Infacrt Ecg Changes

Circ ECG Challenge Response! Regarding the 67 year old man with chest pain: There is a regular rhythm at a rate of 140 bpm. Initally P waves are not obvious, but they become exposed after the 8th QRScomplex as a positive waveform just before the QRS complex (+). This is best seen in lead aVF and the lead II rhythm strip. With the subsequent QRS complexes the P wave becomes more obvious, with anincreasing PR interval. As the PR interval increases, there is a subtle change in the QRS complex morphology, best seen by the 13th- 14th complexes (↓). The changing PR interval means that the P waveis not captured and hence AV dissociation. Complexes 13 and 14 are fusion complexes. From the 15th QRS complex through complex 21 (^) there is a stable PR interval (0.16 sec) and stable QRS complexmorphology. Hence these are captured QRS complexes, representing the native QRS complexes. As seen in the lead II rhythm strip there is a change in the QRS complex morphology as the PR intervallengthens and there is capture.; hence the dissociated complexes are different from those that are captured. Therefore the initial complexes are ventricular and since the atrial rate and ventricular rates areidentical, this represents isorhythmic dissociation. The fact that there ultimately is capture, likely a result from a slight increase in the atrial rate, the likely mechanism is an acceleratedventricular rhythm. The captured QRS complexes have ST segment elevation in leads V3-V6 (↑), indicative of an acute anteroapical and anterolateral myocardial infarction. Although the initial QRS complexesare ventricular, there is slight ST segment elevation in leads I and aVL (*), suggesting that there is also a lateral wall myocardial infarction. An acute myocardial infarction can be diagnosed in thepresence of a left bundle branch block, or indeed any situation in which there is direct myocardial activation, which includes a left bundle branch block, a ventricular paced complex and a...