556 - Pharmacotherapy Ii - Hypokalemia

Front 1

What is the normal range of serum potassium ion?

Back 1

3.5 to 4.8 mmol/L

Front 2

Explain the role of aldosterone in the regulation of sodium and potassium levels.

Back 2

Aldosterone stimulates renal reabsorption of sodium in exchange for potassium.

Front 3

What inadvertent effect can an aldosterone antagonist have on serum potassium levels?

Back 3

Aldosterone antagonists can lead to hyperkalemia.

Front 4

What effect does insulin have on the balance of potassium intracellularly versus extracellularly?

Back 4

Insulin stimulates a shift of potassium from outside cells to inside cells.

Front 5

What effect do beta-2 adrenergic receptors, such as epinephrine, have on Na/K ATPase pumps?

Back 5

Beta-2 adrenergic receptors activate Na/K ATPase pumps, stimulating cellular uptake of potassium.

Front 6

What is a frequent cause of hypokalemia in children?

Back 6

Diarrhea

Front 7

In what manner do prescription steroids affect serum potassium levels?

Back 7

Prescription steroids can cause a loss of potassium and contribute to hypokalemia.

Front 8

What are “mineralocorticoid effects?”

Back 8

Mineralocorticoids, such as aldosterone, cause sodium and water retention, extracellular fluid volume expansion, hypertension, potassium depletion, and metabolic alkalosis.

Front 9

How does a magnesium deficiency effect the serum level of potassium?

Back 9

The reabsorption mechanisms for potassium have magnesium dependencies, so that an individual who is depleted of magnesium will have trouble retaining potassium.

Front 10

According to Professor Ronald Sorkness, what is probably the number one cause of hypokalemia?

Back 10

Diuretic Therapy

Front 11

At what point in diuretic therapy is the risk of hypokalemia greatest?

Back 11

The period of active diuresis, following initiation of a diuretic or an increase in the dose, when there is a net loss of sodium and a concurrent drop in potassium, is the period with heightened risk of hypokalemia.

Front 12

What four categories of effects are of concern with hypokalemia?

Back 12

1) Muscle weakness/paralysis, 2) Cardiac effects, such as arrhythmias, 3) Renal effects (impaired concentrating ability, metabolic alkalosis), & 4) Glucose intolerance (depressed insulin secretion)

Front 13

Explain the role of potassium on vascular function. Given its role, what might hypokalemia lead to with respect to skeletal muscles?

Back 13

Potassium functions as a vasodilator. Absence of potassium, in severe hypokalemia, may lead to low blood flow to the skeletal muscles, i.e. ischemia, resulting in rhabdomyolysis (breakdown (lysis) of muscle cells) followed by myoglobinuria (the presence of myoglobin in the urine). Myoglobin can clog up the kidneys and lead to kidney failure.

Front 14

What effect might hypokalemia have on the gut?

Back 14

Hypokalemia can lead to constipation in the form of an ileus (a partial or complete non-mechanical blockage of the small and/or large intestine).

Front 15

What sign might appear on an electrocardiograph of a hypokalemic individual?

Back 15

A U-wave may develop. A U-wave is an extra little hump after the T-wave.

Front 16

What drug used for heart failure, or rate control in atrial fibrillation, has increased risk of toxicity in the event of hypokalemia?

Back 16

Digitalis [This is one situation where even mild hypokalemia is quite dangerous!]

Front 17

What two renal effects that might occur in severe hypokalemia.

Back 17

First, impaired ability to concentrate urin (free water reabsorption is compromised by severe hypokalemia). Second, metabolic alkalosis. The acid-base balance and potassium balance are very closely linked in the kidney. Metabolic alkalosis can exacerbate potassium losses and hypokalemia can facilitate metabolic alkalosis as well.

Front 18

How might hypokalemia contribute to glucose intolerance?

Back 18

Hypokalemia tends to modulate insulin secretion and in that manner it can contribute to a loss of glucose control in an individual who has diabetes.

Front 19

What signs might present at a serum potassium level between 3.0 and 3.5 mmol/L? How should this level of hypokalemia be managed?

Back 19

Usually asymptomatic. Utilize oral potassium supplements for patients on digitalis. Otherwise, increased dietary intake is recommended.

Front 20

What signs might present at a serum potassium level between 2.5 and 3.0 mmol/L? How should this level of hypokalemia be managed?

Back 20

Some individuals will experience muscle weakness at this level. Treat with oral potassium supplements – 40 to 60 mmol, three to four times per day – until serum K > 3.0.

Front 21

What signs might present at a serum potassium level between 2.0 and 2.5 mmol/L? How should this level of hypokalemia be managed?

Back 21

At this level, nearly everyone will experience muscle weakness. Treat with oral potassium supplements, or IV supplements if oral route is questionable or if IV fluids are being given anyway.

Front 22

What signs might present at serum potassium levels < 2.0 mmol/L? How should this level of hypokalemia be managed?

Back 22

At this level, individuals may have trouble with respiratory muscles. Rhabdomyolysis may occur as well as other serious complicatons. IV potassium supplementation should be administered immediately.

Front 23

What is the preferred potassium salt in most cases?

Back 23

Potassium Chloride (KCl)

Front 24

What is the preferred potassium salt for correcting hypokalemia resulting from gastric losses, i.e. vomiting?

Back 24

Potassium Chloride (KCl)

Front 25

What is the preferred potassium salt for correcting hypokalemia resulting from diuretic therapy?

Back 25

Potassium Chloride (KCl)

Front 26

What is the preferred potassium salt for correcting hypokalemia accompanied by phosphate deficiency?

Back 26

Potassium Phosphate

Front 27

What is an frequently utilized potassium salt for correcting hypokalemia resulting from lower GI losses, i.e. diarrhea?

Back 27

Potassium Bicarbonate

Front 28

Describe four situations in which an effort to correct hypokalemia may result in an increase in potassium levels more rapidly than typically anticipated.

Back 28

1) Use of a potassium-sparing diuretic; 2) Blockade of beta-2 receptors by a non-selective beta blocker, such as propranolol, or by higher doses of a beta-1 selective agent, such as atenolol, will delay intracellular potassium uptake; 3) Decreased renal function (GFR < 30 mL/min; & 4) Use of an ACE inhibitor, or an Angiotensin II Receptor Antagonist, will inhibit potassium secretion by inhibiting aldosterone production.

Front 29

What is the most important safety consideration when treating hypokalemia via IV potassium supplementation?

Back 29

Infusing potassium too quickly can be fatal! Remember that potassium is the drugs used to stop the heart for execution by lethal injection.

Front 30

What is the concentration limit for the administration of potassium ion via peripheral vein?

Back 30

40 mmol/L

Front 31

What is the typical rate of potassium infusion for correcting hypokalemia? What is the limit for urgent situations? What is the limiting factor in this rate?

Back 31

The typical rate is 10 mmol/hr. Up to 20 mmol/hr may be administered via central vein for urgent situations. Cardiotoxicity is the rate limiting factor.

Front 32

Why is dextrose-free fluid used to deliver potassium when correcting hypokalemia?

Back 32

Though dextrose would stimulate insulin production, which facilitates cellular uptake of both dextrose and potassium, this presents a problem in that doing so removes the relatively linear correlation between the serum potassium level and the total body potassium. The serum potassium will appear deceptively low in such a case because the potassium is piling into cells, and when the target serum level is finally reached, and the infusion is stopped, the potassium re-equilibrates and suddenly the patient has a potassium level of 6. So monitoring the correction is easier when delivering the potassium via a dextrose-free fluid.