Acute Coronary Syndromes. Epidemiology Ischemic Heart Disease (IHD) is the leading cause of morbidity and mortality worldwide Ischemic Heart Disease (IHD)

Acute Coronary Acute Coronary SyndromesSyndromes

EpidemiologyEpidemiology

Ischemic Heart Disease (IHD) is the leading cause of Ischemic Heart Disease (IHD) is the leading cause of morbidity and mortality worldwidemorbidity and mortality worldwide

Over the next 10 years, IHD will become the leading Over the next 10 years, IHD will become the leading cause of death and disability in most developing cause of death and disability in most developing countriescountries

IHD is the leading cause of death in USA ; 1 million IHD is the leading cause of death in USA ; 1 million annuallyannually

50 % of all cardiovascular deaths occur in women50 % of all cardiovascular deaths occur in women Despite educational efforts, patients with Acute Despite educational efforts, patients with Acute

Myocardial Infarction (AMI) delay an average of 2 to Myocardial Infarction (AMI) delay an average of 2 to 6 hours before seeking health care6 hours before seeking health care

Diagnosis remains a challengeDiagnosis remains a challenge

Of the 1.25 million AMI’s in the USA yearly, over 80 Of the 1.25 million AMI’s in the USA yearly, over 80 % present to the Emergency Department (ED)% present to the Emergency Department (ED)

The history, exam and ECG can be nondiagnosticThe history, exam and ECG can be nondiagnostic Past studies : 5 to 8% of AMI’s are sent homePast studies : 5 to 8% of AMI’s are sent home Recent studies : 2 to 5% of AMI’s are sent homeRecent studies : 2 to 5% of AMI’s are sent home Mortality doubles when AMI’s are sent home Mortality doubles when AMI’s are sent home

Acute Coronary Syndromes (ACS)Acute Coronary Syndromes (ACS)

Maintain high clinical suspicionMaintain high clinical suspicion Early recognitionEarly recognition Early risk stratificationEarly risk stratification Optimize therapy

4 Areas of Delay4 Areas of Delay

Patient seeking carePatient seeking care Early triage with ECGEarly triage with ECG Delay in clinical decision to treatDelay in clinical decision to treat TreatmentTreatment

Aspirin, oxygen, beta-blocker, Unfractionated Aspirin, oxygen, beta-blocker, Unfractionated heparin or Low Molecular Weight Heparinheparin or Low Molecular Weight Heparin

Thrombolytics (door to drug in under 60 minutes)Thrombolytics (door to drug in under 60 minutes) Intervention (door to cath lab in under 2.2 hours)Intervention (door to cath lab in under 2.2 hours)

ACS : Clinical SyndromesACS : Clinical Syndromes

AnginaAngina Class I (severe exertion) to IV (with any activity or at rest)Class I (severe exertion) to IV (with any activity or at rest) Fixed stenotic lesion ; stable precipitating and relieving factorsFixed stenotic lesion ; stable precipitating and relieving factors

Unstable Angina Pectoris (USAP)Unstable Angina Pectoris (USAP) Increasing frequency, transition to a higher class, pain at restIncreasing frequency, transition to a higher class, pain at rest

Variant (Prinzmetal’s) anginaVariant (Prinzmetal’s) angina AMIAMI

2 of 3 W.H.O. criteria : 2 of 3 W.H.O. criteria : clinical history or setting, ECG changes, positive cardiac clinical history or setting, ECG changes, positive cardiac

markersmarkers Non-ST Elevation (NSTE) ACS versus ST Elevation Non-ST Elevation (NSTE) ACS versus ST Elevation

Myocardial Infarction (STEMI)Myocardial Infarction (STEMI) Various reperfusion and adjunctive therapies are based Various reperfusion and adjunctive therapies are based

on the presence of ST segment elevation in the on the presence of ST segment elevation in the appropriate clinical settingappropriate clinical setting

Pathophysiology of ACSPathophysiology of ACS

Endothelial damage occurs by plaque disruption, Endothelial damage occurs by plaque disruption, irregular luminal lesions or shear injuryirregular luminal lesions or shear injury

Platelet aggregation is followed by thrombus formation Platelet aggregation is followed by thrombus formation Ischemia causing local mediator release and vasospasmIschemia causing local mediator release and vasospasm Reperfusion injuryReperfusion injury In USAP spontaneous thrombolysis occurs rapidly.In USAP spontaneous thrombolysis occurs rapidly. Persistence of occlusive thrombus for 60 to 90 minutes Persistence of occlusive thrombus for 60 to 90 minutes

before spontaneous lysis results in a non-STE AMI.before spontaneous lysis results in a non-STE AMI. Transmural AMI occurs when the thrombus occlusion Transmural AMI occurs when the thrombus occlusion

lasts for 2 to 3 hours.lasts for 2 to 3 hours.

History & Physical……and Atypical History & Physical……and Atypical PresentationsPresentations

History is essential … but not diagnostic of ACSHistory is essential … but not diagnostic of ACS only 20 to 30 % report crushing or pressure painonly 20 to 30 % report crushing or pressure pain

Beware of atypical presentationsBeware of atypical presentations Up to 20 % of ACS present with pain in other areas (arm, back, Up to 20 % of ACS present with pain in other areas (arm, back,

abdomen)abdomen) No pain in 25 % of diabeticsNo pain in 25 % of diabetics Burning pain in 15 % of USAP or AMI (may get relief with Burning pain in 15 % of USAP or AMI (may get relief with

antacids)antacids) Right sided radiation in up to 30 %Right sided radiation in up to 30 % Chest wall tenderness in 15 % of AMI’sChest wall tenderness in 15 % of AMI’s Anginal equivalent symptoms in 30 % of AMI’sAnginal equivalent symptoms in 30 % of AMI’s

Dyspnea, nausea, diaphoresis, back pain, jaw painDyspnea, nausea, diaphoresis, back pain, jaw pain Altered mental status (especially if > 85 y/o)Altered mental status (especially if > 85 y/o) Mortality 3-fold greater (50 % vs 18 %)Mortality 3-fold greater (50 % vs 18 %)

High risk groups : young, elderly, diabeticHigh risk groups : young, elderly, diabetic Physical Exam most helpful in excluding noncardiac causesPhysical Exam most helpful in excluding noncardiac causes

Differential DiagnosisDifferential Diagnosis

Causes of chest painCauses of chest pain Most are noncardiac and not seriousMost are noncardiac and not serious Acute coronary syndromeAcute coronary syndrome Pulmonary embolismPulmonary embolism Aortic dissectionAortic dissection Pericarditis / tamponadePericarditis / tamponade Pneumothorax / tension pneumothoraxPneumothorax / tension pneumothorax Pulmonary parenchymal process : pneumonia, Pulmonary parenchymal process : pneumonia,

inflammatory process, benign and malignant inflammatory process, benign and malignant processesprocesses

Diagnostic StudiesDiagnostic Studies

ECGECG Serial ECG’sSerial ECG’s Cardiac enzymesCardiac enzymes

Risk Stratify for other studies based on Risk Stratify for other studies based on history, ECG, and above studieshistory, ECG, and above studies

The ElectrocardiogramThe Electrocardiogram

Advantages:Advantages: select appropriate therapyselect appropriate therapy determine response to treatment determine response to treatment determine inpatient dispositiondetermine inpatient disposition predict complications / deathpredict complications / death


Beware that the 12-lead ECG is diagnostic of Beware that the 12-lead ECG is diagnostic of transmural AMI in only 25 to 50 % of casestransmural AMI in only 25 to 50 % of cases

Non-specific ST / T-wave abnormalities Non-specific ST / T-wave abnormalities 6 % of transmural AMI’s6 % of transmural AMI’s 30 % of NSTE-AMI 30 % of NSTE-AMI 20 % of cases of unstable angina20 % of cases of unstable angina

Completely normal in 3 to 4 % of transmural AMIsCompletely normal in 3 to 4 % of transmural AMIs Serial ECGs may increase sensitivity by 10 to 20 %Serial ECGs may increase sensitivity by 10 to 20 %


Nondiagnostic ECG seen in 50 %Nondiagnostic ECG seen in 50 % Nonspecific ST-Twave (NSSTTW) changesNonspecific ST-Twave (NSSTTW) changes

Less than 1 mm ST depressionLess than 1 mm ST depression Blunted, flattened or biphasic T wavesBlunted, flattened or biphasic T waves

Low risk of AMI (4 %) yet 20 % risk of USAPLow risk of AMI (4 %) yet 20 % risk of USAP If good story & NSSTTW changes : ADMITIf good story & NSSTTW changes : ADMIT

LVH, LBBB, VPR may mask signs of acute LVH, LBBB, VPR may mask signs of acute ischemiaischemia


Low-risk criteriaLow-risk criteria

(14 % AMI, 0.6 % Cardiac events, 0 % mortality)(14 % AMI, 0.6 % Cardiac events, 0 % mortality) Normal ECGNormal ECG NSSTTW changesNSSTTW changes Unchanged ECGUnchanged ECG

High-risk criteriaHigh-risk criteria

(42 % AMI, 14 % Cardiac events, 10 % mortality)(42 % AMI, 14 % Cardiac events, 10 % mortality) Ischemic ST segment or T wave changesIschemic ST segment or T wave changes LVH, LBBB, VPRLVH, LBBB, VPR

Q :Q : ECG manifestation of STE- AMI ECG manifestation of STE- AMI

Increase R wave voltageIncrease R wave voltage

Hyperacute T wave evolves to Hyperacute T wave evolves to STE over the next 30 minutesSTE over the next 30 minutes

Pathologic Q waves :Pathologic Q waves : Commonly develop 24 Commonly develop 24

hours after infarcthours after infarctMay not occur in up to 50 % May not occur in up to 50 %

of patients with an acute of patients with an acute myocardial infarction.myocardial infarction.

Serial ECG if persistent pain, Serial ECG if persistent pain, atypical symptoms or change atypical symptoms or change in VS. (or ST segment trend in VS. (or ST segment trend monitoring)monitoring)

Differential diagnosis of this ECG tracingDifferential diagnosis of this ECG tracing

Acute myocardial Acute myocardial infarctioninfarction

HyperkalemiaHyperkalemia Subarachnoid Subarachnoid

hemorrhagehemorrhage Benign Early Benign Early

Repolarization (BER)Repolarization (BER) LVHLVH Hypertrophic Hypertrophic

cardiomyopathycardiomyopathy Acute pericarditisAcute pericarditis

Inferolateral MIInferolateral MI

Subendocardial / non-transmural MISubendocardial / non-transmural MI

Cardiac MarkersCardiac Markers

Cardiac PanelCardiac Panel MyoglobinMyoglobin CPKCPK CPK-MBCPK-MB Troponin (T and I)Troponin (T and I)

Rapid bedside assays availableRapid bedside assays available

Cardiac EnzymesCardiac Enzymes

MyogobinMyogobin Increased levels within 2 to 4 hours Increased levels within 2 to 4 hours Peaks at 6 to18 hoursPeaks at 6 to18 hours Returns to baseline by 24 hoursReturns to baseline by 24 hours Elevated levels also found in skeletal muscle Elevated levels also found in skeletal muscle

injury (e.g. rhabdomyolysis)injury (e.g. rhabdomyolysis)


CPKCPK Increased levels within 6 to 8 hoursIncreased levels within 6 to 8 hours Peaks at 12 to 24 hoursPeaks at 12 to 24 hours Returns to baseline by 36 to 48 hoursReturns to baseline by 36 to 48 hours Elevated levels also found in cases of skeletal muscle Elevated levels also found in cases of skeletal muscle

injury (e.g. rhabdomyolysis)injury (e.g. rhabdomyolysis)

CPK-MBCPK-MB Similar time course as for total CPKSimilar time course as for total CPK More specific for cardiac muscleMore specific for cardiac muscle Most specific if elevated and 5 % of total CPKMost specific if elevated and 5 % of total CPK


Troponin T and ITroponin T and I Increased levels within 6 to 8 hoursIncreased levels within 6 to 8 hours Peaks at 18 to 24 hoursPeaks at 18 to 24 hours

Troponin T remains elevated for 5 to7 daysTroponin T remains elevated for 5 to7 days Troponin I remains elevated for up to 10 to 14 daysTroponin I remains elevated for up to 10 to 14 days

More specific for cardiac muscle (troponin I is most More specific for cardiac muscle (troponin I is most specific)specific)

Mild elevations seen in up to 1/3 of cases of unstable Mild elevations seen in up to 1/3 of cases of unstable angina ( “microinfarcts”)angina ( “microinfarcts”)

Prognostic value for cardiovascular complicationsPrognostic value for cardiovascular complications

By 12 hours after onset of symptoms, CPK-MB and By 12 hours after onset of symptoms, CPK-MB and Troponin I have a 100 % sensitivity for detecting AMITroponin I have a 100 % sensitivity for detecting AMI

Additional studies for diagnosing Additional studies for diagnosing AICSAICS

2-D echocardiogram2-D echocardiogram Useful with a nondiagnostic ECG or difficult ECG’sUseful with a nondiagnostic ECG or difficult ECG’s Sensitivity 85 % ; specificity 50 %Sensitivity 85 % ; specificity 50 % Can’t distinguish ischemia, AMI or previous infarctionCan’t distinguish ischemia, AMI or previous infarction Less sensitive for nontransmural.Less sensitive for nontransmural.

Radionuclide scanning : thalium 201, technetium-99Radionuclide scanning : thalium 201, technetium-99 Decreased uptake in ischemic tissuesDecreased uptake in ischemic tissues Normal perfusion and stress nuclide scans carry very low Normal perfusion and stress nuclide scans carry very low

risk risk ETTETT

The more abnormal the baseline ECG, the less useful the testThe more abnormal the baseline ECG, the less useful the test Useful in low and intermediate risk groups stratification and Useful in low and intermediate risk groups stratification and

dischargedischarge

ManagementManagement

Risk StratificationRisk Stratification TIMI risk ScoreTIMI risk Score

Age > 65Age > 65 Documented coronary Documented coronary

stenosis > 50 %stenosis > 50 % Three or more risk Three or more risk

factorsfactors Two or more anginal Two or more anginal

equivalents within 24 equivalents within 24 hourshours

ST segment changesST segment changes Increased cardiac Increased cardiac

biomarkersbiomarkers

High risk features :High risk features : Elevated cardiac biomarkersElevated cardiac biomarkers DiabetesDiabetes TIMI score > 5TIMI score > 5 Refractory symptoms despite Refractory symptoms despite

medical managementmedical management Elevated C reactive proteinElevated C reactive protein

Relative risk features :Relative risk features : Prior CABGPrior CABG Prior MIPrior MI LV dysfunctionLV dysfunction CHFCHF

AHA 2002 GuidelinesAHA 2002 Guidelines

STEMI :STEMI : Aspirin 162 mgAspirin 162 mg LMWH or UFHLMWH or UFH Clopidogrel 300 mg loadClopidogrel 300 mg load NitroglycerinNitroglycerin MorphineMorphine MetaprololMetaprolol Lytic therapyLytic therapy

If PCI :If PCI : AbciximabAbciximab Revascularization (PCA / Revascularization (PCA /

stent)stent)

NSTE-ACSNSTE-ACS If No high-risk If No high-risk

features :features : AspirinAspirin LMWHLMWH ClopidogrelClopidogrel

If Positive high risk If Positive high risk features :features :

Add IIb-IIIa GP Add IIb-IIIa GP inhibitorinhibitor

Other TreatmentsOther Treatments

TiclopidineTiclopidine Inhibits tranformation of IIB-IIIa glycoprotein receptorInhibits tranformation of IIB-IIIa glycoprotein receptor Good for USAP : takes 8 to 10 days to reach maximal Good for USAP : takes 8 to 10 days to reach maximal

benefit.benefit. Recommend to load with 300 mg initially (unless CABG Recommend to load with 300 mg initially (unless CABG

anticipated)anticipated)

LMW heparinLMW heparin Better than unfractionated heparin for USAPBetter than unfractionated heparin for USAP Better inactivation of Factor XaBetter inactivation of Factor Xa Less nonspecific bindingLess nonspecific binding Longer half-life, predictable responseLonger half-life, predictable response Less bleeding complicationsLess bleeding complications

Glycoprotein IIb-IIIa receptor Glycoprotein IIb-IIIa receptor inhibitorsinhibitors

Monoclonal antibodies that more effectively inhibit Monoclonal antibodies that more effectively inhibit platelet function than aspirin. platelet function than aspirin.

CompletelyCompletely inhibit platelet adhesion inhibit platelet adhesion Proven additive benefit in patients undergoing Proven additive benefit in patients undergoing

percutaneous intracoronary vascular procedures percutaneous intracoronary vascular procedures (abciximab).(abciximab).

Increasing evidence that these agents may be helpful Increasing evidence that these agents may be helpful in ischemic episodes not responsive to other agents.in ischemic episodes not responsive to other agents.

ACC / AHA 2002 guidelines for management of NSTE ACC / AHA 2002 guidelines for management of NSTE ACS :ACS : Level 2A recommendation for patients without Level 2A recommendation for patients without

intended early cath / PCIintended early cath / PCI

Management Sequence for ACSManagement Sequence for ACS

Pt arrives to ED

Targeted history

Physical assessment, V.S., EKG

ASA 160 mg PO

Oxygen, IV assess

Cardiac monitoring & send labs

Management of Chest Pain (CP)Management of Chest Pain (CP)

If patient continues with CP and not hypotensive :If patient continues with CP and not hypotensive :

Nitro 0.4 mg SL q 5 min X 3 prn

Morphine 2 to 4 mg IV q 5 min prn

Beta Blocker (Metoprolol 5 mg IV q 5 min x 3)LMWH, Clopidogrel

CEU Protocol

Thrombolytics IIb-IIIa GP inhibitor, PCI

USAP, NSTE-ACSAdmit

ThrombolyticsThrombolytics

Reduce short-term mortality by 18 to 25 %Reduce short-term mortality by 18 to 25 %

Overall :Overall : All agents are effective and should be combined with All agents are effective and should be combined with

antithrombin agentsantithrombin agents Larger the infarct, the greater the mortality reduction with Larger the infarct, the greater the mortality reduction with

thrombolyticsthrombolytics Accelerated t-PA results in better flow at 90 minutes and 15 Accelerated t-PA results in better flow at 90 minutes and 15

% reduction in 30 day mortality % reduction in 30 day mortality TNK (mutant form of t-PA) is as effective as accelerated t-TNK (mutant form of t-PA) is as effective as accelerated t-

PA and single bolus dosing. TNK is 14 x more fibrin PA and single bolus dosing. TNK is 14 x more fibrin specific, 80 x more resistant to PAI-1specific, 80 x more resistant to PAI-1

Thrombolytics : eligibility criteriaThrombolytics : eligibility criteria

Consistent history and physical examConsistent history and physical exam STE STE >> 1 mm in two or more contiguous limb leads or 1 mm in two or more contiguous limb leads or

>> 2 mm in two or more contiguous precordial leads 2 mm in two or more contiguous precordial leads (not ST depression : not ischemic syndromes !)(not ST depression : not ischemic syndromes !)

New LBBBNew LBBB Therapeutic window is 12 hours from symptom Therapeutic window is 12 hours from symptom

onset.onset.

Contraindications (CI) to ThrombolyticsContraindications (CI) to Thrombolytics

Absolute CI :Absolute CI : Prolonged CPRProlonged CPR Major surgery or trauma within the last 10 daysMajor surgery or trauma within the last 10 days Significant coagulopathySignificant coagulopathy Diabetic hemorrhagic retinopathyDiabetic hemorrhagic retinopathy Left heart thrombus, SBE, pericarditisLeft heart thrombus, SBE, pericarditis Oral anticoagulant useOral anticoagulant use Septic thrombophlebitisSeptic thrombophlebitis Previous CVAPrevious CVA

Relative CI :Relative CI : > 12 hours after onset of symptoms> 12 hours after onset of symptoms Age > 75 ???Age > 75 ??? Poorly controlled hypertension (> 180 to 200 / 110 to 120)Poorly controlled hypertension (> 180 to 200 / 110 to 120)

Additional reperfusion strategiesAdditional reperfusion strategies

PCI (percutaneous coronary interventions)PCI (percutaneous coronary interventions) Lower risk of intracranial bleedingLower risk of intracranial bleeding Higher reperfusion ratesHigher reperfusion rates Rapid evaluation of patients not eligible for thrombolyticsRapid evaluation of patients not eligible for thrombolytics Better risk stratification, earlier dischargeBetter risk stratification, earlier discharge Early identification of surgical candidatesEarly identification of surgical candidates Prior CABG patients (grafts thrombose, larger burden of clot)Prior CABG patients (grafts thrombose, larger burden of clot) Superior to thrombolytics if intervention within 90 minutesSuperior to thrombolytics if intervention within 90 minutes Recommended for patients in shock if PCI in 90 to 120 Recommended for patients in shock if PCI in 90 to 120

minutes.minutes. Rescue PCI if poor response to thrombolyticsRescue PCI if poor response to thrombolytics Grab bag of various strategies with no clear conclusions : i.e. Grab bag of various strategies with no clear conclusions : i.e.

lose dose thrombolytics prior to immediate PCI (facilitated PCI), lose dose thrombolytics prior to immediate PCI (facilitated PCI), glycoprotein inhibitor plus thrombolytics, etc. : Long term benefit glycoprotein inhibitor plus thrombolytics, etc. : Long term benefit yet to be proven.yet to be proven.

Radioactive implantsRadioactive implants

Who to transfer ?Who to transfer ?

Transfer to a tertiary care facility with interventional Transfer to a tertiary care facility with interventional and cardiac surgery capabilities is indicated :and cardiac surgery capabilities is indicated : CI to thrombolytics and may benefit from PCI, CABGCI to thrombolytics and may benefit from PCI, CABG Persistent hemodynamic instability or ventricular Persistent hemodynamic instability or ventricular

arrhythmiasarrhythmias Ongoing ischemia following infarction or thrombolyticsOngoing ischemia following infarction or thrombolytics

Patients SHOULD receive the initial standard ED therapy Patients SHOULD receive the initial standard ED therapy includingincluding thrombolytics. thrombolytics.

Final ThoughtsFinal Thoughts

Rapid history, rapid ECG with interpretation, rapid Rapid history, rapid ECG with interpretation, rapid treatmenttreatment

Maintain a high clinical suspicion : 2 to 10 % of Maintain a high clinical suspicion : 2 to 10 % of patients with CP and AMI are released from EDpatients with CP and AMI are released from ED Young, atypical presentations, nondiagnostic ECG’sYoung, atypical presentations, nondiagnostic ECG’s

Single ECG and single set of enzymes can give a Single ECG and single set of enzymes can give a false sense of securityfalse sense of security

ED cocktail : ASA, MSOED cocktail : ASA, MSO44, , ββ-blocker, clopidogrel, -blocker, clopidogrel, LMWH, IIb-IIIa agentsLMWH, IIb-IIIa agents

Target goal of thrombolytics within 30 minutes for Target goal of thrombolytics within 30 minutes for STEMISTEMI

Strongly advocate for PCI when appropriateStrongly advocate for PCI when appropriate

A Comprehensive Approach : A Comprehensive Approach : Goals of the ED Cardiac Goals of the ED Cardiac Evaluation Unit (CEU)Evaluation Unit (CEU)

1.1. Early Systematic Evaluation of All Chest Pain Early Systematic Evaluation of All Chest Pain PatientsPatients

Identification of all reperfusion candidatesIdentification of all reperfusion candidates Reduction of delays in initiation of reperfusion Reduction of delays in initiation of reperfusion

therapy therapy Improved diagnosis and treatment of other dangerous Improved diagnosis and treatment of other dangerous

pathologypathology Early (primary) risk stratificationEarly (primary) risk stratification

ED Evaluation of Chest PainED Evaluation of Chest Pain

5,000,000 visits / year in U.S.5,000,000 visits / year in U.S. 5 % of all ED visits5 % of all ED visits 5 to 15 Chest Pain patients / 5 to 15 Chest Pain patients /

day per EDday per ED Lengthy Differential Lengthy Differential

DiagnosisDiagnosis

Identifying the Problem :Identifying the Problem :

Need for a More Aggressive Approach to Acute MI :Need for a More Aggressive Approach to Acute MI : ““Time is Myocardium”Time is Myocardium” Dramatic Mortality Reduction in STEMI with Early Dramatic Mortality Reduction in STEMI with Early

ReperfusionReperfusion ThrombolyticsThrombolytics Immediate PTCA / stentingImmediate PTCA / stenting

Increasing number of other treatments available for Increasing number of other treatments available for ACSACS Require early risk assessmentRequire early risk assessment

Team Members Team Members

Cardiologist : specialist, algorithmCardiologist : specialist, algorithm ED Physician : team leaderED Physician : team leader

algorithm, educate & motivate staffalgorithm, educate & motivate staff Senior triage nurse : team facilitatorSenior triage nurse : team facilitator

algorithm, educate & motivate staffalgorithm, educate & motivate staff Clinical technician : algorithm, educate & Clinical technician : algorithm, educate &

motivate staffmotivate staff Patient Service Coordinator : algorithmPatient Service Coordinator : algorithm Research coordinator : data collectionResearch coordinator : data collection

CEU Goals (Continued)CEU Goals (Continued)

2.2. Accelerated Rule-out of MI among low risk Accelerated Rule-out of MI among low risk patientspatients

• Reduce LOSReduce LOS• Improve cost-effectivenessImprove cost-effectiveness• Improve patient satisfactionImprove patient satisfaction• Eliminate “missed MI”Eliminate “missed MI”

3.3. Secondary Risk stratificationSecondary Risk stratification4.4. Comprehensive Diagnosis and Treatment Comprehensive Diagnosis and Treatment

CenterCenter5.5. Education and Community OutreachEducation and Community Outreach6.6. Multidisciplinary approachMultidisciplinary approach

Implementation :Implementation :Goal 1 : Early Diagnosis of MIGoal 1 : Early Diagnosis of MI

ALL chest pain patients receive immediate, ALL chest pain patients receive immediate, aggressive evaluationaggressive evaluation Vital signsVital signs Cardiac monitorCardiac monitor Intravenous “lifeline” placedIntravenous “lifeline” placed Oxygen and/or pulse oxymetryOxygen and/or pulse oxymetry

ECG performed under standing orders within 10 ECG performed under standing orders within 10 minutes of arrivalminutes of arrival ECG handed directly to physician for interpretationECG handed directly to physician for interpretation

Goal 1 : Early Diagnosis of MIGoal 1 : Early Diagnosis of MI

Early focused history and physical examEarly focused history and physical exam Blood drawn upon arrival for initial Blood drawn upon arrival for initial

myocardial markers (Cardiac Panel)myocardial markers (Cardiac Panel) CK-MBCK-MB TroponinTroponin MyoglobinMyoglobin

““Reperfusion Checklist”Reperfusion Checklist”

Goal 2 : Evaluation of Low Risk Goal 2 : Evaluation of Low Risk PatientsPatients

““Zero tolerance” for missed MIZero tolerance” for missed MI MI can not be excluded by history, MI can not be excluded by history,

exam aloneexam alone Hospitalization for “Rule-Out MI” Hospitalization for “Rule-Out MI”

expensive, inefficientexpensive, inefficient Several alternative approaches now Several alternative approaches now

existexist

Goal 2 : Evaluation of Low Risk PatientsGoal 2 : Evaluation of Low Risk Patients

Initial Risk Stratification within 1 to 3 hours Initial Risk Stratification within 1 to 3 hours ::1.1. ST segment elevation MI :ST segment elevation MI :

Thrombolytics or cath labThrombolytics or cath lab2.2. High Probability for ACS and / or High Risk :High Probability for ACS and / or High Risk :

Ischemic ECG, positive marker, etc.Ischemic ECG, positive marker, etc. ICU vs in-patient unit, anti-ischemic therapy, ? cathICU vs in-patient unit, anti-ischemic therapy, ? cath

3.3. Low Risk for ACS :Low Risk for ACS : No high risk clinical featuresNo high risk clinical features Non-diagnostic ECGNon-diagnostic ECG Initial myocardial markers negativeInitial myocardial markers negative Hold for further workup or go to CEUHold for further workup or go to CEU

4.4. Negligible Risk :Negligible Risk : Atypical history, no risk factors, normal ECG and Atypical history, no risk factors, normal ECG and

markers, other cause identifiedmarkers, other cause identified Discharge homeDischarge home

Goal 2 : Evaluation of Low Risk Goal 2 : Evaluation of Low Risk Patients Patients

Continuous observation on cardiac monitorContinuous observation on cardiac monitor 12 to 24 hours12 to 24 hours

Accelerated “rule-out” of MIAccelerated “rule-out” of MI Serial ECGsSerial ECGs Serial Myocardial Marker MeasurementsSerial Myocardial Marker Measurements

0, 3, 6, 9 hours0, 3, 6, 9 hours CK-MB, troponinCK-MB, troponin

MI definitively excluded within 12 hoursMI definitively excluded within 12 hours

Goal 3 : Secondary Risk Goal 3 : Secondary Risk StratificationStratification

MI rule-out does not exclude other ACS (Unstable MI rule-out does not exclude other ACS (Unstable Angina)Angina)

Further evaluation often needed prior to Further evaluation often needed prior to dischargedischarge

Stress testingStress testing Screening test for CADScreening test for CAD Accurate predictor of short and long term risk of death, Accurate predictor of short and long term risk of death,

adverse eventsadverse events Reduces need for repeated evaluations Reduces need for repeated evaluations

Stress TestingStress Testing

Standard (Bruce protocol) exercise Standard (Bruce protocol) exercise (treadmill) stress testing(treadmill) stress testing

Stress echocardiographyStress echocardiography Radionucleotide scanningRadionucleotide scanning

ThalliumThallium Sestamibi Sestamibi Dual isotopeDual isotope

Pharmacologic stress testingPharmacologic stress testing

Low Risk Chest Pain Low Risk Chest Pain Evaluation ProtocolEvaluation Protocol

Initial Risk Stratification

History

Physical Exam

ECG

Myoglobin

CK-MB

Troponin

Low Risk Patient

1 hour 3 hours 6 hours 9 hours

ECG ECG ECG

CK-MB CK-MB CK-MB, cTn

Continuous Monitoring

All Negative

Diagnostic Stress Testing Home(-)

(+) Admit

Impact of CEU Approach :Impact of CEU Approach :Low Risk Chest Pain PatientsLow Risk Chest Pain Patients

Problems : “Unnecessary” admission of low risk Problems : “Unnecessary” admission of low risk patients, “Missed” MI’spatients, “Missed” MI’s

Measure : length of stay, % MI’s dischargedMeasure : length of stay, % MI’s dischargedInterventions : accelerated rule-out protocolInterventions : accelerated rule-out protocolImpact : Missed MI’s reduced from 4.5 to 0.4 %*Impact : Missed MI’s reduced from 4.5 to 0.4 %*Length of stay reduced ~ 2.5 days to 1 dayLength of stay reduced ~ 2.5 days to 1 day

* Graff et al. * Graff et al. Am J CardiolAm J Cardiol 1997; 80 : 563-8 1997; 80 : 563-8

Growth of Chest Pain Units in the U.S.Growth of Chest Pain Units in the U.S.

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Documents

Acute Coronary Syndromes. Epidemiology Ischemic Heart Disease (IHD) is the leading cause of morbidity and mortality worldwide Ischemic Heart Disease (IHD)