Acute Coronary Syndrome Flashcards
Define ACS
ACS is a global term for STEMI (30%), non-STEMI (25%) and unstable angina (38%)
ACS Pathogenesis
The common pathology of acute coronary events is the rupture or erosion of a coronary plaque, leading to intracoronary thrombosis. The clinical picture depends on whether the artery is totally occluded (producing an ST- elevation MI) or only partially or transiently (<20mins) totally occluded (producing a non-ST elevation wave MI or unstable angina)
ECG Leads with Coronary Regions
Anterior - V3, V4 Septal - V1, V2 Lateral - I, aVL, V5, V6 Inferior - II, III, aVF
Corresponding ECG Regions with Coronary Vasculature
- Anterior
* Occlusion of left anterior descending (LAD)- Anterolateral
- Occlusion of left circumflex or left circumflex (marginal branch) or LAD (diagonal branch).
- Posterior
- Occlusion of (right) posterior interventricular or right (distal) or left circumflex (distal).
- Inferior (or diaphragmatic)
- Occlusion of right coronary.
- Anterolateral
ACS Clinical Presentation
- Crushing chest pain lasting > 20minutes
* May radiate to jaw and left arm- Dyspnoea
- Sweating
- Nausea
- Atypical in females
- SoB, fatigue & weakness
- Silent in diabetics
ACS Risk Factors
- Atherosclerotic risk factors
* Hypercholesterolaemia
* Smoking
* HTN
* Diabetes
* Male gender
* Age
ACS Management
- Patient Presents w/ Chest pain, etc
- During Transport
- Morphine - IV or IM - 2.5-5mg (max 10mg) & wait 5 minutes.
- Oxygen
- Nitrates - up 3 tablets or 4 sprays
- Aspirin - 100-300mg
- Emergency Department
- ECG 12-lead
- IV access
- Troponin
- Monitoring
- ST Elevation
- Yes
- STEMI pathway
- No
- NSTEACS risk stratification
- Yes
- During Transport
On diagnosis of STEMI Management
- Anti-platelet agents
* Aspirin and clopidogrel (unless CABG likely)- Antithrombin agents
- Enoxaparin or unfractioned heparin
- Beta blockers (in absence of heart failure or heart block)
- Atenolol or metoprolol
- Either immediate PCI or fibrinolytic agent
- Alteplase
- Antithrombin agents
Subsequent management of STEMI
- Statin / Spironalactone
- Anti-platelet agents
- Aspirin and clopidogrel
- (dual therapy for 12months unless on warfarin)
- ACEi or ARBs
- Beta blockers
- Atenolol or metoprolol
- Clexane / warfarin
- Anti-platelet agents
NSTEACS Stratification Assessment
The non-ST elevation ACS (NSTEACS) patients are stratified as high, intermediate or low risk based on troponin (>10 times) or ECG changes and chest pain
On diagnosis of High Risk NSTEACS Management
- Anti-platelet agents
* Aspirin and clopidogrel (unless CABG likely)- Antithrombin agents
- Enoxaparin or unfractioned heparin
- Beta blockers (in absence of heart failure or heart block)
- Atenolol or metoprolol
- Antithrombin agents
On diagnosis of Intermediate Risk NSTEACS Management
- Reassessment repeated to enable classification of high or low risk with subsequent treatment
On diagnosis of Low Risk NSTEACS Management
- Anti-platelet agent
* Aspirin- Repeat troponins in 8 hours and discharge
- Procedural (outpatient)
- Stress ECG or stress echo or nuclear stress
ACS Morphology
Essentially the sequence of events is that of coagulation necrosis and inflammation, followed by the formation of granulation tissue, resorption of necrotic myocardium and, finally, organisation into to a collagen-rich scar (fibrosis).
0-12 hours - No change - No changes are evident 12-18 hours - No change - Coagulation necrosis 18-24 hours - Slight pallor - Coagulation necrosis continues and neutrophils (neutrophils reach a peak on day 3 and then diminish) 24-72 hours - Pallor - Coagulation necrosis is complete 4-7 days - Central pallor with hyperaemic border - Macrophages appear to disintegrate the necrotic fibres 10 days - Yellow, soft, shrunken - Developed phagocytosis and granulation tissue 7-8 weeks - Firm, grey - Fibrosis
ACS ECG Progression
Hours - ST elevation Days - ST elevation - Pathological Q waves - Inverted T waves Weeks - ST flattening off - Pathological Q waves Months - Pathological Q waves
