acute coronary syndrome - bmh/tele

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)


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


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



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


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


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


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


ST-segment depression or T-wave ST-segment depression or T-wave inversioninversion

Elevated Cardiac biomarkersElevated Cardiac biomarkers


STEMISTEMI

Cause:Cause:

Thrombus fully occludes the coronary Thrombus fully occludes the coronary arteryartery


ST-segment elevation or new left ST-segment elevation or new left bundle branch blockbundle branch block

Elevated Cardiac BiomarkersElevated Cardiac Biomarkers


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


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


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


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)


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


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


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


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


HMG-CoA Reductase InhibitorsHMG-CoA Reductase Inhibitors

““Statins”Statins”

Women & Heart Women & Heart DiseaseDisease


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.


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

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


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


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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