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.

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     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.

     Hypernatremia due to water loss is called dehydration. This is different from hypovolemia, in which both salt and water are lost.

     Hypernatremia generally begins with lethargy, weakness and irritability, and may progress to twitching, seizures and coma.

• Unreplaced water loss
• Insensible and sweat losses
• Gastrointestinal losses
• Central or nephrogenic diabetes insipidus
• Osmotic diuresis
• Hypothalamic lesions affecting thirst
• Water loss into cells
• Sodium overload

     Hyponatremia is a low level of sodium caused by loss of salt and water through sweating, use of certain diuretics, chronic or severe vomiting or diarrhea, or osmotic diuresis (DKA). The prehospital management for hyponatremia includes normal saline infusion. Cerebral cells are especially vulnerable to increases in intracellular volume, as the skull provides no relief for edema and pressure increases and may ultimately lead to brain herniation.

     Not all hyponatremia is alike. Different causes and approaches to treatment exist due to acuity, volume status, total body water amount (TBW) and osmolarity.

     The hyponatremic patient seems to have "failure to thrive" with anorexia, nausea, headache, cramps or altered mental status ranging from confusion and status seizures to coma, and potentially death. If the sodium level has dropped gradually, compensatory changes will have occurred. The patient may have mild symptoms and may tolerate serum sodium of 110 mEq/L. If change has occurred in 24–48 hours, patients will be symptomatic at 120 mEq/L and risk of herniation increases with continued fall.¹

     Other symptoms may include thirst, dry membranes, apathy, confusion, restlessness, fever, decreased or absent urine output, hyperventilation, muscle twitching or spasticity, and progressive decrease in mental status.

     Treatment options for hyponatremia are:

• Fluid restriction: limit access to free water=
• Fluid replacement with normal saline=
• Hypertonic saline (3%): give "extra" sodium. This therapy is reserved for patients with impending brain stem herniation or status epilepticus.⁵

• Heat stroke or exhaustion
• Infants given only tap water during gastroenteritis
• Hyperglycemia and diabetic ketoacidosis
• Psychogenic polydipsia
• Beer alcoholism with malnutrition
• Recreational use of MDMA (ecstasy)
• Congestive heart failure
• Malignancy
• CNS disease
• Pulmonary disease, tuberculosis
• Drug effects (good medication history is needed)
• Renal disorders
• Hepatic cirrhosis
• Hypothyroidism
• Adrenal insufficiency
• Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
• Iatrogenic replacement of fluid losses with hypotonic solutions

     Potassium: an electrolyte that is important to the function of nerve and muscle cells, including the heart. Potassium is the chief cation in intracellular fluid.

     Serum potassium concentration is determined by the relationship between potassium intake and urinary potassium excretion. In most patients, dietary potassium is excreted in the urine. The degree of potassium secretion is primarily stimulated by three factors: an increase in serum potassium concentration; a rise in plasma aldosterone concentration; and enhanced delivery of sodium and water to the distal secretory site.⁶

     In EMS, we often see high potassium levels in certain segments of the population, such as dialysis patients. The ability of the renal failure patient to maintain potassium excretion at near-normal levels is generally possible, assuming that both aldosterone secretion and distal flow are maintained. As a result, hyperkalemia generally only develops in someone who produces little to no urine or who has an additional problem, such as a high-potassium diet, increased tissue breakdown, hypoaldosteronism, or fasting in dialysis patients.⁶

     Impaired cell uptake of potassium also contributes to development of hyperkalemia in advanced renal failure. It is believed that diminished sodium-potassium pump activity in skeletal muscles may be mitigated by retained uremic toxins from renal failure.

     A discussion of these two electrolytes would not be complete without discussing the sodium-potassium pump, which is an active transport mechanism. This means it is a molecular machine using a protein in a cell membrane that uses energy in the form of ATP. The sodium-potassium pump moves sodium in one direction while pumping potassium in the other against concentration gradients. The purpose of this pump is to ensure an appropriate balance of sodium and potassium into and out of the cell membrane.⁴

     Hyperkalemia is a potentially life-threatening metabolic problem caused by inability of the kidneys to excrete potassium, impairment of the mechanisms that move potassium from the circulation into the cells, or a combination of these factors.

     Potassium elevation is a common, potentially life-threatening problem most often occurring in patients with chronic renal failure or other illnesses that reduce renal potassium excretion. In these patients, acute hyperkalemia often is precipitated by stressors such as illness, dehydration or medication.

     Symptoms of hyperkalemia include abnormalities in myocardial function. Cardiac abnormalities of mild hyperkalemia (5.0 to 6.5 mM potassium) can be detected by an electrocardiogram. With severe hyperkalemia (over 8.0 mM potassium), the heart may fibrillate or stop beating entirely. Patients with moderate or severe hyperkalemia may also develop nervous symptoms such as tingling of the skin, numbness of the hands or feet, weakness, or a flaccid paralysis, which is characteristic of both hyperkalemia and hypokalemia.

     ECG changes seen in hyperkalemia include a sequential progression of effects, which roughly correlate with the potassium level. ECG findings may be observed as follows:

• Early changes of hyperkalemia include peaked T waves, shortened QT interval and ST segment depression.
• The above changes are followed by bundle branch blocks causing a widening of the QRS complex, increases in the PR interval and decreased amplitude of the P wave.
• Eventually, the P wave disappears and the QRS morphology widens to resemble a sine wave, with ventricular fibrillation or asystole ultimately occurring.

     ECG findings generally correlate with the potassium level, but as already stated above, potentially life-threatening arrhythmias can occur without warning at almost any level of hyperkalemia.⁷

     Factors necessitating emergent treatment of hyperkalemia include changes on ECG, a rapid rise of serum potassium, decreased renal function and presence of significant acidosis.⁵ Urgent ECG changes in a patient with hyperkalemia are of significant concern and may indicate the presence of a potentially fatal arrhythmia; however, hyperkalemia can be life-threatening even if the ECG is normal.⁸ About one-half of patients with potassium levels exceeding 6.0 mEq/L have a normal ECG.⁹

     Urgent treatment of hyperkalemia includes stabilizing the myocardium to protect against arrhythmias and shifting potassium from the vascular space into the cells. After the serum potassium level is reduced to safe levels, treatment focuses on lowering total body potassium. In patients who do not require urgent treatment, lowering total body potassium may be the only step necessary.

     Intravenous calcium is administered to stabilize the myocardium. It lowers the threshold potential, thus counteracting the toxic effect of high potassium. Calcium does not have any effect on the serum potassium level. Improvement in the ECG changes should be visible within two to three minutes of calcium administration.¹⁰ This is an appropriate consideration for an EMS provider with a lengthy transport time and positive ECG changes. Calcium gluconate is preferred over calcium chloride because it is less likely to complicate the ionic chemistry. Caution should be used in patients who take digoxin, as calcium has been reported to worsen the myocardial effects of digoxin toxicity.¹¹

     Although most EMS providers will not administer insulin without a serum potassium level, knowing the therapeutic effects of insulin can help to understand the process at hand. Shifting potassium intracellularly is done with insulin or a beta2 agonist.¹⁰ Insulin typically is given as 10 units intravenously with 50 mL of 50% glucose to counteract hypoglycemia. Repeated doses can be given if the potassium level remains elevated.

     Inhaled beta2 agonists have a rapid onset of action. The effect of beta2 agonists is additive to that of insulin administration, and they can be taken together. Nebulized albuterol (Ventolin) is given in a dose of 10 to 20 mg.

     Sodium bicarbonate is not recommended to lower potassium, but remains a viable treatment option for patients with severe metabolic acidosis.¹²

     Some patients who could benefit from administration of IV calcium and possibly even nebulized albuterol include those with:¹³

• Acute renal failure
• Crush injuries
• Compartment syndrome
• Rhabdomyolysis.

     The most common cause of hyperkalemia is impaired kidney function, such as in acute or chronic kidney failure. Other causes of hyperkalemia include:

• Certain medications like angiotensin-converting enzyme (ACE) inhibitors
• Hormone deficiencies, including adrenal failure (Addison's disease)
• Destruction of red blood cells due to severe injury or burns
• Excessive use of potassium supplements
• Alcoholism or heavy drug use that causes rhabdomyolysis, a breakdown of muscle fibers that results in release of potassium into the bloodstream.

     Hypokalemia is a low level of potassium caused by excessive potassium loss in urine from either a low-potassium diet or through the gastrointestinal tract when the patient is using certain diuretics, has chronic or severe vomiting or diarrhea, impaired kidney function or is overproducing aldosterone (a hormone that causes kidneys to excrete more potassium). There is no prehospital management for hypokalemia. These patients require potassium replacement, which is not common prehospital therapy.

     Mild hypokalemia usually results in no symptoms, while moderate hypokalemia may result in confusion, disorientation, weakness and muscle aches. Severe hypokalemia may result in extreme weakness of the body and, on occasion, flaccid paralysis, or limpness. If paralysis reaches the lungs, death will occur. The most significant result of severe hypokalemia is development of a cardiac arrhythmia leading to cardiac arrest.

     EKG findings in hypokalemia include abnormalities associated with moderate to severe hypokalemia including the triad of:

• decreased T-wave amplitude
• depression of the ST segment (0.5 mm or greater)
• and the appearance of U waves (amplitude greater than 1 mm and amplitude greater than the T wave in the same lead). U waves are often seen in the lateral precordial leads V4 to V6.¹⁴

     Hypokalemia is most commonly caused by the use of diuretics. The severity of hypokalemia tends to be proportionate to the degree and duration of hypokalemia. Symptoms generally do not manifest until the serum potassium reaches a level of below 3.0 mEq/L, unless the serum potassium falls rapidly or the patient has a comorbid factor that predisposes the patient to an arrhythmia:

• Decreased potassium intake
• An elevation in extracellular pH
• Increased availability of insulin
• Elevated beta-adrenergic activity
• Hypokalemic periodic paralysis.

     Manifestations of hypokalemia may be difficult to recognize in the presence of sinus tachycardia. This occurs because ST segment depression and decreased T- and U-wave amplitude are common ECG findings in tachycardia.⁷

     In emergency situations, the management of hypokalemia includes aggressive potassium replacement via an IV.¹⁵ In mild hypokalemia, oral replacement can be undertaken. In either case, potassium replacement only occurs after documented hypokalemia, which will almost never be treated in the field.

     Although clinical presentation and a good history can lead an EMS provider to conclude that an electrolyte imbalance exists, treatment should not be undertaken without confirmed blood chemistry or medical direction.

     Cation: An ion or group of ions having a positive charge and characteristically moving toward the negative electrode in electrolysis.

     Extracellular: Located or occurring outside a cell or cells.

     Hypotonicity: Having the lower osmotic pressure of two fluids.

     Serum: The clear yellowish fluid obtained upon separating whole blood into its solid and liquid components after it has been allowed to clot.

1. Kugler JP, Hustead T. Hyponatremia and hypernatremia in the elderly. Am Fam Physician 61(12):3623–3630, Jun 15, 2000.

2. Lindner G, Funk GC, Schwarz C, et al. Hypernatremia in the critically ill is an independent risk factor for mortality. Am J Kidney Dis 50:952, 2007.

3. Snyder NA, Feigal DW, Arieff AI. Hypernatremia in elderly patients. Ann Intern Med 107:309, 1987.

4. Tortora GJ, Derrickson BH. Principles of Anatomy & Physiology. Hoboken, NJ: John Wiley & Sons, 2009.

5. Lien YH. Hyponatremia: Clinical diagnosis and management. Am J Med 120(8):653–658, 1 Aug 2007.

6. Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, pp. 383-396, 898–910. New York, NY: McGraw-Hill, 2001.

7. Wald DA. ECG manifestations of selected metabolic and endocrine disorders. Emerg Med Clin North Am 24(1): 145–157, vii, 1 Feb 2006.

8. Martinez-Vea A, Bardaji A, Garcia C, Oliver JA. Severe hyperkalemia with minimal electrocardiographic manifestations: A report of seven cases. J Electrocardiol 32:45–49, 1999.

9. Acker CG, Johnson JP, Palevsky PM, Greenberg A. Hyperkalemia in hospitalized patients: Causes, adequacy of treatment, and results of an attempt to improve physician compliance with published therapy guidelines. Arch Intern Med 158:917–924, 1998.

10. Greenburg A, Cheung AK. National Kidney Foundation. Primer on Kidney Diseases, 4th ed. Philadelphia: Elsevier Saunders, 2005.

11. Gennari FJ. Disorders of potassium homeostasis. Hypokalemia and hyperkalemia. Crit Care Clin 18:273–288, 2002.

12. Kim HJ. Combined effect of bicarbonate and insulin with glucose in acute therapy of hyperkalemia in end-stage renal disease patients. Nephron 72:476–482, 1996.

13. Schaider J. Rosen and Barkin's 5-minute Emergency Medicine Consult, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2003.

14. Delk C. Electrocardiographic abnormalities associated with poisoning. Am J Emerg Med 25(6): 672–687, 1 Jul 2007.

15. Holstege CP. ECG manifestations: The poisoned patient. Emerg Med Clin North Am 24(1): 159–177, vii, 1 Feb 2006.

     William S. Krost, MBA, NREMT-P, is director of Emergency Services & Health System Access for Blanchard Valley Health System in Findlay, OH.

     Joseph J. Mistovich, MEd, NREMT-P, is a professor and chair of the Department of Health Professions at Youngstown (OH) State University.

     Daniel D. Limmer, AS, EMT-P, is a paramedic with Kennebunk Fire-Rescue in Kennebunk, ME.

     A 72-year-old female with chronic renal failure has been in the hospital recovering from a heart attack. She has just undergone balloon angioplasty to redilate her left coronary artery and is on an "npo" diet (i.e., not allowed to have food or drink by mouth), but is receiving fluid through an IV line. Late one night, a nurse replacing the woman's empty IV bag misreads the physician's orders and hooks up a fresh bag of IV fluid that is "twice-normal" rather than "half-normal" saline (four times more sodium than it should have been). When you arrive to transport the patient to a tertiary care center, you notice marked pitting edema around her sacral region and inspiratory rales at the base of the lungs on each side. She complains of difficulty breathing. As you are loading the patient for transport, her blood results from earlier this morning come back as follows:

     The nurse also tells you there is fluid in the lung fields on the patient's chest x-ray.

     What is wrong with this patient?

     The patient was given hypertonic saline (high concentrations of saline), which elevated the plasma and interstitial fluid sodium concentrations. As the plasma sodium level rises, more water than normal is passively (osmotically) drawn from the renal tubules into the kidneys. This raises blood volume and blood pressure, causing a shift of water from the plasma into the interstitial spaces and the patient develops edema in tissues and lung fields.

     Why does the patient have fluid in her lungs?

     This process is exacerbated by the patient's underlying chronic renal failure and heart attack. Her failing kidneys have a difficult time excreting the excess sodium and chloride ions introduced into her body. Furthermore, her recent cardiac event places her at increased risk of developing congestive heart failure. Her left coronary artery blockage probably caused damage to her left ventricle. The osmotic increase in blood volume places an increased preload work requirement on an already impaired left ventricle. If this ventricle cannot pump blood out into the aorta at a rate equal to that of blood entering the left ventricle from the left atrium, pressure will rise in the left side of the heart, and ultimately within the pulmonary circuit. As fluid builds up in the pulmonary circuit, it may begin to form pulmonary edema. When this happens, rales (i.e., crackling sounds) will be heard with a stethoscope when the patient inhales.