The document discusses various ECG abnormalities relevant to pulmonary medicine, including normal values for key ECG components and pathological changes associated with conditions like right atrial enlargement and hyperkalemia. It outlines specific characteristics of ECG waves, intervals, and segments that indicate conditions such as myocardial infarction and arrhythmias, as well as the implications of electrolyte imbalances like hypokalemia and hyperkalemia. The effects of these abnormalities on the heart's electrical activity, as well as diagnostic criteria for conditions like right bundle branch block and left bundle branch block, are also highlighted.

1. ECG Abnormalities In
Pulmonary Medicine
Dr. Manjit S. Tendolkar
Dept of Chest Medicine,
Seth G. S. Medical College and K.E.M. Hospital, Mumbai.

2. Normal ECG

3. P-wave = <0.12 sec & <2.5 mm height (limb) <1.5 mm (precordial)
P-R interval = 0.12-0.2 sec
QRS = 0.12 sec
QTc = 0.42 sec (QT/sq root RR)

4. P Wave
P wave is always positive in lead II and
always negative in lead aVR during sinus
rhythm

5. P-Pulmonale
The presence of tall, peaked P waves
(>2.5 mm) in lead II is a sign of right atrial
enlargement, usually due to pulmonary
hypertension (e.g. cor pulmonale from
chronic respiratory disease).

6. Q wave
Considered Pathological if
• > 40 ms (1 mm) wide
• > 2 mm deep
• > 25% of depth of QRS complex
• Seen in leads V1-3
Signifies Old MI

7. R wave
Abnormalities:
1. Dominant R wave in V1
2. Dominant R wave in aVR (TCA,
Dextrocardia)
3. Poor R wave progression

8. Dominant R wave in V1
Normal in Children and Young Adults
Right Ventricular Hypertrophy
- Pulmonary Embolus
- RBBB
Posterior Wall MI
Right Ventricular Hypertrophy

9. Poor R wave Progression
Defined as R wave < 3mm height in V3
Causes:
• LVH
• Prior Antero Septal MI
• Inaccurate Lead Placement
• Normal Variant

10. T wave
Upright in all leads except aVR and V1
Amplitude: < 5 mm in limb leads ; < 10 mm in
precordial leads

11. Peaked T wave (narrow & symmetrically
peaked)
Hyperkalemia

12. Hyperacute T wave (broad &
asymmetrically peaked)
Early stages of ST elevated
MI, often preceding
occurrence of ST elevation
and Q waves.

13. T wave Inversion
Normal in children
Pulmonary embolism
Ventricular hypertrophy
(Strain Pattern)
Raised ICP
T wave inversion in lead III
is normal variant.
Pathological T wave
inversion is usually
symmetrical and deep (> 3
mm)

14. Biphasic T wave
Ischaemia ( up-down )
Hypokalemia ( down-up
)

15. Camel Hump T waves
Prominent U wave fused to
end of T wave ( severe
Hypokalemia)
Hidden P wave embedded in
T wave ( Sinus Tachycardia,
Heart Blocks)

16. U wave
Normally, inversely proportional to heart rate.
Grows bigger as heart rate slows down. (visible at
HR < 65)
Normal, < 25 % T wave voltage or < 1-2 mm
amplitude

17. Prominent U wave
Severe Hypokalemia
Digoxin

18. Abnormalities of
Segments & Intervals

19. QRS
Narrow Complex <100 ms (
Supraventricular)
Broad Complex >120 ms (
Ventricular or aberrant supra
ventricular conduction -
Hyperkalemia,BBB)
Sinus rhythm with frequent ventricular ectopics

20. RBBB
• In RBBB, activation of the right ventricle is delayed as depolarisation has to spread across the
septum from the left ventricle.
• The left ventricle is activated normally, meaning that the early part of the QRS complex is
unchanged.
• The delayed right ventricular activation produces a secondary R wave (R’) in the right
precordial leads (V1-3) and a wide, slurred S wave in the lateral leads.

21. Diagnostic Criteria Of RBBB
• Broad QRS > 120 ms
• RSR’ pattern in V1-3 (‘M-shaped’ QRS complex)
• Wide, slurred S wave in the lateral leads (I, aVL, V5-6)

22. Causes of RBBB
Cor Pulmonale / Right Ventricular Hypertrophy
Pulmonary Emboli
IHD

23. Incomplete RBBB
QRS < 120 ms
Normal Variant, Common in Children.

24. LBBB
Causes:
Hyperkalemia
Digoxin Toxicity

25. Hypokalaemia
Decreased extracellular potassium causes myocardial
hyperexcitability with the potential to develop re-entrant
arrhythmias
• Hypokalaemia is defined as a potassium level < 3.5 mEq/L
• Moderate hypokalemia is a serum level of < 3.0 mEq/L
• Severe hypokalemia is defined as a level < 2.5 mEq/L

26. Changes appear when K+ falls below about 2.7 mmol/l
• Increased amplitude and width of the P wave
• Prolongation of the PR interval
• T wave flattening and inversion
• ST depression
• Prominent U waves (best seen in the precordial leads)
• Apparent long QT interval due to fusion of the T and U
waves (= long QU interval)

27. With worsening hypokalaemia:
• Frequent supraventricular and ventricular
ectopics
• Supraventricular tachyarrhythmias: AF, atrial
flutter, atrial tachycardia
• Potential to develop life-threatening ventricular
arrhythmias, e.g. VT, VF and Torsades de Pointes

28. Hyperkalemia
• Increased extracellular potassium reduces myocardial excitability, with depression of both pacemaking and
conducting tissues.
• Progressively worsening hyperkalaemia leads to suppression of impulse generation by the SA node and
reduced conduction by the AV node and His-Purkinje system, resulting in bradycardia and conduction blocks and
ultimately cardiac arrest.
• Hyperkalaemia is defined as a potassium level > 5.5 mEq/L
• Moderate hyperkalaemia is a serum potassium > 6.0 mEq/L
• Severe hyperkalaemia is a serum potassium > 7.0 mE/L

29. Serum potassium > 5.5 mEq/L is associated
with repolarization abnormalities:
• Peaked T waves (usually the earliest sign of
hyperkalaemia)

30. Serum potassium > 6.5 mEq/L is associated
with progressive paralysis of the atria:
• P wave widens and flattens
• PR segment lengthens
• P waves eventually disappear

31. Serum potassium > 7.0 mEq/L is associated with conduction
abnormalities and bradycardia:
• Prolonged QRS interval with bizarre QRS morphology
• High-grade AV block with slow junctional and ventricular escape
rhythms
• Any kind of conduction block (bundle branch blocks, fascicular
blocks)
• Sinus bradycardia or slow AF
• Development of a sine wave appearance (a pre-terminal rhythm)

32. Serum potassium level of > 9.0 mEq/Lcauses cardiac
arrest due to:
• Asystole
• Ventricular fibrillation
• PEA with bizarre, wide complex rhythm

33. QTc Interval
Prolonged QTc (>440 ms)
• Hypokalaemia
• Hypomagnesaemia
• Hypocalcaemia
• Hypothermia
• Myocardial ischemia

34. ST Segment Elevation
Acute STEMI may produce ST elevation with either concave, convex or
obliquely straight morphology
Reciprocal ST depression in opposite leads.

35. Benign Early Repolarization
Causes mild ST elevation with tall T-waves mainly in the
precordial leads. Is a normal variant commonly seen in young,
healthy patients. There is often notching of the J-point — the “fish-hook”
pattern.
No reciprocal ST depression.

36. Less common causes of ST elevation:
• Pulmonary embolism and acute cor pulmonale
(usually in lead III)
• J-waves (hypothermia, hypercalcaemia)
• Hyperkalaemia

37. ST Segment Depression • ST depression can be either upsloping, downsloping, or
horizontal.
• Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point
in ≥ 2 contiguous leads indicates myocardial ischaemia
(according to the 2007 Task Force Criteria).
• Upsloping ST depression is non-specific for myocardial
ischaemia.

38. Hypokalaemia causes widespread downsloping ST
depression with T-wave flattening/inversion, prominent
U waves and a prolonged QU interval.

39. Treatment with digoxin causes downsloping ST
depression with a “sagging” morphology, reminiscent
of Salvador Dali’s moustache.

40. Thank You