By Ariel Bowman, MD
Case: A 27 year-old female with no past medical history presents with shortness of breath and chest pain and is found to have a heart rate of 240 bpm. BP 104/75, RR 24, O2 sat 93% RA. She is obese, pale, diaphoretic, and appears uncomfortable but she is A+Ox4. The following EKG is obtained.
What’s the diagnosis?
This patient is presenting with a supraventricular tachycardia, a term for any tachycardia that involves atrial or AV nodal tissue for initiation and maintenance. SVT is responsible for approximately 50,000 ED visits in the United States annually,1 and about half of new cases of SVT are diagnosed in the ED.2 In our patient, the rate is quite fast at ~240 bpm, the QRS complex is regular and narrow, there are no discernible P-waves, and there is evidence of ST depression in I, II, aVL, and V2-V6.
As with any tachyarrhythmia, the first question should be whether the patient is hemodynamically stable or unstable (in the latter case, if not sinus tach – electricity!); if the patient is stable, determine if the QRS is wide or narrow and then whether the rhythm is regular or irregular. This patient is (for now) stable, and has a narrow, regular tachycardia.
DIFFERENTIAL DIAGNOSIS OF SVT
The most common etiology of a narrow, regular tachycardia is sinus tachycardia, which usually does not exceed a rate of 220 minus the patient’s age and should have a gradual onset.3 Theoretically, you should be clued in by the P waves preceding the QRS complex, but realistically, at very fast rates, P waves can be hard to see. Other narrow, regular tachycardias include atrial flutter, which is most commonly caused by a reentrant circuit in the right atrium around the tricuspid valve, and typically has an atrial rate of 300 bpm with a ventricular rate of 150 bpm when there is 2:1 conduction through the AV node. Flutter waves can be difficult to see when there is 2:1 conduction as they can be hidden by T waves.
Atrioventricular nodal reentrant tachycardia (AVNRT), orthodromic atrioventricular reentrant (or reciprocating) tachycardia (AVRT), and atrial tachycardia all have rates between 150 to 250 bpm. They are common, occurring in roughly 1 in 500 people in the US,2 and are often what people actually mean when they call a rhythm an “SVT.” AVNRT involves a reentrant loop made possible by fast and slow conducting tissue within the AV node. Retrograde P waves can sometimes be seen after the QRS complex, and can look like an R’.3
AVRT occurs when there is a bypass tract between the atria and ventricles (as in the Bundle of Kent in Wolff-Parkinson-White syndrome). The EKG will only show a delta wave (initial slurring of the QRS complex) if there is anterograde conduction down the bypass tract – turns out some bypass tracts conduct anterograde only, some retrograde only, and some can go both ways.3 The tachycardia of AVRT is narrow only when there is orthodromic conduction down the AV node/Bundle of His and up the bypass tract. Retrograde P waves may be seen after the QRS complex. Atrial tachycardia, unlike the preceding two rhythms, can sometimes have a slightly more gradual onset or “warm-up phenomenon.”3
|DDx: Narrow, regular tachycardia|
|Sinus tachycardia||SA node – Pain, fever, drugs, etc.||Max = 220 – patient’s age||P waves, but often hard to see
Gradual on/off-set, variability in rate
|Atrial flutter||Re-entrant circuit in RA around tricuspid valve||Atrial rate 300
Ventricular rate 150 if 2:1
|Flutter waves, hard to see if 2:1 conduction because hidden by Ts|
|AVNRT (Atrioventricular nodal reentrant tachycardia)*
|Re-entrant loop in AV node||150-250 bpm||Can see retrograde Ps after the QRS, can look like an R’3|
|AVRT (Atrioventricular reentrant (or reciprocating) tachycardia)*||bypass tract between the atria and ventricles||150-250 bpm||Only narrow if orthodromic conduction down AV node/Bundle of His and up bypass tract
Can see retrograde Ps after the QRS
|Atrial tachycardia||Ectopic atrial pacemaker||150-250 bpm||Can have gradual onset or “warm-up phenomenon”|
* Often collectively referred to as PSVT, or paroxysmal supraventricular tachycardia.
So, now we know all about the differential diagnosis of narrow, regular tachycardias. What to do about it?
If the patient is stable, the ACLS algorithm for narrow, regular tachycardias begins with vagal maneuvers, designed to stimulate the vagus nerve and increase parasympathetic input to the AV node. Options include the Valsalva maneuver, carotid sinus massage, and the dive reflex (a.k.a. ice to the face). A recent Cochrane Review of the effectiveness of Valsalva maneuver yielded some interesting points, namely that 1) if you’re going to study the Valsalva maneuver in a standardized manner, you’re going to have some amazingly-named study variables like “strain duration;” 2) the Valsalva maneuver was first described in 1704 by Antonio Maria Valsalva as a method of ejecting pus from the middle ear; and 3) of the three RCTs reviewed, two that induced SVTs in patients in a clinical laboratory setting had rates of conversion to sinus rhythm of around 50% with Valsalva, while the single RCT that studied patients in SVT in the Emergency Department had a successful conversion rate of only 19%.4 One useful pointer is that the way that these studies reliably reproduced adequate pressures throughout the strain duration was to have patients blow into a 10ml syringe. Much easier than telling patients to close their glottis and bear down. A newer valsava technique, called the REVERT technique, combines passive leg raise with valsalva and has a higher reported success rate.
(check it out here: http://rebelem.com/the-revert-trial-a-modified-valsalva-maneuver-to-convert-svt/)
When vagal maneuvers don’t work, the next step is adenosine, which can be both diagnostically as well as therapeutically useful; the response of the patient’s arrhythmia to this super short-acting AV nodal blocking agent can help clarify the underlying rhythm. In sinus tachycardia, atrial flutter, and atrial fibrillation, the administration of adenosine will cause a transient slowing of the rate (of the ventricular rate in the latter two). It should terminate almost all AVNRTs and AVRTs and reportedly 60-80% of atrial tachycardias.
Things to watch out for with adenosine: it will briefly stop your patent’s heart. So, it’s good form to tell them it’s going to feel weird before you push it. Like all drugs that treat arrhythmias, adenosine can actually be pro-arrhythmogenic as well – rates of atrial fibrillation of up to 12% of patients have been reported with higher doses of adenosine.5 The dose of adenosine is 6mg followed by a rapid saline flush, then 12mg if 6 doesn’t work. Higher doses may be required if your patient has a lot of caffeine in her system. Use a lower dose (3mg) if giving via a central line, in the case of a heart transplant, or if your patient also takes dipyramidole or carbamazepine. Options if adenosine doesn’t work, often the case with atrial flutter or atrial fibrillation, include the calcium-channel blockers verapamil or diltiazem, or â-blockers.
This is what happened when our patient got adenosine:
So what about the ST depressions that our patient had when she was going at a rate of 240? Should we care? Should we send troponins?
The answer is, in this otherwise healthy, young patient, probably not. Although positive troponins have been linked to worse outcomes in some non-ACS diseases (sepsis, renal failure, CHF), that’s likely not the case in the setting of SVT. One recent retrospective study that looked at troponin I levels and ST segment depression in patients with SVT who subsequently got either invasive or non-invasive evaluation for coronary artery disease found no association between troponin increase and presence of CAD, and there was no association between ST depression and CAD when controlling for history of CAD, hypertension, and hyperlipidemia.6 Another study showed no adverse 30 day outcomes in ED patients with SVT who had a positive troponin.7 (Although, full disclosure, in that same study, 2 patients with positive troponins were diagnosed with an NSTEMI after they had continued chest pain and dizziness even after resolution of their SVT.)
So, bottom line, in this patient, don’t send a troponin! It might or might not be positive; either way it shouldn’t influence our management/dispo or her outcome. And look what happened to her ST segment depressions after she converted to sinus rhythm:
||1 hour post-adenosine
Speaking of dispo, what is appropriate for our patient? In thinking about this, it’s probably best to think about SVT patients in 2 broad categories – younger patients without any significant comorbidities or underlying heart disease (“lone SVT”), and older patients or patients with underlying or comorbid cardiovascular disease.2 In an older patient or a patient with a history of, say, CHF or valvular disease or CAD, you have to ask yourself if the SVT is really a symptom of another underlying process that needs to be addressed – for example, is your patient going into an SVT because they are having a CHF exacerbation or underlying ischemia?
Overall, however, presuming your patient is not sick, doesn’t have a ton of comorbidities, and is stable after you heroically convert them back to sinus, they’ll probably do well with a brief period of observation and be able to be discharged home. Epidemiological data suggests that about a quarter of patients seen in the ED for SVT will be admitted, a quarter will be discharged with referral, and 44% will be discharged home with no planned follow-up.1 A retrospective study looking at outcomes after ED treatment for SVT found that of the 71% of patients who were discharged home, only 4% had a recurrence, all within 24 hours, and none with any instability. Of the admitted patients, 91% were admitted to an ICU setting, and these patients tended to be older, had higher rates of recurrence of SVT (19%) or needing continued anti-arrhythmic therapy while inpatient (61%).
Overall recurrence of arrhythmia was more likely to occur in admitted patients, older patients, and patients with a known history of cardiac disease.8 But before you do discharge, don’t forget to look at your patient’s EKG after cardioversion – patients with evidence of a bypass tract should probably be referred to cardiology for consideration of an EP study and possible ablation.
1 Murman et al. US Emergency Department Visits for Supraventricular Tachyardia, 1993-2003. Acad Emerg Med. 2007;14:578-581.
2 Orejarena et al. Paroxysmal Supraventricular Tachycardia in the General Population. J AM Coll Cardiol 1998;31:150-7.
3 Link MS. Evaluation and Initial Treatment of Supraventricular Tachycardia. N Engl J Med. 2012;367:1438-1448.
4 Smith GD, Dyson K, Taylor D, Morgans A, Cantwell K. Effectiveness of the Valsalva Manoeuvre for reversion of supraventricular tachycardia (Review). The Cochrane Library. 2013;3.
5 Strickberger SA, Man KC, Daoud Eg, et. al. Adenosine-induced atrial arrythmia: a prospective analysis. Ann Intern Med 1997;127:417-22.
6 Bukkapatnam RN, Robinson M, Turnipseed S, Tancredi D, Amsterdam E, Srivatsa UN. Relationship of Mycocaridal Ischemia and Injury to Coronary Artery Disease in Patients with Supraventricular Tachycardia. Am J Cardiol 2010;106:374-377.
7 Carlberg DJ, Tsuchitani S, Barlotta KS, Brady WJ. Serum troponin testing in patients with paroxysmal supraventricular tachycardia: outcome after ED care. American Journal of Emergency Medicine. 2011;29:545-548.
8 Luber S, Brady WJ, Joyce T, Perron AD. Paroxysmal Supraventricular Tachycardia: Outcome After ED Care. Am J Emerg Med 2001;19:40-42.