Acute Myocardial Acute Myocardial InfarctionInfarction

Septemius A. Pansacola RN, MDSeptemius A. Pansacola RN, MD

Acute Myocardial InfarctionAcute Myocardial Infarction

End result of luminal narrowing of End result of luminal narrowing of coronary arteriescoronary arteries Reduction of blood supplyReduction of blood supply Reductin of O2 supplyReductin of O2 supply

EpidemiologyEpidemiology

WHO estimated that in 2002, 12.6 WHO estimated that in 2002, 12.6 percent of deaths worldwide percent of deaths worldwide

Ischemic heart disease is the leading Ischemic heart disease is the leading cause of death in developed cause of death in developed countriescountries

In the US: In the US: Approximately 1.5 Approximately 1.5 million cases of MI occur each year. million cases of MI occur each year.

Risk factorsRisk factors

Older ageOlder age Male genderMale gender Cigarette smokingCigarette smoking Hypercholesterolemia (more accurately Hypercholesterolemia (more accurately

hyperlipoproteinemia, especially high low hyperlipoproteinemia, especially high low density lipoprotein and low high density density lipoprotein and low high density lipoprotein) lipoprotein)

Diabetes Diabetes High blood pressureHigh blood pressure ObesityObesity

PathophysiologyPathophysiology

Result of AtherosclerosisResult of Atherosclerosis disease affecting arterial blood vessels disease affecting arterial blood vessels It is a chronic inflammatory response in It is a chronic inflammatory response in

the walls of arteries, the walls of arteries, deposition of lipoproteins (plasma proteins deposition of lipoproteins (plasma proteins

that carry cholesterol and triglycerides). that carry cholesterol and triglycerides). formation of multiple plaques within the formation of multiple plaques within the

arteries. arteries.

HEART ATTACKHEART ATTACK

AtherogenesisAtherogenesis

Development of fatty streaksDevelopment of fatty streaks LDL in blood plasma invades the LDL in blood plasma invades the

endothelium and becomes oxidizedendothelium and becomes oxidized free radicals in the endotheliumfree radicals in the endothelium

inflammation response. inflammation response. Monocytes (a type of white blood cell) enter Monocytes (a type of white blood cell) enter

the artery wall from the bloodstream, with the artery wall from the bloodstream, with platelets adhering to the area of insult. platelets adhering to the area of insult.

VCAM-1VCAM-1 monocytesmonocytes differentiate into differentiate into macrophagesmacrophages which ingest which ingest oxidizedoxidized LDLLDL, slowly turning into , slowly turning into

large "foam cells" large "foam cells"

AtherogenesisAtherogenesis

Foam cells eventually die, and Foam cells eventually die, and further propagate the inflammatory further propagate the inflammatory process. process.

smooth muscle proliferation and smooth muscle proliferation and migration from tunica media to migration from tunica media to intima intima formation of a fibrous capsule covering formation of a fibrous capsule covering

the fatty streak. the fatty streak.

AtherogenesisAtherogenesis

Calcification and lipidsCalcification and lipids Intracellular Intracellular microcalcificationsmicrocalcifications form within vascular form within vascular

smooth musclesmooth muscle leads to extracellular calcium deposits leads to extracellular calcium deposits

Cholesterol is delivered into the vessel wall by Cholesterol is delivered into the vessel wall by cholesterol-containing cholesterol-containing low-density lipoproteinlow-density lipoprotein (LDL) (LDL) particles. particles. To attract and stimulate macrophages, the cholesterol To attract and stimulate macrophages, the cholesterol

must be released from the LDL particles and oxidized, a must be released from the LDL particles and oxidized, a key step in the ongoing inflammatory process. key step in the ongoing inflammatory process.

The foam cells and platelets encourage the migration and The foam cells and platelets encourage the migration and proliferation of smooth muscle cells, proliferation of smooth muscle cells,

These capped fatty deposits (now called These capped fatty deposits (now called atheromasatheromas)) produce enzymes that cause the artery to enlarge over produce enzymes that cause the artery to enlarge over

time. time.

AtherogenesisAtherogenesis

leukocytes such as monocytes or leukocytes such as monocytes or basophils begin to attack the basophils begin to attack the endotheliumendothelium

inflammation leads to formation of inflammation leads to formation of atheromatous plaquesatheromatous plaques in the arterial in the arterial intimaintima excess fat, collagen, and elastin. excess fat, collagen, and elastin. Initially, wall thickeningInitially, wall thickening stenosisstenosis

is often the result of repeated plaque rupture is often the result of repeated plaque rupture and healing responsesand healing responses

Rupture and stenosisRupture and stenosis

tissue fragments are exposed and tissue fragments are exposed and released,released,

very clot-promoting, containing very clot-promoting, containing collagen and tissue factorcollagen and tissue factor activate platelets and activate the activate platelets and activate the

system of coagulationsystem of coagulation formation of a thrombusformation of a thrombus

Arterial WallArterial Wall

RUPTURED ATHEROMARUPTURED ATHEROMA

atheromatous plaque: atheromatous plaque: three three distinct components:distinct components:

Atheroma is the nodular Atheroma is the nodular accumulation of a soft, flaky, accumulation of a soft, flaky, yellowish material at the center of yellowish material at the center of large plaques, large plaques,

Cholesterol crystals. Cholesterol crystals. Calcification at the outer base of Calcification at the outer base of

older/more advanced lesions. older/more advanced lesions.

complicationcomplication

plaque ruptures and plaque ruptures and stenosisstenosis (narrowing) of the artery (narrowing) of the artery formation of a thrombus formation of a thrombus

aneurysmaneurysm

Acute Myocardial InfarctionAcute Myocardial Infarction

Major Pathological Types:Major Pathological Types: Transmural InfarctTransmural Infarct

Full thicknessFull thickness Endocardium to epicardiumEndocardium to epicardium Q wave infarctQ wave infarct

Subendocardial infarctSubendocardial infarct Involves the subendocardium, the intramural Involves the subendocardium, the intramural

myocardium or bothmyocardium or both Non Q wave infarctNon Q wave infarct

DiagnosisDiagnosis

HistoryHistory Chest painChest pain

Location: substernalLocation: substernal Radiation: left arm or left shoulderRadiation: left arm or left shoulder Character: crushing, constricting, heavinessCharacter: crushing, constricting, heaviness Intensity: severeIntensity: severe Duration: more than 20-30 minutesDuration: more than 20-30 minutes No relief from nitroglycerineNo relief from nitroglycerine

Rough diagram of pain zones in myocardial Rough diagram of pain zones in myocardial infarction (dark red = most typical area, light red = infarction (dark red = most typical area, light red =

other possible areas, view of the chest).other possible areas, view of the chest).

Accompanying symptoms:Accompanying symptoms: DiaphoresisDiaphoresis Profound weaknessProfound weakness Sense of impending doomSense of impending doom AnxietyAnxiety Vagal symptomsVagal symptoms

N&V, diarrhea, abdominal painN&V, diarrhea, abdominal pain

The most common symptoms of MI in The most common symptoms of MI in women includewomen include shortness of breath, weakness, and fatigue. shortness of breath, weakness, and fatigue.

Approximately one fourth of all myocardial Approximately one fourth of all myocardial infarctions are silent: infarctions are silent: ElderlyElderly diabetes mellitusdiabetes mellitus

differences in pain threshold, autonomic neuropathy, differences in pain threshold, autonomic neuropathy, and psychological factors and psychological factors

after heart transplantationafter heart transplantation

Physical ExaminationPhysical Examination Gen. AppearanceGen. Appearance

Anxious, restless, diaphoretic, cold clammy Anxious, restless, diaphoretic, cold clammy skinskin

Vital SignsVital Signs BP: normal, hypotensive-CHF,vasovagal BP: normal, hypotensive-CHF,vasovagal

reactionreaction HR: slow or fast, regular/ irregular rhythmHR: slow or fast, regular/ irregular rhythm Temp: may be febrileTemp: may be febrile RR: TachypneicRR: Tachypneic

HeartHeart Dyskinetic cardiac impulseDyskinetic cardiac impulse S1 muffledS1 muffled S4 usually presentS4 usually present S3: Heart FailureS3: Heart Failure Systolic murmurSystolic murmur Pericardial rubPericardial rub

LungsLungs Rales: CHFRales: CHF

ECG FindingsECG Findings

Transmural Infarction:Transmural Infarction: Hyperacute T wavesHyperacute T waves ST elevationST elevation Pathologic Q wavePathologic Q wave Loss of R waveLoss of R wave

Subendocardial infarctionSubendocardial infarction ST segment depressionST segment depression Inverted T wavesInverted T waves

ECGECG

ST segment elevations ST segment elevations typically due to complete occlusion of a typically due to complete occlusion of a

coronary artery. coronary artery. NSTEMIs NSTEMIs

typically a sudden narrowing of a typically a sudden narrowing of a coronary artery with preserved (but coronary artery with preserved (but diminished) flow to the distal diminished) flow to the distal myocardium. myocardium.

Anticoagulation and antiplatelet agents Anticoagulation and antiplatelet agents prevent the narrowed artery from occluding. prevent the narrowed artery from occluding.

Exercise Stress TestExercise Stress Test

determine the amount of stress that determine the amount of stress that your heart can manage:your heart can manage: before developing either an abnormal before developing either an abnormal

rhythm rhythm or evidence of ischemiaor evidence of ischemia

Exercise Stress Test Exercise Stress Test

A physician may A physician may recommend an exercise recommend an exercise stress test for various stress test for various reasons:reasons:

diagnose coronary artery diagnose coronary artery disease disease

diagnose a possible heart-diagnose a possible heart-related cause of symptomsrelated cause of symptoms

To determine a safe level of To determine a safe level of exercise exercise

To check the effectiveness To check the effectiveness of procedures done of procedures done

To predict risk of dangerous To predict risk of dangerous heart-related conditions heart-related conditions such as a heart attack. such as a heart attack.

effectiveness of medications effectiveness of medications to control angina and to control angina and ischemia. ischemia.

Types of Stress TestsTypes of Stress Tests Dobutamine or Adenosine Stress Test:Dobutamine or Adenosine Stress Test:

used in people who are unable to exercise. used in people who are unable to exercise. heart respond as if the person were exercising. heart respond as if the person were exercising. no exercise is required. no exercise is required.

Stress echocardiogram:Stress echocardiogram: An echocardiogram (often called "echo") is a graphic outline of An echocardiogram (often called "echo") is a graphic outline of

the heart's movement. the heart's movement. accurately visualize the motion of the heart's walls and accurately visualize the motion of the heart's walls and

pumping action when the heart is stressedpumping action when the heart is stressed Nuclear stress test:Nuclear stress test:

determine which parts of the heart are healthy and function determine which parts of the heart are healthy and function normally and which are not. normally and which are not.

radioactive substance is injected into the patient. radioactive substance is injected into the patient. These pictures are done both at rest and after exercise. These pictures are done both at rest and after exercise. a less than normal amount of thallium will be seen in those a less than normal amount of thallium will be seen in those

areas of the heart that have a decreased blood supply. areas of the heart that have a decreased blood supply.

Cardiac EnzymesCardiac Enzymes

Proteins releases by necrotic Proteins releases by necrotic myocardial muscle cellsmyocardial muscle cells SGOTSGOT

Rise: 8-12 hoursRise: 8-12 hours Peak: 18-36 hoursPeak: 18-36 hours Normal: 3-4 daysNormal: 3-4 days Elevated: Hepatic diseases, skeletal muscle Elevated: Hepatic diseases, skeletal muscle

disorders, pulmonary embolismdisorders, pulmonary embolism

Holter monitoringHolter monitoring

continuous continuous monitoring of the monitoring of the electrical activity of electrical activity of a patient's heart a patient's heart muscle muscle (electrocardiograph(electrocardiography) for 24 hours, y) for 24 hours,

special portable special portable device called a device called a Holter monitor. Holter monitor.

LDHLDH Rise: 24-48 hoursRise: 24-48 hours Peak: 3-6 daysPeak: 3-6 days Elevated: hemolysis, liver and renal disorders, pulmonary Elevated: hemolysis, liver and renal disorders, pulmonary

embolismembolism CPKCPK

Creatine Phosphokinase IsoenzymesCreatine Phosphokinase Isoenzymes MM fraction  - skeletal muscleMM fraction  - skeletal muscle

MB fraction - heart muscleMB fraction - heart muscleBB fraction - brainBB fraction - brain

Rise: 6-8 hoursRise: 6-8 hours Peak: 24 hoursPeak: 24 hours Normal: 3-4 daysNormal: 3-4 days Elevated: alcohol intoxication, trauma, intramuscular injectionElevated: alcohol intoxication, trauma, intramuscular injection MB fractionMB fraction

§ § Rises and returns to normal sooner than total CKRises and returns to normal sooner than total CK§ § Rises in 3-4 hours Rises in 3-4 hours § § Returns to normal in 2 days Returns to normal in 2 days

Troponin I (cTnI) or T (cTnT) are the Troponin I (cTnI) or T (cTnT) are the forms frequently assessed.  forms frequently assessed.  Rises 2 - 6 hours after injuryRises 2 - 6 hours after injury Peaks in 12 - 16 hours Peaks in 12 - 16 hours TnI stays elevated for 5-10 daysTnI stays elevated for 5-10 days TnT for 5-14 daysTnT for 5-14 days

MyoglobinMyoglobin Found in striated muscle. Damage to skeletal or Found in striated muscle. Damage to skeletal or

cardiac muscle releases myoglobin into cardiac muscle releases myoglobin into circulation.circulation.

Time sequence after myocardial infarctionTime sequence after myocardial infarction

§ § Rises fast (2 hours) after myocardial Rises fast (2 hours) after myocardial infarctioninfarction§ § Peaks at 6 - 8 hoursPeaks at 6 - 8 hours§ § Returns to normal in 20 - 36 hoursReturns to normal in 20 - 36 hours

Have false positives with skeletal muscle Have false positives with skeletal muscle injury and renal failure.injury and renal failure.

Other Laboratory FindingsOther Laboratory Findings

LeucocytosisLeucocytosis NeutrophiliaNeutrophilia Elevated ESRElevated ESR

Radiologic Findings Radiologic Findings Chest X-RayChest X-Ray NormalNormal CardiomegalyCardiomegaly Signs of CHFSigns of CHF

Ancillary ProceduresAncillary Procedures

Myocardial Perfusion ScanMyocardial Perfusion Scan Technetium Pyrophosphate ScanTechnetium Pyrophosphate Scan

Confirm the diagnosisConfirm the diagnosis Isotope is taken up by damaged cellsIsotope is taken up by damaged cells (+) 36 hrs, remain for 6-10 days(+) 36 hrs, remain for 6-10 days ECG and enzymes not conclusiveECG and enzymes not conclusive

Hemodynamic Hemodynamic MonitoringMonitoring Swan-Ganz Swan-Ganz

CatheterizationCatheterization Right side of the Right side of the

heartheart Pulmonary artery Pulmonary artery

pressurepressure Pulmonary artery Pulmonary artery

occlusive pressureocclusive pressure Right atrial pressureRight atrial pressure Cardiac outputCardiac output

Coronary Coronary angiogramangiogram allows to visualize allows to visualize

narrowings or narrowings or obstructions obstructions

therapeutic therapeutic measures can measures can follow immediately.follow immediately.

Killip classificationKillip classification Used in individuals with an acute Used in individuals with an acute myocardial infarctionmyocardial infarction

to risk stratify to risk stratify Individuals with a low Killip class are less likely to die within Individuals with a low Killip class are less likely to die within

the first 30 the first 30

The killip classificationThe killip classification Killip class I includes individuals with no clinical signs of Killip class I includes individuals with no clinical signs of

heart failureheart failure. . Mortality rate = 6%.Mortality rate = 6%. Killip class II includes individuals with rales in the Killip class II includes individuals with rales in the lungslungs, an , an

S3 S3 gallopgallop, and elevated jugular venous pressure. , and elevated jugular venous pressure. Mortality Mortality rate = 17%.rate = 17%.

Killip class III describes individuals with frank pulmonary Killip class III describes individuals with frank pulmonary edema. edema. Mortality rate = 38%.Mortality rate = 38%.

Killip class IV describes individuals in Killip class IV describes individuals in cardiogeniccardiogenic shock shock. . Mortality rate = 81% Mortality rate = 81%

TreatmentTreatment

Goal:Goal: Pain reliefPain relief Reduction of myocardial oxygen Reduction of myocardial oxygen

consumptionconsumption Prevention and treatment of Prevention and treatment of

complicatioscomplicatios

Admit to the CCUAdmit to the CCU ActivityActivity

Day 1: bed rest, if stableDay 1: bed rest, if stable Day 2-3: bed rest, but patient may be allowed to sit on a Day 2-3: bed rest, but patient may be allowed to sit on a

chair for 15-20 minuteschair for 15-20 minutes Early mobilization is recommended for uncomplicated AMIEarly mobilization is recommended for uncomplicated AMI

Monitoring Vital SignsMonitoring Vital Signs First 6 hours- q30-60 minutesFirst 6 hours- q30-60 minutes Next 24 hours- q 2 hoursNext 24 hours- q 2 hours Thereafter q 4 hoursThereafter q 4 hours

DietDiet NPO: 1NPO: 1stst 24 hours 24 hours If stable low salt, low cholesterol dietIf stable low salt, low cholesterol diet

IV FluidsIV Fluids D5W to KVOD5W to KVO If unable to take food/fluid per oremIf unable to take food/fluid per orem

1000ml/8 hours1000ml/8 hours K supplementK supplement

Laboratory StudiesLaboratory Studies ECG daily for 3 daysECG daily for 3 days EnzymesEnzymes ElectrolytesElectrolytes BUN/ CreatinineBUN/ Creatinine FBSFBS CXR daily for 3 daysCXR daily for 3 days

MedicationsMedications

Nasal Oxygenation for the 1Nasal Oxygenation for the 1stst 24 24 hourshours

Relief of PainRelief of Pain Morphine SO4 (2-5mg/IV dose)Morphine SO4 (2-5mg/IV dose)

Potent analgesicPotent analgesic Peripheral venous vasodilationPeripheral venous vasodilation Pulmonary venous distentionPulmonary venous distention Inferior wall MI: may increase vagal Inferior wall MI: may increase vagal

dischargedischarge Pethidine HCLPethidine HCL

TranquilizresTranquilizres To decrease anxietyTo decrease anxiety Diazepam (5-10 mg per IV/orem)Diazepam (5-10 mg per IV/orem)

LaxativeLaxative To prevent straining during defecationTo prevent straining during defecation Lactulose (HS)Lactulose (HS)

Drugs to Limit Infarct SizeDrugs to Limit Infarct Size

Beta BlockersBeta Blockers Hyperdynamic states, HPN w/o evidence Hyperdynamic states, HPN w/o evidence

of heart failureof heart failure Reduce myocardial oxygen consumption Reduce myocardial oxygen consumption

by decreasing:by decreasing: Cardiac indexCardiac index Stroke indexStroke index Heart rateHeart rate Blood pressureBlood pressure

Ex: Propranolol, MetoprololEx: Propranolol, Metoprolol

NitratesNitrates Act by augmenting perfusion at the Act by augmenting perfusion at the

border of ischemic zoneborder of ischemic zone Dilating collateralsDilating collaterals

Reducing myocardial O2 demandReducing myocardial O2 demand Lowering preloadLowering preload Lowering afterloadLowering afterload

Ex: IV Nitroglycerine, Sublingual Ex: IV Nitroglycerine, Sublingual Niotroglycerine, Oral/Transdermal Niotroglycerine, Oral/Transdermal NitroglycerineNitroglycerine

ACE inhibitors ACE inhibitors reduce mortality rates after MI. reduce mortality rates after MI. Administer ACE inhibitors as soon as Administer ACE inhibitors as soon as

possible possible ACE inhibitors have the greatest benefit in ACE inhibitors have the greatest benefit in

patients with ventricular dysfunction. patients with ventricular dysfunction. Continue ACE inhibitors indefinitely after MI. Continue ACE inhibitors indefinitely after MI. Angiotensin-receptor blockers may be used Angiotensin-receptor blockers may be used

as an alternative as an alternative adverse effects, such as a persistent cough, adverse effects, such as a persistent cough,

Aspirin and/or antiplatelet therapyAspirin and/or antiplatelet therapy Aspirin has been shown to decrease mortality and re-Aspirin has been shown to decrease mortality and re-

infarction ratesinfarction rates Administer aspirin immediatelyAdminister aspirin immediately Continue aspirin indefinitelyContinue aspirin indefinitely Clopidogrel may be used as an alternative Clopidogrel may be used as an alternative

resistance or allergy to aspirin. resistance or allergy to aspirin. Administer a platelet glycoprotein (GP) IIb/IIIa-receptor Administer a platelet glycoprotein (GP) IIb/IIIa-receptor

antagonistantagonist continuing ischemia or with other high-risk features and to continuing ischemia or with other high-risk features and to

patients in whom a percutaneous coronary intervention patients in whom a percutaneous coronary intervention (PCI) is planned. (PCI) is planned.

Eptifibatide and tirofiban are approved for this use. Eptifibatide and tirofiban are approved for this use. Abciximab also can be used for 12-24 hours in patients with Abciximab also can be used for 12-24 hours in patients with

unstable angina or NSTEMI in whom a PCI is planned within unstable angina or NSTEMI in whom a PCI is planned within the next 24 hours.the next 24 hours.

Heparin (and other anticoagulant agents) Heparin (and other anticoagulant agents) established role as an adjunctive agent in established role as an adjunctive agent in

patients receiving t-PA but not with patients receiving t-PA but not with streptokinase. streptokinase.

Heparin is also indicated in patients Heparin is also indicated in patients undergoing primary angioplasty. undergoing primary angioplasty.

Low–molecular-weight heparins (LMWHs) Low–molecular-weight heparins (LMWHs) have been shown to be superior to UFHs in have been shown to be superior to UFHs in patients with unstable angina or NSTEMI. patients with unstable angina or NSTEMI.

ReperfusionReperfusion

ST segment elevation (STEMI) or ST segment elevation (STEMI) or new bundle branch block on the 12 new bundle branch block on the 12

lead ECGlead ECG presumed to have an occlusive presumed to have an occlusive

thrombosis in an epicardial coronary thrombosis in an epicardial coronary artery. artery.

candidates for immediate reperfusion,candidates for immediate reperfusion, thrombolyticthrombolytic therapy therapy percutaneouspercutaneous coronary intervention coronary intervention bypass surgerybypass surgery. .

Thrombolytic therapy Thrombolytic therapy improve survival ratesimprove survival rates If PCI capability is not available or will cause a If PCI capability is not available or will cause a

delay greater than 90 minutes, delay greater than 90 minutes, optimal approach is to administer thrombolytics within 12 optimal approach is to administer thrombolytics within 12

hours of onset of symptomshours of onset of symptoms ST-segment elevation ST-segment elevation new left bundle-branch block (LBBB), new left bundle-branch block (LBBB), or anterior ST depression consistent with posterior infarction. or anterior ST depression consistent with posterior infarction.

Tissue plasminogen activator (t-PA) is superior to Tissue plasminogen activator (t-PA) is superior to streptokinasestreptokinase

Recent trials show a high patency rate if a IIb/IIIa receptor Recent trials show a high patency rate if a IIb/IIIa receptor antagonist is combined with a half dose of a thrombolytic antagonist is combined with a half dose of a thrombolytic agent as the initial reperfusion strategy. agent as the initial reperfusion strategy.

thombolytic therapythombolytic therapy

The effectiveness:The effectiveness: highest in the first 2 hourshighest in the first 2 hours After 12 hours, the risk associated with After 12 hours, the risk associated with

thrombolytic therapy outweighs any benefitthrombolytic therapy outweighs any benefit contraindicatedcontraindicated

unstable angina and NSTEMIunstable angina and NSTEMI and for the treatment of individuals with evidence of and for the treatment of individuals with evidence of

cardiogenic shockcardiogenic shock streptokinasestreptokinase, , urokinaseurokinase, and , and alteplasealteplase

(recombinant (recombinant tissue tissue plasminogenplasminogen activator activator, , rtPA), rtPA), reteplasereteplase, tenecteplase , tenecteplase

Surgical CareSurgical Care

Percutaneous coronary Percutaneous coronary interventionintervention treatment of choice treatment of choice

STEMI, (door to needle time of less than 90 minutes.)STEMI, (door to needle time of less than 90 minutes.) PCI provides greater coronary patency PCI provides greater coronary patency lower risk of bleedinglower risk of bleeding and instant knowledge about the extent of the underlying and instant knowledge about the extent of the underlying

disease. disease. The widespread use of stenting and adjunctive IIb/IIIa The widespread use of stenting and adjunctive IIb/IIIa

therapy are improving the results of primary PCI. therapy are improving the results of primary PCI. Primary PCI is also the treatment of choice in Primary PCI is also the treatment of choice in

cardiogenic shockcardiogenic shock patients in whom thrombolysis failedpatients in whom thrombolysis failed high risk of bleeding or contraindications to thrombolytic high risk of bleeding or contraindications to thrombolytic

therapy.therapy.

Emergent or urgent Emergent or urgent coronary artery coronary artery graft bypass graft bypass surgerysurgery is is indicatedindicated angioplasty fails angioplasty fails develop mechanical develop mechanical

complications such complications such as a VSD, LV, or as a VSD, LV, or papillary muscle papillary muscle rupture.rupture.

ComplicationsComplications

RESULT:RESULT: InflammationInflammation MechanicalMechanical Electrical abnormalitiesElectrical abnormalities

ArrhythmiasArrhythmias

Major cause of Major cause of mortality in the 1mortality in the 1stst 24 hours24 hours ventricular ventricular

tachycardia tachycardia ventricular ventricular

fibrillationfibrillation complete heart complete heart

block block Atrial FibrillationAtrial Fibrillation Sinus bradycardiaSinus bradycardia

Congestive heart failureCongestive heart failure

Impaired cardiac Impaired cardiac contractilitycontractility

Increased Increased myocardial myocardial stiffnessstiffness

Mechanical Mechanical dysfunction ( MR )dysfunction ( MR )

Cardiogenic shockCardiogenic shock

hemodynamic state in which the hemodynamic state in which the heart cannot produce enough of a heart cannot produce enough of a cardiac output to supply an adequate cardiac output to supply an adequate amount of oxygenated blood amount of oxygenated blood

40% of ventricular mass has 40% of ventricular mass has necrosednecrosed

Myocardial ruptureMyocardial rupture

most common most common three to five days three to five days after myocardial after myocardial infarction infarction

May occur May occur VentriclesVentricles SeptumSeptum papillary musclespapillary muscles atriaatria

Ventricular AneurysmVentricular Aneurysm

Late complicationLate complication Weeks to months Weeks to months

after MIafter MI Left VentricleLeft Ventricle

Mural thrombusMural thrombus Ventricular Ventricular

ArrhythmiasArrhythmias CHFCHF

PericarditisPericarditis

As a reaction to the As a reaction to the damage of the damage of the heart muscle ( 10-heart muscle ( 10-15% )15% ) inflammatory cells inflammatory cells

are attracted. are attracted. may reach out and may reach out and

affect the heart sac.affect the heart sac. Sharp pain, fever, Sharp pain, fever,

pericardial friction pericardial friction rub rub

ThromboembolismThromboembolism

Intracavitary Intracavitary thrombus thrombus formationformation

Result in infarction Result in infarction of peripheral of peripheral organs:organs: BrainBrain KidneysKidneys Peripheral vesselPeripheral vessel

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