Acute Coronary Syndromes & Stable Angina Flashcards
what is hs-TnI
high sensitivity Troponin I released from cardiac myocytes due to necrosis
what is troponin
a protein in myocardium and skeletal muscle
- TnI levels begin to rise 3-4 hours after myocardial damage and stay elevated for up to 2 weeks
also measure CK in STEMI patients
what the parameters for TnI levels in men and women suggesting myocardial necrosis
males: hs-TnI levels greater than 34 ng/L for men suggests a high likelihood of myocardial necrosis
females: hs-TnI levels greater than 16 ng/L for women suggests a high likelihood of myocardial necrosis.
what do rising and/or falling cardiac troponin levels help to differentiate from
acute from chronic cardiomyocyte damage
- the more pronoounced the change, the higher the likelihood of acute MI
- a rise in greater than 5ng/L may indicate ACS
when are hs-TnI levels taken
taken on admission and again at 1 hour
one 1 level is required if the onset of symtpoms was 3 or more hour previously
in which patients may there be a false positive elevation of hs-TnI
- advanced renal failure
- large PE
in which patients may there be an elevated hs-TnI level
- severe congestive cardiac failure
- myocarditis
- prolonged tachyarrhythmias
- aortic dissection
- aortic stenosis
- hypertrophic cardiomyopathy
- severe sepsis
Hs-TnI levels may remain elevated for several days and care should be taken in their interpretation in the context of re-admissions within a couple of weeks of a myocardial infarction
what are the ECG changes seen in STEMI (2)
- ST segement elevation in 2 or more leads from the same zone (ie leads II, III or AVF as inferior leads)
- new LBBB
what ECG changes are seen in an NSTEMI
- ST depression
- T wave inversion or flattening
- T wave pseudo-normalisation
what does ST depression confined to leads V1-V4 suggest
true posterior MI
- should be treated in the same manner as STEMI
what leads should STEMI patients have routinely recorded and why
posterior (V7-V9) and RV leads on or soon after admission
- especially those with inferior STEMI as diagnostic changes may be transient
what is ST elevation in RV4 highly sensitive for
RV infarction
what conditions may mimic STEMI on the ECG (4)
- early repolarisation causes up-sloping ST elevation esp in leads V1/V2 (more commonly seen in younger, athletic patients)
- concave ST elevation in pericarditis; may be widespread
- Brugada syndrome - anterior STEMI
- Takotsubo cardiomyopathy
what do pathological Q waves suggest
deep infarction involving the full thickness of the heart i.e. transmural
- typically appear 6 or more hours after the onset of symptoms
what is the inital management of STEMI
- IV access
- Pain relief e.g. morphine/anti-emetic
- O2
- Aspirin 300mg loading + 75mg OD for life
what antiplatelet therapies can be used in management of STEMI (3)
- prasugrel: thienopyridine inhibits ADP receptors 60mg loading and 100mg daily for up to 12 months
- clopidogrel: inhibits ADP receptors, loading dose 600mg followed by 75mg OD for up to 12 months
- ticagrelor: non thienopyridine loading dose 180mg + 90mg BD for up to 12 months (in pt who cannot have prasugrel or 1st choice NSTEMI)
what is the criteria for prescribing prasugrel
restricted to patients undergoing PPCI for STEMI who are under the age of 75 and who weigh more than 60kg and who have not had a prior TIA or stroke
what investigations are mandatory in patients presenting with STEMI
full biochemical screen on admission
- lipid profile
- random glucose
- HbA1c
- FBC
what medications may be administered as part of management of STEMI
- bisoprolol: reduce HR, avoid in shock! starting dose 1.25mg OD
- ACEi: prevent muscle over-damage, starting dose 2.5mg OD after checking renal function OR ARB starting dose 25mg then uptitrate to max tolerated dose
- statins: 80mg OD target to reduce LDL-C < 1.8mmol/L (total cholesterol target <4.0 mmol/L + ezetemibe if all statins caused side effects