Hyperkalemia and Hypokalemia- paulson Flashcards

1
Q

Hyperkalemia: serum potassium is ______

-Is hyperkalemia dangerous?

A

-> 5.0 mEq/L

**(But there will be some variation in laboratory reference standards)

*Hyperkalemia is a dangerous electrolyte abnormality, potentially leading to life-threatening arrhythmias and death

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2
Q

“emia”=

A

“condition of the blood”

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3
Q

Hyperkalemia refers to high serum potassium, NOT ____

A

whole body potassium

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4
Q

Most (___%) of total body potassium is intracellular

-Less than ___% circulates in the bloodstream

Normal serum K of _______mEq/L is tightly regulated by the kidney

A
  • (98%)
  • 2%
  • 3.5-5.0 =normal
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5
Q

Hyperkalemia: etiology

A
  • Increased intake
  • Decreased excretion
  • Shift from intracellular to extracellular
  • Pseudohyperkalemia
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6
Q

Hyperkalemia:

-describe increased intake

A
  • PO supplementation

- IV potassium

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7
Q

Hyperkalemia:

-describe pseudohyperkalemia

A
  • Mechanical trauma from venipuncture: –>Can see red serum–>Could also be true severe intravascular hemolysis
  • Exercise- repeated clenching of the fist during venipuncture
  • Cooling of sample or deterioration of sample
  • Thrombocytosis
  • Severe leukocytosis
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8
Q

Intracellular to Extracellular Shifts: can occur due to (3 things)

A
  • Any breakdown of cells
  • acidosis
  • Insulin deficiency or resistance
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9
Q

Decreased Excretion (of potassium): describe 3 possible causes

A
  • Renal failure
  • Hypovolemia
  • Hypoaldosteronsism
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10
Q

Describe Renal failure (how it pertains to decreased K+ excretion)

A
  • Acute or chronic

- Kidneys unable to filter and excrete normally

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11
Q

Describe hypovolemia (how it pertains to decreased K+ excretion)

A
  • Dehydration, CHF, cirrhosis

- Low flow to the kidneys

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12
Q

Describe hypoaldosteronism (how it pertains to decreased K+ excretion)

A
  • Everyone’s FAV lecture ;) remember, aldosterone causes secretion of K+
  • RTA4
  • Adrenal insufficiency
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13
Q

Intracellular to Extracellular Shifts:

-Describe any breakdown of cells

A

-Broken cells release potassium when they lyse

  • -Crush injuries/major trauma, rhabdo, tumor lysis syndrome after chemo
  • -Pseudohyperkalemia
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14
Q

Intracellular to Extracellular Shifts:

-Describe Acidosis

A

H+ moves from the blood into the cells in exchange for K+

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15
Q

Intracellular to Extracellular Shifts:

-describe Insulin deficiency or resistance

A
  • Insulin causes K+ entry into cells

- -Diabetes (body doesnt make insulin or is non responsive to insulin–> decreased K+ entry into cells)

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16
Q

Meds that can cause hyperkalemia: KNOW!!!

A

**ACEIs
**ARBs
**NSAIDs
**Spironolactone
Beta blockers
Digitalis
Succinylcholine
**Bactrim
-Amiloride (a diuretic)
Potassium supplements

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17
Q

T/F: hyperkalemia can cause Cardiotoxicity

A

True!!!

  • Hyperkalemia causes cardiotoxicity by ↑ the resting membrane potential of the cardiac myocyte, causing “membrane excitability”
  • *At very high levels, potassium causes the depolarization threshold to rise, leading to overall depressed cardiac function
18
Q

Hyperkalemia:

-clinical features

A

-May have vague and varied symptoms, but is usually totally asymptomatic

-May have:
Nausea/vomiting
Palpitations
Lethargy 
Confusion
Paresthesias
Muscle weakness
Paralysis if advanced
Arrhythmias/Death
19
Q

Hyperkalemia:

-labs/eval

A
  • Repeat the potassium level if there’s doubt about its veracity
  • Serum potassium will be above 5.0
  • BMP to assess renal function
  • EKG
  • Consider ABG if suspecting acidosis
20
Q

EKG changes associated with hyperkalemia

A

**Classic EKG changes (in sequential order):

  • Peaked T wave – K 5.5-6.5 mEq/L
  • Flattened P wave with prolonged PR interval or totally absent P wave – K 6.5-7.5 mEq/L
  • Wide QRS – K 7.0-8.0 mEq/L
  • Sine wave pattern portending imminent cardiac arrest K >8.0 mEq/L
  • Above does not occur in every patient
21
Q

EKG findings

A

image slide 15

22
Q

When is hyperkalemia considered an emergency?

A
  • Clinical s/s from hyperkalemia–> Most serious: muscle weakness or paralysis, arrhythmias
  • Potassium is >6.5
  • Moderate hyperkalemia (>5.5) + significant renal impairment +
  • -Ongoing tissue breakdown –or-
  • -Ongoing potassium absorption –or-
  • -Significant acidosis
23
Q

Hyperkalemia: tx

-If severe hyperkalemia + EKG changes–> tx?

A
  • IV calcium gluconate
  • Continuous cardiac monitoring
  • Options to drive potassium back into the cell:
24
Q

Hyperkalemia: tx

-list options to drive potassium back into the cell

A
  • Insulin + glucose
  • Beta-2 adrenergic agonists (inhaled albuterol)
  • IV sodium bicarbonate–>Temporary, not lasting solutions
25
Q

Hyperkalemia: tx

-Options for removal of Potassium from the body (list 3)

A
  • GI cation exchanger:
  • -Bind K+ in the GI tract in exchange for other cations–> excreted in feces
  • -Sodium polystyrene sulfonate (Kayexalate)
  • -Patiromer (Veltassa)
  • Diuretics: Loop diuretic (ie: Lasix) + saline
  • Hemodialysis–> Hyperkalemic Pts with severe renal impairment
26
Q

Hyperkalemia: tx

-what are some OBVIOUS thoughts regarding tx

A

Stop any potassium supplements or medications that can increase potassium

27
Q

Hypokalemia:

-what is the serum potassium?

A

< 3.5 mEq/L

28
Q

Hypokalemia: pathophysiology

-describe various mechanisms of K+ loss

A

-Increased loss:
Renal: Diuretics, Hyperaldosteronism
GI: Vomiting, Diarrhea

  • Movement of potassium from blood into intracellular compartment
  • Hypomagnesemia
  • Renal tubular acidosis
  • Meds
  • Very LOW calorie diets
29
Q

Hypokalemia: pathophysiology

-describe the methods of Movement of potassium from blood into intracellular compartment (list 3)

A
  • Insulin excess
  • Beta agonist treatment
  • Alkalosis
30
Q

Hypokalemia is often concurrent with _______

A

**hypomagnesemia

Often concurrent Mg & K+ losses ie: diuretics, vomiting

31
Q

Describe renal tubular acidosis:

  • Type 1=
  • Type 2=
A

Type 1 (distal) & 2 (proximal) can cause potassium wasting

32
Q

Hypokalemia 2/2 medications (list ex’s)

A

**Diuretics (except potassium-sparing), amphotericin B, antipsychotics (Risperdal, Seroquel), Barium or chloroquine intoxication

33
Q

Hypokalemia:

-specify caloric input for low cal diet that can cause hypokalemia

A

200-800 calories

34
Q

Hypokalemia:

-clinical features

A
  • No pathognomonic presenting s/s
  • May have muscle fatigue or weakness
  • Often starts in LE, progresses to the trunk/UE, can end in paralysis
  • **Cramps, rhabdomyolysis, and myoglobinuria
  • Respiratory muscle weakness
  • GI muscle involvement
35
Q

Respiratory muscle weakness (seen in some Pts w/ hypokalemia) can lead to _____

A

**respiratory failure/death

36
Q

Hypokalemia:

-describe GI muscle involvement

A

ileus, constipation, n/v

37
Q

Hypokalemia:

-diagnostic tests (list 3)

A
  • **BMP
  • Magnesium
  • EKG
38
Q

Hypokalemia:

-associated EKG changes

A

May have:

  • **Flattened or inverted T waves
  • **More prominent U waves–> Often seen in leads V4-V6
  • ST depression
  • Prolonged QT interval “QU interval”
  • Arrhythmia
39
Q

Hypokalemia: K+ of ___

A

1.7

40
Q

Hypokalemia: tx

A
  • Usually not emergent unless there are cardiac manifestations or K+ level is <2.5
  • Give IV potassium replacement in this situation–> Can cause pain & phlebitis

-Oral potassium chloride preferred for most others

41
Q

Hypokalemia: tx

-if concurrent hypomagnesemia–>

A

also needs to be repleted

42
Q

Hypokalemia: tx

-what needs to be continuously monitored?

A

Needs continuous cardiac monitoring and frequent recheck of K+ level