For the same previous 78-year-old lady, you decided to administer diltiazem to slow down the ventricular rate and also once slowed down carefully scrutinize atrial activity to determine if this truly was AF or atrial tachycardia/flutter with variable AV conduction. While preparing the drug, the monitor started alarming! You walked in along with the nurse. The patient was drowsy, but responsive. She was feeling dizzy and quite diaphoretic. The monitor was showing a rate of 28/min. The repeat 12-lead ECG showed the following:
Interpret the ECG. What is the explanation for the new rhythm abnormality?
Thanks for all your responses!
It appears as though the patient ‘converted’ spontaneously! However, there is a clear change in not only rate, but also the rhythm. There is no clear sinus activity, except perhaps the last beat to the far right end of the rhythm strip. Instead, there are narrow QRS complexes suggesting normal AV nodal and infra-nodal conduction. The atrial activity however, does not appear to arise from the SA node. The P waves are inverted. Those with an inverted P wave appear to conduct with the same degree of AV delay (same PR interval). Then there are atrial beats (different morphology, different PR interval), that occur earlier than the rate at which the ectopic focus is depolarizing (almost a rate of 36/min). These are followed by a long ‘compensatory’ pause which rests the pacemaker. This is consistent with sinus arrest with an ectopic atrial pacemaker taking over.
Some of you did mention ‘junctional’ rhythm, which could still be correct! Therefore, how does one differentiate between an ectopic atrial focus and a junctional focus. The difference lies in the PR interval. With an ectopic atrial focus, the PR interval is >110 msec (AV conduction duration varies and depends on how far the ectopic focus is from the AV node).
Therefore, to sum it up, this elderly lady had a tachycardic episode followed by a post-conversion pause due to sinus arrest with an ectopic atrial pacemaker taking over. The tachy-brady syndrome is a manifestation of sick sinus syndrome. You are right to consider ischemia as a possible etiology. Other etiologies include:
O. Monferdi, et al. J Molecular & Cellular Cardiology 2015.
The following are some common manifestations of sick sinus syndrome:
1. Tachy-brady syndrome
2. Prolonged and symptomatic post conversion/termination pauses
3. Spontaneous sinus arrest
4. Sino-atrial exit block
5. Inappropriate sinus bradycardia
6. Chronotropic incompetence
Some electrophysiologists might argue that the patient should get an EP study to ablate the atrial tachyarrhythmia (if AF then pulmonary vein isolation) because the trigger here is the spontaneous conversion from the tachycardic rhythm, with an SA node that is ‘exhausted’ and therefore non-functional. However, in this particular patient, a pacemaker should be seriously considered (I know I would float a temporary pacemaker followed by arrangement for a permanent one), because not only is the tachy-brady syndrome an issue, but the escape rhythm that maintains forward cardiac output is too slow and rather incompetent, hence syncopal events and dizzy spells that coincided with the slow ventricular rate.
AV node junctional rhythm with variable block /
AF slow ventricular response /
ectopic atrial /
peak T wave ( hyperkalemia/ ischemia )
from lab normal potassium level
Is it ischemia?
I didn't see delta wave !
there is T wave inversion in aVL
possible of myocardial ischemis
symptomatic bradycardia for transcutanous pacing
- pt is symptomatic/unstable Bradycardia. Intiation of Transcutaneous pacing is indicated
- inverted P waves in the inferior leads followed by a narrow QRS
Possible source:
- AV node junctional or
- atrial ectopics
It could be due to the ishemia