Myocardial Infarction. Background Myocardial Infarction if the rapid development of myocardial...
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Transcript of Myocardial Infarction. Background Myocardial Infarction if the rapid development of myocardial...
Myocardial InfarctionMyocardial Infarction
BackgroundBackground
Myocardial Infarction if the rapid Myocardial Infarction if the rapid development of myocardial necrosis by a development of myocardial necrosis by a critical imbalance between oxygen supply critical imbalance between oxygen supply and demand to the myocardiumand demand to the myocardium
ClassificationClassification
Acute coronary syndromes includeAcute coronary syndromes include
ST-elevation MI (STEMI)ST-elevation MI (STEMI)
Non ST-elevation MI ( NSTEMI)Non ST-elevation MI ( NSTEMI)
Unstable AnginaUnstable Angina
Cardiac markers in circulation indicates Cardiac markers in circulation indicates myocardial infarction and help categorize MI myocardial infarction and help categorize MI and is a useful adjunct to diagnosisand is a useful adjunct to diagnosis
ClassificationClassification
Anatomic or morphologicAnatomic or morphologic
Transmural= Full thicknessTransmural= Full thickness
Non-transmural= Partial thicknessNon-transmural= Partial thickness
ECGECG
Q wave MIQ wave MI
Non Q wave MINon Q wave MI
Does not distinguish transmural from a non-Does not distinguish transmural from a non-transmural MI as determined by pathologytransmural MI as determined by pathology
PrevalencePrevalence
In the US, 1.3 million cases of nonfatal MI In the US, 1.3 million cases of nonfatal MI were reported in 2006were reported in 2006
Incidence of 600 per 100,000 peopleIncidence of 600 per 100,000 people
Increase in the proportion of NSTEMI Increase in the proportion of NSTEMI compared to STEMIcompared to STEMI
Approximately 500,000 to 700,000 deaths Approximately 500,000 to 700,000 deaths are caused by heart disease annually in are caused by heart disease annually in the United Statesthe United States
HistoryHistory
The history is critical in making the The history is critical in making the diagnosis of MI and sometimes provide only diagnosis of MI and sometimes provide only the only clues that lead to the diagnosis in the only clues that lead to the diagnosis in the initial phase of presentationthe initial phase of presentation
HistoryHistory
Chest Pain- anterior precordium tightnessChest Pain- anterior precordium tightness
Pain may radiate to jaw, neck and Pain may radiate to jaw, neck and epigastriumepigastrium
Dyspnea- angina equivalent, poor LV Dyspnea- angina equivalent, poor LV functionfunction
Nausea/abdominal pain with posterior MINausea/abdominal pain with posterior MI
AnxietyAnxiety
HistoryHistory
Nausea with and without vomitingNausea with and without vomiting
Diaphoresis or sweatingDiaphoresis or sweating
Syncope or near syncopeSyncope or near syncope
Elderly present with MS changes, fatigue, Elderly present with MS changes, fatigue, syncope or weaknesssyncope or weakness
As many as half of MI are clinically silentAs many as half of MI are clinically silent
PhysicalPhysical
The physical exam can often be The physical exam can often be unremarkableunremarkable
HypertensionHypertension
HypotensionHypotension
Acute valvular dysfunction may be presentAcute valvular dysfunction may be present
RalesRales
Neck vein distentionNeck vein distention
PhysicalPhysical
Third heart sound may be presentThird heart sound may be present
A fourth heart sound poor LV complianceA fourth heart sound poor LV compliance
DysrhythmiasDysrhythmias
Low grade feverLow grade fever
CausesCauses
Most frequent cause is rupture of an Most frequent cause is rupture of an atherosclerotic lesion within coronary wall atherosclerotic lesion within coronary wall with subsequent spasm and thrombus with subsequent spasm and thrombus formationformation
Coronary artery vasospasmCoronary artery vasospasm
Ventricular hypertrophyVentricular hypertrophy
HypoxiaHypoxia
Coronary artery emboliCoronary artery emboli
CausesCauses
CocaineCocaine
ArteriesArteries
Coronary anomaliesCoronary anomalies
Aortic dissectionAortic dissection
Pediatrics Kawasaki disease, Takayasu Pediatrics Kawasaki disease, Takayasu arteritisarteritis
Increased afterload which increases Increased afterload which increases myocardial demandmyocardial demand
Risk factors for atherosclerosisRisk factors for atherosclerosis
AgeAge
Male genderMale gender
SmokingSmoking
Hypercholesterolemia and triglyceridemiaHypercholesterolemia and triglyceridemia
Diabetes MellitusDiabetes Mellitus
Poorly controlled hypertensionPoorly controlled hypertension
Type A personalityType A personality
Risk factors for atherosclerosisRisk factors for atherosclerosis
Family HistoryFamily History
Sedentary lifestyleSedentary lifestyle
DifferentialsDifferentials
Acute coronary syndromeAcute coronary syndrome
AnxietyAnxiety
Aortic stenosisAortic stenosis
AsthmaAsthma
Cholecystitis and biliary colicCholecystitis and biliary colic
CholethiasisCholethiasis
COPDCOPD
DifferentialsDifferentials
Aortic DissectionAortic Dissection
EndocarditisEndocarditis
EsophagitisEsophagitis
ShockShock
MyocarditisMyocarditis
PericarditisPericarditis
Pulmonary embolismPulmonary embolism
Mechanisms of Myocardial damageMechanisms of Myocardial damage
The severity of an MI is dependent of three The severity of an MI is dependent of three factorsfactors
The level of the occlusion in the coronaryThe level of the occlusion in the coronary
The length of time of the occlusionThe length of time of the occlusion
The presence or absence of collateral The presence or absence of collateral circulationcirculation
Cardiac BiomarkersCardiac Biomarkers
Cardiac biomarkers are protein molecules Cardiac biomarkers are protein molecules released into the blood stream from released into the blood stream from damaged heart muscle damaged heart muscle
Since ECG can be inconclusive , Since ECG can be inconclusive , biomarkers are frequently used to evaluate biomarkers are frequently used to evaluate for myocardial injuryfor myocardial injury
These biomarkers have a characteristic These biomarkers have a characteristic rise and fall pattern rise and fall pattern
Troponin T and ITroponin T and I
These isoforms are very specific for cardiac These isoforms are very specific for cardiac injuryinjury
Preferred markers for detecting myocardial Preferred markers for detecting myocardial cell injurycell injury
Rise 2-6 hours after injuryRise 2-6 hours after injury
Peak in 12-16 hoursPeak in 12-16 hours
Stay elevated for 5-14 daysStay elevated for 5-14 days
Creatinine Kinase ( CK-MB)Creatinine Kinase ( CK-MB)
Creatinine Kinase is found in heart muscle Creatinine Kinase is found in heart muscle (MB), skeletal muscle (MM), and brain (BB)(MB), skeletal muscle (MM), and brain (BB)
Increased in over 90% of myocardial Increased in over 90% of myocardial infractioninfraction
However, it can be increased in muscle However, it can be increased in muscle trauma, physical exertion, post-op, trauma, physical exertion, post-op, convulsions, and other conditionsconvulsions, and other conditions
Creatine Kinase (MB)Creatine Kinase (MB)
Time sequence after myocardial infarctionTime sequence after myocardial infarction
Begins to rise 4-6 hoursBegins to rise 4-6 hours
Peaks 24 hoursPeaks 24 hours
returns to normal in 2 daysreturns to normal in 2 days
MB2 released from heart muscle and MB2 released from heart muscle and converted to MB1.converted to MB1.
A level of MB2 > or = 1 and a ratio of A level of MB2 > or = 1 and a ratio of MB2/MB1 > 1.5 indicates myocardial injuryMB2/MB1 > 1.5 indicates myocardial injury
MyoglobinMyoglobin
Damage to skeletal or cardiac muscle Damage to skeletal or cardiac muscle release myoglobin into circulationrelease myoglobin into circulation
Time sequence after infarctionTime sequence after infarction
Rises fast 2hoursRises fast 2hours
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 failureinjury and renal failure
Renal Failure and Renal Renal Failure and Renal TransplantationTransplantation
Diagnostic accuracy of serum markers of Diagnostic accuracy of serum markers of cardiac injury are altered in patients with cardiac injury are altered in patients with renal failurerenal failureCardiac troponins decreased diagnostic Cardiac troponins decreased diagnostic sensitivity and specificity in patients sensitivity and specificity in patients receiving renal replacement therapyreceiving renal replacement therapyCurrent data show levels of troponin I are Current data show levels of troponin I are unaltered while levels of troponin T may be unaltered while levels of troponin T may be elevatedelevated
CBCCBC
CBC is indicated if anemia is suspected as CBC is indicated if anemia is suspected as precipitantprecipitant
Leukocytosis may be observed within Leukocytosis may be observed within several hours after myocardial injury and several hours after myocardial injury and returns returns to levels within the reference returns returns to levels within the reference range within one weekrange within one week
Chemistry ProfileChemistry Profile
Potassium and magnesium levels should be Potassium and magnesium levels should be monitored and corrected monitored and corrected
Creatinine levels must be considered before Creatinine levels must be considered before using contrast dye for coronary angiography using contrast dye for coronary angiography and percutanous revascularizationand percutanous revascularization
C-reactive Protein (CRP)C-reactive Protein (CRP)
C- reactive protein is a marker of acute C- reactive protein is a marker of acute inflammationinflammation
Patients without evidence of myocardial Patients without evidence of myocardial necrosis but with elevated CRP are at necrosis but with elevated CRP are at increased risk of an eventincreased risk of an event
Chest X-RayChest X-Ray
Chest radiography may provide clues to an Chest radiography may provide clues to an alternative diagnosis ( aortic dissection or alternative diagnosis ( aortic dissection or pneumothorax)pneumothorax)
Chest radiography also reveals Chest radiography also reveals complications of myocardial infarction such complications of myocardial infarction such as heart failureas heart failure
EchocardiographyEchocardiography
Use 2-dimentional and M mode Use 2-dimentional and M mode echocardiography when evaluating overall echocardiography when evaluating overall ventricular function and wall motion ventricular function and wall motion abnormalitiesabnormalities
Echocardiography can also identify Echocardiography can also identify complications of MI ( eg. Valvular or complications of MI ( eg. Valvular or pericardial effusion, VSD)pericardial effusion, VSD)
ElectrocardiogramElectrocardiogram
A normal ECG does not exclude ACSA normal ECG does not exclude ACS
High probability include ST segment High probability include ST segment elevation in two contiguous leads or elevation in two contiguous leads or presence of q waves presence of q waves
Intermediate probability ST depressionIntermediate probability ST depression
T wave inversions are less specificT wave inversions are less specific
Localization of MILocalization of MI
ST elevation onlyST elevation onlyInferior wall- II, III, aVFInferior wall- II, III, aVFLateral wall_ I, aVL, V4-V6Lateral wall_ I, aVL, V4-V6Anteroseptal- V1-V3Anteroseptal- V1-V3Anterolateral- V1-V6Anterolateral- V1-V6Right ventricular- RV4, RV5Right ventricular- RV4, RV5Posterior- R/S ratio >1 in V1 and T wave Posterior- R/S ratio >1 in V1 and T wave inversioninversion
TherapyTherapy
The goals of therapy in AMI The goals of therapy in AMI are the expedient restoration of are the expedient restoration of normal coronary flow and the normal coronary flow and the maximum salvage of functional maximum salvage of functional myocardiummyocardium
Antiplatelet AgentsAntiplatelet Agents
Aspirin at lease 160mg immediately Aspirin at lease 160mg immediately
Interferes with function of cyclooxygenase Interferes with function of cyclooxygenase and inhibits the formation of thromboxaneand inhibits the formation of thromboxane
ASA alone has one of the greatest impact ASA alone has one of the greatest impact on the reduction of MI mortality.on the reduction of MI mortality.
Clopidogrel, ticlopidine, have not been Clopidogrel, ticlopidine, have not been shown in any large scal trail to be superior shown in any large scal trail to be superior to Aspirin in acute MIto Aspirin in acute MI
Supplemental OxygenSupplemental Oxygen
Because MI impairs the circulatory function Because MI impairs the circulatory function of the heart, oxygen extraction by the heart of the heart, oxygen extraction by the heart and other tissues may be diminished and other tissues may be diminished
Supplemental oxygen should be Supplemental oxygen should be administered to patient with symptoms and administered to patient with symptoms and or signs of pulmonary edema or pulse or signs of pulmonary edema or pulse oximetry readings less than 90%.oximetry readings less than 90%.
NitratesNitrates
IV nitrates to all patients with MI and IV nitrates to all patients with MI and congestive heart failure, persistent congestive heart failure, persistent ischemia, hypertension, or large anterior ischemia, hypertension, or large anterior wall MIwall MIPrimary benefit vasodilator effectPrimary benefit vasodilator effectMetabolized to nitric oxide in the vascular Metabolized to nitric oxide in the vascular endothelium, relaxes endotheliumendothelium, relaxes endotheliumVasodilatation reduces myocardial oxygen Vasodilatation reduces myocardial oxygen demand and preload and afterloaddemand and preload and afterload
Beta-blockersBeta-blockers
Recommended within 12 hours of MI Recommended within 12 hours of MI symptoms and continued indefinitelysymptoms and continued indefinitely
Reduces Myocardial mortality by Reduces Myocardial mortality by decreasing arrythmogenic deathdecreasing arrythmogenic death
Decrease the rate and force of myocardial Decrease the rate and force of myocardial contraction and decreases overall oxygen contraction and decreases overall oxygen demanddemand
Unfractionated heparinUnfractionated heparin
Forms a chemical complex with Forms a chemical complex with antithrombin III inactivates both free antithrombin III inactivates both free thrombin and factor Xathrombin and factor Xa
Recommended in patients with MI who Recommended in patients with MI who undergo PTCA or fibrinolytic therapy with undergo PTCA or fibrinolytic therapy with alteplasealteplase
Low-molecular weight heparinLow-molecular weight heparin
Direct activity against factors Xa and IIaDirect activity against factors Xa and IIaProven to be effective in treating ACS that Proven to be effective in treating ACS that are characterized by unstable angina or are characterized by unstable angina or non ST- elevation MInon ST- elevation MITheir fixed doses are easy to administer Their fixed doses are easy to administer and laboratory testing to measure their and laboratory testing to measure their therapeutic effect is not necessary makes therapeutic effect is not necessary makes them attractive alternative of un-them attractive alternative of un-fractionated heparinfractionated heparin
ThrombolyticsThrombolytics
Indicated with MI and ST segment Indicated with MI and ST segment elevation greater than 0.1mV in 2 elevation greater than 0.1mV in 2 contiguous ECG leads, or new onset contiguous ECG leads, or new onset LBBB, who present less than 12 hours but LBBB, who present less than 12 hours but not more than 24 hours after symptom not more than 24 hours after symptom onsetonsetThe most critical variable in achieving The most critical variable in achieving successful fibrinolysis is time form successful fibrinolysis is time form symptom onset to drug administrationsymptom onset to drug administration
ThrombolyticsThrombolytics
As a class the plasminogen activators have been As a class the plasminogen activators have been shown to restore coronary blood flow in 50-80% of shown to restore coronary blood flow in 50-80% of patientspatients
Contraindication active intracranial bleeding, CVA Contraindication active intracranial bleeding, CVA 2months, CNS neoplasm, HTN, coagulopathy2months, CNS neoplasm, HTN, coagulopathy
Retaplase slightly higher angiographic patency Retaplase slightly higher angiographic patency but did not translate into survival benefitbut did not translate into survival benefit
Intracranial bleed risk major drawbackIntracranial bleed risk major drawback
Glycoprotein IIb/IIIa AntagonistsGlycoprotein IIb/IIIa Antagonists
Potent inhibitors of platelet aggregationPotent inhibitors of platelet aggregation
Use during PCI and in patients with high Use during PCI and in patients with high risk features ACS have been shown to risk features ACS have been shown to reduce the composite end points of death, reduce the composite end points of death, reinfraction and the need for target lesionreinfraction and the need for target lesion
Percutanous Coronary InterventionPercutanous Coronary Intervention
Alternative if performed by skilled operator Alternative if performed by skilled operator in an experienced centerin an experienced centerStandard is a “ door to balloon” time of 90 Standard is a “ door to balloon” time of 90 minutesminutesPCI can successfully restore coronary PCI can successfully restore coronary blood flow in 90 to 95% of MI patientsblood flow in 90 to 95% of MI patientsPCI definitive survival advantage over PCI definitive survival advantage over fibrinolytics for MI patients who are in fibrinolytics for MI patients who are in cardiogenic shockcardiogenic shock
Surgical RevascularizationSurgical Revascularization
Emergent or surgical revascularization in Emergent or surgical revascularization in setting of failed PTCA in patients with setting of failed PTCA in patients with hemodynamic instability and coronary hemodynamic instability and coronary anatomy amendable to surgical graftinganatomy amendable to surgical graftingAlso indicated of mechanical complications Also indicated of mechanical complications of MI including VSD, free wall rupture, or of MI including VSD, free wall rupture, or acute MRacute MRCarries a higher risk of perioperative Carries a higher risk of perioperative mortality than elective CABGmortality than elective CABG
Lipid ManagementLipid Management
All post MI patients should be on AMA step All post MI patients should be on AMA step II diet ( < 7% of calories from saturated II diet ( < 7% of calories from saturated fats)fats)Post MI patients with LDL > 100 mg/dl are Post MI patients with LDL > 100 mg/dl are recommended to be on drug therapy to try recommended to be on drug therapy to try to lower levels to <100 mg/dlto lower levels to <100 mg/dlRecent data indicate that all MI patients Recent data indicate that all MI patients should be on statin therapy, regardless of should be on statin therapy, regardless of lipid levels or diet lipid levels or diet
Long term MedicationsLong term Medications
Most oral medications instituted in the Most oral medications instituted in the hospital at the time of MI are continued hospital at the time of MI are continued long termlong term
Aspirin, beta blockers and statin are Aspirin, beta blockers and statin are continued indefinitelycontinued indefinitely
ACEI indefinitely in patients with CHF, ACEI indefinitely in patients with CHF, ejection fraction <.40, hypertension, or ejection fraction <.40, hypertension, or diabetesdiabetes