Hyper-K and Shades of Grey

Good morning all…

It's a beautiful fall Sunday morning, and you and your partner are enjoying an nice cup of coffee. But of course, the tones go off, and you are called to the residence of a 52 year old female, "sick". You recognize the address, you've been there before. 

Upon your arrival, you find your patient sitting in a chair in the living room. You remember her. She is a dialysis patient. She does not look well. 

She complains of not feeling well. She says she is weak, and has slight shortness of breath. You don't see any labored breathing or accessory muscle use, and she is able to speak in full sentences for now. Her respiratory rate seems ok, as does her pulse.

As you are getting your history, your partner gets a set of vitals. 

She tells you that she wasn't feeling great yesterday, and missed her scheduled Saturday dialysis (she is on a Tues-Thurs-Sat schedule). 

She thought she would be ok until Tuesday, but it didn't work out that way. She woke up today feeling really rotten and has been progressively feeling worse.

In addition to her renal failure, she also has a history of hypertension and asthma. She has no allergies. She says she has been compliant with her meds, and denies any chest pain or other aches/pains.

Her vitals are as follows:

  • HR         78 regular
  • BP         158/94
  • RR         20
  • SpO2     94 on room air
  • Lungs    very slight expiratory wheezes, but she states she always has that
  • Skin       unremarkable

You acquire an ECG that looks similar to this one:

image credit

You begin packaging your patient.

You are 20 minutes from the closet community hospital.



I am assuming most of you will recognize the above condition and know the available treatments for it. 

So, that is not the question.

The questions are these:

Do we treat this patient prehospitally? 

To be clear, the question is not "could we" but "should we"?

If we did, What would we use and why?

Is there a benefit to treating in the field versus waiting to hospital arrival?


**There is no obvious "right" answer to this… So, let's discuss it and see where we get. Have at it folks!



  • Any B says:

    I'm a paramedic working in the UK.
    i encountered a similar story recently with a dialysis patient feeling weak. The ECG was suggestive of high k. There is no formal protocol or guidline for Paramedics to treat hyperkalaemia per hospital here and paramedics do not carry calcium. We do however carry salbutamol and the drug is recommended for the emergency treatment of hyperklaemia in the ED. I did consider giving salbutamol for my patient but was worried about giving it without the patient having calcium on board, could the salbutamol increase the risk of arrythmia?
    In the end the patient Was transported to the ED with pre alert call. She was diverted by the ED nurse to the majors area and had bloods done 2 hours later. Her potassium was 7.2 and she received supportive care before being transferred for dyalisis. 
    I wonder if she might have been better off being treated pre hospital.

  • Any B says:

    Though that said, I have been told that reanal patients in particular can tolerate high potassium very well…

  • Chance Gearheart says:

    Supportive care unless an arrhythmia develops. Without overt symptoms of impending hyperkalemic collapse or arrest, or iSTAT labs, you can treat a borderline K level and cause more problems.

    For a 20 minute transport, INT access through a large and patent vein, monitoring, and supportive care is the best option with no associated symptoms such as arrhythmia or QRS flattening/widening. Seek expert consultation.

    On a related note, however, she has wheezing, and a normal heart rate with no ischemic symptoms. Albuterol has a nifty side effect when it comes to potassium treatment, doesn’t it?

  • Chance Gearheart says:

    One more thing, this patient is an ESRD patient. She’s not going to pee potassium out very well. Lasix/Bumex or loop diuretics aren’t going to work well. We don’t carry insulin drips. Calcium without a peri arrest situation runs too much risk.

    Sodium Bicarbonate and Albuterol are going to cause intercellular potassium shifting, and might buy time, but bicarbonate has massive risks of its own. Albuterol can also be proarrythmic, and should be used cautiously – no 7.5 or 15mg hour long treatments like in the kiddies.

    Really, they need immediate hemodialysis to slowly remove the potassium and get them to baseline

  • Jason says:

    I would treat it.  The Pt does not feel well.  I correlate it to if the Pt had pain, I wouldn't withhold anelgesics.  Where I am at we are expected to treat the Pt.  Start IV's, administer medications, activate cath labs, activate stroke & sepsis alerts.  If there is ever a question to treat in the field or not, our doctors are a phone call away and are very willing to help.  My system carries Sodium Bicarb and Albuterol for Hyper K treatment.  With this Pt's light wheezes Albuterol could have a double effect.

  • Ben says:

    Personally, I would not treat the hyperkalemia.  She's hemodynamically stable, and the QRS isn't incredibly widened.  This patient has a lot going on that I can't directly measure, and I'm not comfortable giving a relatively large amount of calcium or sodium bicarbonate without having some kind of labs to guide treatment.  This is a similar case to a DKA patient; we can treat one of the side effects of the root problem, but potentially screw up a lot of other things along the way.  Like an above poster mentioned, what this patient really needs is hemodialysis; pushing meds is a stopgap treatment to get the patient to dialysis alive.  This patient doesn't need any stopgaps right now.

  • Brooks Walsh says:

    Good case. Hyperkalemia should be one of those 12-lead diagnoses that paramedic understand inside & out, and feel comfortable aggressively treating. The patient shown here should be treated, and quickly, by EMS.
    Although we would have to look at an old ECG to be sure, we're not just looking at tented T-waves here. The widened QRS, in particular, suggests a dangerously high potassium, and a few leads have the early sine-wave appearance. We also have suppression of atrial activity. I'm not sure if ESRD patients really do tolerate hyperkalemia, but it's clear from the ECG that this patient is not tolerating it now.
    Treatment starts with calcium, the EMS drug of choice. I'm not sure about how calcium "runs too much risk." It's a pretty safe drug, and you should see effects very quickly. Albuterol, by contrast, may transiently raise potassium levels to a minor degree before lowering them. Despite that, it has been shown to be quite effective in treament.
    Sodium bicarb, OTOH, has not been shown to be as effective.
    Again, medics need to know the ECG patterns of hyperkalemia cold. We aren't just looking for STEMIs!

  • ETH says:

    Watch for dysrhythmias.  I am not sure of the benefit for pre-hospital administration of Calcium/D50/Regular Insulin.  I would like to see the potassium level before starting to give medications to correct the hyperkalemic event.  The Doctors have another medication in their arsenal called Kayexalate to reduce potassium that can be administered po, or pr.

  • Chance Gearheart says:

    Hey Brooke. Thanks for the reply. Give me a few hours to get home, and out of class, and ill explain my rationale on why I would not give calcium to this specific patient. It’s hard to type a long discourse on it on an iPhone.

    On that note, calcium chloride is incredibly harsh on veins. If you don’t have a port or central line access to push it, MAKE SURE you have good IV access in a non-varicose or small vein, preferable forearm, AC or EJ. Extravasion of Calcium Chloride or arterial administration can cost someone their arm or leg.

  • Vf says:

    Oxygen, IV calcium chloride drip 8-16 mg/kg, watch her 12 lead closely for arrhythmias.

  • David Baumrind says:

    Thank you for your comments Brooks! I was hoping you would.

    I believe there is much uncertainty in EMS regarding the field treatments of HyperK, and that seems to be reflected in the comments so far!

    I'm looking forward to seeing more.

  • Ben says:

    Brooks, thanks for pointing out the atrial supression…in my pre-coffee state, I totally glossed over that one 🙂  I would like to offer a differing opinion on the patient's tolerance of the hyperkalemia, however….we are seeing clinical signs of hyperkalemia on the ECG, and they definitely are concerning.  However, I think that the patient's blood pressure and mental status presents evidence that the patient is tolerating, or maybe appropriately compensating, for the hyperkalemia.  I agree that we've got to be comfortable treating hyperkalemia aggressively when needed, but looking at the overall presentation of the patient, I'm not ready to pull the trigger on aggressive treatment just yet, just aggressive monitoring.  That being said, I'm still going to use the afternoon off to dig into hyperkalemia in renal disease to see if I'm wrong 🙂

  • Mike Sherriff says:

    Hyperkalemia is a clinical and ECG diagnosis, NOT a laboratory diagnosis.  It is a right-now-baby-cow situation. 
    Early and aggressive treatment of someone with this degree of hyperkalemia (as evidenced by the ECG) or worse may very well prevent a cardiac arrest in the time it takes you to get to the hospital.  According to Garcia, P waves disappear at ~ 8.8 mEq/L, and the rhythm can deteriorate very quickly.  If there is simply T-wave peaking with no other concerning ECG findings, then serial ECG's watching for QRS widening and p wave issues may be okay–you'll certainly know which treatment path to pursue if they code 🙂
    From the number of dialysis patients in cardiac arrest that I have worked, they may not be so tolerant of hyperkalemia.  Of course there are any number of things that can trigger cardiac arrest in these folks at or between their thrice weekly recliner stress tests. 
    So the benefit of prehospital treatment with Calcium (Chloride or Gluconate), Sodium Bicarbonate, and Albuterol is that you may prevent a cardiac arrest in your truck.  I would feel just as uncomfortable, if not more so, watching and waiting on this patient as I would a patient in VTach.
    As always, hyperkalemia can produce a regular, irregular, slow, normal or tachycardic rhythm–don't wait for the bradycardia or the sine wave!

  • akroeze says:

    This is my opinon/views only and does no necessarily reflect what my protocols allow nor what is in my scope.

    I would aggressively treat this patient as we have essentially every standard hyperkalemia sign on one ECG with a clinical picture to support it, this is not a difficult diagnosis.  Calcium, Ventolin, +/- Sodium Bicarb (does it even really do anything?  Jury is out on that one) would be my first line and second line as well if needed.  I would probably have the pads on this patient just in case even though to my understanding these patients respond very poorly to pacing, cardioversion, atropine, etc but I'd rather be prepared regardless.

    I had a call very similar to this in which a 40 minute transport was ahead of me.  The patient was very weak and a rate in the 30s however all other numbers were "normal".  The biggest benefit was rerouting to a dialysis capable facility instead of the community hospital which was closer.  After physician consultation there was no medical intervention performed beyond IV TKO, pads placed, and close monitoring.  Ultimately was this the right thing?  I don't know, the patient survived and to my knowledge was discharged with no issues.  In my region we do not have access to calcium therefore my only options were ventolin and bicarb for which the physician did not feel there was a need.

    If this person were to arrest however, a departure from standard run of the mill ACLS would be in order.

  • doobis says:

    I would pretty much BLS her to the hospital – by that I mean monitor for any major and critical changes and transport.  Being a renal PT I'd assume she probably has a port so I doubt I need to worry about IV access.  I am not going to treat her hyper K+.  I don't have a protocol for it and personally I'd rather let the labs come back and definative treatment be given after the short ride to the hospital.  Try to take down further info such as her dry vs wet weights.
    She always has these wheezing so I'd let it be.  Is that because of the asthma she has  or is it something else, possibly too much fluid in her system and the body preventing the fluid from filling her lungs by constricting?  
    She is compensating so give her the ride.  My philosophy is to do as little as necessary to achieve a stabilized PT.  Go all in if it requires but be judicial in treatments.  No need to try risking things in the back of a truck or expose a PT to medications unnecessairly.  You never can be certain what side effects will occur giving a med.
    If this PT was presenting differently and needed an airway established by RSI, I'd worry more about the hyper K+ and contact medical control so as to get orders or consult with the Dr. about my concerns with using succs with hyper K+.

  • Frank says:

    As a dialysis nurse w/ 26 years experience this is a common scenerio, I see almost daily in hospital. Most patients, especially those who have been on dialysis for awhile, have become acclimated to have higher potassium levels. It is not uncommon for us to see patients with K levels > 7 and even as high as 9 with minimal symptoms other than ECG changes. Yep calcium, albuterol and such are fine but supportive care if unsymptomatic is usually sufficient. Ultimatly what this woman needs is several hours dialysis, sometimes remedied by her contacting regular facility and making up the treatment. Noncompliance is a major problem in this patient population. We tell our patients if you are too sick to go to dialysis then contact MD or go to hospital.

  • Chance Gearheart says:

    Now that I'm home, this is a little easier.
    Okay. So let's establish what's going on with this patient.
    1) Dialysis Patient with ESRD who missed her last treatment, and is now 4-days post treatment.
    2) She has weakness with shortness of breath (voiced air hunger?) with a history of asthma, and ausucltatable wheezing. Yes, she states it's normal, but given everything else, it's something we can treat. This is VERY important for services without HyperK protocols/clinical guidelines, or the inability to call for orders for a treatment plan for it.
    3) She has a normal heart rate, a high but normal blood pressure, and she's satting perfect on room air.

    Now. On to the EKG. The first thing I notice is that we have hyperacute, sharply peaked T-waves, with a defined J point between the ST segment and the QRS, so there is no mixing of the two, and it is not flattening or taking on a sine appearance, the amplitude is normal. While our QRS complex IS slightly delayed (0.10 to 0.12), there is not a sine wave appearance, and it appears to be regular. Rhythm wise, it appears to be an accelerated junctional rhythm – there is no P wave, and the rate is >60. However, the patient is hemodynamically stable.

    So, it's rational to assume we have a problem with hyperkalemia. The question is, do we have mild, moderate, or severe hyperkalemia. ECG changes correlate with serum potassium poorly in stable patients. In this particular study, hyperacute T-Waves began as low as 5.5meq/L. But this patient has EKG changes other than Hyperacute T waves, namely an AJR. However, they are still hemodynamically stable. In addition, what we have is a patient who is clearly unable to clear their own metabolic wastes and maintain an electrolyte balance without the use of regular dialysis. It is safe to assume, in that instance, that we can treat this patient for moderate hyperkalemia. Since you do not have labs to support aggressive treatment, nor instability, I don't believe I would perform it here.
    Treatment Modalities:
    1) Vascular Access. PIV Access through the largest, most patient, nonphlebotic and non-varicose vein you can find. Emergent AV Fistula access, if your service allows, is not indicated. IO is not indicated. Port-a-cath access, or indwelling line access MIGHT be, if you have the tools to do so. I would not put this patient on maintence fluids, but rather maintain patency through an INT.
    2) Continuous Cardiac Monitoring, including continuous 12-lead if your monitor is capable.
    3) We have wheezes! Let's give some albuterol. 2.5mg/3ml is a safe bet with this patient (You can even double up 5mg/6ml), via nebulizer. Set your flow so it delivers slowly. Albuterol will force an intracellular potassium shift of at least 1 meq/L over the next hour after it's stopped, so it will buy you time.
    4) Let's call for orders to infuse or slow push some Sodium Bicarbonate, 8.4%. Don't slam it. This patient deveoped a hyperkalemia over time, and is not in cardiac arrest. Sodium Bicarbonate induces an intracellular potassium shift lasting 20-30 minutes by producing alkalosis. Infuse it over 10 minutes in a small volume, or slowly push it. The dose is usually 0.5-1meq/kg, but in an adult a 50meq dose is usually what they administer. BE AWARE OF YOUR FLUID Is IN THIS PATIENT.
    5) Check your glucoses. DKA, or Hyperglycemic, Hyperosmolar Nonketoacidosis Syndrome can cause hyperkalemia. Really any acidosis will promote a shift from intracellular to extracellular potassium.
    6) Transport. Not necessarily to the closest hospital, but to the one capable of giving CRRT or Dialysis in the ED or Critical Care Setting. Dialysis is going to be the only thing that will fix this patient. Nothing you give will do so, it will only buy time.
    7) During transport, consult with expert (medical control) given patient and changes on administering calcium gluconate. (if you have it.)

    What I would not give:
    1. Lasix or another loop diuretic – It's going to be useless if the patient doesn't make his or her own urine anymore, or has ESRD. All it'll do is lower your BP.
    2. Polystyrine Sulfonate (Kayexalate) – You don't have it on the unit, silly. Plus, you're probibly either going to give it PO, or by an enema.
    3. Insulin/Glucose – You don't have it!
    4. Calcium Chloride, AT THIS TIME.
    So why would I not give calcium chloride? For one, this patient is not peri-arrest, or even hemodynamically unstable. There are no arrythmias noted that are life threatening. Even though the patient is in an AJR, there is nothing warrenting the myocardial protection given by calcium chloride. In addition, Calcium Chloride is a dangerous drug. For one, it has three times the active calcium of calcium gluconate. That's why we give it in arrest situations for hyperkalemia – it reactivates myocardial calcium channels blocked by the relative inability to depolarize from the high K levels. Think of what kind of patient we have here: an ESRD patient who has not been dialyzed in four days. Potassium is not the only problem we are having. You also have issues with sodium, calcium, phosphates, and metabolic wastes. You run the risk of throwing a patient into hypercalcemia, and developing cardiac and muscle toxicity from it. In addition, they can't clear it. It's going to remain in the blood stream far longer than the normal 30-60 minutes it will in a patient with normal renal function. 
    In addition, calcium chloride does NOTHING for the potassium levels. It just buys the myocardium time until they can be lowered.
    In addition to this, calcium chloride poses MAJOR problems in an end stage renal patient for administration. How hard is it to get a good line on these patients? Extravasion of even SMALL amounts of Calcium Chloride, less than 3mls, can cause major tissue necrosis and loss of a limb or part of it. In addition, if it is inadvertantly injected into an artery, it WILL cause a patient to lose their limb – I've seen this personally. In most hosptial systems, you CANNOT give Calcium Chloride 10% outside of a cardiac arrest, unless you're giving it through a central line, large bore centrally located limb IV, or a PICC line.
    At this time, the risks far outweigh the benefits of giving it. 

  • EMT-I says:

    For me…we have a 20 minute transport.  There's really not much other than supportive measures and rapid transport.  Of course she gets the standard O2, IV, Monitor.  I would have the Pads on and ready.  Keep listening to the BS for any changes and monitor her resperatory effort closely.

  • Brooks Walsh says:

    I can't find any studies that suggest that ESRD patients tolerate hyper-K better than others. Some people feel that slow increases in K don't manifest on ECG as dramatically as acute (but small) increases, but that's about it. And that's just opinion in an article in UpToDate.

  • BigWoodsMedic says:

    Good case. I personally would start with supportive care and contact med command at the hospital, who would likely say to monitor and transport and keep up to date. I do like the ideas of continuous monitoring the 12 lead for any changes. 

  • VinceD says:

    @Any B – Do you folks have IV salbutamol over there?

  • Any B says:

    Hi VinceD,
    No we only have nebuliser solution pre hospital. Apparently the recommended starting dose is 10mg by nebuliser, repeated if effective. I am told only about 60% of patients have a response.

  • Justin A says:

    We have Bicarb, Calcium, and Albuterol and a specific protocol for dialysis patients for hyperkalemia. If they’re not in cardiac arrest we can call for orders for a calcium drip and bicarb push. If they are in arrest, it’s 1g Calcium over 3 minutes and Bicarb 1mEq/kg. I would treat this patient because peaked t-waves equals serious signs and symptoms according to protocol, plus a 20min transport time which is a big thing to keep in mind.

  • Mike Sherriff says:

    Just a couple of comments on Chances post:
    "it appears to be an accelerated junctional rhythm – there is no P wave, and the rate is >60."
    Appears is correct; the rhythm is still most likely sinus.  The visible P waves disappear as the hyperkalemia becomes severe, and treating the hyperkalemia will make them reappear right where they should be.
    "Since you do not have labs to support aggressive treatment, nor instability, I don't believe I would perform it here."
    Again, hyperkalemia is NOT a lab diagnosis.  You have to clinically make the dianosis.  You have to see the ECG, not the lab result.  Another good example is: tension pneumothorax is not an xray diagnosis, you have to find it clinically and treat it.

  • David Baumrind says:

    Great discussion guys… One point I think we need to clarify:

    Many of you have correctly identified nebulized albuterol as a treatment option in the field.

    However, our standard dose is 2.5mg.

    Do you guys know what the effective dose is for hyperkelemia? 

    What will happen if we just give the standard dose?

    What other issues will the hyperkalemia dose bring?

  • Chance Gearheart says:

    Mike, I agree with you. The issue here is atrial suppression of the P-waves by hyperkalemia.
    And I agree with you. Given the signs and symptoms, and the EKG presentation, we can safely assume hyperkalemia is present in this patient.
    But I do not agree that this patient warrants administration of Calcium Chloride at this time. They are not unstable, and the vital signs and perfusion status do not indicate cardiac insufficiency. The patient does not meet the diagnostic criteria, given the signs displayed, of Severe or Immediately Life Threatening Hyperkalemia by the information given at this time, at least in my opinion. 
    The whole mechanism behind calcium in hyperkalemia is not elimination of potassium, or even intracellular shifting. It's reactivating calcium channels blocked by the hyperkalemic state, and inability to conduct impulses or depolarize. 
    I do not think it's a diagnosis made necessary by labs. I think it's a mechanism which warrants laboratory investigation to obtain a potassium to SUPPORT the decision to arbitrarily administer a resuscitation drug with substantial risks to that patient, versus administration of Calcium Gluconate, or holding the medicine on stand-by during transport. A bedside potassium takes all of three minutes to run.

  • Chance Gearheart says:

    @Mike Sherriff – Also, I'll say up front that Calcium Chloride, as a drug, scares me. I've witnessed in an ICU setting what happens when it extravases, and I've seen an infant lose a limb from accidental arterial injection. So I'm a little more hesitant to give it versus gluconate or other options outside of an arrest.

  • Mike Sherriff says:

    CaCl scares me too, and D50.  Which is good, because it makes me make sure I have very good IV access 🙂

  • STPEMTP says:

    In my opinion, I wouldn't say that this patient is tolerating the hyperkalemia.  This pt is approx 3 days since their last run of dialysis, which is a "normal" length of time between runs for them (Saturday-tues = 3 days, thurs-sunday = 3 days).  We're looking at approx 20 mins to a hosp that probably isn't able to care for them (dialysis) since it's mentioned as the community hospital.  The patient has signs of hyperK.  HyperK does not follow a specific pattern of peaked T waves then widened QRS, followed by sine wave as the K increases.  (Amal Mattu, MD has multiple video case lectures on this topic.  Unfortunately its yet another medical myth….)
    Albuterol treatment, if you going to use it is 10-20mg dose.  At most, I'm carrying 7.5-10mgs in my truck so probably not going to be very helpful here.
    Calcium chloride is not a drug without risk, but I think the question that is fair to ask here is: What is the bigger risk?  Spontaneous cardiac arrest from hyperK and metabolic acidosis (remember, she's 3 days out since last dialysis) or infiltration of calcium into soft tissue?  I think we can minimize the risk of infiltration by infusing at least 100ml's of saline thru this IV BEFORE we consider giving the calcium.  If you have Calcium gluconate available, this is a moot argument as long as you give it slow to avoid the hypotension it can cause with rapid administration.
    Sodium Bicarb may be a slightly "safer" treatment here, but she is already short of breath.  Right now she is speaking full sentances.  If she drops her tidal volume, is she going to be able to clear the extra CO2 the bicarb will produce.  If she doesn't, then we have just made her more acidotic and worsened her hyperK. 
    Personally (not protocol), I say that we probably should be giving the Calcium Chloide 1 gram and the Bicarb 50meq in this situations with the above caveats.  If I had access to Calcium Gluconate (which I don't), I would use that in place of Calcium Chloride in this case. 
    @Tom B: Lead V3, there is some ST depression with the peaked T that kinda looks like De Winter's T waves.  HyperK is the "sylphillus" of EKG's (Amal again).  Are you aware of any literature saying hyperK can mimic this finding?  I haven't seen much in De Winter's T waves besides a couple of articles.

  • Darren says:

    Our orders for this are, unfortunately, nonexistent.  However, if I had the option, I would treat this patient, but I believe a conservative treatment is warranted here.
    We can't safely give this patient enough albuterol to affect their K, but they are still wheezing, so I might give them a 5 mg dose at most to improve their ventilation.  Again, if I had the choice, I think at that point I would give a small dose of calcium gluconate.  Bicarb doesn't do all that well in some studies; I'm not sure that it helps, and we know that calcium does, so I think I would go with the small calcium dose.
    I say small dose because, while the patient manifestation and 12 lead presentation are diagnostic for hyperkalemia, they are not diagnostic of exactly how much.  The patient is moderately ill and we know that dialysis patients are typically electrolyte nightmares.  I'm not thrilled with the thoughts of giving a whole lot of electrolyte to a patient that I suspect is already a mess.  Hypercalcemia is not as lethal as hyperkalemia, but it's no picnic either.
    I think this is one of the reasons that point of care testing in EMS (iSTAT and other devices) should be pursued.  There are so many instances in which knowing a few basic labs could direct a course of treatment that would be hugely beneficial for patients.  But that's another topic altogether. 🙂

  • VinceD says:

    @Any B – That 60% number is new to me, very interesting. I've seen doses quoted upwards of 20mg, which is where IV albuterol would be wonderful. Maybe it's Australia where they carry that. Who wants to have their patient who's not even in respiratory distress on a noisy nebulizer for an hour?

  • Any B says:

    This article may be of interest. It quotes the 60% figure (40%) of pts are resistant to the hypO k effects..

  • Mike Sherriff says:

    @VinceD   "Even among patients not taking -blockers, as
    many as 40% seem to be resistant to the
    hypokalemic effect of albuterol (42, 48).
    The mechanism for this resistance is unknown,
    and there is currently no basis for
    predicting which patients will respond."
    Crit Care Med. 2008 Dec;36(12):3246-51.
    Management of Severe Hyperkalemia

  • Brooks Walsh says:

    Thanks to this discussion (looking at you Gearheart!), I decided to take closer look at extravasation risks of calcium Cl, D50W, and other EMS/EM drugs.
    First off, I'm surprised by how toxic dextrose can be. I've always tried to be careful with it, giving it in a running line, never "straight", but even the dextrose 10% can be dangerous – check out http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1344036/ for some nasty pictures of bad necrosis in babies.
    Ironically, there's a picture in Annals of Emergency Medicine (Volume 48, Issue 3, September 2006, Page 239) of a patient who received D50 for hyperkalemia, and had necrosis of his AC fossa. No mention of any calcium salts.
    OTOH, another article (http://www.ncbi.nlm.nih.gov/pubmed/17713732) describes 4 episodes of skin necrosis in patients who received IV CaCl for "symptomatic" hypocalcemia after parathyroid surgery. The fact that skin necrosis after IV CaCl administration warrents a case report (in 2007!) suggest to me that this is not a very common event. Even their references only list case reports from 1975 (listed above) and 1957.
    To summarize – while I feel more emboldened to give CaCl intravenously, I'm actually more afraid of D50 now!

  • Christopher says:

    If you're scared of running in CaCl, add it to half a bag or to a bunch of flushes or something.

    We carry D10 bags for pediatrics…and I actually use it on everybody who would get D50. Dirty secret, don't let the textbook authors find me.

    Brooks, that case series is interesting for this tidbit (emphasis added):

    Case 7. Soon after open heart surgery, a 42-year-old woman received an intravenous solution containing calcium chloride through a right frontal scalp vein. Some of the solution estravasated causing a 4 x 6 cm slough of forehead skin and scalp. The necrotic area was kept clean, debrided and gradually healed by ingrowth of scar epithelium.

    Never too old for a scalp IV apparently…

  • forsythfd922 says:

    I was under the impression that CaCl stabilized the cell membrane, Bicarb assists with mediating the acidotic state, insulin/glucose promotes shifting the Potassium into the cell to reduce blood levels, and Albuterol promotes uptake of Potassim into the cells as well, and kayexalate excretes the K+ via diarrhea.  While I would be able to justify administering the Albuterol on a standing order (not HyperK dosing…), I would have to consult with medical control for the rest/the things I carry.   On my truck, I probably would not treat this patient since I typically have a 5-10 minute transport time.  If I had an hour or so, or more, I may consider calling for orders to start a Bicarb drip/ Calcium administration, especially with ECG changes occurring.  While she isn't in arrest, If her myocardium is being affected, and it needs to be stabilized.  I say this one depends on your transport time, and latitude granted by your medical director.  Ours happens to be aggressive towards Dialysis patients.  Good scenario changing the questions up a bit.

  • Nicky J says:

    Great discussion.
    Personally I would sit on my hands in this scenario. If I was more concerned calcium gluconate 10% 10ml over 10/60 and repeat to stabilise myocytes.
    If there was haemodynamic compromise or widened QRS or AV dissociation I would consider sodium bicarbonate 8.4% 100ml and concurrent 20mg neblised salbutamol.
    VinceD- we do cary IV salbutamol in australia however not for this indication. Below is a good review/refresher – free just copy and paste into google scholar.
    Elliott, MJ, Ronksley, PE, Clase, CM, Ahmed, SB, Hemmelgarn, BR (2010). Management of patients with acute hyperkalemia. Can Med Assoc J, 182(15), 1631-35

  • Robert says:

    I'm a little late on this topic, but here's my two cents.
    I'd be very aggressive with this patient! Very! And here's my reason why… ECG changes do not reflect/dictate how high/low the patient's pottasium level is. This patient has significant ECG changes very clearly showing Hyperkalemia. Yeah, maybe it's just above 5.0, but maybe its at 8.0. What happens if you don't treat and your patient goes into VFib/Asystole?  Calcium, Albuterol, Dextrose, Insulin are in no way going to hurt your patient as long as you're not causing tissue necrosis and pushing your calcium at a slow rate.
    Treatment Modalities:
    >Calcium Chloride/Calcium Gluconate
    >Insulin/Dextrose Combo
    >High Dose Albuterol (20mg +)
    >Bicarb is controversial
    I'm adamant on my position and would love to debate anyone who thinks otherwise after listening to Scott Weingarts podcast. Cheers!

  • VinceD says:

    Just doing a final pass through the comments:
    @Mike Sherriff – I've read that article but completely forgot the point about albuterol resistance. Thanks for bringing that up! I've always consider it something that's nice to add but shouldn't be relied upon to really save lives, so that fits in nicely with my thinking.

    @Brooks/Christopher – Our region, which has historically been very resistant to change (bougies are considered the work of the devil) recently allowed itself to be absorbed into a larger region's protocols, so now we only carry D10 on our trucks. It's been working great the past couple of months, but interesting to learn that even 10% isn't as safe as we may have thought…

  • Paul says:

    I would give a gram or two of calcium, because it’s pretty benign, even to a normocalcemic patient. I wouldn’t do much else sans arrhyhmias. Well, I would add the caveat, that I might start a bicarbonate drip (25meq/250cc NS) but I sure wouldn’t be giving any IVP.

  • SA-ECP says:

    It’s strange that so many say she is haemodynamically stable: 158/94 giving a MAP of 115. That to me is a concern on its own. The respiratory system in it self is also a grey area but definitly not normal. I would also treat with calcium chloride: remember every drug you give you should have a patent, well placed IV line. So why use the excuse of this in this case. 10ml of a Calcium chloride 10% solution over 10 minutes. Neb B2 adrenergic stimulant over 10 min. Closely monitor E.C.G and BP. I feel if you don’t treat this and your patient crashes you are responsible and negligent.

  • Ania says:

    I just finished paramedic school and am studying CCProtocols… I would treat the pt even though she appears stable at the moment. I would ensure and maintain patent airway, administer O2 NC at 2 lpm, attach pt to monitor for BP, EtCO2 and SPO2 monitoring, 12 lead, IV access ( 2 large bore IV’s), administer Calcium Chl 1 g slow IVP, D50 15 mg, sodium bicarb 50 mEq in 50 mL of NS over 10 min, albuterol 2.5 mg/ 3 ml; reassess, and if condition does not improve, I would repeat everything but D50. Call en route medical direction… rapid transport and ensure comfort…

  • Ania says:

    D50 25 gm/ 50 ml- it is a mistake… 25 gm is correct

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