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STEMI (from Cameron, Dunn, little bit from Tint) ANTERIOR Commonest site LAD or branches Precordial leads V1-V4 Reciprocal ST depression in 30% (?which leads…?posterior - no) May have marked sympathetic stimulation & require rate control to control ischaemia Large anteriors result in LV dysfunction Prone to mural thrombus May be associated INFERIOR infarction POOR PROGNOSTIC SIGNS: Bradycardia Heart block Note: Antero-septal: ST V1-V4 Anterior: rS in V1, ST V2-V4, low R amplitude V1-V4 Anterolateral: ST V4-V6, I and aVL INFERIOR Inferior leads: II, III, aVF Reciprocal changes in V1-V3 in 80% ST depression in aVL = earliest sign Occasionally Left axis Due to occlusion in: RCA (ST greater in III than II) NB: Proximal RCA lesion (ST V1/V4R) = right ventricular infarction) OR: Circumflex (suggested by ST V5/V6/I/aVL) = infero-lateral NB Reciprocal ST depression in V1-V4 are present in both RCA & Circumflex infarctions Less impairment of LV cf Anterior AMI If associated with RECIPROCAL ST depression in ant leads (V1-V4) likely to have additional LAD disease, poor LV function/incr risk CCF, May present with epigastric pain/n/v (from vagal overactivity) At risk for early complications: Arrhythmias (especially bradycardias – more common in inferiors) Heart Block Cardiogenic Shock RIGHT VENTRICULAR MI In isolation = < 3% of all AMI’s BUT occurs in association with approx 50% of INFERIOR MI’s RCA occlusion prox to marginal branches Or: Circumflex occlusion in left dominant circulation RV Leads RV4-6 ST elevation confirms Dx All patients with Inferior AMI + RHF: ie Hypotension Clear Lung fields Raised JVP Should have RV leads performed RV Infarction complications Shock Heart Block (usually with Inferior) AF PE from RV thrombus TR Pericarditis Must maintain preload in RV Infarction Adequate filling Avoid nitrates/diuretics Maintain Sinus rhythm Inotrope: Dobutamine (after adequate filling) If associated with LV dysfunction: May require IABP or arterial vasodilators (nitroprusside) to reduce afterload POSTERIOR AMI 20% of AMI’s ST Depression or peaked T’s in V1-3, with upright T’s Initial tall wide R in V1-2 (R:S ratio >1) ST elevation in posterior leads V7-9 Usually associated with inferior or lateral AMI In Inferior: less ST elevation in II than III/aVF R/S ratio > 1 in V1-2 without RAD LATERAL AMI: ST elevation in V4-6, I & aVL “High lateral” Changes in I, aVL but not V5-6 Can move leads up one intercostal space – may help make Dx More prone to free ventricular rupture NON STEMI “subendocardial” NSTMI = 40% of AMI’s Tend to be smaller than transmural Better LVEF Less likely to produce new onset CCF Lower in hospital mortality Higher risk of post infarct angina an recurrent infarction CLINICAL FEATURES: Often missed in: Young patients unsuspected 2-6% occur in age < 40 Elderly: Atypical Syx (weakness, syncope, confusion, CVA) Painless: 60-70% of AMI’s over age 85 Difficult Diagnosis in: LBBB Diabetic (autonomic neuropathy) Alt consc state DIAGNOSIS OF AMI: AT LEAST 2 OF: 1) Typical ischaemic chest pain for >30 min 2) ECG: ST ELEVATION a. At least 2mm in 2 or more consecutive chest leads b. At least 1mm in 2 limb leads c. New LBBB 3) Elevation of cardiac markers ECG: 70% Sensitive, increased with repeat ECG incr 10% if RV & Post leads done 99% Specific ST Elevation Mimics: LV Aneurysm: Concave initial ST segment Q waves usually present in same leads as ST elevation Loss of R waves Benign Early Repolarisation Greatest in precordial leads (V2-V5) Usually < 2mm Minimal in limb leads, Usually < 0.5mm Concave shape J point elevated No reciprocal changes, T waves shouldn’t evolve/change, no Q waves Pericarditis/Myocarditis: PR depression Generalised ST changes, not regional LVH: ST similar morphology to BER LBBB (+/- AMI) Hypothermia – Osborne wave Hypertrophic cardiomyopathy Pacemaker Normal variation Serial ECG’s: 15% of Pt’s with initial normal ECG will develop criteria for reperfusion in subsequent 24-48hrs Every 30min if painfree, every 15min with pain ST Depression: In ACS Usually >1mm below J point Usually flat or downsloping Regional (not generalised) May represent NSTMI Posterior AMI Reciprocal changes Ischaemia without infarction ST Depression Mimics: Hypokalaemia Digoxin Cor pulmonale/RH strain BER LVH Paced LBBB ST Depression/T inversion: LV Strain Downsloping ST depression No J point depression Asymmetrically inverted T wave T inversion more marked in V6 than V4 Digoxin Reverse tick More prominent in lateral leads T inversion Mimics: Persistent juvenile pattern Stokes-Adams syncope/seizures Post tachycardia Post pacemeker Intracranial pathology Mitral Valve Prolapse Pericarditis PE PTX Myocardial contusion LBBB RBBB Q Waves: Pathological if: Q’s in 2 contiguous leads V1-3 30ms or more in width 1mm or more in depth in I, II, aVL, aVF, V4-6 LBBB & AMI 15% of Pt with chest pain & LBBB = AMI Higher mortality than non-LBBB “Normal LBBB” ST & T wave will be in opposite direction to QRS (“normal discordance”) LBBB & AMI ST & T will be in SAME direction as QRS (ie CONCORDANT) Sgarbossa Criteria for reperfusion in LBBB: ST elevation 1mm or more in same direction as QRS (concordance) ST depression of 1mm or more in V1-V3 ST elevation >5mm in V1-V3 “New LBBB” new compared to old ECG “Indeterminate LBBB” = when no old ECG available “Old LBBB” proven to have been present on old ECG PACEMAKERS ECG criteria of paced rhythm = same as for LBBB Can try to establish natural rhythm Magnet Atropine to increase rate Dangerous as may increase O2 consumtion NB Troponin: No difference in sensitivity or specificity comp to CKMB at 6 hours But: Troponin stays elevated longer so at 24 hrs: Troponin = 100% sensitive CKMB = 57% sensitive Troponin In Unstable Angina Only 50% sensitive BUT PREDICTIVE (IF ELEVATED) OF: 30 day cardiac complications 1 year prognosis CHEST XRAY: Only use – rule out dissection Cameron: “CxR should not delay administration of thromblytics” MANAGEMENT ABC/IV/O2/Monitoring Aspirin Treat arrhythmias/CCF Reperfusion Therapies that reduce mortality: Aspirin Nitrates B-blockers ACEI Reperfusion (thrombolysis/PTCA) Therapies that don’t reduce mortality: Ca2+ blockers GP IIb/IIIa inhibitors (Abciximab, Tirofiban) – unclear THROMBOLYSIS Most commonly used reperfusion technique Max benefit if started within 1 hour of Syx After 6 hours: some benefit After 12 hours: NO benefit Good idea for ED’s to record & audit “door to needle time” Plasminogen activators (PA’s) or SK? No difference between PA’s (alteplase, reteplase, tenecteplase, lanoteplase) Newer ones have increased fibrin specificity, longer T1/2, and resistance to PA inhibitor. tPA vs SK: tPA better in: Age < 75 Anterior AMI Presenting within 4 hours (ie give SK to older Pt with anterior AMI) INDICATIONS FOR THROMBOLYSIS: Typical pain >30min but < 6hrs ECG criteria as above for Dx of AMI No contraindications CONTRAINDICATIONS FOR THROMBOLYSIS: ABSOLUTE: Uncontrolled HT (>180/120mmHg) Bleeding diathesis Recent GI bleed Haemorrhagic stroke (<6mths) Neurosurgery (<6mths) Trauma, surgery, organ biopsy (<6 wks) Pregnancy (up to 1wk post partum) Aortic dissection Acute pancreatitis RELATIVE Non-compressible vessel puncture site Hx of cerebrovascular disease Controlled HT Acute ventricular thrombus Endocarditis Non-traumatic CPR If any of these prewent – need to balance risks/benefits COMPLICATIONS: 1) Cerebral haemorrhage: 0.5-1.5% Greater when SBP >150mmHg Age > 65 Low body wt tPA Most other bleeding complications are relatively minor 2) Allergy/Anaphylaxis SK = bacterial protein Previous Strept infection or SK use (ie high Ab titres) More likely to have allergic reaction SK less effective Anaphylaxis < 0.5% Serum sickness may develop – treat in usual way 3) Hypotension Due to kinin release during SK use, related to rate of administration Treatment: Slow infusion, Fluid bolus 4) Reperfusion arrhythmias: usually self terminating Seldom require specific therapy Occurrence often signals reperfusion if irritable myocardium PCI/REVASCULARISATION Mild angina & lesser degree of coronary atheroma Medical Mx better Significant LAD stenosis Triple vessel disease (regardless of Syx) Angina that fails to respond to medical Mx ANGIOPLASTY VS CABG? No clear advantage of one vs other in morbidity/mortality PCI better for high risk surgical candidates ANGIOPLASTY 85-90% success depending on site of lesion Restenosis/stent occlusion: 50% in 2-3 years Preferred for: Previous PTCA or CABG NSTMI CABG Preferred for LAD/triple vessel disease: MEDICAL THERAPY ASPIRIN: Reduces death or MI in unstable angina/NSTMI Reduces death in STMI if given early Aspirin + SK = better than either treatment alone Minimum effective dose/formula unknown No benefit in coronary spasm BETA-BLOCKERS Improve survival after AMI Antiarrhythmic Decrease infarct size Earlier is better Blunt CVS response to adrenergic stimulation CI: Heart block Symptomatic bradycardia Low output/LVF/Acute CCF May precipitate coronary spasm So Ca2+ blocker preferred if spasm thought to be cause of ischaemia In Stable Angina: Reduce symptoms – especially with exercise/increased symp activity BUT: Do not reduce AMI rate or mortality ACEI Reduce mortality post AMI Early use after AMI = 6.5% reduction in mortality NITRATES Reduce: VR & LVEDP & myocardial O2 consumption Coronary dilatation – improves flow to sub-endocardium & epicardium Dilate stenotic segments Improve collateral flow May have anti-thrombotic effects Post MI reduce ventricular dilation Reduce pulmonary congestion & MR Early short-term (4-6wk) use may reduce mortality Ca2+ BLOCKERS Do not reduce mortality during/after AMI Useful if can’t tolerate B-Blockers for relief of ischaemic pain/antiarrhytmic GP IIb/IIIa INHIBITORS Abciximab Tirofiban Eptifibatide Lamifiban Efficacy in USA/NSTMI unclear Mixed results for mortality/long term benefit USA/NSTMI – GpIIb/IIIa + PCI = beneficial combination STMI Beneficial when combined with aspirin/heparin/tPA BUT: increased bleeding complications ADP Inhibitors Clopidogrel Ticlopidine