65 year old male CC: Fall with injury

Here's a very interesting case submitted by a faithful reader who wishes to remain anonymous. Some changes have been made to preserve patient confidentiality.

EMS is called to a local breakfast restaurant for a 65 year old male who fell in the parking lot. He was reported to have suffered a head injury.

On arrival the patient is found sitting in his car. He appears critically ill. Skin is pale and diaphoretic. Nail beds are blue. The patient's level of consciousness is significantly diminished. His shirt and pants are wet and it's not clear if he was incontinent of urine or spilled a drink on himself. He has audible expiratory rales without the need for a stethescope. 

The patient states that he tripped and fell. His wife states that he was "fine" prior to falling but she does not impress EMS as a good historian. When asked about his history she says, "heart." 

The head appears atraumatic with the exception of some abrasions to the face. He admits to head pain "all over" and keeps muttering "please take me to the hospital."

Due to the patient's diminished level of consciousness it is not possible to clear the cervical spine with any established criteria. However, the paramedics conclude that the patient cannot be laid flat and elect to defer spinal immobilization. The patient is placed on the gurney with the head elevated and vital signs are assessed.

  • RR: 30
  • HR: 148
  • NIBP: 150/77
  • SpO2: 58 on room air

The patient is placed on a NRB mask @ 15 LPM. The chest is exposed and no chest trauma is apparent. Breath sounds: rhonchi and rales bilaterally

The patient is given a dose of SL NTG and loaded in the back of the ambulance. At this point the patient appears peri-arrest.

The cardiac monitor is attached.

A 12-lead ECG is obtained.

What would you do next?

See also:

65 year old male CC: Fall with injury – Conclusion


  • Susan says:

    A fib with a rapid ventricular response – left bundle branch block.  Need to notify the hospital to try to get an old EKG to check if this is new onset or not.
    Initial priority is the low oxygen saturation and rales.  I'm thinking flash pulmonary edema if he was truly fine earlier.  I would get him on capnography.  My state protocol if he's conscious enough is CPAP, subligual nitro, an inch of nitro paste. (other states lasix).  Transport.  Reassess for trauma.  Does he obey commands, pupils, etc.

  • Daman Deep Singh says:

    acute coronary syndrome with LVF with sinus tachycardia with LBBB with possibly syncope
    Diuresis, NTG
    X Ray Chest
    Echocardiography to confirm
    NCCT to rule out any CVA & hence anticoagulation

  • FB says:

    A-flutter with LBBB vs V-tach. I'd think about getting aggressive with NTG and maybe some diltiazem. If that didn't work quickly or patient loses consciousness I'd cardiovert and if that failed I think I would be forced to RSI patient if CPAP did not help. Scary patient. Anyone else notice how the QRS amplitude varies…possibly with respiration? The variation is almost cyclical.

  • Alex says:

    there are fusion beats so it is VTach

  • achu says:

    this is not AF,This is broad complex tachycadia,Need ABGandCXR for to rule out respiratory causes.

  • Andre says:

    With the diminished LOC, this patient would be a great candidate for KED so thatvu can at least maintain some Cspine. However this is a very critical patient and I would feel as if that would take too long… Secondly the patient is obviously having an acute pulmonary and cardiovascular incident which I would agree when the comment of very aggressive treatment is required… I feel as if this patient is a 100% candidate for RSI, not only due to all the changes in the patients status but due to the altered level of consciousness and the severity of his oxygen levels. This patient won’t tolerate laying flat for a CT therefore intubation is certain.. as we all know a new onset of a LBBB is a very acute problem and should be treated as such …. But we also need to treat our patient… This patient ( as many as we see) is presenting as if he also has a head bleed. I would agree that CPAP is a great place to start but this patient appears to be beyond that point add intubation is not preventable…. I would be careful with anything other then nitro for vasodilation but I would definitely give some lasix…. This sounds like a difficult case and I commend the EMS provider for the quick decisions in which may have saved his life!

  • Firescue231 says:

    Treat the respiratory problem first. The heart rate will come down, the oxygen saturation will come up. The body is compensating by increasing heart and rate and respirations in its best effort to push out the fluid in the lungs. CPAP vs. Intubation, Nitro and Lasix. As for the EKG, seems to be sinus with LBBB and a LVH, with some possible lab abnormalities. Either way, the patient needs more advanced care than an ambulance. 

  • Andre says:

    This is a perfect candidate for a Nitro drip! And I agree with firerescue231

  • Nick Adams says:

    Very difficult 12 lead, but here's my interpretation.  Wide complex tachycardia, Physiological LAD, LBBB, LVH,  There is a disturbance in the TW's, which could be PW's hidden in there, Hyperacute TW's in the precordial leads that look like it would hurt if you sat on them makes me believe this is Hyperkalemia.  Is it VT? Could be, but I doubt it.  It's kinda slow, not ERAD, V1 is negative and V6 is positive so there's no concordance, and the morphology of V1 is not indicative of VT.  Pt is in CHF….so that needs to be addressed first.  Even though the pt and spouse are poor historians, they still may know the meds he is on.  Is he on Spirolactone or any other potassium sparing type diuretics.  While the O2 via NRB is ok initially, CPAP would be better.  Bring the patients O2 up to above 90.  See what it does to his EKG (3 & 12)NTG SL till you get the CPAP on and then NTG gtt starting at 10 mcg/min titrating up to a max of 200 mcg.min.  If he is hyperkalemic, lasix will help remove K+ anyway, and treat the CHF.  Because hyperkalemia is a suspect and the patient has evidence of LVH and Lt. sided CHF, you could talk with med control and see what the doc thought of giving the pt CaCl IVP (slow). Calcium with reduce increased postassium and strengthen myocardial contractions.

  • Fire medic24 says:

    Too slow for flutter with 2:1… Too regular for afib…it is either vtach or sinus tach… Not seeing any p waves and vtach would explain syncope and sudden LV failure. I do see some abnormalities in the t waves, but when you compare with other leads they don’t match up. I am highly suspicious of vtach. If I don’t see any improvement with cpap in the next couple minutes I would cardiovert.

  • Fire medic24 says:

    I suppose flutter 2:1 is a possibility as well, but I don't see any flutter waves in the rhythm strip.

  • Why do you say it's too slow for 2:1 flutter?

  • Helen says:

    I love reading the comments!  I presume that everyone who comments has some level of medical training?  And yet there are (so far) at least 10 different interpretations of the rhythm and as many different treatment plans.  The fact that the responses are so varied helps me illustrate to my students why it is so important to treat the patient, and not the monitor.  When I look at this EKG I see something pretty regular (R-R) with a decent rate.  That's all I need to know…he has a decent BP so whatever the rhythm is it appears to be working for now.  Better get busy fixing the pulmonary edema before he drowns!

  • MaEMTB says:

    Does anyone else think this could be an accelerated junctional with LBBB? If the P-wave is truly hidden I think this would be possible. I would try and get a little history about the fall from some people maybe standing around the area, and bring the wife in the front seat in case she randomly has a med list with her. However, this pt. needs rapid transport obviously. Pt. upright is a good idea medically, but risky. Definite NTG and depending on how severe the crackles are give Lasix IV. CPAP for sure. Transport priority 1, and Prepare for defib. Cardiovert, but  if necessary. Recommend a head CT at the hospital as well as reviewing old ECG's if pt. stable.

  • doobis says:

    Given the PT's vitals I would not worry too much about looking at the EKG trying to fingure out if it is A Fib RVR or a sinus ry.  ABCs is what needs to be the goal.  His sats are so bad he is going to go into arrest if things do not improve.  Oxygen.  CPAP if he can tollerate.  Nitro SL and Tridal drips.  Intubation if he does not improve.
    After that if I have time I'd look more closesly at the EKGs.  I see a sinus tach with LBBB.  I believe there are P waves seen in the T waves.  Also the T waves are concord. in V5, V6, and II.  I'd worry about a new Lateral AMI.  Doubt he will be able to chew up the ASA when he cant breath so I continue the tridal and think about morphine while going emergency to the cardiac hospital.  (very cautious with morphine and I don't like lasix so I would not give it except as a last resort.)

  • Nick Adams says:

    AMAMEDIC –  I agree with you moslty.  CPAP, NTG and Lasix.  CaCl was down on my list.  All other thing woulds be done.  This is a scenerio which is assumed to have a longer transport time then 5 minutes…….lol.  the CaCl is based on the suspicion of hyperkalemia,based on the ECG findings AND a good patient history to include med list..  100mg of CaCl is helpful if Hyperkalemia is suspected, and wouldn't hurt him otherwise.  You don't need lab values if the potassium is high enough to cause EKG changes.  This patient doesn't have the criteria for a STEMI and there was no mention of CP, so an MI is probably not the culprit.  People are trying to come up with treatments that make sense to them and are still ever learning…. so give them a break.  The KED would allow the patient to sit up and still provide the maximum spinal support given this situation.  CaCl as i stated above.  Not so sure about the Echo.  Maybe that person is one who predominantly works in a hospital envionment, and is concerned with looking do hypokinesis or akinesis?  Now is the time that prehospital providers must step it up through education and good prehospital diagnosis and treatment.  We are not just ambulance drivers anymore.  If people are concerned if this is ST, VT or 2:1 AF, Amiodarone could treat all of these things.  Our protocol allows us to give Adenosine @ 6mg to help diagnose an uncertain wide complex tachycardia.  I'd save the cardioversion as a comlete last resort, while the patient is talking to you, so he is stable enough to not do that right now……..it hurts alot. If you have time to medicate for pain and sedation prior to this treatment, you have time for other meds as well.

  • doobis says:

    As an addition to my earlier post:
    The fall did not cause the CHF; almost certainly his hypoxia caused him to fall. The fall was only ground level. The body can be fragile especially in the elderly but not usually so fragile to have to worry about a skull or spinal fracture from a ground level fall. People have those falls all the time and simply get up and keep going. If the fall was 3 times his height or there was obvious ‘real’ external trauma I’d be more concerned. SMR would certainly worsen his condition and would be practically pointless even if the fall was his only complaint excluding s/s of head trauma. EMS and emergency medicine is often more an art based on common sense than a science measured by a textbook written by people that have never truly been in the field. Besides many studies have shown SMR causes more harm than good in most circumstances. We in the USA are just too stubborn and scared of lawyers to always adapt to the best practices!

  • Canuck Medic says:

    The fall could be the cause. With his decreasing LOC, it could be neurogenic pulmonary edema. It’s less likely but you can’t say for sure that it’s not. I agree with the treatment of O2, CPAP, and nitro but I’m curious why the Lasix? Are we treating left sided heart failure or right? Nothing in this call points to systemic fluid overload. It may be a factor but with the description given it points more to a pump issue

  • Firemedic24 says:

    Tom, I corrected myself in the next post… It could be a flutter 2:1, which would make it regular. Generally atrial rates in a flutter are 300 or more and 2 : 1 would yield 150 ventricular rate…

    As far as treating the pt not the monitor… There was a time I would agree with you, but now I am in the school of thought to treat the pt AND the monitor. EKG is another tool just like capnography or blood pressure. There is indeed a great deal of variance in opinions, but that Is not necessarily a bad thing. This seems like a difficult case. I have seen cardiologists argue for hours on end over subtle ECG changes.

    KED? Sure… I don’t think it will make much difference… CPAP, NRB, or RSI… Whatever gets the job done… Antidysrhythmics v cardioversion… Both will do the job. This is a difficult case and there are many ways to proceed. It is difficult to say how someone will act given the limited info provided and an ECG. The truth is we are processing thousands of things that can’t be portrayed in a short text. I have told my basic plan, but I don’t think it is the only way. Ultimately alot of decisions will be made in the ongoing assessment. Don’t get me wrong I still beleive in do no harm and if it ain’t broke don’t fix it, but when the pt is described as pre arrest I better have plan a, b, and c lined up.

  • Robert says:

    12 Lead Interpretation: A Flutter w/ 2:1 AV conduction. Atrial Rate at 290(best seen in lead II), LBBB (Negative deflection in v1, LAD, Broad monophasic R waves in Lateral Leads V6/I QRS>0.12).  Fast, Wide, Regular, Absence of P waves in all leads. Differential Diagnoses: V Tach vs A Flutter. When ever the heart rate is 150 + or – 20, A Flutter should always be considered.
    Treatment: Spinal Immobilization, thankfully, is getting out of our system shortly. Soon, all we'll be using is a Collar. That's for another discussion though.
    CPAP is not indicated for the patient due to his ALOC. This patient immediately needs to be intubated. I'd stay away from the NTG due to his recent fall given the fact he is probably on blood thinners. I wouldn't do anything for the heart rate unless it started to show signs of hemodynamic instability, at that point i'd strongly consider cardioversion since I wouldn't have as much time as I do right now to distinguish between V tach & A Flutter.

  • Patrick W says:

    The EKG is concerning but I’m not prepared to say that the tachycardia is what is causing the symptoms. That said, I would keep an eye on it , if it remains ~147 despite treatment I will be more concerned with the rhythm. As of right now, I’m concerned with his airway and breathing.

    It certainly looks and sounds like CHF. His blood pressure is not as high as I would expect it to be with someone in his condition, so I wonder if it is on the way down as he is peri-arrest. The varying QRS amplitude has me wondering about pericardial effusion.

    I would treat as CHF, CPAP and liberal doses of NTG. RSI if necessary, and peri-arrest is as good a time as any.

  • Nick Adams says:

    If the pt admits to "Pain all over", and says "Please take me to the hospital", he's alert enough for CPAP and too alert for cardioversion.  His AMS is probably due to a RA SpO2 of 58%.  He does have hemodynamic instability in the form of LV failure.  I think the guy has CHF secondary to LV failure from a decrease in contractility and not from fluid overload like Canuck Medic pointed out.  Great comments from Firemedic24.  All is going to be based on pt history and medication list to give us a clue as to what is going on so it can be properly treated.

  • Nick Adams says:

    If the pt admits to "Pain all over", and says "Please take me to the hospital", he's alert enough for CPAP and too alert for cardioversion.  His AMS is probably due to a RA SpO2 of 58%.  He does have hemodynamic instability in the form of LV failure.  I think the guy has CHF secondary to LV failure from a decrease in contractility and not from fluid overload like Canuck Medic pointed out.  Great comments from Firemedic24.  All is going to be based on pt history and medication list to give us a clue as to what is going on so it can be properly treated.  I just love these discussions….lol.  I learn so much from all of you because everyone has some good points.

  • doobis says:

    I keep reading people talking about antiarrythmics and cardioverting the guy.  I just don't see that at all.  He has an good B/P and his HR is only 150.  Why would you try to control that?
    If I was drowning on my fluids I'd probably have an adrenelne response and my HR would go up to 150.  If I was highly hypoxic and I assume that my CO2 exchange is also highly inhibited, I'd imagine my HR would increase to try to compensate for the overall hypoxia just as your HR increases when you perform physical activity to increase gas exchange throughout your cells.  
    Need to get the fluid out of the lungs, oxygenate his blood, aleive the respiratory acidosis, reduce the workload of the damaged and strained heart, and evaluate from there.
    But, we will see the conclusion soon enough!  It has been interesting and fun seeing these comments.

  • Robert says:

    @ Nick: From the story given above, " He appears critically ill. Skin is pale and diaphoretic. Nail beds are blue. The patient's level of consciousness is significantly diminished."
    From reading that statement, he sounds significantly altered. They also say he appears to be in peri-arrest. To me, that's past the point of return. I'd be very aggressive w/ the airway as well as getting the Dopamine set up as he appears to be about to go into cardiogenic shock…

  • Fire medic24 says:

    Ok, I apologize in advanced for being long winded in this response, but I feel like it is important to not only describe what I would do, but why.
    First I will give my observations as to pt condition and pathophisiology.  65 yo m who's max heart rate should be 155 bpm…  Currently the heart rate is below that, but I need to keep in the back of my mind the fact that structural heart disease can make the heart less tolerant of tachyarrhythmias.  Given the hx of "heart" there are quite a few things that pop in my mind…  Previous MI… Helps support vtach dx… Valvular replacement…  Helps support tachyarrhythmias dx.  The general impression is poor as the pt has altered mental status and respiratory distress/failure.  I wish I were good enough at ECGs that I could say with absolute certainty this is x rhythm.  Generally when I have a pt in poor condition and the ECG is wide and fast I think vtach. However there are certain things in the ECG that make me think twice.  First no axis ERAD,second no fusion beats that I can see.  However I don't see any p waves (which may be hidden in the t wave, but the t waves look pretty uniform especially in V1 where p waves should be more pronounced.  A flutter is a possibility albeit less common.  So my three options are vtach, sinus tach, or a flutter.  Moving on, but keeping that in mind there are some things I need to find out quickly in my assessment.  JVD? Cannon waves? Etc…  I also want to listen to heart sounds.  Are they muffled or do I hear any mechanical abnormalities?  Do I see a scar along the chest indicating open heart surgery?  These are important findings that could direct my care.  All of these assessment findings take no time at all and could make a difference in care.
    There are other assessment procedures that may become necessary as time goes on, but this starts me off.  Moving on I would get bipap/cpap started early.  This leads to important discussion.  Firstly some consider bipap/cpap contraindicated due to mental status.  The reason nippv (non invasive positive pressure ventilation) is contraindicated in altered mental status is failure to recognize vomitus aspiration, or airway failure.  In the hospital setting this is important as nurses and doctors tend to leave the room.  In this case I am at the bedside constantly evaluating the pt.  Not only is nippv therapeutic, but it is also diagnostic.  If the patient improves, great! I will keep it there and not move any further.  O2 come up, heart rate go down? Great let's reevaluate the ECG and treat accordingly.
    let's say things aren't so rosy.  With nippv in place I am perfectly set up for Delayed Sequence Intubation.  (a great concept pioneered by Scott Weingart) If you are unfamiliar with DSI I highly reccomend you research this topic for yourself.  Furthermore if the pt does not improve I want to know how things have changed.  If there is a significant drop in pressure (due to intrathoracic) pressure.  That supports cardio genic shock due to heart failure.  The alternative is SCAPE sympathetic crashing acute pulmonary edema due to catecholmine response of a diseased heart.  
    This makes no mention of the trauma.  Judging by the description, the trauma seems like a non issue, but that comes down to assessment.  If I think there might be a bleed no nitro.  If it seems like a non issue, nitro is good.  As I move on with my assessment I may go to lasix, but I will be absolutely sure that this is not vtach before doing that.
    finally, the ECG… I am keeping vtach in the back of my mind, and cardioversion is my panic button.  I.e. nothing I am doing is working the pt is continuing to deteriorate.  As I am continuing toa asses my pt I am looking for more clues as to vtach or not (fusion beats, previous MI, decrease in BP etc.)
    In attempt to respond to the comments about heart rate too low, blood pressure too good for vtach… I would say in the pre arrest patient I trust my eyes and my hands more than anything.  Pre arrest to me means poor perfusion.  There is a lot of unknowns as far as mental status and what I deem pre arrest might be different than the author or you.  Honestly the decision on cardiovert or no can not be made with the information given, but I would not rule it out.  Furthermore blood pressure does not always mean cardiac output.  It is a small piece of a big puzzle.
    I am excited to see the conclusion to this case.  I am humbled by the ECG, but I am learning more every day.  I hope my thought process can help others improve as I try to improve by reading all of your comments.  It is difficult to try and treat life threats without fully understanding them, but sometimes we are limited by what we can do and what we have time to do.

  • Fire medic24 says:

    Also, I mentioned if nippv worked I would reasses ECG and treat accordingly.  Let me specify treat accordingly.  Hopefully the ECG has slowed a bit to help dx the rhythm with more certainty.  If not I think it might be a good idea to consider vagal manouvers or adenosine depending on several factors.  The adenosine is mostly diagnostic, but also could be therapeutic in the rare case this is svt w/ aberrant conduction.

  • Byron Wanstall says:

    Oxygen, IPPV, GTN , Lasix. Morphine if chest pain present. Positive inotrope consider dobutamine and get the pads on him might need to light this guy up like a christmas tree 🙂 neurogenic pulmonary oedema is a possibility but I think that can take a couple hours to develop after neurological insult and papa didnt wet his pants, his sympathetic nervous system is intact. Treat the SVT which has caused the acute pulmonary oedema. If im wrong, game over.

  • CardiacRN/Medic says:

    I can see some very good points and some points that I disagree with on this scenario.  First off, I have to agree that because this was a fall from standing I would not bother with SMR.  This is a sick individual and the KED vest takes time to apply.  I would simply do what we are all taught and do and perform a brief trauma assessment of the spine and neck and assuming no abnormalities would leave it alone.  This pt has bigger problems.  The 12-Lead to me looks like Sinus Tach. with a LBBB.  Sounds to me, that he probably is having an exacerbation of his CHF.  I base this on his lung sounds, and clinical appearance.  Also from the fact that he wet himself, more than likely this guy takes diuretics at home and with the syncopal event just lost control.  Yes he is approaching his max heart rate but as someone else said wouldn’t you if you were drowning.    O2/large bore IV and RSI, this guy has a sat of 58% he needs a tube and secured airway ASAP and then we can treat the underlying conditions.  The tube could also offer us some informal diagnostics; perhaps if his pulmonary edema is bad enough we will see the textbook "pink-frothy sputum" and have a pretty decent diagnosis of HF.  Now with that said, let’s throw some pads on him just to ward off evil spirits and go to work.  I would give him NTG x3 (depending on pressures) and give him Lasix (40mg sounds good to start, we can repeat with another 40mg if he needs it), as it will help with the pulmonary edema and the hyper-K.  We can use MS if we have to at that time.  I would definitely have some Dopamine on stand-by incase this whole thing goes south.  I disagree with what someone was saying about CaCl, yes its good for hyper-K however, it creates other issues such as VF/VT if we don’t have a level and increased MVO2.  Sounds to me that if this guy makes it to the hospital he is going to buy himself a Swan-Ganz and an IABP for at least a week or so.

  • CardiacRN/Medic says:

    Also I dont disagree with the CXR and the ECHO.  By doing those you will find any wall abnormalities in the heart and get a chance to evaluate valve function and %EF.  Those are good clinical tools however, not exactly something you can store in the cabinet of the squad.  Definately, in house diagnostics.

  • Andre says:

    In this Situation as I previously mentioned a KED is Contraindicated due to the severity of the patient. The one thing I think all agree is Lasix and Nitro CPAP or Intubation.. Its so nice to see that Each Paramedic including myself… Has a different ways of getting the job done but in reality we are doing the samething.

  • Andre says:

    Dobutamine is contraindicated in this situation due to the Tachydysrhythmias…. S.E. is also VT, VF and AMI… This is not a drug that I would suggest but it is adequate without the Tachy Dysrhythm

  • 1OregonCoastMedic says:

    Aberrantly conducted ST w/ a LBBB. But this guys primary problem is us treating the monitor… FIRST AND FOREMOST fix the airway/breathing problem. IV, Nitro, CPAP, Lasix if your protocols support it. I would bet that his HR reduces and his SPO2 increases rapidly… If not RSI. I have seen CPAP & Nitro turn 60ish SPO2 into 98 on severe CHF… Remember putting a patient on a vent increases morbidity significantly. I agree that if I do not see a significant difference w/ CPAP then RSI and try to keep PEEP up w/ bagging. I guess we are all looking at is this a cardiac rate/rhythm causing the problem or as I believe exacerbation of CHF causing hypoxia retention which is causing the increased HR. Which is probably going to if not already is causing cardiac damage.

  • 1OregonCoastMedic says:

    Oh, and good CASE!

  • 1OregonCoastMedic says:

    Just re-read my post its supposed to be "morbidity & mortality" not just morbidity…

  • FB says:

    Peri arrest after just 1 NTG? Maybe thinking aortic stenosis? Maybe he took the little blue pill in anticipation of an afternoon delight? Deeply, what do you think the rhythm is? SVT? AF?  Sinus tach? I can understand if you think that the tachycardia is compensatory if it was sinus tach but even an A-fib at 150 would need to slowed down? No? If its A-flutter I doubt that would be compensatory and I don't think you can ignore a possible rate problem if there is this presentation? Given his wide LBBB and heart history any excessive tachycardia can't be helping to pump blood from the LV and prevent backup into the lungs? Your thoughts?

  • techno_medic says:

    Wow.is.right …what a response. I did.like to see everyone’s idea. My thoughts first even though is is a interesting ecg we need to start with airway and breathing. As far as I am.concerned.if.the pt can follow my commands and talk NIPPV is my first choice. I tend ore treat with.zofran during cpap if I worry about vomiting at all. I.do RSI where I.work but I.would start with cpap and.see if the pt improves. If the pt gets worse or.spo2 remains that low. I.would rsi. If cpap works then NTG I.would keep with that. Def keep an.eye on how.much no.drop happens between NTG. We don’t use.lasix or.morphine anymore.for Pulmonary edema in our area. We can use ativan or.fentanyl for pain or anxiety control. As for the echo. I.am thinking stach with lbbb. Also lvh. I am concerned about the t waves and hyper k+
    I.would not treat now but have the pads on and cacl and bicarb ready if the qrs.widens out and the pt.codes. I also have also worry about the greater than 5mm st evel v1-v3 with discordant to the qrs( ami is.possible as underlying cause of LV dysfunction but I.am not going to fix that here) also my eta to.the hospital may effect how far we tx this pt.
    In the end its great to.think and look.fen.zebras, but tx the horses first .

  • techno_medic says:

    Sorry auto correct. That was suppose to be watch bp and.not echo. Suppose.to.be.ecg.
    Again nice to see everyone’s ideas

  • Robert says:

    Here's some information regarding new onset LBBB's. Always interesting to see information constantly changing…

  • techno_medic says:

    Ct medic
    I.don’t know what part of ct you are.from. I.work in north central.. have you xmited a non stemi yet. Just wonder what type.of.response you got from.the hospital for it
    But again I agree. Fix the breathing and I.bet the does.much better than shocking or.give cardiac.meds

  • arnel c says:

    Reqular, momomoprhic wide QRS tachycardia with a cycle lenght of 440 ms (~136/min), QRS alternans prob rate-related, LAD, poor R wave progression, LVH, LBBB, tall T waves in precordial leads, prolonged QTc and a 40 ms notch in the terminal limb of the QRS in V4 which could be Cabrera sign. Difficult to get PRI since P may be hidden or fused with the T waves but tracking the P waves in the T waves, there are some distortions in the the T waves w. The differentials in this case could be ST, AT,  slow AFl in the setting of LBBB and VT. Tackling VT: wide QRS with LBBB morphology, the initial R in precordial is narrow, the RS is about 40 ms, no notch in the downstroke of the QRS in the precordial lead, hard to say if there is AVD.
    In the rhtyhm strip there seems to be a quadrigeminal occurrence (best seen in III). There seems to be retrograde P waves with an RPI of about 140 ms. So could this be ventriculo atrial echo or VA conduction (1:1). Getting that interval, I bevelieve there is AV dissociation. VA conduction (1:1) was found about 64% of cases in a study by Wellens and Lei. It is uncommom when the vent rate is rapid. Thus, with age, wide QRS, probabiliy of an old MI (cabrera sign) and AV dissociation, I will enteratain and manage the case as VT (peri-arrest as mentioned).
    In addition the tall, wider T waves looks very suspicious for hyperacute T wave. Unless the lab comes out with the K, I will also entertain ACS prob Mi on top of this tachyarrhtyhmia.

  • Medic77 says:

    I would apply a NRBM at 15 LPM to see if his Saturation improves.  If his SPO2 does not rise to at least 90% than CPAP him. This is screaming to me CHF or flash pulmonary edema .  AT the same time, I would have my partner apply the monitor and obtain a 12 lead.  I would also have a NC ETCO2 applied to see about his output.  If the wide QRS tachycardia is the cause of the rales and SOB, then Load and Go getting IV access and I would transmit this 12 lead to the ER for review, obvious LBBB.  I would obtain orders for Lasix and give him SL nitro.  If he starts to deteriate further, sedate and Snyc shocks starting at 100 joules.  Also, since you can't lay this guy flat for obvious reasons, apply the KED board with a c-collar and this way you can sit him up while keeping his c-spine immobilized. 

  • firemedic24 says:

    After taking a second look at the initial rhythm strip it is indeed too slow for flutter.  The R to R interval is a little longer than in the 12 lead.

  • UK CCU Nurse says:

    High flow O2 via NRM, on scene thrombolysis and/or get to nearest cath lab.
    Probably AMI with pulmonary oedema. Sats won't pick up 'til artery open. No nitrate as ?AS given age and limited history. IV morphine ans IIb IIIa if at hand.
    Just a thought?

  • medic7044 says:

    I agree with what another comment i read…i believe this is a sinus tach with LBBB. High con oxygen while ur partner sets up cpap, 1 dose SL nitro, CPAP, IV, at least for my protocol 40-80mg lasix…i would try to see if he takes lasix so you can give a more accurate dose. Rapid transport is the highest priority. In my opinion this is a APE 2/2 AMI until proven otherwise, a lot of reevaluation of vital signs and mental status must occur, he seems to be teetering on the borderline of intubation.

  • Adrienne Linn says:

    I’ve been reading all the options and it was interesting to see all the ideas presented and to finally find out what the issue was with cpap for altered patients. I’d just like to note that my first pt I every C-Papped a patient, they had a GCS of 3; 25 minutes later, they were a GCS of 15, signed my paperwork and thanked me for helping them, so I have a hard time buying the altered, don’t C-pap ultimatum.

    On to the case study, I would love to have updated vitals because that will determine my treatment. Peri-arrest indicates to me low BP and poor peripheral pulse, breathing has slowed and needs assistance(BVM and intubate if needed), and patient is most definitely a candidate for sync cardioversion or defibrillation. Otherwise, if vitals are unchanged, C-pap and nitro would seem to be the order of the day, at least in the beginning. This is an unstable patient and consequently a dynamic call…there is no clear, simple answer based on the information we have. I think the key is reassess and treat, or leave off treatment, as necessary.

  • Brooks Walsh says:

    Since there are a large number of educated and thoughtful prehospital responses above, I'll tailor my response to that of the receiving emergency physician. This is a great case for that, as there are no simple interpretations, and a large component of the decision-making would rely on "being there."
    First off, I would prefer that this patient NOT be immobilized. He certainly could have a cervical spine fracture, but there are competing priorities. And while the evidence is zilch that immobilization prevents/treats neuologic damage (http://summaries.cochrane.org/CD002803/spinal-immobilisation-for-trauma-patients), we know for sure that it worsens breathing (http://www.ncbi.nlm.nih.gov/pubmed/10534038), as well as the airway. So, if the paramedic decided to forgo a collar and board for these reasons, I would support them.
    Also, I would support the medic whether or not they cardioverted. This could certainly be a primary arrhythmic problem, and a (small!) dose of a sedative and 200J could go a long way to illuminating the issue. Aggressive NIPPV and NTG, without cardioversion, would also be a viable strategy, which I would support.
    There are a lot of justifiable paths here, and I would mostly about the reasoning that the medic employed, as well as the data collected. Cardioverting is fine, as long as there was a rationale, and plenty of pre- and post-attempt data; e.g. strips, 12-leads, BPs, etc.
    That being said, I wouldn't be so hot with EMS giving calcium-channel blockers, beta-blockers, or antiarrhythmics in this case. Really, any medicine that doesn't wear off in minutes, or relies on a specific diagnosis. No lasix either, but I'm not going to make a huge issue about that. If the medic gave morphine for CHF, I would probably ask what rock he's been living under, since that was long banished in our neck of the woods!
    Speaking to Tom's FB statement earlier today, my response to most of the commentary I read in these scenarios on EMS 12-Lead is "I can't believe these guys are paramedics." Because the commentary is usually on such an advanced level that I realize that the emergency docs have to work to keep up with the field people!

  • medic999 says:


  • 1OregonCoastMedic says:

    I agree Adrienne mostly.. I still want to see what happens when the patients sats come up before I consider cardioversion. A hypoxic heart is a pissed off heart…

  • jdbr78 says:

    Wont repeat whats already been said but…

    This reminds me of a similar patient. Fall, very ill post event, developed APE from what was later Dx as SAH which has also been shown capable of causing ECG changes…

  • Dustin says:

    I think this is AMI with Flash pulmonary Edema…. I initially wouldn’t do anything for rhythm. Doesn’t really matter what you call it at this point (V-tach, sinus tach with LBB, A-flutter 2:1) because the rhythm is perfusing well to have a BP of any sort. I would elect CPAP first and see if anything changes. Then I would go from there whether to treat the rhythm with meds or electricity. I would want an old 12 lead and right sided 12 lead before I would very cautiously give NTG. If the CPAP improved his mental status, oxygen sat and rhythm I would give NTG. I would have fluid and dopamine handy…. I think there are too many unknowns to treat the maybes… meaning that this could be AMI, V-tach, electrolyte imbalance even a head bleed, but we have to initially treat what we have in front of us, A man who cant breath and lungs are full of fluid…..Doesn’t matter what the problem is if he not oxygenating vital organs then things are going to get real easy to treat (i.e cardiac arrest….)

  • Brandon O says:

    Hyperk and CHF exacerbation. Perhaps predisposed but doubt one caused the other. Possibly MI causing both but you’re not going to read it through this. CPAP if you’re really that comfortable with it, nitro, calcium, then reread. Immobilize later if you want. Great case.

  • VinceD says:

    I have a verrrry high suspicion that there is an underlying a-flutter here and would have a very low threshold to cardiovert if he truly appears moribund. First things first though: I’d want HIGH-flow O2 running plus/minus CPAP depending on your regional and personal comfort using it on such a patient. Personally, even though he may very well end up intubated, I’d probably still want to start with it and get that sat up. I’d probably hold most meds to start unless cardioversion fails and I need some rhythm control.

    Of note, T-waves are abnormally upright in V5 and V6.

  • Robert says:

    Interesting comments about the CPAP w/ the ALOC.
    Capnog is ultimately the most essential tool in determining whether i'll go to CPAP vs Intubation. As new evidence and data show increased mortality w/ a CHF'r it is always wise to avoid intubation at all costs, but there is a certain point where CPAP will no longer be useful.
    If a patient has ALOC/Lethargic, it is usually because they are hypoxic and tired. This is a point where they begin to hypoventilate and have an increase in EtCO2. Once the etco2 begins to read in the 60's is a point where i'm going to intubate. In order for CPAP to work appropriately, a patient needs to be able to cooperate and inhale/exhale w/ in the etco2 range.

  • John says:

    Well apparently my comment was deleted.  To Technomedic, I also work in North Central and I have transmitted Non-STEMI's to a recieving facility and patched or called in directly to the ED w/ Medical Control to discuss an ECG.  Not that I wasn't comfortable but to see if the MD could pull up old ECG's.  If your recieving facility is not burried and busy, and depending on your direct repore with the Doctor it can go well.  I have never had a MD complain about being consulted in a case while I was transporting.  In this scenerio obvoiusly the consultation would have to be so quick and patient care would take priority. 
    To Mr Brooks Walsh, I appreciate your comments and wish you worked up in North Central and not down South, we could use more Doc's supportive of EMS like you.  Keep up the good work in your Blogs!!!

  • Jake says:

    My take? Acute CHF, possibly caused by a new MI or some other new cardiac issue.

    Replace the O2 with CPAP ASAP. Get continuous EtCO2 monitoring on him, now – despite his obvious respiratory distress, that SpO2 reading is suspect due to decreased peripheral perfusion as evidenced by his blue nail beds, and EtCO2 will be a better indication of patient improvement or decline. Transmit that ECG. I see possible ST elevation in 3, aVF, V1, V2 and V3, with depression in I and aVL – as Brandon O said above, there may be an MI in there, “but you’re not going to see it through this.” Punt it to the ER doc who hopefully has a little more time to give it a good in-depth evaluation, and may be able to pull an old ECG for comparison before you get to the ER.

    Get an IV, then NTG x3 (if the BP holds). Get online with medical control early, and follow up after a NTG or two with any changes.

    Lasix in my region is an option, but only after consulting with med-control. There’s evidence that it may actually be harmful in acute CHF, anyway. We aren’t equipped for RSI, either.

    Get his lungs emptied of fluid, and the other symptoms may resolve on their own once he’s getting proper O2/CO2 exchange.

    Above all, “treat with diesel.” This is not something we can fix in the field. He needs to be in a hospital for definitive diagnosis and treatment, quickly, or else he’s going to die.

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