ED Risk Stratification for Chest Pain

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Non-ST-Segment Elevation Non-ST-Segment Elevation Acute Coronary Syndromes: Acute Coronary Syndromes: Risk Stratification Based on the Risk Stratification Based on the ACC/AHA ACC/AHA UA / NSTEMI Guidelines UA / NSTEMI Guidelines

description

Non-ST-Segment Elevation Acute Coronary Syndromes: Risk Stratification Based on the ACC/AHA UA / NSTEMI Guidelines. ED Risk Stratification for Chest Pain. For the past 20 years. In 2002: Does this patient need fibrinolytic therapy? - PowerPoint PPT Presentation

Transcript of ED Risk Stratification for Chest Pain

Page 1: ED Risk Stratification for Chest Pain

Non-ST-Segment ElevationNon-ST-Segment ElevationAcute Coronary Syndromes:Acute Coronary Syndromes:

Risk Stratification Based on the ACC/AHA Risk Stratification Based on the ACC/AHA UA / NSTEMI GuidelinesUA / NSTEMI Guidelines

Non-ST-Segment ElevationNon-ST-Segment ElevationAcute Coronary Syndromes:Acute Coronary Syndromes:

Risk Stratification Based on the ACC/AHA Risk Stratification Based on the ACC/AHA UA / NSTEMI GuidelinesUA / NSTEMI Guidelines

Page 2: ED Risk Stratification for Chest Pain

ED Risk Stratification for Chest PainED Risk Stratification for Chest PainED Risk Stratification for Chest PainED Risk Stratification for Chest Pain

In 2002:In 2002:

Does this patient need Does this patient need fibrinolytic therapy? fibrinolytic therapy?

Should this patient get anti-Should this patient get anti-thrombin and anti-platelet thrombin and anti-platelet agents? agents?

Can I safely send this patient Can I safely send this patient home?home?

In 2002:In 2002:

Does this patient need Does this patient need fibrinolytic therapy? fibrinolytic therapy?

Should this patient get anti-Should this patient get anti-thrombin and anti-platelet thrombin and anti-platelet agents? agents?

Can I safely send this patient Can I safely send this patient home?home?

R/O MI

For the past 20 years . . .For the past 20 years . . .For the past 20 years . . .For the past 20 years . . .

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ED ED CCU CCU Cath Lab Risk Stratification for Chest Pain Cath Lab Risk Stratification for Chest PainED ED CCU CCU Cath Lab Risk Stratification for Chest Pain Cath Lab Risk Stratification for Chest Pain

Three levels of risk stratification are pertinent to the ED:Three levels of risk stratification are pertinent to the ED: LowLow, , intermediateintermediate, or, or highhigh risk that ischemic symptoms are a risk that ischemic symptoms are a

result of CADresult of CAD

LowLow,, intermediate intermediate, or , or highhigh risk of short-term death or risk of short-term death or nonfatal MI from ACSnonfatal MI from ACS

Dynamic, ongoing risk-oriented evaluation of low- or Dynamic, ongoing risk-oriented evaluation of low- or intermediate-risk patients for “conversion” to high-risk status intermediate-risk patients for “conversion” to high-risk status that is linked to intensity of treatmentthat is linked to intensity of treatment

Three levels of risk stratification are pertinent to the ED:Three levels of risk stratification are pertinent to the ED: LowLow, , intermediateintermediate, or, or highhigh risk that ischemic symptoms are a risk that ischemic symptoms are a

result of CADresult of CAD

LowLow,, intermediate intermediate, or , or highhigh risk of short-term death or risk of short-term death or nonfatal MI from ACSnonfatal MI from ACS

Dynamic, ongoing risk-oriented evaluation of low- or Dynamic, ongoing risk-oriented evaluation of low- or intermediate-risk patients for “conversion” to high-risk status intermediate-risk patients for “conversion” to high-risk status that is linked to intensity of treatmentthat is linked to intensity of treatment

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History, PhysicalEKG

Chest Pain

STEMI UA/NSTEMI/High Risk

Mod Risk Low RiskDefinite

Non-Cardiac

Initial Risk Stratification SchemeInitial Risk Stratification SchemeInitial Risk Stratification SchemeInitial Risk Stratification Scheme

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Risk Stratification Tools in the EDRisk Stratification Tools in the ED

• History and PhysicalHistory and Physical

• Standard ECG and Non-standard ECG leadsStandard ECG and Non-standard ECG leads

Cardiac BiomarkersCardiac Biomarkers• Troponin I or T, CK-MB, myoglobinTroponin I or T, CK-MB, myoglobin

Predictive Indices / SchemesPredictive Indices / Schemes

Non-Invasive Imaging StudiesNon-Invasive Imaging Studies EchocardiogramEchocardiogram Exercise testingExercise testing Technetium-99m-sestamibi: stress and restTechnetium-99m-sestamibi: stress and rest

• History and PhysicalHistory and Physical

• Standard ECG and Non-standard ECG leadsStandard ECG and Non-standard ECG leads

Cardiac BiomarkersCardiac Biomarkers• Troponin I or T, CK-MB, myoglobinTroponin I or T, CK-MB, myoglobin

Predictive Indices / SchemesPredictive Indices / Schemes

Non-Invasive Imaging StudiesNon-Invasive Imaging Studies EchocardiogramEchocardiogram Exercise testingExercise testing Technetium-99m-sestamibi: stress and restTechnetium-99m-sestamibi: stress and rest

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Initial EvaluationInitial EvaluationRisk Stratification (1)Risk Stratification (1)

Initial EvaluationInitial EvaluationRisk Stratification (1)Risk Stratification (1)

Early risk stratification by symptoms, physical findings, ECG, cardiac markers

12-lead ECG within 10 min for ongoing pain, or ASAP if pain has resolved at presentation

Cardiac markers, Troponins and CK-MB, for initial assessment

Monitoring, repeat ECG and cardiac markers in 6-12 hours, if initial results normal

Early risk stratification by symptoms, physical findings, ECG, cardiac markers

12-lead ECG within 10 min for ongoing pain, or ASAP if pain has resolved at presentation

Cardiac markers, Troponins and CK-MB, for initial assessment

Monitoring, repeat ECG and cardiac markers in 6-12 hours, if initial results normal

IIII IIaIIaIIaIIa IIbIIbIIbIIb IIIIIIIIIIII

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Initial EvaluationInitial EvaluationRisk Stratification (2)Risk Stratification (2)

Initial EvaluationInitial EvaluationRisk Stratification (2)Risk Stratification (2)

If <6 hours after symptom onset, add early myoglobin or CK-MB to troponin

C-reactive protein, other markers of inflammation

Total CK, SGOT, HBDH, LDH

If <6 hours after symptom onset, add early myoglobin or CK-MB to troponin

C-reactive protein, other markers of inflammation

Total CK, SGOT, HBDH, LDH

IIII IIaIIaIIaIIa IIbIIbIIbIIb IIIIIIIIIIII

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Clinical Assessment (1)Clinical Assessment (1)

Rapid, focused evaluationRapid, focused evaluation Decisions based on this evaluation have Decisions based on this evaluation have

substantial clinical and economic consequencessubstantial clinical and economic consequences

Are the symptoms a manifestation of ACS? Are the symptoms a manifestation of ACS? If so, what is the prognosis?If so, what is the prognosis?

Identify signs of life-threatening instabilityIdentify signs of life-threatening instability

Triage to most appropriate areaTriage to most appropriate area Typically an ED or chest pain unitTypically an ED or chest pain unit

Rapid, focused evaluationRapid, focused evaluation Decisions based on this evaluation have Decisions based on this evaluation have

substantial clinical and economic consequencessubstantial clinical and economic consequences

Are the symptoms a manifestation of ACS? Are the symptoms a manifestation of ACS? If so, what is the prognosis?If so, what is the prognosis?

Identify signs of life-threatening instabilityIdentify signs of life-threatening instability

Triage to most appropriate areaTriage to most appropriate area Typically an ED or chest pain unitTypically an ED or chest pain unit

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Clinical Assessment (2)Clinical Assessment (2)Clinical Assessment (2)Clinical Assessment (2)

Risk status determined in the ED by:Risk status determined in the ED by: Assessment of anginal symptomsAssessment of anginal symptoms Careful physical examinationCareful physical examination ElectrocardiogramElectrocardiogram Cardiac biomarkersCardiac biomarkers CAD risk factorsCAD risk factors Illicit drug useIllicit drug use

Initial risk stratification assignment drives pace Initial risk stratification assignment drives pace of subsequent evaluation and treatmentof subsequent evaluation and treatment

Risk status determined in the ED by:Risk status determined in the ED by: Assessment of anginal symptomsAssessment of anginal symptoms Careful physical examinationCareful physical examination ElectrocardiogramElectrocardiogram Cardiac biomarkersCardiac biomarkers CAD risk factorsCAD risk factors Illicit drug useIllicit drug use

Initial risk stratification assignment drives pace Initial risk stratification assignment drives pace of subsequent evaluation and treatmentof subsequent evaluation and treatment

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Clinical Assessment (3)Clinical Assessment (3)

High-risk features apparent in the ED:High-risk features apparent in the ED: Accelerated pattern of anginaAccelerated pattern of angina Ongoing rest pain > 20 minOngoing rest pain > 20 min Signs of CHFSigns of CHF Hemodynamic instabilityHemodynamic instability Arrhythmias - Atrial or ventricularArrhythmias - Atrial or ventricular Advanced age (> 75 years)Advanced age (> 75 years) Ischemic ECG changes Ischemic ECG changes Elevated cardiac markersElevated cardiac markers

High-risk features apparent in the ED:High-risk features apparent in the ED: Accelerated pattern of anginaAccelerated pattern of angina Ongoing rest pain > 20 minOngoing rest pain > 20 min Signs of CHFSigns of CHF Hemodynamic instabilityHemodynamic instability Arrhythmias - Atrial or ventricularArrhythmias - Atrial or ventricular Advanced age (> 75 years)Advanced age (> 75 years) Ischemic ECG changes Ischemic ECG changes Elevated cardiac markersElevated cardiac markers

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ElectrocardiogramElectrocardiogramElectrocardiogramElectrocardiogram

Carries diagnostic and prognostic valueCarries diagnostic and prognostic value

Especially valuable if captured Especially valuable if captured duringduring pain pain

ST-segment depression or transient ST-segment ST-segment depression or transient ST-segment elevation are primary ECG markers of UA/NSTEMIelevation are primary ECG markers of UA/NSTEMI 75% of patients with + CK-MB do not develop Q waves75% of patients with + CK-MB do not develop Q waves Differentiation between UA and NSTEMI relies upon Differentiation between UA and NSTEMI relies upon

positive biomarkerspositive biomarkers Inverted T-waves suggestive of ischemia, particularly Inverted T-waves suggestive of ischemia, particularly

with good chest pain storywith good chest pain story

Carries diagnostic and prognostic valueCarries diagnostic and prognostic value

Especially valuable if captured Especially valuable if captured duringduring pain pain

ST-segment depression or transient ST-segment ST-segment depression or transient ST-segment elevation are primary ECG markers of UA/NSTEMIelevation are primary ECG markers of UA/NSTEMI 75% of patients with + CK-MB do not develop Q waves75% of patients with + CK-MB do not develop Q waves Differentiation between UA and NSTEMI relies upon Differentiation between UA and NSTEMI relies upon

positive biomarkerspositive biomarkers Inverted T-waves suggestive of ischemia, particularly Inverted T-waves suggestive of ischemia, particularly

with good chest pain storywith good chest pain story

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Six-Month Mortality by Baseline ECG Findings -Six-Month Mortality by Baseline ECG Findings -GUSTO-IIb ResultsGUSTO-IIb Results

Six-Month Mortality by Baseline ECG Findings -Six-Month Mortality by Baseline ECG Findings -GUSTO-IIb ResultsGUSTO-IIb Results

0%0%

2%2%

4%4%

6%6%

8%8%

10%10%

00 3030 6060 9090 120120 150150 180180

NS ST-TNS ST-Tss

ST ST

ST ST

Savonitto, JAMA 1999Savonitto, JAMA 1999

% M

orta

lity

% M

orta

lity

Days from RandomizationDays from Randomization

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Biomarkers: CK/CKMBBiomarkers: CK/CKMBBiomarkers: CK/CKMBBiomarkers: CK/CKMB

Until recently the principal serum marker used in Until recently the principal serum marker used in evaluation of ACS despite known limitations:evaluation of ACS despite known limitations: Low levels in healthy persons limits specificityLow levels in healthy persons limits specificity MB band may be elevated in skeletal muscle damageMB band may be elevated in skeletal muscle damage Different MB isoforms exist in myocardium (MBDifferent MB isoforms exist in myocardium (MB22) and ) and

in plasma (MBin plasma (MB11), and differentiating assay is not ), and differentiating assay is not

widely availablewidely available

Until recently the principal serum marker used in Until recently the principal serum marker used in evaluation of ACS despite known limitations:evaluation of ACS despite known limitations: Low levels in healthy persons limits specificityLow levels in healthy persons limits specificity MB band may be elevated in skeletal muscle damageMB band may be elevated in skeletal muscle damage Different MB isoforms exist in myocardium (MBDifferent MB isoforms exist in myocardium (MB22) and ) and

in plasma (MBin plasma (MB11), and differentiating assay is not ), and differentiating assay is not

widely availablewidely available

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Biomarkers: TroponinsBiomarkers: Troponins

Very useful in diagnosis and prognosis of ACSVery useful in diagnosis and prognosis of ACS Normally not detectable in blood of healthy persons; Normally not detectable in blood of healthy persons; cTnI or cTnT can be positive with negative CK-MB = cTnI or cTnT can be positive with negative CK-MB =

“minor myocardial damage”“minor myocardial damage” Predictive of MI and death when elevated, independent Predictive of MI and death when elevated, independent

of CK-MB levelsof CK-MB levels Elevated troponins validated as a predictor of enhanced Elevated troponins validated as a predictor of enhanced

treatment benefit from aggressive therapies (LMW treatment benefit from aggressive therapies (LMW heparins, GP IIb/IIIa inhibitors, early invasive strategy)heparins, GP IIb/IIIa inhibitors, early invasive strategy)

Very useful in diagnosis and prognosis of ACSVery useful in diagnosis and prognosis of ACS Normally not detectable in blood of healthy persons; Normally not detectable in blood of healthy persons; cTnI or cTnT can be positive with negative CK-MB = cTnI or cTnT can be positive with negative CK-MB =

“minor myocardial damage”“minor myocardial damage” Predictive of MI and death when elevated, independent Predictive of MI and death when elevated, independent

of CK-MB levelsof CK-MB levels Elevated troponins validated as a predictor of enhanced Elevated troponins validated as a predictor of enhanced

treatment benefit from aggressive therapies (LMW treatment benefit from aggressive therapies (LMW heparins, GP IIb/IIIa inhibitors, early invasive strategy)heparins, GP IIb/IIIa inhibitors, early invasive strategy)

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Troponin as a Marker of Increased Risk in ACSTroponin as a Marker of Increased Risk in ACS

30%

12% 11%

34%

22%19% 19%

23%

2%4% 4%

12%

1% 0%

6% 6%

0%

10%

20%

30%

40%

Hamm(1992)

FRISC(1996)

TRIM(1999)

Pettijohn(1997)

Hamm(1997)

Hamm(1997)

Polanczyk(1998)

Galvanni(1997)

Dea

th o

r M

I

Troponin +

Troponin -30%

12% 11%

34%

22%19% 19%

23%

2%4% 4%

12%

1% 0%

6% 6%

0%

10%

20%

30%

40%

Hamm(1992)

FRISC(1996)

TRIM(1999)

Pettijohn(1997)

Hamm(1997)

Hamm(1997)

Polanczyk(1998)

Galvanni(1997)

Dea

th o

r M

I

Troponin +

Troponin -

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Long Term Survival and Troponin-T StatusLong Term Survival and Troponin-T Status

80%

85%

90%

95%

100%

0 50 100 150 200 250 300 350

Days from Randomization

Su

rviv

al

80%

85%

90%

95%

100%

0 50 100 150 200 250 300 350

Days from Randomization

Su

rviv

al

GUSTO-IIa ResultsGUSTO-IIa Results

TnT +TnT +

TnT -TnT -

1-Year Mortality Rates:1-Year Mortality Rates:Troponin-T Positive: 14%Troponin-T Positive: 14%Troponin-T Negative: 5%Troponin-T Negative: 5%

1-Year Mortality Rates:1-Year Mortality Rates:Troponin-T Positive: 14%Troponin-T Positive: 14%Troponin-T Negative: 5%Troponin-T Negative: 5%

p < 0.001p < 0.001

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Biomarkers: MyoglobinBiomarkers: MyoglobinBiomarkers: MyoglobinBiomarkers: Myoglobin

Utility limited by release kinetics (early) and by lack Utility limited by release kinetics (early) and by lack of cardiac specificityof cardiac specificity

Isolated elevation of myoglobin 4-8 hours after pain Isolated elevation of myoglobin 4-8 hours after pain onset with a a non-diagnostic ECG must be onset with a a non-diagnostic ECG must be supplemented by a more cardiac-specific markersupplemented by a more cardiac-specific marker

Sufficiently sensitive that a Sufficiently sensitive that a negativenegative myoglobin 4-8 myoglobin 4-8 hours after pain onset is useful in excluding hours after pain onset is useful in excluding myocardial necrosismyocardial necrosis

Utility limited by release kinetics (early) and by lack Utility limited by release kinetics (early) and by lack of cardiac specificityof cardiac specificity

Isolated elevation of myoglobin 4-8 hours after pain Isolated elevation of myoglobin 4-8 hours after pain onset with a a non-diagnostic ECG must be onset with a a non-diagnostic ECG must be supplemented by a more cardiac-specific markersupplemented by a more cardiac-specific marker

Sufficiently sensitive that a Sufficiently sensitive that a negativenegative myoglobin 4-8 myoglobin 4-8 hours after pain onset is useful in excluding hours after pain onset is useful in excluding myocardial necrosismyocardial necrosis

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Integration of Biomarkers with Clinical HistoryIntegration of Biomarkers with Clinical HistoryIntegration of Biomarkers with Clinical HistoryIntegration of Biomarkers with Clinical History

Time since symptom onset should be a factor in Time since symptom onset should be a factor in marker selection and in repeat assay strategymarker selection and in repeat assay strategy

Elevated serum levels of troponins persist for 7-14 Elevated serum levels of troponins persist for 7-14 days after initial releasedays after initial release

Delta values, as close as 2 hours apart, may be Delta values, as close as 2 hours apart, may be sufficiently sensitive to assist with serial sufficiently sensitive to assist with serial evaluationsevaluations

Serial cardiac marker strategy not specifiedSerial cardiac marker strategy not specified

Time since symptom onset should be a factor in Time since symptom onset should be a factor in marker selection and in repeat assay strategymarker selection and in repeat assay strategy

Elevated serum levels of troponins persist for 7-14 Elevated serum levels of troponins persist for 7-14 days after initial releasedays after initial release

Delta values, as close as 2 hours apart, may be Delta values, as close as 2 hours apart, may be sufficiently sensitive to assist with serial sufficiently sensitive to assist with serial evaluationsevaluations

Serial cardiac marker strategy not specifiedSerial cardiac marker strategy not specified

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Serial Cardiac MarkersSerial Cardiac Markers

0%

25%

50%

75%

100%

3 4 5 6 8 12

Myoglobin CK-MB (mass) Troponin T

0%

25%

50%

75%

100%

3 4 5 6 8 12

Myoglobin CK-MB (mass) Troponin T

Serial Testing in 309 Patients with Suspected MISerial Testing in 309 Patients with Suspected MI

Hours After Symptom OnsetHours After Symptom OnsetHours After Symptom Onset

SensitivitySensitivity

Winter, Circulation, 1995Winter, Circulation, 1995Winter, Circulation, 1995Winter, Circulation, 1995

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Biomarkers: Biomarkers: BedsideBedside Testing TestingBiomarkers: Biomarkers: BedsideBedside Testing Testing

Consideration of bedside marker assay recommended Consideration of bedside marker assay recommended when hospital lab turnaround time > 30-60 minuteswhen hospital lab turnaround time > 30-60 minutes

Ready-for-use availability must be balanced against Ready-for-use availability must be balanced against need for stringent QC and training of ED personnel, need for stringent QC and training of ED personnel, CLIA concerns, political hazards, etcCLIA concerns, political hazards, etc

Prognostic value limited because many assays are Prognostic value limited because many assays are qualitative, not quantitativequalitative, not quantitative

Consideration of bedside marker assay recommended Consideration of bedside marker assay recommended when hospital lab turnaround time > 30-60 minuteswhen hospital lab turnaround time > 30-60 minutes

Ready-for-use availability must be balanced against Ready-for-use availability must be balanced against need for stringent QC and training of ED personnel, need for stringent QC and training of ED personnel, CLIA concerns, political hazards, etcCLIA concerns, political hazards, etc

Prognostic value limited because many assays are Prognostic value limited because many assays are qualitative, not quantitativequalitative, not quantitative

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““Vein-to-Brain” Reporting Times Vein-to-Brain” Reporting Times for Cardiac Markers - St. Agnes Hospitalfor Cardiac Markers - St. Agnes Hospital

““Vein-to-Brain” Reporting Times Vein-to-Brain” Reporting Times for Cardiac Markers - St. Agnes Hospitalfor Cardiac Markers - St. Agnes Hospital

00

2020

4040

6060

8080

100100

120120

140140

160160

180180

Test Type Test Type

"Vei

n-t

o B

rain

" "V

ein

-to

Bra

in"

Rep

ort

ing

Tim

es (

min

s)R

epo

rtin

g T

imes

(m

ins)

Bedside Test (mean=15 mins)Bedside Test (mean=15 mins)

Laboratory Test (mean=128 mins)Laboratory Test (mean=128 mins)

n = 939n = 939SD = 46.74SD = 46.74

Christenson R: Md Med 2001 Spring:Suppl:98-103Christenson R: Md Med 2001 Spring:Suppl:98-103

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Distribution of Reporting Times for Distribution of Reporting Times for Cardiac Markers - St. Agnes Hospital Cardiac Markers - St. Agnes Hospital

Distribution of Reporting Times for Distribution of Reporting Times for Cardiac Markers - St. Agnes Hospital Cardiac Markers - St. Agnes Hospital

Range of Lab Reporting TimesRange of Lab Reporting Times

40 mins = Earliest Reporting Time40 mins = Earliest Reporting Time

284 mins = Latest Reporting Time284 mins = Latest Reporting Time

2525thth percentile percentile

(Median , 117 mins)5050th th percentilepercentile

7575th th percentilepercentile

9595th th percentilepercentile (201.3 mins)

(147 mins)

(85 mins)

55thth percentile percentile (62.6 mins)

Christenson R: Md Med 2001 Spring:Suppl:98-103Christenson R: Md Med 2001 Spring:Suppl:98-103

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Noninvasive StudiesNoninvasive StudiesNoninvasive StudiesNoninvasive Studies

Guidelines do not consider use of these tests in Guidelines do not consider use of these tests in the ED setting, although:the ED setting, although: Many EDs now use rest sestamibi scanning in Many EDs now use rest sestamibi scanning in

the risk stratification process the risk stratification process Stress testing used after patients have “ruled out”Stress testing used after patients have “ruled out”

Reality dictates that appropriate provocative Reality dictates that appropriate provocative testing often not likely after patient leaves EDtesting often not likely after patient leaves ED ED is the “first, last, and best shot” at intervening ED is the “first, last, and best shot” at intervening

in patients with risk concernsin patients with risk concerns

Guidelines do not consider use of these tests in Guidelines do not consider use of these tests in the ED setting, although:the ED setting, although: Many EDs now use rest sestamibi scanning in Many EDs now use rest sestamibi scanning in

the risk stratification process the risk stratification process Stress testing used after patients have “ruled out”Stress testing used after patients have “ruled out”

Reality dictates that appropriate provocative Reality dictates that appropriate provocative testing often not likely after patient leaves EDtesting often not likely after patient leaves ED ED is the “first, last, and best shot” at intervening ED is the “first, last, and best shot” at intervening

in patients with risk concernsin patients with risk concerns

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Predictive Indices - Risk Scores in the EDPredictive Indices - Risk Scores in the EDPredictive Indices - Risk Scores in the EDPredictive Indices - Risk Scores in the ED

Combine clinical history, physical exam Combine clinical history, physical exam findings, ECG signs of ischemia, and cardiac findings, ECG signs of ischemia, and cardiac marker resultsmarker results PURSUIT and TIMI Risk ScoresPURSUIT and TIMI Risk Scores

Therapies such as LMW heparin and GP IIb/IIIa Therapies such as LMW heparin and GP IIb/IIIa inhibitors have greater benefit in patients with inhibitors have greater benefit in patients with higher risk scoreshigher risk scores

Have not been tested prospectively in the EDHave not been tested prospectively in the ED

Risk scores not specifically recommended by Risk scores not specifically recommended by the ACC/AHA Guidelinesthe ACC/AHA Guidelines

Combine clinical history, physical exam Combine clinical history, physical exam findings, ECG signs of ischemia, and cardiac findings, ECG signs of ischemia, and cardiac marker resultsmarker results PURSUIT and TIMI Risk ScoresPURSUIT and TIMI Risk Scores

Therapies such as LMW heparin and GP IIb/IIIa Therapies such as LMW heparin and GP IIb/IIIa inhibitors have greater benefit in patients with inhibitors have greater benefit in patients with higher risk scoreshigher risk scores

Have not been tested prospectively in the EDHave not been tested prospectively in the ED

Risk scores not specifically recommended by Risk scores not specifically recommended by the ACC/AHA Guidelinesthe ACC/AHA Guidelines

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Immediate ManagementImmediate ManagementImmediate ManagementImmediate Management

Classify as non-cardiac, chronic stable angina, possible ACS, or definite ACS

Evaluate for immediate reperfusion therapy if definite ACS and ST-segment present

Pharmacological or exercise stress test, if possible ACS and serial biomarkers and ECGs are normal

Admit pts with definite ACS, ongoing pain, biomarkers, new ST or deep T-wave inversion, abnormal hemodynamics, or (+) stress test

Classify as non-cardiac, chronic stable angina, possible ACS, or definite ACS

Evaluate for immediate reperfusion therapy if definite ACS and ST-segment present

Pharmacological or exercise stress test, if possible ACS and serial biomarkers and ECGs are normal

Admit pts with definite ACS, ongoing pain, biomarkers, new ST or deep T-wave inversion, abnormal hemodynamics, or (+) stress test

IIII IIaIIaIIaIIa IIbIIbIIbIIb IIIIIIIIIIII

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The “Key” to Risk StratificationThe “Key” to Risk Stratification

Link ongoing evaluation of risk to changes in intensity of therapy

Develop risk stratification schemes that reflect capabilities of ED and needs/preferences of cardiologists

Develop treatment pathways that provide for independent response of emergency physicians to recognition of higher risk levels

Link ongoing evaluation of risk to changes in intensity of therapy

Develop risk stratification schemes that reflect capabilities of ED and needs/preferences of cardiologists

Develop treatment pathways that provide for independent response of emergency physicians to recognition of higher risk levels

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The “Rallying Cry” for CRUSADE . . .The “Rallying Cry” for CRUSADE . . .The “Rallying Cry” for CRUSADE . . .The “Rallying Cry” for CRUSADE . . .

A seamless transition of optimal care—diagnostic and therapeutic—from the ED to the Cardiology Service . . .A seamless transition of optimal care—diagnostic and therapeutic—from the ED to the Cardiology Service . . .

. . . starts with a successful risk stratification strategy. . . starts with a successful risk stratification strategy. . . starts with a successful risk stratification strategy. . . starts with a successful risk stratification strategy

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