ECG changes in MI Flashcards
Define MI
Definition of MI
- MI is a major cause of death and disability
- It is a significant diagnosis, with major implications (clinical, epidemiological, psychological, legal…)
- It is diagnosed by symptoms, ECG, troponin, imaging OR post-mortem
- Therefore — a precise and consistent definition is required
Criteria for acute MI
Evidence of myocardial injury in a clinical setting that is consistent with acute myocardial ischaemia includes:
- detection of a rise and/or fall of cardiac biomarkers (preferably cTn, most specific/sensitive) — with at least one value above the 99th percentile upper right limit
and at least one of the following:
- symptoms of ischaemia (e.g. chest pain)
- significant ST segment or T wave changes or new LBBB ^[left bundle branch block; also RBBB]
- development of pathological Q waves in ECG (see NurseYourOwnWay site)
- imaging evidence of a new loss of viable myocardium ^[echo] OR new regional wall motion abnormality
- identification of an intracoronary thrombus by angiography OR autopsy
Describe how MI is diagnosed
or see criteria
Diagnosing MI
- clinical evidence of ischaemia + myocardial injury
- injury but not ischaemia = NOT MI e.g. elevated troponin in heart failure
Describe reasons for elevation of cardiac troponin values in the case of MI, and some other causes of elevation
Myocardial injury related to acute myocardial ischaemia is the result of atherosclerotic plaque disruption with thrombosis.
Myocardial injury because of oxygen supply/demand balance is a consequence of reduced perfusion or increased demand.
Other causes of myocardial injury include:
- cardiac conditions: heart failure, myocarditis, pericarditis, any cardiomyopathy, arrhythmias
- systemic conditions: sepsis, infectious disease, stroke, pulmonary embolism
HI
Describe the types of MI
There are five types of MI:
- type 1: athero-thrombotic (plaque rupture with thrombus) myocardial infarction – causing occlusion/near-occlusion – leads to ischaemia and tissue damage
- type 2: MI secondary to oxygen supply/demand imbalance
- type 3: MI resulting in death when biomarker results are unavailable
- type 4: MI related to percutaneous coronary intervention ^[i.e. stenting] i.e. when troponin levels are five times higher than upper right limit
- type 5: MI related to coronary artery bypass grafting i.e. when troponin levels are greater than ten times the upper right limit
Describe type 2 MI
Type 2 is the consequence of
- an oxygen supply-demand imbalance ALONE
- fixed atherosclerosis AND a supply-demand imbalance
- vasospasm or endothelial dysfunction. ^[can also be a result of sepsis]
The following algorithm shows the diagnosis under various conditions where cTn is elevated greater than the 99th percentile upper right limit
- if Tn stable: chronic myo injury e.g. inflammation e.g. structural heart ddisease or chronic jidney disease
- if rise and or fall AND a
Describe ECG changes in ischaemia and MI
Several characteristic changes in MI are either indicative of ischaemic disease:
- ST elevation and acute myocardial injury
- ST depression and myocardial ischaemia
- anterior ST depression and acute posterior injury
- T wave inversion and recent (Resolved) ischaemia
- Q wave formation and completed i.e. old injury
NOTE:
These changes are not specific to ischaemia ^[and are correct ~90% of the time]
AND
ECG machine often overcalls. Therefore take history into account.
HI
Describe how acute coronary syndromes are managed
Management of acute coronary syndromes
For all MI, the following management strategies are relevant:
- patient education
- aspirin and clopidogrel
- intravenous heparin (anti-coagulant)
- statin (later as a preventative measure)
- beta blocker (slow HR, reducing myocardial oxygen consumption, long term– if significant LV dysfunction)
- ACE inhibitor for LV dysfunction, or HTN
For STEMIs:
- urgent PCI
- or thrombolysis of PCI is over 90 minutes away
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For non-STEMIs:
- angiography within 48 hours, with or w
Describe characteristics of anterior MI
- usually LAD occlusion
- ST elevation in anteroseptal leads : V1, V2 (anterior), V3 and 4 (septal) ^[5 and 6 are lateral leads]
Describe characteristics of inferior MI
- ST elevation in inferior leads: II, III, and aVF (and sometimes V6)
Describe characteristics of lateral MI
i.e. occlusion of LCA, marginal/diagonal branch of LAD a.
- ST elevation in lateral leads aka I, aVL, V5-6
Describe characteristics of posterior MI
- ST depression in anterior leads, e.g. V2, 3
Describe criteria for primary PCI
- CHEST PAIN OR other ischaemic symptoms
- within 12 hours of onset
- ST elevation, suggestive of acute MI
- anterior ST depression suggestive of posterior MI
- (or new LBBB ~ if symptoms are highly suggestive)
Note: very important
HI
Describe the evolution of ECG changes of acute MI
- tall T waves in 1-2 minutes
- ST elevation in 1-2 minutes
- T wave inversion in 12 to 24 hours – biphasic T wave
- Q wave formation in 12 hours - little divot before complex
- T wave normalisation in 3 to 6 months
To test, see cases
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