MYOCARDIAL INFARCTION

MYOCARDIAL INFARCTIONPRESENTED BY-SANDEEP KAUR

INTRODUCTIONMyocardial 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.

DEFINITIONMyocardial 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

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

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

NON-MODIFIABLERISKFACTORSMODIFIABLERISKFACTORSETIOLOGYNON-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 FACTORSHIGH BLOOD CHOLESTROL LEVEL

LOW DENSITYLIPOPROTEIN(LDL)DANGEROUSHIGH DENSITYLIPOPROTEIN(HDL)

LIPIDS(LIPOPROTIENS)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. HYPERTENSIONIf 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.

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

Injury to myocardium

PHYSICAL INACTIVITY Improper lipid metabolism

LDL level increases

Starts accumulating in blood vessels

Risk of M.I.

OBESITYMore lipids are produced

LDL level increases

Atherosclerosis

Risk of M.I.

DIABETES MELLITUSGlucose molecules may stick to lumen of artery

Blockage of artery

Risk of having M.I.STRESSSNS stimulation

Release of catecholamine

Increases heart rate & intensify the force of myocardial contraction

Increases O2 demand

Cell death

Risk of M.I.

PATHOPHYSIOLOGYCausative factor: Obesity

Atherosclerosis

Narrowing of lumen

ed heart insufficient blood flow to myocardiumContractility ed O2 demand of myocardial cells

Inadequate creates an O2 deficitBlood supply myocardial cell death inflammationOliguria CK-MB & Troponine released Fever Anaerobic glycolysis

Accumulation of lactic acid

Irritation of myocardial nerve fibers

Transmission of pain massage to myocardium

Chest pain & radiation towards shoulder & armStimulation of vomiting SNS Stimulation center increasedNausea & Vomiting catecholamine

Diaphoresis Increased(perfuse sweating) Heart Rate

Cold & Clammy skin Cold Sweat CLINICAL MANIFESTATIONSCardiovascular-Chest pain/DiscomfortPalpitationsElevated BPECG may show tachycardia, bradycardia and dysarrythmia

CONTD..Respiratory-Shortness of breathDyspnea/TachypneaCracklesPulmonary edema-may be presentGastrointestinal-NauseaVomitingCONTD..Genitourinary-Decreased urinary outputSkin-Cool, clammy skinDiaphoresisPallor, CyanosisCoolness of extremitiesCONTD..Neurogenic-Anxiety, restlenessLight- headednessHeadacheVisual DisturbancesAltered speechAltered motor functionsAltered level of consciousness

CONTD..Psychosocial-

Fear feeling

Pt. may deny that anything is wrong

PAINCharacteristics: 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 & VOMITINGStimulation of vomiting center by severe pain causes nausea & vomiting.

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

SYMPATHETIC NERVOUS SYSTEM STIMULATIONIncreased catecholamine releases.

Diaphoresis (perfuse sweating).

Cold & clammy skin (cold sweat).

CARDIOVASCULAR MANIFESTATIONSHypotension

Decrease cardiac output

Shock

Urine output (Oliguria): 3monthsDementiaPregnancyActive peptic ulcerCurrent use of anticoagulants, the higher the INR the greater the riskAllergic reaction to streptokinase or antistreplase

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 MANAGEMENTPTCA (Percutaneous Transluminal Coronary Angioplasty)

STENT PLACEMENT

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

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.

COMPLICATIONSDysrrythmias

Cardiogenic shock

Heart failure

Pulmonary embolism

Recurrent MI

Dresslers syndrome

NURSING MANAGEMENTNursing 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

Nursing interventions in acute stage-

Obtain a description of chest discomfortAssess vital signsAssess cardiovascular statusPlace client in semi-fowlers positionAdminister oxygenEstablish I/V accessAdminister NTG as prescribed

CONTD..Administer Morphine Sulfate as prescribed.Obtain 12-lead ECGAdminister I/V and anti-dysrrythmics as prescribedMonitor thrombolytic therapyMonitor for signs of bleedingMonitor lab valuesAssess distal peripheral pulses

CONTD..Monitor intake-outputAssess resp. rate and breath soundsProvide reassurance to client and family

CONTD..Interventions following acute stage-

Maintain bed rest for 24-36 hrs.Provide range of motion exercisesMonitor for complicationsEncourage client to verbalize feelings regarding MI

Nursing diagnosisAcute pain R/T myocardial ischemia resulting from coronary artery occlusionOutcome- the client will experience improved comfort as evidenced by dec. in pain rating scale.Interventions- assess characteristics of painAssess 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.

Ineffective tissue perfusion R/T thrombus in coronary arteryOutcome- 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.

Dysrrhythmias R/T electrical instability or irritability secondary to infarcted tissueOutcome- 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.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.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.Assess respiratory status for dyspnea & crackles.Prepare for intubation & mechanical ventilation if hypoxia inc.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. 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.

THANKSTHANKS