Acute coronary syndromes (Unstable angina + STEMI + NSTEMI) Flashcards
What is the epidemiology of ACS?
Coronary heart disease is the single biggest cause of death in the UK
Prevalence of NSTEMI>STEMI
What are some risk factors for ACS?
Non-modifiable (risk factors for atherosclerosis):
- Increasing age, male sex, FHx coronary heart disease, MI 40-50yrs; premature menopause
Modifiable risk factors:
- Smoking, diabetes/impaired glucose tolerance, hypertension, raised LDL + low HDL, obesity, physical inactivity
Increases with age
Male sex
FH of IHD (if symptoms present before 55yrs)
Other non-atherosclerotic causes (often younger patients):
- Coronary artery occlusion secondary to vasculitis, coronary artery spasm, cocaine use, coronary trauma, increased oxygen requirement (e.g. hyperthyroidism), decreased oxygen delivery (e.g. severe anaemia)
What is the pathophysiology of MI?
All caused by the rupture of an atherosclerotic plaque - fibrous cap of plaque gets a superficial injury or ruptures and a thrombus forms on the remaining
area
Platelets in this thrombus release thromboxane A2 and serotonin → vasoconstriction → causing/exacerbation of ischemia and subsequent infarction
Types:
Transmural – infarct that causes necrosis of tissue through full thickness of myocardium (STEMI)
Nontransmural – infarct does not cause full thickness necrosis (NSTEMI)
What is a typical presentation of an MI?
Pain:
- Central, crushing, radiating down left arm and neck/jaw, can last 15mins-2+hrs
- Comes on at rest/from nowhere or may be precipitated by exercise but not resolving on cessation
SOB, Syncope, Sweating, Tachycardia, Nausea + Vomiting
Sudden death – from ventricular fibrillation or asystole; mostly within
1hr
MI (and stroke) are more common in the morning:
BP drops at night and rises upon waking – this is thought to dislodge any thrombus formed in the night; also catecholamines peak meaning maximum platelet aggregability, vascular tone, heart rate and BP
How does a silent MI present?
Most common in diabetics and the elderly
SOB - may be key presenting symptom Absence of pain Syncope Pulmonary oedema Epigastric pain Vomiting Confusion Stroke Diabetic hyperglycaemia
What are some signs of impaired myocardial functioning?
3rd and/or 4th heart sounds Pan systolic murmur Pericardial rub Lung crepitations (pulmonary oedema) Hypotension Quiet first heart sound Narrow pulse pressure (<40mmHg difference) Raised JVP
Signs of sympathetic
activation - pallor,
sweating, tachycardia
What are some complications of MI?
Cardiac arrest, bradycardia, heart block, tachyarrhythmias, LV/RV failure, pericarditis, DVT/PE etc
Cardiac failure - major cause of death in those that survive the first few hours
What is cardiac tamponade?
Fluid (often blood) build up in the pericardium leading to compression
What is Dressler’s syndrome?
Autoimmune pericarditis
5-10% patients → fever, pericardial effusion, anaemia, cardiomegaly, pericardial rub; self limiting, lasts a few days
NSAID +/- steroid treatment
What is a mural thrombus?
Thrombus attached to wall of endocardium or aortic wall; caused by the stasis that results from an MI
Larger infarct = larger risk
Thrombus can embolise into
pulmonary or systemic circulation
What is a ventricular wall rupture?
Post MI, myocardium is soft → blood can exit into pericardium → cardiac tamponade; normal ECG results but no cardiac output or pulse = pulseless electrical activity (PEA) = almost always certain death
What is a ventricular aneurysm?
Late stage complication of transmural MI:
Infracted muscle re-
placed by thin later of scar tissue that will stretch as intraventricular pressure rises during systole → leads to further complications i.e. arrhythmias, LV failure, mural thrombus
What do you find on an ECG in an ACS?
Very early signs:
- Hyperacute or biphasic T waves without ST changes e.g. biphasic V2-V3 = Wellen’s syndrome, critical stenosis of LAD - MI impending
Within hours-days:
- Raised ST segment >1mm in 2+ contiguous limb leads, or >2mm in chest leads OR new LBBB = STEMI
- Non-raised ST; T-wave inversion/flattening; ST depression = NSTEMI (may also be normal)
Within weeks:
- Pathological Q waves >25% height R wave/2mm+ high, 0.04s width)
- T-wave inversion
- Possible normalisation
In general - ST depression = ischemia, ST elevation = infarction
- ST depression in anteroseptal leads with ongoing chest pain should have a posterior ECG to rule out posterior MI
What do you find on bloods in MI?
Troponin (T/I - High Sensitivity):
- Take at 6 and 12hrs post pain onset (as peak at 12-24hrs, stay raised for up to 14d)
- Raised indicating ACS = >99th percentile of the upper limit of normal
- If STEMI on ECG + clinical picture, not needed for Dx but will be increased
- If NSTEMI - ECG may be normal but trops will be raised
- If unstable angina - ECG may be normal and trops will also be normal/slightly raised
Glucose:
- High on admission for ACS = poor prognosis
Lipids:
- May be high, relating to aetiology
FBC:
- Any anaemia? (possible aetiology and will exacerbate ACS)
U+E:
- Baseline renal function
- Any electrolyte abnormalities causing arrhythmias?
- Also trops can be raised in renal disease
Clotting:
- In view of anticoagulation
TFTs, CRP
What other investigations are indicated in MI?
Coronary angiography:
- Presence/severity of coronary artery disease
Echo:
- Motion wall abnormalities due to ischaemia - good evidence if picture is unclear
- Valvular dysfunction, hypertrophy, thrombus?
CXR:
- Complications of ischaemia e.g. pulmonary oedema
- Rule out other pathology e.g. aortic aneurysm, pneumothorax
Cardiac MR:
- Assessment of function and perfusion and detection of scar tissue
- Also can diagnose myocarditis
