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Myocardial Infarction

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BY.DEEPAK_DKRSBY.DEEPAK_DKRS0334702772403347027724

Myocardial infarction (MI)Myocardial infarction (MI)

A lack of oxygen due myocardial perfusion which form of imbalace oxygen suply and demand and development of colatral ciculation.

A clinical syndrom characerized proxymal attack of pain or feeling of chest thightness.

The thrombus often undergoes spontaneous lysis over the course of the next few days, although by this time irreversible myocardial damage has occurred.

Clinical features of myocardial infarction

Symptoms : Prolonged cardiac pain (chest, throat, arms,

epigastrum or back) Anxiety and fear of impending death Nausea and vomiting Breathlessness Collapse/syncope

Myocardial InfarctionMyocardial Infarction

Physical signs : Signs of sympathetic activation :

Pallor, sweating, tachycardia

Signs of vagal activation : Vomiting, tachycardia

Physical signs : Signs of sympathetic activation :

Pallor, sweating, tachycardia

Signs of vagal activation : Vomiting, tachycardia


N.B. : The pain occurs in the same sites as angina but is usually

more severe and lasts longer, it is often described as a tightness, heaviness or constriction in the chest.

Painless or silent myocardial infarction is common in older or diabetic patients.

Sudden death from ventricular fibrillation or asystole may occur immediately and many deaths occur within the first hour.


InvestigationsInvestigations

I.I. ElectrocardiographyElectrocardiography Is usually helpful in confirming the diagnosis.Is usually helpful in confirming the diagnosis.


II. Plasma biochemical markers MI causes a detectable rise in the plasma

concentration of enzymes and proteins that are normally within cardiac cells.

The most widely used are creatine kinase (CK). A cardio-specific isoform of this enzyme (CK-MB) and the cardiospecific proteins troponin T & I.


Serial (usually daily) estimations are particularly Serial (usually daily) estimations are particularly helpful because it is the change in plasma helpful because it is the change in plasma concentrations of these markers that is of concentrations of these markers that is of diagnostic value.diagnostic value.


CK starts to rise at 4-6 hours, peaks at about 12 hours and falls to normal within 48-72 hours.

Troponin T and I are released within 4-6 hours and remain elevated for up to 2 weeks.


III. Other blood tests1. Leucocytosis2. ↑ ESR3. ↑ CRP (C-reactive protein)

IV. Chest X-ray : Cardiomegaly, pulmonary oedema

V. Echocadiography


Management:Management:

Early management of acute myocardial infarction Early management of acute myocardial infarction (AMI) require immediate access to medical and (AMI) require immediate access to medical and paramedical care and defibrillation facilities.paramedical care and defibrillation facilities.


I. Immediate measures High-flow oxygen I.V. access ECG monitoring 12-lead ECG I.V. analgesia (opiates) and antiemetic

Intravenous opiates e.g. morphine sulphate and antiemetics (metoclopramide) should be administered through an intravenous cannula and titrated by giving repeated small aliquots until the patient is comfortable.

Aspirin 300 mg


2.2. Acute reperfusion therapyAcute reperfusion therapyThrombolysis: successful thrombolysis leads to Thrombolysis: successful thrombolysis leads to reperfusion with relief of pain, resolution of acute reperfusion with relief of pain, resolution of acute ST elevation. The sooner the patient is treated ST elevation. The sooner the patient is treated the better the results will be, any delay will only the better the results will be, any delay will only increase the extent of myocardial damage increase the extent of myocardial damage (minutes mean muscle).(minutes mean muscle).


Streptokinase 1.5 million U in 100 ml of saline given as an intravenous infusion over 1 hour is a widely used regimen. Streptokinase is antigenic and occasionally causes serious allergic manifestations, it may also cause hypotension.


Altephase (human tissue plasminogen activator or tPA) is a genetically engineered drug that is not antigenic and seldom causes hypotension.

The major hazard of thrombolytic therapy is bleeding.

(PCI) Primary percutaneous coronary intervention is the treatment of choice.


3. Maintaining vessel patency3. Maintaining vessel patency Antiplatelet therapyAntiplatelet therapy Aspirin 75-300 mg/dAspirin 75-300 mg/d Clopidogrel 75 mg/dClopidogrel 75 mg/d Anticoagulant: subcutaneous heparin twice daily (low Anticoagulant: subcutaneous heparin twice daily (low

molecular weight heparin is now available).molecular weight heparin is now available).

N.BN.B β blockers and nitrates can be used as Adjunctive β blockers and nitrates can be used as Adjunctive

therapytherapy


N.B Complications of infarction Arrythmias Ventricular fibrillation Atrial fibrillation Sinus bradycardia Acute circulatory failure Embolism


II. Late Management:

Life-style modification- Stop smoking- Regular exercise- Diet (weight control, lipid lowering).


Secondary prevention drug therapy- Antiplatelet therapy- Statin blocker- ACE inhibitor- Control diabetes and hypertension

III. Rehabilitation