54 year old female CC: BLS intercept

Tom, our Editor-in-Chief, and David, an Associate Editor, are gone on vacation. As a send-off, I am presenting the following case. I hope you enjoy it!

It is just after 3am when you are called to intercept a BLS unit on scene with a 54 year old female with a low heart rate.

Upon your arrival, you find two EMT-Basics attending to a small woman lying in bed, who appears acutely ill.

<p.The EMTs state that they cannot get a blood pressure and her pulse is slow and weak at her carotid. They have placed their house bag under her legs and have her on oxygen via NRB at 15 L/min.

The patient is alert, oriented, and answers all of your questions appropriately. She states that she woke up not feeling well and called 911 when she could not get out of bed.

Past Medical History: hysterectomy, cholecystectomy, breast cancer
Medications: Ambien and Zoloft (she denies depression)
Allergies: Aspirin gives her heartburn

You ask her if anything else is going on and she states that her chest, “feels funny”.

Onset: woke her up from her sleep
Provocation/Palliation: nothing makes it better or worse
Quality: she points to the middle of her chest as the source of the funny feeling
Radiation: when asked, she mentions her left leg is tingling
Severity: repeated questioning only elicits, “it isn’t that bad”
Time: 20 minutes

Her vital signs are reassessed in the Trendelenburg position.

Pulse: 44, regular, no radial pulses present, however weak brachials are palpable
Respirations: 12, unlabored, bilaterally clear breath sounds
BP: 54/0, unable to accurately auscultate the diastolic
SpO2: 96% on O2 via NRB at 15 L/min

Besides her cold, ashen gray skin, her physical examination is unremarkable.

The cardiac monitor is attached.

Initial Strip

A 12-Lead ECG is acquired.

First 12-Lead

A final 12-Lead ECG is acquired as you arrive at the receiving facility.

Last 12-Lead

What is your interpretation of the initial 3-Lead and 12-Lead? How would you treat this patient?

Given the final 12-Lead, does this change your interpretation?

See Also:

Second Degree or Third Degree Atrioventricular Block?

54 year old female CC: BLS intercept – Conclusion


  • VinceD says:

    Strip shows sinus tach @100 bpm with no sign of AV conduction, indicating 3rd degree AV block. Narrow complex escape (junctional) at 40 bpm with no notable retrograde VA conduction.

    12L #1 – rhythm as above, normal axis, wandering baseline.

    12L #2 – rhythm as above except beat #7 is slightly delayed for whatever reason. Not seeing much in terms of worrisome ST changes; slight depression in I and the first part of aVL is inverted, which prompts me to look inferior where there’s maybe 0.5mm of elevation in aVF if I want to over-read it. Slight depression in V2-3, which I don’t think is acute either. Doesn’t change my treatment.

    Management: Get her out of Trendelenburg, IV, and rapid fluid boluses 500mL at a time. Pacing pads positioned A-P. Since it takes about 20 seconds to get out atropine and push it, I’m giving her 0.5mg, repeated once or twice. The only reason I could see not to give it would be fear of increasing the sinus rate, which would decrease the likelihood of any beats getting through the AV node. Unfortunately, she’s not letting any through to begin with, so it’s not like we’ll make it worse. Plus, it won’t affect our ability to pace her, so why not?

    If no effect, time for TCP. If that doesn’t work, I’ll max her out on atropine. If that doesn’t work, my last line agent is dopamine.

  • VinceD says:

    Whoops I meant ‘maybe 0.5mm of elevation’ in III, not aVF. Haven’t had my coffee yet.

    There’s also an early R-wave transition in the precordials. With depression in V2-V3, a hint of elevation and Q-waves (prolly not significant) inferiorly, slight depression in I/aVL, and complete heart block, infero-postero MI is in the realm of possibility, but I’m pretty far from convinced. I’m curious how it turns out and what everyone else is thinking…

  • Jenny says:

    I’m not really seing the tachycardia w/ a rate of 100, but I can definitely see the possibility of a 3rd degree block. It’s tough to know for sure because I am unable to print it out and march out the complexes. Personally, I think I’d take the time to get out the narcs or benzos and premedicate and go straight for pacing. I don’t think the atropine would work if this is a high degree block and if she’s having an MI, we could control the rate (thus, somewhat, oxygen demand and work) of the heart. Just my opinion. I’d also love to know the outcome.

  • chris T says:

    sinus brady with type 1 AV block. I sometimes screw those up but either way I consider this a high block. Pt is unstable. No atropine, right to pace. I will be agressive with fentanyl for pain, sedation with benzo tends to drop BP so I will hesitate on those for now. Fluids w/o at this time. Improve BP to at least 90 sys. If this takes a vaso pressor after other treatments then so be it. reevaluate and treat accordingly. I would not have delivered this patient without intervention.
    Investigate ST depression with a posterior EKG. With the size of the amplitude in proportion to the ST Dep does no seem excessive i dont think I will find a posterior STEMI but im gunna look for it.

  • 12leadekg says:

    Sinus brady with complete heart block, Place pads, we have to call for orders to pace here, I would anticipate orders for Valium and pacing. IV bolus 300cc’s, per our local protocol, and recheck lung sounds. I would hold off on Atropine due to it not being recommended for high degree AV blocks.

  • chris T says:

    Now i think its more of a morbits 2 av block. I dont think its 3rd yet

  • chris T says:

    Vince i even tried crossing my eyes, where do you get an underlying rhythm of tachcardia at 100? Im not being critical, im curious.

  • Turbodiesel says:

    sinus tachy with 3rd degree AV block.

  • Bob says:

    Any concern at all with sedation for a hypotensive PT?

  • 12leadekg says:

    @Chris there is no AV association and the rhythm is regular. This is consistant with the rules of 3 degree. Mobitz type II should have a constant PRI interval.

  • Turbodiesel says:

    Chris… look at rate of p waves… this give you the sinus rate, which is about 100. Ventricular rate is somewhere around 40 (qrs complex).

  • chris T says:

    Thank You 12 lead. I alway have to review the high blocks to keep them strait.
    Ah now I see what you guys are saying about the rate in relation to the p waves, thank you Turbodiesel

  • ryan says:

    3rd degree, start pacing, fluids for pressure followed by dopamine at 5-10/mcg/kg/min. Blood sugar, find out about polypharmacy, or if there is anything not medication wise she is taking, illicit drugs, someone elses..etc..transport to a PCI facility with early notification and serial 12 leads. O2 at 3LPM via NC, possibly sidestream CO2..just to watch for acidosis with the potentially poor perfusion.

  • Shalom says:

    Complete heart block. get out the combo pads, lots of fluid, maybe dopamine.
    Im not liking the inferior leads and V2-V3 at all, check V4R and posterior leads and remember to perform serial ekgs throughout.
    transport to PCI hospital asap.

  • Brandon O says:

    3rd degree heart block (march out the P waves if you’re not certain — they’re regular, and walk straight through the absolute refractory period of the QRS) with junctional escape. Quality on this first 12-lead is UNACCEPTABLE given the slow rate and importance of this clinical crossroads; it should have been immediately reacquired. As it is, we’re left with two recordings and no ability to determine whether changes are due to time or due to artifact.

    Nevertheless, I’m very concerned for a possible inferoposterior STEMI, due to seeming STE in inferior leads, depression in aVL and septal leads, and early R/S transition. Given the concordance with the clinical picture (bradycardia and hypotension with clear lungs), I would be willing to buy that bridge, although some additional leads would not be a bad idea.

    On arrival, these changes do seem to have largely resolved. So unless it’s just an artifact issue, this may have been an unstable plaque that resolved spontaneously.

  • complete heart block. tcp.

  • Brandon K says:

    Atropine is never indicated in 3 degree block. And the thought process of I’ll give it because it can’t hurt is careless and poor medicine. It’s that attitude that is making it hard for EMS to gain national respect in the medical field.

  • akroeze says:

    My understanding is that Atropie is generally not recommended in high degree block because the escape complex is USUALLY below the AV junction. In this case however the escape rhythm seems be to from the junction, and the vagus nerve does innervate the junction so atropine should have an effect.

    This is just my understanding, please correct me if I’m wrong on this.

  • akroeze says:

    Atropie = Atropine of course

  • Stephen says:

    I think I would try dopamine before pacing since the patient is A&O. I would place pads in case the patient became unresponsive. I find is hard to justify giving a person a benzo to sedate them to pace them. They are already hypotensive don’t want to worsen the problem and don’t want to cause them pain.

  • Shalom says:

    STE in inferior leads(remember that STE is relative to QRS size) + hypotensive patient…
    RVI maybe?

  • Mike says:

    Complete heart block with evidence of possible IWMI – need posterior and R-sided leads for a more complete picture.
    Diesel bolus to a PCI-Center with notification. Fluid and pressors for BP support (NOT Dopamine, Epi drip better) AHA-ACLS says TCP but, even if you get capture, you will then have a patient twitching at 60 times a minute who is still hypotensive – the “fix” for this patient is in the cath lab.

  • VinceD says:

    Brandon K:
    My understanding is that the reason everyone always says “atropine is contraindicated in high-degree heart blocks” is because it will speed up the rate of the sinus node. Increasing the rate of the sinus node would shower the AV node with even more impulses than it is already receiving, decreasing the likelihood of it conducting even further. However aside from the underlying pathology, in a 54yo the node should definitely be conducting at an atrial rate of 100, so I’m fine with sending more impulses its way if I can also utilize atropine’s ability to increase AV nodal conduction.
    If her baseline sinus rate was around 150 or higher, I may think the AV block was perpetuated by the node being overwhelmed with signals, in which case the chronotropic effects of atropine would be much more likely to outweigh it’s AV nodal effects. However, on these tracings, I see plenty of beats that ‘should’ be conducted but aren’t, and reason that increasing her sinus rate to 120 or 130 still wouldn’t overwhelm the AV node if I could just increase it’s conduction. Also, if she does start conducting 1:1, I could live with her tachy in the 120’s, but if the underlying rate was higher and began conducting, I wouldn’t want her running in the 160’s or 170’s.
    The final piece in my rationale is a personal bias, but I’ve seen atropine work in high degree blocks about twice as often as TCP, and I think many medics and doctors out there would agree. While I too frown upon giving medications just because they don’t hurt, in this case I’m pretty sure there’s enough potential benefits to warrant trying. Of course I may be incorrect in my understanding of why high degree blocks are listed as contraindications, in which case my whole reasoning is nonsense…

  • Great comments so far, I’d add the official line on atropine’s contraindication in a 3AVB is:

    “Avoid relying on atropine in type II second-degree or third-degree AV block or in patients with third-degree AV block with a new wide-QRS complex where the location of block is likely to be in non-nodal tissue (such as in the bundle of His or more distal conduction system).”

  • Troy says:

    3rd degree AVB. Due to her being conscious I would probably try dopamine or epi first over TCP.

    As for atropine: Although the QRS is narrow (meaning the block could be anywhere between the SA and AV node) and with our knowledge of the pacemaker cells being in the NBB of His, atropine might work, but it also might just worsten the block. I agree with Chris in not pushing atropine

  • Baron says:

    You guys have covered most of it, but here’s my spin.
    SA node is firing @ 100 ppm with atrial capture.
    3AVB is present.
    Junctional escape rhythm in the low 40s.

    This is an inferior STEMI.

    There is concordant STE in III and aVF, with a straightened upward ST segment in II. There is reciprocal ST depression in aVL with a down sloping ST segment.

    There is possible posterior involvement, given the concomitant ST depression anteriorly and very likely RVI as well. Clear breath sounds, while grossly hypotensive, makes her positive for two of the RVI triad, with having JVD not been mentioned.

    This is likely a very proximal RCA occlusion, high enough to have caused ischemia in the AV node, and is the source of the block.

    Now, something bothered me about the R wave in III. Granted, the bradycardia doesn’t allow us many complexes to look at for ST/T comparisons, and there is a wandering baseline and artifact present in the first 12L, but it seemed to me that the infarction progressed rather quickly.

    In the strip, you have a qR. In the first 12 lead, you have a qr. And in the second 12 lead, you have a Qs. So I looked at the times.
    First strip-0225
    12L one-0347
    12L two-1950

    So either someone reset the monitor mid call, clock included, or they were on scene for 82mins with a transport time of 16 hours and 3 min. Odd.

    Regardless of why, it explains the odd changes between 12Ls. The ST changes (and R wave in III) were gone by the second ECG because the MI had either run its course or came damn close before being spontaneously reperfused. PCI may not even be indicated now, although a permanent pacemaker likely is. Blocks secondary to AMI are generally transient, but my guess is that’s only when circulation is restored within a reasonable amount of time. She probably lost the function of most of her inferior wall as well as here AVN.

  • A note on the times, the hours were cut off but not the minutes and seconds. So it should be XX:02.25, XX:03.47, and XX:19.50. 17.5 minutes from start to finish.

  • VinceD says:

    I’d want to at least check both femoral pulses while I’m evaluating her, and if I’m looking for something to do, a very rough motor/sensation exam of the legs. Very low yield, but I’m not yet convinced this is an MI, and even less convinced it’s due to medications or her electrolytes being out of whack, so I’m gonna keep looking.

    Of course while I’m considering other things, I’m still treating what’s in front of me, which is a woman who would likely benefit from a slightly faster HR.

  • VinceD says:

    Of note, the patient’s position could have changed from when she was first attached (which may have been in Trendelenburg position, depending on the timeline), to her arrival at the hospital. As far as I know, having never tried, my stretchers don’t do Trendelenburg when locked in the ambulance. Could this account for the change in axis and disappearance of those Q’s inferiorly and S-waves high laterally?

  • Darlene says:

    mobitz II, bolus, atropine, pacer pads, just in case most likely want be needed, hold off on pain meds BP is too low

  • javier checo says:

    3rd degree block ; could that be an aaa ?

  • Steven says:

    It seems like we’re all in agreement that this rhythm is a third degree heart block with the possibility of the being posterior inferior STEMI. I’m not 100% sure I would be screaming this over the HERN, but I might transmit it and politely say, “you may want to take a look at this”. It appears that there is minimal J-point STE in inferior leads, STD in AVL with a biphasic T and in leads V1-V4. A third degree heart block by itself would be suggestive of a high RCA occlusion and with this EKG is probably the likely culprit. I do find it very intriguing that most people would go straight to pacing in a patient who doesn’t appear to be that unstable. Although the patient is hypotensive(maintaining), has a dusky skin color, and complains of a funny feeling in her chest; she is still A/O x4, and orthopneic. Since this is a RVI, the patient would likely have positive results strictly do to a fluid bolus. It is safe to give 2 liters of NS do to the fact that the RV isn’t working properly; this would increase the circulating volume and maintain perfusion.

  • Brandon O says:

    Great run-down, Baron.

  • Schenk says:

    She is definitely in 3rd degree. In first strip p waves march out to themselves, r waves are slow and regular, and no p-qrs correlation. 3rd degree. She is hypotensive, ashen, but still talking. Atropine will not work in high degree blocks. O2, Saline bolus 500ml, Sedate and pace.

  • Butchie PA-C says:

    It’s a third degree heart block. There could be questionably inferior ischemia. I would bolus the patient but use caution with the bradycardia. Pace the patient with sedation.

  • Boston says:

    She’s sinus brady with an atrial rate near 100 with a third degree block. Since she’s not perfusing all that well I’d start pacing her right away. Since her lungs are clear I’d giver her a fluid bolus but the pacing should start bringing her b/p back up.

  • Larry Davis says:

    First of all, I qualify this by saying that I’m a very old medic, which doesn’t mean that I’m trying to trump you with age but that I’m pleading possible Alzheimers, so if you violently disagree with me, be gentle because it’s just age.

    First of all, Javier Checo has hit upon something that was my very first thought when I read the scenario, only because I’ve seen it so many times, so when Vince (there was a Vince who was my mentor as well, so you have a good name) suggests checking the LE pulses, that would have come for me early in my assessment.

    Admittedly, as has been pointed out, these are not optimal strips but when do we ever get optimal strips except in cases where it doesn’t really matter. But it was apparent to me that the patient is in complete block – we would have called this AV dissociation back when I started – and that in and of itself points to some sort of inferior wall problem.

    So, what do I do and not do. First thing is the 100% O2 and get the line in, which they did, and start it at 100cc/hr. I think that it is wise to think ahead and put the pads on the patient while I’m moving her to the stretcher just in case I decide to either use them or find it necessary to use them as the case progresses. Then I think the ambulance is a good place to continue with my discussion with myself about the course of care and I’ll take a firefighter-EMT along in case I need an extra pair of hands. Since I’m now in the ambulance, it’s probably wise for it to be going somewhere so we’re off to a center where they can do more with the heart than just talk about it.

    So, what now? The amount of “stuff” that I would consider doing is proportional to transport time: the longer the transport, the more “stuff” I might be inclined to do. Where I practice there are seven cardiac centers and I can usually get there within 20-30 mins from anywhere I might find myself. I would definitely communicate early with the receiving facility if for no other reason that to make sure they’re not on diversion.

    OK, now what? Well, what do I think is happening. It looks like there’s could be a conduction problem which would likely be secondary to some sort of IW occlusion. Or, it’s an AAA – she sure is at the right age range for it – in which case only my driver’s skillfully quick access to a surgical facility will be helping. But going with the other choice: what are my options.

    Do I want to increase the heart rate? Well, she looks like crap but is this patient unstable? Well, all in all, it doesn’t look like she’s unstable, that is, not getting observably worse as we move along. So, in heart which is already evidencing the inability to supply oxygen to the tissues, do I want to increase the rate (and/or contractility)and thus the oxygen demand. Maybe not. And keeping that AAA in the back of my mind, how much do I want to increase the blood pressure? So, no atropine, though I have no theological reasons for not using it. And I’m not going to pace her just yet, but let’s keep it in mind. We’re certainly ready to do so if it seems to become needed. I’m not going to give her anything that would gender to decreased BP so no MSO4 for sure, especially considering that it can exacerbate an inferior wall MI. No, I don’t want my patient to be uncomfortable but at the same time, I don’t want her getting worse either so, it’s going to be a bad few hours for her in any case and it starts now but be gentle and keep explaining what you’re doing and why. “Well-selected words of encouragement” (anyone else remember that phrase) is still sometimes one of the best things you can do.

    Do I want a fluid bolus? Hmmm. Is this a volume problem? Well, if it is, it’s a bad one so I’m not sure I’m going to increase the workload on an already slow heart without increasing the rate. And I’ve already said I don’t want to do that.

    So here’s the conclusion: whatever the underlying problem is, inferior wall MI or, God forbid, an AAA, or something else that we haven’t thought of, I can’t fix it. So the most important thing that I can do is get her quickly to a place that can. So I’m not going to hang out on the scene over-thinking this and trying things out but I’m going to get on the road, with the support that I may need if things deteriorate. Keep in mind, as described here, this patient is in the shape she’s in but doesn’t seem to be getting worse. Also, I will put the line in and attach the pacemaker pads to prepare for the eventuality should she detiorate. I’ll make sure that the receiving facility knows that we’re coming in and is ready for us. Oxygen, lots of oxygen, is indicated here no matter what is going on, so I’m going to administer that, pulse oximetry being unrevealing in this case (we didn’t have that for 2/3 of my tenure anyway, so…).

    Monitor vital signs and keep a close eye on the EKG, serial twelve-leads in case anything changes on the EKG (and let the hospital know), and provide those well-selected words of encouragement. If something changes, treat that as it arises.

    But I think all of your for your comments. I learn a lot reading what you all write. It makes me think, and encourages me that your patients are in the capable hands of intelligent medical providers.

  • Larry Davis says:

    Oh, and in re-reading this as it posted, I apologize for the occasional inadvertent misspellings. The lengthy and convoluted sentences are a lifelong chronic condition that my wife – the English teacher – has tried to treat without much success.

  • Nanner medic says:

    Third degree heart block. Does look like we have some Inferior STE. Look at V4R and posterior. Email 12 lead to receiving hospital early. Let the DR. determine if he wants to activate the STEMI team. O2 continuation as is. IV bilateral big boar. 250ml fluid challenge. Reevaluate lung sounds after each bolus. 0.5mg Atropine once. Probably won’t work but will try real quick. TCP w/ pad A-P. Fentanyl per protocol. Would consider Versed if b/p increases, might try a very small dose for sedation but would be very careful. Monitor very closely. If need be moved to dopamine or Epi infusion. Contact med control for further direction. Monitor in line ETCO2. Ensure that intubation equipment is readily available in case things go south. Transport Emergent to closest hospital.

  • Larry,

    Stream of consciousness is often the best way to come to a conclusion. I definitely enjoy your thorough reasoning for patient management.

  • Ken Bedell says:

    I like your style! This is exactly what I was thinking while reading all these posts! Medics a lot of the time make calls more complicated than they have to be! I go by the KISS method,(KEEP IT SIMPLE STUPID) and it hasn’t let me down yet. The only suggestion I have is coming from my administrative position, a set of pads cost around 40 bucks so I don’t put them on unless I am absolutley going to use them! I don’t think it takes that long to slap them on. Now before I was in this position, I would have slapped them on also. Bottom line, I hope you or someone like you shows up if its my mom!

  • Jwmedic says:

    Two working differentials with similar treatments: MI and AAA.

    3rd degree block with a junctional pacer….. For this I would do high flow, ekg, 2 large bore IV with a bolus. Consider pacing which in her case I would do. If the rate and bp are fixed I would be quick to sedate.

    Yes her mention is hood but her skin signs point to a patient who could be dead in the near future which is what I’m basing my aggressive treatment on.

    Fix the rate, fix the bp (careful to keep it near 90-100 ) and get to a good facility code 3.

    Dopamine could be considered after 500-1000cc NS with her rate being fixed and her bp still not coming up.

  • Larry Davis says:

    Thank you Christopher for your kind remarks.

    I am jealous of you folks who have fentanyl at your beck and call.

    Just a thought in re oxygen. We talk about administering oxygen because, well, because it’s there and it’s on the list. I sometimes forget the truly beneficial effects of oxygen. In this case there are those who say sedate and those who say don’t sedate and those who say maybe sedate, depending. There are those who say atropine, those who say not, those who say maybe, those who say, “That’s stupid.” (not exactly a persuasive case for medical care).

    But we all agree on the oxygen, when anyone mentioned it. It’s worth pointing out that when less blood is getting to some place in the body and we increase the arterial oxygen tension by 100% or so, we increase the amount of oxygen getting to those deprived places. So, in the case of the heart, we can decrease the ischemia and may prevent the extension of an infarct. If the problem is just ischemia, why, we may actually help the problem and, given a few minutes for the PO2 to increase, there may be improvement from that alone.

    Sometimes, oxygen actually is that drug that we always say that it is.

  • Student Medic says:

    I’ll preface this with stating that I’m getting towards the end of my medic class and I welcome any feedback.

    While she may not look unstable, a BP of 54/nada certainly doesn’t scream stability. A patient with a 3AVB @ 44 seems to me may have a problem with cardiac output (as evidenced by her BP) because of the heart rate. By fixing the rate, we increase BP which may eliminate the tingling in the LE, I’m willing to bet, was because the body was starting to compensate for hypotension. So with that said, I’d place her on high flow O2, start a line, administer 0.5mg Atropine per ACLS guidlines and local protocol while setting up TCP and moving the patient to the ambulance.

    While en route to a STEMI center, when the Atropine fails to work, I’d call for 0.15mg/kg Etomidate (where’s the Ketamine when you need it?! I kid, I kid.) and being pacing. I’d consider a 250cc fluid bolus and/or Dopamine as well but as second line interventions.

    It seems to me that 3AVB are rate dependent issues. First attempts should probably be made at increasing heart rate.

  • Jwmedic says:

    A second approach is if you think this is a AAA do treat only with a NS bolus and burn rubber.

    Reason being the arrhythmia is being caused by ishchemia in the heart from a AAA and making the heart beat faster you’re just making things worse for it.

  • Student Medic says:

    There is no mention of an ABD exam but on a small woman (which the scenario says she is), a AAA may be palpatable. Granted, it doesn’t rule it out but it may rule it in if you find something.

  • Brandon O says:

    Hey Larry, I like your style. Just one thought: the idea of transporting to where they can do the good stuff is smart, but for the main two differentials you offered (MI and AAA), those might be different places! Consider the possibility that the nearest STEMI center may not be a trauma center prepared for emergent surgery, or vice versa.

  • Sergio says:

    HR 40, BP 54/0? It looks like a 3rd deg AV Block to me, but regardless of what anyone thinks the rhythm is, she needs aggressive treatment or she won’t be talking for too much longer. Symptomatic, unstable bradycardia = Pace. Check for pulmonary edema, if none, initiate a fluid bolus. If still hypotensive after pacing and bolus, consider a higher dose dopamine for it’s vasoconstricting effects. All that on top of your standard o2, supine or trendelenburg as tolerated, 2 IVs, FSBS, etc etc. Even if it is a STEMI, the lack of systemic perfusion (tissue hypoxia) from the low BP is probably doing more damage than a coronary occlusion at this time. Treat the huge problem in front of you, then go hunting for the other issues. That’s my two cents worth.

    P.S…I would suspect an elevated HR with a dissecting AAA in a patient still talking to me. If it’s to the point of bradycardia with a AAA, that patient would be shaking hands with God at that point and not answering my questions. Even then I’d not suspect a bradycardia with major AV dissociation and no HX of it while having a dissecting AAA.

  • Canada says:

    3rd Degree. atropine as new ACLS states its worth a try, but would most likely go to dopamine, if that doesn’t work, pacing it is.

  • Sean Fiske says:

    I agree with the 3AVB, Sinus Tachycardia at 100, Junctional Bradycardia at 30. I am not a fan of the first 12 lead quality. I wouldn’t go starting my treatment based on any elevation depression found in it. That said, we definitely have a MAP under 60. Whether one coronary artery is blocked or not, none are perfusing appropriately. My transport times are short and to a cath lab/open heart capable facility with EP lab so we are very spoiled.

    Based on new AHA guidelines and past experience, I would be starting a pressor rather than TCP. Probably Dopamine at 3-10mcg/kg/min. This should help increase perfusion to the heart itself as well as the other organs.

    My first thought on the lower extremity is the lack of perfusion but the AAA isn’t a bad place to take my brain.

    2 Large bores with a fluid bolus are definitely in order. benzos, narcs etc have a chance at decreasing perfusion and are really unnecessary with the pressor route so dopamine makes some sense for those in the KISS realm of thinking. We are also lucky to have it prepackaged in a bag decreasing some time to administration. As far as increasing oxygen demand, at least you are getting the oxygen to the cells in the first place if you increase the perfusion. O2 4lpm via cannula for possible issues following reperfusion.

  • VinceD says:

    Awesome discussion everyone!
    Just to clarify, I was thinking more along the line of dissection than AAA with my LE pulse checks. AAA is possible for a patient who’s sick as all get-up, but there’s a particular reason why I’m considering dissection (and also a few reason why I think it’s not likely, but I’d look anyway).

    Anytime someone has the combination of a torso complaint and anything neurologically, dissection should be considered because when the dissection picks off arteries leading leading to any area of the body, it can present with numbness, tingling, or weakness. Also, a dissection could run back into the coronary arteries, usually the RCA, and cause all the problems of an RCA occlusion, including a tendency to develop blocks.
    That being said, in this case, I think it’s highly unlikely that she has dissected all the way from the root of the aorta down to her left iliac to give the rather distant results of a heart block and left leg tingling. If this was indeed caused by a dissection, I’d be much more convinced if she presented with the heart block and facial numbness, tingling, or droop, since the carotid arteries are so close to the coronaries coming off the aorta. Arm numbness, or even the classic bilateral BP or pulse differential would also be possibilities, but as I said, hitting a coronary and an iliac is a pretty wide swath of aorta to dissect.

  • K-dogg says:

    I work in the UK and I agree that this is type 3 (complete) heart block. Atropine is not contraindicated within our guidelines for complete heartblock, it is infact indicated where there is a high risk of asystole; mobitz type II, complete heart block WITH wide QRS, and ventricular pauses >3 secs. I would certainly give a primary dosage (within our guidelines of symptomatic bradycardia – 500mcg, max of 3 doses), record multiple 12 leads and treat the low BP with fluids (aiming for a systolic of around 90).

    This is a great discussion, I believe our guidelines across the pond in the UK are somewhat different and I find it incredibly interesting that there’s so many different methods of treating this case yet all aiming for the same outcome!

  • Nahid says:

    TO me it sounds like a complete heart block. fluid rescus and pacing with caution will do! although the ECG is with artifacts n the baseline.. its hard to give proper answer!

  • Samantha says:

    I’m going with 3rd degree block. I’d skip the atropine, get pads on in preparation to pace, and do a fluid bolus. I’m not rushing into dopamine because with any luck, pacing will improve her pressure. Depending on her pressure after the fluid bolus(es), I may or may not premedicate, but I would then begin pacing and treat changes appropriately.

  • dan says:

    third degree block dopamine will do just as well as pacing, pt is alert and is going to mind being electrocuted

  • Paul says:

    I agree with the majority of the above. I always give a dose of atropine even to CHB patients, because contrary to what is folklore, I have had a fair number of them respond to atropine. I don’t mind if they remain in a complete heart block, as long as the ventricular rate is high enough to adequately perfuse them and generate a “reasonable” blood pressure. Failing that, epinephrine drip and consideration of transcutaneous pacing. I agree that there is a possibility of inferior infarction, but I’m wondering if the ST abnormalities may be rate related. One must also consider that the three lead strip obtain does not accurately reflect ST elevation as it is not obtained in diagnostic mode. There is variability in the height of the QRS complex is as they appear to be buried T-waves in a few of them that are present. I would administer aspirin, fentanyl, and consider clopidogrel if available. Transport to PCI capable facility.

  • Paul says:

    acute inferior MI. A couple of IV’s, baby aspirin and emergent transport

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