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Phase 1 > Ch. 5 Fluid Therapy > Flashcards

Ch. 5 Fluid Therapy Flashcards

1
Q

What percent of body weight constitutes water in an adult cat or dog

A

60%

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2
Q

what is the osmolarity of the two major water compartments (extra and intracellular fluid)

A

similar to each other, they are both about 310 mOsm/L

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3
Q

what are the primary cation and anions of extracellular fluid

A

Na+
Cl-
HCO3-

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4
Q

how does the NaK/ATPase pump contribute to the electrolytes in the cell

A

extrudes Na+ from the cell
brings K+ into the cell
consumes ATP as it does that

End result is that the Na concentration is low within the cell and K is high within the cell

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5
Q

What are the major anions and cations of the intracellular fluid

A

High K+
some contribution by Mg2+ and Na+
PO4-

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6
Q

what is the glycocalyx

A

this is a layer of glycoproteins and proteoglycans produced by the endothelium that aids in the endothelial barrier
it has a negative charge that allows it to act as a sieve

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7
Q

What is the endothelium of the capillary freely permeable to?

A

water
small molecular weight particles (ions, glucose, acetate, lactate, bicarb)
gases like CO2 and O2

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8
Q

what determines hydrostatic pressure

A

related to the volume of blood that is confined within the vessel walls and is determined by intravascular blood pressures and vascular resistance

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9
Q

What is the maximum rate of sodium correction recommended

A

do not increase by more than 0.5 mEq/hr

do not decrease by more than 1 mEq/hr

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10
Q

what is the sequela of loss of hypotonic fluids from the body (loss of water in excess of solute)

A

loss of hypotonic fluids from the body would be a loss of extracellular fluid which would lead to an increase in extracellular tonicity. Fluid will then shift from intracellular to extracellular –> that leads to intracellular fluid deficits like in cerebral obtundation and hypernatremia (this is called a hypertonic dehydration)

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11
Q

what clinical signs are indicative of poor tissue perfusion from intravascular volume deficits

A 
pale mucous membranes
poor pulse quality
tachycardia
prolonged CRT
cold extremities
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12
Q

What clinical signs are associated with 5-8% dehydration

A

decreased skin turgor, dry MM

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13
Q

what perfect dehydration is associated with 8-10% dehydration

A

decreased skin turgor, dry MM, sunken eyes, slight prolongation of CRT

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14
Q

what clinical signs are associated with 10-12% dehydration

A

severe skin tenting, prolonged CRT, dry MM, eyes sunken in orbit, maybe signs of shock

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15
Q

what is the current IV crystalloid rec for cats and dogs under GA

A

5 ml/kg/hr for dogs

3 ml/kg/hr for cats

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16
Q

why is 0.9% NaCl considered an unbalanced isotonic crystalloid

A

it is isotonic because the osmolarity is 308, similar to the body, but the Na and Cl are 154 mEq/L which is higher than the body’s
A mild increase in sodium will occur, a marked increase in Cl, and a moderate decrease of K and bicarb

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17
Q

what is the role of lactate or acetate in LRS, Plyte, and NormR? Which has a greater effect, lactate or acetatew

A

lactate and acetate are bicarb precursors and are metabolized by gluconeogenesis or oxidation mostly in the liver and some in the muscle (more acetate in the muscle) and kidneys. This has an alkalinizing effect on the blood. The effect with acetate is greater than alkalinization by lactate

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18
Q

what isotonic crystalloid might be a good option for a patient with a hypochloremic, hyponatremic, or hypochloremic metabolic alkalosis?

A

0.9% NaCl

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19
Q

what is the composition of LRS

A 
osmolarity: 273
Na: 130
K: 4
Cl: 109
Mg: none
Ca: 3
Lactate: 28
Acetate: none
Gluconate: none
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20
Q

what is the composition of Plyte 148 and normR

A 
osmolarity: 295
Na: 140
K: 5
Cl: 98
Mg: 3
Ca: none
Lactate: none
Acetate: 27
Gluconate: 23
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21
Q

What would be a desirable fluid for a patient with head trauma

A

0.9% NaCl because this is the highest sodium concentration and therefore lease likely to cause a decrease in osmolarity and subsequent water movement into the brain interstitium

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22
Q

What would be a desirable fluid for a patient with severe hyponatremia or hypernatremia for resuscitation

A

a crystalloid with a sodium concentration that matches the patient’s current sodium

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23
Q

what would be a desirable resuscitation crystalloid for an animal with a hypochloremic metabolic alkalosis?

A

0.9% NaCl because highest Cl fluid and will improve blood pH by dilution
also it tends to be acidifying

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24
Q

what would a desirable resuscitation crystalloid for an animal with a metabolic acidosis (not from lactic acidosis) be?

A

a crystalloid with a bugger like acetate, gluconate, or lactate
*large quantities of acetate can cause vasodilation and a decrease in blood pressure in animals with preexisting hypovolemia

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25
Q

How can large quantities of acetate can cause vasodilation and a decrease in blood pressure in animals with preexisting hypovolemia

A

Adenosine is released from muscle tissue as acetate is metabolized and adenosine is a vasodilator

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26
Q

What do all maintenance fluids have in common?

A

Hypotonic crystalloids that are low in sodium, chloride, and osmolarity but might be high in potassium compared with normal plasma concentrations (because losses from the body are usually high in potassium anyway)
Ex. 0.45% NaCl w/ or w/out dextrose, P lyte 56, plyte M with dextrose, normosol M with dextrose, 5% dextrose in water

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27
Q

how can we give free water IV without using a dangerously hypotonic fluid, like for animals with free water deficits

A

D5W which is 5% dextrose to an osmolarity of 252 mOsm/L

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28
Q

What rate of D5W will lead to a decrease in sodium concentration by 1 mEq/hr?

A

3.7 ml/kg/hr of D5W

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29
Q

what can occur from too rapid hypertonic fluid administration

A

rates exceeding 1 ml/kg/min may result in osmotic stimulation of pulmonary c fibers –> vagally mediated hypotension, bradycardia, bronchoconstriction

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30
Q

What other benefits may hypertonic saline have in addition to shifting extravascular water to the intravascular space

A

may reduce endothelial swelling, increase cardiac contractility, cause mild peripheral vasodilation, modulate inflammation, decrease intra cranial pressure

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31
Q

how does hypertonic solution vs colloid solution improve the intravascular volume

A

hypertonic solution will cause a transient osmotic shift of water from the extravascular to intravascular compartment whereas colloids will increase the colloid osmotic pressure of the plasma (those molecules are too big to cross the vascular membrane) and then the plasma is hyperoncotic to the extravascular fluid and then fluid is pulled into the plasma

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32
Q

weight average vs number average molecular weight

A

weight average molecular weight = mean of all particle molecular weights
number average molecular weight = median of the molecular weights and considered more accurate

The ratio of these two is called the polydisperity index

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33
Q

What is the importance of higher molecular weight molecules not getting metabolized or excreted as quickly as smaller particles?

A

the higher weights will persist longer in the intravascular space but that also means they will contribute to the side effects like interference with coagulation

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34
Q

how do synthetic colloids disrupt normal coagulation

A

decrease in factor VIII and vWF
impair platelet function
interfere with stability of fibrin clots making it more susceptible to fibrinolysis

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35
Q

why do hydroxyethyl starch synthetic colloids need their hydroxyl groups replaced with hydroxyethyl

A

replacement of hydroxyl with hydroxyethyl at C2, C3, or C6 will prevent rapid degradation by amylase
the ratio of substitution at the C2 versus C6 prolonges the solution

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36
Q

what is the recommended dose of hypertonic solution?

A

4-6 ml/kg over 10 to 20 min

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37
Q

what is the recommended dose of synthetic colloids

A

0.5 - 2 ml/kg/day

or as a bolus as 5-20 ml/kg in dog or 2.5-10 ml/kg in cats

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38
Q

what is the colloid osmotic pressure, molecular weight, molar substitution, C2/C6 ratio of vetstarch

A

36 osmotic pressure
130 molecular weight (lower than other hydroxyethyl starches)
0.38-0.45 substitution (lower than other hydroxyethyl starches for example Hetastarch is 0.75)
C2/C6 ratio 9:1

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39
Q

what should you measure to monitor response to colloid therapy

A

NOT total protein refractometer readings

measure the colloid osmotic pressure - goal is greater than 16 mm Hg for most animals unless chronically hypoproteinemic

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40
Q

what is oxyglobin

A

not currently available but it was a bovine hemoglobin solution of high molecular weight that did not require blood typing

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41
Q

what is acute normovolemic hemodilution

A

a potential alternative to autologous blood donation
blood is collected immediately before surgery and the volume is replaced with three times the amount in an isotonic crystalloid or the same amount in a colloid solution. Then, when the animal bleeds during surgery, it will contain less protein and red cell volume and the collected blood will be available to replace the loss

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42
Q

how soon does whole blood need to be administered

A

within 8 hours of collection - platelets dont last long and are definitely all gone after 24 hours, clotting factors also decrease greatly by 24 hours

43
Q

what effects do storage have on packed RBCs

A 
decreased ATP concentration
decreased 2,3 DPG concentration
increased ammonia
nitric oxide scavenging 
oxidative damage
RBC deformability 
increased procoagulant properties
44
Q

What is the difference between fresh frozen plasma and frozen plasma?

A

frozen has been stored for more than a year and no longer has the labile coag factors V, VIII, and vWF

45
Q

what is cryoprecipitate high in?

A

factor VIII, vWF, fibrinogen, fibronectin

46
Q

what is cryopoor plasma (cryosupernatent) high in?

A

serine protease clotting factors - the vitamin K dependent factors (II, VII, IX, X), anticoag and fibrinolytic factors, albumin, globulins

47
Q

why do we need to monitor calcium in big transfusion patients?

A

blood products often contain citrate, which can lead to chelation and hypocalcemia

48
Q

theoretically, what percent of first time canine blood transfusions should be associated with an adverse immunologic reaction from naturally occurring alloantibodies

A

15% of first time canine blood transfusions

49
Q

what is CPDA-1

A

citrate phosphate dextrose adenine - the product for anticoagulation in blood storage bags

50
Q

how should whole blood and packed RBC be stored?

A

4 degrees +/- 2 degrees C for up to 35 days

51
Q

What temp should plasma be stored?

A

less than 20 degrees C

52
Q

what size filter should be used for blood transfusion administration

A

170 um pores to remove red cell and platelet aggregates

53
Q

What is TACO?

A

sadly TACO is not a taco. TACO is transfusion associated circulatory overload secondary to fluid overload secondary to a significant oncotic pull from blood products

54
Q

what percent of plasma oncotic pressure is attributable to albumin

A

80%

55
Q

what are causes of pseudohyponatremia

A

hyperproteinemia

hyper lipidemia

56
Q

what is the primary determinant of extracellular osmolarity

A

sodium

57
Q

what is the serum sodium concentration for dogs and cats in hyponatremia

A

less than 140 for dogs

less than 149 for cats

58
Q

what are examples of hyponatremia with hypervolemia

A

heart failure, severe liver disease, nephrotic syndrome, advanced renal failure

59
Q

what is an example of hyponatremia with normovolemia

A

psychogenic polydipsia, inappropriate ADH release, ADH drugs, hypothyroid myxedema coma, hypotonic fluid administration

60
Q

what are clinical signs of acute hyponatremia

A

CNS depression, ataxia, coma, seizures secondary to cerebral edema
cerebral edema usually develops at concentrations less than 120 mEq/L or with decreasing rates more rapid than 0.5 mEq/L/hr

61
Q

what is central pontine myelinolysis

A

osmotic demyelination syndrome from increasing the sodium in a hyponatremic patient too quickly

62
Q

what concentration of sodium is hypernatremia

A

greater than 150 in dogs

greater than 160 in cats

63
Q

what will hyperaldosteronism and hyperadrenocorticism do to serum sodium

A

may result in hypervolemic hypernatremia

64
Q

what percent of the body’s total potassium in the body is within the cells?

A

95%

65
Q

what is the net resting membrane potential

A

-90 mV

66
Q

what shifts potassium from extracellular to intracellular space?

A

glucose, insulin, catecholamines, metabolic alkalosis

67
Q

what shifts potassium extracellularly?

A

nonorganic metabolic alkalosis

hyperosmolarity

68
Q

ECG abnormalities due to hypokalemia

A

increased amplitude and width of P wave, ST segment depression, decreased amplitude of T waves, prolonged PR intervals, prominent U waves, various ventricular and supraventricular arrhythmias

69
Q

what is the most common cause of hyperkalemia

A

decreased renal potassium excretion

70
Q

what is solvent drag

A

diabetes mellitus may be associated with an extracellular hypertonicity from increased serum glucose which will draw water out of cells and bring potassium with it. will result in a hyperkalemia

71
Q

what breeds have increased potassium concentrations in their red blood cells

A

Akitas and English Springer Spaniels

hemolysis in these breeds can lead to hyperkalemia

72
Q

What ECG changes might you see at 5.7-6.0 mEq/L potassium

A

spiked T waves

shortened QT interval

73
Q

What ECG changes might you see at greater than 8.5 mEq/L potassium

A

P wave disappears

R wave amplitude decreases and S wave prominence increases –> sinoatrial wave

74
Q

What ECG changes might you see at greater than 10-12 mEq/L potassium

A

aystole and ventricular fibrillation

75
Q

how does calcium gluconate improve arrhythmias with hyperkalemia?

A

will raise the threshold membrane potential to restore cell excitability
give 10% calcium gluconate at 0.5-1 ml/kg over 10-20 minutes
bradycardia can develop if given too quickly
works within minutes and lasts about an hour

76
Q

how does dextrose help with hyperkalemia

A

give dextrose at 0.5 to 1 g/kg with or without insulin (0.5-1 units/kg) to help drive potassium into cells
works within 30 min and lasts for 1-2 hours

77
Q

how can sodium bicarb treat hyperkalemia

A

drives potassium into cells in exchange for hydrogen to move out to titrate the bicarb
dose is 0.5-2 mEq/kg IV

78
Q

what percent of the body’s calcium is in bone?

A

99%

79
Q

how can a sodium phosphate enema result in hypocalcemia

A

elevated phosphorus levels will precipitate with calcium, decrease PTH mediate bone resorption, and decrease vit D production

80
Q

what ionized calcium levels are considered hypocalcemic in the dog and cat

A

in dogs, less than 1.2 mmol/L (5.0 mg/dL)

in cats, less than 1.1 mmol/L (4.5 mg/dL)

81
Q

what percent of the body’s magnesium is intra vs extracellular

A

99% is intracell and 1% is extracellular

82
Q

what is the concentration for hypomagnesemia

A

less than 1.7 mg/dL in dogs

less than 1.8 mg/dL in cats

83
Q

what are clinical signs of hypomagenesemia

A

ventricular arrhythmias, atrial arryhthmias, hypertension, muscular weakness, hyperesthesia, muscle tremors, ataxia, CNS depression, seizures, nausea, anorexia

84
Q

what are ECG signs of hypermagnesemia

A

prolongation of the PR interval, widening of the QRS complex, heart block and asystole

may also see muscular effects similar to hypercacelmia like weakness and decreased tendon reflexes

85
Q

what percentage of phosphorus is in bone vs intracellular vs extracellular

A

85% in bone
15% in intracellular
less than 15 in extracellular

86
Q

where is phosphorus reabsorbed

A

primarily in the proximal tubule of the kidney - 85% gets reabsorbed
renal excretion is the primary mechanism for regulating total body phosphate levels

87
Q

what clinical signs are seen with hypophosphatemia

A

mild hypophosphatemia may result in weakness, disorientation, joint pain, anorexia
severe hypophosphatemia can result in hemolysis, rhabdomyolysis, coma, seizures, cardiac arryhthmias, acute respiratory failure

88
Q

What kind of dogs will develop hemolysis secondary to hypophosphatemia

A

Japanese or Korean origin - like Akita, shiba, jindo do NOT use a phosphorus independent red blood cell regulation system and

89
Q

what are the clinical signs of hyperphosphatemia

A

usually caused by the associated hypocalcemia

90
Q

what is the most common cause of hyperphosphatemia

A

decreased renal excretion and occurs in animals with acute or chronic renal failure, post renal azotemia, hypoparathyroidism, hyperthyroidism

91
Q

where is chloride reabsorbed

A

it is the primary anion that is reabsorbed in the proximal tubule of the kidney

92
Q

What is Whipple’s triad

A

a low blood glucose concentration
concurrent signs of hypoglycemia
resolution of clinical signs when blood glucose level is normalized

93
Q

How does sepsis induce hypoglycemia

A

increased circulating levels of cytokines like TNF alpha, IL 6 cause increased utilization of glucose by the tissues
decreased hepatic responsiveness to counterregulatory hormones like catecholamines, glucagon, glucocorticoids, and growth hormone lead to a decreased hepatic production of glucose

94
Q

why should you avoid a bolus of glucose in insulinoma patients

A

may actually stimulate insulin production and worsen the hypoglycemia. It is better to give an infusion of glucagon

95
Q

what contributes to stress hyperglycemia in critically ill patients

A

increased secretion of counter regulatory hormones like glucocoricoids, catecholamines
insulin resistance because of circulating cytokines
use of hyperglycemia inducing treatment modalities in critically ill patients like adrenergic agonists or total parenteral nutrition

96
Q

what is a nonvolatile acid?

A

Hydrogen ions are a non volatile acid

they are acids that must be metabolized by the hepatic or renal route and do not rely on the pulmonary system

97
Q

what is a volatile acid

A

carbonic acid is a volatile acid
volatile acids depend on a gas phase component for their concentration
carbon dioxide will act as an acid because it can combine with water to make carbonic acid, which then dissociates to H+ and HCO3-

98
Q

what does a negative base excess represent

A

a base deficit which is a nonrespiratory acidosis

99
Q

what does a base excess represent

A

a non respiratory alkalosis

100
Q

what are the clinical signs of respiratory acidosis

A

usually related to subsequent catecholamine release and include tachyarrhythmias, increased or normal P, increased cardiac output

101
Q

what are the clinical effects of metabolic acidosis

A 
cardiac arrhythmias
decreased cardiac output
refractory hypotension
decreased renal and hepatic blood flow
reduced sensitivity to catecholamines
tighter binding of oxygen by hemoglobin
insulin resistance
ionized hypercalcemia 
CNS depression 
chronic metabolic acidosis can result in bone demineralization
102
Q

what are some adverse reactions of administering sodium bicarb

A

very hyperosmolar so can cause fluid shifts
electrolyte abnormalities such as hypokalemia, hypocalcemia, hypernatremia
iatrogenic metabolic alkalosis can occur

103
Q

what are clinical manifestations of metabolic alkalosis

A

rare but when they do, shows as agitation, disorientation, stupor, coma, muscle twitching, seizures

Phase 1 (35 decks)

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