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X CNT 1 > Fluid Therapy > Flashcards

Fluid Therapy Flashcards

1
Q

what percentage of body weight is made up of water?

A

60%

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2
Q

what two subdivisions can body water be divided into?

A

extravascular and intravascular

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3
Q

what percentage of body water is found extravascularly?

A

55%

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4
Q

what percentage of body water is found intravascularly?

A

5%

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5
Q

what is maintenance of fluid balance in the body an example of?

A

homeostasis

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6
Q

what must fluid intake match?

A

fluid outgoing

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7
Q

give two examples of fluid intake

A

drinking

eating

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8
Q

give three examples of fluid outgoings

A 
urination
defecation
body surfaces (respiratory tract and skin)
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9
Q

what percentage of extravascular fluid is located within cells?

A

40%

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10
Q

what percentage of extravascular fluid is located in between cells?

A

15%

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11
Q

what are the three main causes of fluid imbalance?

A

changes in fluid volume
changes in fluid content
changes in fluid distribution

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12
Q

what is the most common cause of a change in fluid balance?

A

change in fluid volume

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13
Q

what is a change in fluid volume often caused by?

A

dehydration and hypovolaemia

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14
Q

what are the two main physiological consequences of changes in blood volume?

A

hypovolaemia and dehydration

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15
Q

what occurs during hypovolaemia?

A

fluid is lost quickly from the intravascular space

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16
Q

how quickly is fluid lost during hypovolaemia?

A

quickly

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17
Q

what does hypovolaemia lead to within tissues of the body?

A

tissue hypoperfusion (shock)

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18
Q

does treatment of dehydration and hypovolaemia differ?

A

yes

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19
Q

what happens during dehydration?

A

fluid is lost slowly from the extravascular compartment and patient is unable to keep up with fluid gains and losses

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20
Q

during dehydration is there time for fluid levels to be redistributed across all body compartments?

A

yes

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21
Q

is water lost equally from all body compartments during dehydration?

A

yes

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22
Q

what are the main CVS physiological effects of hypovolaemia?

A

blood loss leading to reduced pre-load and so reduced stroke volume. This leads to a reduced cardiac output

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23
Q

what are the main ways which the body compensates for hypovolaemia?

A

vasoconstriction and tachycardia

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24
Q

what physical signs do vasoconstriction and tachycardia lead to?

A

maintenance of blood pressure (TPR)

changes in mucous membrane colour and CRT

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25
Q

what components of triage give information about the patients intravascular volume status?

A 
heart rate
pulse quality
mucous membrane colour
capillary refill time (CRT)
blood pressure
mentation
temperature
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26
Q

what is the average canine heart rate during mild (compensated) hypovolaemia?

A

130-150 bpm

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27
Q

what is the usual mucous membrane colour of a canine with mild (compensated) hypovolaemia?

A

normal or slightly pinker

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28
Q

what is the usual CRT of a canine with mild (compensated) hypovolaemia?

A

<1

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29
Q

what is the pulse quality of a canine with mild (compensated) hypovolaemia?

A

bounding

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30
Q

what is the usual systolic blood pressure of a canine with mild (compensated) hypovolaemia?

A

> 90 mmHg

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31
Q

what is the usual mentation of a canine with mild (compensated) hypovolaemia?

A

normal

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32
Q

what is the average canine heart rate during moderate hypovolaemia?

A

150-170 bpm

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33
Q

what is the usual mucous membrane colour of a canine with moderate hypovolaemia?

A

pale pink

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34
Q

what is the average CRT of a canine with moderate hypovolaemia?

A

2

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35
Q

what is the average pulse quality of a canine patient with moderate hypovolaemia?

A

weak

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36
Q

what is the average systolic blood pressure of a canine with moderate hypovolaemia?

A

> 90 mmHg

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37
Q

what is the usual mentation of a canine with moderate hypovolaemia?

A

normal/obtunded

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38
Q

what is the average canine heart rate during severe (decompensated) hypovolaemia?

A

170-220

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39
Q

what is the usual mucous membrane colour of a canine with severe (decompensated) hypovolaemia?

A

pale pink/white

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40
Q

what is the average CRT of a canine with severe (decompensated) hypovolaemia?

A

> 2 - prolonged

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41
Q

what is the average pulse quality of a canine patient with severe (decompensated) hypovolaemia?

A

very weak

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42
Q

what is the average systolic blood pressure of a canine with severe (decompensated) hypovolaemia?

A

<90 mmHg

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43
Q

what is the normal mentation of a canine with severe (decompensated) hypovolaemia?

A

obtunded as the brain is starved of oxygen and nutrients

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44
Q

what happens when the body is compensating for hypovolaemia?

A

blood pressure is maintained so tissues remain perfused

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45
Q

what environmental factors can alter a physical exam in normal patients?

A

cold or ambient temperatures

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46
Q

what species typically have paler mucous membranes than canines?

A

felines

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47
Q

what must you be familiar with when assessing intravascular volume?

A

to be familiar with what is normal and look at the entrire clinical picture

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48
Q

what components of triage/physical exam will give information about the patients extravascular volume status?

A 
moistness of mucous membranes
skin turgor (skin tenting)
weight
globe position within orbit of skull
(urine output)
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49
Q

what are the signs of <5% body weight estimated dehydration?

A

not clinically detectable, suspected from clinical history

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50
Q

what are the signs of 5-6% body weight estimated dehydration?

A

tacky mucous membranes

mild delay in skin tent return

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51
Q

what are the signs of 6-8% body weight estimated dehydration?

A

dry mucous membranes
mild increase in CRT
mild to moderate delay in skin tent return
+/- sunken eyes

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52
Q

what are the signs of >10-12% body weight estimated dehydration?

A 
dry mucous membranes
CRT >2-3 seconds
\+/- signs of shock
prolonged skin tent
sunken eyes
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53
Q

why may hypersalivation affect the assessment of dehydration?

A

may hide dry or tacky mucous membranes

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54
Q

what are two other factors aside from hypersalivation that can complicate the assessment of dehydration?

A

subcutaneous fat

skin’s collagen content (elasticity)

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55
Q

what haematology/biochemistry parameters may be affected by a patients hydration status?

A

PCV
total proteins
urea and creatinine

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56
Q

what urinalysis parameters may be affected by a patients hydration status?

A

urine specific gravity

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57
Q

what other tools can be used during patient assessment of dehydration?

A

urinalysis
biochemistry
haematology

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58
Q

when assessing a patients level of dehydration/hypovolaemia what must be considered?

A

all physical exam and clinicopathological parameters must be taken into consideration and none interpreted in isolation

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59
Q

can hypovolaemia and dehydration exist in the same patient?

A

yes and they commonly do

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60
Q

how is a patients stability classed if they are hypovolaemic?

A

they are unstable and their condition could become rapidly life threatening

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61
Q

at what speed is hypovolaemia treated with fluid in the patient?

A

quickly - via a bolus

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62
Q

how will fluid be given to the hypovolaemic patient?

A

stabilised with rapid fluid resuscitation of the patient

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63
Q

how is a patients stability classed if hypovolaemia is not present?

A

they are stable

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64
Q

at what speed should extravascular fluid losses be corrected?

A

slowly

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65
Q

what effect can rapid rehydration of dehydrated patients have?

A

intravascular volume increases rapidly raising atrial pressures and causing production of diuretic hormone causing increased urination

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66
Q

why is rapid rehydration of dehydrated patients so dangerous?

A

can cause even more severe dehydration

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67
Q

define hypovolaemia

A

state of decreased intravascular volume

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68
Q

define hypervolaemia

A

also known as fluid overload, the medical condition where there is too much fluid in the blood

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69
Q

define normovolaemia

A

normal blood volume

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70
Q

define hypoperfusion

A

critical condition brought on by sudden and global defecit in tissue perfusion. Results in inadequate delivary of oxygen and nutrients to vital organs

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71
Q

define shock

A

state of cellular and tissue hypoxia, most commonly caused by hypoperfusion

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72
Q

define dehydration

A

excessive loss of body water from the extra vascular compartment

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73
Q

define oncotic pressure

A

form of osmotic pressure induced by proteins

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74
Q

what is appropriate fluid selection influenced by?

A

what is trying to be achieved with the patient

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75
Q

what are the most common types of fluid?

A

crystalliods

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76
Q

what do crystalliod fluid contain?

A

solutes (dissolved compounds e.g. Na)

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77
Q

can crystalloid fluids move between different fluid compartments of the body?

A

yes

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78
Q

what has happened to crystalloid fluids 1hr after administration?

A

distributed throughout all body compartments

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79
Q

what are the 3 main categories of crystalliod fluids?

A

isotonic
hypertonic
hypotonic

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80
Q

which is the most common type of crystalliod fluid?

A

isotonic

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81
Q

what are isotonic crystalliods used for?

A

replacement fluids

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82
Q

give two examples of isotonic crystalliods

A

0.9% NaCl and Hartmann’s

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83
Q

how do crystalloid fluids mimic the intravascular electrolyte concentrations?

A

high Na and low K

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84
Q

what do replacement fluids mimic?

A

intravascular electrolyte concentrations

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85
Q

why may Hartmann’s be seen as more balanced?

A

electrolyte composition is more similar to that of serum

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86
Q

what is useful for acidosis that usually accompanies hypovolaemia?

A

a buffer such as lactate

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87
Q

in what type of crystalloid fluid is lactate found?

A

hartmann’s

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88
Q

what are the three main indications for the use of Hartmann’s and 0.9% NaCl?

A

hypovolaemia
dehydration
replacement of ongoing losses

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89
Q

what are the preferred uses for 0.9% saline over Hartmann’s?

A

management of hypochloraemia, hypercalcaemia and hyperkalaemia

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90
Q

what are the two key things that must not be mixed with Hartmann’s?

A

blood products

sodium bicarbonate

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91
Q

what are the two key issues with 0.9% NaCl?

A

can exacerbate acidosis as no buffer

requires care with hypernatremia and hyponatramia

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92
Q

what electrolyte must be monitored when giving either Hartmann’s or 0.9%NaCl?

A

serum K+ to prevent hypokalaemia

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93
Q

give one example of hypotonic crystalliods

A

0.18% NaCl and 4% glucose

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94
Q

why is glucose included with 0.18% NaCl hypotonic crystalloid?

A

fluid is isotonic at time of administration to prevent damage to tissues around where IV is placed

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95
Q

what electrolyte imbalance are crystalliod fluids commonly used for?

A

management of severe and acute hypernatraemia

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96
Q

what is hypernatraemia?

A

rise in serum Na+?

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97
Q

what are hypotonic crystalloids commonly used for?

A

management of severe and acute hypernatraemia

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98
Q

why are hypertonic crystalloids used often in large animals?

A

speed of correction of hypovolaemia due to the amount of fluid required to replace the loss

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99
Q

give an example of hypertonic crystalloid fluids

A

7.5% NaCl

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100
Q

what is the risk with hypertonic fluids?

A

very dangerous if used by mistake and particularly in already dehydrated patients

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101
Q

what is the main effect of hypertonic saline?

A

prolongs intravascular volume expansion

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102
Q

what do colloid fluids contain?

A

large molecules (proteins or carbohydrates) that cannot pass semi permeable membranes

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103
Q

what is the usual tonicity of colloids?

A

isotonic

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104
Q

what are the two types of colloid?

A

natural (plasma)

artificial (gelatine)

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105
Q

what is the main effect of colloids?

A

exert an increased colloid osmotic pressure

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106
Q

compared to crystalliod fluids, how long do colloids remain in the intravascular space?

A

much longer

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107
Q

how do colloids leave the intravascular space?

A

through kidneys and lymphatic system

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108
Q

what effect does the prolonged length of time in the intravascular space of colloids compared to crystalloids mean for amount of fluid needed for volume resuscitation?

A

smaller fluid volume needed to have same effect

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109
Q

when is the effectiveness of colloids reduced?

A

in disease processes where vascular permeability is increased

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110
Q

what are the potential uses of colloids?

A

management of hypovolaemia
treatment of coagulopathies with plasma
management of hypoproteinaemia

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111
Q

what does the prolonged length of time in the intravascular space mean for the duration of effect of colloids?

A

longer duration of effect

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112
Q

what are colloids not suitable for?

A

treatment of dehydration and management of electrolyte abnormalities

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113
Q

why are colloids not suitable for treatment of dehydration?

A

fluid will not move from intravascular to extravascular space

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114
Q

what are the 7 main risks of colloids?

A

coagulopathy
allergic reactions
anaphylaxis
associated with increased risk of death when patient has sepsis
associated with increased AKI risk in humans (so potentially in animals)
may not be as effective as first thought
expensive and rarely used

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115
Q

what are two key complications of fluid therapy?

A

they are drugs and so require prescribing and come with risks of side effects
co-morbidities must be considered before fluid therapy is prescribed

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116
Q

what are the 3 main co-morbidities that must be considered before prescription of fluid therapy?

A

cardiac disease and heart failure
renal disease
respiratory disease

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117
Q

what is the main complication involved in fluid therapy?

A

volume overload

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118
Q

what are the key effects of volume overload?

A

pulmonary oedema
venous engorgement
peripheral oedema and chemosis
cavity effusions

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119
Q

what are the signs of pulmonary oedema?

A

tachypnoea, dyspnoea and crackles upon lung field auscultation

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120
Q

what are the signs of venous engorgement?

A

jugular distention and pulsations

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121
Q

what is chemosis?

A

oedema of conjunctiva due to fluid excess

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122
Q

how can volume overload be avoided?

A

frequent monitoring and cautious administration

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123
Q

what are the 5 main methods of fluid administration?

A 
per os
subcutaneous
intravenous
central venous access
intra-osseous
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124
Q

how does per os fluid therapy occur?

A

through the mouth either through the animal drinking by itself or feeding tubes (NG or PEG)

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125
Q

what are 2 advantages of per os fluid therapy?

A

natural

body can regulate amount of fluid taken up and electrolytes required

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126
Q

what are 2 disadvantages of per os fluid therapy?

A

slow

trauma to mouth/throat may prevent this method

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127
Q

how does subcutaneous fluid therapy occur?

A

injection of fluids into subcutaneous space where fluid is slowly absorbed into regional capillaries and distributed equally into fluid compartments

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128
Q

what way may subcutaneous fluids be given?

A

through needle and syringe or via needle attached to giving set and bag

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129
Q

what are 2 advantages of subcutaneous fluid therapy?

A

useful in animals with very small vessels or those with mild dehydration (cats and kidney failure)

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130
Q

what are 2 disadvantages of subcutaneous fluid therapy?

A

slow

no infusion possible

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131
Q

how does intravenous fluid therapy occur?

A

absorbed through IV catheter placed in peripheral vein (cephallic, saphenous or marginal ear)

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132
Q

what are 2 advantages of IV fluid therapy?

A

quick access and potential infusion

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133
Q

what are 2 disadvantages of IV fluid therapy?

A

potential infection site

not always easy to place due to anatomy and temperament of animal

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134
Q

how does central venous access fluid therapy occur?

A

IV is placed in larger vessels (e.g. jugular)

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135
Q

when is central venous access often used?

A

critically ill small patients or large patients

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136
Q

what are two benefits of central venous access for fluid therapy?

A

quick

large fluid volumes possible

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137
Q

what are 2 disadvantages to central venous access fluid therapy?

A

infection is more likely/risky due to central location of vessel
requires more skill to place

138
Q

how is intra-osseus fluid therapy administered?

A

into the medullary cavity of the long bone

139
Q

how is fluid absorbed into the blood stream during intra-osseus fluid therapy?

A

medullary cavity is highly vascularised so fluid is absorbed into the blood stream through these vessels

140
Q

what are 2 advantages of intra-osseus fluid therapy?

A

useful in neonates

when vessels have collapsed during resuscitation

141
Q

what are 2 disadvantages of intra-osseus fluid therapy?

A

infection risk is high

requires skill and specialist equipment

142
Q

what are the 6 main factors to consider when choosing a fluid administration route?

A

patients underlying disease process and co-morbidities
desired speed, volume and duration of fluid therapy
the type of fluid and/or drugs being administered
the risks associated with the route of administration
the availability of equipment, expense of equipment, availability of monitoring and technical expertise required for the route of administration
other patient factors e.g. species, breed and temperament

143
Q

for what 5 reasons should supportive diagnostics be used when using fluid therapy?

A

to support assessment of patient shock or dehydration

for investigation of underlying causes of shock or dehydration

some tests may help with prognostication

to help decide which fluids to use

to monitor effects of therapy

144
Q

what is the minimum database?

A

diagnostic tests used when patients are critically ill to assess status and need for fluid therapy

145
Q

what 6 tests are included in the minimum database?

A 
PCV
TP
urea
glucose 
lactate
blood smear
146
Q

what are the 4 key advantages of using the minimum database?

A

quick to perform
requires very little blood
cheap
facilitates decision making to stabilise critical patient

147
Q

how should PCV and TP be interpreted?

A

together and in the context of clinical findings

148
Q

are changes in PCV and TP diagnostic?

A

no

149
Q

what is normal PCV in the dog?

A

35-55%

150
Q

what is normal PCV in the cat?

A

25-45%

151
Q

what is normal TP?

A

50-70g/L

152
Q

what are the possible causes of increased PCV and increased TP?

A

dehydration

153
Q

what are the possible causes of increased PCV and normal TP?

A

normal for breed
polycythaemia
dehydration with concurrent protein loss

154
Q

what are the possible causes of normal PCV and increased TP?

A

hyperglobulinaemia

artefact (e.g. lipaemia)

155
Q

what are the possible causes of normal PCV and decreased TP?

A

acute hemorrhage
hypoproteinaemia
severe vasculitis

156
Q

what are the possible causes of decreased PCV and normal TP?

A

haemorrhagic anaemia

157
Q

what are the possible causes of decreased PCV and decreased TP?

A

haemorrhage
anaemia and hypoproteinaemia
aggressive IVFT

158
Q

why can haemorrhage not be ruled out even if PCV and TP are normal?

A

these are relative values (total blood volume may be lost but levels within could remain the same)
possibility of splenic contraction increasing PCV and TP levels in acute illness

159
Q

what else must happen during a PCV as well as the process itself?

A

visual inspection of serum to look of abnormalities (lipaemia/icteric serum)

160
Q

how can blood urea be quickly tested?

A

dipstick blood urea nitrogen (BUN)

161
Q

are high or low values of BUN more accurate?

A

low, high values should be confirmed with lab methods

162
Q

what are the main causes of rises in blood urea (azotemia)?

A

pre-renal
renal
post renal

163
Q

what is a pre-renal cause of azotemia?

A

dehydration or bleeding

164
Q

what is a renal cause of azotemia?

A

loss of renal function (e.g. AKI)

165
Q

what is a post renal cause of azotemia?

A

obstruction of urinary tract

166
Q

what may low urea be due to?

A

severe hepatic dysfunction (PSS)

167
Q

what may be triggered by abnormal blood urea results?

A

further investigation

168
Q

why must hypoglycaemia be addressed alongside other supportive therapies?

A

animals with hypoglycaemia will not respond to supportive therapy until hypoglycaemia is addressed

169
Q

under what 5 conditions must blood glucose always be checked?

A 
a patient presenting with altered mentation
patients experiencing seizures
patients with distributive shock
paediatric patients
patients with history compatible with DM
170
Q

what are the 7 possible causes of hypoglycaemia?

A 
paediatric patients
sepsis
insulin overdose
hypoadrenocoticism
severe hepatic dysfunction
prolonged seizure activity
insulinoma
171
Q

what is the main cause of persistent hyperglycaemia?

A

uncontrolled diabetes

172
Q

what are the 4 main causes of transient hyperglycaemia?

A

stress hyperglycaemia
head trauma
seizures
severe hypovolaemia or hypoxia

173
Q

in what species does stress hyperglycaemia occur most often?

A

cats

174
Q

what else should be measured in patients with high blood glucose?

A

serum or urine ketones to check for ketosis

175
Q

what is lactate a marker of?

A

tissue hypoxia

176
Q

what can cause an increase in lactate levels?

A

shock

177
Q

what can serial checking of lactate do?

A

monitor response to therapy

178
Q

what 5 areas is a blood smear useful for?

A

if anaemia is regenerative or non-regenerative
to look for RBC morphology changes that may be indicative of disease
change in circulating WBC numbers
adequacy of platelet numbers
to look for blood borne parasites

179
Q

what RBC morphology changes may be indicative of disease?

A

ghost cells
spherocytes
schistocytes (fragmented parts of RBC)
Heinz bodies

180
Q

what can be done with all the information gained from the minimum database tests?

A

interpretation of findings in context of history and physical exam
aim to correct abnormalities or act

181
Q

what are the 5 extra tests that could be used alongside the minimum database?

A 
electrolytes
minerals
acid-base and blood gas analysis
urinalysis
rapid ultrasound scans
182
Q

what are the 3 key electrolytes?

A

potassium
sodium
chloride

183
Q

what electrolyte is most often disturbed?

A

potassium

184
Q

what is the most severe out of hyperkalaemia and hypokalaemia?

A

hyperkalaemia

185
Q

what are the effects of hyperkalaemia?

A

life threatening effects on myocardial conduction

186
Q

what are the 3 overarching causes of hyperkalaemia?

A

decreased urinary excretion
translocation from intracellular to extracellular
increased intake

187
Q

what are the 6 causes of hyperkalaemia due to decreased urinary excretion?

A 
urethral obstruction
uroabdomen
hypoadrenocorticism
anuric/oliguric renal failure
GI disease
body cavity effusion
188
Q

what are the 3 causes of hyperkalaemia linked to translocation of potassium from intracellular to extracellular?

A

massive cell death (e.g. reperfusion injury, tumor lysis syndrome, heat stroke
insulin deficiency
acute acidosis

189
Q

what is the cause of hyperkalaemia due to increased intake of potassium?

A

iatrogenic

190
Q

define iatrogenic

A

caused by medical exam or treatment

191
Q

what is a priority when treating hyperkalaemia?

A

stabilisation and treatment

192
Q

how may hyperkalaemia be treated?

A

IVFT - isotonic colloid
calcium gluconate
glucose +/- soluble insulin
treatment of underlying cause

193
Q

when treating hyperkalaemia what is essential?

A

continuous monitoring including ECG to ensure hypokalaemia doesn’t occur

194
Q

in what patients is hypokalaemia common?

A

critically ill patients - often inappetant and on long term IVFT

195
Q

what are the signs of hypokalaemia?

A

non specific including weakness, lethargy, ileus and anorexia

196
Q

what may be caused by severe hypokalaemia?

A

respiratory muscle weakness and hypoventilation

197
Q

what are the 3 overarching reasons for hypokalaemia?

A

increased loss of K+
translocation from extracellular to intracellular
decreased intake of K+

198
Q

what are the 2 causes of hypokalaemia due to increased loss?

A

GI tract losses e.g. vomiting or diarrhoea

urinary tract losses (e.g. CKD, post-obstructive diuresis, some diuretic

199
Q

what are the 3 causes of hypokalaemia due to translocation from extracellular to intracellular?

A

insulin or glucose containing fluids (care when treating hyperkalaemia!)
alkalaemia
re-feeding syndrome

200
Q

what are the 2 causes of hypokalaemia linked to decreased K+ uptake?

A

inappetance/anorexia

long term IVFT with low potassium conc.

201
Q

how should hypokalaemia be treated?

A

address underlying cause

K+ supplementation (oral or IV)

202
Q

when is IV K+ most often given?

A

in critically ill patients

203
Q

what can potassium be added to during IVFT?

A

saline or Hartmann’s

204
Q

when may oral potassium supplementation be best?

A

patients with chronic disease and hypokalaemia

205
Q

what must never be done with fluids containing potassium?

A

do not bolus!!

206
Q

what does measured serum sodium concentration represent?

A

the amount of sodium relative to the amount of water in the intravascular compartment

207
Q

are mild sodium abnormalities common?

A

yes - and rarely cause clinical signs

208
Q

are severe sodium abnormalities common?

A

no

209
Q

what determines the severity of signs during sodium abnormalities?

A

the rate at which the abnormality develops as opposed to the absolute value of the abnormality

210
Q

what are the main signs of sodium abnormality?

A

neurological - due to movement of water in and out of cells (particularly brain cells - cerebral dehydration or oedema)

211
Q

what are the 3 overarching causes of hypernatraemia?

A

solute gain
pure water deficit
loss of water in excess of sodium

212
Q

what are the 2 main causes of hypernatraemia due to solute gain?

A

salt poisoning

iatrogenic

213
Q

what are the 3 main causes of hypernatraemia due to pure water deficit?

A

hyperthermia
diabetes insipidus
inadequate access to water

214
Q

what are the 4 causes of hypernatraemia due to loss of water in excess of sodium?

A

renal failure
vomiting and diarrhoea
burns
drugs

215
Q

what are the 3 overarching causes of hyponatraemia?

A

impaired water excretion
pure water gains
loss of sodium in excess of water

216
Q

what is a cause of hyponatraemia due to impaired water excretion?

A

congestive heart failure

217
Q

what is a cause of hyponatraemia due to pure water gains?

A

psychogenic polydipsia

218
Q

what are the 3 main causes of hyponatraemia due to loss of sodium in excess of water?

A

hypoadrenocorticism
vomiting and diarrhoea
drugs

219
Q

how can most sodium abnormalities be treated?

A

treatment of underlying disease process

220
Q

what will be required for patients with clinical signs associated with sodium abnormality?

A

specific therapy will be required to correct this

221
Q

how should a sodium abnormality be treated if it is going to be?

A

slow changes as rapid will exacerbate clinical signs (over 24-48 hrs)

222
Q

how should hypovolaemia be addressed in the patient with a sodium disturbance?

A

with fluids of similar sodium concentration as the patients serum

223
Q

what ratio should sodium be to chloride?

A

1:1

224
Q

how do you calculate if changes in chloride are proportionate/disproportionate?

A

chloride needs to be corrected - results are modified to take into account sodium changes. this value is then used to determine differential diagnosis

225
Q

how is chloride disturbance treated if it is proportionate?

A

sodium is corrected and so chloride corrects itself

226
Q

if corrected chloride is normal what does it indicated changes are due to?

A

changes in free water and so the primary cause of hyper/hyponatraemia should be investigated

227
Q

what is corrected hyperchloraemia due to?

A

artefact
iatrogenic
asscoiated with acid-base disturbance

228
Q

what is corrected hypochloraemia due to?

A

iatrogenic (diuretics)

loss of chloride in excess of sodium (e.g pure gastric vomiting)

229
Q

why may pure gastric vomiting cause hypochloraemia?

A

loss of lots of HCl due to pyloric obstruction and vomiting from stomach only. No buffer from duodenum (NaOH) to balance Cl loss

230
Q

what are the main causes of hypocalcaemia?

A

eclampsia
pancreatitis
urethral obstruction

231
Q

what are the clinical signs of hypocalcaemia?

A

tetany
panting
hyperthermia
facial pruritus

232
Q

what is the treatment for hypocalcaemia?

A

calcium gluconate IV

233
Q

what must be monitored when giving calcium gluconate IV?

A

ECG to check for hypokalaemia

234
Q

what are the causes of hypercalcaemia?

A

hyperparathyroid

235
Q

what are the clinical signs of hypercalcaemia?

A 
PUPD
anorexia
lethargy
depression
vomiting
shivering
twitching
236
Q

how can hypercalcaemia be treated?

A

underlying cause treated and correction of dehydration

salmon calcitonin or bisphosphonates considered if severe

237
Q

in what types of patient is metabolic acidosis common?

A

clinically unwell patients

238
Q

in what patients is respiratory acidosis most common?

A

anaesthetised animals

239
Q

how can acidosis be treated using IVFT?

A

Hartmann’s as it contains lactate

240
Q

how may alkalosis be treated using IVFT?

A

0.9% NaCl as it is slightly acidifying

241
Q

how should an acid base disturbance be treated?

A

treat underlying disease
support renal and respiratory systems
manage shock and dehydration

242
Q

define shock

A

imbalance between oxygen delivery to the tissues and oxygen consumption by the tissues

243
Q

what happens when the body’s cells do not receive enough oxygen?

A

switch to anaerobic respiration leading to the production of lactate and free hydrogen ions. This leads to acidosis which can then lead to cell death

244
Q

define hypoperfusion (circulatory shock)

A

a critical condition that is brought on by a sudden and global deficit in tissue perfusion resulting in inadequate delivery of oxygen and nutrients to vital organs

245
Q

what is the most common cause of shock in veterinary patients?

A

circulatory shock

246
Q

what are the 4 types of circulatory shock?

A

hypovolaemic
cardiogenic
obstructive
distributive

247
Q

what causes circulatory shock?

A

any disease process which lowers mean arterial blood pressure (and so tissue perfusion)

248
Q

what does reduced mean arterial blood pressure lead to?

A

reduced perfusion

249
Q

what is blood pressure the product of?

A

cardiac output and total peripheral resistance

250
Q

what determines cardiac output?

A

heart rate and stroke volume

251
Q

what is stroke volume determined by?

A

pre-load, after-load and hearts contractility

252
Q

what is hypovolaemic shock?

A

shock caused by a decreased blood volume

253
Q

what may hypovolaemic shock be the result of?

A

fluid losses or decreased fluid intake

254
Q

what are the 2 types of fluid losses that can lead to hypovolaemia?

A

haemorrhagic - internal/external

non-haemorrhagic - internal/external

255
Q

what may decreased fluid intake that leads to hypovolaemia be due to?

A

restricted water access or conditions where animals are unable to swallow/keep down water

256
Q

how is perfusion reduced in hypovolaemic shock?

A

reduced stroke volume will reduce cardiac output, this leads to reduce MABP and so reduced perfusion

257
Q

what is cardiogenic shock?

A

shock caused by ‘forward’ or pump failure (reduced cardiac output)

258
Q

what are 4 examples of things that may cause cardiogenic shock?

A

conditions with reduced systolic function
conditions with diastolic dysfunction
bradyarrhythmias
tachyarrhythmias

259
Q

what is a condition which can cause reduced systolic function?

A

dilated cardiac myopathy - heart contracts poorly so stroke volume is reduced and therefore perfusion

260
Q

what are 2 conditions with diastolic dysfunction that can cause cardiogenic shock?

A

pericardial tamponade

hypertrophic cardiomyopathy

261
Q

what is hypertrophic cardiomyopathy?

A

enlargement of heart muscle leading to difficulties in the heart pumping adequately

262
Q

what is dilated cardiomyopathy?

A

thinning of heart muscle so that heart is unable to pump strongly enough

263
Q

how do conditions with reduced systolic function lead to cardiogenic shock?

A

reduced pre-load and poor contractility so reduced SV and so reduced perfusion

264
Q

how do conditions with diastolic dysfunction lead to cardiogenic shock?

A

prevention of adequate filling of the heart (small pre-load) so SV is reduced and so is perfusion

265
Q

what is an example of a bradyarrhythima that can lead to cardiogenic shock?

A

AV block

266
Q

what is AV block?

A

when the electrical signal that controls your heartbeat is partially or completely blocked

267
Q

how do bradyarrhythmias cause cardiogenic shock?

A

reduced heart rate so reduced cardiac output and so reduced perfusion

268
Q

what tachyarrhythmias can cause cardiogenic shock?

A

ventricular tachycardia

269
Q

how can tachyarrhythmias cause cardiogenic shock?

A

due to speed of contraction there is reduced stroke volume and so cardiac output leading to reduced perfusion

270
Q

what must be remembered about the link between backward failure and cardiogenic shock?

A

not all patients with ‘backward’ failure are in cardiogenic shock (forward failure)

271
Q

what is an example of ‘backwards’ failure?

A

mitral valve disease so blood is not contained in the left ventricle and can move back into the atria on contraction

272
Q

how is perfusion reduced in cardiogenic shock?

A

reduced cardiac output leads to reduced blood pressure and so tissue perfusion

273
Q

what causes obstructive shock?

A

physical obstructions in blood flow to or from the heart or through the great vessels

274
Q

what are 4 key causes of obstructive shock?

A

GDV (gastric dilation-volvulus)
pericardial tamponade
tension pneumothorax
pulmonary or aortic thromboembolism

275
Q

how does GDV cause obstructive shock?

A

compression of large vessels (IVC and aorta) which affects supply to heart and tissues

276
Q

how does pericardial tamponade cause obstructive shock?

A

rapid development may collapse right atrium and so reduce cardiac output and so tissue perfusion

277
Q

how is perfusion affected by cardiogenic shock?

A

reduced preload and afterload leading to reduced CO and so blood pressure and perfusion

278
Q

what causes distributive shock?

A

maldistribution of blood flow

279
Q

what is maldistribution of blood flow seen in distributive shock usually due to?

A

inappropriate and widespread vasodilation

280
Q

what may distributive shock be caused by?

A 
histamine release (anaphylaxis)
generalised uncontrolled inflammatory responses due to bacterial infection (sepsis) or non infectious insults (pancreatitis, trauma, burns etc)
281
Q

how does distributive shock affect perfusion?

A

reduced TPR leading to reduced pre-load and so reduced SV and blood pressure

282
Q

what can some disease states do with regards to shock?

A

cause it through multiple mechanisms

283
Q

what happens during the bodies physiological response to hypovolaemic shock?

A

body initiates a neurohormonal response to decreased effective circulating volume with the aim to preserve cardiac output

284
Q

what are the 4 key physiological responses of the body to hypovolaemic shock?

A

catecholamine release
activation of renin-angiotensin-aldosterone system
release of ADH
contraction of the spleen

285
Q

how does catecholamine release help the body to compensate for hypovolaemic shock?

A

increased HR, increased cardiac contractility and peripheral vasoconstriction

286
Q

how does activation of renin-angiotensin-aldosterone system aid response to hypovolaemic shock?

A

increases sodium and water retention and peripheral vasoconstriction

287
Q

how does release of ADH aid response to hypovolaemic shock?

A

increases renal water retention

288
Q

how does contraction of the spleen aid response to hypovolaemic shock?

A

releases more RBC into the circulation

289
Q

how can hypovolaemic shock be recognised?

A

understanding of the body’s physiological response will help to understand what the patient may ‘look’ like like upon physical exam

290
Q

what is the patients presentation with hypovolaemia also affected by alongside physiological response?

A

the severity of hypovolaemia

291
Q

how is hypovolaemic shock classified?

A

decompensated

compensated

292
Q

what is happening to a patient with compensated shock?

A

homeostatic mechanisms are successfully maintaining tissue perfusion

293
Q

what is happening to a patient with decompensated hypovolaemic shock?

A

the compensatory physiological mechanisms are failing and the patient is in danger of dying

294
Q

describe how to recognise mild (compensatory) shock in the dog

A 
moderate elevation of HR - 130 to 150 bpm
normal to pinker MM
CRT of <1
bounding pulse
>90 Systolic BP
normal mentation
lactate: 3-5 mmol/l
295
Q

describe how to recognise severe (decompensatory) shock

A 
HR of 170-220
pale pink or white MM
CRT of >2
very weak pulse
<90 Systolic BP
obtunded
Lactate: >8 mmol/L
296
Q

how do cats respond to hypovolaemia?

A

less predictable than dogs and horses

bradycardia and hypothermia are common

297
Q

why is the feline response to hypovolaemia so much more challenging?

A

white coat syndrome (leading to tachycardia)
difficult to charactorise pulse quality
may decompensate more rapidly or just present later

298
Q

what is involved in initial treatment of hypovolaemia?

A

rapid administration of fluids to restore intravascular volume and improve tissue perfusion

299
Q

is there a difference in outcome between crystalliod and colloid therapy for fluid resuscitation?

A

none known

300
Q

where should treatment of hypovolaemia also be directed?

A

at underlying cause

301
Q

what may be required following severe blood loss?

A

blood transfusion as too much fluids may begin to dilute RBC

302
Q

what is a key priority in the hypovolaemic patient?

A

gaining vascular access

303
Q

how should hypovolaemic shock be treated?

A

bolus for cat or dog over 15-20 mins and monitor throughout
reassess for improvement
administer a further bolus if required
monitor throughout
reassess again
once patient is stable move on to maintainence therapy

304
Q

what is the correct bolus volume for dogs to correct hypovolaemia?

A

10-20ml/kg

305
Q

what is the correct bolus volume for cats to correct hypovolaemia?

A

5-10ml/kg

306
Q

why is there such a variety in bolus sizes to correct hypovolaemia?

A

bolus can be tailored to levels of hypovolaemia

307
Q

what is the aim of treatment of hypovolaemic shock?

A

return patient to normal or near normal cardiovascular parameters

308
Q

what should happen if there is evidence of volume overload?

A

therapy discontinued immediately

309
Q

at what volumes of boluses administered should an alternative diagnosis be considered?

A

45-60 ml/kg in dogs

30-35 ml/kg in cats

310
Q

when should the administration of blood products be considered during treatment for hypovolaemia?

A

patient is loosing blood and there is concurrent anaemia (PCV <20%)

311
Q

what does a ‘shock dose’ represent?

A

patients entire blood volume and so is not an aim to be administered

312
Q

how can the efficacy of hypovolaemic shock treatment be determined?

A 
repeat major body system assessment every 15-30 mins during initial stabilisation
check BP
monitor lactate
urine output
ECG
313
Q

what major body system parameters should be assessed during stabilisation of patient with hypovolaemic shock?

A 
mentation
HR
CRT
MM
pulse quality
temperature
314
Q

why should blood pressure be interpreted with caution when monitoring a patient with hypovolaemic shock?

A

BP my return to normal but patient is just compensating

315
Q

what would you expect to happen to lactate levels with effective treatment of hypovolaemic shock?

A

decrease

316
Q

what is a target for urine output that patients should be meeting once hypovolaemia is resolved and the have no underlying conditions to prevent normal urine output?

A

> 0.5ml/kg/hr

317
Q

what is an ECG useful when monitoring the patient recovering from hypovolaemic shock?

A

monitoring arrhythmias which may be responsible for shock state or that may develop as a result of shock

318
Q

what effect do hypertonic fluids have on movement of water?

A

will move water from extravascular to intravascular compartment

319
Q

what are advantages of hypertonic fluids?

A

lowers initial volume required for volume resuscitation

useful for cerebral oedema as will reduce fluid around brain

320
Q

what is the usual bolus of hypertonic fluid for dogs?

A

4-7ml/kg

321
Q

what is the usual bolus of hypertonic fluid for cats?

A

2-4 ml/kg

322
Q

how many times should boluses of hypertonic fluid be given?

A

once

323
Q

over what time period must hypertonic fluid boluses be given?

A

> 5mins

324
Q

what must follow a hypertonic fluid bolus?

A

isotonic crystalloids to reduce the debt to extravascular compartment

325
Q

when are hypertonic fluids contraindicated?

A

if hypernaturaemic or dehydrated

326
Q

why is hypertonic fluid therapy so useful in large animals?

A

difficult to administer required volumes quickly enough

327
Q

what size bolus of hypertonic fluids is given to large animals?

A

4 ml/kg

328
Q

how much isotonic colloid must be given for every litre of hypertonic fluid?

A

10L

329
Q

what is the fluid requirement for dogs and cats?

A

2ml/kg/hr or 50ml/kg/day

330
Q

what is the calculation used to work out dehydration deficit using estimated percentage?

A

body weight (kg) x % dehydrated = deficiency

331
Q

what is 1kg of dehydration deficiency equivalent to?

A

1L

332
Q

what is the equation used to calculate dehydration deficit using PCV?

A

% dehydration x body weight (kg) x 10

333
Q

what does 1% increase in PCV equate to in fluid loss?

A

10ml

334
Q

how are ongoing losses calculated?

A

number of v+/D+ episodes x 4ml x bodyweight (kg)

335
Q

what is the calculation for total fluid req. over 24 hours?

A

dehydration deficit + maintenance + ongoing losses

336
Q

how is total fluid req. converted to ml/hr?

A

TFR/24 hours

337
Q

how is ml/hr converted to ml/min?

A

divided by 60

338
Q

how are drops per min calculated from ml/min?

A

ml/min x giving set factor (20 or 60)

339
Q

how are drops per second calculated from drops per min?

A

60/drops per min

340
Q

what are the most common catheters?

A

over the needle

341
Q

what is the correct size of IV catheter?

A

allow high fluid rate to pass through without occluding vein (too large) or limiting volume (too small)

342
Q

what should be checked when setting up fluid bags and giving sets?

A

correct fluids/set?
in date?
is packaging damaged?
fluids free from contaminants?

X CNT 1 (4 decks)

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