57 year old male: Chest Discomfort

The following is a great case from Mordy E, and as always some details have been changed to protect patient privacy.

You and your partner are refueling your ambulance at a gas station when a woman walks up and asks if you could, "come check out my husband."

As you walk over to their car she states that, "he's had chest pain for almost 5 hours now and didn't want me to call 911."

Your patient is standing, pumping gasoline, and appears unwell and diaphoretic. He seems reluctant to accept care at first, but you encourage him to let you check him out and he admits to chest discomfort.

He sits down in the passenger seat and lets you evaluate him.

  • Onset: 5 hours ago
  • Provocation/Palliation: nothing makes it better or worse
  • Quality: "pressure"
  • Radiation: "to my jaw"
  • Severity: "it isn't that bad"
  • Timing: constant

Your partner puts the monitor on the back seat and places electrodes while you get a set of vitals.

  • Pulse: 150, weak at the radials
  • BP: 102/68
  • Resps: 22, unlabored, clear bilaterally
  • SpO2: 94% r/a

As the initial rhythm strip prints and your partner places electrodes for a 12-Lead, you get a quick medical history.

  • PMHx: hypertension, hyperlipidemia, palpitations
  • Meds: "some pressure medication"
  • Allergies: seasonal allergies, NKDA
  • Last In's/Out's: breakfast
  • Events: sudden onset of chest discomfort which woke him up this morning

Your partner hands you the rhythm strip and leaves to grab the stretcher as the 12-Lead prints.

Round and Round He Goes - Initial Rhythm

You tear off the 12-Lead and the patient asks, "well, is something wrong with my heart?"

Round and Round He Goes - Initial 12-Lead

Your partner places the stretcher in front of the patient and says, "yessir, your heart is going too fast. Let's get you on our cot and into the back of our office so we can do something about that."

As you wheel the patient to the unit, your partner asks:

  • What is our patient's rhythm?
  • What did the 12-Lead show?
  • How should we treat this patient?

71 Comments

  • Nick Adams says:

    Sudden onset. Rate approximately 150. aVR and lead I is highly suspicious for a 2:1 A-Flutter. Treatment would be O2 @ 2 lpm, IV, 0.25mg/kg of Cardizem IVP (slow) to reduce rate and improve CO and therefore symptoms.

  • JCMedic says:

    Alright. Somewhat new medic here. I see a narrow complex tachycardia. Rate seems a little low for true SVT and there does appear to be some irregularity to it but it is too fast to be sure that it is Afib with RVR. I’d call it SVT at this point. Story fits for SVT as well. I’d like some O2, IV with bolus, 6mg Adenosine and watch for the underlying rhythm.

  • MSToflinski says:

    Rate is to slow for SVT, however I would have patient try to bear down to correct rate. I would start a line for fluids. 12-lead show elevation in v3 and v4, I would classify this as a STEMI and get patient to proper closest hospital. I would treat patient with how they present.

  • JHAEMT says:

    Not a medic, but ill give it a shot.  I don't see any p-waves and isn't quite fast enough to be an SVT, so rapid a-fib.  I'd try a 500cc bolus (boarderline hypotension) and O2 . If that doesnt work cardizem drip.

  • Kim says:

    This has been going on too long, he has had a sudden on set, the time is to long to try to convert without  the cathlab on site with you. I see some ischema in the limb leads shows that damage has occured.  Hosptial with fluids and pain control monitor blood pressure, it is ready to fall, convert quickly if pt goes unconscious, be ready.  Always treat the patients symptoms

  • DevKrev says:

    rhythm: SVT
    12-lead: non-diagnostic for stemi, wouldn't expect it for this timeline. No P-waves though, I would try to measure R-R and see how regular it is. It looks like there are J-waves though, especially noticable in lead II and V5, maybe.
    treatment: No rate control, the guy was pumping gas, lie him down and see if his rate/pressure improves. IV with Labs, 324 mg PO ASA, monitor, transport.
    This guy is obviously okay enough to eat breakfast/leave the house/pump gas, so at this point I'm just going to take a wait and see approach.

  • Francis says:

    I am not a medic but I will give this a shot as well. Looks like either rapid afib or sinus tach. I leaning towards rapid afib with the possibility of this becoming a STEMI. Treatment can be IV cardizem adenosein or Amioderone. Transport asap and at monitor ECG every five to ten minutes and monitor vitals every five minutes. Pt appears stable but light not sirens to the ER.

  • Terry says:

    Treat the patient, not the monitor.  Patient appears "unwell and diaphoretic," and has pain (pressure) radiating to the jaw.  I agree with DevKrev about the J waves in II and V5, and possibly in V2 – V4, but not sure that is our problem yet.  You also have possible ST elevation in V1 – V4 as well as peaked T's in V2 – V4.  Patient needs to get to the hospital now for further evaluation, if nothing else, for the rapid heart rate.  All chest pain treated as an MI until proven otherwise, so going with an Antero-Septal Infarct for now, no STEMI activation, but early report to receiving hospital.  Patient has a history of hyperlipidemia and hypertension which definitely could lead to cardiac problems.

  • Christopher says:

    Terry,
    Let's give up the tired dogma of "treat the patient, not the monitor." This is an educational site.

  • Medicts says:

    The rhythm is an SVT, more specifically an AVNRT (slow-fast channel, which is the most common)  Typically, these origonate following an APB. However, we are not able to see the onset in this ECG. As the impulse travels in a circular motion down the slow channel and back up the the fast channel in the AV node, it not only causes depolarization of the ventricles, it depolarized (retrograde) the atria. This continues in a cyclic manner causing the simultanious depolarization of both chambers resulting in the tachycardia.  If you look at several of the QRS complexes you can see what is called a pseudo BBB, and pseudo q wave as a result of the P wave at the end of the QRS.
    It is sad how many so call advanced practitioners out there lack not only clinical judgement but  practice in black and white (treat the pt , not the monitor). This pt could have significant disease reducing his ability to deal with this borderline rate. Typically we treat the rhythm before the pain, but this is based on the clinical picture or totallity of circumstance. See how many responding to this ECG have very little understanding and simply throw out uneducated guesses.  This is why physicians and Nurses dont have the respect for Paramedics that is deserved  . Reading and learning continues after medic school.

  • NinjaMedic says:

    Christopher,

    Terry is correct even though you may call it dogma. As an educational site, we need to remind our practitioners to do exactly that, treat the pt.

  • Christopher says:

    NinjaMedic,
    We learn nothing by espousing "treat the patient, not the monitor." We're here to learn to interpret ECG's. I'd prefer the discussion surround the rhythm interpretation, 12-Lead interpretation, and treatment plan for the patient.

  • Christopher says:

    JCMedic,
    Usually the rate for AF w/ RVR will be variable on the monitor. In this case we can march out the R-R intervals with relative ease and we see that they are drop dead regular.

  • NinjaMedic says:

    I agree with Medicts. This is exactly why we don’t have the respect we deserve. Honestly I could care less of the nurses respect us, but to gain the respect of physicians would advance our profession greatly.

  • Christopher says:

    JHAEMT,
    The rhythm itself is drop dead regular. If you count the little or big boxes between the R-waves, you'll find that it is at almost exactly 150 beats per minute. This excludes atrial fibrillation.

  • Christopher says:

    DevKrev,
    The wait and see approach with this patient may certainly be appropriate given the scenario. Especially if they seem to be maintaining their hemodynamics and have an uncertain rhythm/etiology.
    However, in this case you have a field diagnosis of the rhythm; so what would your treatment plan be if you elected to treat him?

  • Hugh says:

    I see a narrow complex tachycardia here with a regular rhythm at just about 150 bpm, which is a little bit slow for me to be jumping onto the adenosine and is too regular to really be a-fib. He's definitely sick I'm just not sure that it's SVT territory. Large IV 18ga or so and dump 500 cc fluid bolus see if that helps to bring the rate down. even if he isn't showing classic STEMI his S&S is concerning for pretty classic cardiac trouble so probably ASA 324 PO and some O2, say 6 lpm via NC. I think the elevations in V2-V4 are probably early repolarization when you consider them in conjuction with the lateral J wave like deflections at the end of the QRS complex (I,II, V5) rather than a true STEMI. If the fluid doesn't do anything to help bring the heart rate down maybe I'll start thinking about the adenosine.

  • Adam says:

    @Christopher I'm going to support Terry on this one I think that "dogma" is very important and we tend to get too zoned in on our toys.
    I see this patient as a symptomatic (two or more S/S) SVT with a rate of ~150. Treatment: O2, IV (proximal), Vagal Manuver (strip printing), if no conversion>, Adenosine 6mg Rapid IV push, If no slowing again @ 12, If it slows and shows Aflut then cardizem 20mg slow IVP, Another 12 Lead, Continue to appropriate facility. I do NOT see the STEMI criteria as the elevation in V3 & V4 are only a single MM elevated not two MM, but it certainly could have caused an MI or be caused by an MI. So if after the rate is slowed he still has cx pn/sob I would treat as an AMI.

  • Christopher says:

    Medicts,
    The great part about a site like this is you can get better at rhythm interpretation without worrying about affecting an actual patient. Getting the diagnosis wrong here and learning from it allows you to get it right when you see it in the field.

  • Christopher says:

    Hugh,
    Outside of cardiogenic shock or atrial fibrillation with RVR, it is rare to see a STEMI with marked tachycardia.

  • Christopher says:

    Adam,
    I don't see how that dogma helps anyone interpret this ECG :-) Regardless, your diagnosis and treatment plan is quite reasonable.

  • I agree with Christopher that the phase "treat the patient, not the monitor" should be permanently retired and put out to pasture.  For those who are determined to cling on to that statement, I offer up Dr. Ken Grauer's insights that he posted for a previous blog on this website back on May 19th of this year.  He provided a modified version of it.  

    Ken Grauer says:  Perhaps an even better way to say it is, "Treat the patient IN THE CONTEXT OF the monitor". By "treating the patient" – what really is implied is "the whole patient" (with presumption to the thinking clinician that this DOES include the rhythm on the monitor/ECG as well as what the patient 'looks like' ). To ensure optimal thinking by clinicians – perhaps spelling it out by adding "in the context" may help.

  • David Baumrind says:

    I will just add my 2 cents…

    1- On an educational site like this, we improve by attempting to interpret things we do not yet understand. That is the point of this learning exercise. It is not about trying to impress anybody. ALL are encouraged to participate in a constructive way.

    2- There is no room for dogma here. "Treat the patient not the monitor" is not helpful here, as i have written before in posts. There are many causes of chest pain. Many of these causes can be discovered by skillful interpetation of 12 leads. They are certainly NOT all due to MI, and to treat them all as such does your patient no favors. Of course we always assess our patients… but we also integrate our ECG interpretation into our clinical picture to develop the most beneficial treatment plan for our patients.

    Thanks for participating!

  • DevKrev says:

    @Christopher…
    I would "treat the patient, not the monitor" :P
    Depending on what his rate/BP did once supine, I would probably treat his SVT with 5 mg of metoprolol very slow IVP q 5 minutes x 3(or less) PRN. Hopefully that helps with his chest pain.

  • Canmedic says:

    SVT. O2 and 18G AC IV @tkvo. Cardioversion as pt is unstable (chest pain). Other tx as needed depending on cardioversion outcome. Rapid transport.

  • Michelle says:

    It looks too regular for A-Fib. I'm not seeing any P waves but thought that in a couple of the complexes the P's may have been "swallowed" by the T's (possible 1st degree block??). The fact that it's a sudden onset and has been going on for 5 hours with nothing helping and radiation to his jaw, he has HTN but now it's borderline low (Either his BP meds are working too well or he's getting some cardiogenic shock going & I'm going with shock), his O2 sat is too low for my liking too, Let's put him on 15 lpm NRB, 18g or better in the AC with a blood draw, vagal manuvers to see if we can slow the rate a bit, NS bolus to get his pressure up a bit. I am not seeing any ST elevation but that doesn't rule out MI, so I'd consider ASA and probably even a nitro spray if pressure stays above 90 & no contraindications. If the vagals help we'll try to maintain that and get to ER.

  • DevKrev,

    I find the choice of metoprolol interesting in the context of suspected SVT. Is this a protocol based choice? I ask only because the top causes of SVT are more readily and safely terminated with adenosine.

  • cwood says:

    Hello I'm a frequent observer first time follower and a medic in IDPH region 4 in Illinois… Seeing the SVT rhytmn, obviously follow the alogrithm for that.
    1) ECC (O2/IV/)
    2) Vagal if no change
    3) 6/12/12 Adeonsine if no change
    Diesel injection to hospital and alert receiving hospital asap
     

  • Michelle,

    It seems prudent to consider sinus tachycardia and a 1st degree AVB as this patient's rate could potentially be sinus in origin. Are there any safe treatments we could provide to differentiate sinus tachycardia?

  • jon says:

    Sinus tachycardia-some p waves are visible on preceding T wave.
    Would not call this a STEMI without enzymes but there is some elevation noted in anterior leads.
    O2 2lpm, ASA,IV,fluid bolus,nitro trial. If pt doesn’t respond to above,then rate control.

  • DevKrev says:

    @Christopher…
    Good Point…I guess I should start with adenosine. But if I had to move to rate control I would choose metoprolol, given the soft pressure and being prescribed "some pressure medication" which probably isn't Cardizem.
    Speaking of protocols…for tachycardia mine don't kick in until HR is greater than 150, so I would be working in a protocol grey area with this case.
     

  • DevKrev says:

    I guess in my choice to stay away from Cardizem, I skipped Adenosine. I guess it would be prudent to start with that.
    Speaking of protocols, mine for tachycardia don't start until HR is greater than 150, so I would be in a somewhat protocol gray area anyway.

  • Hugh says:

    @Christopher
    I didn't mean to imply that there was evidence of a STEMI here I was looking for evidence against it in fact. Also, if we say that this rhythm is in that AV reentrant tachy range is it possible that those deflections at the end of the QRS complex could be retrograde conductions of P waves conducting back up the slow pathway of the AV node? I don't see P wave preceeding most QRS to my thought is that there could be a 1 degree AVB (as a few others have mentioned) or retrograde conduction of P waves.

  • Nick Adams says:

    WOW……………I am really concerned with all the comments about treating the pt and not the monitor. In order to treat the patient, you have to do a good physical exam to include all your toys…..and pt history……come to a conclusion as to what is going on…..and then provide the best treatment within your ability in the best interests or the patient. This is done by treating the patient AND the monitor. You can’t just treat the patient without a monitor….those days are gone long ago. A pt who is stable who has a potentially unstable rhythm….may not be stable if you wait….then you’re chasing your tail. If you go by the signs and symptoms……….the pt is not stable and should be cardioverted….if you want to be text book about it. Are we gonna do that?…….I hope you don’t.

  • Hugh,

    I was just tacking on to what you were saying, as you brought up good points!

  • Hugh says:

    Christopher,
    Oh, okay. glad to know I was thinking in the right direction then, or at least not totally off base.

  • DevKrev,

    I count out 15 complexes in 6 seconds on the rhythm strip, which is close enough to 150 for me! Keep in mind the monitor counts / miscounts any deflection and keeps a running average. I would put the monitor's count within +/- 5 bpm of the actual rate, depending on the baseline and the size of the complexes.

    As always, protocols exist as guidelines. We use our best judgement when dealing in the gray areas. Dr. Brent Meyers of Wake County refers to protocols as the "foundations of care," with education, experience, clinical judgement, and medical control used to fill in the blanks!

  • Jason R says:

    @ Michelle:  is it in your protocols to use flush O2 for a pt w/an SpO2 of 94% @ RA?  I am sking only because I would use 2-4 L/min via NC if I did anything other than monitor this vital.  We use 94-99% as our target.  Granted, this pt is @ the bottom of that range but and needs to have this vital, among many others, closely monitored but, in my opinion, does not need flush O2.
     
    For the Strip, the rate puts it is the "judgement call" zone which os what we are trained and paid for.  I am going w/SVT: 1) 2-4 L/min O2 via NC, 2) Vasalva while on monitor, 3) if no improvement Adenosine 6, 12, 12  rapid IVP.    Ideally, we will have been administering the tried and true "high flow diesel treatment"  while working through this algorithm and will be arriving shortly @ definitive care.

  • Bryan L says:

    wouldthe lewis lead be helpful in differentiation of Sinus Tachycardia/Atrial flutter/SVT?

  • Dane Wallace says:

    Rhythm Interpretation: High conduction ratio A-flutter. (my differential is Sinus Tach).  There is borderline ST segment elevation in V2 and V3.
    Treatment:  O2 @ 4lpm via NC. IV with NS fluid bolus. Vagal maneuver trial. ASA 324mg PO. NTG 400mcg trial.  Consider Cardizem 0.25mg/kg. Transport to nearest hospital.  Repeat 12-Lead for serial changes and consider diversion to PCI lab if serial EKG bear out true STEMI.
     

  • Adam says:

    @Jason R, I tend to agree with the High flow O2 for a patient with a cardiac problem. Normally my goal is greater than 92% but if its a patient who can benifit from "loading the boat" ie making sure every hemoglobin has 100% of its capacity used w/ O2 I do it. Since this patient has a significant potential for an AMI I would be loading the boat. Just my two cents since Sat monitors only tell you what percentage of hemoglobin have a O2 molecule on them not if those hemoglobin are full.
    @ those of you discussing the dogma here is my point. I had a partner who mis-interpreted an EKG and freaked out was starting to head down the path of calcium channel blockers then a U turn and antidysrhythmics when the patients VS and symptoms had not changed. I agree you need to "use all your toys," but be aware your toys can be wrong. For the record the EKG was artifact w/ an underlying of NSR/SB. This can be avoided w/ proper training and experience.

  • Adam says:

    @ Bryan Adenosine used as a diagnostic tool can help with the interpretation aflut vs SVT.

  • woody says:

    Oxygen 2 ltr/min, start i.v., 500 ml cristalline, 2.5 to 5 mg metoprolol i.v. maybe some morphine i.v. if there is no pain relief , transport to hospital, no need for immediate pci

  • FB says:

    Chris, thank you for a lot of your responses. If this is SVT or A-Flutter, I think that metoprolol or diltiazem are very appropriate (especially if you are leaning towards a-flutter). Adenosine looks like it feels horrible for the patient. I agree that it is probably the safest but since we don't have an irregular, wide complex rhythm, and it is regular without p-waves at a rate of 150, it might be worth assuming this is flutter and skip the adenosine? 

  • FB,

    You prefer adenosine first line in this case as we might actually be looking at sinus tachycardia! Giving a B-blocker or Ca-channel blocker to a patient with a compensatory sinus tachycardia is likely to be far more detrimental than a transient response to adenosine.

    If adenosine breaks the tachycardia, we likely had AVNRT or AVRT (maybe junctional tachycardia). B-blockers and Ca-channel blockers will be unnecessary.

    If adenosine shows excess P'-waves or F-waves, we likely have an ectopic atrial rhythm or atrial flutter. B-blockers and Ca-channel blockers may be indicated.

    If adenosine slows the tachycardia but P-waves remain, we had a compensatory sinus tachycardia and we need to continue searching for causes.

    Does this help?

  • Emergency Doc says:

    This looks like an atrial flutter with 2:1 block – my computer monitor isn't the best (at work at the moment) but certainly looks like regular flutter waves visible in lead III at a rate of about 300/min.
    I certainly wouldn't want to subject the patient to adenosine! If you're worried it could be a sinus tachycardia then might be reasonable to try a fluid bolus, look for any underlying cause to suggest a sinus tach (e.g. sepsis) and also watch for variations in the heart rate – an atrial flutter will remain pretty mch constant whereas a sinus tach will have some variability in rate. The other thing you can do is record an ECG at half speed to improve visualisation of the flutter waves.
    Unless the patient is in extremis (and it sounds like he isn't, given he was standing up filling the car with gas) then I would probably avoid giving him any treatment prehospital and just focus on transferring him into the ED for assessment, assuming you don't have a ridiculously long transfer time to hospital. If he does develop cardio-vascular collapse then DC cardioversion would be an option.
    (I can't see any signs to suggest STEMI on the ECGs posted – there's no ST elevation and no reciprocal ST depression).
     
     

  • Robert says:

    Interpretation: Fast, Narrow, and Regular Rhythm. Rule ins include Sinus Tachycardia, PSVT, A-Flutter. Sinus Tachycardia always has to be less than 220-age, in which case it is, but there is no obvious sinus activity even in leads v1/v2 excluding sinus tach. Whenever a heart rate is 150 +- 20, it is highly suspicious for A-Flutter. A-Flutter is best seen in the inferior leads when the 12 lead ecg is flipped upside down. It appears to be 2:1 AV conduction. This ecg includes A-flutter VS another SVT rhythm.
    Treatment: 02,IV,ASA. We need a AV blocking medication, now short or fast? If you're 100% positive it's A-Flutter, you may start w/ your beta/calcium channel blockers, but if uncertain adenosine should be used first. Christopher shows some excellent points above.
    One of my favorite lectures on SVT rhythms is by Mel Herbert on EMRAP, very simple approach and informative - http://www.emrap.tv/index.php?option=com_content&view=article&id=2202:EMRAPTV62-Tachyarrythmia_Therapy
     

  • Daren says:

    I believe that looking at how the patient is presenting at the time and viewing the monitor … I would provide treatment for his Tachycardia since his symptoms are hypotension, altered mental status, and signs of shock plus chest discomfort.  They are narrow complexes so I would provide O2, gain IV access, and look into Synchronized Cardioversion.  I would get the Adenosine IV and follow the algorithm on page 10 of the ACLS book.  :-)      

  • Patrick says:

    AVNRT.

    My differentials were A-Flutter vs. AVNRT vs. Sinus Tach (in that order).

    Sinus tach just seems unlikely given his history. Also no apparent P waves.

    A-flutter was what I thought I was going to see before looking at the EKG. But I see no flutter waves. Still a possibility though.

    The “J waves” as mentioned earlier have subtle changes to them from beat to beat. I think this is likely due to retrograde depolarization of the atria superimposed on the end of the QRS. Perhaps the pt’s “pressure meds” have resulted in his tachycardia not being at a more profound rate, like we are used to. This is a good example of why tachycardia protocols which only permit treatment if the ventricular rate is greater than 150, for example, hurt patients.

    My treatment would primarily be vagal maneuvers followed by adenosine, keeping a close eye on the monitor and capturing another 12-Lead while the adenosine produces the transient AV block (for rhythm identification if I am wrong).

  • Chris says:

    Slow SVT, possible A-Flutter underlying rhythm. 
    O2, Bilat LB IV 1 @TKO, 1 @ NS Lock, ASA, withhold Nitro, Vagel Manuvers, repeat 12 lead, concider adenosine, monitor, rapid transport.

  • wiggy762 says:

    Going to throw in with the A-Flutter crowd. O2 (NRB @ kbo- keep bag open), IV TKO w/ a 500mL challenge as long as LS remain CTAB. NTG per pain/BP. Serial 12 leads.

  • Michelle says:

    Jason- our protocols are 15 lpm NRB for any "cardiac event". We have be "fussed" at by our cardiologist for not having a pt on 15 lpm when they were 100%sat RA when the C/C was "chest pain" even when it was actually anxiety with hyperventilation. All our chest pain/discomfort calls get "reviewed" by a cardiologist regardless of eventual Dx.  That being said… High flow won't hurt 'em & might help by loading all the hemoglobin up in the event things go very bad very quickly & they need that little extra for later. Being a "green" medic, I make sure to follow as many rules as possible when dictated by the cardiologist (when I can understand what he says since English is his 4th or 5th language)

  • Emergency Doc says:

    Interested in the thought that some people would like to DC cardiovert the patient at this stage – he's GCS 15 with a SBP >100 and only a marginally raised resp rate. He may well need cardioversion but does he really need it right now?
    Assuming you do decide to electrically cardiovert in the back of the ambulance then what agents do you guys have for providing procedural sedation (do you have the authorisation to use propofol / ketamine)? I don't work in the US so not familiar with your protocols and the drugs that EMTs are authorised to use – in the UK paramedics can't use anaesthetic agents and are limited to morphine (+/- midazolam) which wouldn't be an optimal option for this patient. (I work as a PreHospital Care HEMS physician and if we needed to DC cardiovert a patient then we'd probaby go for propofol or ketamine in the field, although with those vitals I'd be keen to avoid electricity unless the patient started to deteriorate significantly).
    Surely it does also depend how far you are from the ED? This patient doesn't sound like he's going to crash in the next 20-30 mins so might be better waiting until you're in the ED with a trained Emergency Physician able to interpret the ECG and provide electrical cardioversion, if required, in more controlled surroundings.

  • VinceD says:

    @Bryan L – Nice call-back! Lewis can certainly play a role in teasing out atrial-flutter vs. sinus tach, but without actually running one here, I wouldn't be able to comment on it's efficacy on this exact patient. If you wanted to go down that route, I would suggest playing around with electrode placement a bit (different intercostal-spaces on either side of the sternum) while looking at different leads on the monitor if you're not seeing what you want right away.

    For an example of subtle a-flutter that JUMPS out with the Lewis lead, click my name above here, check out my first post on atrial flutter, and scroll down to section 4.5. I'd add a link in this comment, but then it would probably get filtered out by this site's spam filter.

  • Robert says:

    @ Emergency Doc -I Wouldn't even consider synch cardio at this point. 
    In our area, we're currently using Etomidate for SC. What are your thoughts on the drug for SC? Currently, we're having a significant drug shortage in the states, and will soon be getting propofol as well as ketamine. 
    Cheers.

  • Robert says:

    @ Michelle – I think you and your cardiologist are living in the prehistoric era (even if he speaks 4 different languages). The AHA guidlines as well as many literature reviews are beginning to show adverse side effects w/ hyperoxygenation. 94% seems very reasonable to me.

  • Emergency Doc,

    Perhaps it is a limited to our region, but if I let a patient ride to the hospital with a tachyarrhythmia without any treatment I would be in serious trouble. Our ED docs expect us to interpret the 3/12-Leads and treat the rhythm. If we're in one of those gray areas–say WPW or maybe a young kid with a WCT–then we call for advice/orders, but rarely we'll be told just to watch and transport.

    Different expectations I guess.

  • Adam says:

    I second that Chris. We are expected to interpret and if the patient is symptomatic (this one is) we are to treat. If I have a borderline patient and I have the ability (radios suck and cell coverage sucks) I contact OLMC if I'm unable to contact OLMC I have a judgement call. I dont see a reason to cardiovert this gentleman yet but it probably wouldnt be a bad plan to have the defib pads placed if my previous treatments did not work.
    Emergency Doc,
    I cant speak for all states but in Oregon Paramedics are allowed to use any medication that their physician advisor approves. e.g. I know of at least one that carries anti-biotics, we carry some heavy hitters for a STEMI but only versed, morphine, and fentanyl for pn/sedation. I agree that adenosine is going to be unpleasent, but I have two options, sit and do nothing IMHO not an option. Or treat the rhythm/symptoms. I would (due to long transports) treat the patient. 150 seems a little fast for hypovolemia either regardless of cause, but I suppose its possible so add in my treatment (earlier post) a fluid challenge prior to the adenosine.

  • Jeff says:

    I am be curious to see why some label the tachycardia to be the problem but then treat with MI protocol.  Why would you use nitroglycerin for MI and then cardizem for rate control.  I believe that if you give the nitroglycerin first, attempting mulitple doses, and then giving meds for rate control your patient's blood pressure is going to tank.  They will then need to be in compensatory tachycardia, which you would have taken and made nearly impossible.  I personally have never seen an MI with tachycardia in a regular rhythm, maybe someone else could bring a scenario to the table with this presentaion. 
    If someone could explain to me the rational for why the earlier method listed would be more appriopriate. 

  • jason says:

    Differentials to include AVNRT vs AFlutter 2:1. Leaning heavily towards AVNRT. AHA guidelines state to withhold O2 in an ACS patient if SPO2 is 94% or higher (unless there is dyspnea or cardiogenic shock). Per protocol (Denver). 12 mg of Adenosine, rapid push. Follow with second dose of 12 mg if necessary. If no conversion then fluid bolus and transport. Don’t think this patient warrants cardioversion in an ambulance. Don’t carry calcium channel or beta blockers.

  • Nick Adams says:

    ST? – Sudden onset. No underlining cause.
    SVT? – Too slow…………really
    A-fib? – Too regular.
    2:1 A-Flutter – Narrow complex tachycardia?…….Check. No decernable PW’s?…..Check. Rate approx 150?…..Check. F-Waves?……Check and best seen in lead I and aVR.

    It’s a 2:1 A-Flutter

  • Gorton says:

    Christopher,
    Telling us that you treat every tachyarrhythmia is very suprising to me.  I suppose that you have a bottomless bag of medicine to appropriatley treat every patient you come across.  More so is that you would get in trouble for using your clinical judgement.  Sorry to hear your service is still forcing medics to work in a tight protocol box without the ability to think things out in a rational manner.  
     

  • Christopher says:

    I'm not sure how an expectation of treatment for symptomatic arrhythmias is being placed in a "tight protocol box." Sitting on your hands simply requires an explanation, just it had better not be, "well I couldn't figure it out so we just took them to this hospital."

  • Gorton says:

    Christopher,
    I actually have a lot of respect for your knowledge, professionalism, and cases you bring forward to this site.  My dark and twisted side wanted to see if I could get you going with my last comment.  Obviously it couldn't and you are a good guy,
    Sorry Chris

  • Christopher says:

    How can you test the limits of our advice if you don't push them? Trust but verify.

  • Gorton says:

    Christopher,
    I have a question for you,
    wiggy762's comment at the top of this page says that he would give a 500 fluid bolus and also treat with Nitro for pain.  I agree with a bit of fluid to increase preload therefore ejection fraction via the Starling mechanism, but to then follow that up with Nitro which may decrease preload?  Would we be chasing our tail here?  
    Also, what do you think is the cause of this guys pain?  Given his history I'm sure his arteries are sclerosed and he may find relief with Nitro, but if his pain is rate related then my thought would be to fix the rate first.  Thoughts?
    Thanks

  • Christopher says:

    I think if you didn't catch that this was not sinus tachycardia, you could fall into the trap of treating it as a problem not related to the rate.
    That being said, if this were sinus tachycardia at 150, nitro is likely contraindicated as the patient is compensating significantly for some pathophysiology! Compensatory tachycardias should be treated by fixing their underlying problem instead and if this were a tachycardia at 150 due to ACS…they probably are in cardiogenic shock.
    Does that help?

  • Gorton says:

    That helps Thank you,
    Another question I have is about the use of Adenosine in an Atrial Flutter with variable conduction or A Fib.   It's my understanding that it can be very dangerous to give Adenosine in WPW where there may be a Kent bundle or accessory pathway.  I believe this happens because Adenosine decreases conduction through the AV node but not the accessory pathway therefore we would be creating a perfect situation for reentry.  Do you know why it is dangerous in AFlutter or AFib?  I understand that it just wouldn't work due to the fact that these rhythms are generated from ectopic foci in the atrium.  But dangerous?  
    Thanks again!
     

  • Christopher says:

    Adenosine could be dangerous in irregularly irregular rhythms where the AVN serves as a buffer against 1:1 ventricular conduction. In regular, narrow complex rhythms it is safe. AF (or AFlut) w/ WPW has a very distinctive look, wide/irregular/bizarre changing morphology. In AF w/ WPW or AFlut w/ WPW you are not worried about reentry but instead that these are automatic (in the view of ventricles, a-flutter is functionally automatic). Adenosine will not stop them nor decrease conduction through a bypass tract.
    Reentry rhythms can be safely terminated with adenosine, whether or not they are dependent on a bypass tract, because they are still dependent on the AVN in order to continue.

  • Kieran says:

    I agree with a possible 2:1 atrial flutter. But can’t rule out a sinus tach… Difficult one. But I’d argue there’s a possibility for cardiogenic shock, and that there’s some possible ischemia in the tracing too (subtle ST changes) there too. Protocol would dictate Aspirin 300mg PO and 400mcg GTN SL for ‘suspected cardiac chest pain’ with morphine being the pain relief of choice. However, concerned about cardiogenic shock in my mind – nil GTN. I’d cannulate, titrate O2 to response (2-4l via nasal specs) and admin 300mg aspirin. Hospital pre alert and get them in.

    In the UK we work from “JRCALC”. So I’d be interested to hear views. Would anyone recommend morphine (careful admin) for pain? I’m just concerned about ‘chasing our tail’ with this guys BP as mentioned above.

  • Chris says:

    I would consider AFlutter (2:1), mostly because the rate is so consistent. The flutter waves may be buried in the Ts. A trial of adenosine is as great diagnostic if you can’t differentiate and it only has a 6 second half life. If you find the rhythm goes to Afib after the rate breaks, you can then decide a tx plan.

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Ivan Rios
The role of 12 lead ECG in Pediatric Pulmonary Hypertension
Thanks for writing Tyler. They are the same thing. Strain pattern is just the result of increased pressures against the ventricles which alters the way repolarization occurs from epicardium to endocardium. Similar to stepping on a puddle of water. Your show spreads the water away from the area of pressure. The ST segment is slightly…
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The role of 12 lead ECG in Pediatric Pulmonary Hypertension
Can you explain how these ST segment and T wave changes can be differentiated from right strain pattern?
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