Prehospital treatment options for hyperkalemic emergencies
Montgomery County Hospital District shares 3 years of results of a hyperkalemia treatment protocol
Let’s review hyperkalemia to:
- Know the red flag historical features suggestive of hyperkalemia
- Recognize EKG features suggestive of severe hyperkalemia and patients at high risk of cardiac arrest
- Understand prehospital treatment options for hyperkalemic emergencies, including IV calcium carbonate, nebulized albuterol and sodium bicarbonate therapy
Hyperkalemia is one of the most dangerous electrolyte emergencies, and severe hyperkalemia can quickly lead to cardiac arrest if not promptly recognized and treated. Before discussing specific treatment options for hyperkalemia, recognition of hyperkalemia in the prehospital setting must be addressed.
The kidneys primarily govern potassium physiology. As a result, acute or chronic kidney disease is the most common cause of hyperkalemia. Many patients with life-threatening hyperkalemia are patients with chronic kidney disease who are dialysis dependent. Missed dialysis can quickly lead to severe and life-threatening hyperkalemia.
Other relatively common causes of hyperkalemia are diseases that lead to acute kidney injury, such as rhabdomyolysis/crush injury. Diabetic ketoacidosis (DKA) can lead to large extracellular potassium shifts and, in turn, severe life-threatening hyperkalemia.
Hyperkalemia is often referred to as the “great imitator” as a result of its wide range in presentation. Some of the more common presenting symptoms of hyperkalemia include generalized weakness, nausea and vomiting, and palpitations. There are no specific physical exam findings specific for hyperkalemia beyond a thorough search for evidence of hemodialysis access. As the presentation for hyperkalemia often consists of vague and nonspecific symptoms, it is important to consider hyperkalemia in patients with a high-risk history, especially those with abnormal EKG findings concerning for hyperkalemia .
Hyperkalemia EKG changes
Potassium is an essential electrolyte for cardiac conduction, and potassium transporters are necessary for cardiac depolarization. As a result, hyperkalemia leads to abnormal cardiac conduction. At mild levels of hyperkalemia, patients may be completely asymptomatic with normal EKG findings. On the extreme end of the spectrum (K > 8.0), most patients will be symptomatic, and EKG changes are more common. At these severe levels of hyperkalemia, cardiac arrest becomes much more likely. Hyperkalemia most commonly leads to asystolic arrest when it occurs but can also result in ventricular arrhythmias and PEA. Even with prompt recognition and treatment, these cardiac arrests have poor survival rates, making recognition and prompt treatment vital [2-5].
An orderly hyperkalemia EKG progression, relative to increasing potassium levels, is typically taught. However, these classic findings can be variable and progress quite erratically in no predictable fashion. Therefore, the clinical concern should not be minimized based on a “mildly” normal EKG in a high-risk patient. Peaked T waves are often thought of as the earliest hyperkalemia EKG finding. These are narrow-based T waves, as contrasted to the hyperacute, wide-based T waves associated with occlusion MI. Other hyperkalemia EKG changes include P wave flattening and PR interval prolongation, followed by QRS widening > 120 ms and ST segment changes. These ST segment elevations can be dramatic and often mimic occlusion MI. At the extreme, hyperkalemia EKG’s will take on a bizarre sinusoidal appearance, and patients will often become significantly bradycardic. At this stage, patients are in danger of imminent cardiac arrest if their potassium is not corrected [2-5].
Other conditions (e.g., intracerebral hemorrhage, sodium channel ingestion) may illicit EKG findings that mimic hyperkalemia, with lab results showing normal potassium levels. Prior studies have shown that the EKG alone is poorly sensitive for detecting hyperkalemia. However, significantly hyperkalemic patients (K > 6.5) are much more likely than less hyperkalemic patients to have the classic EKG changes. Considering the prehospital diagnostic limitations, the EKG is a rapid test that can quickly show cardiac conduction abnormalities and, when positive in high-risk patients, help identify hyperkalemia [2-5].
Prehospital hyperkalemia treatment options
There are multiple treatment options for hyperkalemia. In the prehospital setting, the goal of treatment is to prevent cardiac arrest and temporarily shift potassium/lower extracellular levels until definitive management can be initiated. Intravenous calcium carbonate is the rapidly acting initial option that stabilizes the cardiac membrane, therefore, reducing the likelihood of cardiac arrest. It does not lower the potassium level but allows time for other therapies to take effect. Calcium has a rapid onset effect (within minutes), is short-acting and is relatively safe. Its limited side effects consist mostly of GI symptoms, such as nausea and vomiting. Fears of the “stone-heart” phenomenon with calcium administration to patients taking digoxin are unfounded and not based on current evidence .
Albuterol is another readily available prehospital treatment option for hyperkalemia that acts to shift potassium. Therefore, it temporarily lowers serum potassium levels without excreting any potassium from the body and, like calcium, it buys time to initiate hemodialysis. Nebulized albuterol is also a cheap, relatively safe intervention with mild side effects, including tachycardia and palpitations.
Sodium bicarbonate is also included in many emergent hyperkalemia treatment protocols. It acts by alkalinizing the serum, which may lead to the temporary shifting of potassium into. Many hyperkalemic patients will be significantly acidotic, especially those with chronic kidney disease or in DKA. The standard dose for acute hyperkalemia is 1 ampule, or 50 mEq of sodium bicarbonate intravenously. Side effects commonly include GI symptoms such as nausea and vomiting, and volume retention issues secondary to the high sodium load. While studies have shown a small effect on potassium shifting, bicarbonate is likely a safe option for high-risk patients.
Other emergent treatment options, such as furosemide and a combination of insulin and dextrose, are less commonly found in the EMS setting and more often utilized in the emergency department.
MCHD hyperkalemia treatment protocol evidence
MCHD instituted a hyperkalemia treatment protocol using the previously described prehospital treatment options, which included the option to treat high-risk patients when awake and not just as a part of addressing the “Hs and Ts” in PEA cardiac arrest. Patients were eligible for treatment if they were determined to be clinically high-risk based on history along with having EKG changes concerning for hyperkalemia. EKG changes considered consisted of bradycardia, QRS widening or peaked T waves. Any of the classic hyperkalemia EKG abnormalities qualified the patient to receive treatment under the protocol. They did not have to possess any certain combination.
From February 2018-2021, all MCHD patients treated for hyperkalemia were followed for EMS and emergency department outcomes. Patients were kept on cardiac monitoring with any adverse events during transport. Potassium levels were determined at the ED following EMS treatment. Two independent reviewers assessed all cases for protocol compliance.
A total of 582 patients were treated under the hyperkalemia protocol. Of this group, 533 were excluded as they were in cardiac arrest prior to EMS arrival. The 48 non-arrest patients who received the treatment protocol were included in the analysis. Of these patients, ED potassium levels were found to be greater than 5.0 in 22 patients (45.8%), K of 3.5-5.0 in 23 patients (47.9%), and K of less than 3.5 in 3 patients (6.3%). An independent review showed EKG changes consistent with hyperkalemia in 43/48 patients (89.6%). Five patients (10.4%) either did not meet protocol criteria, either due to a lack of EKG changes or appropriate clinical suspicion.
The results of this study are consistent with prior ED hyperkalemia diagnostic and treatment evidence. EKG changes can be a useful indicator of hyperkalemia when present, especially those patients at a high risk of cardiac arrest, but they are not highly specific for hyperkalemia. Many other diseases can lead to EKG changes typically associated with hyperkalemia. It was also impossible to distinguish if patients with normal ED potassium had a normal potassium level prior to EMS treatment, as prehospital lab obtainment was unavailable.
Despite these limitations, nearly half of the treated patients had lab-diagnosed hyperkalemia upon ED arrival. Additionally, the overall accuracy rate of MCHD medics administering the hyperkalemia treatment protocol was quite high, with 43/48 cases correctly meeting protocol criteria. Given the benign profile for the given treatment options compared to the high mortality rate of hyperkalemic cardiac arrest, it seems reasonable to allow prehospital providers to continue administering a hyperkalemia treatment protocol based on EKG changes and clinical history. Further investigation is warranted to better refine the treatment protocol to improve accuracy.
Listen for more:
HyperK+ and MCHD’s clinical protocol with Jordan Anderson
How do we recognize and treat hyperkalemia in the prehospital setting?
- McArthur, R., Rafique, Z., Ward, B., Rodriguez, L., Dickson, R., & Patrick, C. (2022). Treatment of Presumed Hyperkalemia in the Prehospital Setting. Prehospital and Disaster Medicine, 37(5).
- Varga, C., Kálmán, Z., Szakáll, A., Drubits, K., Koch, M., Bánhegyi, R., Oláh, T., Pozsgai, É., Fülöp, N., & Betlehem, J. (2019, May 31). ECG alterations suggestive of hyperkalemia in normokalemic versus hyperkalemic patients. BMC emergency medicine. Retrieved November 11, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6814982/
- Montague, B. T., Ouellette, J. R., & Buller, G. K. (2008, March). Retrospective review of the frequency of ECG changes in hyperkalemia. Clinical journal of the American Society of Nephrology. Retrieved November 11, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2390954/
- Elliott, M. J., Ronksley, P. E., Clase, C. M., Ahmed, S. B., & Hemmelgarn, B. R. (2010, October 19). Management of patients with acute hyperkalemia. Canadian Medical Association Journal. Retrieved November 11, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2952010/
- ECG changes due to electrolyte imbalance (disorder). ECG & ECHO Learning. (2021, July 21). Retrieved November 11, 2022, from https://ecgwaves.com/topic/ecg-electrolyte-imbalance-electrolyte-disorder-calcium-potassium-magnesium/
- Levine M, Nikkanen H, Pallin DJ. The effects of intravenous calcium in patients with digoxin toxicity. J Emerg Med. 2011 Jan;40(1):41-6.
About the authors
Brad Ward, EMT-P, is the cardiac quality coordinator for MCHD EMS.
Konnor Cue, MD, is a second-year emergency medicine resident at the HCA Houston Healthcare/University of Houston Kingwood Emergency Medicine Program.
Casey Patrick, MD, FAEMS, is medical director for Harris County ESD11 Mobile Healthcare and assistant medical director for the Montgomery County Hospital District EMS service in Greater Houston, where he helped develop and produces the MCHD Paramedic Podcast. Dr. Patrick is board certified in both Emergency and EMS Medicine and works as a community emergency physician in multiple states. Additionally, he is an active member of the Texas NAEMSP State chapter and the national association, and serves as an EMS1 Editorial Advisory Board member.
Robert L. Dickson, MD, FACEP, FAEMS, is an assistant professor of emergency medicine at Baylor College of Medicine in Houston Texas. He serves as EMS medical director of Montgomery County Hospital District EMS and is board certified in emergency medicine. His academic interests include stroke, acute care coordination and resuscitation.