Rhythm Nation March 2015 – Answer!
Congratulations to VTACHomas for being first! Excellent discussion from JFreedman and Eschnitz.
This is a complicated ECG!
Let’s first look at the option of ventricular bigeminy.
Ventricular bigeminy has recurring premature ventricular contractions (PVCs) after every atrial sinus beat. There is then a compensatory pause after every PVC. In this ECG, the coupling interval – the distance between sinus QRS and PVC – is short and fixed which suggests the cause is reentry and explains the regularity of PVC morphology. As for the P waves seen prior to the PVCs in V2 and V3 they could be anterograde conduction from a reentry circuit.
But what if this is atrial bigeminy? As also pointed out by our commenters, there are very short – but present – P waves before the wide-complex beats and could be atrial in origin. Atrial premature complexes (APCs) are followed by non-compensatory pauses. If the APC is close to the AV node the PR interval will be short, and the His-Purkinje system may still be partially refractory from the previous sinus beat. This results in a wide-complex beat consistent with bundle branch block. It is easy to see how atrial bigeminy is sometimes confused for ventricular bigeminy. This ECG has very regular beat morphology which suggests a singular ectopic focus.
If it’s atrial bigeminy there is no need for treatment unless a patient is very symptomatic yet they do not run an increased risk of ventricular fibrillation.
If this is ventricular bigeminy, frequent PVCs carry a short coupling interval, and risk a PVC during the sinus refractory period that could put the heart into ventricular fibrillation (R-on-T phenomenon).
Symptomatic care is indicated by rate control using beta-blockers or calcium-channel blockers.
This young patient had been having anxiety symptoms and intermittent palpitations for months, with this being the first time his arrhythmia was caught on ECG and cardiac monitor. Increasing frequency of PVCs points towards structural heart disease which itself increases the likelihood of sudden cardiac death. Increasing frequency of APCs does not require ablation or emergent admission, but in such an unclear ECG like our patient, it is better to admit for cardiology evaluation of atrial vs ventricular origin of the bigeminy and monitoring until such decision is made.
Cardiology evaluation includes electrophysiologic study with likely radiofrequency ablation for ventricular bigeminy or highly symptomatic atrial bigeminy. Admission to cardiology with telemetry for a stable patient would be sufficient, or cardiac intensive care if unstable.
As suggested in the comments, Catecholaminergic Polymorphic Ventricular Tachycardia is an autosomal dominant genetic condition whereby the faster the heart beats the more ventricular abnormalities present, leading to sudden death. While it’s less likely in our patient as this arrhythmia was captured at rest and remained persistent at rest, the history does fit. Starting usually between 100-120 beats per minute while exercising, these patients will have PVCs, then bigeminy, then runs of nonsustained VT and finally VT.Symptoms range from syncope to sudden cardiac death. An exercise stress test is used to diagnose this condition and/or an electrophysiologic study.
With Dr. Jennifer Martindale.
References:
Dave, Jatin et al. Ventricular Premature Complexes. September 15, 2014. Medscape Emedicine. Accessed: March, 2015 from: http://emedicine.medscape.com/article/158939
Marchlinski, Francis. “Chapter 233. The Tachyarrhythmias.” Harrison’s Principles of Internal Medicine, 18e. Eds. Dan L. Longo, et al. New York, NY: McGraw-Hill, 2012.
Martindale, Jennifer and Brown, David. “Chapter 5. Premature Contractions.” Rapid Interpretation of ECGs in Emergency Medicine. Philadelphia, PA: Lippincott Williams & Williams, 2012.
Napoletano, C et al. Catecholaminergic Polymorphic Ventricular Tachycardia. NIH Genetics Home Reference. Accessed March, 2015 at http://ghr.nlm.nih.gov/condition/catecholaminergic-polymorphic-ventricular-tachycardia
eabram
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