MYOCARDIAL INFARCTION

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PRESENTED BYSANDEEP KAUR

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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.

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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.

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CORONARY ARTERIES OF HEART

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LOCATION / TYPES OF MYPCARDIAL INFARCTION

Obstruction of the left anterior descending artery

(LAD) results in anterior or septal wall MI.

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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.

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ETIOLOGY

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ETIOLOG Y

NONMODIFIABL E RISK FACTORS

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MODIFIAB LE RISK FACTORS

NON-MODIFIABLE RISK FACTORS

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

HIGH BLOOD CHOLESTROL LEVEL

LIPIDS (LIPOPROTIEN S)

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LOW DENSITY LIPOPRO TEIN

HIGH DENSIT Y

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.

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HYPERTENSION
If a persons 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.

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SMOKING
Smoking nicotine catecholamine (epinephrine & nor epinephrine) release increases heart rate & blood pressure increases cardiac workload. + CO decreases O2 available to myocardium

Injury to myocardium

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

OBESITY
More lipids are produced LDL level increases Atherosclerosis Risk of M.I.
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DIABETES MELLITUS
Glucose molecules may stick to lumen of artery Blockage of artery Risk of having M.I.

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STRESS
SNS stimulation Release of catecholamine Increases heart rate & intensify the force of myocardial contraction Increases O2 demand Cell death
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PATHOPHYSIOLOGY

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Causative factor: Obesity Atherosclerosis Narrowing of lumen ed heart Contractility Inadequate Blood supply
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insufficient blood flow to myocardium ed O2 demand of myocardial cells creates an O2 deficit myocardial cell death inflammation

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 center

SNS Stimulation increased

Nausea & Vomiting

catecholamine

Diaphoresis (perfuse sweating) Cold & Clammy skin Cold Sweat

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Increased Heart Rate

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

dysarrythmia

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

Gastrointestinal Nausea Vomiting

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CONTD..
Genitourinary Decreased urinary output

Skin Cool, clammy skin Diaphoresis Pallor, Cyanosis Coolness of extremities

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CONTD..
Neurogenic Anxiety, restleness Light- headedness Headache Visual Disturbances Altered speech Altered motor functions Altered level of consciousness
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CONTD..
Psychosocial Fear feeling

Pt. may deny that anything is wrong

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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.

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NAUSEA & VOMITING

Stimulation of vomiting center by severe pain causes nausea & vomiting.

FEVER
100.4 to 102.2F It is due to inflammatory process caused by Myocardial cell death.

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SYMPATHETIC NERVOUS SYSTEM STIMULATION

Increased catecholamine releases. Diaphoresis (perfuse sweating). Cold & clammy skin (cold sweat).

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

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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,
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family health history

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

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CONTD..

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Contd..

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SERUM CARDIAC MARKERS

CK-MB (ENZYME)

TROPONI NE-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/mm3 ) appears

on second day after MI & diappears in 1 wk.

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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.

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ANGIOGRAPHY
To detect percentage of blockage & type of MI.

CHEST X-RAY
To detect cardiomegaly.

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

assess tissue perfusion.

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MEDICAL MANAGEMENT
MEDICAL MANAGEMENT

DRUG THERAP Y

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FIBRINOL YTIC THERAPY

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)

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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 Take second Tab. After 10
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If pain not relieved take next Tab. at same time

minutes

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 O2 demand of myocardium.
LOW-MOLECULAR-WEIGHT HEPARIN
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(Fragmine)

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.
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Absolute & relative contraindications for thrombolytic therapy

Absolute contraindicationsAny 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

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Relative contraindicationsHistory of chronic, severe, poorly controlled

hypertension presentation

Severe uncontrolled hypertension on History of prior ischemic stroke >3months Dementia Pregnancy Active peptic ulcer Current use of anticoagulants, the higher the
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INR the greater the risk

Pts. with NSTEMI is diagnosed with elevation

of cardiac markers.

They are not candidates for immediate

thrombolytic therapy but should receive antiischemic 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.

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SURGICAL MANAGEMENT
PTCA (Percutaneous Transluminal Coronary Angioplasty)

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STENT PLACEMENT

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

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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.
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COMPLICATIONS
Dysrrythmias Cardiogenic shock Heart failure Pulmonary embolism Recurrent MI
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NURSING MANAGEMENT
Nursing assessmnetSUBJECTIVE 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 9/12/12 signs & findings

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

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

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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

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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. episode of chest pain.

Obtain 12 lead WCG on admission & on each Monitor respond to drug therapy.
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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.
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Dysrrhythmias R/T electrical instability or

irritability secondary to infarcted tissue as evidenced by normal sinus rhythm.

Outcome- the client will have no dysrrythmias 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.
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Decreased cardiac output R/T negativ

einotropic changes in heart secondary to myocardial ischemia. cardiac output as evidenced by normal cardiac rate, rhythm & hemodynamic parameters.

Outcome- the client will have improved

Interventions- assess mental status of pt. Assess lung sounds for crackles & ronchi. Monitor BP . Assess heart sounds for murmur.
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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 clients skin, capillary refill

& level of consciousness. crackles.

Assess respiratory status for dyspnea & Prepare for intubation & mechanical 9/12/12

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
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supply & demand.

Risk for heart failure R/T disease progress as

evidenced by tachycardia, hypotension or hypertension. decreased cardiac output, increased ADH hormone & sodium & water retention. decreased tissue perfusion.

Excess fluid volume R/T reduced GFR,

Risk for impaired skin integrity R/T bed rest &

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THANK

THANK S

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