A wide and notched P wave is typically seen in
Ans. is 'a' i.e., Mitral stenosis Mitral stenosis is icall associated with a Wide and Notched P wave rom Le t Atrial Enlar * ement LAE Cor-Pulmonate, COPD and Pulmonary embolism are all associated with Right Atrial Enlargement resulting in a Tall P wave (not a wide p wave). P wave becomes "tall" in RA enlargement and "wide" with LA enlargement Components of P wave RA component The SA node depolarises the RA first, so the initial pa of P wave represents RA current. After about 40 msec the wave front reaches LA and it begins it's depolarisation. LA component By the time LA is maximally depolarized the RA already stas its repolarisation. So there is overlap and also a sho time lag between these two wave forms. This is very impoant to recognise as, even if the RA conduction is prolonged in pathology the RA component of P-wave still falls within the LA wave. Hence it is not shown in the ECG and P wave is not widened in RA enlargement. This is in contrast to LA enlargement, when the terminal half of P vector delayed it stretches the P wave wide beyond the normal 100ms. Hence LAE widens the P wave. P wave becomes taller in RA enlargement In classical P pulmonale, the P wave is tall > 2.5 mm. It is easy to explain why it not getting wide than why it is getting taller The atrial vector has two components. The initial RA vector, is directed anteriorly. The main reason is due to the anatomical proximity of RA to the chest wall. Fuher the atrial electrical dp/dt is fast, so the slope of forward limb is steep. Any RA voltage increase is easily picked up by the chest leads. LAE can not produce tall P wave The left atrial vector which follows RA vector is mainly directed posteriorly and hence inscribe a descending limb of P wave. This causes the P terminal force. So the direction of vector forces and the anatomical locality make a tall and positive P deflection highly improbable in LAE.
Mitral stenosis
Cor-Pulmonale
COPD
Pulmonary embolism