Fluid Therapy Flashcards

1
Q

How is total fluid requirement calculated?

A

Fluid requirement (ml) = extravascular fluid deficit (ml) + maintenance requirement (ml) + ongoing loss (ml)

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2
Q

How is extravascular fluid deficit calculated?

A

Extravascular fluid deficit (ml) = % dehydration x body weight (kg)

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3
Q

How is the water that make sup 60% of the body split up into compartments?

A
  • 5% = intravascular compartment, due to water inside vessels
  • 55% extravascular, outside blood vessels
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4
Q

How is the intravascular compartment split up?

A
  • 40% = water found inside cells, for maintenance of cellular size and shape
  • 15% found in between cells
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5
Q

What is the generally considered value of maintenance fluid?

A

2ml/kg/h (but many factors affect this)

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6
Q

List the factors influencing the fluid losses in a normal animal.

A

Fluid lost during breathing, normal frequency of urination, sweating, panting, hydration, diet, exercise.

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7
Q

List the factors influencing the fluid gains in diseased animals.

A

Vomiting, inappetence and not drinking, diarrhoea, parasites, kidney disease, leaky valve, abnormal lymph drainage.

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8
Q

What are the 3 main categories of fluid disturbance in sick patients?

A

Changes in volume - dehydration, hypovolaemia
Changes in content - elect5rolyte disturbance, blood glucose, blood protein
Changes in distribution - third spacing

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9
Q

Define hypovolaemia.

A

Fluid is lost quickly from the intravascular space. This results in tissue hypoperfusion/shock.

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10
Q

Define dehydration.

A
  • Fluid is lost slowly from the extravascular compartment
  • Unable to keep up with homeostasis of fluid balance.
  • There is time for fluid to be redistributed across all body compartments, resulting in water being lost equally from all body compartments.
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11
Q

What is the equation involving blood pressure and cardiac output?

A

BP = CO X TPR

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12
Q

What compartments of your triage will give you information about the patient’s intravascular volume status?

A

Heart rate
Pulse quality
Mucous membrane colour
Capillary refill time
Blood pressure
Mentation
(Temperature)

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13
Q

What does a heart rate of above 220bpm indicate?

A

Tachyarrhythmia, as the body won’t use a heart rate of 220 to maintain cardiac output, as refill time in ventricles becomes so small that CO decreases.

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14
Q

What does a suspiciously low heart rate indicate?

A

Hyperkalaemia, as a heart rate that low would have low CO.

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15
Q

What would be the physical exam of a normal animal?

A

6-120 bpm
Pink mmbs
CRT <2s
Normal pulse quality
Systolic BP >90mmHg
Normal mentation

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16
Q

What would the physical exam of a mild shock/compensatory animal?

A

130-150bpm
Normal-pinker mmbs
CRT <1s
Bounding pulse quality
Systolic BP >90mmHg
Normal mentation

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17
Q

What would be the physical examination of an animal with moderate shock be?

A

150-170bpm
Pale pink mmbs
CRT 2s
Weak pulse quality
Systolic BP >90mmHg
Normal-obtunded mentation

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18
Q

What would the physical examination of an animal with severe shock/decompensatory?

A

170-220bpm
Pale pink-white mmbs
CRT >2s
Very weak pulse quality
Systolic BP <90mmHg
Obtunded mentation

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19
Q

What components of your triage/physical exam will give you information about the patient’s extravascular volume status?

A

Moistness of mucous membranes
Skin turgor (tenting) – SA over the head, LA above eye
Weight
Globe position in orbit
(Urine output)

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20
Q

What does <5% dehydration mean?

A

Not clinically detectable, suspected from clinical history

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21
Q

What does 5-6% dehydration mean?

A

Tacky mucous membranes, mild delay in skin tent return

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22
Q

What does 6-8% dehydration mean?

A

Dry mucous membranes, mild increase in CRT, mild to moderate delay in skin tent return and/or sunken eyes

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23
Q

What does >10-12% dehydration mean?

A

Dry mucous membranes, CRT >2-3s, and/or signs of shock, marked prolongation/standing skin tent, sunken eyes

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24
Q

What does a >15% dehydration mean?

A

Incompatible with life

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25
Q

What parameters from haematology, biochemistry and urinalysis may be affected by a patient’s hydration status?

A
  • Increased packed cell volume
  • Increased urea and creatinine
  • Higher urine specific gravity
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26
Q

What are the aims of fluid administration if hypovolaemia is present?

A

Patient is unstable. Proceed stabilisation and rapid fluid resuscitation of the patient = giving boluses of fluid.

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27
Q

What are the aims of fluid administration if hypovolaemia is not present?

A

Patient is stable. Check for extravascular fluid losses. If present, these should be corrected slowly.

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28
Q

Define colloid osmotic pressure.

A

A type of osmotic pressure caused by very large molecules that do not readily cross semi-permeable membranes. The high colloid osmotic pressure of the remaining fluid within the venules, pulls fluid back in.

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29
Q

Define crystalloid.

A

Solutions containing small molecules such as electrolytes dissolved in water. They readily move out of the blood stream through the capillary membrane.

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30
Q

What is the tonicity of crystalloids?

A

Their tonicity is variable, they do not exert any colloid osmotic pressure. - They can be isotonic, hypertonic or hypotonic.

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31
Q

Define colloid.

A

Solutions containing large molecules. These molecules do not readily move out of the bloodstream.

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32
Q

What is the tonicity of colloids?

A

They are isotonic but they do exert colloid osmotic pressure. This varies according to size and number of large molecules within the solution.

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33
Q

Define tonicity.

A

The capability of a solution to modify the volume of cells by altering their water content.

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34
Q

Define hypertonic.

A

Having a higher concentration of solutes, water will flow out of the cell into the extracellular fluid. Cells will shrink until 2 concentrations become equal.

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35
Q

Define hypotonic.

A

Having a lower concentration of solutes, water will flow into the cell from the extracellular fluid. Cells will swell.

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36
Q

Define isotonic.

A

Having the same concentration of solutes. There will be no net shifts of fluid.

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37
Q

What is the composition of an isotonic crystalloid?

A

Mimic intravascular electrolyte concentrations – they are high sodium and low potassium.

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38
Q

What is an example of an isotonic crytsalloid?

A

0.9% NaCl and Hartmann’s

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39
Q

How can isotonic crystalloids be used?

A

For dehydrated and hypovolaemic patients

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40
Q

Why are hypotonic crystalloids rarely used?

A

Can be indicated for the management of hypernatraemia, which is rare.

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41
Q

What is an example of a hypotonic crystalloid and why is it hypotonic?

A

0.18% saline and 4% glucose. Glucose gets metabolised in the body and so is isotonic in your hand but is hypotonic in the body. This is so it does not cause phlebitis/local inflammation.

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42
Q

What can occur if hypotonic crystalloids are used inappropriately?

A

Acute hyponatraemia, leading to causing cerebral oedema and death

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43
Q

What happens to fluid in the body upon hypotonic crystalloid administration?

A

Net shifting of fluid from intravascular to extravascular compartments.

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44
Q

What happens to fluid in the body upon hypertonic crystalloid administration?

A

Net shifting of fluid from the extravascular to intravascular compartment.

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45
Q

What are 2 examples of a hypertonic crystalloid?

A

7.2% NaCl and 7.5% NaCl

46
Q

When are hypertonic crystalloids most commonly used?

A

Small animals: management of raised intracranial pressure

Large animals: rapid intravascular volume expansion

47
Q

Why should hypertonic crystalloids be stored away from other fluids in a practice?

A

Giving this in the wrong situations is very dangerous. Should not be used for management in dehydration, as we are losing fluid from extravascular.

48
Q

What is a colloid?

A

Their large molecules mean that they have an increased colloid osmotic pressure.

49
Q

Why do colloids have a longer duration of action than crystalloids?

A

They stay in the intravascular space for longer

50
Q

What are examples of natural and synthetic colloids?

A

They can be natural, such as plasma. They can be artificial, such as gelatine or hydroxyethyl starches.

51
Q

How can colloids be used for volume resuscitation?

A

A smaller volume of fluid can be used subsequently for volume resuscitation.

52
Q

What are the uses of colloids?

A

Management of hypovolaemia

Plasma can be used for treatment of some coagulopathies

(Not suitable for dehydration or electrolyte abnormalities)

53
Q

What are the risks of colloids?

A
  • Coagulopathy
  • Allergic reactions
  • Anaphylaxis
  • Increased risk of death when used in human patients with sepsis
  • Increased of AKI in people
  • They may not be as effective as once thought
  • They are expensive and rarely used
54
Q

How can fluid be administered per os?

A

Voluntary or feeding tube

55
Q

What are the advantages of per os?

A

Body can fine tune via intestine absorption
Owners can do this at home

56
Q

What are the disadvantages of per os?

A

Cannot do this if no gag reflex – coma, anaesthetised, seizing

Not suitable for hypovolaemic or clinically moderate to severe dehydration as absorption is too slow (in shock, perfusion to gut decreased).

57
Q

What are the advantages of subcutaneous fluid administration?

A

Cheap
Easy
Owners can learn

58
Q

What are the disadvantages of subcutaneous fluid administration?

A

Absorption is slow (not suitable for hypovolaemia or dehydration)

Limit about how much you can administer

59
Q

Name the 4 types of shock.

A

Hypovolaemic
Cardiogenic
Obstructive
Distributive

60
Q

Define hyperperfusion/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. The most common cause of shock in veterinary patients.

61
Q

What is the affect of reduced blood pressure?

A

Reduced perfusion

62
Q

How is blood pressure calculated?

A

Blood pressure = cardiac output x systemic vascular resistance

63
Q

What is stroke volume determined by?

A

By pre-load, afterload and the heart’s contractility.

64
Q

What does shock result in?

A

Shock resulting in decreased blood volume

65
Q

What is cardiogenic shock caused by?

A

Forward or pump failure – reduced cardiac output

66
Q

What are some examples of conditions that result in cardiogenic shock?

A
  • Conditions with reduced systolic dysfunction, such as DCM
  • Conditions with diastolic dysfunction, such as HCM or pericardial tamponade
  • Bradyarrhythmias, such as AV block
  • Tachyarrythmias, such as ventricular tachycardia
67
Q

What is obstructive shock the result of?

A
  • Due to physical obstructions in blood flow to or from the heart or through the great vessels
  • Overlap with cardiogenic shock
68
Q

What are the causes of obstructive shock?

A

GDV – gastric dilation volvulus. Massive gaseous distension of the stomach will compress large intra-abdominal vessels such as the caudal vena cava.

Pericardial tamponade – pericardial effusion, collapse of atria

Tension pneumothorax – gas build up in pleural space, positive pressure on thoracic greater vessels

Pulmonary or aortic thromboembolism

69
Q

What is distributive shock the result of?

A
  • Due to maldistribution of blood flow
  • Usually due to inappropriate and widespread vasodilation
70
Q

What are the causes of distributive shock?

A

Histamine release

Sepsis

Non-infectious insults, such as pancreatitis, trauma, burns

71
Q

What is the physiological response to hypovolaemic shock?

A

The body initiate s a neurohormonal response to the decreased effective circulating volume with the aim to preserve cardiac output

72
Q

How does the body preserve cardiac output?

A
  • Catecholamine release – increased heart rate, increased cardiac contractility, peripheral vasoconstriction.
  • Activation of the renin-angiotensin-aldosterone system – increases sodium and water retention and peripheral vasoconstriction.
  • ADH may be released – increase renal water retention
  • The spleen may contract to release more RBCs into the circulation
73
Q

How is hypovolaemic shock further classified?

A

Compensated – the homeostatic mechanisms are successfully maintaining tissue perfusion

Decompensated – the compensatory physiological mechanisms are failing, and the patient in in danger of dying

74
Q

How is mild shock (compensatory) recognised in canine patients?

A

130-150 bpm
Normal to pinker mmbs
<1 CRT
Bounding pulse quality
>90 BP
Normal mentation
3-5mmol/L lactate conc

75
Q

How is moderate shock recognised in canine patients?

A

150-170 bpm
Pale pink mmbs
2s CRT
Weak pulse quality
>90 BP
Normal-obtunded mentation
5-8 mmol/L lactate conc

76
Q

How is severe shock (decompensatory) recognised in canine patient?

A

170-220bmp
Pale pink-white mmbs
>2 CRT
Very weak pulse quality
<90 BP
Obtunded mentation
>8mml/L lactate conc

77
Q

How is mild shock recognised in equine patient?

A

44-60bpm
Pinker mmbs
<1 CRT
Bounding pulse quality
Normal mentation
3-5mmol/L lactate conc

78
Q

How is severe shock recognised in equine patient?

A

> 60 bpm
Pale mmbs
2 CRT
Weak pulse quality
Depressed mentation
8mmol/L lactate conc

79
Q

What are the stages of hypovolaemic shock in the feline patient?

A
  • The feline response to hypovolaemia is less predictable
  • Bradycardia and hypothermia are common features
80
Q

Why is the feline response to hypovolaemia less predictable than the canine response?

A

The challenge of them being stressed in the practice. Characterising pulse quality is challenging. Do these patients decompensate more rapidly or present later or good at hiding features as prey species?

81
Q

How is hypovolaemic shock treated?

A
  • Initial treatment is rapid administration of fluids to restore the intravascular volume and improve tissue perfusion.
  • Treatments should also be directed at the underlying cause.
  • In severe blood loss transfusion therapy may be required.
  • Thus, getting vascular access is a priority.
82
Q

How are isotonic crystalloids used to treat hypovolaemic shock?

A
  1. Bolus
  2. Reassess for improvement
  3. Bolus again if required. Monitor
  4. Reassess the patient again
  5. If no improvement consider if you have the right diagnosis or if there is ongoing blood loss?
  6. Consider administration of blood products
  7. Once stable, move on to maintenance therapy
83
Q

How is the efficacy of treatment determined?

A
  • Every 15-30 mins: mentation, HR, pulse quality, mmbs colour, CRT, temperature
  • Blood pressure – interpret with caution.
  • Lactate – would expect this to decrease with effective treatment.
  • Urine output >0.5ml/kg/h has been suggested as a target.
  • ECG
84
Q

What must be done after hypertonic fluid administration?

A

Will need to be followed by isotonic crystalloids to replace the debt to the extravascular compartment.

85
Q

How should fluid be administered to horses and cows?

A
  • Administering enough fluid, fast enough is very difficult
  • Use of hypertonic fluid
  • Follow with large volume of isotonic water – stomach tube, voluntary or intravenous
86
Q

Can fluid therapy be used to treat other types of shock?

A

Fluid therapy is not indicated for all types of shock and may even be contraindicated

87
Q

How can fluid therapy be monitored?

A

Body weight
Physical examination
Monitoring urine output
Laboratory tests

88
Q

Which laboratory tests monitor fluid therapy?

A
  • Packed cell volume and total solids
  • Blood urea nitrogen and creatinine
  • Urine specific gravity
  • Lactate
  • Glucose
  • Electrolytes
  • Acid-base status – can’t be commonly assessed
89
Q

What is the most common electrolyte disturbance?

A

Potassium: hyperkalaemia and hypokalaemia. Needs to be maintained in a very narrow range.

90
Q

What are the causes of hyperkalaemia?

A

Decreased urinary excretion: urethral obstruction, uroabdomen, hypoadrenocorticism, anuric/oliguric renal failure, GI disease, body cavity effusion

Translocation from intracellular to extracellular: massive cell death, such as reperfusion injury, tumour lysis syndrome, heat stroke, insulin deficiency, acute acidosis

Increased intake – iatrogenic

91
Q

How is hyperkalaemia stabilised adn treated?

A
  • IVFT – an isotonic crystalloid
  • Calcium gluconate – dilute, can cause arrythmias in own right
92
Q

Why can glucose with/without soluble insulin be used to treat hyperkalaemia?

A

Glucose with/without soluble insulin, glucose can drag potassium back into cells with it. But patients in these situations are so sick that they are not able to produce insulin response so soluble insulin is also given. Risk of hypo/hyperglycaemia afterwards.

93
Q

What are the clinical signs of hypokalaemia?

A

Non-specific clinical signs, such as weakness, lethargy, ileus and anorexia

94
Q

What can severe hypokalaemia cause?

A

If severe can cause respiratory muscle weakness and hypoventilation (respiratory muscle weakness)

95
Q

What are the causes of hypokalaemia?

A

Increased loss: GI tract losses via vomiting or diarrhoea. Urinary tract losses, such as CKD, post obstructive diuresis, some diuretics, mineralocorticoid excess

Translocation from extracellular to intracellular: insulin/glucose containing fluids, alkalaemia, re-feeding syndrome

Decreased intake: inappetence/anorexia, long term IVFT with low potassium concentration

96
Q

How can hypokalaemia be managed?

A
  • Address underlying cause
  • Potassium supplementation
  • Intravenously most common in critically ill patients
  • Oral supplementation available for patients with chronic disease and hypokalaemia, such as CKD
97
Q

How is acidaemia and alkalaemia defined?

A

Acidaemia pH<7.35 and alkalaemia pH>7.45.

98
Q

What can metabolic acidosis be caused by?

A
  • A loss of base – bicarbonate with severe diarrhoea
  • A failure to excrete acid – hydrogen ions in some patients with renal failure
  • An accumulation of acid – lactic acid in patients with shock
99
Q

What is the body’s response to metabolic acidosis?

A

The body tries to achieve this by blowing off more CO2 in hyperventilation

100
Q

How is metabolic acidosis characterised?

A

Low pH and a low pCO2

101
Q

What are the causes of metabolic alkalosis?

A
  • Excessive administration of bicarbonate
  • Loss of acid, such as pyloric obstruction
102
Q

What is the body’s response to metabolic alkalosis?

A
  • By increasing blood CO2 > hypoventilation
  • The ability of the body to compensate in this way is limited. Hypoventilation > hypoxia > stimulation of ventilation
103
Q

How is metabolic alkalosis characterised?

A

Blood gas has high pH and high pCO2

104
Q

What is respiratory acidosis caused by?

A

Any disease/state which results in hypoventilation:
- Upper airway obstruction
- Pleural space disease
- Pulmonary disease
- CNS depression
- Depression of neuromuscular respiratory function

105
Q

What is the body’s response to respiratory acidosis?

A

The kidneys will retain more bicarbonate and excrete more hydrogen ions

106
Q

How is respiratory acidosis characterised?

A

Low pH, high CO2

107
Q

What is respiratory alkalosis caused by?

A

Which is caused by any disease/state which results in hyperventilation: pain, hyperthermia, stress

108
Q

How can acid-base disturbance alter approach to fluid therapy?

A
  • Sodium bicarbonate can be administered to patients with acidosis very rarely needed
  • Great risk of causing metabolic alkalosis
  • Never administer without access to blood gas analysis
109
Q

When orally rehydrating a calf, why do milk and oral life have to be alternated?

A

So as to not dilute this. Milk needs to be appropriately clotted in the abomasum so it can be digested.

110
Q

What are the advantages of giving fluids to a horse orally vs intravenously?

A

More practical in the field

111
Q

What are the disadvantages of giving fluids to this horse orally vs intravenously?

A

Not all horses tolerate repeated tubing

112
Q

Which fluid should be given orally?

A

Don’t give Hartmann’s orally, it is expensive, give pure tap water or Glauber’s salts dissolved in tap water.