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
Describe the evidence/utility/predictability of INSULIN used in setting of emergency hyperkalemia
1. More predictable than sodium bicarbonate or beta-adrenergic agonists. 2. Predictable K+ reduction 3. Can be used as monotherapy
26
Describe the evidence/utility/predictability of BICARBONATE used in setting of emergency hyperkalemia
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
Describe the evidence/utility/predictability of beta-adrenergic agonists used in setting of emergency hyperkalemia
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
What is typical dosing of insulin and glucose in hyperkalemia?
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
Discuss three risks of insulin errors in emergency hyperkalemia
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
In what patients with emergency hyperkalemia can you consider administering insulin alone without glucose?
1. Concomitant hyperglycemia | 2. Monitor for hypoglycemia
31
What is a common adverse effect from insulin and glucose in treatment of emergency hyperkalemia
Hypoglycemia
32
What is typical K+ lowering of 10 units of insulin (magnitude, onset, and duration)
1. 0.5-1.5 mEq/L 2. Within 1 hour 2. May last for several hours
33
Describe dosing of sodium bicarbonate in patients with emergency hyperkalemia
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
Describe onset and duration of K+ lowering of sodium bicarbonate in emergency hyperkalemia
1. Onset: within 30-60 minutes 2. Duration: several hours 3. Can be repeated after 30 minutes if needed
35
What is the dose of albuterol in emergency hyperkalemia
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
What is the onset of K+ lowering of albuterol in patients with hyperkalemia
30 minutes with inhalation
37
What is the expected plasma potassium lowering of albuterol?
0.5-1.5 mEq/L
38
In what type of patients should you avoid albuterol in emergency hyperkalemia and why?
1. Cardiac ischemia | 2. Risk of tachycardia
39
List three strategies to remove excess K+ from the body
1. Diuretics 2. Cation exchange resins 3. Dialysis
40
When is dialysis used in hyperkalemia? (three situations)
1. When other measures or ineffective OR 2. Severe hyperkalemia is present OR 3. advanced kidney disease
41
Which type of dialysis removes K+ fastest?
1. Hemodialysis removes K+ faster than peritoneal dialysis
42
Why should K+ be monitored after dialysis in emergency hyperkalemia?
Monitor for rebound increase in K+ after dialysis
43
What is the expected K+ lowering of dialysis in hyperkalemia?
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
What types of diuretics should be used in hyperkalemia to lower K+?
1. Loop or thiazide diuretics increase K+ renal excretion
45
In what patients are diuretics ineffective at lowering K+ in hyperkalemia?
Ineffective in patients with advanced kidney disease
46
List three cation exchange resins and the cations they exchange
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
How do cation exchange resins work? (Mechanism of action)
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
Describe risk of concomitant oral medication administration with cation exchange resins?
Binders, such as K+ binders, can reduce oral absorption of medications
49
Describe the role of cation exchange resins in emergency treatment of hyperkalemia
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
In what subgroup of patients should increased caution be exercised in the use of Na+-K+ exchange resins (i.e. SPS?)
1. Kidney disease | 2. Heart failure caused by Na+ (and subsequent fluid retention)
51
Describe the evidence for efficacy of Kayexalate
1. Approved by the FDA in 1958 before demonstrated efficacy was required 2. No controlled trials have shown efficacy
52
How is SPS administered in hyperkalemia?
1. Oral dose of SPS is 15 g repeated every 6 hours as needed
53
Describe the mixing of SPS with sorbitol
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
What is the intended purpose of mixing sorbitol with SPS
Common side effect of SPS is constipation. Sorbitol acts as a cathartic to prevent constipation.
55
In what patients is there the highest risk of intestinal necrosis with SPS?
Patients within 1 week of surgery (occurs in about 1.8% of patients)
56
What is the postulated mechanism of bowel injury (e.g. intestinal necrosis) with using SPS?
Bowel injury is linked to the deposition of drug crystal in the GI tract
57
Can bowel injury occur from SPS without sorbitol?
A systematic review found that GI injury is also associated with SPS without sorbitol
58
Describe an alternative way to administer SPS in a patient with hyperkalemia (how to prepare, how to administer)
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.