Cardiology: ACS Flashcards
How can ACS be categorised?
1) STEMI
2) NSTEMI
3) Unstable angina
What does a new left bundle branch block on an ECG indicate?
Always pathological:
1) MI
2) HTN
3) aortic stenosis
4) cardiomyopathy
5) rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
A new LBBB due to ischaemia is the result of the occlusion of what artery?
Proximal left anterior descending (LAD) or left main stem artery.
Why is a new LBBB indicate a worse prognosis in MI?
A large amount of myocardium and conductive tissue needs to be affected to cause this ECG appearance and these patients are usually acutely unwell.
What ECG changes may be seen in an MI?
1) hyperacute T waves (often the first sign of MI but often only persists for a few minutes)
2) ST elevation
3) T wave inversion
4) pathological Q waves
What is often the first ECG sign of an MI?
Hyperacute T waves
When does T wave inversion on an ECG typically appear in an MI?
How long do they last?
The T waves typically become inverted within the first 24 hours.
The inversion of the T waves can last for days to months.
When do pathological Q waves on an ECG in an MI typically appear?
How long do they last?
Pathological Q waves develop after several hours to days.
This change usually persists indefinitely.
What does the Q wave reflect?
Septal depolarisation.
This is usually hidden behind the much more forceful and electrically active ventricular wall depolarisation.
How does an MI lead to the development of Q waves on an ECG?
The Q wave reflects septal depolarisation. This is usually hidden behind the much more forceful and electrically active ventricular wall depolarisation.
If the ventricular wall is dead, a ‘window’ is created that allows the septal depolarisation to show up on the surface ECG.
The sequence of changes and signs of ischaemia (the ischaemic cascade) in an MI
1) Flow disruption (start of the MI)
2) Hypoperfusion (detectable on sensitive scanning but not particularly clinically relevant)
3) Diastolic dysfunction
4) Systolic dysfunction
5) ECG changes
6) Angina
7) Identification of intracoronary thrombus by angiography or at autopsy
Give some causes of a raised troponin
1) MI
2) Tachy/bradyarrhythmias
3) Aortic dissection
4) Severe aortic valve disease
5) Hypertrophic cardiomyopathy
6) Severe respiratory failure
7) Severe anaemia
8) Coronary spasm
9) Heart failure
10) Takotsubo cardiomyopathy
11) Sepsis
12) Renal failure
13) Stroke
14) Subarachnoid haemorrhage
What are the 5 classifications of MI?
1) Spontaneous MI
2) MI 2ary to ischaemia
3) MI diagnosed post-mortem
4a) MI related to percutaneous coronary intervention
4b) MI related to stent thrombosis
5) MI related to bypass (CABG) operation
What occur in a spontaneous (type 1) MI?
This is your ‘typical’ myocardial infarction.
1) Atherosclerosis originates from damage to the endothelium and a build-up of cholesterol.
2) The inflammatory reaction to atherosclerosis by macrophages causes a plaque of foam cells, lipids, cellular debris and (eventually) calcium to build up with a fibrous cap on top.
3) When this cap cracks, the exposed debris triggers thrombus formation in the confines of the affected coronary artery (which are only typically between 2 and 5mm in diameter)
4) This causes partial or total occlusion of the artery.
What is an MI 2ary to ischaemia (type 2)?
A common event in hospitals where patients with stable coronary artery disease +/ previous coronary intervention (PCI or CABG) are unwell and put additional stress on their heart that would not normally be present.
The myocardium can become ischaemic without a plaque rupture event.
What is a type 4a MI?
This is related to percutaneous coronary intervention (i.e. caused by an angioplasty procedure blocking a side branch or damaging the main coronary artery causing ischaemia)
What is a type 4b MI?
This is related to stent thrombosis.
If patients stop anti-platelets early post-angioplasty or continue to smoke, stents can occlude (this usually results in a STEMI if complete sudden thrombosis or NSTEMI if gradual re-stenosis over time).
Clinical features of ACS?
1) chest pain:
- classically on the left side of the chest
- pressure, tightness, or crushing sensation
- may radiate to the left arm or neck
2) dyspnoea
3) N&V:
- due to vagal activation or gastric distension
4) sweating (poor indicator as signifies sympathetic activation)
5) palpitations
In which patients may chest pain not be present in ACS?
Diabetics & elderly
What are 3 atypical symptoms that may be seen in ACS?
1) epigastric pain
2) fatigue
3) syncope or presyncope
Who may epigastric pain in an MI be seen in?
Diabetics, elderly, & women
Who may fatigue in an MI be seen in?
Generalised fatigue without chest pain can sometimes be the sole symptom, particularly in older adults.
What may syncope or presyncope indicate in MI?
may indicate arrhythmias or severe ischemia affecting cardiac output.
An MI can cause hypotension or hypertension.
What may each indicate?
Hypotension: cardiogenic shock
HTN: stress response
MI can cause tachycardia or bradycardia.
What type of MI would bradycardia indicate?
inferior myocardial infarction due to vagal activation.
What causes a STEMI?
Complete occlusion of an epicardial coronary artery by thrombus causing immediate myocardial death relating to the territory affected.
What criteria is required for a STEMI diagnosis
Clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
1) 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
2) 1.5 mm ST elevation in V2-3 in women
3) 1 mm ST elevation in other leads
4) new LBBB (LBBB should be considered new unless there is evidence otherwise)
Give the artery affected & ECG leads affected in the following MIs:
1) Anterior
2) Inferior
3) Lateral
4) Posterior
5) Anterolateral
1) Anterior:
- left anterior descending artery
- V1-V4
2) Inferior:
- right coronary artery
- II, III, aVF
3) Lateral:
- left circumflex artery
- I, aVL +/- V5-V6
4) Posterior:
- usually left circumflex, also right coronary artery
- Tall R waves V1-2
5) Anterolateral:
- left anterior descending or left circumflex
- V4-6, I, aVL
What is the initial management when ACS is suspected?
1) 12 lead ECG
2) Morphine
3) Oxygen; only if low O2
4) Nitrates (e.g. GTN)
5) Aspirin (300mg) and a second rapid-acting antiplatelet such as Ticagrelor or Prasugrel
Define a STEMI
ST-segment elevation + elevated biomarkers of myocardial damage
Define an NSTEMI
ECG changes but no ST-segment elevation + elevated biomarkers of myocardial damage
What is the common management of all patients with ACS?
1) aspirin 300mg
2) O2 (only if sats <94%)
3) morphine: only if in severe pain
4) nitrates:
- sublingually or IV
- useful if the patient has ongoing chest or HTN
- caution if patient hypotensive
Then determine whether they meet the ECG criteria for STEMI.
Is morphine given routinely in ACS?
No, only in severe pain.
Evidence suggests that giving IV morphine routinely may be associated with adverse outcomes
Once a STEMI has been confirmed, what is the next step?
Assess elegibility for coronary reperfusion therapy.
What are the 2 types of coronary reperfusion therapy?
1) primary coronary intervention (PCI)
2) thromboylsis
Who should PCI be offered to in STEMI patients?
1) if the presentation is within 12 hours of onset of symptoms
AND
2) PCI can be delivered within 120 minutes of the time when thrombolysis could have been given
Also, if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered.
If patients with STEMI present after 12 hours but still have evidence of ongoing ischaemia, can they be considered for PCI?
Yes
