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ASPEN Clin 2 Readings > Chapter 7 > Flashcards

Chapter 7 Flashcards

1
Q

ICF

A

2/3 TBW

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2
Q

ECF

A

1/3 TBW

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3
Q

Most clinically important fluid compartment

A

ECF, because the ECF includes the interstitial and intravascular spaces

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4
Q

Dominant extracellular osmole?

A

Sodium

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5
Q

Dominante intracellular osmole?

A

Potassium

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6
Q

How is 1L of dextrose IV solution dispersed?

A

1/3 ECF, 2/3 ICF

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7
Q

Of the 1/3 ECF from the 1L of dextrose IV solution, how much to interstitial and intravascular space?

A

2/3 Interstitial,1/3 intravascular

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8
Q

How is 0.9% NaCl (Isonic) solution dispersed? What is the clinical significiance?

A

100% to ECF, where 1/4 to intravascular, 3/4 to interstitial. To establish blood pressure as it is 3x more effective in expanding the intravascular space

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9
Q

1000 ml of dextrose solution, how much in intravascular space?

A

Approximately 83 ml

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10
Q

1000 ml of NaCl 0.9% isotonic solution, how much in intravascular space?

A

Approximately 250 ml

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11
Q

When is edema common?

A

Severe blood volume depletion, as it can cause capillary permeability to increase

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12
Q

Explain edema, after a reduction in blood volume.

A

Increased permeability of capillaries causes the leakage of albumin to interstitial space (still in ECF), reducing plasma oncotic pressure which further favours movement of fluid from the intravascular to interstitial space.

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13
Q

What is third spacing?

A

The accumulation of the excess fluid in the interstitial space (edema) or in the potential fluid spaces (effusion)

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14
Q

Why is water needed?

A

To support individuals LBM

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15
Q

Why should energy-based fluid calculations be avoided in those older than 65 years old?

A

To prevent dehydration

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16
Q

What does dehydration cause in the elderly?

A

Hypotension, confusion, extreme thirst and constipation

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17
Q

What are the three formulas that may be used for fluid calculations in the older adult?

A

1) Adj. Holliday-Segar
2) 30ml/kg, min of 1500 ml
3) 1500-2000 ml/day

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18
Q

Holliday-Segar formula?

A

1500 ml for first 20 kg, 15ml/kg for remaining BW

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19
Q

Why must obesity-adjusted weight be used when calculating fluid req?

A

We are hydrating lean mass, not adipose tissue

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20
Q

Obesity Adj. BW (lbs) =

A

[(ABW - IBW) x 0.25] + IBW

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21
Q

Give examples of increased fluid needs

A
  • Severe diarrhea, emesis
  • Large draining wounds
  • High gastric fistula
  • Ostomy outputs
  • High fevers
  • Lactating women
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22
Q

The more energy-dense a formula is, the lower ____

A

percentage of water volume

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23
Q

Heart failure patient fluid restriction?

A

20-25 ml/kg

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24
Q

Heart failure patient on fluid restriction, sodium restriction?

A

<2000 mg /day

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25
Q

In heart failure, what would not meeting the fluid restriction cause?

A

Contribute further respiratory decompensation, which would require diuresis and ICU transfer

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26
Q

How does fluid restriction help in HF?

A

Decreased O2 requirements, less stress on pumping blood through lungs

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27
Q

What else should HF patients be put on?

A

Loop diuretics

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28
Q

What is the normal range of serum osmolality?

A

280-295 mOSm/kg

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29
Q

What is elicited when serum osmolality changes?

A

Change in thirst and ADH secretion

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30
Q

When does volume depletion, or hypovolemia occur?

A
  • GI hemorrhage
  • Vomiting
  • Diarrhea
  • Diuresis
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31
Q

What are primary contributors to electrolyte balances?

A
  • Losses from GI tract

- Abnormalities in renal excretion

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32
Q

What are the electrolytes found in the greatest amounts in the stomach, duodenum, ileum and bile

A

Cl, Na+

-More Cl in stomach compared to Na+

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33
Q

What are the predominant electrolytes in the pancreas?

A

Na+, HCO3-

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34
Q

What are the predominant electrolytes in the colon?

A

Na+, K+, Cl-

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35
Q

_____ trends in electrolytes are the most important, where acute electrolyte imbalance can be _____ if corrected too rapidly

A
  • chronological

- harmful

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36
Q

When is IV electrolyte replacement preferred?

A

When patients have impaired GI tract absorption, nil os, and critically low electrolyte levels

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37
Q

When is conservative electrolyte replacement preferred?

A

In patients with impaired renal function, unles if they are receiving renal replacement therapy

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38
Q

(T/F) Magnesium should be repleted prior to correcting potassium levels

A

T

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39
Q

How can we correct hypokalemia and hypophosphatemia while minimizing electrolyte replacement?

A

potassium phosphate

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40
Q

Normal sodium

A

135-145 mEQ/L

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41
Q

Hyponatremia symptoms

A

Dizziness, headache, N/V, muscle cramps, lethargy

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42
Q

When electrolytes are above, how can we correct?

A
  • Remove exogenous source
  • Discontinue agents, meds
  • Facilitate elimination
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43
Q

When electrolytes are below, how can we correct?

A
  • IV
  • Assess GI function for oral supplement
  • Assess fluid status, renal function
  • See if there are concurrent elect abnormalities
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44
Q

What is hypertonic hyponatremia?

A
  • > 290 mOSm/L
  • Caused by osmotically active substance other than sodium in the ECF
  • Common causes is mannitol and hyperglycemia
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45
Q

What is isotonic hyponatremia?

A
  • Serum osmolality is normal
  • Fraction of serum compose of water is reduced
  • Rare
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46
Q

What is hypotonic hyponatremia?

A
  • <275 mOsm/L
  • Can be hypervolemic or hypovolemic
  • More serious
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47
Q

Hypovolemic hypotonic hyponatremia?

A
  • More sodium loss than water, but water also decreases

- Treat with isotonic fluids to expand ECF volume

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48
Q

Hypervolemic hypotonic hyponatremia?

A
  • Retain more water than sodium, but sodium is also retained
  • May cause edema forming states and renal failure
  • Treat with fluid and sodium restriction
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49
Q

Why sodium restriction in hypervolemic hypotonic hyponatremia?

A

To avoid further water retention, as there is already more water retained than sodium

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50
Q

Euvolemic hypotonic hyponatremia?

A
  • sodium remains the same, while total body water increases
  • urine osmolality > serum osmolality, which indicates that the kidneys are inappropriately concentrating urine
  • Treat with fluid restriction
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51
Q

What is euvolemic hypotonic hyponatremia usually associated with?

A

SIAD (Syndrome of innappropriate diuresis), where there are excessive levels of ADH

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52
Q

What is more common, hypo or hypernatremia?

A

Hypo, but hyper has a lower threshold to see clinical manifestations

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53
Q

What is euvolemic hypernatremia?

A

Diabetes insipidus, where water losses exceed sodium losses

54
Q

Hypovolemic hypernatremia?

A
  • Total body water decreases more that total body sodium

- Treat with volume expansion with isotonic saline

55
Q

Euvolemic hypernatremia?

A
  • Total body sodium unchanged, total body water decreases

- Treat with water replacement

56
Q

Hypervolemic hypernatremia?

A
  • Total body sodium increases, total body water remains unchanged
  • Treat with diuretics, water replacement
57
Q

Hypokalemia?

A

When serum potassium less than 3.6 mEQ/L

58
Q

What often causes hypokalemia?

A

Loss of potassium in urine or stool, less often caused by trans-cellular shift or inadequate dietary intake

59
Q

What can cause trans cellular shift of K+ into cells?

A
  • Catecholamines
  • Metabolic alkalosis
  • Insulin increase
60
Q

Hypokalemia and hypo___ are often seen together

A

magnesemia

61
Q

In the presence of metabolic acidosis, what potassium salt is used to treat hypoK? Why?

A

Potassium acetate instead of potassium chloride, because acetate is converted to bicarbonate

62
Q

Why should dextrose solutions be avoided within the context of hypokalemia?

A

insulin facilitates trans-cellular shift of K+ to intracellular space

63
Q

What can hypomagnesemia result in?

A

Refractory hypokalemia

64
Q

Clinical manifestations of hyperK?

A

Changes in neuromuscular and cardiac function

65
Q

What is the most common context of hyperK?

A

Chronic kidney disease

66
Q

Extracellular shifts of K+ are relatively commonn, and due to what?

A
  • Metabolic acidosis
  • Tissue catabolism
  • PseudohyperK
67
Q

Explain why we see HyperK in metabolic acidosis

A

ECF flux of K+ to maintain electroneutrality due to excess of H+ ions (remember that outside the cell is usually more positive)

68
Q

How can those with HyperK have their membrane excitability be restored to normal (making K+ shift back intracellularly?)

A
  • IV calcium gluconate
  • Insulin, dextrose
  • Sodium bicarbonate
  • Loop diuretics
69
Q

Normal mg? where is it found?

A

1.8-2.8 mg/dl, mostly found in ICF, and up to 60% in bone

70
Q

Where does most Mg absorption take place?

A

In the distal jejunum and ileum

71
Q

What is the primary symptom of mg deficiency?

A

Neuromuscular hyper-excitability

72
Q

What must be corrected prior to correcting mg?

A

Calcium and potassium

73
Q

What is hypomg’s impact on CHO and lipid metabolism?

A
  • Reduce insulin sensitivity and secretion and glucose cellular uptake
  • Reduce LPL
74
Q

When may hypomg occur?

A
  • Alcoholism
  • PEM
  • Ileostomy, colostomy
  • Short bowel syndrome
  • Reduced mg intake, mg-free IV fluids or TPN
75
Q

When can intra-cellular shifts of mg be seen?

A
  • Refeeding
  • Diabetic ketoacidosis
  • Hyperthryoidism
  • MI
76
Q

Normal serum calcium?

A

8.6-10.2 mg/dl

77
Q

Most abundant cation in the body?

A

Calcium, accounts for 1-2% of total body weight

78
Q

Metabolically active form of calcium? Is it impacted by hypoalbuminemia?

A
  • Ionized calcium

- NO

79
Q

Low serum calcium stimulates ___ high serum calcium stimulates ___

A

PTH

Calcitonin

80
Q

For each 1 g/dl decrease in albumin below 4 g/dl, there is an decrease of total serum calcium of ___

A

0.8 mg/dl

81
Q

Direct measurement of ____ is the most critical in the ICU patient

A

ionized calcium

82
Q

Hypocalcemia is not usually clinically significant if the _____ remains the same

A

ionized calcium

83
Q

Options to correct hypocalcemia?

A
  • IV calcium gluconate

- Calcium chloride table

84
Q

What calcium supplement may cause tissue necrosis if exacerbation occurs?

A

CaCl, 3 x more elemental calcium than IV calcium gluconate

85
Q

When does hypercalcemia occure?

A
  • Hyperparathyroidism
  • Cancer w/ bone mestases
  • Vit A or Vit D toxicity
  • CaCl and renal insufficiency
86
Q

How should hypercalcemia be treated?

A

Isotonic solution, as it often causes volume depletion

87
Q

What is the main intracellular anion?

A

Phosphorous

88
Q

Normal range of phosphorous?

A

2.7-4.5 mg/Dl, reflects less than 1% of total body phosphorous

89
Q

What causes intracellular shifts of phosphorus?

A
  • CHO and insulin administration
  • Catecholamine
  • Alkalosis
90
Q

When is hypophophatemia observed?

A
  • Chronic alcoholism
  • Critically ill
  • Diabetic ketoacidosis
91
Q

When is hypophosphatemia likely to be caused?

A

After administration of CHO load or PN without phosphate, especially in the context of a malnourished patient (refeeding)

92
Q

What can agressive feeding in malnourished patients cause?

A

major shifts of potassium, magnesium and phosphorus into the intracellular space

93
Q

How should nutrition support be administered to avoid re-feeding?

A

500 kcal/day, increase by 150% per day if OK, and add thiamine supplementation to aid in CHO metabolism

94
Q

____ should be corrected prior to nutritional therapy

A

Electrolyte imbalances

95
Q

When does hyperphosphatemia occur?

A

CKD usually, trauma, cytoxic agents, metabolic acidosis

96
Q

When can the administration of high quantities of phosphate containing laxatives cause severe hyperphospatemia and end-organ damage?

A

In the elderly

97
Q

What is the most serious complication of hyperphosphatemia?

A

Soft tissue and vascular calcification

98
Q

pH for acidemia of blood?

A

<7.35

99
Q

pH for alkalemia of blood?

A

> 7.45

100
Q

What are the three ways the body regulates H+?

A

1) Buffering through ECF and ICF
2) PCO2, by changing breathing
3) HCO3- changes through kidneys

101
Q

What is the principle buffer system?

A

H2CO3 –> HCO3-

102
Q

What is the principle role of the lungs?

A

Maintain acid-base balance by regulating the pressure of dissolved CO2 gas in the blood –> when the respiratory system is compromised, we risk acid-base balance

103
Q

What is the slowest mechanism to regulate H+?

A

Excretion of H+ and reabsorption of HCO3- by the kidneys

104
Q

What is the only organ that can regulate alkaline substances and eliminate metabolic acids?

A

The kidneys

105
Q

What are arterial blood gases? (ABGs)

A

Ability of lungs to oxygenate the blood

106
Q

What are venous blood gases (VBGs)

A

Reflect tissue oxygenation

107
Q

PCO2 indicated what?

A

Lungs ability to excrete CO2

108
Q

Increased PCO2?

A

Acidosis

109
Q

Decreased PCO2?

A

Alkalosis

110
Q

PO2 indicates what?

A

Ability of hemoglobin to carry oxygen

111
Q

The PO2 values is directly related to __

A

O2 saturation

112
Q

Increase HCO3-?

A

alkalosis

113
Q

Decreased HCO3-?

A

Acidosis

114
Q

Steps to analyze acid base disorder?

A

1) Measure pH
2) Assess PCO2 to see if resp. disorder
3) Assess serum HCO3- to see if met. disorder
4) Calculate anion gap to see if metabolic acidosis is present

115
Q

What is resp. acidosis characterized by?

A
  • Decreased pH
  • Increased PCO2
  • Variable increase in HCO3-
116
Q

What is resp. acidosis caused by?

A

Decreased alveolar ventilation

117
Q

What is resp. alkalosis characterized by?

A
  • Increased pH
  • Decreased PCO2
  • Variable decrease in HCO3-
118
Q

Whet is resp. alkalosis caused by?

A

Effective alveolar ventilation is increased beyond the level necessary to eliminated metabolically produced CO2

119
Q

What is metabolic acidosis?

A
  • Reduced pH
  • Reduced serum HCO3-
  • Compensatory hyperventilation, causing decreased PCO2
120
Q

How can met. acidosis be induced?

A
  • Inability of kidneys to excrete H+ load

- Increase in the generation of H+ by addition of H+ or loss of HCO3-

121
Q

Anion gap equation?

A

(serum Na+) - (Serum Cl-) + (Serum HCO3-)

122
Q

What affects anion gap? What must be added?

A
  • Hypoalbuminemia

- 2.5 mEQ/L of anion gap added for each 1 g/dL decrease

123
Q

What does the anion gap distinguish between?

A

Normal and elevated anion gap acidosis

124
Q

What is normal anion gap acidosis?

A

Replacement with HCO3- by Cl-, thus anion gap does not change as sum remains constant

125
Q

How is elevated anion gap resolved?

A

Arises from the increased endogenous acid production

126
Q

What should the PN formula for patient with high output ileostomy be in the context of metabolic acidosis?

A

-Maximum amounts of acetate salts, the acetate will be converted into bicarbonate in the functioning liver

127
Q

What should the PN formula for patient with high output ileostomy be in the context of avoiding refeeding?

A

start at 500 kcal/day, then increase. Correct electrolyte abnormalities before

128
Q

What should the PN formula for patient with high output ileostomy be in the context of ileostomy output?

A

Should be at an isotonic solution 0.9% which is the same as the ileostomy fluid

129
Q

Why are those with high-output ileostomy at risk for acid-base disturbances?

A

Anatomical changes

May require fluid replacement

130
Q

What is metabolic alkalosis characterized by?

A
  • Elevated pH
  • Increase in serum HCO3-
  • Compensatory hypoventilation, increased PCO2
131
Q

How can metabolic alkalosis occur?

A
  • Loss of HCL through vomiting and diarrhea
  • Nasogastric suction
  • Diuretic use
  • Hypokalemia, H+ shifts
132
Q

What is usually required for metabolic alkalosis to occur ?Why?

A

Some degree of renal impairment, as the kidney can usually excrete HCO3-

ASPEN Clin 2 Readings (6 decks)

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