ROLE OF ECG IN

CHEST PRACTISE

DR S RAGHU M.D.,ASST PROF DEPT. T B & CDGUNTUR MEDICAL COLLEGEGUNTUR

Dr s. raghu m.d.,Associate professor Department of TB & CDR I M S medical collegeONGOLE

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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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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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ECG BASICS• Normal Impulse Conduction

Sinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers

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• The “PQRST”

P wave - Atrial depolarization

QRS - Ventriculardepolarization

T wave - Ventricular repolarization

U wave- uncertain origin (? Repolarization of papillary muscles)

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• The PR Interval

Atrial depolarization +

delay in AV junction (AV node/Bundle of His)

(delay allows time for the atriato contract before the ventricles contract)

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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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• 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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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

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What to look for?

• Rhythm• P wave abnormalities• Cardiac axis• QRS complex• ST segment• T waves• U waves

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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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• Step 1 : Calculate rateOption 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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• 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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• 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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• Step 4: Determine PR intervalNormal: 0.12 - 0.20 seconds.

(3 – 5 small boxes)

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• Step 5: QRS durationNormal: 0.04 - 0.12 seconds.

(1 - 3 small boxes)

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• Normal sinus rhythm parameters:

Rate 60 - 100 bpmRegularity regularP waves normalPR interval 0.12 - 0.20 sQRS duration 0.04 - 0.12 s

Any deviation from above is sinus tachycardia, sinus bradycardia or an arrhythmia

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Normal ECG

• Normal sinus rhythm, normal PR interval• Normal QRS duration, normal QRS complexes• Normal cardiac axis, normal T waves

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Abnormal ECG

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P wave abnormalities• Peaked & tall P waves: Right atrial hypertrophy

eg: Tricuspid stenosis Pulm. Hypertension

• Notched & broad P waves: Left atrial hypertrophyeg: mitral stenosis

II

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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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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)

R

R1

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• 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

RVH LVH

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• 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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• 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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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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Pericarditis

• Widespread ST elevation

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• ST segment depression:- Horizontal depression : Indicates ischemia- Down-ward sloping(reversed tick):digitalis treatment

ISCHEMIA DIGITALIS EFFECT

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T waves

• Peaked T waves : Hyperkalemia

• Flat and prolonged T waves : Hypokalemia

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• 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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U waves

• U waves : normal or hypokalemia

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Pathophysiology and ECG findings of pulmonary dysfunction

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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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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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What do you notice about P waves ?

> 2 ½ boxes (in height)

> 1 ½ boxes (in height)

Combination of P pulmonale and RAE

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44 yr old Male with 60 pack-year smoking

• P Pulmonale (P >0.25 mV in II)• No RAE by V1 criteria or by echo04/15/2023

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ECGs of Patient with COPDExacerbation Before and After Treatment

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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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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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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.

Normal RVH

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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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Left atrial enlargement

• The P waves in lead II are notched and in lead V1 they have a deep and wide negative component.

Notched

Negative deflection

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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

Normal LAE

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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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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.

* The “poor precordial R-waveprogression” sign is least specific

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Sensitivity and Specificity of theseECG 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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69y Male with COPD : Limb Lead Low Voltage Transition Shifted Leftward

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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 Findings1.Sinus tachycardia2.P pulmonale3.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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ECG changes of acute PE

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Pulmonary Embolism: ECG Score

• Score > 9 suggests PA systolic Pressure>50 (normal=24)and correlates with amount of perfusion deficits

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Post-Pneumonectomy Changes• New RBBB, New

ST segment and T wave Abnormalities in leads V1-V3

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ECG Changes in Pneumothorax

• 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.

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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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44y Male Developed Severe ChestPain and Dyspnea while Jogging

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Same Patient after Left ICDT Insertion

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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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Dextrocardia

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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.

Pericardial effusion

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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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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

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Multifocal Atrial Tachycardia with Block in Patient with COPD (note at least 3 different P Wave Morphologies)

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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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• 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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Abnormal ECG ? -----------------

WHAT IS IT ?

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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

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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.

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Inferior wall MI

• Q waves, Elevated ST segments in II, III, aVF

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Posterior wall MI

• Dominant R waves in lead V1• Non-specific T wave flattening in leads I, aVL.04/15/2023

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Pulmonary embolism & RVH

• Right axis deviation• RSR1 pattern in lead V1 & deep S waves in lead V6• Inverted T waves in leads V1- V404/15/2023

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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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67y Male with Massive PE; no MI

• Initial diagnosis was acute anterior STEMI