Electrolyte Imbalances—Part 2: Potassium Balance Disorders

Last month EMS World began a four-part look at electrolyte imbalances with a focus on sodium. This month we look at potassium balance disorders.

Potassium Balance Disorders

Potassium is the primary intracellular electrolyte, and because of its positive charge it is considered the primary intracellular cation. The total amount of potassium in the body is related to the person's size, but it averages 3,200 mEq in males and 2,200 in females. Of the body's potassium, 70% is found in skeletal muscle, and 28% is found in the liver and red blood cells, which means that 98% of the potassium in the body is in the intracellular fluid. The remaining 2% is found in the extracellular fluid. It is this 2% that is critical to normal cardiovascular and neuromuscular function, and it is what is measured in a serum potassium reading.

The normal serum potassium is 3.5 to 5.0 mEq/L. Having too little potassium (less than 3.5 mEq/L) is called hypokalemia, while having too much (more than 5.5 mEq/L) is called hyperkalemia. Even minor variations in serum potassium levels can have significant impact on cardiovascular and neuromuscular function. This is because the ratio of intracellular to extracellular potassium is an important determinant of cellular membrane potential. Potassium is constantly moving between the ICF and ECF by way of the sodium-potassium pump.

Adequate renal function is necessary to maintain normal potassium levels. There are two methods by which the kidneys regulate potassium balance. First, potassium and hydrogen ions compete for exchange with sodium ions in the renal tubules. The urine salt content is adjusted by the distal convoluted tubules of the kidney. Second, aldosterone causes the kidneys to retain sodium, which in turn causes retention of water. To retain sodium, the kidneys excrete potassium. Nine-tenths of the potassium excreted daily is excreted in the urine, while the other 10% is lost through the feces and sweat glands. Because the body cannot store potassium, it must be ingested daily—the body needs 40 mEq a day. The normal diet contains 60 to 100 mEq a day, and the potassium balance is maintained by a daily intake and output of 50 to 100 mEq.

Hypokalemia is one of the most common electrolyte disorders. It clinically defined as a serum potassium level of less than 3.5 mEq/L. Moderate hypokalemia is a serum level of 2.5 to 3.0 mEq/L; severe hypokalemia is a serum level of less than 2.5 mEq/L (although life-threatening hypokalemia is rare). Hypokalemia is generally the result of a decrease in total stored potassium, but it can also occur when the body has normal potassium stores in the presence of an alkalotic state. For causes of hypokalemia, see Figure 1.

Potassium plays a key role in the maintenance of pH levels. In alkalosis, where the percentage of hydrogen in the ECF is low, the cells will release hydrogen into the ECF to increase acidity, and will absorb potassium from the serum. This results in a lowering of serum potassium levels. Although total body potassium is normal in this situation, the serum potassium will be lower. If the level drops below 3.5 mEq/L, the patient may exhibit signs and symptoms of hypokalemia despite the fact that alkalosis was their original condition. In the setting of hypokalemia, potassium is released from the ICF to maintain serum potassium levels. In response to this, hydrogen is absorbed into the ICF, creating an alkalotic state. Therefore, regardless of the original condition, hypokalemia and alkalosis commonly coexist, as either condition may cause the other.

The signs and symptoms of hypokalemia are nonspecific and depend on the individual patient. They generally originate in the nervous and muscular systems and are often not present until the potassium levels are less than 3.0 mEq/L. A good history and physical exam are required in the absence of actual potassium levels. As the hypokalemia progresses, the cardiovascular system may become involved. Early symptoms often noted by patients are muscular fatigue and weakness, particularly in the lower extremities (for signs and symptoms, see Figure 2). Death from hypokalemia is usually caused by anoxia secondary to paralysis of the respiratory muscles, which in turn leads to cardiac arrest.

The prehospital treatment of hypokalemia is difficult and rare. The only potassium-containing fluid that may be found in the prehospital setting is lactated Ringer's (LR); however, this is not a very effective treatment and is not commonly stocked on ambulances. Even if LR is available, attempts at correction should be avoided in the setting of unknown potassium levels. General treatment includes addressing any immediate life threats, avoiding hypoxia and anoxia by supporting respirations as needed, and providing standard treatment for cardiac arrhythmias. Treatment of hypokalemia in the hospital is through oral potassium supplements whenever possible. If the patient is severely hypokalemic, potassium chloride may be administered intravenously.

Hyperkalemia, a serum potassium level of greater than 5.5 mEq/L, most commonly occurs secondary to an increase in total potassium stores and can be classified as mild (5.5. to 6.0 mEq/L), moderate (6.1 to 7.0 mEq/L) or severe (greater than 7.1 mEq/L). It can also occur with normal potassium stores in the presence of metabolic acidosis. In the setting of acidosis, the cells will absorb hydrogen ions in an attempt to raise the serum pH, releasing potassium in exchange. On the other hand, during hyperkalemia the cells will absorb potassium in an effort to reduce serum potassium levels and thereby release hydrogen, causing a metabolic acidosis. Because of this mechanism, shifting hydrogen and potassium between the ICF and ECF, acidosis can cause hyperkalemia, and hyperkalemia can cause acidosis.

As with hypokalemia, it is nearly impossible for someone with normal renal function to spontaneously become hyperkalemic. Although it is much less common than hypokalemia, hyperkalemia is much more dangerous, and when unrecognized or untreated it may result in cardiac arrest. It is therefore imperative that signs, symptoms and history suggestive of hyperkalemia are recognized, and immediate treatment is provided if indicated.

Hyperkalemia is generally caused by decreased or impaired renal excretion, the addition of potassium to the extracellular space or transmembrane shifts of potassium. Simply increasing the dietary intake of potassium rarely causes hyperkalemia, as it is rapidly excreted by the kidneys. However, if the patient has a history of renal failure or is taking potassium-sparing diuretics or ACE inhibitors, an increase in dietary potassium can result in hyperkalemia. For causes of hyperkalemia, see Figure 3.

The signs and symptoms of hyperkalemia extend from the neuromuscular and cardiovascular systems. The most common finding is vague muscle weakness starting in the legs and ascending to the trunk and arms, and which can result in flaccid paralysis. The respiratory muscles may become involved, leading to hypoventilation, but this is often a late finding. Bradycardia in the hyperkalemic patient is often a preterminal event. Death is generally secondary to cardiac arrhythmias which may include various heart blocks, ventricular tachycardia, ventricular fibrillation and asystole. For signs and symptoms of hyperkalemia, see Figure 4. 

It is imperative that the medical practitioner understand that the signs and symptoms of hyperkalemia relate poorly to actual potassium levels. As with most electrolyte emergencies, the best treatment may simply be to monitor the patient and notify the receiving facility of your suspicions. Initial treatment of hyperkalemia includes the resolution of any compromise to the airway, breathing or circulation. Cardiovascular effects such as EKG changes, cardiac dysrhythmias or hypotension in the setting of suspected hyperkalemia deserve a heightened awareness of the possible need for intervention. Indicators of imminent arrest, such as a widening QRS complex, warrant immediate treatment aimed at stabilization of the cardiac resting membrane potential (RMP) and movement of potassium into the ICF. Specific therapies to achieve this include:

• 10 to 20 ml of 10% calcium gluconate, or 5 to 10 ml of 10% calcium chloride: Calcium does not promote the movement of potassium into the cells, but rather restores the cardiac RMP by antagonizing the cardiotoxic effects of hyperkalemia. Calcium should be avoided in patients who take digitalis or if digitalis toxicity is suspected, as it can potentiate the effects of digitalis.

• 1 mEq/kg of sodium bicarbonate with a maximum dose of 100 mEq: Increasing the pH of the blood causes cells to excrete hydrogen ions to the ECF in an attempt to lower it. In this way, potassium will be absorbed into the cell, effectively lowering ECF potassium concentrations.

• 25 g of 50% dextrose, unless hyperglycemic: As glucose enters the cells, it will promote the movement of potassium as well, effectively lowering ECF concentrations of potassium.

• 10 units of regular insulin: This is not generally available in the prehospital setting. Insulin is administered to stimulate the movement of glucose, and therefore the movement of potassium, into the cells. While glucose can be administered in the absence of insulin (it will stimulate intrinsic insulin release), insulin should not be administered without glucose, as it can precipitate hypoglycemia.

• 2.5 mg of nebulized albuterol: Albuterol increases plasma insulin levels, which can be beneficial when insulin administration is not an option. Albuterol alone lowers potassium levels by 0.5 to 1.5 mEq/L.

• 20 to 40 mg of furosemide: Furosemide is a potassium-wasting diuretic that promotes excretion by the kidneys.

Maintain an increased suspicion of hyperkalemia in patients presenting with weakness or in arrest if they have chronic renal failure or are on dialysis.

Next month: Magnesium Balance Disorders

Bibliography

1. Braunwald E, Fauci AS, Kasper DL, et al. Harrison's Principles of Internal Medicine, 15^th ed. New York, NY: McGraw-Hill, 2001.

2. Marx JM, Hockberger RS, Walls RM, et al. Rosen's Emergency Medicine: Concepts and Clinical Practice, 6^th ed. Philadelphia, PA: Mosby, 2006.

3. Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: A Comprehensive Study Guide, 6^th ed. New York, NY: McGraw-Hill, 2004.

Robert Vroman, BS, NREMT-P, has been involved in all levels of EMS for almost 20 years, working with both rural and urban services as a provider and educator. He has a Bachelor’s degree in Emergency Medical Care from Western Carolina University, and is currently pursuing a Master’s of Education, specializing in Adult Education and Training at Colorado State University.