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Pharmacology Test 1 > Fluid Management & Blood Therapy > Flashcards

Fluid Management & Blood Therapy Flashcards

1
Q

How much is TBW of lean body weight?

A

60% of lean body weight

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2
Q

What is ICV of normal body weight?

A

40% body weight (2/3)

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3
Q

What percentage is EVC of TBW?

A

20% body weight (1/3 TBW)

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4
Q

What percent is plasma volume?

A

4% (1/4 of ECV)

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5
Q

What percent is interstitial volume?

A

16% (3/4 of ECV)

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6
Q

How many mL/kh/day necessary for homeostasis for health adult?

A

25-35 mL/kg/day (about 2-3 L)

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7
Q

What is also contained in ECV in small amounts?

A

Trans cellular fluids, CSF, synovial fluid, GI secretions, intraocular fluid

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8
Q

Normal Na in plasma?

A

142 mEq/L

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9
Q

Normal Na in ICF?

A

10 mEq/L

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10
Q

What is ECF Na amount?

A

140 mEq/L

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11
Q

Normal K amount plasma

A

4 mEq/L

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12
Q

Normal K amount intracellular fluid

A

150 mEq/l

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13
Q

Normal K ECF?

A

4.5 mEq/L

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14
Q

Normal Mg plasma?

A

2 mEq/L

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15
Q

Normal Mg intracellular?

A

40 mEq/L

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16
Q

Normal Mg ECF?

A

2 mEq/L

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17
Q

Normal Ca plasma?

A

5 mEq/L

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18
Q

Normal Ca ICF

A

1 mEq/L

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19
Q

Normal Ca ECF?

A

5 mEq/L

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20
Q

Normal Cl Plasma?

A

103 mEq/L

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21
Q

Normal Cl ICF

A

103 mEq/L

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22
Q

Normal Cl ECF?

A

117 mEq/L`

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23
Q

Normal bicarb Plasma?

A

25 mEq/L

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24
Q

Normal Bicab IF?

A

7 mEq/L

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25
Q

Normal Bicarb ECF?

A

28 mEq/L

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26
Q

Primary cation and anion ICF?

A

K (cation), phosphate (anion)

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27
Q

Primary cation and anion ECF?

A

Na (cation), Cl (anion)

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28
Q

Normal range K in plasma?

A

3.5-5.5 mEq/L

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29
Q

What is value for hypokalemia?

A

<3.5 mEq/L

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30
Q

Etiology of hypokalemia?

A 
Poor intake: diet
GI loss (v/d/ NG sxn, kayexalate)
Renal loss: diuretics, metabolic alkalosis, licorice

Intracellular shift: beta2 agonist, insulin, alkalosis

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31
Q

Presentation of hypokalemia?

A

Skeletal muscle cramps–> weakness–> paralysis

Worsens dig toxicity

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32
Q

EKG findings for hypokalemia?

A

PR interval- short
QT- Long
T wave- flat
U wave

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33
Q

How to treat hypokalemia?

A

Potassium supplementation

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34
Q

Etiology of hyperkalemia

A

Poor excretion : renal failure, K sparing diuretics
Extracellular shift: acidosis
Iatrogenic: succ
Misc tumor lysis

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35
Q

Presentation of hyperkalemia?

A

Cardiac rhythm disturbances

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36
Q

Early EKG findings of hyperkalemia

A

PR long, T wave peaked, QT short

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37
Q

Middle stage EKG findings hyperkalemia?

A

P flat, QRS- wide

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38
Q

Late stage EKG findings hyperkalemia?

A

QRS- sine waves–> VF

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39
Q

Treatment for hyperkalemia?

A 
Calcium FIRST to stabilize membrane (does not affect K directdly)
Insulin + D50
Hyperventilation
Bicarbonate
Albuterol
Potassium wasting diuretics
Dialysis
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40
Q

Normal range sodium level blood?

A

135-145 mEq/L

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41
Q

Etiology of hyponatremia

A

SIADH, CHF, cirrhosis, TURP sydrome, cushings

Need to evaluate plasma osm and ECF volume to determine cause

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42
Q

Presentation of hyponatremia

A

N/V
Skeletal muscle weakness
Mental status changes–> seziures–> coma
Cerebral edema (cell SWELLING)

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43
Q

Treatment of hyponatremia?

A

Depends on specific cause. Do slowly to prevent extreme shifts

Restore Na by manipulating serum Osm and fluid balance with H2O restriction

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44
Q

Etiology of hypernatremia?

A

DI, Impaired thirst, NaHCO3 administration

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45
Q

Presentation of hypernatremia?

A 
Thirst
Mental status changes--> sz--> coma
Cerebral dehydration (cell shrinkage)
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46
Q

Treatment hypernatremia?

A

Depends on cause

Goal to restore Na by fluid balance and Na restriction

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47
Q

Normal range Ca in blood?

A

8.5 mg/dL- 10.5 mg/dL

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48
Q

Etiology of hypocalcemia?

A 
Hypoparathyroidism ( i.e. parathyroidectomy)
Vitamin D def.
Renal osteodystrophy
Pancreatitis
Sepsis

Blood product adminEtio

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49
Q

Presentation of hypocalcemia?

A

Skeletal muscle cramps
Nerve irritability– paresthesia and tetany (circumferential numbness/tingling)
Chvostek sign (tap face and twitch)
Trousseua sign (carpal spasm with BP cuff on)
Laryngospasm
Mental status changes–> sz

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50
Q

EKG findings of hypocalcemia?

A

QT LONG

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51
Q

Treatment of hypocalcemia?

A

Admin calcium

Vit D

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52
Q

Etiology hypercalcemia

A 
Hyperparathyroidism
Ca
Thyrotoxicosis
Thiazide diuretics
Immobilization
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53
Q

Presentation of Hypercalcemia

A 
nausea
ABD pain
HTN
Psychosis
Mental status changes
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54
Q

EKG findings hypercalcemia

A

QT SHORT

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55
Q

Treatment of hypercalcemia

A

NS, furosemide

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56
Q

Normal range of Mg in blood?

A

1.3-2.5 mEq/L

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57
Q

Etiology hypomagensimia?

A 
poor intake
Alcohol abuse
Diuretics
Critical illness
Commonly occurs with hypokalemia
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58
Q

Presentation of hypomagnesemia?

A

Skeletal muscle weakness

Arrythmia (torsade to pointes)

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59
Q

EKG findings of hypomagnesemia?

A

Not very significant unless very low, then long QT

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60
Q

Treatment hypomagnesemia?

A

Mg sulfate

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61
Q

Etiology hypermagnesemia?

A

Excessive admin (iatrogenic)
Renal failure
Adrenal insufficiency

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62
Q

When do you lose deep tendon reflexes in hypermagnesemia?

A

4-6.5 mEq/L or 10-12 mg/dL

lower levels of hypermagnesemia

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63
Q

When do you see respiratory depression in hypermagnesemia?

A

6.5-7.5 mEq/L or >18 mg/dL

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64
Q

When do you see cardiac arrest in hypermagnesemia?

A

> 10 mEq/L or >25 mg/dL

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65
Q

Treatment for hypermagnesemia?

A

Calcium chloride

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66
Q

How is interstitial fluid pressure relative to atmospheric pressure?

A

Negative; believed to be due to contraction of lymphatic vessels

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67
Q

How does plasma communicate with interstiital fluid?

A

Capillary pores

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68
Q

What dictates fluid movement?

A

Osmotic forces and hydrostatic pressure

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69
Q

What is most important oncotically active constituent of ECF?

A

Albumin

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70
Q

What favors filtration of fluid into interstitial space?

A

Increases in capillary hydrostatic pressure and interstitial oncotic pressure

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71
Q

What favors absorption of fluid into intravascular space?

A

Increase in interstitial fluid hydrostatic pressure and plasma oncotic pressure.

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72
Q

What accounts for small amount of fluid diff b/w arteries and venous ends of capillary?

A

Lymph vessels absorb some fluid

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73
Q

What is the sum of filtration and absorption?

A

Net filtration pressure (NFP)

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74
Q

What is main determinant of extracellular osmotic pressure?

A

Na

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75
Q

What is main determinant of intracellular osmotic pressure?

A

K

76
Q

What does positive net filtration favor?

A

Fluid exudation into tissue

77
Q

What does negative net filtration favor?

A

Fluid absorption into vasculature

78
Q

How much intravascular volume is constantly filtered into interstitial space?

A

2mL/min; returned to intravascular system via lympatic system

79
Q

What is endothelial glycocalyx?

A

Gel layer in capillary epithelium that creates physiologically active barrier within vascular space.
-Creates barrier between vessel and blood

  • Plays role in transcapillary fluid excahnge, microcirculatory flow, blood component rheology, plasma oncotic pressure, signal transduction, immune modulation and vascular tone (GEEZ)
  • Composed glycoproteins, polysaccharides, hyaluronic acid
80
Q

How does EGL preserve oncotic pressure and decrease capillary permeability to water?

A

Binds to circulating plasma albumin

81
Q

What is also contained in EGL?

A

inflammatory mediators, free radical scavenging, activation of anticoag factors

82
Q

What can destory EGL?

A

Hyperglycemia

Stress, critical illness

83
Q

How does EGL contribute to laminar blood flow?

A

dyanmic barrier repels negatively charged polar compounds in addition to blood components.

-This prevents blood component adhesion to vascular wall

84
Q

What are some neurohormonal influences in fluid dynamics (general overview)

A

RAAS- reabsoprtion of sodium and water
ADH- hold onto water
ANP– inhibit renin and ADH when atria stretch receptors stimulated

85
Q

Why might intraoperative UOP not be a good indicator of fluid status?

A

Stress causes increase in ADH
- Increased abd pressure from lap surgery can also release ADH

May see abrupt drop in UOP even in health, euvolemic patients

86
Q

Normal pH ABG

A

7.35-7.45

87
Q

Normal CO2 ABG

A

35-45

88
Q

Normal bicarb ABG

A

22-26

89
Q

Cardiac effects acidosis?

A

Increased p50 (right release o2)
Decreased contractility
Increased SNS tone
Increased risk of dysrhythmia

90
Q

CNS effect of acidosis?

A

Increased CBF

Increased ICP

91
Q

Pulmonary effects acidosis?

A

Increased PVR

92
Q

Other effect acidosis?

A

Hyperkalemia

93
Q

Cardiac effects of alkalosis?

A

Decreased p50 (left= love, holding onto o2)
Decreased coronary blood flow
Increased risk dysrhythmia

94
Q

CNS Effect alkalosis

A

Decreased CBF

Decreased ICP

95
Q

Other effects alkalosis?

A

Hypokalemia

Decreased ionized calcium

96
Q

What do we use hypotonic solutions for?

A

Replaces water loss
called MAINTENANCE fluids
ex: D5W

97
Q

What do we use iotonic? What Osm is considered isotonic?

A

REPLACEMENT fluids
Replaces water and electrolyte loss

Ex: LR, NS

(275-295 mOsm/L)

98
Q

What do we use hypertonic fluids for?

A

Hyponatremia, shocks

D5 1/2NS (405 mOsm/L) , 3% NS (1026 mOSM/L)

99
Q

Why might crystalloids be preferred for fluid restoration?

A
  • Lack of allergenic potential
  • Ease of metabolism and renal clearance (compared to colloids)
  • Preservation of electolyte balance despite active intraoperative plasma losses
100
Q

What is consequence of low molecular weight of crystalloid?

A

Crystalloid solutions contribute to hemodilution of plasma proteins and loss of capillary oncotic pressure. This causes filtration of 75-80% of volumes into interstitial space.

Ability of crystalloids to expand plasma volume is transient

101
Q

What are hypotnic solutions and their osmolarity?

A

NaCl 0.45%- 154

D5W- 253

102
Q

What are isotonic solutions (crystalloid and colloid) and OsM

A

NaCl 0.9%- 308
LR- 273
Plasmalyte A- 294

Colloids:
- Albumin 5%- 300
Voluven 6%- 296
Hespan 6%- 309

103
Q

What are hypertonic solutions and Osm

A 
Crys:
NaCl 3%- 1026
D5 NaCl 0.9%- 560
D5 NaCl 0.45%- 405
D5 LR- 525

Colloid:
Dextran 10%- 350

104
Q

Which solutions will cause cells to swell?

A

Hypotonic

105
Q

Which solutions cause cell to shrink?

A

Hypertonic

106
Q

What is plasmalyte/normosl/isolyte composed of? OsM?

A

Na, K, Cl, phosphat,e Mg, acetate, gluonate

OsM- 294-295

107
Q

What is LR composed of? OsM?

A 
Na
K
Cl
Calcium
Lactate
OSM- 275
108
Q

What is 0.9% NS composed of? OsM

A

Na, Cl

Osm- 310

109
Q

What crystalloids cannot be used with blood products?

A

Anything with Ca (LR)

110
Q

Which crystalloids can be used to admin blood products?

A

Plasamalyte, NS

111
Q

Key points for NS?

A

Isotonic (308 mOsM/L) (but least physiologic)

  • in large volumes, can increase Cl content in blood. Causes hyperchloremic acidosis
  • Typical solution for diluting PRBC
112
Q

Hazrds with NS?

A
  • Hyperchloremic acidosis- high amount of Cl contribute to acid-base imbalance
  • Studies show does-dependent association with renal impairment and postop bowel dysmotility- effects more pronounced in pt with preexisting renal dx
113
Q

Key points LR?

A
  • NS with electolyes (K, Ca) and buffer (lactate)
  • 273 mOsM/L, provides 100 cc free water/L, tends to lower Na
  • Considered isotonic but actually slightly hypotonic
  • Lactate can convert to bicarb, cause slight met. alkalosis
114
Q

Cautions of LR?

A

Limit in ESRD since contains K
Avoid large volume in diabetic
-byproduct of hepatic metabolism of lactate is gluconeogenic\

-Don’t mix with prbc

115
Q

When is LR contraindicated?

A

Patient with TBI or other neurovascular insults.

Avoid use in any pt at increased risk for cerebral edema

116
Q

Which is more effective in preserving intravascular volume, LR or NS?

A

LR

117
Q

Key points D5W?

A

Hypotonic 260mOsM/L
- little place perioperatively (except neonates and pt receiving IV insulin)
Provides 170-200 cal/L

118
Q

Caution in D5W?

A

Free water intoxication

hyponatremia

119
Q

Key points 3% and 5%

A

3% Na/Cl 513 mEq
5% 856 mEq

Used for low volume resuscitation(rarely)
Main use os txmt of hyponatremia

120
Q

Risk of 3% and 5%

A 
Hyperchloremia, hypernatremia
Cellular dehydration (generally wanted in head-injured pt)
121
Q

What can happen if hypertonic solution infused too fast?

A

Sudden fluid shifts into intravascular space can cause dehydration of neural cells leading to osmotic demyelination syndrome

122
Q

Half life of colloid solutions?

A

In circulation 16 hours but can be 2-3 hours

123
Q

How do colloid solutions produce volume expansion?

A

Increasing plasma oncotic pressure and interacting with endothelial glycocalyx to decrease transcapillary filtration

124
Q

What is only naturally occuring colloid solution available?

A

Albumin

125
Q

What is dextran?

A

Synthetic colloid solution made from bacterial metabolism of sucrose. Hyperosmolar

1/2 life 6-12 hours
Largely abondoned use

126
Q

Side effects dextran?

A

ACUTE RENAL FAILUR

  • Anaphylactoid rection
  • PLT inhibition (was used to small antithrombotic effects)
  • Noncardic pulmonary edema
  • Interference with crossmatching from biding to RBC and changing morphology
127
Q

What is hespan?

A

-Synthetically derived form starchy plants (potatoes)

128
Q

Side effects hespan?

A
  • Huge allergy risk
  • Coaguloathy
  • Pruritis
  • BLACK BOX for nephrotoxicity

MAX DOSE <20 mL/kg/day<

129
Q

What is difference between different generations of synthetic collods?

A

Molecular weight gets lighter. Lighter molecular weight has slightly less side effects

130
Q

What is albumin?

A

Colloid derived from pooled human plasma

- heat treated to eliminate risk of disease transmission

131
Q

What is critical to consider when considering administering albumin?

A

If EGL is intact or not. Only increase in pulmonary edem and end-organ complications with damaged EGL.

Colloid solutions should be avoided in patient with hyperglycemia or sepsis. Cochrane review”Cannot justify cost in crtiically ill patient.” However, use of albumin in small allotments is warranted in goal-directed admin in volume-responsive patients

132
Q

Propoenents of crystalloids say…

A
  • cryst equally as effective as colloid in restoring intravascular volume
  • support u/o better
  • less likely to cause pulmonary edema
  • inexpensive
133
Q

Proponents of colloids say…

A
  • prolonged increase in plasma volume by maintaining plasma oncotic pressure
  • half life 3-5 hr colloid vs 20-30 min cryst
  • fluid of choice with hypoporteinemia
  • less tissue edema
  • less volume infused
134
Q

What is impact on vascular flow and organ perfusion during surgery and anesthesia

A
  • Stress activates hypothalamus-pituitary release cortisol
  • release of catecholamines- increased HR, increased SVR, vasoconstriction, release ADH, reabsoprtion water

-Damages EGL, and impairs wound healing, contributes to osmotic diuresis

135
Q

Why are historical intraoperative fluid management requirements antiquated?

A
  • Leads to substantial disruption of EGL and leads to pathologic fluid overload
136
Q

What are the 4 step components of traiditonal fluid replacment?

A

1) Find baseline maintenance (wt- 20 )+60= ?mL/hr

2) Find fasting NPO def (maintenance dose from #1 x hours NPO)
replace 1/2 in 1st hour
replace 1/4 in 2nd
replace 1/4 in 3rd hr

3) Replacement of blood loss (starts hours 2)
3: 1 crystalloid of 1:1 colloid

4) evaporative losses (based on invasiveness sx)

137
Q

What is formula for fluid replacmeent?

A

Holiday-Segar 4:2:1
<10 kg- 4mL/kg
11-20kg 40 + next 10kg@ 2mL/kg
>20 60 mL +anything over 20kg @1mL/kg

Quick way wt-20 + 60

138
Q

When should you treat fluid deficit from preop NPo status

A

If prolonged i.e. kid vomiting 3 days prior to intussiception sx

139
Q

How is NPo deficit replaced in sx?

A

1/2 in 1st hour
1/4 in 2nd hour
1/4 in 3rd hr

140
Q

How much blood can soaked gauze hold (4x4)

A

10 cc

141
Q

HOw much can soak lap pads hold?

A

100-150 cc blood

142
Q

How do you find estimated blood volume in adults?

A

70 mL/kg

Wt * 70= EBV in adults

143
Q

How do you find allowable blood loss?

A

EBV x (starting hgb-target hgb)/ starting hgb

Can replace HGB with HCT and find target HCT for transfusion

144
Q

What is evaporative loss for superficial trauma (simple sx)

A

1-2 mL/kg/hr

145
Q

Evaporative estimate for minimal trauma (minor sx)

A

2-4 mL/kg/hr

146
Q

Evaporative loss for moderate trauma (non major abd sx, lap sx)

A

4-6 mL/kg/hr

147
Q

Evaporative loss for major surgery?

A

6-8mL/kg/hr

148
Q

What is ratio for blood loss replacement?

A

3: 1 crystalloid
1: 1 colloid

149
Q

What is ERAS and goal directed fluid therapy (GDFT)

A

“Utilize individualized hemodynamic end points to support oxygen transport blanace by minimizing oxygen demand and optimnizing CO, tissue oxygenation, capillary and macrovascular flow, oxygen and nutrient deliver, end organ perfusion”

  • MAP , CVP, UOP do not have good predictive value for fluid responsiveness
150
Q

Consequences of too little volume resus?

A 
Hypovolemia
Decreased O2 delivery
Decreased organ perfusion
Hemoconcentration (increased blood viscosity)
MI
Renal impairment
PONV
151
Q

Too much volume resus consequences?

A 
Hypervolemia
Decreased O2 deliver (microvascular congestion)
IMpaired glycocalyx
Hemodilution (hgb, coag factors, plasma proteins)
impaired wound healing
increased extravascular lung water
VAP
ABD compartment syndrome
liver congestion
152
Q

At what point on frank starling curve will patient be responive to fluid?

A

Steep slope

153
Q

At the plateau of frank starling curve, will pt be fluid responsive?

A

No

154
Q

What is frank starling curve based on?

A

Length-tension relationship of sarcomeres

155
Q

What is preload dependence?

A

When patient is on lower-end of frank starling curve and needs more sarcomere stretch in order to achieve more contraction

Sarcomeres are too tight together, need more volume to “stretch” sarcomeres and allow stronger contraction

156
Q

What is preload independence?

A

Plateau of frank starling curve that suggest optimal balance between ciruclating volume and myocardial performance.

  • additional fluids would not improve hemodynamics or oxygen delivery
157
Q

What is overshoot on frank starling curve?

A

Impaired myocardial performance, placing pt at risk of pulmonary edema and CHF

158
Q

Where do we want our patients to stay in frank starling curve?

A

Top left quadrant= “safe quadrant”

159
Q

How is pulse contour analysis used for GDFT?

A

<9% SVV non responsive to fluid
9-13%- gray zone
>13% responsive to fluid

160
Q

Hemodynamic factors to guide GDFT?

A

Dilution techniques- thermodilution (invasive)
Pulse contour
ECHO, TEE (gold standard)
Tissue oxygenation

161
Q

When are pulse contour readings inaccurate?

A
  • Spontaneous ventilation
  • Small TV <8mL/kg
  • Open chest
  • Sustained arrhyhtmia
  • High level PEEP
  • Right heart dysfunction

May be able to trend, but can’t take absolute value

162
Q

Goal Directed Fluid protocls want what preop, intraop and postop?

A

Preop- limit NPO time (2hr clear liquid)

Intraop- baseline assessment of target hemodynamic. Small boluses to assess responsiveness
vasopressors and inotropes as needed

Post op- quick discontinuation of IV fluids and encouraging PO intake

163
Q

Recommendation for transfusion based on HGB?

A

> 10 g/dL- not recommended
<6 always recommended

6-10- depends on patients risk for complication and inadequate oxygenation

Single transfusion trigger not recommended

164
Q

What is purpose of crossmatch?

A

Evaluate patient’s blood response to specific unit of blood

165
Q

How much will 1 unit increase hgb/hct

A

Increase Hgb 1 gm/dL
HCT 2-3%

HCT 65-70%/unit

166
Q

What preservatives are in PRBC?

A

Citrate
Dextrose (substrate for glycolysis)
Phosphate (buffers combats acidosis)
Adenine (helps RBC synthesize ATP)

167
Q

What is citrate toxicity?

A

Causes hypocalcemia

Monitor ionized Ca

168
Q

Universal donor, recipient?

A

O- donor

AB+ recipient

169
Q

What does irradiation of PRBC prevent?

A

Graft vs host dx

170
Q

What does leukocyte reduced blood do?

A

Decrease rate of complications and HLA alloimmunization

171
Q

When do we see more complications with blood storage?

A

> 14 DAYS

We start to see:
- decrease 2,3 DPG
- Depletion ATP
-oxidative damage
-Increased adhesion to human vascular endothelium
- acidosis
-altered morphologyRBC
-hyperkalemia
- absence viable plt
-absence factor V and VIII
hemokylsis
172
Q

Potential complications of autologous blood transfusion?

A
  • Anemia
  • Preop MI
  • Admin wrong unit
  • Need for more frequent blood transfusion
  • febrile/allergic reaction
173
Q

When can we not use cell save

A

Sx with wounds with bacteria, amniotic fluid, malignant cells or patient with sepsis, chemical contaminants

174
Q

What is acute normovolemic hemodilution?

A

Remove blood from pt

  • Replace BV with crystalloid/colloid
  • After sx blood loss slowed/stopped, blood transfused back to pt
175
Q

What composes bag of platelets?

A

Either multi donor pooling (6-10)

or single donor aphersis units<

176
Q

Shelf life plt?

A

5 days

HIGH bacterial contamination risk 1:12,000

177
Q

How much should PLT increase after transfusion?

A

7,000-10,000 one hour after transfusion

178
Q

Uses for plt?

A
  • Thrombocytopenia
  • Dysfunctional plt
  • Active bleeding
  • PLT count <50,000 for low, mod risk
  • Plt count <100,000 for high risk
179
Q

What is contained in FFP?

A

Clotting factors (no plt)

180
Q

How long can we store FFP?

A

Frozen for up to 1 yr

181
Q

Volume of FFP?

A

200-250 CC

182
Q

Use of FFP?

A
  • Reversal warfarin
  • Known coag factor deficiency
  • microvascular bleed in presence of increased PT or PTT
183
Q

What is cryoprecipitate?

A

Derived from precipitate remaining after FFP thawed

184
Q

What does cryo contain?

A

Factor VIII

  • XIII
  • Fibrinogen
  • von willebrand
  • plasma
  • fibronectin
185
Q

Most common risk of transfuion?

A

CMV 1-3% of transfusions

186
Q

Risk for TRALI? Product at highest risk?

A

1:8000

FFP/PLT highest risk

Pharmacology Test 1 (3 decks)

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