![New onset of LBBB suggests acute MI.
In patients with documented LBBB earlier,it is
difficult to diagnose AWMI due to masking
effect of LBBB on QRST changes.
CRITERIA USED FOR ACUTE AWMI WITH PRIOR
LBBB IS SGARBOSSA CRITERIA
1.ST elevation in atleast one lead of >1mm
concordant to positive QRS complex[5]
2.ST depression of >1mm in V1 to V3[3]
3.Discordant ST elevation >5mm in atleast one
leads with prominant negative QRS[2]
A total of >= 3 points suggests](https://image.slidesharecdn.com/ecgchangesinmi-170418202712/85/Ecg-changes-in-mi-26-320.jpg)
Ecg changes in mi
- 2. M.I denotes cellular damage due to prolonged ischaemia .Sudden cardiac death is a frequent presenting feature of MI with most of deaths occuring within one hour due to ventricular arrythymias. In presence of ischaemic symptoms the diagnosisof MI is based upon one of the following 1.Development of new pathological Q waves. 2.Presence of ST segment elevation or depression 3.Development of new LBBB
- 3. The changes in ECG should be present in two contiguous leads. Confirmation by diagnosis can be done by demonstration by elevation in cardiac enzymes,ECHO,or by coronary angiography.
- 4. Based on ECG, MI is further differentiated as STEMI and NSTEMI. Evolution of NSTEMI into STEMI is possible and therefore both subsets should be treated as aggresively as possible
- 5. The ECG changes evolve over a period of time and are described as 1.HYPERACUTE PHASE(over minutes-hours) 2.EVOLVED PHASE(over hours) 3.CHRONIC STABILISED PHASE(over days-weeks) The changes in ECG of chronic stabilised phase persists throughout life and generally represent changes of changes of old MI in absence of further progession of disease.
- 6. The ECG changes in this phase are 1.Tall,symmetrical,peaked and widened T waves 2.Slope elevation of ST segment 3.Increased amplitude of R wave/changes in Terminal QRS complex 4.Increased ventricular activation time This phase is critical because complication of Ventricular fibrillation is most likely to occur and Coronary reperfusion during this phase totally reverses changes without any residual myocardial damage.
- 7. The Twaves are tall and wide sometimes itmay exceed amplitude of associated R wave. Although for individual leads,different thresholds of calling tall T waves exist,roughly >0.5mv in limb leads and >1mv in precordial leads can be considerded tall.
- 8. -One of most noticeable and characteristic feature is slope elevation of ST segment,which loses its upwards concavity and becomes straightened with upward slope -New onset J point and ST elevation of >0.1m in leads ll,III,aVF,V4,V5,V6,I and aVL and in leads V2,V3 of >0.2mv in males >40yr and>0.25mv in Males <40yrs and >0.15mm in females -in absence of ventricular hypertrophy or LBBB represent best variables for diagnosis of MI.
- 9. The R wave becomes taller than normal. Tall R wave,slope elevated ST segment and tall widened T wave at times merge with each other so that it is difficult to separate 3 deflections and the resulting wide complex is result of QRS-ST-T fusion.
- 10. There is increase in ventricular activationtime, the time from beginning of QRS complex to apexof the R wave The ventricular activation time is delayed beyond 40ms
- 11. This phase is characterised by 1.Appearance of new q waves and decrease in R wave height 2.J point and ST segment elevation 3.T wave inversion 4.Increase in ventricular activation time and appearance of new conduction defects,blocks 5.QT prolongation
- 12. Appearance of new q waves is considered pathognomic of myocardical necrosis and indicates irreversible myocardial damage. Q waves >20ms in V1 to V4 and >30ms in other leads except III and aVR is considered pathological. J point and ST elevation decreases in this phase
- 13. Tall peaked wave of hyperacute phase start to decrease in amplitude and becomes inverted in the infarcted area which occurs simultaneously along with new q waves and decrease in ST segment The QRS complex becomes wider due to increase in ventricular activation time due to slow conduction and delayed depolarization in affected area.
- 14. QT interval may be prolonged due to increase in durationof depolarization and repolarization and appearance of new conduction defects.
- 15. This phase is characterised by 1.Changes in QRS complex: the q waves evolve maximally in QS, QR or Qr pattern and sometimes disappear. 2.Changes in J point and ST segment: elevated J point and ST segment returns to baseline and isoelectric 3.Changes in T wave :the inverted T waves regains its positivity 4.Normalization of QT interval :occurs once ischaemia is relieved
- 18. LEFT MAIN CORONARY ARTERY : 1.Left anterior descending:upper 2/3 septum, anterior wall, lateral wall and apex of L.ventricle 2.Left circumflex:lateral wall and posterior/ inferior wall RIGHT CORONARY ARTERY: right ventricle, inferior/posterior wall and lower 1/3 septum
- 23. 1.ST elevation in lead III>aVF>II 2.ST depression in lead I and aVL. 3.Sum of ST depression in lead I –III /sum of ST elevation in lead inferior leads <1 4.S/R ratio in lead avl >3 1.ST elevation in lead II>aVF>III and leads V5 V6 2.No ST depression or sometimes ST elevation in lead I and aVL 3. 3.Sum of ST depression in lead I –III /sum of ST elevation in lead inferior leads >1 4.S/R ratio in lead avl <3
- 26. New onset of LBBB suggests acute MI. In patients with documented LBBB earlier,it is difficult to diagnose AWMI due to masking effect of LBBB on QRST changes. CRITERIA USED FOR ACUTE AWMI WITH PRIOR LBBB IS SGARBOSSA CRITERIA 1.ST elevation in atleast one lead of >1mm concordant to positive QRS complex[5] 2.ST depression of >1mm in V1 to V3[3] 3.Discordant ST elevation >5mm in atleast one leads with prominant negative QRS[2] A total of >= 3 points suggests
- 27. An acute IWMI in presence of LBBB can be diagnosed as there is no masking effect of LBBB in inferior leads.
- 28. Characterised by ST segment depression dueto Myocardial ischaemia of subendocardial region. Following are ECG changes in NSTEMI: 1.ST segment depression 2.T wave inversion There is little or no alternation of QRS complex.
- 29. New horizontal or down sloping ST segment of >0.05mv in two contiguous leads suggests ongoing myocardial ischaemia
- 30. T wave inversion of >0.1mv in two contiguous leads with prominent R wave suggests myocardial ischaemia. T wave inversion accompanies changes of ST segment depression in NSTEMI
- 31. RISK OF ASSESSMENT IN NSTEMI BASED ON ECG 1.LBBB 2.ST segment deviation of >0.05mv(1/2 small sq) 3.T wave inversion of >0.3mv(3 small sq)
- 32. Descibed in a patient who presents with history of chestpain. ECG during during episode appears to be normal, with ST segment in V2 and V3 being either concave or straight and which is Isoelectric or minimally elevated. Following chest pain symmetric and deep T Wave invwesion may develop in pain free periods with no pathological Q waves and there is no significant biochemical alternation. This is due to tight proximal LAD stenosis.
- 33. The ECG dignosis reinfarction following initial infarction may be confounded by the initial evolutionary ECG changes. Reinarction should be considered when ST elevation of 0.1mv reoccurs in a patient having lesser degree of ST elevation or new pathognomic Q waves appear in atleast two contiguous leads when associated with Ischaemic symptoms for >= 20 min