Hypokalemia, defined as plasma [K+] less than 3.5 mEq/L, can occur as a result of (1) an intercom-partmental shift of K+ (see above), (2) increased potassium loss, or (3) an inadequate potassium intake (Table 49–8). Plasma potassium concentration typi-cally correlates poorly with the total potassium deficit. A decrease in plasma [K+] from 4 mEq/L to 3 mEq/L usually represents a 100- to 200-mEq deficit, whereas plasma [K+] below 3 mEq/L can represent a deficit anywhere between 200 mEq and 400 mEq.
Hypokalemia due to the intracellular movement of potassium occurs with alkalosis, insulin therapy, β2-adrenergic agonists, and hypothermia and dur-ing attacks of hypokalemic periodic paralysis (see above). Hypokalemia may also be seen following transfusion of previously frozen red cells; these cells lose potassium in the preservation process and take up potassium following reinfusion. Cel-lular K+ uptake by red blood cells (and platelets) also accounts for the hypokalemia seen in patients recently treated with folate or vitamin B12 for mega-loblastic anemia.
Excessive potassium losses are usually either renal or gastrointestinal. Renal wasting of potassium is most commonly the result of diuresis or enhanced mineralocorticoid activity. Other renal causes include hypomagnesemia , renal tubular acidosis , ketoacidosis, salt-wasting nephropathies, and some drug therapies (carbenicil-lin and amphotericin B). Increased gastrointestinal loss of potassium is most commonly due to nasogas-tric suctioning or to persistent vomiting or diarrhea. Other gastrointestinal causes include losses from fis-tulae, laxative abuse, villous adenomas, and pancre-atic tumors secreting vasoactive intestinal peptide.
Chronic increased sweat formation occasionally causes hypokalemia, particularly when potassium intake is limited. Dialysis with a low-potassium-containing dialysate solution can also cause hypo-kalemia. Uremic patients may actually have a total body potassium deficit (primarily intracellular) despite a normal or even high plasma concentra-tion; the absence of hypokalemia in these instances is probably due to an intercompartmental shift from the acidosis. Dialysis in these patients unmasks the total body potassium deficit and often results in hypokalemia.
Urinary [K+] less than 20 mEq/L is generally indicative of increased extrarenal losses, whereas concentrations greater than 20 mEq/L suggest renal wasting of K+.
Because of the kidney’s ability to decrease urinary potassium excretion to as low as 5–20 mEq/L, marked reductions in potassium intake are required to produce hypokalemia. Low potassium intakes, however, often accentuate the effects of increased potassium losses.
Hypokalemia can produce widespread organ dysfunc-tion (Table 49–9). Most patients are asymptomatic until plasma [K+] falls below 3 mEq/L. Cardiovascular effects are most prominent and include an abnormal ECG (Figure 49–5), arrhythmias, decreased cardiac contractility, and a labile arterial blood pressure due to autonomic dysfunction. Chronic hypokalemia has also been reported to cause myocardial fibrosis.
ECG manifestations are primarily due to delayed ventricular repolarization and include T-wave flat-tening and inversion, an increasingly prominent U wave, ST-segment depression, increased P-wave amplitude, and prolongation of the P–R interval.
Increased myocardial cell automaticity and delayed repolarization promote both atrial and ventricular arrhythmias.
Neuromuscular effects of hypokalemia include skeletal muscle weakness, flaccid paralysis, hypo-reflexia, muscle cramping, ileus, and, rarely, rhab-domyolysis. Hypokalemia induced by diuretics is often associated with metabolic alkalosis; as the kidneys absorb sodium to compensate for intra-vascular volume depletion and in the presence of diuretic-induced hypochloremia, bicarbonate is absorbed. The end result is hypokalemia and hypo-chloremic metabolic alkalosis. Renal dysfunction is seen due to impaired concentrating ability (resis-tance to ADH, resulting in polyuria) and increased production of ammonia resulting in impairment of urinary acidification. Increased ammonia pro-duction represents intracellular acidosis; hydrogen ions move intracellularly to compensate for intra-cellular potassium losses. The resulting metabolic alkalosis, together with increased ammonia pro-duction, can precipitate encephalopathy in patients with advanced liver disease. Chronic hypokalemia has been associated with renal fibrosis (tubulointer-stitial nephropathy).
The treatment of hypokalemia depends on the presence and severity of any associated organ dysfunction. Significant ECG changes such as ST-segment changes or arrhythmias mandate con-tinuous ECG monitoring, particularly during intravenous K+ replacement. Digoxin therapy—as well as the hypokalemia itself—sensitizes the heart to changes in potassium ion concentration. Muscle strength should also be periodically assessed in patients with weakness.
In most circumstances, the safest method by which to correct a potassium deficit is oral replace-ment over several days using a potassium chloride solution (60–80 mEq/d). Intravenous replacement of potassium chloride is usuallybe reserved for patients with, or at risk for, signifi-cant cardiac manifestations or severe muscle weakness. The goal of intravenous therapy is to remove the patient from immediate danger, not to correct the entire potassium deficit. Because of potassium’s irritative effect on peripheral veins, peripheral intravenous replacement should not exceed 8 mEq/h. Dextrose-containing solutions should generally be avoided because the resulting hyperglycemia and secondary insulin secretion may actually worsen the low plasma [K+]. More rapid intravenous potassium replacement (10–20 mEq/h) requires central venous adminis-tration and close monitoring of the ECG. Intrave-nous replacement should generally not exceed 240 mEq/d. Potassium chloride is the preferred potas-sium salt when a metabolic alkalosis is also present because it also corrects the chloride deficit discussed above. Potassium bicarbonate or equivalent (K acetate or K citrate) is preferable for patients with metabolic acidosis. Potassium phosphate is a suit-able alternative with concomitant hypophosphate-mia (diabetic ketoacidosis).
Hypokalemia is a common preoperative finding. The decision to proceed with elective surgery is often based on lower plasma [K+] limits somewhere between 3 and 3.5 mEq/L. The decision, how-ever, should also be based on the rate at which the hypokalemia developed as well as the presence or absence of secondary organ dysfunction. In general, chronic mild hypokalemia (3–3.5 mEq/L) without ECG changes does not substantially increase anes-thetic risk. The latter may not apply to patients receiving digoxin, who may be at increased risk of developing digoxin toxicity from the hypokalemia; plasma [K +] values above 4 mEq/L are desirable in such patients.
The intraoperative management of hypokale-mia requires vigilant ECG monitoring. Intravenous potassium should be given if atrial or ventricular arrhythmias develop. Glucose-free intravenous solutions should be used and hyperventilation avoided to prevent further decreases in plasma [K +]. Increased sensitivity to neuromuscular blockers (NMBs) may be seen; therefore dosages of NMBs should be reduced 25–50%, and a nerve stimulator should be used to follow both the degree of paralysis and the adequacy of reversal.
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