzymes

• Cardiac imaging

Normal Sinus Rhythm

STEMI

• ST segment elevations

• T wave changes

• Q wave development

• Enzyme elevations

• Reciprocals

NSTEMI

• ST segment depressions

• T wave changes

• No Q wave development

• Mild enzyme elevations

• No reciprocals

STEMI vs. NSTEMI

Phases of a STEMI

• Hyperacute Phase– Occurs within the first few hours of MI onset.– Leads facing the infarcted surface: ST

segment elevation.– Leads facing the uninjured surface: ST

segment depression (reciprocals)– T waves become tall, widened and might be

taller than the R wave.

Phases of a STEMI

• Fully Evolved Phase– Q wave development– ST elevation – T waves start to become inverted in leads

facing the injury.

Phases of a STEMI

• Resolution phase– Weeks after there will be a gradual return of

ST segments to baseline. – T waves will gradually return to normal but are

the last to change back.

Localization of MI

• ST elevation only• Inferior wall- II, III, aVF• Lateral wall- I, aVL, V4-V6• Anteroseptal- V1-V3• Anterolateral- V1-V6• Right ventricular- RV4, RV5• Posterior- R/S ratio >1 in V1 and T wave

inversion

Serum Cardiac Markers

• Myocardial cells produce certain proteins and enzymes associated with cellular functions.

• When cell death occurs, these cellular enzymes are released into the blood stream.

• CPK and troponin

CPK

• Creatine Phosphokinase

• CPK-MB more specific for STEMI

• Begin to rise 3 to 12 hours after acute MI.

• Peak in 24 hours

• Return to normal in 2 to 3 days

Troponin

• Troponin-T & Troponin-I

• Myocardial muscle protein released into circulation after injury.

• These are highly specific indicators of MI.

• Troponin rises quickly like CK but will continue to stay elevated for 2 weeks.

• Myoglobin-lacks cardiac specificity.

Serum Cardiac Markers

Within the first 10 minutes upon arrival to the hospital:

• Check vital signs and evaluate oxygen saturation

• Establish IV access• Obtain and review 12-lead ECG• Take a brief focused history and perform a

physical exam• Obtain blood samples to evaluate initial cardiac

markers, electrolytes and coagulation

Pre Hospital Management

• Aspirin 300 mg stat

• S/L nitrates 0.4 mg up to 3 doses

• Analgesia morphine 5-10 mg IV + metaclopramide 10 mg IV

In Hospital

• High flow O2 .

• Analgesia morphine 5-10 mg IV + metaclopramide 10 mg IV.

• S/L GTN• IV β-blockers metoprolol 5 mg every 5 min

for 3 doses, 15 min after the last IV dose oral regimen is started 50 mg/6h for 48 hrs followed by 100 mg/12h.

Fibrinolytic Therapy

• Indicated for patients with STEMIs.

• Should be given within 12 hours of symptom onset.

• Fibrinolytics will break down clots found within the vessles

Types of fibrinolysis• Fibrin specific agents

tPA, tenecteplase, reteplase. rtPA indicated if patients received previously SK > 4 days or reacted to SK, 15 mg loading followed by 50 mg IV over 30 min followed by 35 mg over 60 min. rPA double bolus regimen 10 MU bolus over 2 min followed by 2nd 10 MU over 30 min. TNK single IV bolus of 0.53 mg/kg over 30 min. UFH is usually indicated after thrombolysis.

• Non-fibrin specific agent1.5 MU SK over 1h in 100 ml N/S. S/E nausea, vomiting, hemorrhage, stroke, disarrythmias & allergic reactions. No indication of UFH after SK

Contraindications

Absolute•H/O CVA hemorrhage , Non-hemorrhagic stroke•Marked hypertension systolic > 180 & diastolic > 110 at presentation•Suspicion of aortic dissection , Active internal bleeding

Contraindications

Relative•Current use of anticoagulant , Recent surgical procedure•Prolonged or traumatic CPR•Bleeding diathesis, pregnancy, diabetic retinopathy, peptic ulcer disease

Hospital phase management

Activity: •First 12 hrs. Complete bed rest•12-24 hrs. Resume upright posture by hanging their feet over the side of the bed & sitting in the chair•By the 2nd & 3rd day patients are walking in the room with increasing duration & frequency and may take shower or bath.•By 3rd day after infarction patient should increase their walk progressively to 600 ft 3 times a day.

Diet: •Either nothing or only clear fluids by mouth for the 1st 4-12h to prevent emesis or aspiration.•Food enriched with K, Mg and fibers but low in Na.Bowels: •Diet rich in bulk and the routine use of stool softner to prevent constipationSedation: •Benzodiazepines

Subsequent Management• Daily exam for complication• Daily 12 lead ECG, cardiac enzymes for 2-

3 days• Prophylaxis against thrombolysis, UFH

until fully mobilized. If large anterior MI consider warfarin for 3 months against systemic embolism from mural thrombus. Daily low dose Aspirin 75-150 mg indefinitely

• Start oral β-blocker, Metoprolol 50 mg/6h if contraindicated Verapamil Continuous ACE inhibitor

• Modify risk factors, discourage smoking, encourage exercise, treat DM, HTN, hyperlipidemia

• Discharge after 5-7 days• May return to work after 2 months• Few occupations should not be restarted

after MI like pilots, drivers, divers, air traffic controllers

• Avoid air travel for 2 months• Start Statin

Cardiac Catheterization

• A diagnostic angiography which includes angioplasty and possible stenting.

• Performed by an interventional cardiologist with a cardiac surgeon on stand by.

• Percutaneous procedure through the femoral or brachial artery.

Complications

• Recurrent ischemia or failure to reperfuse

• Cardiac arrest ,cardiogenic shock

• Arrythmias

• LVF,RVF

• Pericarditis

• DVT,PE,systemic embolism

• Cardiac tamponad

• MR,VSD

• Dressler's syndrome

• LV aneurysm