Ann Crawford in her article "Balancing act: Sodium and Potassium" in the July issue of Nursing (pp. 44-50) describes the pump as the main mechanism of moving sodium "from inside cells to the extracellular compartments, and returns potassium from the extracellular compartments into cells using adenosine triphosphate (ATP) as an energy source."
She likewise explains that electrolytes tend to move from areas of high concentrations to lower concentrations. So the body naturally works to maintain potassium inside cells 35 times greater than outside cells so potassium has a tendency to want to get out of cells. Likewise, sodium outside cells is kept 14 times greater than inside cells so sodium has a natural tendency to want to go into cells.
Sodium attracts water. So if sodium levels inside the cell were to get too high the cells would absorb water and would swell and ultimately explode. Obviously this wouldn't be good.
Rene Fester Kratz in his book "Molecular & Cell Biology for Dummies" explains the pump as a protein in cellular walls and "for every round of action, the sodium potassium pump moves three sodium ions out of the cell and two potassium ions into the cell. Thus the pump creates a higher concentration of sodium outside the cell, a higher concentration of potassium inside the cell, and a greater positive charge outside the cell. These differences in ion concentration and electrical charge are important in the functioning or nerve and muscle cells in animals."
To understand how albuterol can decrease your potassium levels, you need to understand how certain hormones, known as catecholamines, affect potassium. Catecholamines, such as the hormone epinephrine and adrenaline, increase the activity of a protein known as a sodium-potassium ATPase. When this protein is activated, it pumps potassium into cells while also pumping sodium out of cells. The movement of potassium into the cells causes a decrease in the amount of potassium in the blood.
Albuterol (and Levalbuterol) is known as a beta-2 agonist. This means that it is able to bind to and mimic the effects of adrenaline on certain cells, including its ability to trigger the transport of potassium out of the blood. Consequently, taking albuterol can lower your potassium levels. This may make your muscles weak or cause muscle spasms, and it can also cause an abnormal heart rhythm. Other symptoms of hypokalemia include fatigue, constipation and the breakdown of muscle fibers.
Growing evidence suggests that there may be a role for albuterol in the treatment of patients with severe hyperkalemia. Catecholamines activate Na-K ATPase pumps through β2 receptor stimulation in a manner that is additive to the effect of insulin.(1, 2) In a study by Montoliu and coworkers, (3) 0.5 mg of intravenous albuterol was given to patients with hyperkalemia, leading to a 1-mEq/L decrease in serum potassium levels with minimal adverse effects. (4) Because there are no approved intravenous forms of β agonists available in the United States, studies have been performed to determine whether nebulized β agonists would have a similar effect on serum potassium levels. One such study found that albuterol, when given in very high doses (10–20 mg vs the normal 0.5 mg), decreased potassium levels by 0.62 to 0.98 mEq/L.45 The onset of action for inhaled albuterol was immediate and lasted for 1 to 2 hours. Although in these studies the effects varied among individuals, β2agonist administration was found to be safe and was associated with a significant decrease in serum potassium levels. Therefore, β2 agonist therapy should be considered as an adjunctive treatment for patients with severe hyperkalemia.
Nonetheless, we have reservations about the use of β2 agonists as a first-line therapy in emergency treatment of hyperkalaemia. First, 20–40% of patients studied have a decline in PK of <0.5 mM and it is not possible to predict who will fail to respond. Secondly, there are safety concerns because the doses used are 4–8 times those prescribed for the treatment of acute asthma. Although no severe adverse events were reported, most of these studies were performed in stable patients. Some of these studies excluded patients on β-blockers and those with significant coronary heart disease or unstable heart rhythms. Therefore, the safety of these agents was determined in a group of patients that may not resemble the general ESRD population.
Allon and Copkney (5) examined whether the effect of nebulized β2 agonists is additive to that of insulin. There was a similar decrease in PK with insulin (0.65 mM) or albuterol (0.66 mM). There was a substantially greater fall in PK with the combined regimen (1.2 mM). The dose of intravenous regular insulin used in this study was only 10 units, and PK fell less than in studies when higher doses of insulin were used (6). Thus, it remains uncertain whether β2 agonists would have a PK-lowering effect additive to that of insulin if insulin were given at the higher doses.