Potassium Disorders

The total body content of potassium (K) is about 3500 mEq,y and roughly 98 percent is intracellular, two thirds of which is intramuscular. [9 Because cell membranes are more permeable to K than to Na and Cl, K is primarily responsible for the resting transmembrane potential and is therefore critical to the function of excitable tissue.

HYPOKALEMIA

Hypokalemia, the most frequent electrolyte disorder encountered by the clinician, is defined as a plasma K concentration below the normal range (3.5 to 5.5 mEq/L).

Pathogenesis and Pathophysiology. Whenever K losses exceed intake, total body K decreases and hypokalemia results. Each 1-mEq/L decrement in the plasma K level roughly correlates to a total body K decrease of 100 to 300 mEq (.Ta..ble..3.8.-2. ). K influx increases intracellular positivity, thereby producing a mild depolarization. This lessened state of electrical excitability underlies the muscle weakness and hyporeflexia that can be seen clinically.

Epidemiology and Risk Factors. Approximately 2 percent of normal adults, 21 percent of hospitalized patients, 25 percent of patients taking 50 mg of hydrochlorothiazide daily, and nearly 100 percent of patients taking more than one class of diuretic have hypokalemia. y Although acute hypokalemia is an uncommon cause of weakness, certain scenarios increase its risk of development, including rapid correction of systemic acidosis (e.g., hyperventilation, bicarbonate administration), postoperative patients unable to take food by mouth (because K excretion cannot be stopped), and the chronic use of beta-2 agonists (e.g., asthmatics).

Clinical Features and Associated Disorders. The clinical features of hypokalemia are predominantly muscular and occur more frequently when the extracellular K level changes rapidly. The magnitude is also influential. y K levels of 3 to 3.5 mEq/L are associated with weakness, myalgias, and easy fatigability; those of 2.5 to 3.0 mEq/L are associated with more pronounced weakness; and those below 2.5 mEq/L (and especially if below 2.0 mEq/L) are associated with structural muscle damage (rhabdomyolysis and myoglobinuria). Areflexic quadriplegia and respiratory insufficiency may also occur at these lowest levels. The cranial musculature is rarely involved. Tetany may be observed in some hypokalemic patients, especially those with concomitant systemic alkalosis. Because hypokalemia can mask the tetany of hypocalcemia, tetany may appear as the hypokalemia is corrected.y Sensory disturbances and encephalopathic features are not expected in hypokalemia and, when present, should prompt a search for an underlying cause. Because hypokalemia can increase renal ammonia

_TABLE 38-2 -- MAJOR CAUSES OF HYPOKALEMIA_

Inadequate intake

Transcellular shifts (systemic alkalosis, thyrotoxic and hypokalemic periodic paralysis) Renal loss

Gastrointestinal losses

Other (drugs, head trauma, burns, hypomagnesemia, hypocalcemia)

Modified from Zull DN: Disorders of potassium metabolism. Emerg Med Clin North Am 1989;7:771-794.

production, it can aggravate a pre-existing hepatic encephalopathy (HE). y

Differential Diagnosis and Evaluation. Frequently, the cause of hypokalemia is apparent by history, and a full general and neurological examination, with particular emphasis on muscle strength and deep tendon reflexes, is necessary. The possibility of Cushing's syndrome or hyperaldosteronism is suggested by hypertension, and the presence of thyrotoxic periodic paralysis (TPP) is indicated by evidence of hyperthyroidism. Laboratory evaluation should include Na, K, Cl, bicarbonate, BUN, Cr, glucose, calcium (Ca), and magnesium (Mg), as well as an arterial blood gas (ABG) and an electrocardiogram (EKG). Thyroid function tests (TFTs) identify the rare TPP, and muscle biopsy may demonstrate vacuolar change but generally is not indicated.

Management. Therapy includes correction of the underlying cause and replacement therapy. Replacement therapy is usually recommended once the K level is below

3.5 mEq/L. Oral supplementation is preferred, but IV supplementation may be required when GI dysfunction exists or when the K deficiency is severe (with arrhythmias and neuromuscular manifestations).

Prognosis and Future Perspectives. Although respiratory failure and death can occur when hypokalemia goes unrecognized, complete recovery is expected when K replacement can be provided and the underlying disorder corrected. For disorders that cannot be corrected (e.g., aldosterone-secreting tumors), the prognosis is related to the underlying disorder.

HYPERKALEMIA

Pathogenesis and Pathophysiology. Hyperkalemia may result in three ways: (1) increased entry of K into the ECF, (2) intracellular K efflux, or (3) decreased K output. Of these three processes, intracellular K efflux and decreased K output predominate. Because the renal capacity for kaliuresis adapts to increasing K intake, hyperkalemia usually is not seen unless a massive amount of K is ingested, parenteral replacement in provided too rapidly, or co-existent adrenal or renal dysfunction exists. Even in the setting of complete RF, the rise in serum K is slow, ranging from 1 mEq/L per week to 0.5 mEq/L per day. y In the setting of hyperkalemia, the chemical gradient for K efflux is lessened and, therefore, intracellular positivity increases. This results in a minimal depolarization which, in turn, makes the tissue less excitable by causing a reduction in Na influx.

Epidemiology and Risk Factors. Among hospitalized patients, the incidence of hyperkalemia approaches 10 percent, one fifth of which is above 6.0 mEq/L. y Risk factors for the development of hyperkalemia include (1) renal or adrenal insufficiency, (2) K supplementation at rates and quantities above the suggested values, (3) situations resulting in tissue destruction (e.g., induction of chemotherapy), and (4) the use of beta-2 antagonists (e.g., propranolol) or other medications known to cause hyperkalemia (e.g., heparin, K-sparing diuretics).

Clinical Features and Associated Disorders. The usual manifesting feature of hyperkalemia is cardiac toxicity. '9! EKG features include peaked T waves, increased PR (atrioventricular block) and QRS (interventricular block) intervals, and arrhythmias. Cardiac arrest represents the major problem and may be the initial symptom. y Like hypokalemia, the major neurological manifestations of hyperkalemia are peripheral. Hyperkalemia may cause loss of strength and deep tendon reflexes, although this is observed less commonly than with hypokalemia. Muscle cramping is not uncommon, and both paresthesias'27' and focal neurological signs y have been reported.

Differential Diagnosis and Evaluation. Systemic acidosis and adrenal or renal insufficiency are the more frequently encountered etiologies of hyperkalemia. Once hyperkalemia is noted, an EKG must be obtained, followed by continuous cardiac monitoring until causes of pseudohyperkalemia are excluded. This requires a complete blood count (CBC) with smear for the presence of red blood cell hemolysis, thrombocytosis (> 500,000/mm 3 ), or leukocytosis (> 50,000/mm3 ). Tourniquet-induced stasis and forearm exercise may also produce hyperkalemia. '2'

Management. The treatment of hyperkalemia includes addressing its cardiac manifestations, reversing the underlying disorder, decreasing the K input, increasing the intracellular influx of K, and increasing K excretion.

Coping with Asthma

Coping with Asthma

If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.

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