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Board Review 2020 > AcidBase.Fluids.Lytes > Flashcards

AcidBase.Fluids.Lytes Flashcards

1
Q

What is the composition of LRS: Include osmolarity, organi anions and pH

A

Na: 130 Cl 109 K 4 Ca 3
Os: 272 mOsm/L
Lactate 28
pH 6.5

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2
Q

What is the composition of Norm-R: Include osmolarity, organi anions and pH

A

Na: 140 Cl 98 K 5 Mg 3
Os: 296 mOsm/L
acetate 23 / Gluconate 27
pH 6.4

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3
Q

What is the composition of Plyte-A: Include osmolarity, organi anions and pH

A

Na: 140 Cl 98 K 5 Mg 3
Os: 294 mOsm/L
acetate 23 / Gluconate 27
pH 7.4

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4
Q

What is the composition of Plyte 148: Include osmolarity, organi anions and pH

A

Na: 140 Cl 98 K 5 Mg 3
Os: 296 mOsm/L
acetate 23 / Gluconate 27
pH 5.5

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5
Q

What is the composition of 0.9% NaCl: Include osmolarity, organi anions and pH

A

Na: 154 Cl 154
Os: 308 mOsm/L
pH 5.0

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6
Q

What is the composition of 0.45%: Include osmolarity, organi anions and pH

A

Na: 77 Cl 77
Os: 154 mOsm/L
pH 5.0

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7
Q

What is the composition of D5W: Include osmolarity, organi anions and pH

A

Na: 0 Cl 0
Os: 252 mOsm/L
pH 4.0

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8
Q

What is the composition of 7.5% NaCl: Include osmolarity, organi anions and pH

A

Na: 1282 Cl 1282
Os: 2564 mOsm/L
pH 5.0

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9
Q

Summarize some of the recent controversies associated with the use of 0.9% sodium chloride in hospitalized human patients. What is the proposed mechanism for acute kidney injury (AKI) after administration of 0.9% NaCl?

A

Large volumes can lead to hyperchloremic metabolic acidosis results in greater extravascular expansion, increasing risk for interstitial edema. May also see hyperchloremic metabolic acidosis due to chloride load, AKI with reduced urine output, damaged vascular permeability and stiffness, increased in proinflammatory mediators, detrimental gastrointestinal perfusion and function.
Renal vasoconstriction and reduced GFR resulting in NaCl retention and water retention.
When compared to a balanced electrolyte solution has been shown to result in significantly increased in hospital mortality in critically ill people.

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10
Q

0.9% sodium chloride is commonly called “physiologic” saline. What are three reasons why “physiologic” saline is considered a misnomer?

A
  • Cl level is much higher than physiologic values
  • pH is lower (5.0) than physiologic pH 7.4
  • NaCl are not the only electrolytes that matter in a physiological basis such as K, Ca, MG
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11
Q
  1. VetStarch 6% 130/0.4/9:1 is a currently available synthetic colloid solution. What do the numbers associated with VetStarch indicate?
A

6% =6 g of HES/ 100 ml
130 = Molecular weight
0.4 = tetrastarch- average number of hydroxethyl residues per glucose
9:1= C2:C6 Ration. Higher ratio will be slower to breakdown.

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12
Q

What three factors would increase the plasma half-life of a synthetic starch colloid

A

High C2:C6 Ratio
High molecular weight
High Molar substitution

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13
Q

Why might dogs have different HES metabolism than people

A

Dogs have more amylase therefore may breakdown more quickly.

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14
Q

What is the Henderson Hasselbach equation

A

pH = 6.1 + log [HCO3/ (0.03 x PCO2)]

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15
Q

How does hemoglobin affect buffering

A

More hemoglobin more buffering effect

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16
Q

Where is the most carbonic anydrase located

A

in RBCs

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17
Q

What are the compensation calculations in the standard approach for respiratory disturbances

A

Acute acidosis 0.15 increase in bicarb
Acute alkalosis 0.25 decrease in bicarb
Chronic acidosis 0.35 increase in bicarb
Chronic alkalosis 0.55 decrease in bicarb

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18
Q

What are the compensation calculations in the standard approach for metabolic disturbances

A

0.7 (increase/decrease) in PCO2 for acidosis/alkalosis

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19
Q

What is the primary underlying causes of Respiratory acidosis

A

alveolar hypoventilation (decreased alveolar minute ventilation)

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20
Q

What is the primary underlying causes of Respiratory alkalosis

A

hyperventilation, high altitude

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21
Q

What is the primary underlying causes of metabolic acidosis

A

acids added to blood (DUEL) for High anion gap
Bicarbonate loss - normal AG hyperchloremic metabolic acidosis (diarrhea, renal tubular acidosis, dilutional acidosis- 0.9% NaCl, addisons)

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22
Q

What is the primary underlying causes of metabolic alkalosis

A

Loss of gastric acids, renal retention of bicarb

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23
Q

Calculate the free water deficit

A

ml= [(Na measured/Na normal)-1] x BW x 0.6

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24
Q

Calculate the Anion Gap

A

Na+K - (Cl- + HCO3-)

Normal 12-20 mmol/L

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25
Q

Define base excess

A

Amount of acid or base that must be added to a sample of oxygenated whole blood to restore the pH to 7.4 at 37C and at a PCO2 of 40 mmHg
Normal 0 +/- 2
Neg = acidosis
Positive= alkalosis

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26
Q

What does base excess tell us

A

Provides a measure of metabolic componenet of acid/base that is independent of PCO2

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27
Q

How much sodium bicarbonate do you give

A

0.3 x BW x base deficit
0.3= approx value for the distribution of bicarbonate
Give about 50% of calculated dose
Dilute as hyperosmolar

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28
Q

How does PvCO2 compare to PaCO2

A

Generally close, but will see an increase in PvCO2 vs PaCO2 due to poor cardiac output not hypoventilation

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29
Q

How does hypoalbuminemia affect AG

A

It will increase less and may even be normal

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30
Q

Does serum potassium reflect whole body K

A

No. Primarily stored intracellularly

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31
Q

How does the body maintain normal serum K

A

Distribution of K between extracellular and intracellular compartments
renal excretion of excess K

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32
Q

What are causes of hypoK

A

decreased intake
Intracellular shift
Increased renal excretion

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33
Q

How do you treat a metabolic acidosis with a signficant hypo K

A

Treat the hypo K,

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34
Q

If pateint is not responding to treatment for ventricular arrhythmia and has Hypo K what should you do

A

Hypo K leaves myocardium refractory to the effects of Class 1 antiarrhythmic agents and serum K concentrations should be corrected

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35
Q

What is the max rate of K supplementation

A

0.5 mEq/Kg/hr

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36
Q

What other electrolyte is needed to be supplemented if K is not improving

A

Magnesium

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37
Q

What are causes of hyperkalemia

A

Increased supplementation/intake
Increased extracellular movement (repurfusion injury, insulin deficiency, metabolic acidosis)
Decreased renal excretion
Tumor lysis syndrome

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38
Q

What is pseudohyperkalemia

A

K+ shift from cells after blood draw (RBCs, Platelets, WBCs)
Most commonly seen with thromobcytosis, but also Leukocytosis
Japaneses origin breeds have functional Na/K atpase pump that with hemolysis

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39
Q

What electrolyte abnormalities occur with repeated draining of effusions

A

Hyper K and hypo Na

Due to a decrease in circulating volume

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40
Q

Differentials for a Na/K ratio < 27:1

A

Primary is addison’s disease

r/o GI disease - trichurasis, salmonellosis, perforated duodenal ulcers

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41
Q

What are ECG abnormalities in HyperK

A

Generally seen > 8 mEq/L but does not correlate with increase.
Tall tented T waves, depressed p-wave, prolonged QRS and PR interval
In severe get atrial standstill, bradycardia, and ventricular astolye

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42
Q

What is the MOA for Ca Gluconate treatment with HyperK

A

restablishses normal gradient between resting membrane potential and threshold potential
Does not decrease K

43
Q

What is the MOA for dextrose and insulin dextrose with Tx of Hyper K

A

Insulin (both endogenous and exogenous) promotes intracellular shift of K through ativation of NaK atpase pump

44
Q

What is the MOA of Na bicarbonate with tx of hyperK

A

Increase extracelluar pH and promotes intracellular shift of K+ in exchange for H+

45
Q

What is the MOA of beta adrenergic agonists in the tx of Hyper K

A

Promotes intracellular shift of K through activation of NaK ATPase pump

46
Q

Where is phosphorus stored in the body

A

80% skeletal
19-20% intracellular
1% plasma

47
Q

What regulates storage and absorption of phosphorus

A

Vitamin D- enhances GI absorption

PTH, VitD, and calcitonin regulate storage

48
Q

What regulates excretion of phosphorus by the kidney

A

PTH

fibroblast growth factor 23 (FGF 23

49
Q

How does Fibroblast growth factor (FGF) 23 work

A

Secreted by osteoblasts in response to increase phos intake
Inhibits production and stimulates 1-25 dihydroxyvitamin D (calcitriol)
Promotes excretion in the kidneys indepent mechanism of PTH and Vit D

50
Q

What is the main site of renal Phosphorus regulation

A

Renal tubular NaPO4 co transportor

Inhibited with metabolic acidosis

51
Q

What are the causes of hypophosphatemia

A 
Transcellular shfits (refeeding, respiratory alkalosis)
Increased renal excretion (eclampsia, etc)
Decreased intake/abosrption
52
Q

What rate of supplementation is generally started for phos

A

0.03 mmol/kg/hr

53
Q

What are causes of hyperphosphatemia

A

Increased endogenous release (tumor lysis syndrome, crush injury)
increased exogenous uptake ( vit d toxicosis, phsophate enemas
Decreased renal excretion (CKD)

54
Q

How does furosemide alter phosphorus in the kidneys

A

May promote phosphorus excretion

55
Q

How does calcium levels affect voltage gated ion channels

A

Extracellular low Ca: open too easily

Extracellular high Ca: prevent/reduce opening

56
Q

What are the concentrations of calcium in the plasma

A

55% ionized
10% non ionized
35% protein bound (albumin)

57
Q

what is believed to be the mechanism of hypo Ca with pancreatitis

A

Soponafication

58
Q

What do you want to avoid in treating hypocalcium

A

at calcium x phosphorus ration of > 70

59
Q

What are causes of HyperCa

A

1) generally increase PTH or hormonally related peptide
2) bone destruction, bone inflammation, or bone infection
Thiazied diruetics, toxicity: Vit D analogues rodenticides

60
Q

In life threatening hyperCa what are treatment options

A

calcium chelating agents
calcium channel blockers
extracorpeal therapies
bisphosphonate agents (pamidronate)

61
Q

Where is Magnesium found in the body

A

Most is intracellular second highest to K

62
Q

How is Magnesium uptake regulated

A

Dogs- colonic absorption Cats unknown

Active uptake when whole body stores are low; Passive uptake with normal to high Mg

63
Q

Signs attributed to HypoMg

A 
ECF composition-- HypoK, HypoCa
Neuromuscular signs
Neurologic- nystagmus
CV
GI ileus unresponsive to traditional tx
64
Q

How to treat HypoMg with normal whole body stores

A

If not whole body deficiency then oral supplementation won’t work and will act as laxative
Cellular uptake of Mg slow and may take 24hrs to equilibrate. Therefore need CRI

65
Q

What is the recommended supplementation of Mg

A

Daily dose
Small 0.5 g/day
Dog 6-20 kg 1 g/day
Dogs > 20 kg 2 g/day

66
Q

What are causes of HyperMg

A

decrease renal function/GFR

Less likely due to increase uptake due to passive nature

67
Q

What are signs of hyper Mg

A

weakenss, hypotension, respiratory difficulty

rarely asytole—- Mg is a calcium channel blocker

68
Q

What is the treatment for hyperMg

A

Diruresis/ increase GFR
Insulin/dextrose improves cellular uptake
Ca gluconate if signs are severe

69
Q

Bicarbonate therapy potential adverse effects

A 
increase hemoglobin affinity for Oxygen
increase blood lactate concentration
paradoxical intracellular acidosis (CO2 into the cell )
Hypercapnia
Hypervolemia
Hyperosmolarlity
HypoiCa, HypoK, Pheblitis
70
Q

If you didn’t get base deficit on your machine how can you estimate the bicarb to give a patient

A

replace base deficit with Bicarb patient- normal bicarb

71
Q

In the stewart approach to Acid/Base what are the 3 independent determinants

A

Partial pressure of CO2 (PCO2)
Strong ion difference
Total weak acids Atot

72
Q

In the Stewart approach to acid/base what are the possible abnormalities

A 
Increased SID metabolic alkalosis
Decreased SID metabolic acidosis
Decreased Atot metabolic alkalosis
Increased Atot Metabolic acidosis
Increased SIG metabolic Acidosis
73
Q

What is a strong ion

A

Ions that fully dissociate at physiologic pH

74
Q

What is used to calculate SID

A 
Cations: Na + K + Ca + Mg
subtract anions
anion Cl-
If Atot remains constant the change in SID will reflect changes in HCO3
Normal 40-45 mEq/L
75
Q

Define total weak acids

A

partially dissociated at physiologic pH

albumin and phosphate

76
Q

How do you calculate SIG

A

SID- (HCO3- + Atot)

77
Q

How is Atot estimated

A

Dogs (Albx4.9) - AG
Cats (Alb x 7.4) - AG

If phos is elevated need to adjust AG
AG + (2.52 - .58 x phos concentration)

78
Q

What are the semiquantitive formulas

A 
Free water effect
Chloride effect
albumin effect
Phosphorus effect
lactate effect
79
Q

How due you calculate the semiquantative approach

A

Sum = free H20 + Chloride effect + Alb effect + Phosphate effect + Lactate effect

80
Q

How do you measure unmeasured anions in the semiquantative approach

A

Base excess - sum

81
Q

How doe you calculate the free H2O effect in the semiquantitive approach

A

(Na measured - Na normal)/4

82
Q

How doe you calculate the chloride effect in the semiquantitive approach

A

Corrected chloride= Measured cl x (Normal Na/Measured Na)

Chloride effect= normal Cl - corrected chloride

83
Q

How doe you calculate the albumin effect in the semiquantitive approach

A

(normal alb- measured alb)/ 4

84
Q

How doe you calculate the phosphorus effect in the semiquantitive approach

A

(Normal phos - Measured phos)/2

85
Q

How doe you calculate the lactate effect in the semiquantitive approach

A

Measured lactate x (-1)

86
Q

What are the systemic consequences of acidemia

A

Decreased cardiac contractility, decreased cardiac output, increased susceptibility to arrythmias
impairs response to catecholamines
Promotes systemic inflammatory state
pH < 7.15 decreases systemic and increases pulmonary vascular resistance— hypotension worse

87
Q

What are the sources of fluid acidity

A

Container- PVC generates acid- small amount
CO2 absorbed from air (largest contributor)
Salts added increase hydronium ions (H3O+) favoring H+ actitivity- decrease pH

88
Q

What is the SID of IV fluids

A

In vitro is 0 due to law of electroneutrality

In vivo is 0-50 mEq/L because of metabolizable organic anions

89
Q

What is the mechanism that IV fluids change plasma pH

A

primarily due to change in SID, not in dilution

90
Q

What is the in vivo SID of PLyte and Norm R

A

SID 50

Increases plasma pH

91
Q

How is the water in the body divided

A 
Total body water 60% of BW
Intracellular= 67%
Extracellular= 33%
     Interstitial= 75%
      Intravasculature= 25%
92
Q

What is the difference of osmoalitlity and osmolarity

A

Osmolality: number of particles (mOsm) per kg of water

Osmolarity- Number of particles per liters of H20

93
Q

What are the two mechanism for ADH release

A

Osmotic: hyperosmolarity
Nonosmotic: decrease in circulationg volume

94
Q

how to calculate sodium deficiency

A

BW(kg) x 0.6 x (Normal na- patient Na)

95
Q

How to calculate change serum Na expected with 1 Liter

A

(infusate Na + K - patient Na)/ (BWx0.6 +1)

96
Q

What is the equivilant volume of cyrstalloid to 1 colloid

A

3-4 times crystalloid to 1 collowed to get equal intravascular volume

97
Q

How much plasma is needed to increase albumin 1 g/dl

A

40 ml/kg

98
Q

What are possible adervese effects with human serum albumin

A

type III hypersensitivity reactions in healthy dogs

But reported in critically ill dogs

99
Q

What are adverse effects of crystalloids

A

Specific fluid tyype complications: Saline, LRS (hypotonic) Acetate may cause vasodiluation/hypoperfusion with rapid admin
Resuscitation injury, upregulation of pro inflammatory cytokines, augmented neutrophil adhesion to vascular endothelium, stimulate neutorphil oxidative burst, increase cellular apoptosis
Fluid overload

100
Q

What are adverse effects of HES

A

Coagulopathy, AKI, Tissue accumulation, trends toward mortality

101
Q

What is the proposed MOA for HES induced AKI

A

hyperviscosity mediated, ischemic injruy, osmotic nephrons

renal uptake by interstial reticuloendothelial system

102
Q

What is the MOA for HES induced coagulopathy

A

decrease vWF, F VIII activity and acquired fibrinogen deficiency

103
Q

What are the coefficents in the starlings equation and what do they mean

A 
K= filtration- ease with which fluids moves across membranes
sigma= represents the pore size or permeability of the membrane

Board Review 2020 (37 decks)

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