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Acute Coronary Syndrome PowerPoint Presentation
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Acute Coronary Syndrome

Acute Coronary Syndrome

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Acute Coronary Syndrome

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  1. ER medical lecture series September 21st 2006 Dr. Cernik presenting Slides by Brian A. Romito, DO IM/EM PGY4 Acute Coronary Syndrome

  2. 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

  3. 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

  4. 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!!!

  5. 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

  6. 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

  7. 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

  8. 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

  9. 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

  10. 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

  11. 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

  12. 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

  13. 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

  14. 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.

  15. 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

  16. 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

  17. 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

  18. 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

  19. 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[¶]

  20. 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

  21. 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

  22. 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

  23. 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

  24. 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)

  25. ECG abnormalities in ACS

  26. 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

  27. 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

  28. 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)

  29. 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

  30. 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

  31. 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

  32. 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

  33. ST elevation

  34. ST segment depression

  35. Inverted T wave

  36. 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,

  37. Q wave

  38. Q waves • 1/3 the amplitude of the QRS complex pathologic • May disappear w/ time

  39. Anterior AMI

  40. 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

  41. Lateral AMI

  42. 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

  43. INF AMI

  44. 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

  45. 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

  46. 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

  47. 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

  48. 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

  49. 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

  50. 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