slide1 l.
Skip this Video
Loading SlideShow in 5 Seconds..
Acute Coronary Syndrome PowerPoint Presentation
Download Presentation
Acute Coronary Syndrome

Loading in 2 Seconds...

play fullscreen
1 / 70

Acute Coronary Syndrome - PowerPoint PPT Presentation

  • Uploaded on

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;

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

Acute Coronary Syndrome

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
ER medical lecture series

September 21st 2006

Dr. Cernik presenting

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

Acute Coronary Syndrome
acute coronary syndrome acs
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
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
acs by the numbers
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!!!
spectrum of dz stable angina
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
canadian cardiovasc society classification
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
unstable aka preinfacrt accelerating or cresendo angina
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
unstable angina
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
acute myocardial infarction
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
acute myocardial infarction classification
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
ami pathophysiology
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
ami pathophysiology12
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
acs vasospasm
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
more myocardial damage
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.
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
ed eval hx
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
classical hx
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
atypical hx
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

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

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


Chest pain 515 51 75 75


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


No symptoms 17 1

Total 777[*] 87[¶] 102[**] 387[¶]

atypical sx
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
missed dx of acs
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
early complications of ami
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
early complications of ami cont
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
early complications of ami cont24
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)
ecg changes in acs
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
ecg changes in acs27
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
ecg changes in acs28
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)
ecg changes in acs29
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
ecg changes in acs30
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
ecg changes in acs31
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
ecg changes in acs32
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
inverted t waves
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,
q waves
Q waves
  • 1/3 the amplitude of the QRS complex pathologic
  • May disappear w/ time
anterior ami40
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
lateral ami42
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
inferior ami
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
posterior ami
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
cardiac markers troponins i t
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
cardiac markers creatinine phosphokinase
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
cardiac markers myoglobin
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
mngt goals acs
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
time to tx w outcomes
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
time to tx w outcomes51
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
time is short move swiftly decide
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
groovy drugs ntg
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
i feel good morphine
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
the big dog rx b blocker
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
ace is the place ace inhibitors
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
think long hard calcium channel blockers
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
great minds think alike antiplatelet therapy
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
glycoprotein iib iiia receptor blockers
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!!!
along came plavix antiplatelets cont
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
  • 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
  • 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
low molecular wt heparins
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
direct thrombin inhibitors hirudin bivalirudin
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
fibrinolytic therapy
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
ekg fibrinolytic therapy eligibility
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
when to initiate
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
when to when not to
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!
when to when not to69
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
primary percutaneous coronary intervention
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