Chapter 9: Fluids and Electrolytes Flashcards

1
Q

Water weight distribution

A

2/3: intracellular (mostly muscle)

1/3: extracellular

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2
Q

Extracellular water distribution

A

2/3: Interstitial

1/3: plasma

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3
Q

Determine plasma/interstitial compartment osmotic pressures

A

Proteins

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4
Q

Determines intracellular/extracellular osmotic pressure

A

Sodium

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5
Q

MCC is iatrogenic; first sign is weight gain

A

Volume overload

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6
Q

What is the first sign of volume overload?

A

Weight gain

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7
Q

Can release a significant amount of water

A

Cellular catabolism

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8
Q

Normal saline:

[Na], [Cl]

A
[Na] = 154
[Cl] = 154
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9
Q

3% Normal saline

[Na], [Cl]

A
[Na] = 513
[Cl] = 513
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10
Q

Lactated ringer’s

[Na], [K], [Ca], [Cl], [Bicarb]

A
[Na] = 130
[K] = 4
[Ca] = 2.7
[Cl] = 109
[Bicarb] = 28
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11
Q

Calculate plasma osmolarity

A

(2Na) + (Glucose/18) + (BUN/2.8)

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12
Q

Normal plasma osmolarity

A

280 - 295

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13
Q

How does water achieve osmotic equilibrium?

A

Water shifts from areas of low solute concentration (low osmolarity) to areas of high solute concentration (high osmolarity) to achieve osmotic equilibrium.

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14
Q

Estimates of volume replacement

A

4 cc/kg/h for 1st 10kg
2cc/kg/h for 2nd 10kg
1 cc/kg/h for each kg after that

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15
Q

Best indicator of adequate volume replacement

A

Urine output

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16
Q

Fluid loss during abdominal operations

A

0.5 - 1.0 L/h unless there are measurable blood losses

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17
Q

When should you think about replacing blood?

A

> 500 cc

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18
Q

What are insensible fluid losses?

A

10 cc/kg/day; 75% skin, 25% respiratory, pure water

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19
Q

Replacement fluids after major adult gastrointestinal surgery:
1st 24 hours ->
After 24 hours ->

A

1st 24 hours: LR

After 24 hours: D5 1/2 NS with 20 mEq K+

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20
Q

Why switch to D5 1/2 after 24 hours with replacement fluids after major adult gastrointestinal surgery?

A
  • 5% dextrose will stimulate insulin release, resulting in amino acid uptake and protein synthesis (also prevents protein catabolism)
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21
Q

How much glucose does D5 1/2 NS @ 125/h provide?

A

150g glucose per day (525 kcal/day)

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22
Q

GI fluid secretion:

Stomach

A

1-2 L/day

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23
Q

GI fluid secretion:

Biliary system

A

500 - 1,000 mL/day

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24
Q

GI fluid secretion:

Pancreas

A

500 - 1,000 mL/day

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25
GI fluid secretion: | Duodenum
500 - 1,000 mL/day
26
Normal K+ requirement
0.5 - 1.0 mEq/kg/day
27
Normal Na+ requirement
1 - 2 mEq/kg/day
28
Electrolyte loss: sweat
Hypotonic (Na concentration 35-65)
29
Electrolyte loss: saliva
K+ (highest concentration of K+ in body)
30
Electrolyte loss: stomach
H+ and Cl-
31
Electrolyte loss: pancreas
HCO3-
32
Electrolyte loss: bile
HCO3-
33
Electrolyte loss: small intestine
HCO3- and K+
34
Electrolyte loss: large intestine
K+
35
Replacement: gastric losses
Replacement is D5 1/2 NS with 20 mg K+
36
Replacement: pancreatic / biliary / small intestine losses
Replacement is LR with HCO3-
37
Replacement: large intestine losses (diarrhea)
Replacement is LR with K+
38
Replacement: GI losses
Should generally be replaced cc/cc
39
Replacement: Dehydration (eg marathon runner)
Replacement with normal saline
40
Replacement: urine output
Should be kept at least 0.5 cc/kg/h; should not be replaced, usually a sign of normal postoperative diuresis
41
Peaked t waves on EKG; often occurs with renal failure | Tx?
Hyperkalemia - Calcium gluconate (membrane stabilizer for heart) - Sodium bicarbonate (causes alkalosis, K enters cell in exchange for H) - 10U insulin, 1 amp D50 (K driven into cells with glucose) - Kayexalate - Dialysis if refractory
42
T waves disappear (usually occurs in setting of overdiuresis)
Hypokalemia | - May need to replace magnesium before you can correct K+
43
Usually from dehydration; restlessness, irritability, seizures - Correct with D5 water slowly to avoid brain swelling
Hypernatremia
44
Usually from fluid overload; headaches, n/v, seizures.
Hyponatremia
45
First-line treatment for hyponatremia
Water restriction, then diuresis
46
Why correct sodium slowly?
Avoid central pontine myelinosis (no more than 1 mEq/h)
47
How does sodium affect sugar?
Hyperglycemia can cause pseudohyponatremia - for each 100 increment of glucose over normal, add 2 points to the sodium value
48
How does SIADH affect sodium?
SIADH: syndrome of inappropriate antidiuretic hormone can cause hyponatremia
49
MC malignant cause of hypercalcemia
Breast cancer
50
MC benign cause of hypercalcemia
Hyperparathyroidism
51
Tx: hypercalcemia - General disease - Malignant disease
- General: NS at 200-300 cc/h and Lasix | - Malignant: mithramycin, calcitonin, alendrotnic acid, dialysis
52
Why no LR or thiazide diuretics in hypercalcemia?
LR: contains calcium | Thiazide diuretics: retain calcium
53
Hyperrelfexia, Chovstek's sign, perioral tingling and numbness, Trousseau's sign, prolonged QT
Hypocalcemia
54
Dx: hypercalcemia
Ca usually > 13 or ionized > 6-7 for symptoms (causes lethargy)
55
Dx: hypocalcemia
Ca usually
56
Causes lethargic state; usually in renal failure patients taking supplements. Tx: calcium
Hypermagnesemia
57
Usually occurs with massive diuresis, chronic TPN without mineral replacement or ETOH abuse; signs similar to hypocalcemia
Hypomagnesemia
58
Calculate anion gap
Na = (HCO3 + Cl) | Normal:
59
DDx: high anion gap acidosis
MUDPILES | Methanol, uremeia, DKA, paraldehydes, isoniazid, lactic acidosis, ethylene glycol, salicylates
60
Acidosis usually secondary to loss of Na/HCO3- (ileostomies, small bowel fistulas).
Normal anion gap acidosis
61
Tx: normal anion gap acidosis
Tx: underlying cause, keep pH > 7.20 with bicarbonate, severely decreased pH can affect myocardial contractility.
62
Usually a contraction alkalosis
Metabolic alkalosis
63
Electrolyte changes: nasogastric suction
Hypochloremic, hypokalemic, metabolic alkalosis, and paradoxical aciduria
64
Pathophys: electrolyte changes nasogastric suction
- Low Cl/H: NGT suction (hypochloremia, alkalosis) - Low H2O: kidneys reabsorb Na in exchange for K, (Na/K ATPase) thus losing K (hypokalemia) - Na/H exchange to reabsorb H2O with K/H to reabsorb K -> paradoxical aciduria
65
Tx: electrolyte disturbance s/t nasogastric suction
Normal saline (need to correct the Cl- deficit)
66
Time: respiratory compensation
Minutes (CO2 regulation)
67
Time: renal compensation
Hours-days (HCO3- regulation)
68
Best test for azotemia
FeNa
69
Calculation: FeNa
(urine Na/Cr)/(plasma Na/Cr)
70
Dx: prerenal azotemia - FeNa - Urine Na - BUN/Cr ratio - Urine osomolality
Prerenal azotemia: - FeNa 20 - Urine osmolality > 500 mOsm
71
%: renal mass damaged before you see increased Cr and BUN
70% of renal mass must be damaged before you see changes
72
Prevent renal damage secondary to contrast dyes
Prehydration best prevents renal damage; HCO3- and N-acetylcysteine
73
Converted to ferrihemate in acidic environment, which is toxic to renal cells. Tx: alkalinize urine.
Myoglobin
74
- Release of purines and pyrimidines leads to increased phosphate and uric acid and decreased calcium. - Can result in increased BUN/Cr (from renal damage), EKG changes
Tx: hydration (best), rasburicase (converts uric acid in inactive metabolite allantoin), allopurinol (decreases uric acid production), diuretics, alkalization of urine
75
Converts uric acid in inactive metabolite allantoin
Rasburicase
76
Decreases uric acid production
Allopurinol
77
- Made in skin (UV sunlight converts 7-dehydrocholesterol to cholecalciferol) - Goes to liver for (25-OH), then kidney for (1-OH). This creates the active form
Vitamin D (cholecalciferol)
78
Increases calcium-binding protein, leading to increased intestinal calcium absorption
Active form of vitamin D
79
- Decreased active vitamin D (decreased 1-OH hydroxylation) -> decreased calcium reabsorption from gut (decreased calcium-binding protein) - Anemia: from low erythropoietin
Chronic Renal Failure
80
Transporter of iron
Transferrin
81
Storage form of iron
Ferritin