role of ECG in chest practice

2. DR S RAGHU M.D.,
ASST PROF
DEPT. T B & CD
GUNTUR MEDICAL
COLLEGE
GUNTUR
Dr s. raghu m.d.,
Associate professor
Department of TB & CD
R I M S medical college
ONGOLE

3. Introduction
• Electrocardiography is a valuable, non-invasive
graphical representation of the heart’s electrical
activity.
• ECG helps with the cause of chest pain and
breathlessness.
• ECG can provide evidence to support a diagnosis
and in some cases it is crucial for patient
management.
• However, it is important to see the ECG as a tool
and not as an end in itself.
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4. The electricity of the heart
• Contraction of any muscle is associated with
electrical changes called depolarization, and
these changes can be detected by electrodes
attached to the surface of the body
• Although heart has four chambers, from the
electrical point of view it can be thought of as
having only two, because the two atria
contract together and then two ventricles
contract together.
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5. ECG BASICS
• Normal Impulse Conduction
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
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6. • The “PQRST”
P wave - Atrial
depolarization
QRS - Ventricular
depolarization
T wave - Ventricular
repolarization
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U wave- uncertain origin (? Repolarization of papillary muscles)

7. • The PR Interval
Atrial depolarization
+
delay in AV junction
(AV node/Bundle of His)
(delay allows time for the atria
to contract before the ventricles
contract)
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8. Pacemakers of the Heart:
SA Node - Dominant pacemaker with an
intrinsic rate of 60 - 100 beats/minute.
AV Node - Back-up pacemaker with an intrinsic
rate of 40 - 60 beats/minute.
Ventricular cells - Back-up pacemaker with an
intrinsic rate of 20 - 45 bpm.
*Impulse generation rate is highest in SA node and
lowest in purkinge system
* The conduction velocity is fastest in purkinge
system and slowest in AV node.
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9. • The ECG Paper:
• Horizontally (Duration)
– One small box - 0.04 s
– One large box - 0.20 s
• Vertically (Voltage)
– One large box - 0.5 mV
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10. 5/29/2015 10
 Every 3 seconds (15 large boxes) is marked
by a vertical line.
 This helps when calculating the heart rate.
Normal ECG paper speed – 25 mm/s

11. What to look for?
• Rhythm
• P wave abnormalities
• Cardiac axis
• QRS complex
• ST segment
• T waves
• U waves
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12. The Rhythm
• Step 1: Calculate rate.
• Step 2: Determine regularity.
• Step 3: Assess the P waves.
• Step 4: Determine PR interval.
• Step 5: Determine QRS duration.
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13. • Step 1 : Calculate rate
Option 1
– Count the no. of R waves in a 6 second rhythm strip, then multiply
with 10.
-9x10=90/min
Option 2
– Find a R wave that lands on a bold line.
– Count the no. of large boxes to the next R wave. If the second R
wave is 1 large box away, the rate is 300, 2 boxes - 150, 3 boxes -
100, 4 boxes - 75, 5 boxes -50.
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14. • Step 2: Determine regularity
• Look at the R-R distances (using a caliper or
markings on a pen or paper).
• Regular (are they equidistant apart)?
Occasionally irregular? Regularly irregular?
Irregularly irregular?
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15. • Step 3: Assess the P waves
• Are there P waves?
• Do the P waves all look alike?
• Do the P waves occur at a regular rate?
• Is there one P wave before each QRS?
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16. • Step 4: Determine PR interval
Normal: 0.12 - 0.20 seconds.
(3 – 5 small boxes)
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17. • Step 5: QRS duration
Normal: 0.04 - 0.12 seconds.
(1 - 3 small boxes)
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18. • Normal sinus rhythm parameters:
Rate 60 - 100 bpm
Regularity regular
P waves normal
PR interval 0.12 - 0.20 s
QRS duration 0.04 - 0.12 s
Any deviation from above is sinus tachycardia, sinus
bradycardia or an arrhythmia
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19. Normal ECG
• Normal sinus rhythm, normal PR interval
• Normal QRS duration, normal QRS complexes
• Normal cardiac axis, normal T waves
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20. Abnormal ECG
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21. P wave abnormalities
• Peaked & tall P waves: Right atrial hypertrophy
eg: Tricuspid stenosis
Pulm. Hypertension
• Notched & broad P waves: Left atrial hypertrophy
eg: mitral stenosis
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II

22. Cardiac axis
• Right axis deviation:- QRS complex predominantly
downward in lead I.
-Mainly with pulmonary
conditions that cause a strain
on the right side of the heart &
with congenital heart diseases.
• Left axis deviation:- QRS complex predominantly
downward in leads II and III.
- left ventricular hypertrophy
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23. The QRS complex
• Abnormalities of width:
-Wide QRS complexes
Bundle branch block(BBB)
(i) Right BBB:
Best seen in lead V1 (RSR1 pattern)
(ii) Left BBB:
Best seen in lead V6 ( M pattern)
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R
R1

24. • Abnormalities of height:
- An increase of muscle mass in either ventricle
will lead to increase in height of QRS complex.
- tall R waves in lead V1 : RVH
- tall R waves in lead V6 : LVH
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RVH LVH

25. • Transition point:
- R and S waves are equal in chest leads over inter
ventricular septum ( leads V3/V4)
- If the right ventricle is enlarged and occupies more
of the precordium, transition point will move from
its normal position of leads V3/V4 to leads V4/V5 or
V5/V6(clockwise rotation)
- Characteristic of chronic lung disease.
- Dominant S wave
in V6
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26. • Q waves :
- Q waves > 1 small square in width(40 ms) and
>2mm in depth indicates myocardial infarction.
-Leads in which Q waves appear give some indication of the part of
the heart damaged
- anterior wall MI : V2-V4/V5
- anterolateral MI : I, aVL, V3-V6
- inferior wall MI : III, aVF
- posterior wall MI : NO Q waves.
But dominant R wave in lead V1
(similar to RVH)
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27. The ST segment
• Lies between the QRS complex and the T wave
• Should be isoelectric
• Elevation of ST segment:
- Acute MI ( anterior MI – V leads)
( inferior MI – leads III, aVF)
- Pericarditis ( ST elevation in all leads)
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28. Pericarditis
• Widespread ST elevation
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29. • ST segment depression:
- Horizontal depression : Indicates ischemia
- Down-ward sloping(reversed tick):digitalis treatment
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ISCHEMIA DIGITALIS EFFECT

30. T waves
• Peaked T waves : Hyperkalemia
• Flat and prolonged T waves : Hypokalemia
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31. • Inverted T waves :
- Normal in some leads ( leads aVR & V1,
sometimes in leads III & V2)
- Ischemia & infarction
- Ventricular hypertrophy
- Bundle branch block
- Digoxin treatment
- May be in pulm embolism ( leads V1-V3)
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32. U waves
• U waves : normal or hypokalemia
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33. Pathophysiology and ECG findings
of pulmonary dysfunction
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34. P-wave abnormalities
• RAE vs ‘P pulmonale’. Are they same??
 RAE :
P-wave > 0.15 mV in V1 or V2 (best criterion)
 P Pulmonale (frequently indicative of transient RA
strain/dilatation):
Peaked P-waves ≥ 0.25 mV in II, III, or aVF
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35. Note:
• Degree of rightward P-wave axis correlates
better with lung disease severity than P-wave
amplitude
• P-wave amplitude correlates better with RA
strain (may be transient)
• Overlap of the two criteria
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36. 5/29/2015 36
What do you notice about P waves ?
> 2 ½ boxes (in height)
> 1 ½ boxes (in height)
Combination of P pulmonale and RAE

37. 44 yr old Male with 60 pack-year smoking
• P Pulmonale (P >0.25 mV in II)
• No RAE by V1 criteria or by echo
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38. ECGs of Patient with COPD
Exacerbation Before and After Treatment
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39. ECG Findings Pulmonary Hypertension
 Depends on:
• Severity and duration of the process
• Whether PH is primary (PAH) or secondary to
other conditions (e.g. Mitral Stenosis)
• Primary: various degrees of RVH
• Secondary: combination of RVH and other
findings (e.g. in MS: RVH and LAE)
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40. Right Ventricular Hypertrophy
ECG showing
• There is right axis deviation ( QRS is negative in I,
more positive in III).
• Also tall R waves in V1, V2.
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41. Right ventricular hypertrophy
– Notice the R wave is normally small in V1, V2 because the
right ventricle does not have a lot of muscle mass.
– But in the hypertrophied right ventricle the R wave is
tall(>0.7mv/7mm) in V1, V2.
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Normal RVH

42. Right Ventricular Hypertrophy Criteria
• Right Axis Deviation (QRS is negative in I, more
positive in III)
• Tall R wave in lead V1 (R wave > 7 mm & R/S > 1)
• T wave inversions in leads V1-V2, sometimes V3/V4
• S-wave in lead V2 < 2 mm
• Deep S waves in lead V6 (R/S ratio ≤ 1)
• Sometimes RBBB(RSR1 pattern in lead V1 & R1>7mm)
• Note: Need at least two criteria for definite diagnosis.
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43. Left atrial enlargement
• The P waves in lead II are notched and in
lead V1 they have a deep and wide negative
component.
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Notched
Negative deflection

44. Criteria for diagnosing LAE
• II  > 0.04 s (1 small box) between notched peaks
or
• V1  Neg. deflection > 1 small box wide x 1 box deep
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Normal LAE

45. Type A : 40y old woman, severe PAH & RVH
• Peaked P waves, best seen in lead II.
• Right axis deviation,Dominant R waves in lead V1
• Deep S waves in lead V6.
• Inverted T waves in leads II, III, VF, V1-V3
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46. Pathophysiology and the ECG in COPD
Pathophysiology
• Right atrial “strain”
• Right atrial enlargement
• “Clockwise” rotation of the
heart
• RVH (usually mild or mod.
unless end-stage)
• Lung hyperinflation
• Intermittent hypoxia and
pulm. vasoconstriction
• Depressed diaphragms
ECG findings
• P Pulmonale (peaked &
>0.25 mV) in II, III, aVF
• Shift of transition leftward*
• Rightward QRS axis
• RVH (late)
• Low voltage in limb leads
• Transient atrial arrhythmias
(MAT is pathognomonic)
during decompensation.
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* The “poor precordial R-wave
progression” sign is least specific

47. Sensitivity and Specificity of these
ECG Criteria
• For single criterion – specificity is low (54% false
positive)
• With two or more criteria specificity much better.
♥ COPD likely to be present if one P and one QRS
criterion present
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48. 69y Male with COPD : Limb Lead Low Voltage
Transition Shifted Leftward
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49. Acute Pulmonary Embolism
Pathophysiology
• Sympathetic stimulation
• RA & RV strain/dilatation
• Acute pulmonary
hypertension
• Spatial changes (clockwise
rotation)
• ↑ RV wall stress leading to
RV ischemia
• RV dysfunction
ECG Findings
1.Sinus tachycardia
2.P pulmonale
3.S1Q3T3 pattern (? IMI)
• RBBB (complete or incomplete)
4.Acute rightward axis shift
5.↓ T V1-V3 (frequently
persistent) (? Ac STEMI)
6.Atrial arrhythmias (AFib or
AFlutter)
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50. ECG changes of acute PE
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51. Pulmonary Embolism: ECG Score
• Score > 9 suggests
PA systolic
Pressure>50
(normal=24)and
correlates with
amount of
perfusion deficits
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52. Post-Pneumonectomy Changes
• New RBBB,
New ST
segment and T
wave
Abnormalities
in leads V1-V3
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53. ECG Changes in Pneumothorax
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• The ECG changes in pneumothorax
depends on the size and site of the
pneumothorax.
• A tension pneumothorax is able to
induce a hypotensive state with a
resulting reduction of coronary
blood flow. The consequent
myocardial ischemia results in ECG
changes like T wave inversions.

54. ECG Changes in Pneumothorax
• ECG abnormalities may be different
in relation to site of the PNTX also.
• Left sided pneumothorax: Axis
deviation is more common &
reduction of amplitude of QRS
complexes.
• Right sided pneumothorax :
Changes in morphology of QRS
complex ( new RBBB) & T wave
(inversions)
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55. 44y Male Developed Severe Chest
Pain and Dyspnea while Jogging
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56. Same Patient after Left ICDT Insertion
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57. Dextrocardia
• Right axis deviation
• Positive QRS complexes (with upright P and T waves) in
aVR
• Lead I: inversion of all complexes, also known as ‘global
negativity’ (inverted P wave, negative QRS, inverted T
wave)
• Absent R-wave progression in the chest leads
(dominant S waves throughout)
(These changes can be reversed by placing the precordial
leads in a mirror-image position on the right side of the
chest and reversing the left and right arm leads.)
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58. Dextrocardia
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59. Pericardial effusion
ECG changes:
• Normal axis
• Normal width but generally small QRS complexes
• T wave inversion in leads I, II, III, VF, V5-V6
Small QRS complexes are sometimes also in
patients with chronic lung disease but The
widespread T wave changes are consistent with
pericardial disease.
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60. Pericardial effusion
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61. Atrial fibrillation
• Atrial muscle fibres contract independently.
• No P waves on ECG, only irregular baseline.
• AV node conducts impulses irregularly but of
constant intensity.
• So QRS complexes are irregular but normally
shaped
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62. Atrial fibrillation
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• Atrial fibrillation, Ventricular rate 75-200/min
• Normal axis, Normal QRS complexes
• Downward-sloping ST segment depression(digitalis effect) , especially
in leads V5, V6

63. Multifocal Atrial Tachycardia with Block in
Patient with COPD (note at least 3 different P
Wave Morphologies)
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64. Take Home
• ECG is a simple and cost-effective, bedside
investigation for the early detection of heart
changes in the course of pulmonary diseases.
• The presence of ECG changes alerts the chest
physician to take measures which helps in the
reversal of cardiac changes or preventing the
further cardiac compromise.
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65. • Acute breathlessness or chest pain associated
with acute severe asthma, pulmonary
thromboembolism, pneumothorax commonly
shows ECG abnormalities which increases the
specificity of the pulmonary disease and helps in
early intervention.
• But the clinical examination and chest X-ray are
must to confirm the diagnosis and the ECG serves
the supportive findings.
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66. Abnormal ECG ? ------
-----------
WHAT IS IT ?
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67. Anterior wall MI
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• Q waves in leads V2-V4
• Raised ST segments in leads V2-V4
• Inverted T waves in leads I, aVL, V2-V6

68. Antero-lateral wall MI
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• Q waves in leads V3-V5.
• Raised ST segments in I, aVL, V3-V6
• Depressed ST segments in leads III, aVF.

69. Inferior wall MI
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• Q waves, Elevated ST segments in II, III, aVF

70. Posterior wall MI
• Dominant R waves in lead V1
• Non-specific T wave flattening in leads I, aVL.
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71. Pulmonary embolism & RVH
• Right axis deviation
• RSR1 pattern in lead V1 & deep S waves in lead V6
• Inverted T waves in leads V1- V4
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72. 57y Female, with Massive PE (Severe RV
dysfunction by Echo)
DDx: Anterior wall ischemia
• ↓ T-waves in V1-
V4 and leftward
displaced
transition are the
only ECG findings
here
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73. 67y Male with Massive PE; no MI
• Initial diagnosis was
acute anterior STEMI
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