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APA > Electrolyte Abnormalities > Flashcards

Electrolyte Abnormalities Flashcards

1
Q

T/F fluid control is one of the most influential aspects of what we do.

A

True

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2
Q

How is total water broken down in the body by weight?

A
  • 60% of total body weight is water
    • 40% intracellular
    • 20% extracellular
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3
Q

How much of extracellular fluid is interstitial vs plasma?

A
  • 75% interstitial

- 25% plasma volume

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4
Q

How does total body water vary with men, women and infants?

A
  • 55% of mans weight
  • 45% of woman’s weight
  • 80% of infants weight
    Obese individuals have less total body water than non obese
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5
Q

What electrolytes dominate in intracellular fluid?

A
  • high concentration of K+
  • mg+
  • Na/K+ ATPase pump and active transport maintain high [K+] inside cell and [Na] outside of cell
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6
Q

Extracellular fluid primarily contains which electrolytes?

A
  • high concentration of Na+ (primary cation) and Cl- (primary anion)
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7
Q

Intravascular fluid (plasma) controls fluid movement how?

A
  • high concent. Of osmotically active plasma proteins—-> albumin
    • capillary membrane not permeable to albumin- remains in vascular space
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8
Q

Fluid movement is affected by:

A
  • properties of membranes separating compartments

- concentration of osmotically active substances within a compartment

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9
Q

What is the chief focus of fluid treatment for us?

A
  • intravascular fluid space—> it the only thing we can get into and control
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10
Q

What is the difference between hydrostatic pressure and oncotic pressure?

A
  • hydrostatic pressure: pushing pressure, water pressure, pressure of fluid going out—-> BP
  • oncotic pressure: pulling pressure from proteins
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11
Q

What are starling forces effected by?

A
  • hydrostatic pressures in capillary vs interstitium

- oncotic pressures in capillary vs interstitium

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12
Q

Which factors affect fluid movement?

A
  • osmolarity
    • # of osmoles of solute/Liter of solution
  • osmolality
    • # of osmoles of solute/Kg of solvent
  • tonicity
    • how solution affects cell volume
    • isotonic, hypotonic, hypertonic
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13
Q

What is an isotonic solution?

A

-285mosm/L

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14
Q

How do you increase osmolarity or osmolality?

A

-increase the amount of solute (water value will remain the same, 1L or 1kg)

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15
Q

What is the difference between hypovolemia and dehydration?

A
  • hypovolemia: fluid body has is still at normal balance
    • loss of extracellular fluids, decrease in circulation fluid
      • absolute loss of fluid from the body.
  • dehydration: unbalanced
    • concentration disorder
    • insufficient water present in relation to Na levels
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16
Q

What is the most common electrolyte abnormality in hospitalized patients?

A

Hyponatremia

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17
Q

What causes hyponatremia?

A 
Vomiting
Diarrhea
Diuretics 
Adrenal insufficiency
SIADH
Renal failure/nephrotic syndrome
Water intoxication
CHF 
Liver failure
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18
Q

What are clinical manifestations of hyponatremia?

A
  • neuro-
    • HA. - coma
    • malaise. - cerebral edema
    • agitation. - confusion
  • GI-
    • anorexia
    • n/v
  • Muscular-
    • cramps, weakness
  • *** since Na doesn’t cross the BBB, you get higher levels of Na inside the brain comparatively. H2O follows Na—> cerebral edema that can lead to DEATH
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19
Q

What is the treatment of hyponatremia?

A
  • fluid restriction
  • admin hypertonic saline and osmotic or loop diuretic
  • correction of serum Na level too quickly can lead to neuro damage and demyelination
    —> correct slowly: 1-2 mEq/L
    • no more than 10-15 mmol in 24 hours
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20
Q

What causes hypernatremia?

A
  • most common cause I’d water deficiency d/t:
    • excessive water loss or inadequate intake
      Also caused by:
  • extra Na intake/administration
  • 1Ëš hyperaldosteronism
  • DI
  • renal dysfunction
  • impaired thirst
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21
Q

What are clinical manifestations of hypernatremia?

A
  • Neuro:
    • thirst
    • weakness
    • seizures
    • hallucinations
    • irritability
    • coma
    • disorientation
    • intracranial bleeding
  • CV:
    • hypervolemia
  • renal:
    - polyuria or oliguria
    • renal insufficiency
22
Q

In hypernatremia, what happens to the brain?

A

Na+ in vasculature is in excess relative to brain Na+ levels
—> H2O in brain follows this Na+, dehydrating the brain, and pulls so hard it can rip the vessels- causing intracranial bleeding

23
Q

How is hypernatremia treated?

A

Replace the water deficit

- increase 1-2mEq/hr until pt clinically stable, gradually over a 24 hr time frame

24
Q

What is a major function of K+?

A

Largely responsible for resting membrane potential

- balanced by GI absorption and renal excretion

25
Q

What causes hypokalemia?

A
  • GI losses
  • systemic alkalosis
  • DKA
  • diuretics
  • SNS stimulation
  • poor dietary intake
    • most common electrolyte abnormality in our clinical practice ***
  • thiazide diuretics —>11xs more likely to have low K+
  • men 2xs as likely as women
26
Q

What are clinical manifestations of hypokalemia?

A 
-CV:
ST depression
Presence of U wave
Flattened/inverted T waves
Ventricular ectopy
-Neuromuscular:
Weakness (resp. Muscle)
Depressed reflexes 
Confusion
** serum k <2.5–> parasthesias, fasiculations, muscle weakness
27
Q

How is hypokalemia treated?

A
  • slow IV supplementation
    Anesthesia related concerns:
    • increased risk of myocardial irritability when K+ <2.6
    • avoid hyperventilation of lungs—> alkalosis causes low K(uses k in blood to drive pH one way or another)
    • avoid rapid infusion of K (40 mEq/hr MAX)
      —> too fast will hyperpolarize the heart and stop it from beating
28
Q

What causes hyperkalemia?

A
  • increased total body K+
    • renal failure
    • K sparing diuretics
    • excessive IV K
    • excessive salt substitutes
  • Altered distribution of K+
    • metabolis/resp. Acidosis
    • dig. Intox, ACE inhibitors, ARBS
    • insulin deficiency
    • hemolysis
    • tissue/muscle damage after burns
    • succinylcholine administration
      —> normal k increase is 05.mEq- with muscle disorder and burns, up regulation of receptors can increase K up to 10mEq
  • DO NOT GIVE SUCC. TO QUADS/PARAS OR BURN PTS ***
29
Q

What are clinical manifestations of hyperkalemia?

A
  • CV:
    • tall peaked and elevated T waves
    • widened QRS
    • prolonged PR
    • flattened/absence P waves
    • ST depression
    • cardiac arrest
30
Q

What is the treatment of hyperkalemia?

A
  • 1Ëš goal—>avoid adverse cardiac effects.
    1. ) stabilize cardiac membrane with IV Ca++
    2. ) drive K+ into cells with insulin and glucose
    3. ) get K+ out with Kayexalate
31
Q

What are anesthesia/surgical related concerns for hyperkalemia?

A

If k+ >5.5 reschedule

5.5 is max for elective procedures

32
Q

What is the role of magnesium, and where is it found?

A
  • 40-60% stored in muscle and bone
  • 30% intracellular
  • 1% in serum
    Regulated by kidneys and intestines
  • roles:
  • co-factors in enzymatic reactions
  • energy metabolism
  • protein synthesis
  • neuromuscular excitability
  • function of Na/K ATPase
33
Q

What causes hypomagnesemia? (<1.7 mEq/L)

A
  • inadequate intake, starvation
  • TPN without Mg+
  • GI losses:
    • diarrhea
    • fistulas
    • NG sanctioning
    • vomiting
    • chronic ETOH
34
Q

What are chronic manifestations of hypomagnesemia?

A
  • EKG:
  • flat T waves
  • U waves
  • prolonged QT
  • wide QRS
  • atrial and ventricular PVCs
35
Q

What is the treatment for hypomagnesemia?

A

IV Mg+: 1-2 G over 5 min, then 1-2 G/hr continuous infusion

36
Q

What causes hypermagnesemia?

A
  • Iatrogenic administration
    • pre-eclampsia
    • antacids/laxatives (tums, mag citrate, MOM)
  • renal failure
  • adrenal insufficiency
37
Q

What are clinical manifestations of hypermagnesemia?

A
  • 3-5 mEq/l ———> flushing, N/V
  • 4-7 ——> drowsy, decreased deep tendon reflexes, weakness
  • 5-10—-> bradycardia, hypotension
  • 7-10——> loss of patellar reflex
  • 10———> Respiratory depression
  • 10-15—> respiratory paralysis
  • 15-20—> cardiac arrest

( huge doses required to have these effects)

38
Q

What is the treatment for hypermagnesemia?

A
  • DC Mg supplement
  • use Ca as an antagonist in urgent situations (bradycardia, heart block, resp depression)—-> Mg decreases resting potential, Ca increases resting potential
  • Ca potentiates ND NMBs
39
Q

How does Mg work for pain control?

A

Makes muscles relax (muscle pain)

  • settles down NMDA receptors
  • can eliminate acute migraines, pancreatic CA pain, and fibromyalgia pain
  • enhances action of analgesics (IV, gas and spinal)
40
Q

What is the norm for Mg?

A

1.4-2.2mEq/L

41
Q

What is the function of calcium,and where is it found?

A
  • 99% found in bones
  • 1% in plasma and body cells
    Function:
  • structural integrity of bones
  • second messenger that couples cell membrane receptors to cellular responses
    —-> muscular contraction, hormones, neuro transmission, coagulation, myocardial contractility
42
Q

Which lab value is best to use for Ca and why?

A

Ionized Ca: physiologically active portion

- normal ionized Ca is 9-10.5 mg/dL

43
Q

What drives Ca into bones? What pulls it out of bones?

A
  • calcitonin drives Ca into bones

- parathyroid hormone pulls Ca out of bones

44
Q

What causes hypocalcemia?

A
  • hypoparathyroid
  • malignancy
  • chronic renal insufficiency
  • hyperventilation—> alkalosis—>protein binding of Ca
  • citrate of blood (transfused) binds to Ca and lowers Ca levels
45
Q

What are clinical manifestations of hypocalcemia?

A

Neuromusc. Irritability:

  • resting membrane potential and threshold potential narrow—> doesn’t take much to fire an impulse
  • cramps
  • weakness
  • Chvostek’s sign
  • Trousseau’s sign
  • numbness
  • tingling
46
Q

What are clinical manifestations of hypocalemia?

A 
CV: 
- dysrrhythmias
- prolonged QT
- T wave inversion
- hypotension
- decreased myocardial contractility
Pulm:
- laryngospasm
- bronchospasm
- hypoventilation
47
Q

What is the treatment of hypocalcemia?

A
  • infusion of Ca salts
    • Ca chloride: best if available—> more bioavailable and quicker
    • Ca gluconate: slower
      - 3 G Ca gluconate = 1 G CaCl
48
Q

What are causes of hypercalcemia?

A
  • HYPERparathyroid (>50% cause)
  • tumors/malignancy
  • Ca mobilization from bone d/t immobility
49
Q

What are clinical manifestations of hypercalcemia?

A 
CV: 
- HTN
- heart block
- shortened QT
- dysrhythmias
Neuro musc:
- muscle weakness
- depressed deep tendon reflexes
- sedation
50
Q

How is hypercalcemia treated?

A
  • treat underlying cause
  • volume expansion with NS—> manage intraoperatively with enough IVF to maintain adequate UOP
    • loop diuretics
  • HD can filter out Ca if really bad *

APA (8 decks)

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