Acute Coronary Syndromes (ACS) Flashcards
(23 cards)
What is the definition of ACS?
ACS refers to a spectrum of acute myocardial ischaemia and/or infarction and encompasses unstable angina and evolving MI (STEMI/new onset LBBB and NSTEMI).
What are the causes of ACS?
- Atherosclerotic plaque development, rupture, thrombosis and inflammation.
- Rarely due to coronary spasm.
What are the signs & symptoms of ACS?
- Signs/symptoms include central/left chest pain radiating to left arm or jaw, nausea, sweating, dyspnoea, palpitations, anxiety, pallor, tachy/bradycardia, ↓/↑BP, 4th heart sounds, signs of LVF, syncope and delirium.
- Risk factors include HTN, DM, smoking, hypercholesterolaemia, obesity, advancing age, male sex and FHx of MI <55yrs.
- NB - patient may not experience typical chest pain and is called a ‘silent MI’
What is the pathophysiology of ACS?
- The most common cause is rupture of atherosclerotic plaques leading to exposure of subendothelial matrix elements (such as collagen) stimulating platelet activation and thrombus formation. Release of tissue factor directly activates the coagulation cascade and promotes the formation of fibrin. If an occlusive thrombus forms, the patient may develop an acute STEMI unless the myocardium is richly collateralised. If the thrombus formation is not occlusive, the patient may develop UA or NSTEMI. Arterial inflammation, caused by or related to infection, may cause plaque destabilisation and rupture and precipitate ACS. Activated macrophages and T lymphocytes located at the shoulder of a plaque increase the expression of enzymes such as metalloproteinase that may cause thinning and disruption of plaque, leading to ACS.
- NSTEMI can also be caused by dynamic obstruction, such as in vasospasm, progressive luminal narrowing (i.e. chronic narrowing from restenosis), inflammatory mechanisms (i.e. vasculitis) or extrinsic factors leading to poor coronary perfusion (such as hypotension, hypovolaemia or hypoxia).
How is ACS investigated?
- 12-lead ECG
- STEMI sequence; normal, ST elevation, tall T waves, Q waves (full thickness infarct), normalisation of ST segments, T wave inversion
- NSTEMI; ST depression, deep T wave inversion, pathological Q waves
- UA; no pathological changes
- Troponin T/I
- Elevated from 3-12hrs (need 12hr trop to exclude MI)
- Normal in UA
- CXR
- Cardiomegaly
- Pulmonary oedema
- Widened mediastinum (aortic rupture)
- U&Es
- Glucose
- Lipids
- Coagulation Screen
- CT coronary angiography
What are the complications of ACS? (Remember DREAD)
- Death
- Rupture of the heart septum or papillary muscles
- ‘Edema’ (heart failure) or embolism
- Arrhythmia or Aneurysm (ventricular)
- Dressler’s Syndrome
- Also pericarditis
How is ACS prevented?
- Primary prevention
- Adjust/manage modifiable risk factors
- Secondary prevention (6 A’s)
- Aspirin
- Another antiplatelet (clopidogrel, ticagrelor)
- Atorvastatin
- ACE-inhibitor
- Atenolol (or other BB)
- Aldosterone antagonist for those with clinical HF
- NB - Includes lifestyle factors
- Prognosis
- STEMI 30-day mortality ~15%
- NSTEMI overall mortality 1-2%
How are STEMI’s treated? (remember FATMAN)
- Fondaparinux
- Aspirin
- Ticagrelor (or clopidogrel)
- Morphine
- Anti-emetic
- Nitrate
- Primary PCI with coronary angioplasty (if available within 2 hours of presentation)
- Thrombolysis (if PCI not available within 2 hours of presentation)
What does the right coronary artery supply?
- Right atrium
- Right ventricle
- Inferior aspect of left ventricle
- Posterior septal area
What does the circumflex artery supply?
- Left atrium
- Posterior aspect of left ventricle
What does the left anterior descending artery supply?
- Anterior aspect of the left ventricle
- Anterior aspect of septum
Which artery and ECG leads are affected in an anterolateral STEMI?
- Left coronary artery
- I, aVL, V3-V6
Which artery and ECG leads are affected in an anterior STEMI?
- LAD
- V1-V4
Which artery and ECG leads are affected in an lateral STEMI?
- Circumflex
- I, aVL, V5-V6
Which artery and ECG leads are affected in an inferior STEMI?
- Right coronary artery
- II, III, aVF
What are 5 alternative causes of raised troponins?
- Chronic renal failure
- Sepsis
- Myocarditis
- Aortic dissection
- Pulmonary embolism
How are NSTEMIs treated? (Remember BATMAN)
- Beta blockers (unless contraindicated)
- Aspirin
- Ticagrelor (or clopidogrel)
- Morphine
- Anticoagulant (LMWH)
- Nitrates
Which scoring system is used to asess for PCI in NSTEMI?
- GRACE score
- Medium-high risk considered for early PCI (within 4 days)
What is Dressler’s Syndrome?
- Also called post-myocardial infarction sndrome
- Usually 2-3 weeks after MI
- Localised immune response and causes pericarditis
- Presents with pleuritic chest pain, low grade fever and pericardial rub
- Can cause pericardial effusion and rarely tamponade
- Global ST elevation and T wave inversion
- Management with NSAIDs and steroids
- May require pericardiocentesis
What are the different types of MI?
1) Traditional due to an acute coronary event
2) Ischaemia secondary to increased demand or reduced supply of oxygen (i.e. anaemia)
3) Sudden cardiac death or cardiac arrest suggestive of ischaemic event
4) MI associated with PCI/coronary stenting/CABG
How is stable angina (not an example of ACS) treated? (Remember RAMP)
- Refer to cardiology
- Advise about diagnosis and management
- Medical treatment (GTN for short term, BB or CCB for long term)
- Procedural or surgical interventions
How is stable angina treated?
- Immediate
- GTN spray
- Long-term
- BBs (i.e. bisoprolol)
- CCBs (i.e. amlodipine)
- Long acting nitrates (i.e. isosorbide mononitrate)
- Ivabradine
- Nicorandil
- Ranolazine
- Secondary prevention
- Aspirin
- Atorvastatin
- ACE-I
- BB (already on for symptomatic relief)
Which vessel disease causes which type of MI?
- RCA or LCx causes inferior
- Cx or RCA causes posterior
- LCx causes lateral
- LAD causes anteroseptal
- LAD causes anterior
