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Acute Coronary Acute Coronary SyndromesSyndromes
Natalie Bermudez, RN, BSN, MSNatalie Bermudez, RN, BSN, MSClinical Educator for Cardiac Clinical Educator for Cardiac
TelemetryTelemetry
Learning ObjectivesLearning Objectives
Define the differences of ischemia, Define the differences of ischemia, injury, and infarct.injury, and infarct.
Define angina pectoris, etiology, s/s, Define angina pectoris, etiology, s/s, diagnosis, and treatmentdiagnosis, and treatment
Differentiate between UA, NSTEMI, & Differentiate between UA, NSTEMI, & STEMI: s/s, diagnosis, and treatmentSTEMI: s/s, diagnosis, and treatment
Localize area of infarct on a 12-lead Localize area of infarct on a 12-lead EKGEKG
Discuss women & heart diseaseDiscuss women & heart disease
National StatisticsNational StatisticsCoronary Artery DiseaseCoronary Artery Disease
Cardiovascular disease is the leading Cardiovascular disease is the leading cause of death among men and women cause of death among men and women
in all racial and ethnic groups.in all racial and ethnic groups.
Affects approximately 58 million Affects approximately 58 million Americans and costs the nation $274 Americans and costs the nation $274
billion each year, including health billion each year, including health expenditures and loss of productivityexpenditures and loss of productivity
(Woods et al, 2005, p.115)(Woods et al, 2005, p.115)
National StatisticsNational Statistics
According to the AHA, According to the AHA, 785,000 Americans will 785,000 Americans will
have an MI this year, and have an MI this year, and nearly 500,000 of them nearly 500,000 of them will experience anotherwill experience another
(Overbaugh, 2009, p. 42)
National StatisticsNational Statistics
In 2006, nearly 1.4 million In 2006, nearly 1.4 million patients were discharged patients were discharged
with a primary or secondary with a primary or secondary diagnosis of ACS, including diagnosis of ACS, including
537,000 with unstable 537,000 with unstable angina and 810,000 with angina and 810,000 with either NSTEMI or STEMIeither NSTEMI or STEMI
(Overbaugh, 2009, p. 42)
Atherosclerotic PlaqueAtherosclerotic Plaque
The usual cause of an acute The usual cause of an acute coronary syndrome is the coronary syndrome is the
rupture of an atherosclerotic rupture of an atherosclerotic plaqueplaque
(Phalen and Aehlert, 2006, p. 61)
ANGINA PECTORISANGINA PECTORIS
Angina PectorisAngina Pectoris
Latin phrase literally means “pain Latin phrase literally means “pain in the chest”in the chest”
Many different conditions are Many different conditions are responsible for causing angina responsible for causing angina
pectorispectoris
Stable (Classic) AnginaStable (Classic) Angina
Remains relatively constant and predictable Remains relatively constant and predictable in terms of frequency of episodes, in terms of frequency of episodes,
severity, duration, time of appearance, severity, duration, time of appearance, precipitating factors, and response to precipitating factors, and response to
therapytherapy
Usually related to emotional upset, exercise Usually related to emotional upset, exercise or exertion, exposure to cold weather, or exertion, exposure to cold weather,
consumption of heavy mealsconsumption of heavy meals
Duration of symptoms is typically 2 – 5 Duration of symptoms is typically 2 – 5 minutes; occasionally 10 – 15 minutesminutes; occasionally 10 – 15 minutes
Stable (Classic) AnginaStable (Classic) Angina
Treatment Includes:Treatment Includes:
Lifestyle Modifications (Diet & Lifestyle Modifications (Diet & Exercise)Exercise)
Antiplatelet Agents (aspirin)Antiplatelet Agents (aspirin)
Beta-Adrenergic BlockersBeta-Adrenergic Blockers
Antianginal Meds (SL nitroglycerin)Antianginal Meds (SL nitroglycerin)
Prinzmetal’s AnginaPrinzmetal’s AnginaAKA Variant AnginaAKA Variant Angina
It is the result of intense spasm of a It is the result of intense spasm of a segment of an epicardial coronary arterysegment of an epicardial coronary artery
Occurs exclusively at rest; early morningOccurs exclusively at rest; early morning
Lasts only a few minutes; however long Lasts only a few minutes; however long enough to produce dysrhythmias including enough to produce dysrhythmias including
v-tach or v-fib, as well as sudden deathv-tach or v-fib, as well as sudden death
Prinzmetal’s AnginaPrinzmetal’s Angina
Difficult to identify this type of anginaDifficult to identify this type of angina
Has been reported to occur with Has been reported to occur with migraine, Raynaud’s phenomenon, migraine, Raynaud’s phenomenon,
and aspirin-induced asthmaand aspirin-induced asthma
It is relieved by administration of It is relieved by administration of nitroglycerinnitroglycerin
Silent AnginaSilent Angina
Objective evidence of ischemia Objective evidence of ischemia (i.e. EKG changes with stress (i.e. EKG changes with stress
test)test)
No reports of symptomsNo reports of symptoms
ACUTE CORONARY ACUTE CORONARY SYNDROMESSYNDROMES
Acute Coronary Acute Coronary SyndromesSyndromes
ACS’s are a physiologic continuum ACS’s are a physiologic continuum of conditions caused by a similar of conditions caused by a similar sequence of pathologic events: a sequence of pathologic events: a
transient or permanent transient or permanent obstruction of a coronary arteryobstruction of a coronary artery
(Phalen and Aehlert, 2006, p. 60)
Acute Coronary Acute Coronary SyndromesSyndromes
These conditions are characterized by These conditions are characterized by an excessive demand or inadequate an excessive demand or inadequate
supply of Osupply of O22 and nutrients to the and nutrients to the heart muscle associated with:heart muscle associated with:
Plaque DisruptionPlaque Disruption
Thrombus FormationThrombus Formation
VasoconstrictionVasoconstriction
(Phalen and Aehlert, 2006, p. 60)
ACS’s: 3 CategoriesACS’s: 3 Categories
Unstable AnginaUnstable Angina
Non-ST-Segment Elevation MI Non-ST-Segment Elevation MI (NSTEMI)(NSTEMI)
ST-Segment Elevation MI (STEMI)ST-Segment Elevation MI (STEMI)
Blood Vessel Wall LayersBlood Vessel Wall Layers
Coronary Artery Coronary Artery ObstructionObstruction
How does it happen?How does it happen?
Fatty Streak
Fibrous Plaque
Ruptured Plaque
Advanced Atheromatous Plaque
Endothelial Damage Endothelial Damage
Progression from a fatty streak to Progression from a fatty streak to an advanced lesion is associated an advanced lesion is associated
with injured endothelium that with injured endothelium that activates the inflammatory activates the inflammatory
responseresponse
(Phalen and Aehlert, 2006, p. 61)
Rupture of Plaque Rupture of Plaque
Rupture of the plaque surface Rupture of the plaque surface occurs frequently during plaque occurs frequently during plaque growth and is probably the most growth and is probably the most
significant mechanism significant mechanism underlying the progression of underlying the progression of
coronary lesionscoronary lesions
(Phalen and Aehlert, 2006, p. 61)
Stable & Unstable Stable & Unstable Plaque Plaque
As plaque builds up, it can become either stable or unstable. As plaque builds up, it can become either stable or unstable.
Unstable plaque is more prone to sudden rupture, a potentially Unstable plaque is more prone to sudden rupture, a potentially life-threatening even.life-threatening even.
Stable PlaqueStable Plaque
Hard, consist primarily of Hard, consist primarily of collagen-rich sclerotic tissue, collagen-rich sclerotic tissue, and have a thick fibrous cap and have a thick fibrous cap
over the lipid core that over the lipid core that separates it from contact separates it from contact
with bloodwith blood
70%-diameter stenosis is 70%-diameter stenosis is required to produce anginal required to produce anginal
symptomssymptoms
(Phalen and Aehlert, 2006, p. 62)(Phalen and Aehlert, 2006, p. 62)
Unstable PlaqueUnstable Plaque
Soft and have a thin fibrous Soft and have a thin fibrous tissue over the lipid core tissue over the lipid core that separates it from the that separates it from the
vessel lumenvessel lumen
Rupture tends to occur near Rupture tends to occur near the normal part of the the normal part of the
vessel wallvessel wall
It is unknown whether plaque It is unknown whether plaque rupture is triggered on rupture is triggered on
spontaneouslyspontaneously
(Phalen and Aehlert, 2006, p. 63, 64)(Phalen and Aehlert, 2006, p. 63, 64)
Ischemia, Ischemia, Injury, and Injury, and InfarctionInfarction
IschemiaIschemia
Myocardial ischemia is the result of an Myocardial ischemia is the result of an imbalance between the metabolic needs imbalance between the metabolic needs
of the myocardium and the flow of of the myocardium and the flow of oxygenated blood to itoxygenated blood to it
EKG Changes:EKG Changes: ST-segment depression ST-segment depression & T-wave inversion& T-wave inversion
(Related to delays in depolarization and (Related to delays in depolarization and repolarization)repolarization)
IschemiaIschemia
May occur as a result of either or both of the May occur as a result of either or both of the following:following:
Demand Ischemia:Demand Ischemia: Increased myocardial O Increased myocardial O22 demand demand
(Anemia, hypoxemia, coronary artery narrowing due to a (Anemia, hypoxemia, coronary artery narrowing due to a thrombus, vasospasm, or rapid progression of thrombus, vasospasm, or rapid progression of
atherosclerosis)atherosclerosis)
Supply Ischemia:Supply Ischemia: Reduced myocardial O Reduced myocardial O22 supply supply(Exercise, smoking, heavy meals, fever, HF, (Exercise, smoking, heavy meals, fever, HF,
tachydysrhythmias, OCM, cocaine, amphetamines, tachydysrhythmias, OCM, cocaine, amphetamines, emotional stress, hypertension, cold weather, aortic emotional stress, hypertension, cold weather, aortic
stenosis, pheochromocytoma, thyrotoxicosis)stenosis, pheochromocytoma, thyrotoxicosis)
InjuryInjury
Ischemia prolonged more than just a few Ischemia prolonged more than just a few minutes results in myocardial injury.minutes results in myocardial injury.
Injured myocardial cells are still alive but will Injured myocardial cells are still alive but will infarct if the ischemia is not quickly correctedinfarct if the ischemia is not quickly corrected
EKG Changes:EKG Changes: ST-segment elevation ST-segment elevation
(Injured myocardial cells do not depolarize (Injured myocardial cells do not depolarize completely, remaining electrically more completely, remaining electrically more
positive than the uninjured areas positive than the uninjured areas surrounding them)surrounding them)
InfarctionInfarction
A myocardial infarction occurs when blood A myocardial infarction occurs when blood flow to the heart muscle stops or is flow to the heart muscle stops or is
suddenly decreased long enough to cause suddenly decreased long enough to cause cell deathcell death
Infarcted cells are without function and Infarcted cells are without function and cannot respond to electrical stimulus or cannot respond to electrical stimulus or
provide any mechanical functionprovide any mechanical function
(Thalen and Aehlert, 2006, p, 67)(Thalen and Aehlert, 2006, p, 67)
EKG Changes:EKG Changes: ST-segment elevation, ST-segment elevation,
T-wave inversion, abnormal Q wavesT-wave inversion, abnormal Q waves
Abnormal Q WavesAbnormal Q WavesAn abnormal Q wave indicates the presence of
dead myocardial tissue and subsequently a loss of electrical activity (Thalen and Aelhert, 2006, p. 77)
Pathological Q waves represent transmural MI and are most commonly seen with STEMI (Davis,
2004)
Sometimes occurs within hours of onset of chest pain
More commonly appears 1-3 days after the event
Most Post MI Q waves are permanent
Pathologic Q WavesPathologic Q Waves
1/3 or greater than the amplitude of an R wave
And/or greater than 40 ms (0.04 secs)
Q Wave
2.5 mm
R Wave
5 mm
Risk Factors for Risk Factors for DevelopingDeveloping
CORONARY ARTERY CORONARY ARTERY DISEASEDISEASE
Risk FactorsRisk FactorsNon-Non-
ModifiableModifiable
HeredityHeredity AgeAge
Race Race GenderGender
ModifiableModifiable
ETOH IntakeETOH Intake HypertensioHypertensio
n n Lipids & Lipids & CholesterolCholesterol
SmokingSmoking Drug UseDrug Use
StressStress
ContributingContributing
Inactive Inactive LifestyleLifestyle
DiabetesDiabetes ObesityObesity
Causes and Causes and Diagnostic Findings Diagnostic Findings
forfor
Unstable AnginaUnstable AnginaNSTEMINSTEMISTEMISTEMI
Unstable AnginaUnstable Angina
Cause:Cause:
Thrombus partially or intermittently Thrombus partially or intermittently occludes the coronary arteryoccludes the coronary artery
Diagnostic Findings:Diagnostic Findings:
ST-segment depression or T-wave ST-segment depression or T-wave inversioninversion
Normal Cardiac MarkersNormal Cardiac Markers
(Overbaugh, 2009, p. 46)(Overbaugh, 2009, p. 46)
NSTEMINSTEMI
Cause:Cause:
Thrombus partially or intermittently the Thrombus partially or intermittently the occludes coronary arteryoccludes coronary artery
Diagnostic Findings:Diagnostic Findings:
ST-segment depression or T-wave ST-segment depression or T-wave inversioninversion
Elevated Cardiac biomarkersElevated Cardiac biomarkers
(Overbaugh, 2009, p. 46)(Overbaugh, 2009, p. 46)
STEMISTEMI
Cause:Cause:
Thrombus fully occludes the coronary Thrombus fully occludes the coronary arteryartery
Diagnostic Findings:Diagnostic Findings:
ST-segment elevation or new left ST-segment elevation or new left bundle branch blockbundle branch block
Elevated Cardiac BiomarkersElevated Cardiac Biomarkers
(Overbaugh, 2009, p. 47)(Overbaugh, 2009, p. 47)
Cardiac MarkersCardiac Markers
Cardiac EnzymesCardiac Enzymes
Cardiac EnzymesCardiac EnzymesA.K.A. ACP (Acute Cardiac Profile)A.K.A. ACP (Acute Cardiac Profile)
Normal Ranges:Normal Ranges:
CPK: 39 – 308CPK: 39 – 308
CK-MB: 0 – 3.60CK-MB: 0 – 3.60
**Troponin I: 0 – 0.099****Troponin I: 0 – 0.099**
Cardiac EnzymesCardiac EnzymesOrdered for patients c/o chest pain and Ordered for patients c/o chest pain and
suspected AMIsuspected AMI
CE’s are drawn in sets of three 6 to 8 CE’s are drawn in sets of three 6 to 8 hours aparthours apart
Sometimes initial results are negativeSometimes initial results are negative
CK-MB & Troponins are released within CK-MB & Troponins are released within hours of a cardiac eventhours of a cardiac event
Cardiac EnzymesCardiac EnzymesCK-MB or CPK-MBCK-MB or CPK-MB
Creatine PhosphokinaseCreatine Phosphokinase
Rise within 4-6 hours after an AMIRise within 4-6 hours after an AMI
Peak @ 18 – 24 hours (6x > normal)Peak @ 18 – 24 hours (6x > normal)
Return to normal within 3 – 4 daysReturn to normal within 3 – 4 days
Cardiac EnzymesCardiac EnzymesTroponin ITroponin I
Rise within 3 hours of an AMIRise within 3 hours of an AMI
Preferred cardiac enzyme in Preferred cardiac enzyme in diagnosis of an AMI diagnosis of an AMI
Cardiac EnzymesCardiac Enzymes
Lab will call nursing for critical lab Lab will call nursing for critical lab valuesvalues
Physician needs to be notified Physician needs to be notified immediately for elevated immediately for elevated
Troponin levelsTroponin levels
Cardiac EnzymesCardiac Enzymes
Patients with elevated CE’s usually Patients with elevated CE’s usually undergo a stress test and/or undergo a stress test and/or cardiac catheterization for cardiac catheterization for
further investigation of cause of further investigation of cause of chest pain.chest pain.
Signs and Symptoms ofSigns and Symptoms of
Unstable Angina,Unstable Angina,NSTEMI, &STEMINSTEMI, &STEMI
Signs & SymptomsSigns & Symptoms
UA, NSTEMI, & STEMIUA, NSTEMI, & STEMI
Pain with or without radiation to arm, Pain with or without radiation to arm, neck, back, or epigastric regionneck, back, or epigastric region
SOB, tachypnea, decreased SaOSOB, tachypnea, decreased SaO22
Tachycardia, hypotension or Tachycardia, hypotension or hypertensionhypertension
Diaphoresis, nausea, lightheadedness,Diaphoresis, nausea, lightheadedness, Rhythm abnormalitiesRhythm abnormalities
Signs & Symptoms: Chest Signs & Symptoms: Chest PainPain
UA:UA: Occurs with Occurs with
rest or rest or exertion; limits exertion; limits
activityactivity
NSTEMINSTEMI Occurs with Occurs with rest or exertion; rest or exertion;
limits activitylimits activity Longer duration Longer duration
and more and more severe than in severe than in
unstable anginaunstable angina
(Overbaugh, 2009, pp. 46, (Overbaugh, 2009, pp. 46, 47)47)
STEMISTEMI Occurs with rest Occurs with rest
or exertion; or exertion; limits activitylimits activity
Longer duration Longer duration and more severe and more severe than in unstable than in unstable
angina angina (irreversible tissue (irreversible tissue
damage damage [infarction] occurs [infarction] occurs if perfusion is not if perfusion is not
restored)restored)
Treatment ofTreatment of
Unstable AnginaUnstable AnginaNSTEMINSTEMISTEMISTEMI
Goals for TreatmentGoals for Treatment
Minimize Infarct SizeMinimize Infarct Size
Salvage ischemic MyocardiumSalvage ischemic Myocardium
Alleviate VasoconstrictionAlleviate Vasoconstriction
Reduce Myocardial OReduce Myocardial O22 Demand Demand
Prevent & Manage ComplicationsPrevent & Manage Complications
Improve Chances of SurvivalImprove Chances of Survival(Phalen and Aehlert, 2006, p. 60)
TreatmentTreatmentUAUA
Oxygen to Oxygen to maintain Omaintain O22 sat sat
> 90%> 90% NTG or MSO4 NTG or MSO4
to control painto control pain BB’s, CCB’s, BB’s, CCB’s, ACEI’s, statins, ACEI’s, statins,
clopidogrel, clopidogrel, unfractionated unfractionated
heparin or heparin or LMWH, LMWH,
glycoprotein glycoprotein IIb/IIIa IIb/IIIa
inhibitorsinhibitors
NSTEMINSTEMISame as UA plus:Same as UA plus: Cardiac cath & Cardiac cath &
possible PCI for possible PCI for patients with patients with ongoing CP, ongoing CP,
hemodynamic hemodynamic instability, or instability, or
increased risk of increased risk of worsening worsening
clinical conditionclinical condition
(Overbaugh, 2009, pp. 46, (Overbaugh, 2009, pp. 46, 47)47)
STEMISTEMISame as UA & Same as UA & NSTEMI except:NSTEMI except:
No glycoprotein No glycoprotein IIb/IIIa inhibitorsIIb/IIIa inhibitors
PCI should be PCI should be done within 90 done within 90
minutes of minutes of medical medical
evaluationevaluation Fibrinolytic Fibrinolytic therapy within therapy within 30 minutes of 30 minutes of
evaluationevaluation
Beta-Adrenergic BlockersBeta-Adrenergic Blockers
Negative Inotropic and Chronotropic Negative Inotropic and Chronotropic EffectsEffects
Reduces myocardial contractility and Reduces myocardial contractility and heart rate resulting in decreased heart rate resulting in decreased
demand for oxygendemand for oxygen
Pharmacologic Pharmacologic TreatmentTreatment
Calcium Channel BlockersCalcium Channel BlockersNon-dihydropyridinesNon-dihydropyridines
Negative Inotropic and Chronotropic EffectsNegative Inotropic and Chronotropic Effects
Reduces myocardial contractility and heart Reduces myocardial contractility and heart rate resulting in decreased demand for rate resulting in decreased demand for
oxygenoxygen
Also work to decrease workload of the heart Also work to decrease workload of the heart by coronary arteriolesby coronary arterioles
Pharmacologic Pharmacologic TreatmentTreatment
NitroglycerinNitroglycerin
Promotes decrease OPromotes decrease O22 demand by demand by dilating veins which decreases venous dilating veins which decreases venous
return to the heart thus decreasing return to the heart thus decreasing ventricular filling (decreases preload)ventricular filling (decreases preload)
Decrease in wall tension decreases ODecrease in wall tension decreases O22 demanddemand
(Frank-Starling Effect)(Frank-Starling Effect)
Pharmacologic Pharmacologic TreatmentTreatment
Morphine SulfateMorphine Sulfate
Decreases pain and anxiety – decreasing Decreases pain and anxiety – decreasing heart rate and oxygen consumptionheart rate and oxygen consumption
Reduces cardiac preload and afterload – Reduces cardiac preload and afterload – decreasing workload of the heartdecreasing workload of the heart
Relaxes bronchioles – increasing Relaxes bronchioles – increasing oxygenationoxygenation
Pharmacologic Pharmacologic TreatmentTreatment
Antiplatelet AgentsAntiplatelet Agents
Aspirin (acetalsalicylic acid):Aspirin (acetalsalicylic acid): Low dose, Low dose, long-term aspirin use irreversibly long-term aspirin use irreversibly
blocks formation of thromboxane Ablocks formation of thromboxane A22 in in platelets, producing an inhibitory effect platelets, producing an inhibitory effect
on platelet aggregation on platelet aggregation
Pharmacologic Pharmacologic TreatmentTreatment
Antiplatelet AgentsAntiplatelet Agents
Plavix (clopidogrel):Plavix (clopidogrel): Inhibits 1 Inhibits 1stst and 2 and 2ndnd Phases ADP-induced affects of platelet Phases ADP-induced affects of platelet
aggregationaggregation
Pharmacologic Pharmacologic TreatmentTreatment
Decreases the rate of Decreases the rate of cholesterol productioncholesterol production
Liver needs HMG-CoA Liver needs HMG-CoA reductase to make reductase to make
cholesterolcholesterol
When less cholesterol is When less cholesterol is produced liver needs to produced liver needs to “recycle” LDL from the “recycle” LDL from the
blood circulationblood circulation
Pharmacologic Pharmacologic TreatmentTreatment
HMG-CoA Reductase InhibitorsHMG-CoA Reductase Inhibitors
““Statins”Statins”
Women & Heart Women & Heart DiseaseDisease
National StatisticsNational Statistics
American Heart Association:American Heart Association:
About 7.3 million females About 7.3 million females alive today have a history of alive today have a history of
heart attack, angina heart attack, angina pectoris, or bothpectoris, or both
NationalNational StatisticsStatistics
Women with diabetes and CVD, especially Women with diabetes and CVD, especially African American and Hispanic, die at a African American and Hispanic, die at a
higher rate than men or non-diabetic womenhigher rate than men or non-diabetic women
Since 1984, the number of CVD deaths for Since 1984, the number of CVD deaths for females has exceeded those for males. females has exceeded those for males.
In 2004, CVD was the cause of death in In 2004, CVD was the cause of death in 459,096 females. Females represent 52.8 459,096 females. Females represent 52.8
percent of deaths from CVD.percent of deaths from CVD.
National StatisticsNational Statistics
According to the American Heart Association:According to the American Heart Association:
More women than men have angina More women than men have angina pectoris in total numbers (4.6 pectoris in total numbers (4.6
million versus. 4.4 million)million versus. 4.4 million)
About 25,000 females diagnosed with About 25,000 females diagnosed with angina pectoris were discharged angina pectoris were discharged from short-stay hospitals in 2005from short-stay hospitals in 2005
Atypical Chest PainAtypical Chest PainWomen experience cardiac chest pain differently!!Women experience cardiac chest pain differently!!
Discomfort varies greatly and be more Discomfort varies greatly and be more generalized or subtlegeneralized or subtle
Chest heaviness, squeezingChest heaviness, squeezing Pain in left chest, midabdomen, back, or Pain in left chest, midabdomen, back, or
shouldershoulder Arm painArm pain
Sharp, fleeting painSharp, fleeting pain PalpitationsPalpitations
(Cheek and Sherrod, 2008)(Cheek and Sherrod, 2008)
Atypical Chest PainAtypical Chest Pain
During an MI:During an MI:
Discomfort is more likely to occur in neck, back, Discomfort is more likely to occur in neck, back, arm, shoulder, jaw, or throatarm, shoulder, jaw, or throat
Sometimes occurring with n/v, indigestion, Sometimes occurring with n/v, indigestion, upper abdominal pain, dyspnea, fatigue, upper abdominal pain, dyspnea, fatigue,
diaphoresis, dizziness, or faintingdiaphoresis, dizziness, or fainting
(Cheek and Sherrod, 2008)(Cheek and Sherrod, 2008)
Atypical FindingsAtypical Findings
An older women or one with diabetes may not An older women or one with diabetes may not experience any pain during an MIexperience any pain during an MI
EKG findings are different for men and womenEKG findings are different for men and women
Women are less likely to have ST-segment Women are less likely to have ST-segment elevationelevation
(Cheek and Sherrod, 2008, pp. 38, 39)(Cheek and Sherrod, 2008, pp. 38, 39)
Aspirin within 24 hoursAspirin within 24 hours PCI within 90 minutes for STEMIPCI within 90 minutes for STEMI
LVF Assessment (echocardiogram)LVF Assessment (echocardiogram) ACEI or ARB for EF < 40%ACEI or ARB for EF < 40%
If +MI, aspirin & BB ordered at D/CIf +MI, aspirin & BB ordered at D/C ““STATIN” prescribed at dischargeSTATIN” prescribed at discharge
Discharge medications to include aspirin & Discharge medications to include aspirin & beta-blocker if positive for MIbeta-blocker if positive for MI
Adult smoking cessation advice/counselingAdult smoking cessation advice/counseling
TJC Core Measures TJC Core Measures for AMIfor AMI
Cardiac Catheterization Cardiac Catheterization ProceduresProcedures
Cardiac Catheterization Cardiac Catheterization ProceduresProcedures
Cardiac Catheterization Cardiac Catheterization ProceduresProcedures
Before & AfterBefore & After
Post Myocardial Post Myocardial Infarction Infarction
ComplicationsComplications
Post MI ComplicationsPost MI Complications
ArrhythmiasArrhythmias
Cardiac ArrestCardiac Arrest
Cardiac Muscle Cardiac Muscle DysfunctionDysfunction
Cardiogenic Cardiogenic ShockShock
(Haworth and Pratowski, 2000 p. 90)
Heart FailureHeart Failure
Mitral Mitral InsufficienciesInsufficiencies
PericarditisPericarditis
ThromboembolisThromboembolismm
GI ComplaintsGI Complaints
Post MI: Common Post MI: Common ArrhythmiasArrhythmias
Atrial FibrillationAtrial Fibrillation
Premature Ventricular ContractionsPremature Ventricular Contractions
Ventricular TachycardiaVentricular Tachycardia
Accelerated Idioventricular RhythmAccelerated Idioventricular Rhythm
Ventricular FibrillationVentricular Fibrillation
Atrioventricular BlockAtrioventricular Block(Haworth and Pratowski, 2000 p.
91)
Localizing the Localizing the Affected Area of Affected Area of
Ischemia and Ischemia and InfarctionInfarction
12-Lead EKG: 12-Lead EKG: Precordial & Limb LeadsPrecordial & Limb Leads
Limb Leads: Limb Leads: I, II, III, aVR, aVL, aVFI, II, III, aVR, aVL, aVF
I, II, III
aVR, aVL, aVF
EKG
Limb Leads: I, II, IIILimb Leads: I, II, III
BipolarBipolar
Each of these leads has a distinct Each of these leads has a distinct negative pole and a distinct negative pole and a distinct
positive polepositive pole
These were the 1These were the 1stst leads to be used leads to be used when EKG’s were developedwhen EKG’s were developed
(Phalen and Aehlert, 2006, p. 24)
Limb Leads
Limb Leads: aVR, aVL, Limb Leads: aVR, aVL, aVFaVF
““a” = augmenteda” = augmented
““V” = voltageV” = voltage
““R” = right armR” = right arm
““L” = left armL” = left arm
““F” = left foot F” = left foot (leg)(leg)
(Phalen and Aehlert, 2006, p. 24, 26)
UnipolarUnipolar
Have a distinct Have a distinct positive pole positive pole
but do not have but do not have a distinct a distinct
negative polenegative pole
Limb Leads
Chest Leads: VChest Leads: V11-V-V66
V1-V6
Chest Leads: VChest Leads: V11-V-V66
Aka Precordial LeadsAka Precordial Leads
UnipolarUnipolar
The positive electrode for each lead The positive electrode for each lead is placed on a specific location on is placed on a specific location on
the chest and the heart is the the chest and the heart is the theoretical negative electrodetheoretical negative electrode
(Phalen and Aehlert, 2006, p. 25)
Chest Leads
R-wave ProgressionR-wave Progression
Localizing EKG ChangesLocalizing EKG Changes
I: lateralI: lateral
II: inferiorII: inferior
III: inferiorIII: inferior
aVR: noneaVR: none
aVL: lateralaVL: lateral
aVF: inferioraVF: inferior(Phalen and Aehlert, 2006, p. 86)
VV11: septum: septum
VV22: septum: septum
VV33: anterior: anterior
VV44: anterior: anterior
VV55: lateral: lateral
VV66: lateral: lateralLimb Leads
ILateral
LAD or RCA branch
aVRNone
V1SeptalLAD
V4Anterior
LAD
IIInferior
RCA
aVLLateral
LAD or RCA branch
V2SeptalLAD
V5Lateral
LAD or RCA branch
IIIInferior
RCA
aVFInferior
RCA
V3Anterior
LAD
V6Lateral
LAD or RCA branch
Anterolateral Wall Anterolateral Wall MIMI
Leads: I, VLeads: I, V33-V-V66, AVL, AVL
Reciprocal ST-segment Depression in Reciprocal ST-segment Depression in Inferior LeadsInferior Leads
Inferior/Posterior Wall MIInferior/Posterior Wall MILeads: II, III, AVFLeads: II, III, AVF
Reciprocal ST depression in Posterior LeadsReciprocal ST depression in Posterior Leads
If ST elevation is seen in II, III, and/or AVF, then look for reciprocal If ST elevation is seen in II, III, and/or AVF, then look for reciprocal changes (ST-depression) in V1 – V4, indicates a posterior MIchanges (ST-depression) in V1 – V4, indicates a posterior MI
Posterior Wall MIPosterior Wall MIHyperacute: Mirror image of acute injury in leads VHyperacute: Mirror image of acute injury in leads V11--
VV33
Fully Involved: Tall R-wave, Tall upright T-wave in Fully Involved: Tall R-wave, Tall upright T-wave in leads Vleads V11-V-V33
STEMI & New BBBSTEMI & New BBB
Infarct-induced BBB – increased Infarct-induced BBB – increased mortality rate between 40% and 60%mortality rate between 40% and 60%
Increased rate of cardiogenic shock – Increased rate of cardiogenic shock – up to 70%up to 70%
New-Onset BBB is an indication of a New-Onset BBB is an indication of a bigger problem – extensive infarctionbigger problem – extensive infarction– Tissue lost due to infarct is what Tissue lost due to infarct is what
increases the mortality rate and increases the mortality rate and cardiogenic shockcardiogenic shock
STEMI & New BBBSTEMI & New BBB
Patients that have septal or Patients that have septal or anteroseptal infarcts are more likely to anteroseptal infarcts are more likely to develop new-onset BBBdevelop new-onset BBB
New-Onset BBB also indicates a higher New-Onset BBB also indicates a higher likelihood of developing AV blockslikelihood of developing AV blocks
On the other hand, an old LBBB can On the other hand, an old LBBB can produce ST-segment elevation and wide produce ST-segment elevation and wide Q waves that are similar to infarctionQ waves that are similar to infarction
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