Acute Coronary Syndromes - Illinois College of Emergency ......Acute Coronary Syndromes Page 3 iii....

Acute Coronary Syndromes

Henry Pitzele, MD, FACEP

Associate Director, Section of Emergency Medicine, Jesse Brown VA Medical Center, Chicago; Clinical Assistant Professor, Department

of Emergency Medicine, University of Illinois at Chicago

Notes

Acute Coronary Syndromes Page 1

ACUTE CORONARY SYNDROMES

I. INTRODUCTION

A. Epidemiology

1. 5 million annual ED visits for CP a. 15% AMI b. 25-30% UA

2. IHD leading cause of death in US a. 500,000 annual deaths b. MI still 35% mortality

3. Released MI = malpractice payouts

B. History

1. Early 1900s: advent of arrhythmia control 2. Revolution in the ’60s

a. Catheterization b. CPR c. CCU d. EMS

3. Active reperfusion begun in 1980s

C. Definitions

1. All definitions necessarily retrospective 2. Stable angina

a. Chest pain (or ischemic angina variant) b. Transient c. Episodic d. Reproducible e. Extinguishable f. Unchanged from previous g. Canadian Cardiovascular Society

i. Class I Strenuous activity ii. Class II Slight limitation iii. Class III Severe limitation (1 block/flight) iv. Class IV Any activity/pain at rest

3. ACS a. Unstable angina: any change from previous

i. New onset angina ii. Any change in provocation iii. Increased duration iv. Increased severity

Notes


v. Resistance to previous treatment vi. Synonyms

• Preinfarction angina • Accelerating angina • Crescendo angina • Intermediate coronary syndrome • Preocclusive syndrome

v. Evolution • 40% progress to AMI • 17% mortality without diagnosis

b. Variant angina i. AKA Prinzmetal’s Angina ii. Nonocclusive coronary vasospasm iii. STE with clinical features of AMI

c. Acute MI (WHO definition from 1960s): two of three i. Chest pain > 15-20 mins ii. No relief with NTG or rest iii. EKG changes +/- enzyme bump

d. Acute MI (2000 ACC definition) = troponin elevation plus one of the following: i. Ischemic symptoms ii. Q waves iii. ST deviation iv. PCI

II. PATHOPHYSIOLOGY

A. Mechanism: Tissue ischemia

1. Lack of oxygen delivery to tissue/muscle 2. Usually secondary to lack of blood flow 3. Continuum of hypoxia to cell death 4. Occlusion of coronary arteries 5. Usually by thrombus

B. Anatomy

1. Coronary vasculature review a. Left

i. LAD ii. Circumflex

b. Right 2. Two types of thrombi

a. White i. Platelet rich ii. Gradual onset

Notes


iii. Only partially occlusive iv. Like rings of tree v. Thought to be cause of UA/NSTEMI

b. Red i. Caused by plaque rupture

• Change in intraluminal pressure • Mechanical shearing forces • Size/thickness of fibrous cap • Lipid content • Statins: possible plaque stabilizer?

ii. Clotting factors involved iii. Not more likely with larger lesions iv. Causes complete occlusion v. Sudden vi. Thought to be responsible for STEMI

C. Tissue Damage

1. Three steps of damage a. Acute ischemia b. Vasospasm c. Reperfusion injury

2. Two main complications a. Dysrhythmias b. Pump failure

i. No CHF 5% mortality ii. Mild CHF 15-20% mortality iii. Pulm edema 40% mortality iv. Cardiogenic shock 80% mortality

c. Rarer: papillary muscle/valvular rupture

III. DIAGNOSIS

A. History

1. Risk factors a. Age / sex b. Traditional coronary risk factors

i. HTN ii. DM iii. HL iv. Smoking v. FMH vi. Obesity

c. Known CAD 2. Pain Quality

Notes


a. Angina ≠ ‘Chest Pain’ i. Choking / Strangulation / Constriction ii. Pressure iii. Squeezing iv. Fullness v. Burning vi. Heaviness

b. If described as ‘pain’ i. Dull / Aching ii. Less likely sharp / stabbing

c. Location i. Sternal ii. Left chest

d. Radiation i. Shoulder ii. Neck iii. Mandible iv. Arm

e. ‘Atypical’ isn’t so atypical i. Above are suggestive; 24% of patients presenting this

way have MI; 30% have UA ii. However, of all presenting with sharp / stabbing chest

pain, 5% have MI / 17% have UA iii. Up to 20% ACS for “burning” type pain iv. 19% MI’s describe as stabbing

f. Duration guidelines i. Angina < 15 min ii. MI > 15 min iii. Generally not ACS when < 1 second iv. Hours of pain = large differential

g. Provocation i. Exertion ii. Cold iii. Food

h. Relief i. Rest ii. NTG iii. (reperfusion)

i. Associated symptoms i. Diaphoresis ii. N/V iii. Dizziness iv. Anxiety v. Dyspnea

j. Anginal Equivalents i. Dyspnea (30% AMIs!)

Notes


ii. Radiation pain alone iii. Dizziness iv. Weakness v. Diaphoresis

3. Special populations a. Elderly

i. Pain sensory mechanisms decreased • Nerve damage • Cortical damage • High pain thresholds • Baseline MS decrease

ii. Silent / variant ischemic syndromes more common as age increases

iii. Often present to evaluate complication, not original event b. Young

i. Symptoms often typical ii. No age immune

c. DM i. More MIs ii. Earlier MIs iii. Asymptomatic MIs iv. Polyneuropathy v. Altered perception cardiac pain vi. Extensive comorbidities

4. Prior exams a. ‘Negative’ cath

i. Good for 6-12 mos ii. Negative must be truly negative; subcritical 40% lesion

could rupture at any time b. Negative stress

i. Reliable for less than 6 mos ii. And only 60-70% sensitive for CAD at time of test!

c. In either case, no result is gold

B. Physical

1. Differential a. Pleuritic / positional / palpable b. Signs

i. DVT ii. AAA

2. Complications i. CHF ii. Dysrhythmia iii. New murmur

Notes


C. Tests

1. EKG a. Electrophysiology

i. Anatomic correlations

Anatomic Location EKG Location Coronary Artery

Septal V1-2 LAD lesion

Anterior V3-4 LAD lesion

Lateral V4-6, I, aVL Circumflex branch of LAD

Inferior II, III, aVF RCA (90%)

Posterior V8-9 Circumflex or dominant branch of RCA

Right Ventricular V4R RCA

ii. Evolution of ischemia

• ST Depression • T wave inversion • Biphasic T waves / nonspecific changes • Hyperacute T wave • ST Elevation / reciprocal depression • T wave inversion • Q waves

b. EKG’s of typical localizations of AMI i. Anteroseptal STEMI

Notes


ii. Anterior STEMI

iii. Anterolateral STEMI

iv. Inferior STEMI

Notes


v. Right Ventricular STEMI

vi. Posterior MI

• STD in V1, STE in V8, V9 • pathologic R’s • R/S ratio > 1 in V1-V2

c. Limitations i. Totally normal EKG: 5% have ACS ii. Nonspecific: 25% have ACS iii. 50% AMI had nondiagnostic initial EKGs iv. Immediate risk stratification: low

• Totally normal • Nonspecific ST/T wave changes • No change

i. Immediate risk stratification: higher • ST deviation • Pathologic Q • T-wave changes • LBBB • Pace • LVH

d. Confounds and Mimics

Notes


i. LBBB • Difficult to read EKG for ischemia due to baseline ST

changes • Sgarbossa criteria for diagnosing acute ischemia in

face of LBBB → STE > 1mm concordant with QRS = 5 pts → STD > 1mm V1, V2, or V3 = 3 pts → STE > 5mm discordant with QRS = 2 pts → Score > 3 suggests MI → Score < 3 not so clear

• Presumably new LBBB with clinical MI → Acute reperfusion therapy → Historically, LBBB and AMI get less therapy

ii. Paced rhythm • Similar to LBBB

→ Reverse depolarization → Mimics and masks

• Sgarbossa criteria also predict suggest ischemia in paced rhythm—same criteria apply

iii. LVH: Features less suggestive of ischemia • Precordial leads V1-V3 should be mirror image of

V4-V4 • Concave ST • Asymmetric TWI

iv. Mimics • Benign early repolarization • Pericarditis • Left ventricular aneurysm

2. Biomarkers a. Creatine Kinase: specifically, CK-MB

i. MB fraction specific for myocardium ii. Earlier rise iii. Earlier fall iv. False positives

• Trauma • Muscular dystrophies • Rhabdomyolysis • Vigorous exercise

v. Still need serial testing b. Troponin

i. Highly sensitive and specific (definitionally) ii. Last longer in the serum iii. Predict mortality for all comers

c. Markers out of favor i. Myoglobin

Notes


• Very early rise • Specificity too low • Does not rule out UA

ii. New markers—as yet unproven or disproven • ST2 • CRP

3. CXR a. Useful to rule out diagnoses in differential

i. Pneumonia ii. Pneumothorax iii. Rib fracture iv. Dissection

b. Seek out complications i. Pulmonary edema ii. Cardiomegaly

4. ECHO a. Ischemia begins with hypokinesis b. Progresses to paradoxic akinesis c. Relatively cheap and safe d. Disadvantages

i. Not always readily available ii. Highly operator dependent iii. Cannot differentiate AMI from

• Noninfarctional ischemia • Nontransmural infarction • Old infarct

D. Schemata / Protocols

1. Accepted standard: “Rule-out MI” a. ED enzymes triage bed type for admit b. One to two more sets at q6-8h c. Rule out UA with provocative stress vs. cath

i. Provocative factor • Exercise • Chemical

→ Persantine → Dobutamine

ii. Sensing factor • EKG • ECHO • Nuclear scintography

2. Current Trend: The Chest Pain Unit a. Goals

i. Sensitively and specifically Dx

Notes


ii. Decrease utilization by decreasing hospital stays b. Procedure

i. Initial risk stratification ii. Rapid protocol ROMI iii. Stress before D/C

c. Prototype: The Erlanger Protocol i. Two hour rule-out ii. Initial 5-level risk stratification iii. Serial ECG’s q15 minutes iv. Comparative delta CK-MB v. Re-stratification at 2h vi. Stress almost all groups vii. Still miss a few ACS

3. Future Goal: Magic Bullet? a. Sensitivity approaching 100% b. Noninvasive c. Cheap d. Plentiful e. Fast

IV. TREATMENT

A. Management—Goals

1. Reperfuse a. Goal of TIMI-3 flow (equal flow before and after lesion) b. Outcome data obtained by bench research / tPA c. ‘Open Artery Theory’: Time = Muscle

i. Limit infarct size ii. Decreased CHF iii. Decreased mortality iv. 2 hours is watershed time—large benefit if reperfuse <

2h • Prehospital delays significant • ED delays less so

→ EKG in 10 minutes → Decision time minimization → Action time minimization

• Door to drug / balloon • 90 minutes

2. Halt clot formation / progression 3. Decrease current ischemia

a. Dilate vasculature b. Decrease myocardial demand

4. Prevent / treat complications

Notes


B. Reperfusion Therapies

1. Thrombolysis a. Mechanism

i. Binds to fibrin-bound plasminogen ii. Turns to plasmin iii. Plasmin breaks fibrin strands iv. Clot busted

b. Drug Choice i. tPA (alteplase, Genentech 1984)

• Recombinant version of naturally occurring endothelial enzyme

• Highly fibrin specific • ‘Front-load’ 1.5h supplanted old 3h protocol

→ Bolus 15mg → .75 mg/kg over next 30 min → .5 mg/kg over subsequent 60 minutes → Max of 100mg

• Circulating half-life of 5 minutes • Always coadminister IV heparin

ii. rPA (reteplase, Boeringer 1996) • Mutant recombinant tPA • Less fibrin-specific

→ Faster → Diffuses through entire clot

• Less bleeding • Easier administration

→ ‘Double bolus’ of 10 Units, 30 minutes apart • Only inferior to tPA in presentation > 4h

iii. TNKase (tenecteplase, Genentech 2000) • Third-generation mutant (2000) • Longer half life: single 30-50mg bolus • Extremely fibrin-specific (14x tPA) • Outcomes ≥ tPA

iv. No longer commonly used for ACS • Streptokinase

→ Antigenic; allergic reaction common with recent strep infection

→ Inferior outcome data compared to tPA products • Urokinase • APSAC

c. Indications: STEMI with EKG showing i. STE ≥ 1mm in ≥ 2 contiguous standard limb leads OR ii. STE ≥ 2mm in ≥ 2 contiguous precordial leads

Notes


OR iii. (presumed) New LBBB

• Left bundle outcomes worse • Treated less frequently • Concern for lytic side effects in face of uncertain Dx

d. Absolute contraindications i. Active internal bleeding ii. CVA history

• Previous hemorrhagic CVA • Ischemic CVA < 1y ago

iii. Known intracranial mass • Neoplasm • AVM • Aneurysm

iv. Suspected • Aortic dissection • Suspected pericarditis

e. Relative contraindications i. HTN

• Acutely > 180/100 • Chronically uncontrolled

ii. Old CVA due to intracranial pathology iii. INR > 3 iv. Known bleeding diathesis v. Trauma < 2 wks vi. CPR > 10 min vii. Major surgery < 3 wks viii. Noncompressible vascular puncture ix. Internal bleed < 4 wks x. Pregnancy xi. Active PUD

f. Complications i. Bleeding ii. Allergy (streptokinase)

2. PCI / PTCA a. Background

i. Mechanical revascularization ii. Balloon expansion of arterial lumen iii. Greater dilatation gives

• Less restenosis • More complications: dissection, thrombus, rupture

iv. Often leave fenestrated stent as scaffold b. Has become industry standard

i. Primary PTCA: outcomes better than lytics, IF • Performed within time window (90-120 min)

Notes


• Performed by experienced operator ii. Need to have staffing / backup iii. Less bleeding complications iv. Hard indication for cardiogenic shock

3. Combinations a. Rescue angioplasty

i. Diagnostic: check flow after lytics (rarely used) ii. Therapeutic: mechanically dilate artery if not resolved

after lytics b. Facilitated PCI

i. Half-dose front-load tPA or other lytic followed by cath ii. Used if PCI imminent, but expecting delay past 90 min iii. Shown to be both safe and effective

4. Emergent CABG a. Last resort b. Failed PCI with continued symptoms / instability

C. Anticoagulants / Antiplatelets

1. Aspirin a. Features

i. Potent irreversible antiplatelet ii. Cheap iii. Extremely effective

• Alone decreases mortality 23% • Synergizes with lytics (42% mortality reduction)

b. Dosages i. 160mg - 325mg ii. Chewed preferable (faster onset)

c. Contraindications i. Acute GI bleed ii. Allergy to ASA (use Plavix)

2. Plavix (clopidogrel) a. Inhibits GP IIb/IIIa transformation to high-affinity state b. Routine ED use not proven c. Credible antiplatelet backup in ASA allergy (300mg load)

3. GPIIb/IIIa inhibitors a. Mechanism

i. Inhibits receptor on surface of platelet ii. Prevents crosslinking of fibrinogen / vWf iii. Therefore decreases platelet adhesion

b. Drug choices i. Eptifibatide (Integrillin) ii. Tirofiban (Aggrastat) iii. Abciximab (try saying several times in a row) (ReoPro)

c. Indications

Notes


i. Improves outcome if PCI performed ii. Some centers using routinely for all MI

4. Heparins a. Mechanism

i. Binds antithrombin III, eventually preventing fibrin formation

ii. Stops new clot formation • Keeps newly revascularized arteries patent (a

necessity when using lytics) • Prevents mural thrombus formation in anterior MI • Prevents formation and dissemination of clots to CNS • Does nothing to break up existing clot • Indicated in UA and MI

b. Unfractionated heparin i. Load at 60 U/kg, infuse at 12 U/kg/hr ii. Max of 5000 U bolus / 1000 U/hr iii. Goal of PTT 1.5 to 2.5 times control

c. Low molecular weight heparins i. Inactivates factor Xa ii. Equal or greater efficacy to UFH

• Not all LMWH are the same • Literature supports Lovenox (enoxaparin) over others

iii. Easier to administer, less frequent checks, fewer complications: overall cheaper

iv. Indicated in UA, used often. v. Not routinely used in AMI: many interventionalists loath

subsequent cath (long half-life, unclear reversal characteristics)

D. Maximize oxygen delivery / minimize oxygen consumption

1. Nitrates: nitroglycerin a. Decrease preload and dilate coronary vasculature

i. Contraindicated in hypotension below 90mm syst ii. Seriously consider holding in inferior/RV infarct, as

decreasing preload may induce severe hypotension b. Historically shows some mortality benefit in AMI c. Three SL’s followed by IV

i. Start at 10 ug/min ii. Titrate until pain free, max 200

2. Beta adrenergic blockade a. Decrease myocardial oxygen demand

i. Decrease catechol-induced tachycardia ii. Decrease contractility

b. Contraindications i. Severe COPD / asthma

Notes


ii. CHF iii. Bradycardia / AV nodal blockade iv. Hypotension v. Contraindications may explain why this proven

therapy is often not given in clinical situations c. Any β-Blocker will do

i. Most commonly metoprolol 5mg IV ii. Esmolol gtt is ultra-short acting, consider in presence of

contraindications 3. Opioid analgesia

a. Theoretically decreased myocardial O2 consumption by decreasing pain and anxiety

b. Some vasodilatory effects c. Never proven in trials d. Why not?

4. Oxygen a. Goal is to maximize O2 delivery b. Attempt to maximize PaO2

E. Treat complications 1. Antiarrhythmics: routine administration not indicated 2. Pressors

a. Begin with fluids, especially in RV infarct syndromes b. Each vasoactive has its indications and side effects c. Norepinephrine

i. Increases SVR ii. Indicated in hypotension below 80mm systolic iii. Increased myocardial O2 demand iv. Switch to dopamine when you hit 80

d. Dopamine i. Vasoactive of choice above 80mm systolic ii. Increases HR, but overall best profile of the vasoactives in

face of MI e. Dobutamine

i. Can consider coadministration with DA above 90mm systolic to decrease amount of DA needed

ii. Dilates coronary vasculature iii. Less myocardial O2 demand than others

3. Mechanical intervention a. Endotracheal intubation b. Intraaortic balloon pump

i. Used in refractory cardiogenic shock ii. Inflates in diastole, deflates for systole iii. Vacuum assists LV iv. Overall improves CO and EF, increases coronary

perfusion pressure, and decreases myocardial O2 demand

Notes


ACUTE CORONARY SYNDROMES

PEARLS

1. ACS is common, and the cause of large amounts of morbidity,

mortality, and litigation. 2. UA is any change in symptoms from that patient’s previous baseline. 3. Acute MI is now defined mainly by an increase in serum troponin. 4. Incompletely occlusive white thrombus is thought to cause UA,

completely occlusive red thrombus is thought to case AMI. 5. Typical anginal symptoms include exertional squeezing/choking and shortness of breath. 6. ‘Atypical’ anginal equivalents are extremely common, especially in

the old and diabetic. 7. Prior stress / cath results are of limited use in ‘ruling out’ ACS in the

ED. 8. EKG is the foremost risk-stratification and diagnostic tool for ACS, but

alone cannot ‘rule out’ MI/UA. 9. Consider concordance and the Sgarbossa criteria in evaluation for

ischemia in the face of LBBB or paced rhythm. 10. Cardiac enzymes are the standard for ruling-in MI, but one set never

rules it out. 11. The goal for reperfusion of AMI is 90 minutes, whether by balloon or

chemical. 12. Don’t forget ASA, heparin, and β-blocker unless they are

contraindicated—all have a significant mortality benefit in AMI.

Notes


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Notes


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Notes


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