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Fluids, coags, transfusions > Apex- fluids, lytes, acid-base > Flashcards

Apex- fluids, lytes, acid-base Flashcards

1
Q

How many L of total body water in a 70kg person

what’s the equation to remember

A

42L

60/40/20 (15/5)

60% TBW = 42L

40% ICV = 28L (40% x 70kg = 28L)
20% ECV= 14L

15% of ECV is intersistal fluid - 11L
5% of ECV is plasma - 3L

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2
Q

Major intracellular (3) vs extracellular (4) ions

A

intracellular = K, Mag, Phosphate
extracellular = Na, CA, Cl, HCO3-

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3
Q

What populations have the highest TBW (1)
vs lowest TBW (3)

A

Highest = neonates
Lowest = olds, fats, females

Think low muscle mass = less body water = less total body water

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4
Q

What forms a protective layer on the interior wall of the blood vessel

what happens when this is disrupted and what could distrupt it

A

glycocalyx

disruption > capillary leak (sepsis)

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5
Q

What does the lymphatic system do?

A

It pretty much filters out proteins, fluids, bacteria, and debris that have entered the intersistium (fluid filled space between structures such as cell membranes)

takes the extra fluid thats lost in the capillary exchange going on in the tissue and mops it up and returns it to the lymphatic ducts

-returns about 3L/day of fblood fluid per day to your ciruclatory system; without it functioning well, all that fluid is going to be outside the vasculature and in the interestial spaces
>swelling, hypotension

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6
Q

How does staph from your skin get into your blood stream from a scrape - outside of direct exposure to vessels

A

tissue is full of intersistal fluid that drains into your lymphatics which then drain to your heart

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7
Q

What is lymph?

how does it get cleared out from the tissues?

A

it’s essentally plamsa that leaks out of the capillaries

-see your circulatory system is a pressurized system, so everytime blood circulates through the capillaries, the capillaries have small holes in them that plasma (ECF) will leak out of the vessels and into the surrounding tissues

-small holes allows for larger molecules to get into the cells that are too big to diffuse through the walls of the capillaries like o2 and co2 can (like nutrients such as glucose from the RBCs and other waste products like nitrogen to get back into the vessels)

there are lymph vessels that clear it from the tissues

-build up of lymph fluid in the tissues, compresses the lymphatic vessels which have pressurized valves that open once lymph reaches a certain presssure in the tissues, then gets forced into the lymphatic vessels ; then when the pressure accumulates inside, it forces the valves shut and it cant escape back out

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8
Q

jobs of lymphatic system

A
  1. clears lymph from tissues and gets it back into the circulatory system via the veins
  2. immunity- lymph nodes serve as check points throughout the lymphatic system that will filter out any bacteria that may be in the lymph so it’s not deposited into your bloodstream
  3. transfers fat - carbs and proteins can leave the intestines and enter the capillaries; but fat cannot, the lymph picks it up and drops it off into the blood stream

your lymphnodes get big as an early sign of infection because once it has bacteria , it recruits RBCs to those lymph nodes to help destroy the bacteria

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9
Q

which pushes vs pulls fluid: onctoic vs hydrostatic

A

hydrostatic PUSHES fluid out
oncotic PULLS fluid in

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10
Q

The intracellular compartment is what % plasma and what % blood?

what is hematocrit?

what increases/decreases it?

A

60% plasma , 40% blood

the fraction of blood volume that is occupied by erythrocytes

increased hct = increased # of RBCs (chronic hypoxia) or decreased plasma volume (dehydration)
decreased hct = decreased # RBCs (anemia) or increased plasma volume (hemodilution)

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11
Q

Where is the thoracic duct?

A

at the juncture of the internal jugular vein and subclavian veins

*left = larger (risk of chylothorax during left IJ placement)

thoracic duct is where lymph is returned to venous circulation

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12
Q

What is fluid that accumulates in a potential space called?

A

an effusion

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13
Q

Label

A
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14
Q

Osmolarity vs Osmolality

A

OsmolaRity = # of osmoles per liteR of a solution
Osmolality- # of osmoles per kg of a solution

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15
Q

What is osmosis

A

the movement of water across a semipermeable membrane

not solute

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16
Q

T/F- osmotic pressure is a function of molecular weights

A

false - it’s a function of the number of osmotically active particles in a solution

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17
Q

Calculate the plasma osmolarity:

Sodium= 150 mEq/L
Glucose = 108g/dL
BUN= 14mg/dL

A

311 mOsm/L

(NA+ x 2) + (Glucose/18) + (BUN/2.8)

so youre adding everything
just remember
NA x 2
Glucose / 18
BUN / 2.8

*from the image you can see sodium is most important determinant and that hyperglycemia nad uremia can also increase the plasma os

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18
Q

Normal Plasma osmolarity

A

280-290 mOsm/L

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19
Q

What is the most important determinant of plasama osmolarity

A

Sodium

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20
Q

3 conditions that increase plasma osmolarity

A

hypernatremia, hyperglycemia, uremia

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21
Q

Rank the tonicity for each fluid, 1 being highest and 4 being lowest:

Albumin 5%
D5 0.45%
D5W
NaCl 3%

A
  1. NaCl3%
  2. D5 0.45%NS
  3. Albumin 5%
  4. D5W
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22
Q

Hypo (2) vs Iso (3) vs hypertonic solutions (4)

A

Hypotonic - lower osmolarity than plasma/cells (cells swell)
→ D5W & NaCl 0.45%

Isotonic- similar osmolarity to plasma/cells (no change)
→ 0.9% NaCl, LR, Plasmalyte

Hypertonic- higher os than plasma/cells
→ 3%NaCl, D5NS, D51/2NS, D5LR

so pretty much the only hypotonic ones are D5W and 0.45%NaCl by themselves
-add them together and its hypertonic

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23
Q

T/F: Albumin 5%, Voluven 6%, and Hespan 6% are all isotonic solutions

A

True

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24
Q

T/F: Dextran 10% is considered hypertonic

A

True

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25
Q

How long to crystalloids tend to remain in the intravascular space?

A

for ~ 30 minutes

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26
Q

Why is LR a better choice for large volume resussitation over NS?

A

bc NS can cause hyperchloremic metabolic acidosis if given in large amounts

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27
Q

What happens with the lactate in LR?

A

it’s converted to bicarb by the liver and kidneys and acts as a buffer to reduce the risk of metabolic acidosis .

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28
Q

Is it okay to give LR with blood? why or why not

A

yes

it used to be avoided due to the calcium content but clinical research shows that LR can be used safely when rapidly transfusing PRBCs

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29
Q

Hetastarch dose should not exceed what?

A

20ml/kg

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30
Q

True or false: Albumin causes hypocalcemia

A

True

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31
Q

True or false: Dextran increases blood viscosity

A

false - reduces blood viscosity

interesting…

it can improve microcirculatory flow during some vascular surgeries

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32
Q

T/F- albumin has pro-inflammatory properties

A

false- anti-inflammatory

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33
Q

when comparing colloids to crystalloids, which outcomes are shown to be better

A

both are the same

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34
Q

How long do crystalloids vs colloids expand plasma volume for?

A

crystalloids = 20-30 mins
colloids 3-6hrs

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35
Q

true or false- colloids have anti-inflammatory effects

A

true

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36
Q

downside to albumin

A

it binds calcium and can cause hypocalcemia

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37
Q

black box warning on Dextran 40

A

risk of renal injury

Coagulopathy & Anaphylaxis
(Dextran > Hetastartch > Hextend)

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38
Q

Which synthetic colloids is coaulopathy not an issue with?

A

volvulen

dont have to worry about keeping below a rate of 20ml/kg

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39
Q

max dose of dextran/hetastartch/hextend?

A

20ml/kg

risk of coagulopathy

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40
Q

how does NSS create a hyperchloremic metabolic acidosis?

A

high chloride load tells kidneys to get rid of bicarb

(too much Cl - ; kidney gets rid of HCO3 - )

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41
Q

True or false- Albumin does not contain antibodies or increase the risk of infectious disease transmission

A

True

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42
Q

Normal Serum K

A

3.5-5.5meq/L

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43
Q

What is the most abundant intracellular cation?

A

Potassium

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44
Q

Which hyperpolarizes cell membranes vs depolarizes them?

Hypo vs Hyperkalemia

A

Hypokalemia - hyperpolarizes them
Hyperkalemia- depolarizes them

okay so theink with hypokalemia there is less K in the blood, this creates a wider potassium gradient which is going to cause more K to seep outside of the cell and into the ECF, making the inside of the cell more negative

with hyperkalemia, there is more K in the ECF, creating LESS of a gradient, so less K is going to leak out of the cell, making the inside of the cell more positive and more easier to depolarize

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45
Q

What is the most important regulator of potassium homeostasis?

A

the kidney

*explains why renal failure and decreased GFR, increases seum K

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46
Q

etiologies of hyperkalemia (general categories 5)

A
  1. pseudohyperkalemia (hemolysis of lab specimen)
  2. increased intake (diet)
  3. reduced clearance (renal failure)
  4. cellular injury (tumor lysis syndrome)
  5. transcellular shift (acidosis)
47
Q

How is the PR effected with potassium disturbances?

what about Calcium?

A

↓K = long PR

(P wave flattens and PR prolonges once K hits 6.5-7.5 range)

Hypocalemia = short PR (long QT- spreads out)
Hypercalcemia = long PR (short QT-quick and efficient)

48
Q

How do serum K levels affect the T-wave?

A

hypokalemia = flat
5.5-6.5 = peaked
6.5-7.5 = flat again (+prolonged PR)

49
Q

At what K levels would you see QRS prolongation

A

7-8

50
Q

Does hypokalemia or hyperkalemia worsen dig toxicity?

A

hypokalemia

51
Q

What is the most common electrolyte disorder in clinical practice?

A

hypokalemia

52
Q

Potassium rate of administration through a peripheral line vs central line?

A

peripheral line = 10meq/hr
central line = 20meq/hr

53
Q

if you have a 20meq K-rider in 100ccs - how fast can you give it through a central line vs peripheral line?

(dose and volume)

what if its 40 in 250?

A

centrally - 100ccs/hr (20meq in 1hr)
peripherally - 50ccs/hr (10meq/hr x 2 hours)

centrally 40 in 250 can be given over 2 hours (125mls/hr)

peripherally over 4 hours (62.5ml/hr)

54
Q

When administering 3% hypertonic saline for hyponatremia, the serum NA level shouldnt be permitted to increase faster than how many mEq/L

A

1-2mEq/L/hr

55
Q

Someone asks you what’s the big deal with giving hypertonic saline that they have to be monitored closely for?

A

if the fluid shifts from ICF to ECF too quickly, it can cause this central pontine myelinolysis

56
Q

what happens if you treat hypernatremia too quickly?

A

fluid can shift from the ECF to the ICF and cause cerebral edema

57
Q

What is the most abundant extracellular cation?

A

Sodium

58
Q

You should consider delaying surgery is the serum sodium is less than what?

A

130meq/L

59
Q

T/F- the symptoms of hypernatremia are based on serum sodium levels

A

false- serum os levles

60
Q

Normal serum os

A

275-295

61
Q

T/F- acidosis increases ionized calcium levels

A

true

*Albumin binds calcium; however, In the setting of acidosis, albumin binds H+ ions, which displaces calcium into the plasma

just remember often when acidosis resolves, you are repleating calcium as it falls

62
Q

Calcium is what factor in the coagulation cascade?

A

4

63
Q

Normal total calcium levels vs ionized

A

total = 8.5-10.5mg/dL
Ionized = 4.65-5.28

(think ionized is around 5- you could prob even get away with remembering ~ 4.5 to 5.5 - which is what the normal total calcium is in mEq/L)

64
Q

PTH (raises/lowers) serum CA, calcitonin (raises/lowers) serum CA

A

PTH- increases
calcitonin lowers

  1. osteoclast activity is inhibited (bone wont release calcium into blood)
  2. tells kidney to decrease caclium reabsorption
65
Q

Primary treatment for hypercalcemia (2)

A

IVF (0.9%NaCl) + a loop diuretic

66
Q

Primary treatment for mag toxicity and why

A

Calcium bc it antagonizes mag at the NMJ

67
Q

Calcium - what % of it is ionized, bound to albumin, and bound with an anion?

A

50% ionized
50% bound: 40% to albumin, 10% with an anion

68
Q

What is the most abundant electrolyte in the body?

A

Calcium

69
Q

How does acid-base balance affect ionized calcium levels?

A

acidosis inccreases ionized calcium (albumin will bind H+ ions and dispalce calcium into blood)

alkalosis decreasis ionized calcium levels (binds more Ca+ to displace more H+ ions into the plasma)

70
Q

What is PTH released by and when?

what happens when it’s released?

A

PTH is released by the ParaTHyroid glands in response to hypocalcemia to increase calcium levels

  1. activate osteoclasts to release calcium from bone
  2. tells kidneys to reabsorb calcium
  3. increases vitamin D synthesis > increased calcium absorption from the small intestines
71
Q

What releases calcitonin and when?

what happens when it’s released

A

thyroid releases calcitonin when high levels of calcium are detected in the blood

72
Q

Why do you need to take both calcium AND vitamin D supplements?

A

bc viamin D is necessary to absorb the calcium from the gut

73
Q

Chvostek Sign

what does it indicate

A

tap on the angle of the jaw
(facial nerve/masseter muscle) –> ipsilateral facial contraction

hypocalcemia

74
Q

Trousseau’s sign

what does it indicate

A

BP cuff on upper extrem for 3 mins; the decreased blood flow will enhance neuromuscular irritability resulting in muscle spasms of forearm and hand

75
Q

Normal mag levels in mg/dL vs mEq/L

A

1.8-2.5mg/dL

1.5-3mEq/L

76
Q

What antagonizes the effects of calcium?

A

Magnesium

77
Q

4 clinical uses for magnesium

A
  1. pre-eclampsia
  2. opioid sparing techniques
  3. acute bronchospasm
  4. cardiac rhythm distrubances (torsaddes)

  1. 4g bolus for 10-15 mins then 1g/hr x 24 hrs
  2. antagonizes NMDA receptor
  3. antagonizes calcium
78
Q

What symptoms are seen at a mag < 1.2mg/dL (3)

what about 1.2-1.8 (3)

A

tetany, seizures, dysrhythmias

hypokalemia
hypcalcemia
neuromuscular irritability

79
Q

mag level where you’d see diminished vs loss of DTR’s

A

diminished 5-7
loss 7-12

80
Q

Signs of hypermagneisa dont typically present until what level

A

5-7

81
Q

When would respiratory and apnea be seen - at a mag level of what

A

> 12mg/dL

+CHB, cardiac arrest, coma, paralysis

82
Q

What 3 other things would you likely see if somone has loss of DTRs

what mag level

A

hypotension
EKG changes
somnolence

7-12mg/dL

83
Q

What 3 other things would you likely see if somone has loss of DTRs

what mag level

A

hypotension
EKG changes
somnolence

7-12mg/dL

84
Q

what should you be thinking about for a pre-eclamptic mom on a mag drip and your anesthetic?

A

if it’s a crash section- mag can potentiate both sux and NDMRs

85
Q

Does hypermagensemia potentiate sux or NDMRs?

A

both

86
Q

How is acid-base and potassium related?

A

H+ is transported into the cells
K+ is transported out of the cells

increased H+ (acidosis) → increased H+ going into cells → increased K+ coming out of cells → hyperkalemia

decreased H+ (alkalosis/hypervent) → less H+ going into cells → less K coming out of cells → hypokalemia

87
Q

Normal anion gap

how to claculate it

A

8-12meq/L

NA - (Cl + HCO3)

88
Q

Mneumonic for anion gap metabolic acidosis

gap > what

whats the mneumonic for non-anion gap

A

MUDPILES
Methanol
Uremia
DKA
Paraldehyde
Isoniazid
Lactate (sepsis, cyanide)
Ethanol
Salicylates (inhibits krebs cycle)

> 12

HARDUP

89
Q

Mneumonic for non-anion gap metabolic acidosis

gap of what

whats the mneumonic for anion gap acidosis?

A

HARDUP
Hypoaldosteronism
Acetazolamide
Renal tubular acidosis
Diarrhea
Uterosigmoid fistula
Pancreatic fistula

8-12meq/L

MUDPILES

90
Q

Mechanical ventilation is indicated with respiratory acidosis with a pH of less than what?

A

7.20

91
Q

3 general eitiologies of respiratory acidosis

A
  1. increased co2 production
  2. decreased co2 elemination
  3. rebreathing

1 → sepsis, MH, thyroid storm
2 → airway obstruction, COPD, opioid OD
3 → incompenent unidirectional valve, exhausted soda lime

92
Q

In acute respiratory acidosis, for every 10mmHg increase in PaCO2, how much does pH decrease by?

what about for chornic respiratory acidosis?

A

0.08 (respiratory quotient)

0.03

93
Q

Where in the body does CO2 have an opposite effect compared to the vasodilation in the periphery?

A

pulmonary vasculature - co2 = vasoconstriction

94
Q

most common cause of respiratory alkalosis vs acidosis

A

acidosis = hypoventilation
alkalosis = iatrogenic (mechanical ventilation)

95
Q

3 things that can lead to metabolic acidosis

A
  1. accumulation of NONvolatile acids
  2. loss of bicarbonate
  3. large volume resussitation with NaCl
96
Q

3 situations that can lead to metabolic alkalosis

A
  1. increased bicarbonate (iatrogenic)
  2. loss of nonvalatile acids (vomitting/ngt)
  3. increased mineralocorticoid activity (Cushing syndome)

Cushing syndrome = being crushed by ACTH
-increased aldosterone = increased NA+, decreaed K and loss of H+ ions

97
Q

3 things that could be used to treat metabolic alkalosis

A
  1. acetazolamide
  2. spironolactone
  3. dialysis

  1. carbonic anhydrase inhibitor - increases renal excretion of bicarb
  2. mineralocorticoid antagonist (decreases sodium, increases reabsorption of K and H ions)
98
Q

T/F- preoperative fasting causes dehydration

A

false- more recently it has been shown that intravascular fluid volume is minimally affected

99
Q

T/F: third spaces loses aren’t as much as we once thought they were

A

true- likely are overloading patients as a result

100
Q

What’s the fundamental objective of goal-directed fluid therapy?

A

optimizing oxygen delivery to the tissues by means of optimizing patients position on the Frank Starling curve

101
Q

Key principle of goal-directed fluid therapy (act)

A

administering 200-250mls to determine preload dependence or independence

*and because fluid blance can change acutely during surgery, you’ll need to monitor preload responsiveness throughout the case

102
Q

T/F- post-induction hypotension should be corrected with fluids first

A

false- vasopressors

  1. anesthesia vasodilates
  2. preop fasting is shown to minimally affect intravascular fluid volume (pts arent coming in as dehydrated as we orginally thought)
103
Q

why is urine output an unreliable measure of renal perfusion intraop?

A

bc surgical stress releasing ADH- which reduces UOP

just make sure your MAPs are adequate and you should be good

104
Q

HR, MAP, and CVP are reliable measures of fluid blance- T/F

A

False- fluid responsiveness provide a better assessment of fluid status

105
Q

what’s the problem with giving too much fluid to a healthy person who can “handle it”

A

excess circulating volume promotes microvascular congestion, impairing o2 delivery to tissues

106
Q

A patient has a blood pH of 7.4. If it decreases to 7.32; then his PaCO2 has:

A. increased by 5mmHg
B. decreased by 5mmHg
C. decreased by 10mmHg
D. increased by 10mmHg

A

D. increased by 10mmHg

for every 10mmHg increase in PaCO2, the pH will decrease by approximately 0.08 (respiratory quotient)

this is so stupid- when will i ever have to see a pH and GUESS how much the CO2 has increased …it will say it… right there….. on the abg result… eyeroll

107
Q

match each fluid with its sodium concentration
-LR, 0.9% NaCl, Plasmalyte

140, 154, 130

A

LR = 130
Plasmalyte = 140
0.9% NaCl = 154

*any solution that contains 0.9% NaCl has a sodium of 154: 5% albumin, NS, D5NS

*any solution that contians LR has a sodium of 130 - LR and D5LR

108
Q

Which IVF is most physiologic?

A

Plasmalyte

sodium 140

109
Q

What is the MOST common electrolyte abnormaility seen in clinical practice:

A. Hypernatremia
B. Hyponatremia
C. Hyperkalemia
D. Hypokalemia

A

D. Hypokalemia

110
Q

Rank each substance in terms of its vD (1 smallest, 3 largest)

  • 0.9% NaCl
  • 5% albumin
  • D5W
A

1- albumin
2- NaCl
3- D5W

Albumin remains in the intravascular space- smallest Vd
NS distributes throughout the entire extracellular space (plasma + intersistial space)
D5W (glucose) distributes into the total body water - largest Vd

111
Q

Use the following data to calculate the net filtration pressure in the capillary:

Plasma oncotic pressure = 26
Plasma hydrostatic pressure = 35
Interistial oncotic pressure = 3
Intersistial hydrostatic pressure = 0

A

12

(plasma oncotic pressure - intersistial oncotic pressure) + (plasma hydrostatic pressure - intersistial hydrostatic pressure)

112
Q

Calculate the plasma osmolarity
Sodium = 115
Glucose = 90
Bun = 14

normal plasma os

A

2 [ NA+] + (glucose/18) + (Bun/2.8)
240

280- 290

113
Q

Why does large amounts of 0.9% NaCl cause hyperchloremic metabolic acidosis

is it gap or non-gabp

A

bc the chloride concentration in 0.9% Na Cl is 154 which is higher than the normal plasma value (96-106)

when the kidneys are faced with an increased chloride load, they excrete bicarb to maintain electroneutraility -> acidosis

non anion gap

non anion gap results from loss of bicarb
anion gab results from loss of acid

Fluids, coags, transfusions (5 decks)

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