A 64-year-old female with a past medical history of hyperthyroidism status post partial thyroidectomy on levothyroxine initially presented to urgent care for two episodes of vaginal spotting over the last two weeks. At urgent care, she was noted to be tachycardic to the 130s bpm and was thus instructed to go to the Emergency Department (ED). The patient reported left lower quadrant pain but denied any chest pain, shortness of breath, or fevers. An ECG was obtained on arrival (Figure 1).
Interpretation:
Rate: 116 bpm; Rhythm: regular narrow complex rhythm with P waves before every QRS; Axis: normal axis (I: pos, II: pos., aVF: pos); Intervals: PR: 104, short; QRS: 86, normal; QTc: 384, normal; P-Waves: present and associated with every QRS, inverted in leads II, III, aVF, V3-V6; QRS Complex: normal; ST Segment/T-waves: normal
Additional work-up included a CBC, which was remarkable for a leukocytosis of 12.0 and hemoglobin of 11.8; a BMP, which was unremarkable; a TSH/T4, which was normal; and a CT of the abdomen and pelvis, which demonstrated findings consistent with sigmoid colon diverticulitis, for which the patient was treated with IV ceftriaxone and metronidazole. The patient had intermittent episodes of tachycardia to 130s bpm while in the ED. A repeat ECG was ordered (Figure 2).
Figure 2. Repeat ECG.
Interpretation:
Rate: 135 bpm; Rhythm: regular narrow complex rhythm with P waves before every QRS; Axis: normal axis (I: pos, II: pos., aVF: pos); Intervals: PR: 118, short; QRS: 85, normal; QTc: 410, normal; P-Waves: present and associated with every QRS, inverted in leads II, III, aVF, V2-V6; QRS Complex: normal; ST Segment/T-waves: normal
This patient was admitted for diverticulitis and further management of atrial tachycardia. Cardiology was consulted by Internal Medicine for tachycardia despite IV fluids and antibiotics. They recommended metoprolol succinate 25mg daily for focal atrial tachycardia in the setting of acute diverticulitis.
Discussion:
The initial ECG shows focal atrial tachycardia (FAT). FAT is a type of atrial tachycardia, a broader term referring to any form of supraventricular tachycardia (SVT) originating within the atria but outside of the sinus node. Focal atrial tachycardia can arise from any one or a combination of the three mechanisms causing tachyarrhythmias: enhanced automaticity, triggered, or micro-reentrant circuit. It can be paroxysmal or sustained. The causes are many, including digoxin toxicity, atrial scarring due to ischemic heart disease, alcohol, catecholamine excess, infections, stimulants such as cocaine and caffeine, or idiopathic.
On ECG, the atrial rate will be over 100 bpm. There will be abnormal P wave morphology and axis, with P wave inversion in the inferior leads. The P waves will be identical (differing from multifocal atrial tachycardia). There should be normal QRS morphology unless there is a pre-existing bundle branch block, accessory pathway, or aberrant conduction pathway.
Having a P wave before each QRS alone does not mean the rhythm is sinus. The inverted P wave in the inferior leads shows it is likely originating from lower in the atria and not at the SA node.
Normal pacemaking impulses arise from the sino-atrial node and are transmitted to the ventricles via the AV-node and His-Purkinje system. The initial ECG above demonstrates that, once the atrial tachycardia resolves, an upright sinus P wave precedes the final QRS. This confirms the patient had a sustained episode of atrial tachycardia.
Figure 3. Normal pacemaking.
A normal P wave axis is between 0° and +75°. P waves should be upright in leads I and II and inverted in aVR. In Figure 4 below, the normal vector of depolarization is shown by the yellow arrow. As the heart depolarizes down and to the left towards leads I, II, aVF you will get positive P waves in leads I, II, aVF; and as it moves away from aVR, you will get a negative P wave in aVR.
Figure 4. Heart depolarization vectors.
Initial management of focal atrial tachycardia should focus on addressing underlying causes: treating acute illness, cessation of stimulants, stress reduction, appropriately managing digoxin toxicity, or chronic disease management. If the tachycardia is persistent or symptomatic, you may treat with beta blockers or calcium channel blockers. Ablation may be done in patients that fail medication therapy.
Authored by Taylor Wahrenbrock, MD, Michael Hohl, MD, and Ari Edelheit, MD.
References:
Buttà C et al. Electrocardiographic diagnosis of atrial tachycardia: classification, P-wave morphology, and differential diagnosis with other supraventricular tachycardias. Ann Noninvasive Electrocardiol. 2015 Jul;20(4):314-27
Life in the Fast Lane: Focal Atrial Tachycardia https://litfl.com/atrial-tachycardia-ecg-library/
ECG Weekly: ECG Stat Atrial Tachycardia https://ecgweekly.com/ecgstat/atrial-tachycardia/
EM in 5: EKG Interpretation QRS/P Wave Axis https://emin5.com/2015/02/02/ekg-interpretation-qrs-p-wave-axis/