Introduction

Hyperkalemia (HK) is potentially life-threatening, characterized by elevated serum potassium (K) levels, and currently accounts for up to two-to-three percent of emergency department (ED) visits with more than 800,000 annual visits in the United States. ^{Reference Singer, Thode and Peacock1–Reference Collins, Pitt and Reaven3} Prior work has shown that HK is associated with increased rates of hospitalization and health care costs. An analysis of data from the Nationwide Emergency Department Sample (NEDS) ⁴ found HK was estimated to account for US$1.18 billion of aggregate health care charges. ^{Reference Rafique, Weir and Onuigbo5} The incidence of HK among patients transported by Emergency Medical Services (EMS) is currently unknown.

Potassium is the most abundant cation in the body with large concentrations located intracellularly. ^{Reference Brown6} A significant gradient between intracellular and extracellular K concentration is required for normal cellular functions including nerve excitation and muscle contraction. ^{Reference Giebisch7} The loss of K gradient across the cell membrane impedes normal nerve, muscle, and cardiac function. ^{Reference Yan, Lankipalli, Burke, Musco and Kowey8} Most importantly, a loss of normal K gradient in myocytes accelerates repolarization leading to “peaked” T waves and delays conduction leading to depolarization abnormalities seen as prolonged PR and QRS intervals. ^{Reference Dittrich and Walls9–Reference Diercks, Shumaik, Harrigan, Brady and Chan11} While the electrocardiogram (ECG) is only 34%-50% sensitive for identifying patients with HK, the presence of conduction changes on ECG is associated with higher risk of progression to arrhythmia. ^{Reference Montague, Ouellette and Buller12–Reference Ettinger, Regan and Oldewurtel17} In cases of severe HK (usually K >6.5mEq/L), ventricular arrhythmias may occur and lead to sudden cardiac death. ^{Reference Mattu, Brady and Robinson10,Reference Rafique, Peacock and Armstead18}

Normal K homeostasis is maintained by renal excretion and redistribution of K into the intracellular space. ^{Reference Brown6,Reference Giebisch7} Patients at risk for HK include conditions limiting the ability of the kidney to excrete K, such as chronic kidney disease (CKD), and conditions which shift potassium from the intracellular to extracellular space, such as metabolic acidosis or diabetic ketoacidosis (DKA) and medications which alter K homeostasis. ^{Reference Jain, Kotla and Little19–Reference Medford-Davis and Rafique23}

Patients with HK are asymptomatic in >50% of cases ^{Reference An, Lee and Jeon14} or can have nonspecific symptoms including fatigue, muscle cramps, paresthesia, flaccid paralysis, vomiting, or diarrhea. ^{Reference Jain, Kotla and Little19,Reference Pepin and Shields24,Reference Weisberg25} Of symptomatic patients with severe HK, the most common presenting symptoms include arrhythmia and cardiac arrest. ^{Reference An, Lee and Jeon14}

In the hospital setting, HK is usually identified through routine laboratory testing, however routine laboratory testing is not available in the prehospital setting. Historically, EMS protocols only allowed for empiric management of presumed HK in settings of cardiac arrest, however, delaying treatment can be dangerous and may lead to cardiac arrhythmia and eventual arrest.

Initial treatment of HK includes the use of calcium to stabilize the myocytes and restore normal cardiac electrical conduction along with medications to drive K intracellularly including insulin and beta agonists such as albuterol. ^{Reference Jain, Kotla and Little19,Reference Weisberg25,Reference Ahee and Crowe26} Intravenous (IV) sodium bicarbonate may aid intracellular redistribution of K, especially in cases of HK resulting from acidosis. Although clinical data on the effectiveness of sodium bicarbonate are mixed and effect is likely to be delayed by hours. ^{Reference Rafique, Weir and Onuigbo5,Reference Mahoney, Smith, Lo, Tsoi, Tonelli and Clase27} Rapid treatment of HK lowers serum K level and has been shown to decrease mortality. ^{Reference An, Lee and Jeon14} Given the high risk of untreated HK when associated with ECG changes and relatively low risk of empiric HK treatment, prior studies have encouraged empiric treatment of presumed HK when classic ECG findings are present. ^{Reference Mattu, Brady and Robinson10}

An EMS protocol for empiric treatment of HK in patients presenting with both a clinical concern for HK and ECG findings consistent with HK was implemented. The purpose of this study is to assess protocol compliance and accuracy of prehospital HK treatment in non-cardiac-arrest patients transported by a single EMS system.