Porth's Essentials of Pathophysiology, 4e

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Disorders of Fluid, Electrolyte, and Acid–Base Balance

C h a p t e r 8

Manifestations of Hypokalemia and Hyperkalemia

TABLE 8-5

Hypokalemia

Hyperkalemia

LaboratoryValues

LaboratoryValues

Serum potassium <3.5 mEq/L (3.5 mmol/L) Thirst and Urine Increased thirst Inability to concentrate urine with polyuria and urine with low specific gravity Effects of Changes in Membrane Potentials on Neural and Muscle Function

Serum potassium >5.5 mEq/L (5.5 mmol/L)

Effects of Changes in Membrane Potentials on Neural and Muscle Function

Gastrointestinal

Gastrointestinal

Anorexia, nausea, vomiting

Nausea, vomiting Intestinal cramps

Constipation, abdominal distention Paralytic ileus (severe hypokalemia)

Diarrhea

Neuromuscular

Neuromuscular

Muscle weakness, flabbiness, fatigue Muscle cramps and tenderness Paresthesias Paralysis (severe hypokalemia)

Muscle weakness

Paresthesias

Paralysis (severe hyperkalemia)

Central Nervous System Confusion, depression Cardiovascular Postural hypotension

Cardiovascular

Electrocardiogram changes

Electrocardiogram changes

Risk of cardiac arrest with severe hyperkalemia

Cardiac arrhythmias Predisposition to digitalis toxicity Acid–Base Balance Metabolic alkalosis

attempt to regulate ECF potassium levels within a more normal range. The signs and symptoms of hypokalemia seldom develop until serum potassium levels have fallen to less than 3.0 mEq/L (3.0 mmol/L). 3 They are typi- cally gradual in onset, and therefore the disorder may go undetected for some time. The renal mechanisms that serve to conserve potas- sium during hypokalemia interfere with the kidney’s ability to concentrate urine. Urine output and plasma osmolality are increased, urine specific gravity is decreased, and complaints of polyuria, nocturia, and thirst are common. Metabolic alkalosis and renal chlo- ride wasting are signs of severe hypokalemia. There are numerous signs and symptoms associated with gastrointestinal function, including anorexia, nau- sea, and vomiting. Atony of the gastrointestinal smooth muscle can cause constipation, abdominal distention, and, in severe hypokalemia, paralytic ileus. When gas- trointestinal symptoms occur gradually and are not severe, they often impair potassium intake and exagger- ate the condition. Complaints of weakness, fatigue, and muscle cramps, particularly during exercise, are common in moderate hypokalemia (serum potassium 2.5 to 3.0 mEq/L [2.5 to 3.0 mmol/L]). Muscle paralysis with life-threatening respiratory insufficiency can occur with severe hypokalemia. Leg muscles, particu- larly the quadriceps, are most prominently affected. Some people complain of muscle tenderness and

paresthesias rather than weakness. In chronic potas- sium deficiency, muscle atrophy may contribute to muscle weakness. The most serious effects of hypokalemia are on the heart. 3,31–33 Hypokalemia produces a decrease in the rest- ing membrane potential, causing prolongation of the PR interval (see Chapter 17). It also prolongs the rate of ventricular repolarization and lengthens the relative refractory period, causing depression of the ST segment, flattening of the T wave, and appearance of a promi- nent U wave. Although these ECG changes usually are not serious, they may predispose to reentry ventricular arrhythmias. Hypokalemia also increases the risk of digitalis toxicity in persons being treated with the drug, and there is an increased risk of ventricular arrhyth- mias, particularly in persons with underlying heart dis- ease. The dangers associated with digitalis toxicity are compounded in persons who are receiving diuretics that increase urinary losses of potassium. In a rare genetic condition, called hypokalemic familial periodic paralysis , episodes of hypokalemia cause attacks of flaccid paralysis that last 6 to 48 hours if untreated. 30 The paralysis may be precipitated by situations that cause severe hypokalemia by produc- ing an intracellular shift in potassium, such as inges- tion of a high-carbohydrate meal or administration of insulin, epinephrine, or glucocorticoid drugs. The paralysis often can be reversed by potassium replace- ment therapy.