A 66-year-old female with a past medical history of acute myeloid leukemia on chemotherapy complicated by tumor lysis syndrome and myelofibrosis presents for a concern of hypotension and tachycardia which was noted on presentation to the outpatient infusion clinic. The patient states she has been feeling well and her last chemo was a month ago. The patient denies any physical manifestations including shortness of breath, chest pain, nausea, vomiting, or other symptoms at present. She does have a history of supraventricular tachycardia (SVT).
Vital signs at the time of assessment are notable for: BP: 90/57, HR: 164, RR: 18, SO2: 100 on RA: Temp 36.6.
Laboratory results are notable for mild hyperkalemia to 5.3, AKI with creatinine of 1.3. Leukocytosis to 11.3, hemoglobin of 6.9 and platelet count of 9. The troponin was negative and the BNP was largely unremarkable. An EKG (Figure 1) is performed.
Interpretation: Rate: 160bpm; Rhythm: regular tachycardia with buried p-waves; Axis: normal axis (I: pos., II: pos., aVF: neg) Intervals: PR: 163, normal; QRS: 85, normal; QT: 368, normal; P-Waves: buried in T waves; QRS Complex: normal, good R wave progression; ST Segment/T-waves: normal morphology, no elevations or depressions
This EKG is consistent with a diagnosis of SVT. At first look, it can be easy to miss the P waves. However, upon further inspection, the abnormal morphology of the T waves is a clue to examine more closely, which reveals evidence of buried P waves (Figure 2).
Figure 2. EKG with highlighted “buried” P-waves
Figure 2 shows the buried P waves indicated by a black arrow. The P waves in this EKG are best visible in lead V2, however, when we follow these P waves down the page, we can more easily identify the P waves in other leads, as indicated by the yellow highlight.
On presentation to the emergency department, the patient was noted to be tachycardic on the monitor with hypotension. However, per patient report and chart review, she did have a history of hypotension and was asymptomatic at the time, so she was not cardioverted. The emergency team attempted Valsalva maneuvers with no change, and the patient was subsequently given adenosine, after which she converted to normal sinus rhythm. The post-conversion EKG (Figure 3) as seen below.
Figure 3. Post-conversion EKG
Interpretation: Rate: 80 bpm; Rhythm: normal sinus rhythm, p waves before every QRS; Axis: left axis deviation (I: pos., II: pos., aVF: neg) Intervals: PR: 154, normal; QRS: 102, normal; QT: 370, normal; P-Waves: normal; QRS Complex: normal, good R wave progression; ST Segment/T-waves: normal morphology, no elevation or depressions
After conversion, the patient’s blood pressure improved. She was admitted to the floor on telemetry, where she was followed by cardiology and EP. She did have an additional episode of atrial tachycardia on the floor, which again resolved with adenosine. Unfortunately, given her significant comorbidities, she was not a candidate for ablation and was started on metoprolol. The patient was given follow-up with EP in the outpatient setting.
Discussion
This patient presented with concern for a supraventricular tachycardia, which was effectively converted to NSR after adenosine administration. When distinguishing types of SVT, it can be helpful to have a framework to evaluate these arrhythmias. As seen in the August 15, 2025 Heart of the Matter, the flowchart (Figure 4) below can help to differentiate these subtypes.
Figure 4. SVT differential algorithm
In the index EKG, the patient was noted to have a regular, narrow complex tachycardia. As discussed above, there is evidence of discernible P waves buried in the T waves. Further analysis (Figure 5) demonstrates that the SVT is a long RP tachycardia, giving us a differential including Atypical AVNRT, AVRT, and AT. [1]
Figure 5. PR and RP intervals of the index EKG
This patient was seen by EP in the inpatient setting and diagnosed with a “Long RP Tachyarrhythmia." However, to take it a step further and to distinguish between types of long RP tachyarrhythmias, we can look at key aspects of the EKG. [2]
AVRT:
Rate normally 200-300
Retrograde P waves, with short PR (usually <120)
Narrow QRS
Atypical AVNRT
Rate normally 140-280
Retrograde P waves: normally either after the QRS and before the T wave, or less commonly preceding the subsequent QRS complex
Atrial Tachycardia
Rate normally greater than 100
Abnormal, but consistent, P wave morphology
Isoelectric baseline
Given that the P wave in the tachycardia ECG (Figure 1) is upright in V1 and is down with return to sinus rhythm (Figure 3), this suggests these sinus P waves originate in a different atrial location than in the tachycardia. This is most consistent with a diagnosis of ectopic Atrial Tachycardia, however, this cannot be determined solely from a surface ECG. This is what EP is for! [3,4,5]
Atrial Tachycardia is a tachyarrhythmia originating in the atria, at a focus other than the sinus node. This ectopic atrial activation can occur through three different processes: enhanced automaticity, triggered activity, or a re-entry pathway within the atria. While there may be subtle differences to suggest specific types of atrial tachycardia seen on EKG, an electrophysiology study will be diagnostic for identifying the type of ectopic focus. [5,6]
Treatment for atrial tachycardia varies based on the presentation. As with all arrhythmias, the patient should undergo cardioversion if unstable. Adenosine may be used for these patients as well. However, for certain subtypes of atrial tachycardia, particularly if they bypass the sinus node altogether, it may only provide transient improvement. The mainstay of treatment for these patients is going to be beta-blockers and calcium channel blockers and for patients who fail medical management, the definitive treatment will be ablation. [6]
Take Away Points:
Atrial tachycardia can be difficult to distinguish from other types of SVT including atypical AVNRT and AVRT, however, the location and morphology of the P waves are generally suggestive of one diagnosis over another
Adenosine is a good first line for most types of SVT, however, if it is not resolving the tachyarrhythmia, the rhythm may be atrial tachycardia, in which case you should consider beta blocking as a second line treatment
References
Irum D Kotadia, Steven E Williams, Mark O'Neill, Supraventricular tachycardia: An overview of diagnosis and management, Clinical Medicine, Volume 20, Issue 1, 2020, Pages 43-47, ISSN 1470-2118, https://doi.org/10.7861/clinmed.cme.20.1.3.
Buttner, R. Atrioventricular Re-entry Tachycardia (AVRT). Life in the Fast Lane. May 20, 2022. https://litfl.com/atrioventricular-re-entry-tachycardia-avrt/
Burns E, Buttner, R. Focal Atrial Tachycardia. Life in the Fast Lane. Oct 8, 2024. https://litfl.com/atrial-tachycardia-ecg-library/
Burns E, Buttner R, Buttner EB and R. Supraventricular tachycardia (SVT). Life in the Fast Lane. October 8, 2024. https://litfl.com/supraventricular-tachycardia-svt-ecg-library/
Liwanag M, Willoughby C. Atrial Tachycardia. [Updated 2023 Jun 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542235/
Engelstein ED, Lippman N, Stein KM, Lerman BB. Mechanism-specific effects of adenosine on atrial tachycardia. Circulation. 1994 Jun;89(6):2645-54. doi: 10.1161/01.cir.89.6.2645. PMID: 8205677.
Authored by Erica Dolph MD and Ari Edelheit MD