The paramedic crew on Medic 3, dispatched to a bus stop for a “sick person,” arrives to find an approximately 25-year-old male sitting alone on a bench. He’s in obvious respiratory distress and complaining of worsening dyspnea, as well as weakness, fatigue and muscle spasms in his extremities.
The patient reports that he just traveled across the country by bus. He also reports extensive medical history and says he “sees a bunch of doctors,” but is unable to give further details.
Upon initial assessment, the patient is awake, with diminished lung sounds in all fields, but no obvious rales, rhonchi or wheezing. His pulse is irregularly irregular. A tunneled dialysis catheter (TDC) is noted in the patient’s right chest.
Upon further questioning, the patient reveals that he suffers from glomerulosclerosis, which led to end stage renal disease (ESRD), causing him to require regular dialysis. However, his last dialysis treatment was over a week ago.
The crew quickly places the patient on a cardiac monitor and obtains vital signs which reveal blood pressure of 130/70 mmHg, heart rate ranges from 35-125, labored breathing with a respiratory rate of 26, with an oxygen saturation of 88% on room air.
The patient is placed on oxygen at 4 Lpm via nasal cannula, and his oxygen saturation quickly improves to 97%. His blood glucose level is found to be 76 mg/dL.
The patient is moved to the ambulance where IV access is obtained and a 12-lead ECG is performed. The patient continues to have a highly variable heart rate, and the crew notes peaked T-waves and multifocal ectopic beats. They see no evidence of ST elevation myocardial infarction or acute ischemic pattern. (See Figure 1.)
Given the ECG changes and the patient’s history, you’re concerned about hyperkalemia. After consultation with online medical control, the patient is given 1 gram of IV calcium chloride and a 5 mg nebulized albuterol treatment.
Transport & Hospital Course
Transport to the hospital is initiated and the crew continues to monitor the patient. While en route to the ED the patient’s heart rate stabilizes to 70 bpm and a repeat 12-lead ECG is captured. The T-waves remain peaked but there’s less ectopy. The patient’s blood pressure increases to 168/110 mmHg and his oxygen saturation improves to 100%. He remains stable until arrival at the ED.
In the ED, the patient is found to have multiple lab abnormalities, including a potassium level of 7.8 mEq/L (normal range is 3.5-5.0 mEq/L). He’s given additional doses of albuterol and calcium, as well as insulin and glucose.
Nephrology is consulted, and arrangements are made for emergent dialysis. The patient is admitted to the ICU, and after dialysis treatment the patient’s potassium level normalizes to 4.4 mEq/L. After six days in the hospital, the patient is released.
The kidneys function to filter the blood and create urine. Blood flows from the renal arteries into the kidneys. Within the kidney, the functional structure of filtration is the glomeruli.
There are approximately 1 million glomeruli in each kidney. Within the individual glomeruli blood flows in and then water, potassium, sodium, magnesium, urea and other waste products diffuse out across the cell membrane. The fluid that diffuses out is urine, and the filtered blood then flows back into systemic circulation through the renal veins. Any disruption in this process can upset the body’s delicate homeostasis.
This patient suffers from glomerulosclerosis, a genetic disorder that causes catastrophic scarring of the kidneys, leading to ESRD, which is characterized by complete or near-complete failure of the renal system to produce urine.
In order to survive, ESRD patients must maintain strict fluid restrictions and receive a regular schedule of dialysis treatment. Because of the significant comorbidities associated with dialysis, these patients have a mortality rate of approximately 23% per year.1
To facilitate the dialysis process, patients will typically have an arteriovenous fistula in an upper extremity or a TDC in their chest wall. When evaluating dialysis patients, it’s important for the EMS provider to protect the fistula by not using that extremity for blood pressure measurement or IV access. Fistula sites can be easily damaged, are susceptible to infection, and bleeding from these sites can be life threatening.
When ESRD patients fail to receive dialysis treatment, fluid overload and significant electrolyte imbalances can quickly occur. Excess fluid may first settle in the extracellular spaces within the lower extremities causing pedal edema. As fluid levels continue to increase it may also leak into the lungs causing pulmonary edema.
Hyperkalemia, or elevated potassium, is perhaps the most serious complication of severe kidney failure. Potassium is important in creating and maintaining the resting potential of cardiac myocytes, and elevation of potassium levels disturbs this potential, making cardiac cells more prone to arrhythmia.2
The normal serum potassium level found in the blood is 3.5-5.0 mEq/L. Without removal through dialysis, potassium levels can quickly rise above normal levels. Patients with severe hyperkalemia may present with multiple vague symptoms such as muscle weakness and spasms, headache, dyspnea, nausea, vomiting. They may also show signs of arrhythmia.
In the prehospital setting, a 12-lead ECG is the best way to evaluate for signs of hyperkalemia. Patients who present with ECG changes that are indicative of hyperkalemia are experiencing a true emergency that requires rapid and aggressive management.
The earliest manifestation of hyperkalemia on an ECG is narrow, peaked T-waves, which typically occur when the potassium level is > 5.5 mEq/L. As the potassium level continues to increase, the QRS widens and may appear identical to a bundle branch block, occurring when potassium level is > 6.5 mEq/L. Above that level, the QRS complex becomes wider and wider until it takes on the appearance of a sine wave.2
In a patient with ECG changes and history consistent with hyperkalemia, the most rapidly effective treatment is intravenous calcium, which works within minutes and acts to stabilize the cardiac membrane potential. This effect lasts 30-60 minutes.3 However, calcium doesn’t affect how much potassium is in the extracellular space.
Albuterol is an adrenergic agonist and shifts potassium into the intracellular space-it can lower the serum potassium level by 0.5-1.0mEq/L.4 The onset of action is around 30 minutes and the duration of action is two hours.3 Sodium bicarbonate is an electrolyte preparation that acts as a buffer and will increase metabolic pH, which causes a temporary shift of potassium into the cell. This effect is short-lived and should only be used in patients with known acidosis.4
In the hospital, hyperkalemic patients are also frequently given insulin and dextrose. Regular insulin stimulates the cellular uptake of potassium and takes effect within 20 minutes. A standard 10-unit dose will lower potassium levels by approximately 0.6 mEq/L.3 Dextrose is given to patients with normal blood glucose to prevent hypoglycemia.
It’s important to note that the pharmaceutical therapies described are all temporary and are used to buy time until the patient can receive the definitive treatment, which is dialysis. When prehospital providers are considering the transport destination for the ESRD patient suffering from hyperkalemia, a facility capable of providing emergent dialysis should
Hyperkalemia is a potentially life-threatening condition that can be successfully managed with several prehospital interventions. It’s important to maintain a high index of suspicion in patients at high risk such as those on dialysis or with prolonged crush injuries. Administration of calcium is the most effective and rapid prehospital intervention, but paramedics should be aware of other possible therapies such as nebulized albuterol and intravenous sodium bicarbonate. When ECG changes consistent with hyperkalemia are noted in these patients, aggressive management should be quickly initiated to protect cardiac function.
1. Zhang H, Schaubel DE, Kalbfleisch JD, et al. Dialysis outcomes and analysis of practice patterns suggests the dialysis schedule affects day-of-week mortality. Kidney Int. 2012;81(11):1108-1115.
2. Parham WA1, Mehdirad AA, Biermann KM, et al. Hyperkalemia revisited. Tex Heart Inst J. 2006;33(1):40-47.
3. Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008;36(12):3246-3251.
4. Pfenning CL, Slovis CM: Electrolyte disorders. In Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s emergency medicine: Concepts and clinical practice, 8th edition. Mosby: St. Louis, pp. 1636-1653, 2014.