Emergency - Acute coronary syndromes Flashcards
Describe the pathophysiology of coronary artery disease.
- Atherosclerotic plaque formation narrows the coronary artery. The atherosclerotic plaque may rupture and lead to thrombus formation, further narrowing the coronary artery.
- This reduces blood flow and hence the delivery of oxygen and glucose to the myocardium, resulting in ischaemia.
- Depending on the extent of narrowing, the ischaemia may:
- only be present when there is an increased demand for oxygen and glucose during exertion (stable angina)
- or may be present at rest (acute coronary syndrome)
- If the narrowing is severe enough, ischaemia can result in necrosis and the myocardium undergoes infarction.
- Partial occlusion of the artery (NSTEMI)
- Complete occlusion of the artery (STEMI)
Describe the formation of an atherosclerotic plaque.
- Chronic endothelial injury - raised LDL, toxins, hypertension
- Endothelial dysfunction with platelet adhesion and monocyte acccummulation, causing release of growth factors and cytokines
- Smooth muscle emigration from tunica media to tunica intima
- Macrophages and smooth muscle cells engulf lipid to form foam cells
- Smooth muscle proliferation, collagen and matrix deposition, extracellular lipid deposition and neovascularisation
What is meant by the stability of an atherosclerotic plaque?
An unstable atherosclerotic plaque is more likely to rupture and lead to thrombus formation.
- Rupture of the plaque allows blood to enter the plaque
- This causes smooth muscle constriction which narrows the artery
- Thrombus formation can occlude the artery completely
Which clinical syndromes are classed as acute coronary syndromes?
Unstable angina
Non-ST-elevation myocardial infarction
ST-elevation myocardial infarction
How can unstable angina present?
- Angina on exertion with increasing frequency over a few days, provoked by less exertion (crescendo angina)
or - Angina occurring recurrently and unpredictably - not specific to exercise
or - Unprovoked and prolonged episode of chest pain
ECG and Troponin in unstable angina?
- Non-specific ECG change OR commonly, a normal ECG
- T wave inversion
- ST segment depression suggests high risk of progressing to MI
- No troponin release
ECG and Troponin in NSTEMI?
- Non-specific ECG abnormalities (usually these are present, though ECG can be normal)
- ST segment depression
- T wave inversion
- Troponin release
What differentiates unstable angina and NSTEMI?
Unstable angina - no troponin release (no myocardial cell death)
NSTEMI - TROPONIN RELEASE (MYOCARDIAL CELL DEATH)
Does a STEMI require troponin to confirm diagnosis?
NO
Does an NSTEMI require troponin to confirm diagnosis?
YES
What are the typical features of an acute MI?
- prolonged chest, throat or arm pain
- usually lasts for 20 mins or longer
- SOB
- clammy
- nauseous
Is the immediate management of an NSTEMI and STEMI the same?
NO
ECG and Troponin in STEMI?
- ECG - Acute ST-segment elevation / new LBBB
- Q waves likely to develop
- Troponin release
(ECG shows STEMI in lateral limb leads and anterior chest leads, the anterior chest leads show pathological q waves)
What do pathological q waves represent?
myocardial necrosis
What is the difference between the immediate management of an NSTEMI and STEMI?
STEMI - immediate reperfusion therapy
Early effective treatment (including reperfusion therapy) may limit myocardial damage and prevent Q wave development in STEMI.
True or False?
TRUE
What is common to the immediate management of ALL acute coronary syndromes?
ABCDE approach + MONA
M – morphine 2-5mg IV PRN
O – oxygen if indicated (sats<94%) 2-4L via nasal cannula
N – nitrate 0.4mg sublingual (GTN spray) / IV
A – aspirin 300mg chewable/crushed
A patient presents with suspected ACS. ABCDE + MONA immediate management is initiated. Once diagnosis of NSTEMI or Unstable angina is confirmed, what are your next steps in management?
Partial occlusion so prevent the clot from getting bigger:
- Second anti-platelet drug - clopidogrel, prasugrel or ticagrelor
- Enoxaparin/fondapurinax for 48 hour
Urgent invasive intervention for high risk patients (recurrent chest pain, uncertain ECG features):
- Tirofiban and urgent angiography within 96 hours with probable stent insertion
Continue with MON:
- Nitrate - sublingually or infusion
- Morphine - if pain does not respond to above
- Oxygen - if hypoxic
Myocardial protection:
- Beta-blocker - bisoprolol
- Coronary angiography/PCI in most patients - not as an emergency but usually during same admission
Frequently reassess patient and cardiac monitoring is required
A patient presents with suspected ACS. ABCDE + MONA immediate management is initiated. Once diagnosis of STEMI is confirmed, what are your next steps in management?
Call cath-lab immediately and activate PPCI pathway for emergency reperfusion therapy (PCI/thrombolysis).
- Percutaneous coronary intervention (PCI)
- Fibrinolytic therapy only if no access to primary PCI
Avoid delay, coronary artery is occluded and needs to be opened up - “Time is muscle”. If there is any doubt about PCI or fibrinolysis, discuss with cardiology team at nearest hospital offering PCI.
A patient presents with chest pain and this ECG. A previous ECG from a few months ago showed sinus rhythm. Diagnosis?
New LBBB - treated as STEMI
Immediate primary percutaneous intervention or fibrinolysis if PCI is not available
What are the absolute contraindications for fibrinolytic therapy?
- Previous haemorrhagic stroke
- Other stroke or CVA within six months
- CNS damage or neoplasm
- Active internal bleeding
- Aortic dissection
- Recent major surgery or trauma
- Known bleeding disorder
What should be done if a patient presents with a STEMI and has a known bleeding disorder?
Primary PCI is a priority in this patient as fibrinolysis is absolutely contraindicated.
If there is PCI providers nearby, consider other anti-thrombotic drugs with the advice of a cardiologist.
What is the long-term management of a patient who has been treated for an acute coronary syndrome?
- Lifestyle advice – cardiac rehabilitation after MI
- Dual anti-platelet – aspirin (lifelong) + prasugrel/ticagrelor (1 year)
- Statin – atorvastatin
- Beta-blocker – bisoprolol. If asthma verapamil or diltiazem. If blood pressure drops too low then ivabradine
- ACEi/ARB – ramipril
- GTN spray PRN
- If they have not already had angiography then this will be done on discharge
Name 3 non-modifiable risk factors for ACS.
Age
Male
Family history of IHD – MI in 1st degree relative <55 years
Name 5 modifiable risk factors of ACS.
Smoking
Hypertension
Hypercholesterolaemia
Diabetes
Obesity
Previous MI, CABG or stent
Which initial investigations would you request for all suspected ACS patients?
- Bloods - troponin T and I, creatine kinase, FBC, U&E’s, HbA1c, lipids
- 12-lead ECG
Describe the evolving ECG changes seen in a STEMI.
hyperacute T waves, T wave inversion, ST elevation, ST segment recovers, T wave recovers, pathological Q waves
What are the complications of an MI?
ACT RAPID
Arrhythmias – Bradycardias, heart block, tachychardia
Congestive heart failure
Tamponade
Rupture of ventricle – ventricular septal defect
Angina
PE
Infection – pericarditis
Death/Dressler’s syndrome
Which coronary artery supplies the inferior aspect of the heart?
RCA
Which coronary artery supplies the lateral aspect of the heart?
Circumflex (Left coronary artery)
Which coronary artery supplies the anteroseptal aspect of the heart?
Left anterior descending artery (Left coronary artery)
Which coronary artery supplies the postero-inferior aspect of the heart?
RCA
What is cardiac rehabilitation?
- It is available to anyone that has had an MI, coronary angioplasty or heart surgery
- Should include: Health education, Lifestyle advice, Stress management, Physical exercise
- It is done because: Improves clinical outcomes, Cost saving through less re-admissions
Where are patients with an acute MI usually managed?
Coronary care unit
