Slowed the Node
Brian Smith, DO
Today we’ll review management of narrow-complex tachyarrhythmias:
The Case:
A 62 F is sent in from a cardiologist's office for abnormal ECG. She reports intermittent palpitations x 3 weeks. She denies any PMH but also states she had not seen a doctor in 7 years prior to today. She is AAOx3 and appears mildly anxious, but comfortable.
VS: HR 185, RR 18, BP: 100/68, SPO2 98% on RA, Temp: 36.7, weight 47 KG. You place her on tele monitoring and draw labs.
Her ECG is shown below:
Question: What is your next step in management?
A) Vagal Maneuvers
B) Adenosine
C) Rate-Controlling Agents
D) Synchronized Cardioversion
When presented with a tachyarrhythmias, it’s important to ask yourself 3 questions to guide management:
Is the patient stable or unstable?
If unstable (Hypotension or mental status changes) perform synchronized cardioversion. If stable, move on to question 2.
Are the QRS complexes wide (>120ms) or narrow (<120ms)?
The management of stable atrial vs ventricular dysrhythmias have many differences so it is important to recognize if QRS complexes are narrow (suggesting atrial origin) vs wide (suggesting ventricular origin)
Is the rhythm regular or irregular?
When patients are this tachycardic, it can be hard to identify the underlying rhythm. However, by distinguishing regular vs irregular rhythm can help clue us into the underlying rhythm and guide management
For our patient:
The patient’s blood pressure is soft, but she is thin and mentating well, so the decision was made not to perform synchronized cardioversion.
The QRS complexes are narrow, suggesting an atrial tachyarrythmia
While it is difficult to tell when the rate is this high, the rhythm does appear regular. With no discernible P waves and a rate of 185, this is suggestive of Paroxysmal supraventricular tachycardia (SVT)
Back to the question:
For this patient, a case could be made to pursue option A, B, C, or D. However, given the patient was stable and with a narrow-complex regular tachyarrythmia, the decision was made to first perform Vagal Maneuvers.
Before scrolling down, think above which vagal maneuver you would perform and why.
Vagal Maneuvers:
With so many options to choose from, how do you decide which vagal maneuver to perform? Is there any evidence supporting one over another?
Luckily, EM physicians in England had the same question; and thanks to them, we have the REVERT Trial.
This was a Multicenter, randomized controlled, parallel-group trial in 10 emergency departments in England. that asked the question: Does modified valsalva maneuver have a higher conversion rate to sinus than regular valsalva?
The modified valsalva (pictured right) is a strain of 40 mm Hg pressure for 15 seconds (either into a syringe or a manual BP machine) with the patient in the semi-recumbent position, followed by supine repositioning with 15 seconds of passive leg raise at a 45-degree angle
Turns out, it does! The modified valsalva maneuver had a 42% conversion rate to sinus compares to 17% for standard valsalva maneuver.
Not only is the modified valsalva 3 times as successful, but it also comes at no additional cost and with no added risk to the patient!
So, as long as the patient can tolerate the modified valsalva, this should be your go-to vagal maneuver to convert a patient back to sinus.
However, we attempted the modified valsalva on our patient and were not able to convert her back to sinus rhythm
What do you want to do next?
A) Adenosine
B) Rate-controlling Agents
C) Synchronized Cardioversion
Adenosine
Given our concern for PSVT, we decided to pursue adenosine next. A couple tips for pushing adenosine:
Dosage: First try 6 mg. If unsuccessful, attempt again with 12 mg. (If still ineffective, can try 12 mg one more time)
Preparation:
Warn our patients that they will feel like they’re dying when adenosine is pushed.
Have the patient connected to the Zoll and the ECG machine. You want to capture the rhythm when adenosine is pushed
Setup: The half life of Adenosine is 10 seconds! So it needs to be pushed QUICKLY in order to reach the heart before it is metabolized. You can increase your chance of success with these measures
Establish good IV access
Techniques to flush adenosine quickly:
Set up a 3-way stopcock with adenosine in one port and a 10cc flush in the other. After pushing Adenosine, quickly switch the stopcock and push a 10 cc flush.
Push Adenosine through running IV line and then push 2 10 cc flushes
Draw adenosine and saline in the SAME 20 cc syringe and push together (a study done in 2019 showed this was noninferior to the 2 other techniques)
After pushing adenosine, raise the patient’s arm to expedite venous return
For our patient, we pushed adenosine through a running IV line then pushed 2 10 cc flushes. Her ECG obtained while pushing adenosine is shown below:
Recognize the rhythm?
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Yup - that’s atrial flutter with variable conduction
We were surprised because the rhythm did seem regular, but that’s OK
While adenosine is THERAPEUTIC for PSVT, it can also be useful in DIAGNOSIS of other atrial tachyarrhythmias
In this case, the adenosine helped us slow the rate to uncover the patient’s atrial flutter.
After 5 minutes, the patient again become tachycardic to the 180s, BP: 98/60, still mentating well and comfortable-appearing.
Given this new information, how would you proceed in controlling the rate?
A) Pharmaceutical rate-controlling agents
B) Synchronized Cardioversion
Rate-Controlling Agents:
We need to slow our patient’s heart rate. But what is the goal HR?
The RACE-II trial demonstrated lenient BP control (HR <110) was noninferior to tight BP control (<80) in preventing major adverse cardiac events.
There are many rate-controlling agents to choose from, but Metoprolol and Diltiazem are our two first line agents. We’ll dive deeper into different options for rapid atrial fibrillation and atrial flutter in a future post.
For now, just know that Diltiazem is the preferred 1st-line agent- as recent meta-analyses have demonstrated Diltiazem achieves rate control faster, more effectively, and with the same incidence of hypotension and bradycardia as metoprolol
We attempted rate control with 0.25 mg/kg IV Diltiazem along with 60 mg PO Diltiazem with no improvement of HR or BP
We then gave 0.35 mg/kg IV Diltiazem with temporary improvement of HR to 140s and BP to 110/70. However, the rate again returned to 180 and BP decreased a few minutes later.
At this point, EP and CCU were consulted. EP advised against synchronized cardioversion in ED, as they planned for TEE-guided cardioversion vs ablation in the AM. CCU recommended additional doses of IV Diltiazem and giving digoxin. However, these interventions did not improve the patient’s HR and she was admitted to CCU.
This 2022 meta-analysis concluded: “Intravenous diltiazem is associated with increased achievement of rate control target in patients with AF-RVR compared to metoprolol, while both medications are associated with similar incidence of hypotension and bradycardia”
Take-Home Points:
When a tachycardic patient presents to your ED, ask:
Is the patient stable or unstable
If stable, are the QRS complexes wide or narrow
If the QRS complexes are narrow, is the rhythm regular or irregular?
It can be difficult to distinguish PSVT vs atrial flutter on ECG. Adenosine can be therapeutic for PSVT and diagnostic for Atrial Flutter
If attempting vagal maneuvers, use the modified valsalva
When pushing adenosine, make sure it goes in QUICKLY
If the patient is unstable, perform synchronized cardioversion
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References:
https://wikem.org/wiki/Atrial_fibrillation_with_RVR
https://wikem.org/wiki/Paroxysmal_supraventricular_tachycardia
The REVERT Trial: A Modified Valsalva Maneuver to Convert SVT", REBEL EM blog, September 14, 2015
Sharda SC, Bhatia MS. Comparison of diltiazem and metoprolol for atrial fibrillation with rapid ventricular rate: Systematic review and meta-analysis. Indian Heart J. 2022 Nov-Dec;74(6):494-499. doi: 10.1016/j.ihj.2022.10.195. Epub 2022 Nov 2. PMID: 36334652; PMCID: PMC9773285.
Van Gelder IC, et al. "Lenient versus Strict Rate Control in Patients with Atrial Fibrillation". The New England Journal of Medicine. 2010. 362(15):1363-73.