Beyond the Basics: Electrolyte Disturbances

     This CE activity is approved by EMS Magazine, an organization accredited by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS), for 1.5 CEUs.

To earn your credits, sign up for this RapidCE course online or log in to your account directly at www.rapidce.com. Or, to print and mail a copy, download the test here. The deadline to take this test is June 5, 2009.

     OBJECTIVES

• Review causes of hypernatremia and hyponatremia
• Review causes of hyperkalemia and hypokalemia
• Discuss case reviews of these conditions

     Garnering a thorough understanding of the way electrolytes function within the body and the way they interact with each other can significantly impact your patient's survivability and overall outcome. There are numerous scenarios where front-line EMS providers can see the impact of electrolyte disturbances. Although many electrolytes influence normal physiology, this article focuses on sodium and potassium.

     Sodium: An electrolyte that is important to the regulation of body water distribution and nerve transmission.

     The balance of water within the body is proportional to the serum sodium concentration of blood. Sodium is the dominant cation in extracellular fluid and the primary determinant of serum osmolality (amount of sodium or other electrolyte in the plasma).In simple terms, hypernatremia (high blood sodium levels) and hyponatremia (low blood sodium levels) are caused by shifts of sodium in the body and can result in an imbalance in body fluid. An easy way to remember this is to remember that sodium always follows water; if the water is moved, sodium will also be moved.

     In normal physiology, water intake and water losses should be equal. If losses exceed intake, thirst is stimulated and fluid intake increases. Thirst is stimulated when the serum osmolality rises above 290–295 mmol per kg.¹ Serum osmolality changes associated with hypotension and hypovolemia will also produce a symptom of thirst as fluid is drawn from the interstitial space into the intravascular space, disturbing the solvent to solute ratio. Renal water conservation is the first line of defense against water depletion and is quickly followed by the stimulation of thirst, which will ultimately maintain a normal fluid balance. In volume depletion, secretion of antidiuretic hormone (ADH) from the posterior pituitary gland causes an increase in renal reabsorption of sodium, resulting in water retention. ADH, often referred to as vasopressin, is the hormone that regulates this sodium/water balance. This produces a more concentrated composition of urine and a decrease in urine output. In conditions of volume overload and hypotonicity, ADH is typically suppressed, resulting in greater excretion of sodium and, with it, increased water excretion. This patient would experience diluted urine with an increase in urine output.

     Hypernatremia, a high level of blood sodium (serum sodium >145 mEq/L), represents a relatively common problem.² Hypernatremia is seen primarily in patients who cannot express thirst normally, namely infants and adults with impaired mental status.³ Prehospital management for hypernatremia includes water (D₅W) infusions.

     If the sodium level drops, ADH secretion drops and the kidneys dump free water (the urine becomes more dilute), thus increasing the blood sodium concentration. If sodium concentration increases, the ADH secretion increases, the kidneys hold on to more free water and sodium concentration returns to normal. When the ADH mechanism is engaged, the water extraction discussed above also happens in the brain, which may cause the brain cells to shrink and result in neurologic changes and impaired neuronal functioning. Brain tissue shrinkage can also pull on dural veins and sinuses, which can cause intracranial hemorrhage.