interpretation of ecg in pulmonary disease. cor pulmonale .. pul hypertension

1. Interpretation of ECG in Pulmonary
Disease

6. Normal PR interval and QRS complex
• The normal P interval is 120-220 ms represented by 3-5
small squares.
• Most of this time is taken up by delay in the AV node.
• If the PR interval is very short either the atria have been
depolarized from close to the AV node or there is
abnormally fast conduction from the atria to the ventricles.
• The duration of QRS complex is normally 120ms
,represented by 3 small squares.
• QT interval is a measure of the time between the start of
the Q wave and the end of the T wave in the heart's
electrical cycle.

8. The ECG in Chronic Obstructive Pulmonary
Disease
ECG changes occur in COPD due to:
1.The presence of hyperexpanded emphysematous lungs within
the chest.
2.The long-term effects of hypoxic pulmonary vasoconstriction
upon the right side of the heart, causing pulmonary hypertension
and subsequent right atrial and right ventricular hypertrophy (i.e.
cor pulmonale).

9. • 3.Lung hyper expansion causes external compression
of the heart and lowering of the diaphragms, with
consequent elongation and vertical orientation of the
heart.
• 4.Due to its fixed attachments to the great vessels, the
heart undergoes clockwise rotation in the transverse
plane, with movement of the right ventricle anteriorly
and displacement of the left ventricle posteriorly.
• 5.The presence of increased air between the heart and
recording electrodes has a dampening effect, leading
to reduced amplitude of the QRS complexes.

10. Lung hyper expansion and vertical orientation
of the heart

11. The most typical ECG findings in emphysema
are:
•Rightward shift of the P wave axis with prominent P
waves in the inferior leads and flattened or inverted P
waves in leads I and aVL.
•Rightward shift of the QRS axis towards +90 degrees
(vertical axis) or beyond (right axis deviation).
•Exaggerated atrial depolarisation causing PR and ST
segments that “sag” below the TP baseline.

12. •Low voltage QRS complexes, especially in
the left precordial leads (V4-6).
•Clockwise rotation of the heart with delayed
R/S transition point in the precordial leads
+/- persistent S wave in V6. There may be
complete absence of R waves in leads V1-3
(the “SV1-SV2-SV3″ pattern).
•Right atrial enlargement (P pulmonale)
•Right ventricular hypertrophy

15. •Rightward QRS axis (+90 degrees).
•Peaked P waves in the inferior leads > 2.5 mm
(P pulmonale) with a rightward P-wave axis
(inverted in aVL)
•Clockwise rotation of the heart with a delayed
R/S transition point (transitional lead = V5).
•Absent R waves in the right precordial leads
(SV1-SV2-SV3 pattern).
•Low voltages in the left-sided leads (I, aVL,
V5-6).

16. Right Atrial Enlargement
Right atrial enlargement produces a peaked
P wave (P pulmonale) with amplitude:
•> 2.5 mm in the inferior leads (II, III and
AVF)
•> 1.5 mm in V1 and V2

17. • Causes
• The principal cause is pulmonary
hypertension due to:
• Chronic lung disease (cor pulmonale)
• Tricuspid stenosis
• Congenital heart disease (pulmonary
stenosis, Tetralogy of Fallot)
• Primary pulmonary hypertension

18. Right atrial enlargement: P wave amplitude > 2.5mm in leads II, III and aVF
Right atrial enlargement: P wave amplitude > 1.5 mm in V2

19. Right Ventricular Hypertrophy
Diagnostic criteria
•Right axis deviation of +110° or more.
•Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
•Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).
•QRS duration < 120ms (i.e. changes not due to RBBB).

20. Supporting criteria
•Right atrial enlargement (P pulmonale).
•Right ventricular strain pattern = ST depression / T
wave inversion in the right precordial (V1-4) and
inferior (II, III, aVF) leads.
•S1 S2 S3 pattern = far right axis deviation with
dominant S waves in leads I, II and III.
•Deep S waves in the lateral leads (I, aVL, V5-V6).
Other abnormalities caused by RVH
•Right bundle branch block (complete or incomplete).

21. Causes
•Pulmonary hypertension
•Mitral stenosis
•Pulmonary embolism
•Chronic lung disease (cor pulmonale)
•Congenital heart disease (e.g. Tetralogy of
Fallot, pulmonary stenosis)
•Arrhythmogenic right ventricular
cardiomyopathy

23. Right Axis Deviation
•QRS axis between + 90 and + 180 degree
•Normal QRS axis is between – 30 and + 90
•QRS is positive (dominant R wave) in leads III and aVF
•QRS is negative (dominant S wave) in leads I and aVL

25. Causes
•Left posterior fascicular block
•Lateral myocardial infarction
•Right ventricular hypertrophy
•Acute lung disease (e.g. PE)
•Chronic lung disease (e.g. COPD)
•Ventricular ectopy
•Hyperkalaemia
•Sodium-channel blocker toxicity
•WPW syndrome

26. RIGHT VENTRICULAR HYPERTROPHY
1.In RBBB, activation of the right ventricle is delayed as
depolarisation has to spread across the septum from
the left ventricle.
2.The left ventricle is activated normally, meaning that
the early part of the QRS complex is unchanged.
3.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.

27. 4.Delayed activation of the right ventricle also
gives rise to secondary repolarization
abnormalities, with ST depression and T wave
inversion in the right precordial leads.
5.In isolated RBBB the cardiac axis is
unchanged, as left ventricular activation
proceeds normally via the left bundle branch.

29. Tall R' wave in V1 ("M" pattern) with wide, slurred S wave in
V6 ("W" pattern)
ECG changes in RBBB
Diagnostic Criteria
•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)
Associated Features
ST depression and T wave inversion in the right precordial leads
(V1-3)
T

30. Typical pattern of T-wave inversion in V1-3
with RBBB
Typical RSR' pattern ('M'-shaped QRS) in V1

31. •Right ventricular hypertrophy / cor pulmonale
•Pulmonary embolus
•Ischaemic heart disease
•Rheumatic heart disease
•Myocarditis or cardiomyopathy
•Degenerative disease of the conduction system
•Congenital heart disease (e.g. atrial septal defect)
Causes of RBBB

32. •Incomplete RBBB is defined as an RSR’ pattern in
V1-3 with QRS duration < 120ms.
•It is a normal variant, commonly seen in children
(of no clinical significance).

33. Right Ventricular Strain
Repolarisation abnormality due to right ventricular hypertrophy or
dilatation.
Electrocardiographic Features
•ST depression and T wave inversion in the leads corresponding
to the right ventricle, i.e
•The right precordial leads: V1-3, often extending out to V4
•The inferior leads: II, III, aVF, often most pronounced in lead III
as this is the most rightward-facing lead.

34. Causes
Associated with increased pulmonary artery
pressures in the setting of acute or chronic right
ventricular hypertrophy or dilatation:
•Pulmonary hypertension
•Mitral stenosis
•Pulmonary embolism
•Chronic lung disease (cor pulmonale)
•Congenital heart disease (e.g. Tetralogy of
Fallot, pulmonary stenosis)
•Arrhythmogenic right ventricular
cardiomyopathy

35. Typical right ventricular strain pattern: ST depression and T-wave inversion in V1-4
(plus lead III), in this case due to right ventricular hypertrophy.

36. Right ventricular strain pattern involving both the precordial and inferior leads: T-wave
inversions are seen in the right precordial (V1-4) and inferior leads (III, aVF) in this
patient with acute right ventricular dilatation due to massive pulmonary embolism.

37. The ECG in Pulmonary Embolism
• Sinus tachycardia – the most common abnormality; seen in
44% of patients.
• Complete or incomplete RBBB – associated with increased
mortality; seen in 18% of patients.
• Right ventricular strain pattern – T wave inversions in the
right precordial leads (V1-4) ± the inferior leads (II, III, aVF).
This pattern is seen in up to 34% of patients and is
associated with high pulmonary artery pressures.
• Right axis deviation – seen in 16% of patients. Extreme
right axis deviation may occur, with axis between zero and -
90 degrees, giving the appearance of left axis deviation
(“pseudo left axis”).

38. • Dominant R wave in V1 – a manifestation of acute
right ventricular dilatation.
• Right atrial enlargement (P pulmonale) – peaked P
wave in lead II > 2.5 mm in height. Seen in 9% of
patients.
• SI QIII TIII pattern – deep S wave in lead I, Q wave in III,
inverted T wave in III. This “classic” finding is neither
sensitive nor specific for pulmonary embolism; found
in only 20% of patients with PE.
• Clockwise rotation – shift of the R/S transition point
towards V6 with a persistent S wave in V6 (“pulmonary
disease pattern”), implying rotation of the heart due to
right ventricular dilatation.

39. 1. Atrial tachyarrhythmias – AF, flutter, atrial tachycardia. Seen in 8% of patients.
2. Non-specific ST segment and T wave changes, including ST elevation and
depression. Reported in up to 50% of patients with PE.

40. •RBBB
•Extreme right axis deviation (+180 degrees)
•S1 Q3 T3
•T-wave inversions in V1-4 and lead III
•Clockwise rotation with persistent S wave in V6
•Sinus tachycardia.
•Simultaneous T-wave inversions in the anterior (V1-4) and inferior leads
(II, III, aVF).
•Non-specific ST changes – slight ST elevation in III and aVF.

41. A 23 year-old man is brought in by paramedics after an episode of syncope at home. On
arrival he is in severe respiratory distress, extremely pale and dripping with sweat. BP
is 125/70, HR is 80bpm, RR 40, SaO2 95% on 15L O2 via NRB. Portable CXR is normal.
His ECG is presented below:

42. Describe the ECG

43. • Sinus rhythm at 80 bpm
• Left axis deviation (-70 degrees)
• RBBB with wide QRS (150ms), tall R wave in V1, RSR’
complexes in leads V1-3
• Right ventricular strain pattern with deep T wave
inversions in V1-3
• Widespread ischaemic changes with 1-2mm ST elevation
and early Q waves in the anterior leads (V2-5) and 1-2 mm
ST depression in inferior leads (II, III and aVF). There is also
significant ST elevation in leads aVR and aVL with formation
of Q waves.
• .

44. • Q2. What is your interpretation of the ECG findings given the
clinical context?
• The combination of new RBBB with signs of right ventricular
strain (deep T wave inversions in V1-3) in a patient presenting
with dyspnoea and syncope is strongly suggestive of acute
pulmonary hypertension secondary to massive PE.
• Widespread myocardial ischaemia/infarction is likely related
to severe global tissue hypoxia from obstructive shock (VBG
in this patient showed venous saturations of 10%, venous PO2
10mmHg with a lactate of 8mmol/L).
• Left axis deviation may represent left anterior fascicular block

45. THANK YOU