Adenosine given for a narrow-complex tachycardia over 150

This case comes to me from a paramedic trainee. Many elements have been altered to preserve anonymity. In the following, the narrative from the run-form is interspersed with questions that I put to the student afterwards.

I was trying to draw out how a student understood the evaluation and management of tachyarrhythmias. But I don’t think this case should be viewed as a reflection on any one student, preceptor, instructor, or even school.

Rather, I want to use this case to highlight some common beliefs about SVT, and the potential pitfalls. We’re looking for a constructive dialogue in the comments here, so keep it positive!

The Case

Run-Form:

“A 34 year-old male presented to EMS sitting upright in a chair. He was conscious, alert, oriented, states ‘I feel like a garbage truck is on my chest.’ Respirations rapid, pulse rapid and strong. Lungs clear bilaterally with slight shallow breathing. A rhythm strip shows sinus tach at a rate of 150.”

EKG_1

Sinus tachycardia, aprox 150 bpm.

Question 1. At this point, what was your overall impression, given his complaint and his rhythm strip?

Answer 1. “The initial impression was respiratory problem, given the rapid respirations. We noticed the tachycardia on the rhythm strip. At that point we knew we had a potentially unstable patient, but we hadn’t been convinced it was 100% cardiac yet. With the clear bilateral lung sounds we began to lean cardiac. The clinical impression then became a symptomatic SVT.”

Run-Form (cont.):

“Patient transferred to ambulance. BP 153/98, pulse 166, spo2 98% room air. At this time patient states he feels like he is going to pass out, monitor observed to be at a rate of 170.“

Question 2. You noted that the rate was higher at this point. How did this change your impression and treatment plan?

Answer 2 “The increase in rate drove us to a more aggressive treatment because the symptoms grew with the rate. However, we still wanted to try less invasive procedures to break or slow the rhythm to determine if the symptoms were solely from the SVT.”

Run-Form (cont.):

“IV established, and normal saline ran, O2 via nasal cannula. I asked the patient if he has ever been cardioverted, patient states ‘Yes, they gave me some drug that stops my heart in the hospital a couple years ago.’ Vagal maneuvers attempted to lower rate. 12-lead obtained shows sinus tach at 150 now post vagal maneuver.”

ECG_2

Question 3. The vagal maneuver lowered the heart rate. What did this demonstrate to you?

Answer 3 “The vagal maneuvers working for the short period of time drove us further down the SVT treatment plan, with the rhythm being refractory to fluids, O2 and now vagal maneuvers, and with the sudden increase in symptoms we proceeded to adenosine. “

Run-Form (cont.):

“Rate shortly returned to 170, patient began to feel impending doom and stating ‘I’m going to pass out.’ Patient now states constant crushing chest pain at an 8/10. 6 mg adenosine given.“

Question 4. Why was adenosine given? What was the hoped-for effect?

Answer 4 “The impending doom and feeling of passing out, coupled with the now constant crushing chest pain. The adenosine was given with the hope of relieving the symptoms, and breaking to rate to search for a possible underlying cause for this dysrhythmia.”

ECG_3

Pre-adenosine

During adenosine push

During adenosine push

Immediately post-push

Immediately post-push

Run-Form (cont.):

“Constant monitor print showed rate broke for brief period of sinus bradycardia and returned to a rate that did not exceed 135. Patient stated relief of chest pain, now a 5/10, still heavy crushing feeling. Patient no longer feels impending doom and states he no longer feels like he is going to pass out. Post medication 12-lead shows sinus tachycardia at 135.”

ECG_6

Question 5. Last question! Was the adenosine helpful?

Answer 5 “I would have to say yes, the rate decreased and symptoms began to dissipate allowing for the patient to become more comfortable and the impending doom subsided.“

Conclusion

An echocardiogram and CT scan showed that the patient had a massive pulmonary embolus, blocking much of both pulmonary arteries. He had a history of PE and DVT, but was non-adherent with the anticoagulant medication.

Questions:

  1. Was this rhythm a “SVT?”
  2. Were the therapies (vagal maneuver and adenosine) helpful for diagnosis or treatment?
  3. What is the “ACLS approach” to the arrhythmia in this patient?
  4. What would your approach be?

 

26 Comments

  • Andrew Merelman says:

    Relly interesting case presentation that highlights an important problem. That problem is the widespread teaching that any narrow complex rhythm above 150 BPM is “SVT”. The initial rhythm strip does not show SVT. It shows sinus tachycardia at about 150 bpm. All subsequent strips also show sinus tachycardia. It is hard to say whether this patient did have an episode of SVT when his heart rate was reported to have been 170 BPM as there are no strips during this time however, it is unlikely given the clinical information. Sinus tachycardia is almost always a compensatory mechanism for another problem. The ACLS strategy for sinus tachycardia reflects this as they recommend investigating other possible causes. The therapies given including vagal maneuvers, and adenosine were likely not helpful for this patient. This patient’s presentation was suggestive of acute pulmonary embolus, especially with the known history of DVT and PE with medication non-compliance. It is hard to say what my approach would have been as I have not actually seen this patient. However, it likely would have consisted of management, anxiolysis, and treatment of respiratory distress and hypoxia. Thanks for sharing, Brooks!

  • Jeff Garcia says:

    By definition the rate, narrow complex and it being a regular R to R interval it is considered SVT of an unknown etiology. After reading the run form I believe what would have been more helpful in suspecting this rhythm to truly be of a cardiac origin would have been a thorough history gathering and an OPQRST of the pressure/pain. Not saying it wasn’t done but it’s not documented for the reader. My approach would be to add a more in depth history and present illness assessment, have a high index of suspicion this could very well be cardiac, put the pt in as high priority considering his past medical hx. Reduce anxiety as mch as possible place pt in POC, 02 via NC titrated for adequate perfusion, cardiac monitor, 12 lead, secondary to rule out infection, temp, sores, sepsis, and so on. Venous access, fluid bolus, depending on transport time to closest facility consider adenosine. Consult an MD to address suspicion of PE vs cardiac. And to add I honestly believe Id try a vagal maneuver. Without being on that call and seeing the Pt this is my attempt to appropriately tx this pt.

    • I agree that it is narrow complex, with regular R-R intervals, and tachycardia. But this has another feature – it’s a SINUS tachycardia. Does it seem reasonable to give adenosine, or try vagal maneuvers, with a sinus rhythm?

  • Anthony Savarese says:

    The common criteria taught for SVT, faulty as it is, is a heart rate of 150/min with the absence of p waves. We can debate the faults or benefits of the simplicity of this definition another time. But I think the p-student, for a variety of possible reasons got some tunnel vision in his/her diagnosis. While I’m reading the run excerpts the given pulse or heart rates (?), aren’t really corresponding to what’s seen on the EKG. There seem to be distinctive p waves and the rates hovering under 150. So like or hate that definition, it didn’t quite meet that. I don’t know of any outright harm, of adenosine or Vagal maneuvers in this siuation (I’m sure I can look up something, nothing is without negative potential), but if the sinus tach were clearly identified it would have been a moot point to go further down the wrong road, searching for more clues for something not there, which could possibly lead to more harm than just time wasted.
    Irregardless of the EKG, I think this seems to be a case of seeing the tree not the forest. If the student saw the bark, they would have seen the sinus tach, but instead they saw the tree a fast rhythm and pt with some S/Sx of a cardiac etiology. If they saw the forest, they would have saw a bunch of other differentials, including PE. Some patients omit history conveniently, to the chagrin of the clinician, and often to their own detriment. Perhaps if they said DVT and pulmonary emboli, or disclosed meds it would have opened another door. Instead the pt only recalled prior rhythm mgmt, which only further led down the wrong path (taking the patient’s self diagnosis and running with it).

    It’s no condemnation to any preceptor, student, or program, because this issue is a matter of perspective when faced with an emergent challenging patient, to try to keep perspective. In fairness this happens to providers of all levels in EM at times. It comes down to training that stresses avoiding preconceptions and combatting complacency and running auto pilot. Bottom line it’s an education issue; and something with my own perspective is neglected to be addressed in much of EMS education.

  • Nate Murray says:

    Let’s not forget that the “SVT” that we give adenosine for is a re entrant circuit phenomenon. This means that the variation in rate throughout the call rules out an adenosine sensitive etiology of the patient’s complaint. I teach new medics to give a liter of fluids first for suspected SVT and only continued down the stable SVT pathway if the rate stays exactly the same. Helps avoid these types of issues…

    • ADunn says:

      I have been a medic for 18 years, seeing a rhythm rate of 170/180 as stated would have me administering adenocard also. However it sounds like by the time they were ready to do that, he was back down to 150’s. The change in rates throughout the call is an excellent point that I would have tunneled away from. Thank you for bringing that up.

  • Natalie says:

    Anyone else ever learn 220 minus the pts age is the top limit of a sinus tach. Anything over is SVT. Not to say anything below isn’t but ruling out anything that could potentially cause a reg sinus tach vs SVT should be considered. So this guy was 35 if I recall. So 220-35 is 185. So up to 185 can be considered just a sinus tach. This guy even at 170 hr would allow him to fall into this category.

    • Katie says:

      The 220-age equation is use for max heart rate. This patients max heart rate would be 185 not the limit of his sinus tach. The equation has + or – 12 beats per minute of error so it isn’t the best equation but I have never seen it used for anything other than estimating heart rate max.

  • Will Roberts says:

    I’m just going to ask this. When I looked at the final 12 lead this is what I see. Lead I I see very slight ST elevation (nothing to cry home to mom about or scream STEMI) in lead III I see a prominent Q wave and flattened T wave present along with a low voltage QRS. The axis is normal. Good R wave progression in precordial leads. So with the ecg revealing what I think is a q1 s3 t3 (on the fence because there really wasn’t T wave inversion however there was some flattening of the T wave) What is the sensitivity and specificity of that finding? And if I’m over analyzing I apologize and feel free to correct me. thanks 😀

  • Brad says:

    Versed is helpful in calming patients that all they can think is “I’m going to die”. Calm them and properly assess afterwards.

  • dan says:

    I was always taught that svt was greater than 160 but regardless, I would have been looking for another reason for the tachycardia. An increase of rate from 150 to 170 post movement would not concern nor surprise me considering the exertion on the patient during movement. Also we must not forget about the anxiety factor from a patient who feels like he is going to die.

    One concern regarding treat is the description of a classic MI but no treatment for ACS. Was the potential for a non ST elevation MI considered?

    One thing I always teach new medics is that criteria is set because there has to me a something that defines a condition. Is a heart rate of 149 less important than a rate of 151? Look at your patient, consider all possibilities, make a decision, then prove yourself right. Don’t be afraid to change course if what you thought should happen isn’t happening or if the evidence no longer supports your conclusion.

    This crew did nothing wrong, but I think their inexperience allowed them to rely on what the book says and they followed that algorithm. Which, is what they are supposed to do.

  • Charlie says:

    SVT aren’t always “reentrant” in nature-atrial rhythms that are rapid and may have a rapid ventricular response are SVTs with problem(s) concerning automaticity not reentry. ACLS guidelines would have clinician attempt to correct the rate first and foremost, assuming any clinical presentation/symptomology is of a cardiac origin. The question is of stability, or lack thereof. This patient’s system is compensating initially. Vagas maneuvers (mechanical intervention) are always the initial tx for symptomatic tachycardias. If not successful then the next option is adenosine (chemical intervention) at the initial 6 mg dose. Depending on the patient’s stability the next option would be cardioversion (electrical intervention). If vitals are stable then a second dose of adenosine at 12mg can be attempted. The key to managing the PE patient pre-hospital is doing everything you can to find out it’s a PE first. Then it’s O2, IV, monitor (12 lead, too), and…. diesel bolus! This patient’s hx and overall presentation is high risk of PE. But, ACLS was followed well.

  • Gene Iannuzzi says:

    I agree with all who stated that this was indeed a sinus tach and thus adenosine was not indicated. What I think was happening is that the providers fell into the trap of treating the monitor rather than the patient, in the sense that the question of what might be causing the rapid rate was never really answered. My question to medic students is always “is the rate causing the problem or is the problem causing the rate”, and in this case the latter was true. Dont know what the patient said during the history, and we know they often change their tune, but the DVT and PE should have been red flags, as well as the non comliance with meds issue. I’m also wondering if more than one pulse oximetry reading was documented and if so, was there a downward trend, which might have been another tip off. Again, no intent to dump on any of these folks, just observations to contribute to the discussion.

    • Pam says:

      I agree that the monitor strip shows sinus tach. I think everyone should ask their self the questions is the rate causing the problem of is the problem causing the rate. We all need to look at this on every call. Maybe the patient’s anxiousness was due to the crew’s anxiousness.

  • Nile Barnes says:

    So a couple of things jump out. 1) whenever I hear rate 150, I think Aflutter…. this is quickly ruled out, but flutter waves are typically at 300 bpm so a 1:1 Aflutter would have a ventricular rate of 150. 2) this is a variable rate, it is NOT an AVNRT, therefore adenosine is not going to break any reentry pattern and allow a sinus pattern to emerge. In fact, every strip I see shows p waves. AVNRTs have a reentry circuit. The rate will remain the same in AVNRTs, despite movement, fluid status, anxiety or other sympathetic or parasympathetic input.

  • Chris says:

    Crushing chest pains, dyspnea, near syncope. This would equal an AMS protocol in my system. 12 lead, Aspirin, nitro.

  • Josh says:

    I was wondering why nobody thought about asa, nitro, 02 and then everything else. The guy is complaining of crushing chest pain…

  • BT says:

    Chest Pain call straight up…rate not high enough IMO to warrant SVT therapy. Should be worked per CP protocol

  • Terry says:

    Why hasn’t there been any mention of oxymetry? Wouldn’t hypoxia with adequate respirations and clear lung sounds be an indication of a PE?

  • Terry says:

    Sorry… I didn’t see the SpO2 reading!

  • John says:

    If things such as Sepsis, Drug Use, Medication issues, Anxiety, Pain, etc.. have been ruled out, and the rate is still >160 (or whatever number you use). How else do you determine S-Tach Vs. SVT? Does a 12 Lead Help (QRS Complexes facing different directions due to different pathways etc..) or a simple 4 Lead? If there is a P-Wave does that automatically rule out SVT?

  • Joe says:

    The initial impression of this pt, to me, is not immediately of a PE (besides that tachycardia and shallow, rapid breathing). It’s at the end of the case that we learn that pt experienced a PE that was “blocking much of both pulmonary arteries”. Pt is complaining of CP, near syncope, tachycardia, tachypnea, shallow breathing. As providers, how do we know that the rate of ~150 is not symptomatic for this pt? The pt has a hx of being administered adenosine and obviously the administration of Adenosine relieved a lot of the symptoms. But, If you truly followed ACLS guidelines for Adult Tachycardia (with pulse), whether you personally say it’s Sinus Tach or PSVT, this Paramedic student did the right thing in administering Adenosine. Instead of just sitting there trying to figure out why the pt is tachycardic, the student administered Adenosine based on the pt’s hx, vital signs, 12 lead, presentation. Would you administer D50 to a pt with AMS and a BGL of 60? For the majority of the other people who posted on here, it sounds like they would have not administered Adenosine and let the pt keep experiencing crushing CP, tachycardia, tachypnea, shallow breathing all because of a number.

  • Ian B says:

    This was never SVT. Too many students are taught that SVT is a number (HR>150) and not that it has anything to do with absent P waves or other underlying conditions. There are many other options to consider before you call a fast sinus rhythm an intrinsic cardiac issue and begin down the ACLS pathway.

    The transient vagal response slowing the heart rate should have clued you in that this was NOT a cardiac issue (SVT). Vagal maneuvers should either break the rhythm or do nothing (personally I have never seen vagal maneuver transiently slow a true SVT, even in PTs that know they have it and can vagal themselves).

    Technically speaking, you could have tried Edison before medicine due to “ischemic chest discomfort”. However, the ACLS protocol was followed since this is a “regular, narrow complex” rhythm. As stated previously, I would not define this a tachydysrhythmia – it is sinus tach – sinus tach has extrinsic causes that must be considered and corrected first. Adenosine was inappropriate.

    While the PTs vitals and EKG do not show many of the expected signs of a PE, a better history (from a cooperative PT) would clearly help. Hearing blood thinners from a 35yo would definitely clue you in to a PE/DVT issue. However, given HR>100, Q3 (though generally isoelectric, lead III has a Q wave), severe chest discomfort, med noncompliance, rapid shallow breathing – first impression is respiratory.

  • Tommy says:

    PE was tricky as a ddx being that pt was RA 98%. Someone on this thread used the looking at the tree instead of the forest example, great analogy! My interpretation was that this was SVT, and adenosine was not a bad option, it did relieved pt symptoms. However, the heart was not the problem, and how would one know out in the field if it’s PE or not? So I would give the trainee credit for following his gut!

  • Iliyas says:

    S.tachycrdia
    T wave inversion in lead v1 to v3
    That leads to thinking over P.E

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