This Cyclist Felt Dizzy and Stopped at the Hospital

Philip J. Podrid, MD

Disclosures

June 08, 2018

Figure 2. Courtesy of Dr Podrid.

Discussion

The diagnosis is nonsustained atrial tachycardia and left ventricular hypertrophy (LVH) with associated ST-T wave changes.

There is a regular narrow complex tachycardia at a rate of 240 beats/min. At this rate, the etiology may be either atrial tachycardia (slightly faster than usual) or atrial flutter with 1:1 conduction (slightly slower than usual). Atrial waveforms are seen before each QRS complex (^) and they appear to be positive in lead II and aVF, making an atrial tachycardia a more likely diagnosis. The tachycardia abruptly terminates without atrial activity (↓). This is the mode of termination of atrial arrhythmias. The atrial focus stops generating an impulse and hence the arrhythmia terminates.

Following the termination is a P wave (+), followed by a QRS complex with the same morphology as the other QRS complexes. This is a sinus complex followed by a second sinus complex.(*) The P-wave morphology is different from the P-wave morphology during tachycardia, confirming that the rhythm is not sinus tachycardia. After this second sinus complex, the atrial tachycardia occurs again. The QRS complexes are narrow (0.08 sec) with normal morphology and axis between 0° and +90° (positive QRS complex in leads I and aVF). The QRS complex amplitude is increased to 25 mm with an S wave ( ] ), and the R wave in V5 is 12 mm ( [ ) (SV2 + RV5 = 37 mm), which meets a criterion for LVH. There are ST-T wave changes in leads V4-V6 (↑) which are associated with LVH. Often referred to as "strain," they actually are the result of chronic subendocardial ischemia. The endocardium (the last layer of myocardium to receive blood and oxygen) becomes ischemic when the myocardial muscle mass increases with increased oxygen demand and reduced supply to the subendocardial layer.

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