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BCPS Exam > FEN: Hyperkalemia > Flashcards

FEN: Hyperkalemia Flashcards

1
Q

Define hyperkalemia based on K+ level

A

K+ concentration greater than 5 mEq/L

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2
Q

At what K+ level do symptoms typically first begin to manifest?

A

6 mEq/L

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3
Q

What are typical early ECG changes in hyperkalemia

A
  1. peaked, narrowed T waves

2. widening of the QRS

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4
Q

What are typical late ECG changes in hyperkalemia

A
  1. ventricular fibrillation

2. asystole

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5
Q

At what K+ should emergency treatment be considered despite normal ECG? and why?

A
  1. K+ greater than 6.5

2. For some patients, initial manifestation can be ventricular fibrillation

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6
Q

List four factors that can increase risk of conduction disturbances in hyperkalemia

A
  1. Hypocalcemia
  2. Hyponatremia
  3. acidosis
  4. rapid elevation in the concentration
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7
Q

At what plasma potassium concentration do neuromuscular conduction changes start to occur? What are those changes?

A
  1. K+ greater than 8 mEq/L

2. Muscle weakness or paralysis

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8
Q

List three principle causese of hyperkalemia

A
  1. Increased intake
  2. Shift of K+ from IC to the EC compartment
  3. Reduced urinary excretion of K+
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9
Q

List six causes of shift of K+ from IC to the EC compartment

A
  1. Acidosis
  2. Insulin deficiency
  3. B-adrenergic blockade
  4. Digoxin overdose
  5. Rewarming after hypothremia (e.g. after cardiac surgery)
  6. Succinylcholine
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10
Q

List six causes of reduced urinary excretion of K+

A
  1. Kidney dysfunction
  2. Intravascular volume depletion
  3. Hypoaldosteronism
  4. K+ sparing diuretics
  5. Angiotestin-converting enzyme inhibitors and angiotensin receptor blockers
  6. Trimethoprim
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11
Q

What is pseudohyperkalemia?

A

Laboratory assigned hyperkalemia but no apparent cause or symptoms

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12
Q

List three causes of pseudohyperkalemia

A
  1. K+ relased after obtaining blood specimen (e.g. trauma during venipuncture)
  2. K+ release during coagulation (e.g. measuring serum rather than plasma concentration, where serum is plasma minus clotting factors)
  3. Contamination of blood specimen with K+ containing IV fluids or parenteral nutrition
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13
Q

What patients are eligible for nonurgent/ non emergency treatment of hyperkalemia?

A
  1. Asymptomatic elevation (K+ 5-6.5 mEq/L) AND

2. No signs or symptoms (muscle, ECG)

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14
Q

What three kind of situations warrant emergency treatment of hyperkalemia?

A
  1. Plasma potassium greater than 6.5 mEq/L
  2. Severe muscle weakness
  3. ECG changes
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15
Q

What treatment modality is used for patients in nonemergency cases?

A

Cation exchange resins

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16
Q

What three general treatment strategies are standard for symptomatic/emergency hyperkalemia?

A
  1. Prevent hyperkalemia-induced arrhythmias
  2. Transiently shift K+ into cells
  3. Remove excess K+
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17
Q

What agent is preferred for prevention of hyperkalemia-induced arrhythmias?

A

IV Calcium gluconate

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18
Q

Compare calcium gluconate to calcium chloride for prevention of hyperkalemia-induced arrhythmias

A
  1. Calcium gluconate has a lower risk of tissue necrosis than calcium chloride
  2. Calcium gluconate can be administered peripherally (CaCl2) is central only)
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19
Q

What is the route and dosing for calcium gluconate in prevention of hyperkalemia-induced arrhythmias? (give in milliliter/concentration and also in milliequivalents of Ca2+)

A
  1. 10 mL of 10% calcium gluconate
  2. 1 g of calcium gluconate, 90 mg elemental Ca2+, or 4.65 mEq)
  3. administered over 2-10 minutes
  4. can be given peripherally
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20
Q

What is the onset and duration of action of calcium gluconate?

A

Onset: minutes
Duration: 30-60 minutes

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21
Q

How does IV calcium help prevent hyperkalemia-induced arrhythmias?

A
  1. Does NOT reduce plasma K+

2. Antagonizes the effect of K+ in cardiac conduction in cells

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22
Q

Patients receiving which drug require increased caution when using IV calcium to prevent hyperkalemia-induced arrhythmias?

A

Digoxin

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23
Q

Describe the risk of IV calcium and digoxin

A
  1. Hypercalcemia can precipitate digoxin toxicity

2. There are reports of sudden death

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24
Q

What three agents are given in setting of emergency hyperkalemia to shift K+ into IC compartment?

A
  1. Insulin and glucose
  2. Sodium bicarbonate
  3. B-adrenergic agonists
25
Q

Describe the evidence/utility/predictability of INSULIN used in setting of emergency hyperkalemia

A
  1. More predictable than sodium bicarbonate or beta-adrenergic agonists.
  2. Predictable K+ reduction
  3. Can be used as monotherapy
26
Q

Describe the evidence/utility/predictability of BICARBONATE used in setting of emergency hyperkalemia

A
  1. Efficacy is disputed
  2. Least effective in advanced kidney disease
  3. Most effective in underlying metabolic acidosis
  4. Has recently been limited by shortages
27
Q

Describe the evidence/utility/predictability of beta-adrenergic agonists used in setting of emergency hyperkalemia

A
  1. 40% of patients do not respond to inhaled albuterol
  2. Especially patients taking beta blockers
  3. Not recommended as a single agent for urgent treatment of hyperkalemia
28
Q

What is typical dosing of insulin and glucose in hyperkalemia?

A
  1. Dose is regular insulin 10 units IV

2. Plus 25-50 g of dextrose administered as a 50% dextrose IV push to prevent hypoglycemia

29
Q

Discuss three risks of insulin errors in emergency hyperkalemia

A
  1. Correct route is IV
  2. Should be administered using an insulin syringe marked in units, which requires a luer-lock insulin syrine compatible with the needless access device.
  3. Order should be written as 10 units. Errors involving calculations are possible.
30
Q

In what patients with emergency hyperkalemia can you consider administering insulin alone without glucose?

A
  1. Concomitant hyperglycemia

2. Monitor for hypoglycemia

31
Q

What is a common adverse effect from insulin and glucose in treatment of emergency hyperkalemia

A

Hypoglycemia

32
Q

What is typical K+ lowering of 10 units of insulin (magnitude, onset, and duration)

A
  1. 0.5-1.5 mEq/L
  2. Within 1 hour
  3. May last for several hours
33
Q

Describe dosing of sodium bicarbonate in patients with emergency hyperkalemia

A
  1. Route: IV
  2. Infused slowly over 5 minutes
  3. 50 mEq of IV sodium bicarbonate
  4. Can be repeated after 30 minutes if needed
34
Q

Describe onset and duration of K+ lowering of sodium bicarbonate in emergency hyperkalemia

A
  1. Onset: within 30-60 minutes
  2. Duration: several hours
  3. Can be repeated after 30 minutes if needed
35
Q

What is the dose of albuterol in emergency hyperkalemia

A
  1. albuterol 10-20 mg nebulized over 10 minutes (much higher doses than used in bronchospasm)
  2. IV albuterol 0.5 mg (not available in the US)
36
Q

What is the onset of K+ lowering of albuterol in patients with hyperkalemia

A

30 minutes with inhalation

37
Q

What is the expected plasma potassium lowering of albuterol?

A

0.5-1.5 mEq/L

38
Q

In what type of patients should you avoid albuterol in emergency hyperkalemia and why?

A
  1. Cardiac ischemia

2. Risk of tachycardia

39
Q

List three strategies to remove excess K+ from the body

A
  1. Diuretics
  2. Cation exchange resins
  3. Dialysis
40
Q

When is dialysis used in hyperkalemia? (three situations)

A
  1. When other measures or ineffective OR
  2. Severe hyperkalemia is present OR
  3. advanced kidney disease
41
Q

Which type of dialysis removes K+ fastest?

A
  1. Hemodialysis removes K+ faster than peritoneal dialysis
42
Q

Why should K+ be monitored after dialysis in emergency hyperkalemia?

A

Monitor for rebound increase in K+ after dialysis

43
Q

What is the expected K+ lowering of dialysis in hyperkalemia?

A
  1. Plasma K+ falls by more than 1 mEq/L in the first hour of dialysis
  2. And by about 2 mEq/L after 3 hours of dialysis
44
Q

What types of diuretics should be used in hyperkalemia to lower K+?

A
  1. Loop or thiazide diuretics increase K+ renal excretion
45
Q

In what patients are diuretics ineffective at lowering K+ in hyperkalemia?

A

Ineffective in patients with advanced kidney disease

46
Q

List three cation exchange resins and the cations they exchange

A
  1. Sodium polystyrene sulfonate (Kayexalate, SPS) (exchanges Na+ for K+)
  2. Patiromer (exchanges Ca2+ for K+)
  3. Sodium zirconium cyclosilicate (exchanges H+ and Na+ for K+)
47
Q

How do cation exchange resins work? (Mechanism of action)

A

They exchange other ions in the GI lumen for K+ (e.g. swapping out the Na+, Ca2+ or H+ in the gut for K+), which increases GI excertion of K+

48
Q

Describe risk of concomitant oral medication administration with cation exchange resins?

A

Binders, such as K+ binders, can reduce oral absorption of medications

49
Q

Describe the role of cation exchange resins in emergency treatment of hyperkalemia

A
  1. Because of slow onset and unpredictable efficacy, cation exchange resins are not indicated for emergency treatment of hyperkalemia.
  2. Can be used as a temporizing agent while waiting for dialysis.
50
Q

In what subgroup of patients should increased caution be exercised in the use of Na+-K+ exchange resins (i.e. SPS?)

A
  1. Kidney disease

2. Heart failure caused by Na+ (and subsequent fluid retention)

51
Q

Describe the evidence for efficacy of Kayexalate

A
  1. Approved by the FDA in 1958 before demonstrated efficacy was required
  2. No controlled trials have shown efficacy
52
Q

How is SPS administered in hyperkalemia?

A
  1. Oral dose of SPS is 15 g repeated every 6 hours as needed
53
Q

Describe the mixing of SPS with sorbitol

A
  1. SPS 15 g can be mixed with 20-100 mL or water or syrup
  2. No longer recommended to mix in 70% sorbitol because of risk of interstinal necrosis
  3. Comes as premixed 33% sorbitol suspension, which also have reports, but less concerning
54
Q

What is the intended purpose of mixing sorbitol with SPS

A

Common side effect of SPS is constipation. Sorbitol acts as a cathartic to prevent constipation.

55
Q

In what patients is there the highest risk of intestinal necrosis with SPS?

A

Patients within 1 week of surgery (occurs in about 1.8% of patients)

56
Q

What is the postulated mechanism of bowel injury (e.g. intestinal necrosis) with using SPS?

A

Bowel injury is linked to the deposition of drug crystal in the GI tract

57
Q

Can bowel injury occur from SPS without sorbitol?

A

A systematic review found that GI injury is also associated with SPS without sorbitol

58
Q

Describe an alternative way to administer SPS in a patient with hyperkalemia (how to prepare, how to administer)

A
  1. Retention enema
  2. Mix 30-50 g of SPS in 100-200 mL of an aqueous vehicle (water, 10% dextrose)
  3. Do not use sorbitol, increased risk of serious GI adverse events
  4. Warm to body temperature
  5. Keep in colon for 30-60 minutes, up to 3 hours.
  6. Irrigate colon afterward.

BCPS Exam (34 decks)

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