Potassium plays an important role in the resting membrane potential of excitable cells such as cardiac myocytes, and disorders of potassium balance can cause life-threatening arrhythmias. Hypokalemia in hospitalized patients is associated with a 10-fold increased mortality. Hyperkalemia is associated with increased mortality of 14% to 41%, and accounts for 2% to 5% of deaths in patients with end-stage renal disease. Acute changes in the ratio of extracellular to intracellular potassium concentration are more dangerous than chronic changes. The chapter presents examples of hypokalemia and hyperkalemia in perioperative patients, reviews the symptoms and causes for each condition, and discusses the appropriate preoperative, intraoperative, and postoperative management.
Keywordshyperkalemia, hypokalemia, potassium chloride, potassium disorders, serum potassium level
A 70-year-old man with hypertension is anesthetized for emergency surgery for a bowel obstruction. His only daily medication is hydrochlorothiazide. His preoperative serum potassium concentration was 3.4 mEq/L. Intraoperative oliguria is treated with 10 mg of intravenous furosemide. He produces 900 mL of urine in the next hour, and his electrocardiogram (ECG) shows new U waves and five premature ventricular systoles per minute. A repeat serum potassium concentration is 2.8 mEq/L.
A 55-year-old woman with end-stage renal disease presents for revision of a left femoral-popliteal artery bypass. She was dialyzed this morning via her left forearm arteriovenous fistula. Her serum potassium before surgery was 5.6 mEq/L. At hour 4 of surgery the femoral artery cross-clamp is released, and her ECG develops peaked T waves and widened QRS complexes. A repeat serum potassium is 7.0 mEq/L.
Potassium plays an important role in the resting membrane potential of excitable cells such as cardiac myocytes, and disorders of potassium balance can cause life-threatening arrhythmias. Hypokalemia occurs in up to 20% of hospitalized patients and is associated with a tenfold increased mortality risk, chiefly due to arrhythmias and cardiovascular events. Hyperkalemia is reported in 1% to 10% of hospitalized patients, and 10% of these have severe hyperkalemia with a K + greater than 6.0 mEq/L. Hyperkalemia accounts for 2% to 5% of deaths in patients with end-stage renal disease.
Perioperative serum potassium concentration abnormalities are common, and the recognition and treatment of hypokalemia and hyperkalemia are important skills. Maintenance of total body potassium is accomplished by a balance between the intake of K + and the renal or gastroenterologic excretion of K + . Potassium is the principal intracellular cation. More than 98% of the total body potassium is located within cells, largely in muscle cells. Total body potassium stores equal 50 mEq/kg; thus a 70-kg man contains approximately 3500 mEq of K + . The normal serum potassium concentration is 3.5 to 5.3 mEq/L. The normal intracellular potassium concentration is about 30 to 40 times higher than the serum concentration. The Na + -K + -ATPase pump inside cell membranes actively pumps sodium out of cells and potassium into cells and maintains the extracellular-intracellular ratio of potassium.
Any change in the extracellular-intracellular K + concentration ratio is of greater concern than the measured extracellular K + serum concentration. Acute changes in the ratio are more dangerous than chronic changes. The most significant risks are to cardiac electrophysiology, resulting in both arrhythmias and depressed contractility. The clinical history that accompanies acute serum potassium decrease or increase is of critical importance, as the two case synopses illustrate.
The first case synopsis illustrates chronic hypokalemia complicated by acute hypokalemia. Chronic hypokalemia is associated with a reduction in both total body stores and measured serum potassium levels, while a normal ratio of extracellular to intracellular potassium concentration is maintained. Diuresis with furosemide causes the renal loss of potassium, with a drop in the serum K + from 3.4 mEq/L to 2. 8 mEq/L. This acute hypokalemia causes a change in the extracellular-intracellular ratio, which leads to an increased resting potential, hyperpolarization across the cell membrane, and a predisposition to cardiac arrhythmias.
In the awake patient the most common symptoms of a serum K + less than 3 mEq/L are weakness and fatigue. Other symptoms relate to cardiovascular, central nervous system, neuromuscular, renal, or metabolic function ( Box 87.1 ). In a patient under general anesthesia, ECG changes, decreased cardiac output, or a decreased response to vasopressors may be the initial presentations of hypokalemia. Abnormal ECG changes or a clinical scenario such as the acute diuresis in the first case synopsis prompt the clinician to measure a serum K + and confirm the diagnosis of hypokalemia. ECG changes in hypokalemia may include the following ( Fig. 87.1 ):
The appearance of U waves
Flattened or inverted T waves, concave ST-segment depression
Increased amplitude of QRS complexes
Premature atrial or ventricular extrasystoles
With severe hypokalemia, supraventricular tachycardias, atrial fibrillation, atrial flutter, and potentially ventricular tachycardia or fibrillation
Decreased cardiac contractility
Electrical conduction abnormalities
Orthostatic hypotension and decreased response to vasopressors
Increased risk of digitalis toxicity
Neuromuscular and Central Nervous System
Weakness and fatigue
Confusion and depression
Respiratory depression (at serum K + <2.5 mEq/L)
Peripheral neuropathy and hyporeflexia
Potentiation of neuromuscular blocking drugs
Rhabdomyolysis (at serum K + <2.0 mEq/L)
Renal and Gastrointestinal
Polyuria; reduced urine concentrating ability
Potentiation of hypomagnesemia and hypocalcemia
Causes of hypokalemia are listed in Box 87.2 . These include inadequate oral intake due to alcoholism or malnutrition, potassium loss via the gastrointestinal tract due to excessive diarrhea, potassium loss via the kidney because of thiazide or loop diuretics, glucocorticoid or mineralocorticoid excess, and potassium loss due to excessive dialysis. An extracellular to intracellular shift of potassium is caused by acute alkalosis, β 2 -catecholamine therapy, or insulin therapy.
Inadequate Dietary Intake
Intracellular Shift of K +
Acute respiratory or metabolic alkalosis
β 2 -Catecholamine agonists
Increased insulin levels
The patient in the first case synopsis developed arrhythmias at a serum K + of 2.8 mEq/L. There is no empiric serum K + concentration below which the risk of arrhythmias is a certainty. The clinical implication of any low K + level depends on the following factors:
The medical comorbidities of the patient
Whether the potassium deficiency is acute or chronic
The cause of the hypokalemia
The planned surgery or procedure
Whether scheduled surgery is urgent or emergent
Any additional acute imbalance that urgent or emergent surgery/anesthesia may bring
Clinically important arrhythmias are the chief risks of hypokalemia. Acute decrease in the extracellular-intracellular potassium ratio increases the transmembrane K + gradient and transmembrane potential of excitable cells, which can stimulate automatic, triggered, or reentrant arrhythmias in cardiac cells.