Hyperkalemia (2024)

November 14, 2024November 26, 2024 ~ iEM Education Project Team ~ Leave a comment

by Chelsea N. Allen

You have a new patient!

A 58-year-old female is brought into the emergency department (ED) by her family for dizziness and fatigue that started today. She has a history of hypertension for which she takes a calcium channel blocker and end-stage renal disease (ESRD) and has been on dialysis for the last four years. She did miss her dialysis session today due to her symptoms, with her last session four days ago.

At triage, her vital signs are as follows: BP 170/90 mmHg, HR 30/min, RR of 18/min, temperature 37.1 degrees Celsius, SpO2 of 98% on room air. She appears fatigued but is able to answer questions appropriately and has no obvious focal neurologic deficits.

Triage EKG is below

What do you need to know?

Hyperkalemia is one of the most important electrolyte abnormalities you will encounter in the emergency department (ED), given the potential for cardiac arrest in these patients. It refers to when the serum potassium (K) is greater than 5.5mEq/L. In all patients suspected of hyperkalemia, it is essential to place them on a cardiac monitor, obtain IV access, and perform an EKG due to the significant role potassium plays in the cardiac cycle. These patients may have non-specific symptoms, such as weakness and fatigue, and thus can make it hard to discern the diagnosis up front. Patients with a high pretest probability, such as those who miss dialysis or have had prior episodes of hyperkalemia, are usually treated for hyperkalemia before lab results are available due to the potential life-threatening nature of the condition. Potassium is stored in the body’s cells. It can be excreted during cellular damage, such as in rhabdomyolysis, or during certain physiologic states to balance the body’s pH when the serum becomes acidotic (e.g., DKA) [1,2]. Potassium is then excreted from the body by the kidneys/urinary system, so in patients whose kidney function has declined, such as ESRD, or in patients with an obstruction (bladder stone, enlarged prostate), potassium must be excreted through dialysis or by removal.

Medical History

Patients with hyperkalemia often present with non-specific symptoms, such as fatigue, muscle weakness, and cramps, which can often lead to a delay in the diagnosis and can be detrimental, even fatal to the patient. Elevations of potassium in a patient’s serum can be caused when there is a disruption in the storage or excretion mechanisms in the body and can cause cardiac arrhythmias, such as premature beats (PVCs), irregular beats (atrial fibrillation) or cardiac arrest (ventricular fibrillation) due to the role of potassium in regulating the cardiac membrane potential [1-5]. Since an underlying elevation in potassium can cause these non-specific symptoms, it is imperative to do a thorough history, keying in on a history of kidney issues, dialysis appointments, and urinary symptoms.

Physical Examination

The most crucial physical exam components in patients with hyperkalemia are the cardiac and skin exam, especially in patients who may not be able to give you much information, as a thorough skin exam can elicit an AV fistula/graft or tunnel catheter, which would clue you into the patient being on dialysis. If the patient does not have a history of ESRD on dialysis, the cardiac exam could be another clue, elucidating irregular rhythms or bradycardia and prompting you to get further evaluation with an EKG.

Alternative & Differential Diagnoses

Given that hyperkalemia can cause a myriad of non-specific symptoms, patients can sometimes have a long list of differential diagnoses. Outside of the cardiac complications, hyperkalemia can cause muscle cramping, fatigue, or feeling weak. Unless you have a high index of suspicion, these symptoms can be attributed to muscle strains or viral illnesses, which in patients who are otherwise healthy or have a good history of these may be more likely than hyperkalemia [5].

Acing Diagnostic Testing

One of the most important tests for patients suspected of having hyperkalemia is the EKG, given how quickly this bedside test can be performed and the wealth of information that can be obtained, especially regarding electrolytes [4,5]. The classic EKG finding in patients with hyperkalemia is peaked T waves. However, hyperkalemia can mimic many EKG changes, and other findings suggest hyperkalemia are a widened QRS, flattened P waves, and heart blocks [3,4,5]. The EKG may follow a step-wise pattern of peaked T waves, followed by progressively lengthening QRS. However, generally, they do not always follow this pattern, so it is important to have a high index of suspicion when you see these changes. The next step is usually laboratory testing with a basic metabolic panel to confirm hyperkalemia. It can also indicate the patient’s electrolyte levels, provide insight into their acid-base balance, and suggest other potential diagnoses. You may also get other testing depending on the cause of the hyperkalemia, such as CT or US imaging, if urinary tract obstruction is the suspected cause. However, in general, imaging is not needed to make the diagnosis.

Risk Stratification

Most of the patients with hyperkalemia are going to be chronic kidney disease or dialysis patients, which are inherently at higher risk given their underlying disease process as well as the fact that the kidneys process and excrete potassium in the body. Specifically, anuric patients within this group are going to be at higher risk for complications, given that the only way to excrete potassium is through dialysis, putting them at risk for the potentially fatal complications of hyperkalemia [1,2].

Management

As always, following the ABCs of emergent patient management is crucial in deciding how quickly you need to intervene, especially in hyperkalemic patients, where cardiac arrest is a high possibility. Once you have assessed that your patient has a patent airway by speaking to them, their breathing by listening for bilateral breath sounds, and their circulation by ensuring they have a pulse, the next critical step in managing hyperkalemia is the reduction of potassium within the body and serum. This is achieved in two ways: shifting and elimination [2,3,4,5]. One medication we use in hyperkalemia where we have EKG changes attributed to elevations in potassium is Calcium (gluconate or chloride) which the sole purpose of this medication is stabilization of the cardiac membrane to prevent further deterioration into unstable rhythms and is usually given first in the line of medications [2]. Its onset is rapid (15-30 min) with a duration of 30-60 min. Monitor closely as it does not lower potassium but rather protects the heart. Calcium chloride is more concentrated than calcium gluconate, so it requires a central line due to the risk of tissue damage.

Shifting medications will be Insulin and Albuterol, given that these medications work in the cAMP pathway on the cell membranes, causing extracellular potassium to shift intracellularly, thereby transiently decreasing serum potassium. Dextrose is usually given with insulin to prevent the drop in glucose associated with insulin use, and it does not shift/eliminate potassium, but it is still vital. If your patient is able to make urine, giving a dose of Furosemide (or another potassium-depleting diuretic) is useful to help start the process of potassium elimination, as these medications will pull extracellular potassium into the waste product (urine). If your patient is unable to make urine, giving Sodium zirconium cyclosilicate, a potassium binder in your gastrointestinal tract, to help eliminate potassium is another way to help deplete body potassium. If severe enough (e.g., arrhythmias/cardiac arrests, ESRD patients), most patients will need to undergo hemodialysis for definitive treatment/removal of potassium. Listed below are the medications mentioned above, as well as the recommended doses and frequency.

Table: Medications frequently used in hyperkalemia treatment [5,6]

Drug generic Name	Dose	Effect	Duration	Pregnancy	Cautions / Comments
Calcium gluconate	1-3gm IV	15-30min	30-60min	C, only if clearly needed
Calcium chloride	1gm IV	15-30min	30-60min	C, only if clearly needed	Concentrated Calcium, needs central line
Albuterol	15-20mg nebulized	30min	2hrs	C
Insulin/Dextrose	10u Regular insulin IV; 25-50gm of 50% dextrose IV	30min-45min	3-6hrs	B (insulin); C (dextrose)	Usually given together, but can be omitted if Glucose >300
Furosemide	40-80mg IV	15-20min	2hrs	C
Sodium zirconium cyclosilicate	10mg TID PO	Can take up to 48hrs		Not Assigned	Usually not first line in the ED

Special Patient Groups

Given its life-threatening nature, hyperkalemia is generally treated the same way in all patient populations, including children and pregnant patients [5]. The above medications are all for adults, but they do have weight-based dosing for pediatric patients that is easily accessible on Broselow tapes found in the Emergency Department. Additional considerations for each group as follows;

Pediatrics

Hyperkalemia in children is often linked to kidney insufficiency, acidosis, and certain genetic conditions affecting potassium balance [7]. Pediatric hyperkalemia treatment includes insulin-glucose therapy, calcium gluconate, and sometimes sodium bicarbonate for acidosis [7]. Dosing is weight-based; careful monitoring is essential to prevent hypoglycemia following insulin administration [7].

Geriatrics

Older adults are prone to hyperkalemia due to decreased renal function and polypharmacy, especially with medications like ACE inhibitors and potassium-sparing diuretics [8]. Geriatric patients require slower dose titration and close monitoring of cardiac function. Reducing or discontinuing potassium-elevating medications may be prioritized before more invasive treatments. Assessing patient’s medication profile carefully to minimize potential interactions and electrolyte disturbances is important.

Pregnant Patients

Hyperkalemia is rare in pregnancy but may occur due to conditions like preeclampsia or excessive potassium supplementation. Treatment is similar to that of the general population but focuses on the safety of both the mother and fetus. Agents like insulin-glucose therapy are used with caution, and glucose and potassium levels are monitored closely to avoid fetal complications.

Caution!

The drugs listed in the table do have specific considerations for pediatric, geriatric, and pregnant patients, as follows:

Calcium Gluconate and Calcium Chloride:
- Pregnant Patients: Generally considered safe for use when needed (Pregnancy Category C), but only administered if benefits outweigh the risks due to limited data on safety in pregnancy.
- Pediatrics: Dosing is usually adjusted based on weight, and administration must be done with caution due to the risk of tissue necrosis with calcium chloride if extravasation occurs.
Albuterol:
- Pregnant Patients: Classified as Category C. Used in asthma or bronchospasm, but risks must be considered, as inhaled bronchodilators are typically preferred.
- Pediatrics and Geriatrics: Pediatric dosing is weight-based, while elderly patients may require lower doses due to sensitivity to stimulants.
Insulin/Dextrose:
- Pregnancy: Insulin is preferred for managing blood glucose in pregnant women with diabetes, categorized as B for insulin, while dextrose is safe when needed.
- Pediatrics: Used in hyperkalemia or diabetic ketoacidosis with dose adjustments based on age and weight.
Furosemide:
- Geriatrics: Lower doses are generally recommended due to increased risk of dehydration and electrolyte imbalance.
- Pregnancy: Considered Category C, used only if necessary as it may affect fetal renal development.
Sodium Zirconium Cyclosilicate:
- Limited data on its use in pediatric and pregnant populations, and generally not a first-line treatment in the emergency department for these groups.

Infographic

When To Admit This Patient

There are very few instances where hyperkalemic patients will be discharged from the ED, given the potential life-threatening arrhythmias. However, ESRD patients who receive dialysis, are back to their baseline and have to follow up/able to make it to their scheduled dialysis sessions will most likely be able to be discharged if a cause for their hyperkalemia is something simple, such as missed dialysis appointments. Ensure clear, specific follow-up arrangements to minimize recurrence risk. Confirm with her dialysis provider for her next sessions. Most other patients will be admitted for monitoring to ensure their potassium levels are normalizing and to identify a cause.

Revisiting Your Patient

As you recall, we had a 58-year-old female with dizziness/fatigue who had missed her dialysis session and was found to be bradycardic and hyperkalemic on her initial workup. She was initially treated with calcium gluconate with improvement in her EKG as well as her symptoms and was able to receive dialysis in the ED. After a brief period of observation after her dialysis sessions and repeat BMP showing normalization of her potassium, she was discharged home with her family to continue her outpatient dialysis schedule.

Author

Chelsea N. Allen, DO

Originally from Adel, GA, USA, graduated college with a degree in biology from Columbus State University in Columbus, GA, USA. Then attended medical school at the Edward Via College of Osteopathic Medicine in Auburn, AL before completing her emergency Medicine residency at the University of Florida, Jacksonville, in Jacksonville, FL, USA. She is currently the Assistant Program Director for the Emergency Medicine program at UF-Jacksonville as well.

Listen to the chapter

References

Harris AN, Grimm PR, Lee HW, et al. Mechanism of Hyperkalemia-Induced Metabolic Acidosis. Journal of the American Society of Nephrology. 2018;29(5):1411-1425. doi:https://doi.org/10.1681/ASN.2017111163
Mount D. Potassium balance in acid-base disorders. Accessed: November 14, 2024. https://www.uptodate.com/contents/potassium-balance-in-acid-base-disorders.
Lindner G, Burdmann EA, Clase CM, et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med. 2020;27(5):329-337. doi:10.1097/MEJ.0000000000000691
Helman, A, Baimel, M, Etchells, E. Emergency Management of Hyperkalemia. Emergency Medicine Cases. September, 2016. Accessed November 14, 2024. https://emergencymedicinecases.com/alcohol-withdrawal-delirium-tremens/
Wachira BW. Fluids, Electrolytes, and Acid-Base Disorders. In: Cydulka RK, Fitch MT, Joing SA, Wang VJ, Cline DM, Ma O. eds. Tintinalli’s Emergency Medicine Manual, 8e. McGraw-Hill Education; 2017. Accessed November 14, 2024. https://accessemergencymedicine-mhmedical-com.uaeu.idm.oclc.org/content.aspx?bookid=2158&sectionid=162269029
Rafique Z, Peacock F, Armstead T, et al. Hyperkalemia management in the emergency department: An expert panel consensus. J Am Coll Emerg Physicians Open. 2021;2(5):e12572. Published 2021 Oct 1. doi:10.1002/emp2.12572
Lederer Hyperkalemia. Accessed: November 14, 2024. https://emedicine.medscape.com/article/240903-overview?form=fpf
Ortiz A, Galán CDA, Carlos Fernández-García J, et al. Consensus document on the management of hyperkalemia. Nefrologia (Engl Ed). 2023;43(6):765-782. doi:10.1016/j.nefroe.2023.12.002

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

From Missed Hemodialysis to Multiple Arrhythmias

November 2, 2020October 23, 2020 ~ Gayatri Lekshmi Madhavan, India ~ 2 Comments

Case Presentation

A 78-year-old male, known case of Chronic Kidney Disease on maintenance hemodialysis, presented to the Emergency Department with dizziness and lethargy complaints about 2 days. He had missed his last hemodialysis session due to personal reasons. We could not elicit any further history details as was significantly dyspneic (no bystanders with him at the time of presentation). Hence, the patient was received in Bay 1 for immediate resuscitative measures. The patient was afebrile, conscious, and well oriented, but unable to communicate because of severe dyspnea.

Vitals

HR – 142 beats/min
BP – not recordable
RR – 36 breaths/min
SpO2 – poor tracing, intermittently showed 98% on room air (15 LO2 via Non Rebreathing Mask was initiated nevertheless)

ECG

He was immediately connected to a defibrillator in anticipation of possible synchronized cardioversion. Simultaneously, the cause of the possible rhythm was being evaluated for and a thorough examination was carried out. On examination, his lung fields were clear. His left arm AV Fistula had a feeble thrill on palpation.

In suspicion of hyperkalemia as the cause of VT, patient was immediately started on potassium reduction measures while the point of care ABG report was awaited. He was treated with salbutamol nebulization 10mg, sodium bicarbonate 50 ml IV and 10% calcium gluconate 10ml IV. In view of hemodynamic instability, he was also started on intravenous noradrenaline infusion.

ABG Findings

pH – 7.010, pCO2 – 20.8 mmHg, pO2 – 125 mmHg, HCO3 – 7 mmol/L, Na – 126 mmol/L, K – 9.6 mmol/L

As hyperkalemia was confirmed, the patient was also given 200 ml of 25% dextrose with 12 units of Rapid-acting insulin IV. With the above measures, the patient’s cardiac rhythm came to a sine wave pattern.

He was later taken up for emergency hemodialysis (HD) – Sustained Low Efficacy Dialysis (SLED) in the ICU, using a low potassium dialysate. Since his AV fistula was non-functioning, HD was done after placement of a femoral dialysis catheter. 2 hours into HD, the patient’s cardiac monitor showed a normal sinus rhythm. His hemodynamic status significantly improved. Noradrenaline infusion was gradually tapered and stopped by the end of the HD session, and repeat blood gas analysis and serum electrolytes showed improvement of all parameters.

The patient was discharged 2 days later, after another session of hemodialysis (through AV fistula) and a detailed cardiology evaluation (ECHO – LVH, normal EF).

For the Inquisitive Minds

The patient underwent a detailed POCUS evaluation, both in the ER and ICU. What findings do you expect to find on the RUSH examination for this patient?
His previous ECHO report (done 1 month ago) mentioned left ventricular hypertrophy and normal ejection fraction. So what would be the reason behind the POCUS findings? Is it reversible?
Why was the AV fistula non-functioning at the time of presentation? When would it have started to function again?
Despite not having hypoxia, this patient was given supplemental oxygen. Did he really require it, and if so, what was the rationale?
What was the necessity for carrying out SLED for this patient?
Why was this patient not immediately cardioverted in the ER?
If this patient had gone into cardiac arrest, what drugs would you have given for management of hyperkalemia?
How differently would you have managed this patient?

Please give your answers and comments into "leave a reply" area below.

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The EKG Case of No Symptoms

October 26, 2020October 23, 2020 ~ Anthony Rodigin, USA ~ Leave a comment

Case Presentation

A 52-year-old woman presents to the ED from an outpatient dialysis center with a rather vague history. She has no symptoms and feels normal, but she was told something “was either too low or too high” on her vital signs at dialysis, so dialysis staff did not perform her scheduled dialysis session. No one had called ahead to alert the emergency department, and the patient had driven herself to the ED, as she was instructed. Vitals show a normal temperature, respiratory rate, oxygen saturation, blood pressure of 102/47 mm Hg, and a heart rate of 138 beats per minute. The physical exam is normal besides a mild regular tachycardia and a working AV dialysis fistula on the right arm. EKG is done, and a representative portion is shown below:

EKG from the prior year is shown for comparison.

How would you interpret the first EKG, and what are your next steps?

Discussion

While you are thinking, I will discuss a few of my practical observations from working in the pit. I want to focus not so much on the diagnosis but on working with these types of scenarios.

Treat the patient and not the chief complaint, vitals, labs, EKGs, studies, or referral information.

Anthony Rodigin Tweet

When they are feeling great and have no symptoms, they are feeling great and have no symptoms! Your nurses will not necessarily think this way, but one does not feel great while having a real STEMI apparent on the triage EKG. So what is it then, if the patient is here for a contact lens stuck in their eye, but has an EKG STEMI? Worst case – a prior STEMI that never corrected or evolved on the EKG. A ventricular aneurysm? Leads misplaced? Did your EKG tech do an EKG on themselves? A silent MI can occur, but an incidental STEMI is unlikely.

Of course, the patient has to be alert, competent, and not intoxicated. They should not be lying about or hiding their symptoms and should not have a secondary interest like the need to make it to a daughter’s wedding - live or die. The easiest thing is to ask directly.

What is the rhythm's rate doing when it is left alone?

Afibs and MATs will tend to vary greatly in the second to second heart rate, sinus tachycardias will fluctuate some, while A-flutters and SVTs will tend to stick to a single number no matter what you do and no matter if the patient is walking, talking, or snoozing. Stable Vtachs will depend on a number of factors like being monomorphic or polymorphic – but we are talking about narrow QRS dysrhythmias or ones with an obvious bundle.

So if you cannot tell from the EKG – observe what the thing does while left alone. As long as the patient is otherwise stable or has had symptoms for a while, you have some time.

Adenosine – not just for SVT conversion

“SVT = adenosine” should not be an automatic equation. First of all, there are contraindications to adenosine based on past history or current medications taken. But adenosine can also be used to “stretch out” weird or equivocal fast rhythms to make flutter waves or hidden P waves come out, so you can see and diagnose the arrhythmia vs. sinus.

You have to have continuous EKG recording going or printing the monitor strip to spot the temporary effect.

Hypotension + tachy-dysrhythmia: does not necessarily add up to Joules.

The textbook mantra of shocking any dysrhythmia associated with hypotension does not hold up in reality. In reality, you will find that most of your Afibs with a rapid response, your new-onset atrial flutters and your SVTs will have a lousy blood pressure: systolic of 80s and 90s are almost to be expected, and may even dip down to 70s on occasion. It also depends on a prior BP baseline, if the person is petite or dehydrated. But if the patient is mentating well and is not suffocating or experiencing crushing chest pain with diaphoresis, please don’t feel like you have to shock them. The body is not used to the new arrhythmia, and the rapid rate compromises the cardiac output.

Yes, you can still use your rate and rhythm controllers. Give the patient a gentle fluid bolus if you must. Of course, pacer pads do have to be on ahead of time.

Be afraid of shocking dialysis patients. Check electrolytes.

Hypotension with normal mentation is much better than a PEA arrest. Shocking extremes of electrolyte and acid/base abnormalities, whether due to TCA and other overdoses or in dialysis patients, will give you exactly that. This is especially true for the so-called “slow-X” arrhythmias: slow Afib, slow SVT, or even V-slow (Vtach with a rate of 130) that dialysis patients like to present in.

Just like airplane travel in transportation, electricity is in general the safest rhythm conversion strategy. But there are exceptions, and you only need to crash once.

A-flutter and the stuck rate of 150

You already know this, but just as a reminder. If the rate is a steady 150, plus or minus, and it is stuck there, you should think of atrial flutter.

Even if you do not see obvious classic flutter waves, there is a high chance of 2:1 conduction. In this case, I thought of it. Fortunately, it did not think of me.

Adenosine (again)….the 6, the 12…the 24??

Sometimes adenosine is not pushed correctly, but sometimes it just does not work or only works for a few seconds. Sometimes the patient’s Mom knows best what works, so you should listen. Sometimes the last time it was used, the patient really did feel like they were going to die – so they do not ever want it again. Ever. That you should try 6mg, then 12mg, then stop is generally true, but it is also a dead-end. What is your back up plan? Electricity? In the past I have given the doses in reverse, combined 6mg with the Valsalva maneuver and had given a preemptive beta-blocker or calcium channel blocker dose 10-15 minutes before adenosine to massage a stubborn heart into adenosine submission. It is ok to experiment a little. Another practical point – how much does your ED freak an SVT patient out while he or she is being triaged and roomed? I still do not completely understand why an SVT tends to be rushed up in the same fashion as a STEMI with cardiogenic shock and bradycardia, judging from staff adrenaline levels.

Calm the patient down, turn the lights off and let them change. It's like a kid with croup. Remember, it is lack of the sympathetic influx that we want, not an excess. Otherwise, why try the Valsalva at all? Has anyone attempted a stellate ganglion block Vfib-style for a refractory SVT? An overkill, I know….but could be fun, and practice for the real deal.

Aren’t all AVNRTs verapamil sensitive?

Years ago, in my first year of solo practice, I had a case of a refractory SVT in a young teenager, which a pediatric cardiologist consulting by phone called a “verapamil-sensitive AVNRT” based on the EKG alone. I was impressed. Hours later, I decided to flash my newly acquired cool knowledge and relayed the same to my in-house cardiologist, who looked at me with a grin and a raised eyebrow and said, “Anthony, all AVNRTs are verapamil sensitive”. At that time, I was also sensitive, and so my feelings were hurt. Lately I have gotten into the habit of treating my SVTs with diltiazem – as a purer verapamil relative. With generally good results and no need to stand in front of the patient during administration by the nurse.

The bottom line is – you have choices. Especially, if the patient is already on a beta-blocker or a calcium channel blocker, give them a beta or a calcium blocker IV, see what happens.

Case Concluded

Despite a single nadir of blood pressure of 75 systolic, the rest holding steadily in the high 90s, the patient received a single dose of IV diltiazem and a small IV fluid bolus. Labs reviewed prior showed normal potassium, calcium, sodium, magnesium and the rest of them. Her average heart rate reduced to about 106 and a repeat EKG is shown, accidentally capturing an event:

She, of course, had a “verapamil sensitive” SVT. The patient’s new right bundle block had also improved to an incomplete, proving to be either SVT- or rate-related. The patient had never experienced any symptoms while in the ED. She was observed for a short time, scheduled for an out-of-sequence dialysis the next day and discharged home with a normal heart rate. I guess, in this case, we did treat the EKG and not the patient.

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