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Acute Coronary Syndrome PowerPoint PPT Presentation


ER medical lecture series September 21 st 2006 Dr. Cernik presenting Slides by Brian A. Romito, DO IM/EM PGY4 Acute Coronary Syndrome Acute Coronary Syndrome (ACS) ACS includes spectrum of clinical presentations from common pathophys Myocardial Ischemia/Necrosis;

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Acute Coronary Syndrome

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ER medical lecture series

September 21st 2006

Dr. Cernik presenting

Slides by Brian A. Romito, DO IM/EM PGY4

Acute Coronary Syndrome


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Acute Coronary Syndrome (ACS)

  • ACS includes spectrum of clinical presentations from common pathophys Myocardial Ischemia/Necrosis;

  • Dz Range; continuum from asymptomatic CAD & Stable Angina to unstable angina & STEMI/NSTEM

  • ACS/AMI--> Leading cause of death in US


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Hx ACS

  • Hx; selective coronary arteriography Sones 1959 & External Cardiac Massage 1960 Kouwenhoven

  • Day est 1st Cardiac Arrest team 1960 & 1st CCU 1962  AMI mortality 50%

  • 1980s Coronary angiography in AMI showing occlusion in infarct-related artery... Rentrop intracoronary Streptokinase in AMI

  • 1980s prehospital portable 12 lead ECG's


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ACS- by the Numbers

  • Ischemic Heart Dz/CAD; leading cause death US 1 million/yr; 160k in 65yrs or younger

  •  mortality 40yrs; 25%  AMI &  survival AMI ; smoking, CTRL lipids, better HTN/DM mngt, resusitation, Cardiac Care

  • 6 million US pts/yr Chest Pain eval in ED2 million dx ACS

  • 2% (120,000) w/ ACS d/c home by ED

  • 900,000 AMI/yr; 20% die b/f ED + 30% die in 30 days= 450K

  • Majority pre-hospital deaths w/in 2hrs of Sx, others disabled

  • Cost for eval & care pts w/ ACS $100-120 Billion!!!


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Spectrum of Dz; Stable Angina

  • Transient, episodic chest discomfort via Myocardial Ischemia

  • Typically predictable & reproducible w/ frequency of attacks

  • Attacks provoked by STRESS; physical, emotional, anemia, environmental, dysrthymias

  • Resolves predictable time; spontaneously, w/ Rest, w/ NTG


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Canadian Cardiovasc Society Classification

  • Class I; No Agina w/ ordinary activity

  • Class II; slight limitation ordinary activity ; anina w/ climbing stairs, emotional stress, walking

  • Class III; severe limitation of ordinary activity; angina w/ walking 1-2 blocks on level surface, 1 flight steps

  • Class IV; inability any physical activity w/o discomfort; anginal symptoms at rest


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Unstable aka preinfacrt, accelerating, or cresendo Angina

  • Harbinger AMI so Tx Aggressively

  • If pt has dx Angina assume Unstable till proven otherwise

  • Plaque rupture accompanied by thrombus formation & vasospasm; intraocoronary events... ECG abnormalities; T wave & ST changes.

  • Variant aka Prinzmetal's Angina; coronary artery vasospasm at rest w/ min fixed coronary artery lesions; may be relieved by exercise or NTG. ST elevation not possible to discern from AMI


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Unstable Angina

  • Occurs w/ min exertion or at rest, new onset, worse than prior stable angina ( freq, longer, resists prior meds, starts w/ < stress/exertion)

  • Rest Angina; occurs at rest, > 20 minutes, w/in 1 week presentation.

  • New Onset Angina; at least Class II, onset w/in 2 months

  • Increasing Angina; previous angina more freq, > 20 min despite stopping activity, increase in class w/in 2 months to class III


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Acute Myocardial Infarction

  • cell death/necrosis myocardium

  • Typical rise/fall of CK-MB, Trop w/ clinical Sx, ECG changes, or coronary artery abnormality w/ 1 below:

  • 1) Ischemic Sx

  • 2) Dev Q waves

  • 3) ST elevation or depression

  • 4) Coronary artery intervention

  • Est MI; Dev New pathologic Q's on serial ECGs or Path findings of healed or healing MI


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Acute Myocardial Infarction classification

  • Old; Transural (transmural process assoc w/ ST elevation) or Non-transmural (subendocarial, ECG changes other than ST elevation-assume smaller infarct size), presumed tissue damage

  • Old; Q-wave or Non-Q-wave MI; based on ECG

  • Preferred nomenclature is STEMI or non-STEMI preferrable


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AMI Pathophysiology

  • Myocardial ischemia; too little perfusion for O2 demand usually due to coronary vessel stenosis 2 CAD

  •  coronary blood flow- NO Ischemic 's w/ rest until stenosis >95%; activity ischemia can occur at 60% stenosis

  • CAD characterized by thickening/obstruction of Coronary arterial lumen by atherosclerotic plaque.

  • Plaque composition varies; Fibrous plaques stable but can produce angina w/ exertion b/c stenosis


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AMI Pathophysiology

  • Initiation of ACS by Endothelial damage & atherosclerotic plaque disruption

  • Fibrolipid plaques rupture from arterial lumen inflammation thrombus & platelet aggregation; acute obstruction cell death

  • Thrombus formation is Integral factor in ACS & platelet rich thrombi > Resistance to throbolysis than fibrin/RBC rich thrombi

  • Damage extent depends on collateral circulation, plaque character, amount vessel obstruction


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ACS Vasospasm

  • 10% of MI's w/ thrombus formation w/o significant CAD

  • Induced by local mediators/vasoactive substances after occlusion; >  in blood flow

  • Vasomotor hyperactivity

  • Sympathetic stimulation; Epi & Serotonin;  platelet clot & neutrophil-mediated vasoconstriction


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More myocardial damage...

  • Calcium, Oxygen, & cell debris occlude distal vessel...

  • Neutrophils & inflammation further decease perfusion causing further inury & Ventricular dys-fxn... by ROS, proteolytic enzymes, and chemoattractants

  • AKA Myocardial Stunning or reperfusion dysrhythmias.


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Pre-hospital

  • Tx: NTG, ASA (oral), IV Morphine

  • 12-lead EKG (99% specific) & + predictive value (93%); AMI pts- atraumatic CP...  EMS time at scene 3 minutes

  • Earlier detection ST segment elevation in AMI, hence more rapid reprofusion therapy, esp w/ long route times


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ED Eval & Hx

  • Type of pain, on set, location, radiation, duration, what makes better/worse, same Sx before???

  • CAD Risk; male, age, smoking, HTN, DM, FmHx, lipids, menopause, cocaine use.

  • 80/122,000 CAD have 1 of 4 (DM, smoking, HTN, lipids)

  • Note; Risk factors are population phenomenon and have no ability to  or  likelyhood of condition of any 1 pt

  • Risk Hx not as impt as HPI, ST/T wave changes or markers


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Classical Hx

  • Angina- term means “tightening”

  • Discomfort; squeezing, pressure, fullness, heaviness or burning sensation

  • Substernal/precordial location +/- radiation; jaw arm neck if down arm; ulnar aspect

  • Location L chest but can be R

  • Initiated by; heavy meal, exertion, cold, relieved w/ rest, lasting 5 to 20 minutes

  • Assoc Sx; SOB, N/V, diaphoresis, weakness, fatigue, dizzy... can be considered anginal equivalent syndrome


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Atypical Hx

  • atypical features of pain;pleuritic, positional, or reproduced by palpation, burning, indigestion, sharp, or stabbing

  • Large Study 435,000 pts dx AMI, 1/3 did NOT have CP at presentation

  • More often in older pts >85yr old, or 40% Diabetics (no CP), or 60% female (No CP) at time of AMI

  • c/o indigestion/anxiety/sleep disturbance/dizziness in women

  • Nonwhite populations likely to have atypical Sx


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Table 77-2 -- Symptoms of Acute Myocardial Infarction: Typical and Atypical

Symptom Bayer et al[*],[†] Tinker[‡] Uretsky et al[§] Pathy[||]

Typical

Chest pain 515 51 75 75

Atypical

Dyspnea 118 19 14 77

Syncope 72 4 1 27

Confusion 46 1 51

Stroke 32 6 2

Fatigue 36 2 4 10

Nausea or emesis 28 1 10

Sudden death 31

Giddiness 18 3 22

Diaphoresis 18 2

Arterial embolus 3 19

Palpitation 4 14

Renal failure 11

Pulmonary embolus 8

Restlessness 4

Abdominal pain 5

Arm pain only 1

Cough 1

Silent

No symptoms 17 1

Total 777[*] 87[¶] 102[**] 387[¶]


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Atypical Sx

  • Atypical presentation pts w/ ACS delayed & poor outcomes

  • 2nd Nat Registry of MI study (NRMI-2): MI w/o CP significantly more likely to die in hospital (23% vs 9%)

  • More likely to have stroke, hypotension, CHF requiring intervention

  • Typical presentation; Less likely to receive ASA, ß-blocker, Heparin, thromboysis & 1 angioplasty


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Missed Dx of ACS

  • 2 to 8% pts w/ AMI to ED are DC'd w/o proper ID diagnosis

  • Pts signif younger, women, nonwhite, atypical complaints, less likely to have ECG evidence of acute ischemia

  • 53% missed AMI & 62% pts w/ unstable angina had normal ECG

  • 11% of MI pts; ED physician failed to detect ST elevation 1 to 2mm

  • Docs w/ > risk; < ED experience, < documented Hx, admitted fewer pts, difficulty in ECG interpretation


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Early complications of AMI

  • Bradydysrythmia & AV Block; 25-30% pts w/ AMI have sinus brady

  • AMI + AV Block = respond poorly to TX; poor prognosis

  • Tachydysrythmias; Atrial (afib, sinustach) or Ventricular (VT, Vfib); 1 Vfib 4-5% of AMI w/ 60% in 1st 4 & 80% 12

  • Cardiogenic shock risk; large MI, Low EJF, DM, age, prior MI

  • LV wall rupture 1/3 in 1st 24 rest in 3-5 days; sudden death, PEA, repetitive vomiting, precipitous decline, nearly 100% fatal... percardialcentesis temporary measure till surgery


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Early complications of AMI cont

  • Infarct Pericarditis assoc w/ AMI = transmural & infarct zone near epicardium. ST changes may be obscured

  • Infarc Pericarditis- new CP 1st week post MI. Pleuritic & worse supine.  risk embolization b/c  risk Ventricular Aneurysm

  • Dressler's Syndrome- does not need to be transmural. Uncommmon 1week-months; Fever, malaise, pleuro-pericardial pain, +/- Rub

  • Dresslers..ESR & WBC ECG; pericarditis & PR depression. ? bloody or serous Pericardial/pleural effusions... immune mediated, use NSAIDS


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Early complications of AMI cont

  • Stroke may complicate AMI. Ischemic, thromboembolic most common. Emboization from LV mural thrombus w/  LVEJ or atrial w/ Afib.

  • Higher rate in AMI (0.9 to 0.1% at day 28 after MI) vs control (0.014%)

  • Hemorrhagic stroke rate w/ fibrinolytics is < 1%, rate w/ age

  • Percutaneous intervention  risk vs fibrinoytic (1.6% tpA vs 0.7 angioplasty), over all (1% fibrinolytic vs 0.1% angioplasty)


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ECG abnormalities in ACS


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ECG changes in ACS

  • Hyperacute T wave changes- earliest findingT wave tall/peaked w/in min. of occlusion

  • Progresses to ST elevation seen in a classic MI

  • Differential dx tall T's; ischemia, high K, benign early repolarzation, LVH, LBBB, & pericarditis

  • Morphologic varations of ST segment elevation seen from the J point at end of QRS to apex of T wave; convex, concave or scooped.

  • Concave morphology is commonly seen w/ other ST segment elevation syndrolmes


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ECG changes in ACS

  • ST seg. Elevation measured in mm's: 1 block=1mm in ht

  • ST elevation benign/pathologic is common

  • Men 90% have ST elevation, in precordial leads; 1mm or

  • more in men. 1Mm less in women

  • ST segment is concave/more prominent the deeper the corresponding S wave


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ECG changes in ACS

  • Differentiating normal/pathologic ST elevation of AMI is a new EKG change

  • ST depression represents subendocardial/nononfarction ischemia

  • NSTMI, may elevate segment in a ST segment elevation AMI, reflect “mirror image” of ST elevation of a post. MI, or represent recipocal ST depression seen in INF wall MI. (seen best in aVL)


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ECG changes in ACS

  • T wave inversion are can be non-specific, can suggest myocardial ischemia.

  • T waves inversion of ACS are narrow,symmetrically inverted

  • Inversions best viewed by comparison to recent EKG


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ECG changes in ACS

  • T wave inversion are can be non-specific, can suggest myocardial ischemia.

  • T waves inversion of ACS are narrow,symmetrically inverted

  • Inversions best viewed by comparison to recent EKG


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ECG changes in ACS

  • Ischemic ST depression is horizontal/downsloping

  • Subendocardial ischemic ST depression is difffuse

  • D/dx: ischemia/infarction, repolarization abn. LVH/RVH, BBB, pacer, dig FX, K, ↓K, PE, ICH, myocarditis, rate-related ST depression, post cardioversion, pneumo


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ECG changes in ACS

  • T wave inversion are can be non-specific, can suggest myocardial ischemia.

  • T waves inversion of ACS are narrow,symmetrically inverted

  • Inversions best viewed by comparison to recent EKG


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ST elevation


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ST segment depression


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Inverted T wave


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Inverted T waves

  • Can be inverted Norm in AVR, V1 & sometimes V2

  • ACS narrow & symmetrically inverted

  • Wellen's Synd; deep symmetric T wave inversion, biphasic T in Anterior precordial leads... No Q's... indicated LAD lesion

  • D/dx; WPW, ACS, BBB,


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Q wave


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Q waves

  • 1/3 the amplitude of the QRS complex pathologic

  • May disappear w/ time


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Anterior AMI


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Anterior AMI

  • V1-V4

  • Septal involvement V1 & V2

  • Reciprocal ST segment depression in III & AVF

  • ANT wall supplied by LAD

  • May involve lateral wall too b/c 1st diagonal branch from LAD is likely to be involved when ST elevation extends to I & AVL


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Lateral AMI


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Lateral AMI

  • Freq seen w/ ANT AMI, INF infarct or INF/POST infarcts

  • Lat wall served by LAD, RCA, and L circumflex arteries.

  • LAT involvement leads; I, AVL, V5, & V6 (high lat infarcts); occlusion L circumflex

  • Reciprocal ST segment depression III, AVF, V1


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INF AMI


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Inferior AMI

  • Changes in II, III, AVF

  • INF Wall heart & AV node; both RCA involved in 90%

  • 10% L circumflex artery

  • Reciprocal changes in AVL, I


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Posterior AMI

  • 15% to 20% of all AMI's

  • Seen w/ INF or INF-LAT infarcts

  • Lesion in RCA; it's POST branch, or L Circ

  • Reciprical changes in V1 to V3

  • Additional leads V8 or V9 increases sensitivity


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Cardiac Markers- Troponins I & T

  • best markers for myocardial cell injury; genetically distinct from Trop in skeletal Musclek

  • Majority bound to muscle fiber, cytolsol amounts smaller released 1st after cell injurty, hence biphasic raise in Trop level

  • Begin to raise ~ 3 Release for 5-7 days, elevation > 7 days

  • Serial measure highly sensitive, TnT 50% 3-4h, 75% 6h & 100% at 12h

  • Linear correlation b/t Trop elevation & Infarct. TnT can be elevated in Renal Failure pts or sketetal muscle dz, TnI not found in Rneal Failure > cardiac specific


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Cardiac Markers- Creatinine Phosphokinase

  • Large quantity in cardiac & Skeletal Muscle  w/in 3-8 w/ peak 20-24 after injury; normalize 3 to 4 days

  • ED presentation 37% sensitive 87% specific for Dx AMI; 12 50% spensitive

  • CK-MB subtype specific for Myocardial cells...w/in 3 only 25% to 50% sensitive > 3 more sensitive 40-100% esp 12-16

  • Also elevated; rhabdo, Musc Dystrophy, Trauma, myosistis, extreme exercise

  • Do Not rely on a single measurement


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Cardiac Markers- Myoglobin

  • Found in muscle rapidly released in circulation after cell injury

  • Raise 1-2 peaks 5-7 & returns to base line 24

  • Myocardial Myo not distinguishable from Skeletal Mus levels

  • Elevated in renal failure b/c reduced clearance & trauma, exercise, signif systemic illness

  • Sensitivity 21-100% Serial testing 2-4 after intial improves diagnostic power... doubling 1-2 still nonspecific

  • Excellent negative predictive value for AMI not ACS


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Mngt Goals ACS

  • Inc Mycardial Oxygen supply w/ O2

  • Dec Oxygen Demand/F contractions via B-Blocker

  • Inc Metabolic substrate to mycardium; NTG, MSO4, Fibrinolytic, Angioplasty

  • Dec inflamm or tox injury... anti-inflammatory Rx

  • Prevent reocclusion of Coronary A w/ Antiplatelet & Anticoagulants


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Time to Tx w/ Outcomes...

  • 1970s wave phenomenon- ischemic cell death... myocardial necrosiss went subendocardium epicardium. Release of occlusion earlier smaller infarct & > transmural progression

  • Beneficial reperfusion; shorter time of AMI & Tx; early patency--> > Myocardial salvage.

  • GUSTO; Preserved LV fxn, & improved at 24 & 30 days related to angiographic patency in 1st 90 minutes. Fibrinolytic Th w/ AMI signif > benefit w/ Tx in 1st 1-2

  • Myocardial Infarction Triage & Intervention (MITI) trial; mortality rate AMI w/ Tx w/in 70 min 1.3% vs 8.7% later Tx


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Time to Tx w/ Outcomes...

  • Pts tx in 1st hour have 40 -50% dec mortality. Tx 2-12 after AMI have modest yet beneficial

  • Pt-bystander delays in seeking Tx via EMS 2-6.5

  • 26-44% AMI pts delay > 4 b/f seeking care. Signif delay due to self Tx ~ 1/3 of pts w/ AMI & sudden Death!!!

  • Prehospital Delay- calling PCP 1st Only ½ of AMI pts call EMS Many drive themselves, or live far distance from Hospital

  • In hospital AVG time to fibrinolysis 45 to 90 minutes AHA recommends tx w/in 30-60 minutes of ED arrival, or PTCA < 90 minutes


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Time is short, move swiftly & decide...

  • 4 D's:

  • Door (events prior to ED arrival)

  • Data (obtain ECG, Lab)

  • Decision (AMI dx & decide Th)

  • Drug (Fibrinolytic or passing Angioplasty Cath)

  • Triage ID AMI, Have Rx ready, Immediate Cardio consult


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Groovy Drugs-NTG

  •  Preload & sml fx on afterload,  venous compliance, hence reduction myocardial oxygen demand

  • Vasodilation Coronary Arteries... pos  collateral blood flow. Meta-analysis small trials show 35%  mortality w/ IV NTG

  • Pts w/ SBP >90 should receive SL NTG 0.4mg on presentation. If no relief of Sx w/ 3 NTG SL then IV NTG

  • CAUTION; Hypotension, INF MI, RV MI, Bradycardia

  • Initial infusion 10mics/min titrate SX free; 10% reduction Normotensive and 20-30% reduction in HTN


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I Feel Good- Morphine :)

  • Use in Unstable Angina NOT eval in Large randomized Trials!

  • Opioid Analgesic w/ weak sympathetic blocker, anxiolytic fx, systemic Histamine realease... all can benefit ACS

  • Use if continued Sx w/ NTG & anti-ischemia Therapy

  • Relieve Pain & Anxiety  Oxygen demand & myocardial work, Some Vasodilatory FX w/ preload reduction

  • 2 to 5 mg IV dose Q 5-30 min prn

  • Caution: Hypotension (mngt IVF bolus), allergic RXN


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The Big Dog Rx; B-Blocker

  • Relieves Catecholeamine-induced Tachycardia,  contractility & myocardial Oxygen demand!

  • Beta-1-Receptors in Myocardium, SA-node AV conduction

  • Beta-2 located in vascular muscle & Lungs

  •  mortality pts w/ AMI &Meta-analysis 13%  risk develop AMI

  • IV metoprolol 5mg over 1-2 min x3. Alt are Atenolol (longest acting), Esmolol (shortest acting; use in COPD, CHF; pts < likely to tolerate B-blockers)

  • CI; AV block, Hypotension, Bradycardia, Pulm Edema, +/-COPD/Asthma


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ACE is the Place: ACE Inhibitors

  • Benefit CHF also may reduce M&M in AMI, best in 1st 24

  • Reduction cardiovascular mortality,  CHF develop, fewer recurrent AMI's

  •  benefit when used w/ other agents; ASA, fibrinolytics

  • MOA, thought  in plaque rupture related to < intracoronary shear force or neurohumoral factors

  • Use in ED especially if long stay in ED

  • Caution; Hypotension, watch Renal Fxn


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Think long & hard: Calcium Channel Blockers

  • 1 benefit is Sx relief.

  • Significant Vasodilatory FX Hypotension worsen Coronary Ischemia

  • Neg Inotropic FX perfusion

  • AV block significant in pts treated w/ B-Blocker

  • DO Not Use Unless for Rate Control in Supraventricular dysrhythmia in pt unable to tolerate B-blocker


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GreAt mindS think Alike; Antiplatelet Therapy

  • In non-ACS pts, > reduction in progression to acute Infarction w/ aggressive antiplatelet Therapy

  • Pts in ACUTE phase of AMI, signif reduction Mortality 25-50%

  • ASA give early. Irreversibly acetylates platelet cyclooxygenase life of platelet (8-10 days)  Stops production Thromboxane A2 & indriect antithrobotic agent too!

  • ASA blocks endothelial cyclooxygenase &  prostacyclin

  • 2nd International Study of Infarct Survival shows 23% reduction Mortality AMI w/o Fibrinolytics and 43% with. 325Mg chewed & swallowed


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Glycoprotein IIb-IIIa Receptor Blockers

  • Activated Platelet Membrane surface proteins that cross-link platelets to form platelet plug

  • 3 drugs abciximab, eptifbatide, and tirofiban, aka GPI's... monoclonal Ab's specific for glycoprotein Iib/IIIa provides proloonged inhibition platelet aggregation

  • Numerous studies bottom line... use if plan PCA, bennefits 35% or greater mortality benefit. Studies to show benefit w/o PCA (even w/ fibrinolysis, ASA, heparin) NONE!!!


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Along came Plavix; Antiplatelets cont...

  • Potent platelet inhibitor... > than ASA, ASA+ Plavix > effectiveness than ASA alone in  cardiovac death

  • Inhibit transformation of glycoprotein Iib/IIIa receptor into high-afinity ligand-binding state, irreversibly inhibiting platelet aggregation

  • Rapid onset, Max platelet inhibition after 3 to 5 days of 75mg earlier onset of platelet inhibition w/ loading dose 300-600mg

  • Use often when PCA is not anticipated due to bleeding complications when mechanical interventions done... ask cardiologist


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Antithrombins

  • Signif dec in progression to Acute/recurrent/extension of infarction and death

  • Unfractionated Heparins, Low Molecular Wt Heparin, and direct Thrombin Inhibitors (Hirudin and bivalirudin).

  • Recurrent Anginal pain, AMI (STEMI & NSTEMI), + serum markers, & dynamic EKG changes


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Heparins

  • Mixture of several mucopolysaccaride chains various lengths & mol wts unfractionated – antithrombotic properties

  • Std dose binds Antithrombin III then inactivates Thrombin (factor II) & active factor X... prevents fibrinogenfibrin, thus clot propagation

  • Heparin by itself has no Anticoagulant property.

  • Synergistic FX w/ ASA in  mortality in ACS

  • Initial dose 60U/kg & 16U/kg/hr maintenance


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Low Molecular Wt Heparins

  • LMW heparins~ 1/3 Mol Wt of Unfractionated < size difference

  • Inhibit coagulation similar to Heparin; 1/3 of molecules bind both antithrombin III & thrombin, remainder bind factor Xa, hence differences in activity

  • High-ratio preps have advantage over heparin... Lovenox highest ratio & better bioavailability & longer half life

  • Inhibtion eariler in coagulation cascade > the antithrobotic FX

  • LMH esp Lovenox w/ Anti Xa/IIa ratio >short term benefit over Heparin. 1mg/Kg BID dose


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Direct Thrombin Inhibitors; Hirudin & bivalirudin

  • Antithrombin anticoagulants; signif advantage over heparin

  • Derivitive of leech salivary gland, but sythesized & recominant

  • Higher affinity to thrombin & inactivates already fibrin-bound thrombin (clot bound thrombin).

  • DOES NOT need endogenous cofactors (antithrombin III)

  • Inhibits thrombin-induced platelet aggregation

  • NOT assoc w/ HIT as Heparin is, however no signif benefit as adjuct therapy in ACS pts, use in Heparin-Thrombocytopenia


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Fibrinolytic Therapy

  • Reopening infarct related artery w/ fibrinolytic or PCI, gives the best opportunity for salvage ischemic myocardium;  M&M

  • C/I & other limitations... PCI Tx of choice w/ or w/o stenting

  • Agents; tPA, Streptokinase; GUSTO-1; 15% reduction in death w/ t-PA up to 1 year

  • Trials; r-PA vs accelerated t-PA; r-PA no adjustment for wt advantage GUSTO-III showed rPA = to tPA, EXCEPT pts >4

  • TNK vs tPA; TNK longer t-1/2, 14X more fibrin specific, 80X resistant to plasminogen activator inhibitor than tPA

  • ASSENT-2; no diff in 30 d M&M, except for pts >4 Sx b/f ED


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EKG fibrinolytic Therapy eligibility

  • ST elevation 1mm+ in 2 or more anatomically contiguous limb leads & 2mm+ in 2 or more contiguous precordial leads

  • OR New or presumed new LBBB

  • No benefit w/ ischemic CP who lack above EKG findings

  • LBBB + AMI = poorer outcome due to likely proximal LAD occlusion, putting Signif portion LV in ischemic jeapordy

  • DO NOT USE in ST-depression... Signif poorer outcomes!!!

  • Remember Age is NO longer excluder, but age > 75  ICH


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When to initiate

  • Gen accepted from time onset ST elevation AMI 12 Earlier use though better outcome. Esp 1st 6 AMI

  • No signif benefit 12 to 24 after Sx onset

  • If BP controlled or can be lowered... b/c risk ICH, initial SPB > 150 (15/1000 lives saved);  SPB > 175mm Hg or > (11/1000)

  • Persistently BP 200/120 Absolute C/I

  • Heart failure, shock, Hypotension (60/1000 lives saved) NOT an absolute C/I per FTT Collaborative Group Meta-analysis


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When TO & When NOT TO

  • Active Diabetic Retinopathy... strong relative C/I risk blindness

  • DM pts w/ AMI 2X more likely to DIE

  • CPR > 10 minutes long or extensive Chest Trauma from CPR Hemithorax/cardiac tamponade Not dx in fibrinolytic survivors

  • Prior Stroke/TIA, major risk for ICH, relative C/I, prior Hemorrhagic stroke ABSOLUTE C/I

  • Prior MI in setting AMI ISIS-2; 26%  Mortality; even if prior fibrinolytics... Hx CABG combo lysis & Angioplasty may be needed!


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When TO & When NOT TO

  • Recent Surgery/Trauma/GI Bleed w/in 10 days is absolute C/I

  • Women menses w/ AMI consider use; excessVag bleeding after Fibrinolytics CTRL w/ Vag packing compressible site of bleeding

  • GI bleed in 10 days Absolute C/I

  • HTN; SBP > 180 or DBP 110

  • Significant liver Dysfunction


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Primary Percutaneous Coronary Intervention

  • Consider in pts w/ C/I to Fibrinolysis, Cardiogenic shock, unstable angina

  • Many advantages over Fibrinolysis... > # pts applies to, lower risk ICH, signif higher initial reperfusion rate, faster hospital D/C

  • Disadvantages; $$$, location specific, time to application

  • Meta-analysis 10 major studies; 30 day mortality less in PTCA vs Fibrinolysis 4.4% vs 6.5% & signif reduction in total stroke or ICH


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