24 year old male: "Anxiety Attack"

This great case comes from a long time reader who wishes to remain anonymous. As always, details have been changed to protect patient and provider privacy.

You're dispatched on an ALS quick response vehicle by law enforcement requesting EMS to check up on a subject. Dispatch notes indicate officers were called reference a domestic disturbance and have two subjects in custody. A BLS ambulance just around the corner from the call checks on scene and requests ALS continue.

You're directed into a small apartment by an officer and find the BLS crew obtaining vitals from a young man, who appears pale, seated on a couch, uncuffed. The officer says, "he started complaining of chest pain and his hands tingling after we arrested him, might be an anxiety attack. He and his girlfriend really got into it."

You check in with the BLS crew who are obtaining his vitals and introduce yourself to the patient. He looks up at you and simply states, "It's SVT."

One of the crew looks up and nods his head while giving the vitals:

  • Pulse: too fast to count
  • BP: 118/64
  • Resps: 18, unlabored
  • SpO2: 94% r/a, cap refill normal
  • JVD: moderately elevated

A quick assessment is made:

  • Signs and Symptoms: Palpitations and SOB
  • Allergies: None
  • Medications: None
  • PMHx: "I've had SVT a lot, like twice already this month."
  • Last In's and Out's: Dinner
  • Events: verbal altercation with girlfriend

During your exam the BLS crew has placed the patient on the monitor for you:

Happens All the Time Man - Initial Rhythm Strip

As it prints out, you tell one of the officers that he's definitely a patient and will be going with you to the hospital.

A 12-Lead is acquired:

Happens All the Time Man - Initial 12-Lead

  • Is this patient actually in SVT?
  • What is your treatment plan?
  • What sort of medical problems could this patient have?


  • Lee Hart Jr says:

    By the patinet stating he has svt and it has happened twice this month. I would probaby beleive him. I wouls plae th epateint on oxygen and the ask the patient how do you control or stop your svt's. I would consult my protocols and confer with his treament plan and probably transport him while monitor all vtal signs. I would also try to get the pateint to calm/slow his breathing down and see if this resolves the svt issue.If this does not I would strongly consider drug therapy and then maybe inform the patient to get rid of unneeded/enwarranted stimulas that is creating this issue. This would my response

  • Andrew says:

    Oxygen. IV. Attempt vagal manuevers. Adenosine.

  • Paul McKeever says:

    Yep, it looks like an SVT.  However he is stable with it for a heart rate of 180, and he is young, so I am not getting overly concerned at this time.  I'd try and gain more history on his previous episodes, and this one, was there any triggering factor? Did it self revert?  His breathing is fine at 18bpm.
    also try and gain some family history, any heart problems??  Is he a smoker, is he generally fit, what if any other health complaints.  Get some 02 on, get the SA02 a bit higher.  Start with some simple vagal maneuvers, dependent on underlying issue here whether vagal will revert or not.  If  not he is Going to need some adenosine.  This could be left to the ER if transport times are short, as he is otherwise clinically stable.
    whats concerning is his raised JVP.  This could be due to slow filling of the heart, or a possible link with his right side hypertrophy.  Due to the hypertrophy and several episodes now of SVT, raised JVP,  I would start to have a concern about cardiomyopathies.  He certainly needs prompt evaluation at a cardiac centre.

  • Cliff says:

    I think Anxiety attack , just for the fact that BP is unchanged if it was PSVT the BP would have increased .

  • Paul McKeever says:

    Possible cardiomyopathy underlying.
    SVT with ST depression, possibly due to fast heart rate and enlarged ventricle.  Raised JVP due to slow filling time in the right ventricle, or due to hypertrophied ventricle?
    02, simple vagal maneuvers first, followed by adenosine if unsuccessful.  Defo needs an urgent referral to a cardiac specialist as this is his 3rd episode, and now with ECG changes.

  • Paul McKeever says:

    BP would not increase with PSVT, it would drop due to shorter filling times in the heart.  

  • Floyd says:

    I would say svt because it is a relatively regular rate with little variations. Also believe the st depression could be rate related also. Would probably just attempt vagal maneuvers, adenosine and transport.

  • Cliff says:

    I have PAT , after each episode my BP is through the roof , just out of my own experience that i mention the BP .

  • Sksmedic says:

    I would remove him from the situation. Get him away from the police and the girlfriend. Maybe she was caught banging his friends. If that doesn’t change the presentation I would consider other causes. Question the circumstances of the previous episodes of SVT. Did he have SVT secondary to Meth,Bath Salts, Spice? Iwould probably consider benzo’s if this were the case. What is his hydration status? What us his mountain dew to water intake ratio? I am not super worried about a rate of 180 in a 20 something guy with otherwise normal vitals. That being said, i will still be prepared chemically /electrically cardiovert if he becomes unstable. I would attempt vagal maneuvers and fluids and go from there. The important thing here is going to be good assessment and history taking.

  • Paul McKeever says:

    Cliff, your probably not wrong.  Initially as the heart rate increase in SVT you will become hypertensive, but when you have been rattling along for a while at that rate the filling times of the ventricle become shorter, leading to normotensive or hypotensive dependent on age and hydration status.
    it is possible this guy is an athlete, hence the large ventricle, and he's been doing drugs.  Despite that, management remains the same, but be cautious with cardio version as he has just had his dinner.  Would like an anesthetist handy if this was the case!

    • Dwayne Armstrong says:

      And be careful because you mentioned in your statement that he has been doing drugs which is the reason for his heart rate, not a heart issue. Are you going to be able to convert him out of a drug induced rhythm with electricity? Just a thought!

  • Christopher says:

    I would caution against using blood pressure to rule in or rule out a cardiac rhythm.

  • slime says:

    just finished my field internship, in our county we dont carry adenosine for svt, and we only sync cardiovert if they are symptomatic. i wanted to get a perspective on this from some of you guys with experience. would you code 2 or code 3 this patient to the hospital? obviously if it is symptomatic it would be a C3, but this patient, other than o2, iv, and vagal maneuvers, we cant do much else in this county for him. Would it look terrible to bring in a patient to the er c2 who is in an arrhythmia, even though it is asypmtomatic? what about someone who WAS symptomatic, was cardioverted and then in a sinus tach with a good BP. should they be transported c3? hemodynamically stable, but altered due to the versed given for sedation, nice easy ride c2 or c3 due to the severity of the call before interventions. thanks!

  • DevKrev says:

    Does he have WPW?

  • Cliff says:

    Thanks for the info Paul 😉 Forsure BP shouldnt be the only thing to look at and as Christopher said it should be used with caution. In this instance the pax should be treated as PSVT as previous episodes have terminated on their own.Pax stable , so vaguel stim probably more appropriate then drugs. The only people who can really rule out the cause is a Cardiologist or a Cardiac Electro Physiologist.

  • ParamedFred says:

    Young Male…possibly a posterior rt sided M.I…ST dep 2, 3, avf (refractory from somewhere and the lateral leads are depressed)I would initiate a heart alert to the appropriate e.d. I would assess RV4 and if time available do a posterior ECG. In the meantime, IV access, high flow O2, further med or drug abuse hx. Ask him what they did to resolve the situation the 1st and second time that happened to him and then take appropriate action. Priorty 1 transport if Vagal manuevers and bolus IV, O2 did not help. I would be very vigilant on blood pressure. If pt’s blood pressure falls enroute to E.D. I would syncronized cardiovert him but of course attempt benzodiazepine Valium to see if it had any effect in slowing his heart down prior to synchronize cardioverting him. And ultimately of course, contact Med director enroute and notify what when and what actions were done and see if he recommends anything else. As for the patient in SVT, yes he is till he is definitively confirmed at an e.d. He may have A-fib to which he may have been treated for the previous times and may need to have an ablation done to remedy his fast heart.

  • Lance says:

    I spy retrograde P waves in lead III.  Suggestive of AVNRT.  Rule out sympathomimetic overdose, trial bolus of NS, adenosine.

  • robert fielding says:

    Interp: tachydysrhthmia is narrow complex regular rhythm includes st, a flutter, & svt.

    St ruled out by 220-age. A flutter ruled out by absence of flutter waves. Svt highly probable based on retrograde p waves seen in a few leads. Also, another common finding in svt is st depression which is sometimes referred to as rate related ischemia. “This abnormality is not a reliable indicator of ischemia and does not reproduce during exercise.” (From Dr amal mattus book ecg for emergency physicians)

  • Paul says:

    With slight hesitation, I am calling this atrial flutter with 1:1 possibly 2:1 conduction. Leads III and AvF provide the most convincing evidence of this. The T waves have the same downsloping as the ST segment just prior to them. Additionally, abnormalities originating at the initiation of the T wave, are seen throughout this 12-lead.

    In any case, atrial flutter is BY DEFINITION, an SVT. IV -> NS/LR Bolus(at any point during this) -> Right-sided 12-Lead -> Adenocard -> Diltiazem or Metoprolol -> Sedate and Cardiovert. (Preferably with maybe 8-10mg of Etomidate and 5-7mg of Ketamine, or just a hearty dose of Fentanyl since this is a very stable patient, but use whatever is available to you.)

    I would not even think of giving amiodarone, as this patient’s EKG is not suggestive of anything that would benefit from amiodarone administration. Additionally, I would be very leery of giving a medication with a half-life of 158 days to any patient, unless I was absolutely convinced it was necessary, and all other pharmacological therapies had failed.

  • Christopher says:

    That should definitely be on our mind, however, it would not change our initial treatment in this patient.

  • Christopher says:

    Thank you for bringing up what I feel to be one of the most underappreciated problems with amiodarone: it's ridiculously long half-life!

  • deezy says:

    Implying that emotions can trigger a heart rate of 200?
    No, more like 100-130.

  • Paul says:

    Thank you Christopher. I am not a fan of amiodarone at all, because of its multi-organ toxicity, as well as its ridiculously long half life. I am also of the opinion that it causes dementia, based on the fact that it is so toxic, it stores itself in fat for up to 158 days even after a patient only receiving one dose of the medication. That said, the brain is 50 percent fat by composition. Given the above information, I feel it a reasonable conclusion that amiodarone would cause neurogenic toxicity.

    Back to the topic at hand… There are much better medications such as lidocaine(for VT), procainamide, sotalol, metoprolol, and even diltiazem, that could and should be administered to this stable patient, without the risk of making a relatively healthy 20-something year old, a dialysis patient.

    The reason I mentioned a fluid bolus is to increase preload(LVEDV) and perfusion to the heart to see if that would have any effect, prior to dumping meds into a 24 year old patient, and potentially making him a cardiac cripple. Decreased perfusion can cause arrhythmias, and when combined with catecholamine surge from the argument, is a perfectly plausible reason for this arrhythmia.

    In any case, a liter of NS/LR will have the least potential side effects, compared to all of the other options. Failing that, I would proceed as I have outlined above.

  • Oliver Hawksby says:

    Paul – do you have any references for your belief regarding amiodarone and dementia? I can find 3 case reports regarding its use over several days causing delirium which cleared after cessation of the amiodarone but none of it causing dementia.

  • Jason says:

    He is clearly having an MI. ST depression and elevation.

    ASA, Nitro, Morphine, O2

    • Christopher Watford says:

      This ECG may have depression and elevation, however, these changes are not consistent with a coronary artery occlusion. Instead, these changes are secondary to increased demand on the myocardium due to the markedly elevated rate.

  • Moe.morrison says:

    Yes, svt. Slow it down, check for MI.
    Are those not peaked T waves in the precordial leads as well?

  • Mike says:

    Some of the assessments and treatments don’t seem to follow evidence-based medicine. First and foremost, there is no STEMI on this EKG. With a HR of 180, there won’t be “normal” repolarization of the ventricles and any suggestion of T-wave abnormalities is premature until the patient can be converted into a normal rhythm. As others have already pointed out, any ST-T wave changes are secondary to the rapid HR, not likely primary changes from coronary artery disease. Furthermore, any patient under the age of 35 is highly unlikely to be having an MI. So let’s focus on more likely causes for the patient’s presentation.

    Based on the patient’s history, physical exam, age of patient, and EKG, this appears to be a classic case of SVT. We could consider both a rapid AFIB too fast to notice any irregularities, a sinus tachycardia (remember a max HR is = 220 – patient’s age [in years], so it could be sinus in origin for this patient) or an SVT. AFIB is unlikely in this patient without a history of such, and sinus tachycardia is unlikely due to the patient’s lack of exertion when assessed by EMS. Add in the patient telling EMS that he has “SVT”, the stronger case supports this clinical impression. BP alone will not be able to rule in or out any of these. I’m glad to see a 12-lead EKG was performed before any further treatment. Since the patient doesn’t appear to be in acute distress or poor mentation, we can take some time to fully assess the electrical disturbance of the patient’s heart. With an SPO2 of 94%, please don’t apply O2 to this patient. More and more evidence suggests that supplemental O2 is unnecessary with adequate oxygen saturation measurements and in some cases may be detrimental, such as in an AMI (recent study: http://www.theage.com.au/victoria/oxygen-damaging-for-heart-attack-patients-study-says-20141120-11qgzl.html). 12-lead interpretation: without discernable P-waves, I wouldn’t call this sinus (although it COULD be). Regular complexes which are fast and narrow = narrow-complex tachycardia without ectopy and within a normal axis suggestive of SVT.

    It would be very prudent to consider gathering HPI from this patient to screen for toxins (e.g. cocaine), history of thyroid disorders, any history of WPW (which would generally lead us to skip over adenosine), past experiences in treatment for his “SVT” episodes. However, due to the narrow complex of the 12-lead, it doesn’t appear that this patient is conducting through an accessory pathway consistent with WPW. So while he may have WPW, he may not be conducting through those pathways currently.

    First line treatment for SVT would be the least invasive: vagal maneuvers. Ocular pressure and carotid massage can be dangerous in the field setting and shouldn’t be attempted by EMS. The valsalva maneuver may be the simplest and easiest to perform in an adult patient who can obey commands. It’s important, however, to coach the patient clearly and to lay the patient supine in a controlled environment for maximum effectiveness. Should this be ineffective, 6mg Adenocard rapid IV would be the second line treatment. IV should be large bore if possible and as proximal as possible followed by a 10mL NS flush immediately after medication administration. Following AHA recommendations, and not any specific local or regional protocol, a second dose of 12 mg Adenocard rapid IV push would then also be administered with a third dose of 12 mg Adenocard administration if still no change. Consulting medical control after the first dose of 12 mg Adenocard would be prudent and skipping medication treatment altogether might be appropriate in this young, healthy patient, if transport time is < 10 mins.

    Cardioversion with administration of a Benzodiazepine would be a last resort as we are now sedating a patient. While the cardioversion itself would be very safe, compared with many side effects of medications, but uncomfortable for the patient. If the patient's rhythm remains unchanged after Adenocard administrations, re-evaluate the patient and consider an alternative course of treatment for a narrow-complex tachycardia. Be sure the rhythm hasn't changed, or slowed, indicating another underlying rhythm (e.g. AFIB). If still no change in rhythm, another arrhythmic medication may be appropriate, such as Diltiazem (my next choice for narrow-complex tachycardias), Amiodarone (try to avoid due to prolonged half-life), Procainamide (difficult to administer due to drip calculations instead of bolus, depending on comfort and training of course), or perhaps even a Beta-Blocker (in case this really is an AFIB). This may be deferred in lieu of transport if the patient seems to remain stable. Certainly, if at any point in time the patient's mental status declines, be prepared to cardiovert. Emergency cardioversion due to a rapidly decompensating patient would skip over administration of Benzodiazepines, at least until after the successful rhythm conversion.

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