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Pre-Hospital STEMI

Steven Fisher, MD

Abington Memorial Hospital

October 10, 2009

Lecture Goals

• It’s just supply and demand

• Early reperfusion saves lives

• PCI is superior to fibrinolytic therapyp y py

• Delay in PCI diminishes efficacy

• D2BT is key indicator of quality care

• Pre-hospital EKGs expedite care

Epidemiology

• 60 M Americans with cardiovascular disease

• Leading cause of death among adultsg g

• 1 M lives claimed in 1997

• 95 M ER visits annually in U.S.• 8 M for chest pain (8.4%)

Epidemiology

• 3 M non-cardiac causes• Of 5 M with probable cardiac etiology

• 20% AMI• 16% Unstable Angina• 6% will die suddenly

• Mortality diminishing but…

Economic Implications

• An estimated 5 million years of life are lost annually

• The cost of CVD exceeded $300 billion in 2000

• $118 billion attributed to CAD

• The average 5-year cost of AMI per patient is estimated at $50,000 and increasing

Myocardial Infarction, Defined

• Defined as myocardial necrosis• Requires 2 of 3 WHO criteria:

– HistoryI h i EKG h– Ischemic EKG changes

– Positive myocardial enzymes

• In 2000: Elevated Troponin and– Ischemic symptoms or– EKG changes or– PCI

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• STEMI: total occlusive thrombotic obstruction/ necrosisNSTEMI l i th b i

Acute Coronary Syndrome

• NSTEMI: non-occlusive thrombosis– ST segment depression– T wave inversion– elevated enzymes

• Unstable Angina: crescendo angina• Chronic Stable Angina

Assess Initial 12-Lead ECG Findings

• ST elevation or new or presumably new LBBB:

• ST depression or dynamicT-wave inversion:

• Nondiagnostic ECG:absence of changes

Classify patients with acute ischemic chest pain into

1 of the 3 groups above ASAP.

strongly suspicious for injury

• ST-elevation AMI

strongly suspicious for ischemia

• High-risk unstable angina/non–ST-elevation AMI

gin ST segment or T waves

• Intermediate/low-riskunstable angina

Anatomy of an MI• Coronary artery with atherosclerosis

Anatomy of an MI

• Plaque may rupture with abrupt changes in blood flow

Anatomy of an MI

• Platelets are activated by factors within the plaque released into the bloodstream

Anatomy of an MI

• Platelets and clotting factors aggregate and form a thrombus

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Pathophysiology

• Endothelial damage and plaque rupture

• Platelet aggregation and thrombus formation

• Occlusion of coronary arteryy y

• Restriction of blood flow and, therefore, delivery of oxygen

• Resultant infarction is due to an imbalance of myocardial oxygen supply and demand

Pathophysiology

• Myocardial death begins after 20 min

• Process complete after 6 hours

Timing may be extended with:• Timing may be extended with:

– Intermittent and transient reperfusion

– Collateral circulation

– Ischemic preconditioning

• Timely reperfusion limits cell death!

Cardiac anatomy Cardiac anatomy

Lead placement: precordial leads Relationship to precordial leads

V1

V2 V3V4

V5

V6

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Relationship to limb leadsEKG Leads & AMI Location?

• Anterior:

• Lateral:

• Inferior:• Inferior:

• RVMI:

• Posterior:

EKG Leads & AMI Location

• Anterior

• Lateral

• Inferior

• V1-V4

• I, AVL, V5-V6

• II, III, AVF

• RVMI

• Posterior

, ,

• V4R

• V8-V9

• Depression V1-V3

Intervals: diagram

STEMI Criteria

• High clinical suspicion

• Chest pain

• 1mm ST elevation in contiguous limb• 1mm ST elevation in contiguous limb leads

• 2 mm ST elevation in 2 contiguousprecordial leads

• New left bundle branch block

Recognition of AMI

ST-segment deviation= 4.5 mmJ point

PR baseline

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12-Lead ECG Variations in AMI and Angina

Baseline

Ischemia—tall or inverted T wave (infarct),ST segment may be depressed (angina)

Injury—elevated ST segment, T wave may invert

Infarction (Acute)—abnormal Q wave,ST segment may be elevated and T wavemay be inverted

Infarction (Age Unknown)—abnormal Q wave,ST segment and T wave returned to normal

The EKG Evolution of AMI

• Hyperacute T waves

• ST segment elevation

• Loss of R’s development of Q’s and• Loss of R s, development of Q s, and inverted T’s

• Resolution of inverted T’s

What Does This 2-Lead ECG Show?What Does This 2-Lead ECG Show? What Does This 12-Lead ECG Show?What Does This 12-Lead ECG Show?

What Does This 12-Lead ECG Show?Damn, that’s heavy!

42 y/o male complains of unrelenting chest pain and states:unrelenting chest pain and states:

"I think I pulled my chest muscles when moving furniture."

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Damn, that’s heavy!

• The patient appears slightly anxious and diaphoretic • PMH - HTN• Meds - HCTZ• BP 190/122 HR 64 RR 20• BP 190/122 HR 64 RR 20• Chest: CTA B • CV: S1 S2, +S4 gallop, grade 2 SEM• Abd: S, NT, ND• No edema

Damn, that’s heavy!

Anterior AMI

• Greater number of leads and reciprocal changes reflect more extensive necrosis, worsened EF, and poor prognosis

• New conduction abnormalities are high risk

• Involvement of the first septal branch of the LAD may precipitate RBBB, LAFB, or type II second degree AVB

Doc, It's Just My Ulcer!

62 y/o man has epigastric pain "just like my ulcer." He is in obvious distress and

diaphoretic…

Doc, It's Just My Ulcer!

• The patient is in distress and markedly diaphoretic. • PMH: PUD, high cholesterol.• Meds: Zocor, Zantac.• Soc: + tob (1 PPD)• Soc: + tob (1 PPD)• Afebrile BP 90/60 HR 68 RR 22• CV: regular without murmurs• Chest: CTA B• No peripheral edema.

Doc, It's Just My Ulcer!

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Inferior AMI

• Patients with EKG evidence of more extensive infarction have in-hospital mortality rates of 23-29%y

• Such patients can also develop high-degree AVB

• RCA supplies the AV node and the inferior wall of the LV in 90% of people

What about Posterior Involvement?

Doc, It's Just My Ulcer!Posterior AMI

• LCX or Dominant RCA

• Commonly occurs with lateral or inferior infarctioninfarction

• Isolated posterior AMI may occur and should be considered for lytics or PTCA

Posterior AMI, EKG criteria

• Wide R wave in V1

• RS ratio >1 in V2

• ST depression V1 V3• ST depression V1-V3

• ST elevation in V8-V9

• V8 and V9 are superior to reciprocal findings in V1-V3

What clinical evidence is there that this patient may have RV

extension?

Hypotension without evidence of pulmonary congestion

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RVMI

• Most commonly seen with Inferior MI• 48% of patients with inferoposterior AMI’s have

coexistent RVMI• Hypotension and cardiogenic shock may occur due to yp g y

decreased LVEDP• 5-10% of patients with RVMI experience

hemodynamic compromise• Avoid Nitrates• Aggressive hydration to promote preload

Inferior AMI with RV extension

• Large amount of jeopardized myocardium

• High rate of in-hospital mortality andHigh rate of in hospital mortality and high-grade AVB

• Few demonstrate extension clinically so it must be sought with V4R

Swooning at Church

74 y/o female was singing in church when she became light headed andwhen she became light-headed and

collapsed to the floor. Upon your arrival, she is complaining of shortness

of breath and lightheadedness.

Swooning at Church

• PMH: MI, HTN, NIDDM• Medications: Digoxin, Lasix, Glyburide.• BP 100/60 HR 80 irregular R 22• Neck: No JVD• Neck: No JVD• Chest: CTA• CV: irregular, 2/6 SEM @ LLSB• ABD: benign• Extremities: trace edema.

Swooning at Church

So you identified the STEMI…

…Now What???

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Therapies

• Reduce myocardial oxygen demand

• Interrupt or reverse thrombosis

Traditional

• Oxygen

• ASA

• Nitrates• Nitrates

• Morphine

• B-blockers

Additional Therapies

• Plavix (clopidogrel)

• Heparin/Lovenox

• GIIbIIIa inhibitors• GIIbIIIa inhibitors

• Fibrinolytic Therapy

• PCI

Oxygen

• Increases supply of oxygen to ischemic tissue

Aspirin

• Irreversibly blocks formation thromboxane A2

• ISIS-2 demonstrated the importance of ASA

• 23% reduction in mortality from AMIy

• 66% decrease in recurrent MI

Nitrates

• GISSI-3, ISIS-4, ESPRIM showed no reduction in mortality

• Dilates coronary arteriesI di ll t l fl• Increases cardiac collateral flow

• Increases venous dilation• Decreases venous blood return to heart • Decreases preload and cardiac

oxygen consumption • Decreases pain of ischemia

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In whom should nitrates be avoided? What type of infarct or

infarct extension might they identify?

RVMI

Morphine Sulfate

• Reduce pain/anxiety• Lessens extension of ischemia by reducing

oxygen demandsyg

ß-Blockers

• Mechanism of action– Blocks catecholamines from binding to

ß-adrenergic receptors

R d HR BP di l t tilit– Reduces HR, BP, myocardial contractility

– Decreases AV nodal conduction

– Decreases incidence of primary VF

ß-Blockers

• Severe CHF/PE

• HR <60 bpm

• Mild/moderate CHF

• History of asthma

AbsoluteContraindications Cautions

• SBP <100 mm Hg

• Acute asthma (bronchospasm)

• 2nd- or 3rd-degree AV block

y

• IDDM

• Severe peripheral vascular disease

ß-Blockers

• 15mg load of Metoprolol

• 5mg increments, observe 2-4 minutes

• If hemodynamic stability continues after• If hemodynamic stability continues after 15 minutes, patient may receive oral load of 50mg

Plavix (Clopidogrel)

• Inhibits ADP activation of platelets

• Binds to platelet receptor

• Onset 2 hours• Onset 2 hours

• Role now for those intolerant of ASA

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Heparin/ LMWH

• Mechanism of action– Indirect thrombin inhibitor (with AT III)

• Indications– PTCA or CABG– With fibrin-specific lytics – UA / NSTEMI

LMWH

• More specific

• Give easier and more safely

• More expensive• More expensive

• Can’t use with renal failure

• Patient should be under 100kg

GIIbIIIa inhibitors

• Blocks fibrinogen receptor that is exposed by platelet shape changes caused by thromboxane and ADPy

• Platelets have no “glue”

• Expensive

• Reopro- lasts longer than others

• Integrelin/Aggrastat from snake venom

GP IIb/IIIa Inhibitor

Fibrinolytic Therapy

• Breaks up the fibrin network that binds clots together• Indications: ST elevation >1 mm in 2 or more

contiguous leads or new LBBB – Time of symptom onset must be <12 hours– Caution: fibrinolytics can cause death from brain

hemorrhage• Agents differ in their mechanism of action, ease of

preparation and administration; cost; need for heparin• Advantage: universally available in ED, unlike cath

labs, and comparatively cheap

Time to Reperfusion

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TIMI Flow

• Grade 0: complete occlusion• Grade I: some penetration of contrast• Grade II: delayed flow to entire vesselGrade II: delayed flow to entire vessel• Grade III: normal flow

• Grade III flow is markedly superior to grade II in terms of infarct size reduction and mortality benefit

PCI

• D2BT less than 90 minutes ideal

• Early delays most significant as myocardium is most salvageablemyocardium is most salvageable

• D2BT delays are associated with worse outcome including in-hospital mortality

PCI

• When D2BT < 90, in-hospital mortality was 3%

• 91-120 minutes: 4 2%91 120 minutes: 4.2%

• 121-150 minutes: 5.7%

• >150 minutes: 7.4%

• Each 15 minute REDUCTION in D2BT resulted in 6.3 fewer deaths per 1000

Core Measures

• Health Quality Alliance Program– CMS and Joint Commission

• July 2006 shifted D2BT goal from 120 to 90 minutesminutes

• Allows exclusion of patients where delays are inevitable

• 1999-2002 <15% of hospitals had median D2BT of <90 minutes

PCI Delays

• Patients who present during “off-hours”

• Transfers <5% are treated in < 90 min

• Not coordinated like that of trauma• Not coordinated like that of trauma

• Emergent transfer, however, appears better than onsite fibrinolytic therapy

PCI

• Better reestablishment of coronary flow

• Lower risk of reinfarction

• Reduced risk of ICH• Reduced risk of ICH

• Minimal contraindications as compared with TPA

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Strategies to reduce D2BT

• EP activation of catheterization lab

• Single-call notification and activation

• On site cardiologist• On-site cardiologist

• Pre-hospital EKG interpretation

• Field transmission of EKG

• Data collection and feed-back

Percutaneous Coronary Interventions (PCIs)

2. PTCA + stent

1. PTCA: Percutaneous Transluminal

Coronary Angioplasty

placement

3. Atherectomy: “grinds away”

the plaque

Angioplasty: the stentAngioplasty and stent: before

and after

Lecture Goals

• It’s just supply and demand

• Early reperfusion saves lives

• PCI is superior to fibrinolytic therapyp y py

• Delay in PCI diminishes efficacy

• D2BT is key indicator of quality care

• Pre-hospital EKGs expedite care

The End!