Myocardial infarction

MYOCARDIAL INFARCTION: 

MYOCARDIAL INFARCTION PRESENTED BY- SANDEEP KAUR

INTRODUCTION: 

INTRODUCTION Myocardial infarction (MI) refers to the process by which areas of myocardial cells in the heart are permanently destroyed. It occurs when myocardial tissues are abruptly and severely deprived of oxygen.

DEFINITION: 

DEFINITION Myocardial infarction is a diseased condition which is caused by reduced blood flow in a coronary artery due to atherosclerosis and occlusion of an artery by an embolus or thrombus.

CORONARY ARTERIES OF HEART: 

CORONARY ARTERIES OF HEART

LOCATION / TYPES OF MYPCARDIAL INFARCTION: 

LOCATION / TYPES OF MYPCARDIAL INFARCTION Obstruction of the left anterior descending artery (LAD) results in anterior or septal wall MI.

Contd…..: 

Contd ….. Obstruction of the circumflex artery results in posterior wall MI or lateral wall MI. Obstruction of the right coronary artery results in inferior wall MI.

ETIOLOGY: 

ETIOLOGY

PowerPoint Presentation: 

NON-MODIFIABLE RISK FACTORS MODIFIABLE RISK FACTORS ETIOLOGY

NON-MODIFIABLE RISK FACTORS: 

NON-MODIFIABLE RISK FACTORS

PowerPoint Presentation: 

AGE: More than 40 years . FAMILY HISTORY: Myocardial infarction can be inherited from parents to children. GENDER: Myocardial infarction is 3 times more in men than women.

MODIFIABLE RISK FACTORS: 

MODIFIABLE RISK FACTORS

PowerPoint Presentation: 

HIGH BLOOD CHOLESTROL LEVEL LOW DENSITY LIPOPROTEIN (LDL) DANGEROUS HIGH DENSITY LIPOPROTEIN (HDL) LIPIDS (LIPOPROTIENS)

PowerPoint Presentation: 

HDL is not dangerous because it contains more proteins & very less lipids. Secondly it carry lipids away from arteries to the liver for metabolism. So it prevents lipids accumulation within arteries. LDL is dangerous because it contains more lipids & has capacity to deposit fat within arteries. So, LDL level more than 160mg/dl will place a person at a risk of myocardial infarction.

HYPERTENSION: 

HYPERTENSION If a person’s blood pressure is more than 140/90 mmHg continuously for 4-5 years Sustained stress on arterial walls injury to endothelial lining atherosclerosis narrowed & thickened arterial walls risk of M.I. Also salt consumption 5gms/ day cause M.I.

SMOKING: 

SMOKING Smoking nicotine catecholamine (epinephrine & nor epinephrine) release increases heart rate & blood pressure increases cardiac workload. + CO decreases O 2 available to myocardium Injury to myocardium

PHYSICAL INACTIVITY: 

PHYSICAL INACTIVITY Improper lipid metabolism LDL level increases Starts accumulating in blood vessels Risk of M.I.

OBESITY: 

OBESITY More lipids are produced LDL level increases Atherosclerosis Risk of M.I.

DIABETES MELLITUS: 

DIABETES MELLITUS Glucose molecules may stick to lumen of artery Blockage of artery Risk of having M.I.

STRESS: 

STRESS SNS stimulation Release of catecholamine Increases heart rate & intensify the force of myocardial contraction Increases O 2 demand Cell death Risk of M.I.

PATHOPHYSIOLOGY: 

PATHOPHYSIOLOGY

PowerPoint Presentation: 

Causative factor: Obesity Atherosclerosis Narrowing of lumen ed heart insufficient blood flow to myocardium Contractility ed O 2 demand of myocardial cells Inadequate creates an O 2 deficit Blood supply myocardial cell death inflammation Oliguria CK-MB & Troponine released Fever

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Anaerobic glycolysis Accumulation of lactic acid Irritation of myocardial nerve fibers Transmission of pain massage to myocardium Chest pain & radiation towards shoulder & arm

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Stimulation of vomiting SNS Stimulation center increased Nausea & Vomiting catecholamine Diaphoresis Increased (perfuse sweating) Heart Rate Cold & Clammy skin “Cold Sweat”

CLINICAL MANIFESTATIONS: 

CLINICAL MANIFESTATIONS Cardiovascular- Chest pain/Discomfort Palpitations Elevated BP ECG may show tachycardia, bradycardia and dysarrythmia

CONTD…..: 

CONTD….. Respiratory- Shortness of breath Dyspnea / Tachypnea Crackles Pulmonary edema-may be present Gastrointestinal- Nausea Vomiting

CONTD…..: 

CONTD….. Genitourinary- Decreased urinary output Skin- Cool, clammy skin Diaphoresis Pallor, Cyanosis Coolness of extremities

CONTD…..: 

CONTD….. Neurogenic - Anxiety, restleness Light- headedness Headache V isual Disturbances Altered speech Altered motor functions Altered level of consciousness

CONTD…..: 

CONTD….. Psychosocial- Fear feeling Pt. may deny that anything is wrong

PAIN: 

PAIN Characteristics: Severe, immobilizing chest pain. Usually prescribed as heaviness, pressure, tightness, burning. Location : Substernal , Retrosternal or Epigestric . Radiation: It may radiate to neck, jaw, arm or back . Duration: Lasts for 20 minutes or more.

NAUSEA & VOMITING: 

NAUSEA & VOMITING Stimulation of vomiting center by severe pain causes nausea & vomiting. FEVER 100.4 to 102.2°F It is due to inflammatory process caused by Myocardial cell death.

SYMPATHETIC NERVOUS SYSTEM STIMULATION: 

SYMPATHETIC NERVOUS SYSTEM STIMULATION Increased catecholamine releases. Diaphoresis (perfuse sweating). Cold & clammy skin (“cold sweat”).

CARDIOVASCULAR MANIFESTATIONS: 

CARDIOVASCULAR MANIFESTATIONS Hypotension Decrease cardiac output Shock Urine output ( Oliguria ): <30ml/day . Dyspnoea

DIAGNOSTIC TESTS: 

DIAGNOSTIC TESTS

ASSESSMENT/DIAGNOSTIC FINDINGS: 

ASSESSMENT/DIAGNOSTIC FINDINGS It is generally based on presenting symptoms, ECG and laboratory test results. Patient history-it includes Description of presenting symptoms History of previous illness, family health history

CONTD…..: 

CONTD….. Electrocardiogram- ECG provides information that assists in diagnosing acute MI. The classic ECG changes are- T wave inversion ST segment elevation Abnormal Q wave

CONTD…..: 

CONTD…..

Contd…..: 

Contd …..

SERUM CARDIAC MARKERS: 

SERUM CARDIAC MARKERS CK-MB (ENZYME) TROPONINE-T (PROTEIN)

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CK-MB- increases 3-6 hrs after onset of chest pain, peaks in 12-18 hrs & return to normal within 3-4 days. Cardiac troponin T- increases 7-14 hrs after MI & persists for 5-7 days.

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LDH- it increases 14-24 hrs after onset of MI, peak within 48-72 hrs & slowly return to normal over next 7-14 days. AST- it increases within several hrs after onset of pain, peaks within 12-18 hrs & return to normal within 3-4 days. Leukocytosis - (10,000-20,000/mm 3 ) appears on second day after MI & diappears in 1 wk.

ECHOCARDIOGRAM: 

ECHOCARDIOGRAM PURPOSE: it is useful to assess the ability of heart muscles to contract & relax. It is done to evaluate ventricular function by checking ejection rate. MEGNATIC RESONANCE IMAGING (MRI) PURPOSE: To detect site & extent of myocardial cells.

ANGIOGRAPHY: 

ANGIOGRAPHY To detect percentage of blockage & type of MI. CHEST X-RAY To detect cardiomegaly .

PowerPoint Presentation: 

Positron emission tomography- (PET scan) It is used to evaluate cardiac metabolism & to assess tissue perfusion.

MEDICAL MANAGEMENT: 

MEDICAL MANAGEMENT DRUG THERAPY FIBRINOLYTIC THERAPY MEDICAL MANAGEMENT

MEDICAL MANAGEMENT: 

MEDICAL MANAGEMENT The goal of medical management is to minimize myocardial damage, preserve myocardial function and prevent complications. Pharmacological management- Thrombolytics Analgesics ACE Inhibitors(ACE-I)

DRUG THERAPY: 

DRUG THERAPY ANALGESIC: Morphine Sulphate . NITRATES I/V Nitroglycerine : 4 ampules of NTG are dissolved in 100 ml normal saline to reduce pain by dilating coronary arteries. Sublingual Nitroglycerine: ( Sorbitrate ) At one time patient can take 3 tablets . if pain relieved If pain not relieved Take second Tab. After 10 take next Tab. at same time minutes

BETA ADRENERGIC BLOCKERS: 

BETA ADRENERGIC BLOCKERS ( Propanolol ) it inhibit SNS stimulation of heart. reduces both heart rate & contractility CALCIUM CHANNEL BLOCKERS ( Verapamil , Nifedipine ) It causes coronary artery vasodilatation & decreases myocardial contractility. Increases blood supply to myocardium & decreases O 2 demand of myocardium. LOW-MOLECULAR-WEIGHT HEPARIN ( Fragmine ) These inhibit conversion of fibrinogen into fibrin.

FIBRINOLYTIC THERAPY: 

FIBRINOLYTIC THERAPY TIME OF ADMINISTRATION: Thrombolytics are given to the patient upto 12 hours of onset of chest pain but for best results it should be given within 1 hr after onset of chest pain. ACTION: These will dissolve & do lysis of thrombus in coronary artery. It includes streoptokinase , urokinase , t-PA, alteplase . After thrombolytic therapy, IV heparin is continued.

Absolute & relative contraindications for thrombolytic therapy: 

Absolute & relative contraindications for thrombolytic therapy Absolute contraindications- Any prior ICH Ischemic stroke within 3 months Known structural cerebral vascular lesion Known malignant intracranial neoplasm Active bleeding or bleeding dissection Significant closed head trauma within past 3 months

PowerPoint Presentation: 

Relative contraindications- History of chronic, severe, poorly controlled hypertension Severe uncontrolled hypertension on presentation History of prior ischemic stroke >3months Dementia Pregnancy Active peptic ulcer Current use of anticoagulants, the higher the INR the greater the risk Allergic reaction to streptokinase or antistreplase

PowerPoint Presentation: 

Pts. with NSTEMI is diagnosed with elevation of cardiac markers. They are not candidates for immediate thrombolytic therapy but should receive anti-ischemic therapy. If STEMI is present, the goal is to achieve a door- to –drug time of 30 min & a door-to –balloon time of within 90 min.

SURGICAL MANAGEMENT: 

SURGICAL MANAGEMENT PTCA ( Percutaneous Transluminal Coronary Angioplasty)

STENT PLACEMENT: 

STENT PLACEMENT

ATHERECTOMY: 

ATHERECTOMY With Atherectomy the plaque is shaved off using a type of rotational blade.

PowerPoint Presentation: 

CORONARY ARTERY BYPASS GRAFT (CABG) A portion of saphenous vein from leg is removed & is anastmosed proximally to the ascending aorta & distally to coronary artery.

COMPLICATIONS: 

COMPLICATIONS Dysrrythmias Cardiogenic shock Heart failure Pulmonary embolism Recurrent MI Dressler’s syndrome

NURSING MANAGEMENT: 

NURSING MANAGEMENT Nursing assessmnet - SUBJECTIVE DATA: Past history of M.I., Angina, hypertension. Medication: use of nitrates, calcium channel blockers, antihypertensive drugs. Chest pain: squeezing, sharp & radiation to jaw, neck, arm. OBJECTIVE DATA: General: anxiety, diaphoresis. Integumentary : cool, clammy skin. Cardiovascular signs & findings

PowerPoint Presentation: 

Nursing interventions in acute stage- Obtain a description of chest discomfort Assess vital signs Assess cardiovascular status Place client in semi-fowler’s position Administer oxygen Establish I/V access Administer NTG as prescribed

CONTD…..: 

CONTD….. Administer Morphine Sulfate as prescribed. Obtain 12-lead ECG Administer I/V and anti- dysrrythmics as prescribed Monitor thrombolytic therapy Monitor for signs of bleeding Monitor lab values Assess distal peripheral pulses

CONTD…..: 

CONTD….. Monitor intake-output Assess resp. rate and breath sounds Provide reassurance to client and family

CONTD…..: 

CONTD….. Interventions following acute stage- Maintain bed rest for 24-36 hrs. Provide range of motion exercises Monitor for complications Encourage client to verbalize feelings regarding MI

Nursing diagnosis: 

Nursing diagnosis Acute pain R/T myocardial ischemia resulting from coronary artery occlusion Outcome- the client will experience improved comfort as evidenced by dec . in pain rating scale. Interventions- assess characteristics of pain Assess respiration, BP, heart rate with each episode of chest pain. Obtain 12 lead WCG on admission & on each episode of chest pain. Monitor respond to drug therapy. Limit visitors. As morphine as ordered. Administer nitrates as ordered.

PowerPoint Presentation: 

Ineffective tissue perfusion R/T thrombus in coronary artery Outcome- the client will demonstrate improved cardiac tissue perfusion as evidenced by dec . rating of pain. Interventions- provide bed rest. Administer oxygen as prescribed. Administer thrombolytics . Monitor ST segments.

PowerPoint Presentation: 

Dysrrhythmias R/T electrical instability or irritability secondary to infarcted tissue Outcome- the client will have no dysrrythmias as evidenced by normal sinus rhythm. Interventions- teach client & family about need for continous monitoring. Assess apical heart rate. Give antidysrrythmic agents as ordered. Monitor effects of antidysrrythmics . Monitor serum K levels. Maintain patent IV line. Monitor ST segments & document changes.

PowerPoint Presentation: 

Decreased cardiac output R/T negativ einotropic changes in heart secondary to myocardial ischemia. Outcome- the client will have improved cardiac output as evidenced by normal cardiac rate, rhythm & hemodynamic parameters. Interventions- assess mental status of pt. Assess lung sounds for crackles & ronchi . Monitor BP . Assess heart sounds for murmur. Monitor urine output. Assess for peripheral perfusion-cyanosis, peripheral pulses. Monitor ABG. Maintain hemodynamic stability & duration.

PowerPoint Presentation: 

Impaired gas exchange R/T decreased cardiac output. Outcome- the client will demonstrate improved gas exchange as evidenced by absence of dyspnea . Interventions- administer oxygen as ordered. Monitor ABG. Continue to assess client’s skin, capillary refill & level of consciousness. Assess respiratory status for dyspnea & crackles. Prepare for intubation & mechanical ventilation if hypoxia inc.

PowerPoint Presentation: 

Risk for bleeding R/T coagulopathies with thrombolytic therapy. Powerlessness R/T a near-death experience & anticipated lifestyle changes. Anxiety & fear R/T hospital admission & fear of death. Risk for constipation R/T bed rest, pain medications & NPO or soft diet. Ineffective health maintenance R/T MI & implications for lifestyle changes. Risk for activity intolerance R/T an imbalance b/w oxygen supply & demand.

PowerPoint Presentation: 

Risk for heart failure R/T disease progress as evidenced by tachycardia, hypotension or hypertension. Excess fluid volume R/T reduced GFR, decreased cardiac output, increased ADH hormone & sodium & water retention. Risk for impaired skin integrity R/T bed rest & decreased tissue perfusion.

THANKS: 

THANKS THANKS