32 - Electrolyte Disorders Flashcards

1
Q

Describe what happens to potassium in the body

A
  • Total body stores = 3000-4000 mmol
  • 98% intracellular, 2% extracellular
  • Na+/K+/ATPase pump results in 3:2 ratio of Na+ out to K+ in
  • Normal serum level = 3.5-5 mmol/L, intracellular = 150 mmol/L
  • Intracellular & extracellular levels are in dynamic flux
  • Many important roles including protein synthesis, cell metabolism, action potential across cell membrane, & BP
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2
Q

Describe potassium homeostasis

A
  • Intake through diet
  • Elimination usually 90% renally (secretion from distal tubules) & 10% GI
  • Homeostasis affected by – hormones, acid-base status, hyperosmolality
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3
Q

Which hormones affect potassium hormones and how?

A
  • Insulin, catecholamines, & aldosterone affect homeostasis
  • Insulin stimulates Na+/K+/ATPase pump to transport K+ intracellularly
  • Catecholamines (ex: epinephrine) = beta-receptor stimulation, which:
    • Activates Na+/K+/ATPase pump -> drives potassium intracellularly
    • Causes glycogenolysis -> increases glucose -> releases insulin, drives potassium intracellularly
  • Aldosterone – acts at distal tubule, increased urinary potassium excretion
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4
Q

Describe how acid-base and osmolality affect potassium homeostasis

A
  • Acid-base status affects K+ shifting; in simple terms:
    • Decreased blood pH – body responds by moving H+ into cells & K+ out (0.1 unit decrease in pH = ~0.6-0.8 mmol/L increase in serum K+ = false hyperkalemia b/c not actually changing amount in body, just shifting)
    • Increased blood pH – body responds by moving H+ out of cells & K+ in (0.1 unit increase in pH = ~0.6 mmol/L decrease in serum K+ = false hypokalemia)
  • Hyperosmolality – K+ shifts to extracellular fluid
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5
Q

Hypokalemia definition

A
  • Definition = serum K+ < 3.5 mmol/L
    • Mild = 3.1-3.5 mmol/L
    • Moderate = 2.5-3 mmol/L
    • Severe < 2.5 mmol/L
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6
Q

Causes of hypokalemia

A
  • Due to total body K+ deficit or intracellular shift
  • Most common cause = medications
  • Other causes = excessive GI loss (diarrhea, vomiting, metabolic alkalosis can develop & decrease serum K+ further); hypomagnesemia (increases renal excretion of potassium; **important – need to correct underlying magnesium deficiency to correct potassium)
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7
Q

Why is hypokalemia a problem?

A
  • Moderately low = cramps, weakness, myalgias

- Severely low = EKG changes, arrhythmias, increased digoxin toxicity

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8
Q

Hypokalemia tx

A
  • Non-pharms = adequate dietary intake of K+, potassium salt substitutes
  • Pharm = oral supplementation when mild & N/V not a concern; IV replacement for severe and/or vomiting; replacement of magnesium first if hypomagnesemia (oral or IV)
  • General rule of thumb = 100 mmol of oral replacement increases serum K+ by ~1 mmol/L
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9
Q

Hypokalemia monitoring

A
  • Acute inpatient setting correcting severe hypokalemia = can monitor serum levels numerous times/day, EKG w/ high rate infusions
  • Inpatient setting w/ mild to moderate acute deficiency = replace & check serum levels daily to q3days
  • Remember to check Mg2+ levels if K+ replacement isn’t correcting serum levels
  • Ambulatory setting (ex: K+ supplementation w/ diuretic) = check serum level, renal function q1-2 months if levels have been stable
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10
Q

Hyperkalemia definition

A
  • Definition = serum K+ > 5 mmol/L
    • Mild = 5.1-5.9 mmol/L
    • Moderate = 6-7 mmol/L
    • Severe > 7 mmol/L
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11
Q

Why is hyperkalemia a problem?

A
  • Mildly elevated = usually asymptomatic

- Moderately to severely elevated = EKG changes, arrhythmias, mortality

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12
Q

Main causes of hyperkalemia

A
  • Increased K+ intake
  • Decreased K+ excretion
  • Decreased effect of aldosterone
  • Extracellular movement of total body K+ (pseudohyperkalemia)
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13
Q

How can increased K+ intake cause hyperkalemia?

A
  • Increased intake usually only a problem in severe renal impairment or dialysis
  • Non-compliance w/ diet restriction (ex: products w/ high K+ content like potato, sweet potato, prunes, carrots, plain yogurt, orange juice)
  • Unwittingly using KCl salt substitutes (200 mmol K+ pet 5 mL)
  • OTC/alternative products containing potassium
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14
Q

How can decreased K+ excretion cause hyperkalemia?

A
  • Impaired excretion in renal failure alone or in conjunction w/ medications (ex: ACEis, ARBs, K+ sparing diuretics, NSAIDs; less common = digoxin, TMP-SMX, heparin)
  • Caution w/ additive effects of > 1 medications (ex: TMP-SMX added short term to pt already receiving ACEi + NSAID
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15
Q

What is important to note about K+ lab tests?

A
  • Blood sample hemolysis = falsely elevated serum K+
  • Intracellular K+ can spill from RBCs
  • Lab will usually note if sample appear hemolyzed
  • Consider false elevation if other labs (blood CO2, renal function) normal
  • Redraw sample before making tx decision
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16
Q

Hyperkalemia tx

A
  • Mild = may self-correct w/ monitoring, may or may not op to treat
  • Hyperkalemia w/ EKG changes = emergency, immediate tx needed
  • Available therapies aim to either reduce total body stores of K+ or correct extracellular (serum) levels by temporarily driving K+ intracellularly
17
Q

Severe hyperkalemia tx

A
  • First, stabilize cardiac membrane (reverse EKG changes) w/ IV calcium gluconate
    • Acts w/in 5 minutes, lasts 30-60 mins
    • Doesn’t change serum K+ level
  • Next, drive serum potassium intracellularly w/ regular insulin 10 U IV x1 (if not already hyperglycemic, give dextrose 25 g IV x1 concurrently to avoid hypoglycemia) +/or beta-2 agonists (salbutamol 10 mg nebule inhaled x1)
    • Don’t use subcut insulin b/c duration is too long for what its being used for (will cause hypoglycemia)
  • For metabolic acidosis (decreased extracellular pH), can also give sodium bicarbonate 50-100 meq IV x1
    • Raises pH, potassium moves into cells
    • Not tx of choice outside of metabolic acidosis px
    • Doesn’t work as well in px w/ ESRD
18
Q

Mild hyperkalemia tx

A
  • Sodium polystyrene sulfonate (commonly known by brand name Kayexalate)
    • Cation exchange resin
    • Exchanges sodium for potassium 1:1 in intestine
    • Takes many hours to see full effect
    • Can give PO or PR, typically 15-45 g per dose
    • CI in bowel dysfunction or constipation
    • Risk of colonic necrosis
    • May bind other medications
  • Furosemide (ex: 40 mg IV x1) to increase urinary K+ loss – onset w/in minutes, duration 4-6 h
19
Q

Describe what happens to sodium in the body

A
  • Human body requires ~1.5 g per day
  • Predominant extracellular cation
  • normal serum concentration 135-147 mmol/L
  • Kidneys normally function to excrete excess sodium or conserve it in a deficit situation, keeping concentration tightly controlled
20
Q

What is hyponatremia?

A
  • Serum sodium < 135 mmol/L
  • Most common electrolyte abnormality
  • Associated w/ significant morbidity & mortality, especially w/ rapid swings in sodium levels
21
Q

Categories of hyponatremia

A
  • Hypovolemic hypotonic hyponatremia (common w/ thiazide diuretics)
  • Euvolemic hyponatremia (associated w/ SIADH, syndrome of inappropriate ADH secretion)
  • Hypervolemic hyponatremia (associated w/ cirrhosis, HF, nephrotic syndrome
22
Q

Hyponatremia – clinical presentation

A
  • Mild (> 125 mmol/L) = usually asymptomatic; impairment of attention & gait & increased fall risk
  • Moderate (115-124 mmol/L) = headache, lethargy, restlessness, disorientation
  • Severe (< 115 mmol/L) = seizures, coma, respiratory arrest, brain damage, death
23
Q

Hyponatremia tx

A
  • Treat underlying cause to correct level
  • Hypovolemic hyponatremia – treat w/ IV NaCl (0.9% or sometimes 3% if severe)
  • Euvolemic or hypervolemic = try fluid restriction first
  • Rapid swings in sodium levels (normally caused by correcting deficiency too rapidly) can cause osmotic demyelination syndrome (damage to myelin sheath of brainstem) -> can result in paralysis or death in minutes
  • Rule of thumb – never increase serum Na+ level more than 12 mmol/L/24 h
24
Q

Describe the options for K+ replacement

A
  • Oral – consider tablet vs. liquid, tolerance can be an issue (split doses to minimize GI irritation) – potassium chloride = 8 meq per tablet (avoid giving more than 24 meg per dose to minimize GI irritation and wait at least 2 h before giving additional doses; chronic deficiency may often give ~8-16 meq oral replacement daily)
  • IV – severe hypokalemia, inpatient setting, high replacement rates need EKG monitoring; ex: 1 L bags of 40 meq KCl in 0.9% NaCl (not in D5W b/c dextrose will increase blood glucose and cause insulin release, which will decrease K+)