SEMINAR ON MYOCARDIAL INFRACTION

Conducted byHelen Lalrinpuii .

I.INTRODUCTION TO THE TOPIC – MYOCARDIAL INFRACTION

II. DEFINITION OF MYOCARDIAL INFARCTION

Myocardial infarction refers to a dynamic process by which one or more region of the heart experiences a severe and prolonged decrease in oxygen supply because of insufficient coronary blood flow, subsequently, necrosis or death to death to the myocardial tissue occurs.

III.EPIDEMIOLOGY OF MI

• Myocardial infarction is a common presentation of heart disease.

• WHO(2004) -12.2% death; 3 million ST-Elevated Myocardial Infarction & 4 million of Non-ST Elevated Myocardial Infarction.

• (American Heart Association) – USA 1 million have heart disease, of which ¼ die at hospital & half of these do not reach hospital.

• India (2004)- 1.46 have myocardial infarction & 14% die, death rate expected to double in 2015.

• Heart disease is a leading cause of death in India.

IV.ETIOLOGY & RISK FACORS OF MI

MODIFIABLE FACTORS: • Stress.• Obesity.• Sedentary lifestyle.• Tobacco user.• Hypertension. • Diabetes mellitus.

NON MODIFIABLE FACTORS:

• Age.• Gender.• Family history.

V. ANATOMY & PHYSIOLOGY OF THE HEART

•Lies in thoracic cavity in obliquely.•Upper part is base and lower part is apex.• Apex is 9cm to the left midline at level of 5th intercostals space & base at the level of 2nd rib. •Size is that of owner fist.

ORGANS ASSOCIATED WITH THE HEART

• Inferior-> diaphragm. • Superior-> blood vessel-aorta, superior vena

cava, pulmonary vein & artery.• Posterior-. esophagus, tracheae, bronchus,

descending aorta, inferior vena cava & thoracic vertebrae.

• Anterior –> sternum, ribs & inter costal muscle.

•STRUCTURE OF THE HEART

A. The heart wall: -Composed o three layer:a. Pericardium. b. Myocardium.C. Endocardium.

Pericardium- *Outer most layer. * Has two sacs-AS TWO SACS- -Outer fibrous sac. . -Inner membrance sac.

2. Myocardium -Composed of specialised muscle. -Network of specialised conducting fibre.

3.Endocardium -Lines chamber, valves & blood vessel.

INTERIOR OF THE HEART•Heart is divided left and right by septum.•Atrioventricular divided it into atrium and ventricles.• Right ventricular valves has 3 flaps and left ventricles has 2 cusp/ flap, which open when pressure in atrium is greater than ventricles.•This valves are guarded by tendinous cord called chordae tendinae.

FLOW OF BLOOD THROUGH THE HEART

(CONTD)

• Superior & inferior vena cava empty their content in right atrium.

• Right atrium to right ventricles valves via right atrio ventricles & pump into pulmonary artery.

• Leaving the heart divided into left & right pulmonaries arteries, carry venous blood to the lungs.

• Changes in the gases take place in the lungs.• 2 pulmonary veins back to left atrium, passed through left

atrio ventricles valves enter the left ventricles & pump into aorta .

• Aorta -> the different part of the body.

BLOOD SUPPLY TO THE HEART:1. Arterial supply:• Right & left coronary arteries..• Receives 5% of total blood via coronary

arteries.• Coronary arteries form vast network of

capillaries.

2.Venous drainages:• Most venous blood is collected in cadiac vein

forming coronary sinus open onto right atrium.

• Remainder passes- heart chamber via venous chamber

NERVES SUPPLY TO THE HEART

• Autonomic nerves originated in cardio vascular centre in medulla oblongata.

• Vagus nerve (parasympathetic nervous system ) .

• Sympathetic nervous system.

VI.PATHOPHYSIOLOGY OF MIPlaque ruptured / thrombus formation.

Occlusion of the artery.f

Vasospasm of the blood vessel's .

Decrease oxygen supply.

Increase oxygen demand.

Myocardial infarction.

VIII. DEGREE /ZONE OF DAMAGES IN MI

A.ZONE OF NECROSIS:• Extensive & complete O2 deprivation.• Irreversible damage zone.

B. ZONE OF INJURY:• Area surrounding necrosis.• Inflamed & injured but viable.

C. ZONE OF ISCHEMIA:• Surrounding injury area.• Not endangered & viable.

VII. CLASSIFICATION OF MIA. ST Segment Elevated MI (STEMI)

B. Non ST Segment Elevated MI (NSTEMI)

IX. CLINICAL MANIFESTATION OF MI

X. COMPLICATION

• Severe arrhythmias.• Cardiac failure.• Ventricular wall ruptured.• Pulmonary / cerebral embolism.• Pericarditis.• Angina pectoris.• Recurrent infarction.• Psychiatric disorder.

• SEVERE ARRHYTHMIAS.• CARDIAC FAILURE.• VENTRICULAR WALL RUPTURED.• PUL. / CEREBRAL EMBOLISM.• PERICARDITIS.• ANGINA PECTORIS.• RECURRENT INFRACTION.• PSYCHIATRIC DISORDER.

XI. PROGNOSIS OF MI

• Depend on intensity & extensity of damages.• Complicated with heart block & Right

Ventricular failure has worst prognosis.• Definitive & prompt intervention has good

prognosis.

XII. DIAGNOSTIC EVALUATION

A. Patient history.B. Electro cardiogram (ECG).C. Echo cardiogram.D. Laboratory test: *Ck-MB. *Myglobulin. *Troponin. *Lactate Dehydrogenase

Total (LDH). *Aspartate Amino

Transferase (AST). *Prothrombin time. * White blood cell (WBC).E. Magnetic Resonance Imaging

(MRI).

XIII. MANAGEMENT OF MI.

I. Medical management:

A.Baseline Rx -MONA:-

M=Morphine.O= Oxygen.N= Nitrate.A= Aspirin.

B. OTHER MEDICATION-• Anti- plateletNTI-PLATELET AGENT.• Thromboyitic.• Glco Protein Receptor Inhibitor.• Anti-coagulant.• Direct Thrombin Inhibitor.• Nitrate.• Beta Blocker.• Calcium Channel Blocker.• Angiotensin Converting Enzymes Inhibitor.• Analgesic.• Anxiolytic.• Cholesterol Lowering Agent.• Oxygen Therapy.

II. SURGICAL MANAGEMENT:a) Intra- aortic baloon pump.b) Percutneous Coronary Intervention /

Angioplasty. c).Transmyocardial Laser Revascularization.d).Coronary Artery By –Pass (CABG).e) Minimal Invasive Direct Coronary Artery By-

Pass.

A. Intra aortic balloon pump.

B. Percutaneous coronary intervention / Angioplasty

C.TRANSMYOCAR-DIAL LASER REVASCULARIZATION.

•This surgery use laser to create channel through the left ventricle free wall into the ischemic myocardium.

D. CORONARY ARTERY BY PASS GRAFT

E. MINIMAL INVASIVE DIRECT CORONARY ARTERY BYPASS

• Its different from CABG is that median sternotomy is eliminated.

• Its has smaller incission.• A robotic system endoscopic technique is used

to place by-pass graft.• Its advantage is that it has fewer

complication.

1. XIV. NURSING MANAGEMENT OF MI USING NURSING PROCESS.

1. Acute pain (chest) r/t imbalance oxygen supply & demand as evidenced by patient verbalization of chest pain.

2. Decreased cardiac output r/t impaired contractility as evidenced by facial pallor & fainting in patient.

3. Altered tissue perfusion r/t coronary restenosis & extension of infarction as evidenced by shortness of breath & hypo/hypertension.

4. Activity intolerance r/t fatigue secondary to decreased cardiac output & poor lung & tissue perfusion as evidenced by fatigue with minimal activity, inability to care for self without dyspnea & increases heart rate.

5. Risk for injury (bleeding) r/t dissolution of protective clot.

6. Knowledge deficit r/t home care & treatment modalities as evidenced by asking numbers of question to health personnel.

XV. CONCLUSION

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Thank you