Right and left atrial enlargement in ecg

Right and left atrial enlargement in ecg

1. ECG CHANGES IN ATRIAL ENLARGEMENT MOHAMED ASHIF A 1ST YEAR CARDIO RESIDENT

2. ECG & ATRIUM ATRIAL DEPOLARIZATION~ P WAVE ATRIAL REPOLARIZATION~ Ta WAVE Ta WAVE Normally obscured by QRS complex due to its Low amplitude <100uV.

3. DETERMINANTS OF P WAVE MORPHOLOGY Origin of Rhythm (~RA Depolarisation Vector) LA Breakthrough (~LA Depolarisation Vector) Atrial Geometry ( Determines the course & duration of depolarization process)

4. SA NODE SA Node, the Primary Pacemaker of the heart, lies at sub-epicardium level of RA near the entrance of SVC. It generate Spontaneous Electrical impulse at the rate of 60-100/min due to the presence of P cells. 60-70% blood supply by RCA “Electrical Activity of SA Node doesn’t produce any Deflection in ECG”

5. SA NODE ACTION POTENTIAL Action potential of SA Node cells are different from other myocardial cells by -Less Negative resting potential of -60mV (Ventricle muscle cell -90mV) -Slow Spontaneous Diastolic Depolarization in Phase 4 due to slow entry of Na+ ions.

6. ATRIAL ACTIVATION The SA Node is connected to the AV Node by 3 tracts - Bachmann’s bundle(Anterior tract) - Wenchebach’s bundle(Middle tract) - Thorel bundle’s(Posterior tract) Atrial activation begins in SA Node and proceed -Anteriorly & Inferiorly in RA -Posterior & Leftwards in LA

7. Duration of -RA activation ~20 to 40ms. -LA activation ~50 to 60ms. Interval between RA & LA activation ~30ms. BACHMANN’S BUNDLE connects both atrium & maintain the interatrial synchrony.

8. P WAVE~ ATRIAL DEPOLARISATION Initial half of P wave is due to RA Activation and terminal half due to LA Activation.

9. SINUS P WAVE FRONTAL PLANE(Lead II) AXIS- +45*to +60* CONTOUR- Smooth & Rounded AMPLITUDE- <2.5mm(<0.25mV) DURATION- <120ms (60ms in Pediatric) HORIZONTAL PLANE(Lead V1) Inverted or Biphasic with Negative portion <1mm(<0.1mV) in depth & duration.

10. SINUS P WAVE

11. RIGHT ATRIAL ENLARGEMENT Frontal Plane AXIS- Shifted to Right of +60* (P3>P1) as RA enlarges downward & to the right CONTOUR- Peaked & Pointed ( P-Pulmonale ) DURATION- Not Prolonged AMPLITUDE- >2.5mm(>0.25mV) Horizontal Plane Peaked Initial upright portion of P wave >1.5mm(> 0.15mV) in V1. Increased area under initial positive portion of P wave in V1 > 0.06 mm-sec qR in V1 ECG features of RA Enlargement have Low Sensitivity (7-10%) and High Specificity (96-100%)

12. RIGHT ATRIAL ENLARGEMENT RA ENLARGES DOWNWARD & TO RIGHT

13. P WAVE AMPLITUDE ~4MM(0.40mV)

14. Lead II P wave~ 3mm(0.30mV) Lead V1- Biphasic P with Upright part ~1.5mm(0.15mV)

15. CAUSES Tricuspid & Pulmonary valve disease Pulmonary hypertension Pulmonary embolism RVH Obstructive Pulmonary Disease Congenital Heart Diseases-TOF, Ebstein’s anomaly.

16. LEFT ATRIAL ENLARGEMENT Frontal Plane AXIS- Shifted to Left of +45*(P1>P3) as LA enlarges left & posteriorly CONTOUR- Prominent Notching with >1mm(>40ms) interval between notches ( P- Mitrale ) (Sensitivity 8% & Specificity 90%) DURATION- >120ms (Sensitivity 84% but Specificity 35%) Horizontal Plane Increased Depth & Duration of Negative portion of P in V1 of >1mm (Sensitivity 37% & Specificity 88%)

17. INDICES FOR LAE MACRUZ INDEX Ratio of P wave duration in lead II and duration of PR segment >1.6 (Normal 1.0 to 1.6) MORRIS INDEX Product of Amplitude & Duration of terminal negativity of P wave in lead V1 > 0.04 mm-sec. “Morris Index differentiates LAE from IAB”

18. LEFT ATRIAL ENLARGEMENT LA ENLARGES POSTERIORLY & TO LEFT

19. Lead II-Bifid P wave with Duration ~3mm(~120ms ) V1-Negative P terminal is >1mm in depth & duration

20. BIFID P WITH 40mm INTERVAL BW NOTCHES DURATION ~120ms TERMINAL NEGATIVE P ~2mm DURATION ~2mm DEPTH

21. CAUSES Mitral stenosis. Mitral regurgitation. LV systolic and diastolic dysfunction.

22. BIATRIAL ENLARGEMENT FRONTAL PLANE CONTOUR- Peaked & Notched( First peak taller than the second– P tricuspidale ) DURATION- >120ms AMPLITUDE- >2.5mm HORIZONTAL PLANE Initial Positive wave is Peaked Negative terminal wave is >1mm in depth & width

23. BI ATRIAL ENLARGEMENT

24. CAUSES Mitral stenosis with pulmonary hypertension Mitral stenosis with tricuspid regurgitation Mitral stenosis with tricuspid stenosis Atrial septal defect .

25. ATRIAL ENLARGEMENT RIGHT ATRIAL ENLARGEMENT Frontal Plane AXIS- Shifted to Right of +60*(P3>P1) CONTOUR- Peaked & Pointed DURATION- Not Prolonged AMPLITUDE- >2.5mm Horizontal Plane Initial upright portion is Peaked of >1.5mm LEFT ATRIAL ENLARGEMENT Frontal Plane AXIS- Shifted to Left of +45*(P1>P3) CONTOUR- Bifid with 2 humps separated by >1mm DURATION- >120ms AMPLITUDE- Not Increased Horizontal Plane Negative portion is >1mm in depth & duration

26. ATRIAL ENLARGEMENT IN AF Coarse AF – f wave is usually >1mm in Amplitude. Fine AF – f wave is <1mm amplitude or ECG baseline is almost Flat “Course AF is often associated with Atrial Enlargement”

27. INTERATRIAL BLOCK PARTIAL IAB Conduction via Bachmann’s bundle was delayed, resulting in Prolonged P wave duration >120ms ADVANCED IAB Conduction via Bachman’s bundle was completely blocked, resulting in Caudocranial activation of LA via Inferior branches P-wave duration was Prolonged with Biphasic morphology in Lead II. “TERMINAL P WAVE is NEITHER DEEP NOR WIDE in IAB”

28. INTERATRIAL BLOCK

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