Which of the following conditions will make a patients more prone to developing hypokalemia?

Hypokalaemia

Hypokalaemia is commonly found in ill animals and causes include endotoxaemia,18 anorexia, diarrhoea and starvation.19 It is frequently present in horses with heat exhaustion along with hypochloraemia, hypocalcaemia and metabolic alkalosis. Hypokalaemia leads to prolongation of the Q–T interval and both supraventricular and ventricular dysrhythmias can be seen in horses with hypokalaemia. Supraventricular tachycardia, ventricular tachycardia, torsades de pointes and ventricular fibrillation can all occur with severe hypokalaemia. If severe hypokalaemia is present, the calculated potassium deficit should be replaced slowly intravenously at a maximum rate of 0.5 mEq/kg/hour while monitoring serum potassium concentrations.

Hypokalemia

Hypokalemia is the most frequent electrolyte disorder encountered in clinical practice and is produced by a variety of mechanisms, including inadequate potassium intake or excessive renal or gastrointestinal potassium loss. Neurologic symptoms of hypokalemia are typically muscular.35,36 Serum potassium concentrations of 3.0 to 3.5 mEq/L may be associated with mild muscle weakness, myalgia, and ease of fatigue. Serum potassium concentrations of 2.5 to 3.0 mEq/L are associated with the development of clinically significant muscle weakness, particularly of the proximal limb muscles, and with muscle cramps. The cranial musculature is characteristically spared in hypokalemia-induced muscle weakness. When the serum potassium level falls below 2.5 mEq/L, and usually below 2.0 mEq/L, structural muscle damage, including rhabdomyolysis and myoglobinuria, may occur.37

Tetany occurs in some patients with hypokalemia, particularly when associated with alkalosis. Hypokalemia may mask the tetany of hypocalcemia. Paradoxically, tetany may occur during the treatment of hypokalemia in patients who are also hypocalcemic.

Cerebral symptoms in hypokalemia are distinctly unusual. Reference to symptoms such as lethargy, apathy, drowsiness, confusion, irritability, delirium, and coma in hypokalemia are rare1 and suggest that an associated acid-base disturbance or other electrolyte abnormality may have been responsible for these encephalopathic symptoms. Brain concussion has been shown to lead to a mild transient hypokalemia.38

Hypokalemia

Hypokalemia is often listed as a cause of nephrogenic DI. However, it is possible that chronic hypokalemia causes a renal concentrating defect rather than true nephrogenic DI.

Hypokalemia diminishes cAMP formation in response to vasopressin in MCD segments from rats in vitro. In addition, rats with hypokalemia have a decreased density of AQP2 in the luminal membrane of the distal nephron. To conclude, however, that the observed decreased expression of AQP2 is rate-limiting for the reabsorption of water, data are needed to show that the osmolality of the luminal fluid in the inner MCD is distinctly lower than the osmolality in the medullary interstitial compartment.

On the other hand, patients with chronic hypokalemia may have a lower medullary interstitial osmolality resulting from the effect of chronic hypokalemia to cause medullary interstitial damage. In addition, potassium depletion has been shown to reduce the abundance of urea transporters in the renal medulla in mice. Therefore, urea may become an effective osmole in the inner MCD and obligate the excretion of water.

Hypokalaemia

Hypokalaemia results in a more negative resting potential. The duration of phase 3 repolarization is increased, increasing the duration of the action potential. Hypokalaemia also results in increased levels of intracellular sodium and calcium. In the clinical setting, hypokalaemia results in a wide spectrum of atrial and ventricular ectopic rhythms. The ectopy is due to enhanced automaticity of latent pacemaker fibers.

The cardiac effects of hypermagnesaemia and hypomagnesaemia mimic those of hyperkalaemia and hypokalaemia, respectively; however, the mechanisms for this have not been clearly described.49 In humans, magnesium treatment has been reported to prevent early afterdepolarizations induced by quinidine, providing a possible explanation for the demonstrated effectiveness of treatment with magnesium salts for torsades de pointes.50

Hypokalemia

Hypokalemia is believed to render the terminal portion of the nephron less responsive to AVP by causing downregulation of aquaporin-2 water channels, thereby interfering with the ability to concentrate urine (Robben et al, 2006; Sands and Bichet, 2006). Hypokalemia may also alter the hypertonic medullary interstitial gradient by causing downregulation of urea transporters and interfering with solute accumulation and may interfere with release of AVP from the pituitary. Polyuria and polydipsia are not common clinical signs of hypokalemia. The most common clinical signs are related to neuromuscular dysfunction of skeletal, cardiac, and smooth muscle (e.g., weakness, cervical ventriflexion). Hypokalemia usually develops secondary to another disorder, many of which also cause polyuria and polydipsia.

Definition and Causes

Hypokalemia occurs when the serum potassium concentration is less than 3.5 mEq/L (normal range 3.5 to 5.5 mEq/L). The general causes of hypokalemia are (1) disorders of internal balance and (2) disorders of external balance. The clinical conditions most commonly associated with each of these are provided in Box 51-1. Recently there has been a heightened recognition of feline hyperaldosteronism as the cause of marked hypokalemia, usually secondary to either an aldosteronoma or adrenocortical hyperplasia. It has also been associated with an adrenocortical adenoma in ferrets.3

Potassium Balance

Hypokalemia is the most common abnormality of serum potassium in patients with CRF; it is more common in cats than in dogs. Hypokalemia most likely results from decreased oral intake, as well as excessive urinary loss of potassium.

If the patient is not vomiting, oral administration of potassium is preferred.

Administer potassium gluconate (Tumil-K) at a dose of 2 to 6 mEq/cat once or twice daily, depending on severity of hypokalemia and the cat's size.

Initially, monitor serum potassium weekly to determine the appropriate maintenance dose; 2 to 4 mEq/cat once daily often is adequate.

If parenteral potassium is necessary due to vomiting or severe hypokalemia, administer potassium chloride with IV fluids (see Chapter 5 for details).

Hypokalemia.

Hypokalemia increases resting membrane potential, resulting in muscle weakness, impaired urine concentration ability, and arrhythmias. Hypokalemia may result from depletion of the body's potassium stores or from a redistribution of potassium from the ECF into the ICF space (Box 22.3). Hypokalemia is most commonly seen with altered intake and absorption and with excessive potassium losses from the gastrointestinal tract caused by vagal indigestion, torsion of the abomasum, ileus, or diarrhea. Excessive renal loss may result from mineralocorticoid excess, certain diuretics, or altered renal function, as reported in horses with renal tubular acidosis. Marked hypokalemia develops when reduced dietary intake caused by anorexia is associated with excessive potassium losses (e.g., causing muscle paresis in dairy cows early postpartum). A hypokalemia syndrome has been observed in cattle,14 mainly in postpartum lactating cows, but also in younger animals. The exact causes have not been completely elucidated except for isoflupredone administration. The syndrome is characterized by muscle weakness, severe depression, recumbency, tachycardia, cardiac arrhythmia, and abnormal neck posture. The lowest reported serum potassium concentration levels are between 2.2 and 2.5 mmol/L.

Hypokalemia without potassium depletion results from the movement of extracellular potassium to the intracellular space. This form of hypokalemia occurs in response to an acute alkalosis and the administration of insulin or glucose. Overzealous and rapid administration of sodium bicarbonate can produce an alkalosis with a profound and rapidly developing hypokalemia. Animals with moderate potassium deficits that are vigorously treated with sodium bicarbonate to correct a coexisting mild metabolic acidosis may be particularly prone to this problem. The initial response to catecholamine administration is a modest, transient increase in potassium caused by α-adrenergic stimulation, which is often followed by hypokalemia caused by β-adrenergic receptor responses.

Pseudohypokalemia is seen in severe lipemia with potassium measured with indirect potentiometry (e.g., older automated profile chemistry analyzers).

10. How often does hypokalemia complicate diuretic use? Is potassium supplementation necessary for animals receiving diuretics?

Hypokalemia is the most common electrolyte abnormality associated with diuretic use. Sodium and chloride levels are less likely to become abnormal, although they certainly can. Maintaining potassium levels is more difficult in those patients that have depressed appetites. This problem results from a combination of diuretic-driven potassium loss and reduced intake. Cats are especially sensitive to this phenomenon and serum electrolytes must be carefully monitored. Dogs that are on furosemide and have good appetites very rarely have a problem with hypokalemia. In general, potassium supplementation is not recommended unless hypokalemia has been documented through the measurement of serum potassium levels.

Clinical Pathology.

Hypokalemia, hyperglycemia, increased plasma insulin, hypomagnesemia, and increased free fatty acids have been associated with therapeutic albuterol use in humans. Hypokalemia is secondary to the intracellular movement of potassium, not a net loss of potassium.16 Hypokalemia has been reported in numerous canine albuterol overdoses. Serum potassium levels as low as 0.9 mmol/L have been reported in some cases in which the tablet formulation was ingested. Hyperglycemia has been associated with albuterol overdoses only rarely in the dog. Hypomagnesemia has not been reported in the dog following albuterol overdoses, presumably because testing for serum magnesium has not been routine.4