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CAUSES OF ABNORMAL WAVES
P WAVE ABNORMALITIES:
1. Tall P wave: The P wave exceeding 2.5mm in height are seen in
a. Right atrial hypertrophy
b. Hypokalemia
2. Wide P wave: P waves exceeding 0.11 seconds in width are observed in
a. Left atrial hypertrophy
b. Hyperkalemia
3. Inverted P wave:
a. Occurs in nodal rhythm (impulses of AV nodal origin),
b. Impulses of ventricular origin,
c. Impulses bypass to SA node after activating AV node (WPW syndrome)
4. Absent P Wave
a. Atrial fibrillation
b. AV nodal rhythm
c. Ventricular tachycardia
d. Hyperkalemia
e. SA block
5. Abnormal P wave axis
a. With right atrial hypertrophy, the axis is +60 degrees to +90 degrees
b. With left atrial hypertrophy, the axis is –30 degrees to +40 degrees
6. Change in P wave morphology
a. P-pulmonale is common in pulmonary hypertension
b. P-mitrale seen in left atrial hypertrophy

QRS COMPLEX ABNORMALITIES
1. Wide QRS complex: The normal QRS width is 0.04 to 0.08sec
a. Interventricular conduction defect or hemi block
b. Left ventricular hypertrophy
c. Myocardial infarction
d. Incomplete bundle branch block
e. WPW syndrome

2. Abnormal QRS Amplitude
a. Tall R wave in lead V1
i. Right ventricular hypertrophy
ii. Right bundle branch block
iii. WPW syndrome type A
iv. Persistent juvenile pattern of right ventricular dominance
v. Mirror image dextocardia
vi. Duchenne’s muscular dystrophy with cardiomyopathy
vii. Hypertrophic obstructive cardiomyopathy
viii. Left ventricular extra systole
ix. Posterior wall myocardial infarction

b. Tall R wave in lead V6
i. Left ventricular systolic overload
ii. Left ventricular diastolic overload
iii. Left bundle branch block
c. Deep S wave in lead V1 (rS pattern): The normal S wave in V1 does not exceed 2.5 mV. Deep S waves in V1 with tall R waves in lead V6 is a feature of left ventricular hypertrophy.
d. Deep S wave (rS pattern) in lead V6:

The normal S wave voltage in V6 does not exceed 0.7mV and the R wave is generally taller than the S wave. A deep S wave in V6 may be due to
i. Right ventricular dominance
ii. Mirror image dextrocardia
iii. Right bundle branch block with left anterior hemi block
iv. Ventricular ectopy
v. Marked clock wise rotation
e. Non-progression of R wave from V1 to V4:
i. Anterior wall myocardial infarction
ii. Diffuse myocardial disease
iii. Pulmonary emphysema
iv. Left ventricular hypertrophy
v. Left bundle branch block
vi. WPW syndrome Type B
vii. Anomalous pulmonary origin of left coronary artery

f. Low QRS voltage: The voltage of QRS complex should be atleast 5mm in the standard leads and atleast 10mm in the precordial leads. Voltage below these values are considered as low.
i. With normal T wave
1. Thick chest wall
2. Marked obesity
3. Pulmonary emphysema
ii. With inverted T wave
1. Pericardial effusion or constrictive pericarditis
2. Hypothyroidism
3. Hypopitutarism
4. Diffuse myocardial disease
g. Electrical Alterans: A condition in which the voltage of the P wave, T wave, and the QRS complex re all variable in the same lead. Reasons
i. Paroxysmal atrial tachyarrhythmia with fast heart rate like atrial tachycardia, flutter or fibrillation
ii. Serious organic heart disease e.g. ischaemic or hypertensive heart disease, cardiomyopathy or myocarditis.
iii. Pericardial effusion e.g. malignant or tubercular.

3. Prolonged Ventricular Activation time:
a. Ventricular hypertrophy
b. Bundle branch block or hemi block
c. Hyperacute phase of myocardial infarction
4. Abnormal QRS morphology:
a. Abnormal R wave Peak:
i. RSR’ Pattern or ‘M’ pattern in the presence of bundle branch block. The RSR’ pattern is observed in lead V1 in right bundle branch block and in lead V6 in left bundle branch block.
b. Delta wave on Ascending limb:
i. Occurs in WPW syndrome due to Bundle of Kent
c. Osborne wave on Descending limb:
i. A hump like deflection on the descending limb of R wave due to prolonged intra ventricular conduction observed in hypothermia.
5. Wide QRS complex:
a. Occurs from various myocardial diseases and conduction defects.


Q WAVE ABNORMALITIES:
1. Q waves in Myocardial infarction:
a. Necrosed myocardial tissue is electrically inert and cannot be depolarized. If the full myocardial thickness is necrosed (transmural infarction), there is an electrical hole in the muscle wall. If an electrode is placed over this hole (area of transmural necrosis) it reflects activation of the opposite ventricular wall. Since the activation is in a direction away from the electrode, it is reflected as a Q wave, which is negative, and not followed by R wave, the so called QS complex. The location of Q waves on the ECG can help to localize the area of myocardial infarction.
i. V1-2: septal;
ii. V3-4: anterior;
iii. V5-6, L1, aVL: Lateral;
iv. V1-4: Antero septal;
v. V3-6, L1, aVL: Antero lateral;
vi. V1-6, L1, aVL: Extensive anterior;
vii. L1, aVL: High lateral;
viii. L2, L3, aVF: Inferior

CAUSES OF T WAVE INVERSION:
1. Non specific causes:
a. Anxiety
b. Hyperventilation
c. Heavy metals
d. Smoking
e. Tachycardia
f. Cerebro vascular Haemorrhage
g. Pancreatitis, cholecystitis
h. Pulmonary embolism
i. Myxoedema
j. Shock
2. Specific Causes
a. Primary
i. Digitalis and Quinidine poisoning
ii. Hypokalemia
iii. Cardiomyopathy
iv. Myocarditis
v. Pericarditis
vi. Pericardial effusion
vii. Acute coronary insufficiency
viii. Acute myocardial infarction
b. Secondary
i. Ventricular hypertrophy
ii. Bundle branch block
iii. WPW syndrome
c. Giant T wave inversion
i. Myocardial ischaemia or infarction
ii. Cerebrovascular accident
iii. Apical myocardiopathy
iv. After resuscitation from ventricular fibrillation

CAUSES OF TALL T WAVE
1. Tall T wave:
a. Hyperkalemia
b. Myocardial ischaemia / injury
i. Hyperacute myocardial infarction
ii. Prinzmetal’s angina
iii. Coronary insufficiency
iv. Recovering inferior wall infarction
c. True posterior wall myocardial infarction (in V1 & V2)
d. Left ventricular diastolic overload (in V5 & V6)
e. Cerebrovascular accident
f. In psychotic individuals
g. As a normal variant in vagotonic persons.
2. Notched or Broad T waves
a. Pericarditis
b. CNS disorders
c. Prolonged Q-T interval
d. Alcoholic Cardiomyopathy
e. Quinidine effect
f. Myocarditis

U WAVE ABNORMALITIES:
1. Prominent U wave:
a. Hypokalemia
b. Sympathetic stimulation
c. Intra-cranial events
2. U wave inversion
a. Coronary artery disease and myocardial ischaemia
b. Aortic and / or mitral valve regurgitation
c. Hypertension with left ventricular hypertrophy
d. Right ventricular hypertrophy

P-R SEGMENT DEPRESSION:
1. Secondary causes
a. Sinus tachycardia in normal persons
b. Atrial enlargement or hypertrophy
2. Primary causes
a. Acute pericarditis
b. Atrial infarction
c. Mechanical injury

S-T SEGMENT DEPRESSION:
1. Non specific causes:
a. Physiological
i. Anxiety
ii. Hyperventilation
iii. Heavy metals
iv. Smoking
v. Tachycardia
b. Extra cardiac causes
i. Subarachnoid haemorrhage
ii. Pancreatitis, cholecystitis
iii. Pulmonary embolism
iv. Myxoedema
v. Shock
2. Specific causes
a. Primary
i. Digitalis, Quinidine effect
ii. Hypokalemia
iii. Cardiomyopathy
iv. Myocarditis
v. Acute coronary insufficiency
vi. Non-Q myocardial infarction
b. Secondary
i. Ventricular hypertrophy or systolic overload
ii. Bundle branch block
iii. WPW syndrome

S-T SEGMENT ELEVATION:
1. Myocardial infarction
2. Prinzmetal’s angina
3. Acute pericarditis
4. Early repolarization variant
5. Ventricular aneurysm
6. Post cardiotomy syndrome

CAUSES OF P-R INTERVAL CHANGE
1. Prolonged P-R interval:
a. Prolonged P-R interval in all beats:
i. Acute rheumatic fever and diphtheria
ii. Drug acting on the A-V node – digitalis, verapamil, propranolol
iii. Coronary artery disease
iv. Congenital heart disease
v. Hyperkalaemia or hypokalemia
vi. Vagotonia
vii. Sympathetic blockade
viii. Rapid atrial placing
ix. Hypothyroidism and hypothermia
b. Prolonged P-R interval in isolated beats:
i. Atrial ectopic
ii. A-V dissociation
iii. Interpolated ventricular ectopic
c. Progressive prolongation of P-R
i. Second degree A-V block
2. Shortened P-R interval
a. Shortened P-R interval in all beats
i. A-V nodal rhythm
ii. Accessory by-pass tract
iii. Vagolytic drugs – atropine, quinidine
iv. Sympathetic stimulation
b. Shortened P-R interval in Isolated beats
i. Atrial ectopic
ii. A-V dissociation
iii. End-diastolic ventricular ectopic
c. Progressive shortening of P-R interval
i. Isorhythmic A-V dissociation
ii. Reverse Wenckebach phenomenon
3. Variable P-R interval
a. With Identical P waves
i. A-V dissociation
b. With changing P wave morphology:
i. Multiple supraventricular ectopics
ii. Wandering pacemaker rhythm
iii. Chaotic atrial rhythm or multifocal atrial tachy cardia.

CAUSES OF Q-T INTERVAL CHANGE:
1. Shortened Q-T interval
a. Hyperkalaemia
b. Hypercalcaemia
c. Digitalis effect
d. Acidosis
e. Hyperthermia
f. Vagal stimulation
2. Prolonged Q-T interval:
a. Acquired causes:
i. Hypocalcaemia and hypomagnesaemia
ii. Acute myocardial infarction or coronary insufficiency
iii. Acute myocarditis and rheumatic fever
iv. Intra-cranial events – head injury, cerebral or subarachnoid haemorrhage.
v. Liquid protein diet
vi. Sympathetic stimulation
vii. Hypothermia
viii. Bradyarrhythmias e.g. third-degree A-V block, marked sinus bradycardia.
 

References:
1. Essentials of applied electrocardiography – Athul Luthra
2. Introduction to electrocardiography – U.N. Panda and Laxmi chand
3. ECG pocket guide – Bradford C. Lipman and Bernard S. Lipman
4. A primer of Electro cardiography – Natoobhai.J.Shah and Sailesh.N.Shah
5. The ECG made easy – John R. Hamptom
6. Electrocardiography -Leo schamroth
7. Text book of medicine – K.V. Krishnadas
8. Clinical Medicine – K.V.Krishnadas
9. Hutchison’s Clinical Methods – Michael Swash
10. Davidson’s Principles and practice of Medicine

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