ECG Abnormalities In

Pulmonary Medicine

Dr. Manjit S. Tendolkar

Dept of Chest Medicine,

Seth G. S. Medical College and K.E.M. Hospital, Mumbai.

Normal ECG

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)

P Wave

P wave is always positive in lead II and

always negative in lead aVR during sinus

rhythm

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).

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

R waveAbnormalities:

1. Dominant R wave in V1

2. Dominant R wave in aVR (TCA,

Dextrocardia)

3. Poor R wave progression

Dominant R wave in V1Normal in Children and Young Adults

Right Ventricular Hypertrophy

- Pulmonary Embolus

- RBBB

Posterior Wall MI

Right Ventricular Hypertrophy

Poor R wave ProgressionDefined as R wave < 3mm height in V3

Causes:

• LVH

• Prior Antero Septal MI

• Inaccurate Lead Placement

• Normal Variant

T wave

Upright in all leads except aVR and V1

Amplitude: < 5 mm in limb leads ; < 10 mm in

precordial leads

Peaked T wave (narrow & symmetrically

peaked)

Hyperkalemia

Hyperacute T wave (broad &

asymmetrically peaked)

Early stages of ST elevated

MI, often preceding

occurrence of ST elevation

and Q waves.

T wave InversionNormal 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)

Biphasic T wave

Ischaemia ( up-down )

Hypokalemia ( down-

up )

Camel Hump T wavesProminent U wave fused to

end of T wave ( severe

Hypokalemia)

Hidden P wave embedded in

T wave ( Sinus Tachycardia,

Heart Blocks)

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

Prominent U wave

Severe Hypokalemia

Digoxin

Abnormalities of

Segments & Intervals

QRSNarrow Complex <100 ms (

Supraventricular)

Broad Complex >120 ms (

Ventricular or aberrant supra

ventricular conduction -

Hyperkalemia,BBB)

Sinus rhythm with frequent ventricular ectopics

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.

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)

Causes of RBBB

Cor Pulmonale / Right Ventricular Hypertrophy

Pulmonary Emboli

IHD

Incomplete RBBB

QRS < 120 ms

Normal Variant, Common in Children.

LBBBCauses:

Hyperkalemia

Digoxin Toxicity

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

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)

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

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

Serum potassium > 5.5 mEq/L is associated

with repolarization abnormalities:

• Peaked T waves (usually the earliest sign of

hyperkalaemia)

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

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)

Serum potassium level of > 9.0 mEq/Lcauses cardiac

arrest due to:

• Asystole

• Ventricular fibrillation

• PEA with bizarre, wide complex rhythm

QTc Interval

Prolonged QTc (>440 ms)

• Hypokalaemia

• Hypomagnesaemia

• Hypocalcaemia

• Hypothermia

• Myocardial ischemia

ST Segment Elevation

Acute STEMI may produce ST elevation with either concave, convex or

obliquely straight morphology

Reciprocal ST depression in opposite leads.

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.

Less common causes of ST elevation:

• Pulmonary embolism and acute cor pulmonale

(usually in lead III)

• J-waves (hypothermia, hypercalcaemia)

• Hyperkalaemia

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.

Hypokalaemia causes widespread downsloping ST

depression with T-wave flattening/inversion, prominent

U waves and a prolonged QU interval.

Treatment with digoxin causes downsloping ST

depression with a “sagging” morphology, reminiscent

of Salvador Dali’s moustache.

Thank You