69 year old male CC: Chest pain

Christopher A. Watford from the My Variables Only Have 6 Letters blog has submitting a very interesting case study (actually he submitted two but you’ll have to wait for the other one).

EMS is called to the residence of a 69 year old male complaining of chest pain.

On arrival the patient is found sitting in a kitchen chair.

He appears acutely ill.

Skin is ashen, cool, and very diaphoretic.

Levine’s sign is present.

It is obvious that the patient is anxious and in severe pain.

Onset: Sudden onset approx 20 minutes before EMS arrival
Provoke: Nothing makes the pain better or worse
Quality: Severe pressure
Radiate: The pain does not radiate
Severity: 10/10
Time: No previous episodes

Breath sounds are clear bilaterally.

Vital signs are assessed.

RR: 20
Pulse: 60 R
BP: 142/68
SpO2: 90 on RA (increases to 96 with oxygen via NRB @ 15 LPM)

BGL: 104

No known drug allergies.
Denies any significant medical history other than “indigestion”.

The cardiac monitor is attached.

A 12-lead ECG is captured.

Another 12-lead ECG is captured with modified chest leads V4R, V5R and V6R.

How would you treat this patient?

Is there anything about this case that surprises you?

*** Update 12/13/2010 ***

What Christopher and I both found unusual about this case is that the GE-Marquette 12SL interpretive algorithm was not giving the ***ACUTE MI SUSPECTED*** message, even though it was giving messages like “ST-elevation consider anterolateral or acute infarct” and “inferior injury pattern” which I had always thought automatically trigged an accompanying ***ACUTE MI SUSPECTED*** message.

This is especially important because some EMS systems require the ***ACUTE MI SUSPECTED*** message in order for paramedics to bypass the local non-PCI hospital for the STEMI Receiving Center!

So, I contacted a friend at Physio-Control who put me in touch with the person responsible for the computerized interpretive algorithm. He was also surprised that the ***ACUTE MI SUSPECTED*** message was not present on these 12-lead ECGs. So he turned to a “veteran 12SL designer”.

Together they figured out the problem.

Mystery solved! The 12SL expert said that the 12SL algorithm would definitely give the Acute MI statement for the first cse that you sent me. So I turned to the setup choices (LP12 Operating Instructions, chapter 9). One of the setup menu items is “ACUTE MI”. The description is “Print Acute MI message”. Further explanation says, “ON: Prints on the 12-lead reports when criteria are met.”

I think that the LP12 is set up with the ACUTE MI option turned off. I suggest that you get back to the customer and have them turn ACUTE MI on in the setup menu for this LP12 and any others that they have.

So, if you have a Lifepak 12 and you’re not receiving the ***ACUTE MI SUSPECTED*** message for obvious acute STEMIs, you might want to check this parameter.

LIFEPACK 12 Defibrillator/Monitor – Operating Instructions

28 Comments

  • Troy says:

    Well for sure this guy has an inferior MI with RVI with recipricol changes in I and aVL. I would want a cleaner 12 lead to see the anteriolateral wall. ASA and oxygen for sure. I would start bilateral IV’s, Fluid bolus as needed, and fentanyl for the pain. Early STEMI activation. Personally, I hold off on nitro with RVI due to them being more preload dependent.

  • Dave B says:

    looks like an IWMI, with RVI and lateral extension (STE in V3-V6, although the wandering baseline in left precordials complicate the interp).. all the usual RVI suspects: ste III > II, flattish ST in V1, with depression in V2, and of course elevation in right sided leads..
    the company it keeps: i am a little surprised at the elevated BP in the setting of what looks to be a clear RVI..there are clear lungs, but no hypotension that is typical…is there any JVD? also, i am surprised that the O2 sats are so low, in the absence of pulmonary or cardiac hx… and if so low, why isn’t the patient tachypneic? and if the low heart rate is due to the conduction system being affected by the infarct, i am again surprised at the pressure the patient is making. seems to be an odd presentation.
    after ASA, O2, do we give NTG? RVI requires caution, but as has been pointed out before on this blog, not always restricted if the systolic is high.

  • Brandon says:

    Case is pretty solid by the comments already provided by Dave & Troy. Early activation is critical w/ making a STRONG patch to the cath center; this gentleman deserves to have the cath team WAITING upon his arrival as opposed to being activated upon arrival.

    What I don’t like about this scenario is the application of O2 at 15 l/min via NRBM. The spO2 I assume is the rationale, but I am leary of relying on a number w/o other supporting signs/symptoms to justify the application of 15 l/min. Inundation w/ excessive free radicals aren’t going to help this individual, particularily at this critical moment of his life.

  • Brandon O. says:

    What’s going on with the precordials? Depression in V2? Anterolateral elevation? And are those spurious P waves I see in the extremity leads? What did you do to this poor guy?

  • Christopher says:

    Brandon,

    I didn’t send Tom many details about how we handled it so he’s filled them in where I did not provide them. Also, the fellow was so profoundly diaphoretic we changed out electrodes twice (they fell off when he stood up)…therefore any I-waves (imaginary waves found during deep introspection of a 12-Lead) should be attributable to poor skin-electrode contact.

  • Billy Hatchell says:

    For sure hold off on the nitro. This guy is preload dependent right now and nitro will bottom him out….Look how long the ST segment is too. There is a real delay in the action potential also. A Ca/KCL imbalence also…..

  • EMT- I Tech says:

    PUCKER UP THE GOOD OLE’ BUTT CHEEKS HOLD ON AND LETS GO FOR A RIDE……….FLUID FLUID FLUID GIVE LOTS OF FLUID……(just watch out for fluid overload). Problem with this pt is that it is showing RVI..Excellent job on the 15 lead, but the question was it nec. Is it not true if the lead 3 elevation is higher then lead 2 that it should already be assumed that the right vent. is envolved…But hey thinking outside the box is a good thing….. Anyways treatment plan…. Fluid fluid Fluid, D-Fib pads in place, 2 18 gauge or larger I.V.(one in each arm pref.)transmitt 12 lead, activate cath, conatact med control for nitro admin.. But if I am not mistaken if the right vent. is involved it fluid is more important then nitro…. Again I am not a medic nor a medic student so if wrong please let me know.

  • Donna says:

    Well textbook anterolateral infarction is present. He is preloaded dependent so nitro would be done very cautiously. His BP supports it now but maybe a bolus would be in order before any nitro would be given. He needs the whole gambit of oxygen, ASA, morphine or something for the pain based on what is carried in your unit, 2 IV’s, and a rapid trip to the cath lab. I am not sure what the issue is with oxygen as was presented by one commentor. When it comes to cellular perfusion the more oxygen, the better. I think free radicals aren’t this patients concern right now. If we don’t get him perfusing his myocardium soon, well the free radicals are a mute point. He is showing perfusion issues with being pale, cool, and diaphoretic regardless of what the pulse ox says. I would be curious to know how he responded after any and all interventions.

  • AJCalhoun says:

    While pt. presents as acute inferior MI, there are EKG inconsistencies. Not unheard of, but: good BP with almost wide pulse pressures, evolving EKG pattern and poorish O2 sat, along with sudden onset and remarkably severe pain rating and extreme diaphoresis all could be consistent with IWMI with extension lateral and RVI, which should be presumptive. Would hold nitro, give IV fluids, O2, monitor and transport to cath center, BUT — with an eye toward alternate possibility of ascending aortic dissection (sudden onset, extreme pain, wider than expected pulse pressure). Look for trachial tug and ask serially for description of pain, expecting possible “tearing” description. Finally, MCA might be culprit vessel, and again could be due to dissection at aortic takeoff. Angiogram will clarify all this, but only once pt. is in the cath lab. Talk to them early on. Treat as RVI to cover majority of bases and hit the road.

  • Geoff says:

    Leaning towards IWMI w/ RVI along with others. Same treatment, ASA, O2 (based on protocols), IVs, Pain Control, STEMI Center. Here is what surprises me, is the Acute MI detection feature turned off? I also noticed the elevation in V3 increased significantly between the 1st and 2nd 12 lead.

  • EMT- I Tech says:

    I keep hearing mona…. ok oxygen yes ASA yes… But in studies that are out am I not correct in saying that morophine increases the death rate in stemi’s, and that we should start holding off on morophine…. also nitro… Ok just really watch the Pt. because you dont want to have the pt brady down…or become hypotensive…..If anyone thinks that is wrong please correct me…

  • Billy Hatchell says:

    This is true…..MS04 is showing to be very bad with a 50% mortality rate after hopsitalized….Fentanyl is showing to be the drug of choice for pain because it does not cause a drop in BP…However, lookout for chest rigidity when administered. A side effect but doesnt last long.

  • Caleb D. says:

    Let’s see, this individual here is definitely going to the cath lab PDQ. Oxygen (Don’t need 15lpm by any means, but definitely 4 or so.) Aspirin. But fortunately with that 15 lead showing what we all have clearly stated, I’m not dropping any SL nitro on this poor fellow, he doesn’t need any help circling the drain, instead, I’m going to be skipping the SL nitro in exchange for a good old nitro drip, I’d kind of like to be able to control just how much nitro he’s going to absorb in a minute. Fentanyl for pain, Zofran prior to the Fentanyl, start him out at 100mcg, and let’s go find this gentleman a hospital bed to rest his head in for a day or 2.

  • Dr. Alo says:

    The initial EKG clearly demonstrates an INF, POST, and RV infarct. A proximal RCA lesion. You don’t need a right sided EKG.

    NO MORPHINE, NO NITRO.

    Tons and Tons of fluids. Patients are allowed to be in pain. Please do not give them morphine or fentanyl. You are just killing them faster. We now have an answer to the question about Opiates. The Crusade trial has clearly shown that morphine kills in any and all MIs. So no more OPIATES.

    Nitro should not be given to RV infarcts, they are very nitro sensitive and will bottom out. They are allowed to be in pain. The only thing that will help will be opening up the artery.

    Give them tons and tons of fluids. The biggest help the EMS and ER world can do for these patients is to scoop them up quickly, get the EKG, give them tons of fluids and activate the cath lab quickly. Don’t hesitate on the fluids.

    How do you know they received enough fluids? When you can hear it in their lungs. Once you hear crackles in their lungs or their O2 requirement goes up, or they need to be intubated, they have received the right amount of fluids. Studies have shown that in 95% of the population, this is normall between 18-20 LITERS of normal saline.

    Don’t waste time getting a right sided EKG. There is no need and no point. If you can’t tell from the original EKG that it is an RV infarct, then send the EKG to someone who can. Don’t waste time teaching an EKG how to do a right sided EKG.

  • Brandon says:

    Donna,

    Certainly the pt needs a cathlab, no dispute there. My comment about the free radicals lies in a concern over exascerbation of the reperfusion injury that is already going to happen, with or without the additional flow of concentrated O2. “The more oxygen, the better” doesn’t hold true as an absolute for ACS, especially when it has an impact on the dreaded M’s. Quality of life is ultimately the “save” for this pt, and by no means a “moot point”. We need to look beyond getting them to the table.

  • harrison says:

    dr alo do you have a source for the 18-20 liters of fluid study?
    i want to present that to my medical director

  • Terry says:

    Dr. Alo,

    I agree with not doing right side V leads if it is clearly an IWMI. I don’t agree with the 18-20 liters of fluid—you know you have given them enough when you can hear it in their lungs. If this is a new approach with documented proof then so be it but it is not taught anywhere that I know of in prehospital. Morphine is definitely losing favor but in every cardiology lecture I go to I ask the cardiologists about not giving NTG to pts with a RVI and everyone of them says to give it. I am just a Paramedic working under local protocols and am restricted by these protocols as to what I can and can’t do. Does anyone know if the new AHA ACLS guidlines follow this approach? We are also taught that it is inhumane to leave pts in pain.

  • Stephen says:

    I agree that it’s a MI. I thought we learned from the studies that patient’s that received morphine did worse but it was never decided if that was because of the morphine or because the patient population was sicker in general. A good alternative would be fentanyl. That seems like a lot of fluid and I would be interested in reading the article if provided. As to the nitro, I would give a trial run after judicious fluid administration, not all proximal RCA occlusions drop their pressure with nitro administration. I am not sold that all STEMI patient’s need 15L of oxygen. I feel that it should be titrated to their saturation assuming that the patient is perfusing well. 15 leads i think should be done because it can give you a better idea of the culprit artery. It doesn’t take that much time to move leads. What is weird to me is that the machine did not pick up on the MI.

  • Aharon says:

    first he have inf.+ant+lat STEMI so we have to give nirro SL 2.5 mg , aspirin chew give O2 vein line with 0.9% NS for be save slowly heparin 4000IU I.V transport to the catheterization romm in ICCU

  • Brandon O says:

    LOL at “I-waves,” Chris 🙂

    Love to hear the other shoe drop on this one — very curious to know what hypothetical occlusion is causing infero-antero-low-lateral-right-sided injury with septal and reciprocal changes. Maybe vasospasm but that seems extreme. To paraphrase Dr. Weingart, this looks like the work of the devil; we may need a priest rather than a cath lab.

  • CanMedic says:

    I agree that this screams right ventricle. I also agree that this screams anterolateral STEMI too. What could cause so many leads to have elevation like this? Left main disease in a patient that falls into the 10-15% of patients with the circumflex supplying portions of the right ventricle perhaps?

    I’m half asleep after a long night shift but a thought also occurred to me: when we get “funny” results with ecg’s part of our trouble shooting is lead placement. In this case let’s assume that the leads are properly placed (as I’m sure they are) but what about the heart? Consider human anatomy- is it possible that this patient has lived for 69 years and never knew that he has dextrocardia? I’ve tried to imagine these ecg’s completely reversed and I keep seeing a bonafide anterolateral MI. I think although I do need lots or sleep. Either way he needs a cath lab yesterday.

  • arnel says:

    If the extra p waves that I see are not artifacts then this could be ST vs AT with a 2:1 AVB. If this is a 2:1 AV block with this short PR then this could be a bad sign (an infranodal problem). STE III>II, SDT aVL>I all points to RCA as culprit artery.STD V1-V2 could be reciprocal changes. STE V4-V6 (V3-V4 STE could be artifacts, hard to tell in a 10 second snapshot) and the STE in V5-V6 could indicate extension to the lateral apical myocardial zone (bad). The cause of such extension (if this is the case) may be occlusion of the LCX or RCA (which is more likely in this case) with a posterior descending or a posterolateral branch that extends to the apical zone. STE in V6 in an inferior infarct is associated with larger infarct size and major arrhytmias. Yes V4R speaks for itself.

  • nadams says:

    Hello everyone, I am really enjoying reading the responses that have been written here……..learning alot. I would like to point out a couple of things that I’ve been reading.

    1. “You don’t need to right-sided leads to verify a RVMI”. With all the literature that I’ve read in cardiology and 12 lead interpretation, I never heard of such a thing. The normal 12-lead EKG ONLY looks at the left side of the heart……not the right. Reciprocal changes in the anteroseptal leads only verifies that the occlusion is a mid RCA occlusion….not a proximal one. Even in the absense of reciprocal changes of a posterior wall MI(involvement), the patient may be left-sided dominant. The ONLY way to verify a proximal RCA occlusion (RVMI) is by doing, at a minumum, a V4R. How long does it take to throw one patch in the V4R position and push the 12-lead button?………..10 seconds? The information you get by verifying a RVMI is good information to know before you start your treatment.

    2). Not all RVMI patients are preload “dumping”. The patient’s SBP is 142? Is RV dysfunction evident? The only way to find out if the pt’s heart function is NTG sensitive, is to give a trail dose of SL NTG. I would have an 18 and 16g bilateral IV established with 1000 mL’s NS connected and running while administering the SL NTG. If the pt’s B/P dumps, lay the pt down and elevate the legs and continue the bluid boluses (pressure bags?). I would not, however, give the patient fluids to the point of fluid overload and pulmonary edema. This compromises the patients breathing and oxygen exchange….exacerbating the whole situation. The pt does need NTG to dilate the coronary arteries for myocardial perfusion. A Tridil gtt would be easier to titrate to effect and SBP.

    3) “Patients are allowed to be in pain”. Really? This is the number one under treated condition in prehospital and interhospital care….pain control. If the patient is sensitive to NTG, I would not give the patient Morphine. Instead, Fentanyl would be a good substitue for pain control. The patient DOES have pain. Pain increases anxiety. Anxiety increase heart rate, O2 demand and consumption. Releiving the pain, you reduce these things. Fentanyl does not have the vasodilation effects that morphine has. Chest wall rigidity is a result of pushing the medication too fast.

    4) There is definately evidence of an anterior wall MI also, which indicates multiple vessel involvement of the proximal RCA and the LAD……it happens.

    5) Someone had a very good point that this may be secondary to an aortic aneurism. While this may be true. The aneurism blocks the opening to the RCA thus creating a proximal RCA occlusion. There is only one problem with that theory…….Why the anterior STEMI? The anterior STEMI gives evidence that this is secondary to an ACS. Also, no radiation, especially to the back.

    So what are you going to do? You can do O2(4 lpm NC or 15 lpm NRB, keeping the SpO2 98-99%), ASA, IV’s, fluid boluses, EKG, and transport. Or, you can be a prehospital clinician and do a proper, more thorough, patient assestment and treatment based on your findings. Do what’s best for your patient with the tools, knowledge and experience that you have.

    Everyone agrees that the definitive treatment for this patient is reprofusion in a cath lab with PTCA or even CABG.

  • Dave B says:

    for what it’s worth, in the setting of IWMI, I believe the ST elevations in V3-V6 are reflective of lateral extension of the IWMI rather than an “anterior” stemi many are referencing. for that to be the case, you are implying an occlusion of both the right and left coronary arteries, which would be a very uncommon occurrence. considering the patient presentation and the pressure they are still making, the “company it keeps” would seem to go against this.
    Tom, i’d love for you to comment on this if you could.

  • Ed Eno says:

    humm,I/Mi,No morphine,no nitro.Fentenal is your drug of choice.Fluid to B/p,don;’t over do it.ekg,Iv,O2 with no pulmanary hx.even so ,tube em.Barf bag ready,alert hosp for cath team.and place your pads just to be safe.

  • this is a rare but good reason why mandating the message “ami suspected” be present before transporting to a stemi hospital is not wise policy. there should be an allowance for crew judgment. but of course, the flip side is that crew judgment, it seems, is often suspect, and false activations more often than not piss hospitals off, especially the really ridiculous ones, like artifact, pacemakers, etc.

  • Troy says:

    Granted I’m just a poor meager medic, I can’t agree with the doctor on this one. I believe fentanyl is totally plausible to this patient and prudent. If you leave the pain, you leave the extreme catacolamine releases and all the bad side effects of it. Fentanyl has no vasodilation effects and can be titrated to effect. The fluid overload to the point of pulmonary edema is asinine in my opinion. Fluid overload causes secondary issues that could be detrimental to the patient who has underlying conditions and if you don’t carry RSI and PEEP, well your going to be way behind the 8 ball. Sure, maybe I could take it being young and healthy but how often do you pick up a young and healthy MI patient….

    I hope anyone who treats me would treat my pain. Otherwise your just a torturous jerk in my mind. Anyone who doesn’t treat pain is negligent in my book

  • Troy says:

    Hey Doc,

    I too would like to know where your study on opiates came from. The only peer-reviewed article I read was on MORPHINE ONLY not Fentanyl in increased mortality in MI patients. Yes, there was an increased mortality in patients suffering from MI who were given morphine but it was specifically the NSTEMI that suffered the highest mortality, hence the 2010 AHA guidelines are now 2-4mg MS in STEMI patients and 1mg cautiously titrated in NSTEMI patients with no relief from NTG

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