Hyperkalemia and Hypokalemia- paulson Flashcards by Sammy B

Hyperkalemia: serum potassium is ______

-Is hyperkalemia dangerous?

-> 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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“emia”=

“condition of the blood”

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Hyperkalemia refers to high serum potassium, NOT ____

whole body potassium

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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

(98%)
2%
3.5-5.0 =normal

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Hyperkalemia: etiology

Increased intake
Decreased excretion
Shift from intracellular to extracellular
Pseudohyperkalemia

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Hyperkalemia:

-describe increased intake

PO supplementation

- IV potassium

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Hyperkalemia:

-describe pseudohyperkalemia

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

Any breakdown of cells
acidosis
Insulin deficiency or resistance

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Decreased Excretion (of potassium): describe 3 possible causes

Renal failure
Hypovolemia
Hypoaldosteronsism

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

Acute or chronic

- Kidneys unable to filter and excrete normally

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

Dehydration, CHF, cirrhosis

- Low flow to the kidneys

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

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

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Intracellular to Extracellular Shifts:

-Describe any breakdown of cells

-Broken cells release potassium when they lyse

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

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Intracellular to Extracellular Shifts:

-Describe Acidosis

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

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Intracellular to Extracellular Shifts:

-describe Insulin deficiency or resistance

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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Meds that can cause hyperkalemia: KNOW!!!

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

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T/F: hyperkalemia can cause Cardiotoxicity

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

Hyperkalemia:

-clinical features

-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

Hyperkalemia:

-labs/eval

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

EKG changes associated with hyperkalemia

**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

EKG findings

image slide 15

When is hyperkalemia considered an emergency?

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

Hyperkalemia: tx

-If severe hyperkalemia + EKG changes–> tx?

IV calcium gluconate
Continuous cardiac monitoring
Options to drive potassium back into the cell:

Hyperkalemia: tx

-list options to drive potassium back into the cell

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

Hyperkalemia: tx | -Options for removal of Potassium from the body (list 3)

- 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

Hyperkalemia: tx | -what are some OBVIOUS thoughts regarding tx

Stop any potassium supplements or medications that can increase potassium

Hypokalemia: | -what is the serum potassium?

< 3.5 mEq/L

Hypokalemia: pathophysiology | -describe various mechanisms of K+ loss

-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

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

- Insulin excess - Beta agonist treatment - Alkalosis

Hypokalemia is often concurrent with _______

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

Describe renal tubular acidosis: - Type 1= - Type 2=

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

Hypokalemia 2/2 medications (list ex's)

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

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

200-800 calories

Hypokalemia: | -clinical features

- 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

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

**respiratory failure/death

Hypokalemia: | -describe GI muscle involvement

ileus, constipation, n/v

Hypokalemia: | -diagnostic tests (list 3)

- **BMP - Magnesium - EKG

Hypokalemia: | -associated EKG changes

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

Hypokalemia: K+ of ___

1.7

Hypokalemia: tx

- 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

Hypokalemia: tx | -if concurrent hypomagnesemia-->

also needs to be repleted

Hypokalemia: tx | -what needs to be continuously monitored?

Needs continuous cardiac monitoring and frequent recheck of K+ level