U1 O2 - Shock, vascular access and fluid therapy

Question 1

Give an example of a hypertonic crystalloid?

Answer 1

7.2-7.5% NaCl

Hypertonic saline

Question 2

What does hypertonic crystalloids do when entering the body?

Answer 2

It results in a large osmotic gradient that draws water from the interstitial and Intracellular fluid compartments

This results in rapid expansion of intravascular volume

There is a NET movement of fluid into the vascular space

Question 3

In what cases can hypertonic saline be used?

Answer 3

Severe hypovolaemia

Resuscitation of dogs with GDV

Head trauma - increased intracranial pressure, small volumes call reduce risk of cerebral oedema whilst restoring blood pressure and cerebral perfusion

Question 4

What does hypertonic saline rely on for its effect?

Because of this what cases would it not be recommended?

Answer 4

It relies on interstitial fluid for effect so not recommend in patients with dehydration

Hypernatraemia

Question 5

Due to the rapid rise in blood pressure hypertonic saline would give in what situation would you not use it?

Answer 5

Worsen any bleeding so should be used cautiously with ongoing haemorrhage

Question 6

How can hypertonic saline effect the heart?

Answer 6

It can cause dysarrhthmias, ECG should be used whilst administering

Question 7

How long do the effects of hypertonic saline last?

Answer 7

30 mins

Useful when rapid intravascular volume expansion needed

Question 8

What are the hypertonic crystalloid bolus rates for dogs and cats?

What is this equivalent to?

Answer 8

Dogs- 4-7ml/kg

Cats- 2-4mg/kg

Over 2-5 minutes

Equivalent to 60-90ml/kg of isotonic crystalloid

Question 9

Is hypertonic saline administered alone?

Answer 9

No it is administered just before or alongside isotonic crystalloids.

It should be carefully labelled so that it doesn’t get confused with normal saline

Question 10

What do hypotonic fluids do when entering the body?

Answer 10

Net movement of fluid from vascular space to the interstitial and extracellular space

Question 11

In what cases are hypotonic fluids not suitable for?

Answer 11

Hypovolaemia

Question 12

What are the benefits of hypotonic fluids?

Answer 12

Primary water replacement

Dehydration

Carriers for medicine

Question 13

Give some examples of hypotonic fluids?

Answer 13

5% dextrose in water

4% dextrose/0.18% NaCl

0.45% saline

(Dextrose rapidly metabolised so patient only really getting the water)

Question 14

What are the potential hazards associated with hypotonic fluids?

Answer 14

Overhydration

Cerebral/pulmonary oedema

Electrolyte derangements

NOT TO BE USED WITH HYPOVOLAEMIA

Question 15

What are colloids and what do they do?

Answer 15

Can be natural or synthetic

Colloids are macromolecules (in solution)
Retained intravascular Due to size

Mimics role if albumin, which provides the main oncotic potential of blood

Create effect of volume expansion

Stay in IV space longer than crystalloids

Question 16

In what cases are colloids suitable?

Answer 16

Volume expansion

Haemorrhage

Burns

Severe GI disease

Question 17

What are the three types of synthetic colours used?

Answer 17

Gelatins

Dextrans

Hydroxyethyl starches

However synthetic colloids not used as much anymore as there was a worry that it caused renal dysfunction and mortality in critical patients in the human world.
Use if currently questionable

Question 18

What are the contraindications and side effects of synthetic colloids

Answer 18

Hypocoaguable state

Potential for anaphylaxis

Not advised for patients with vascular leaks SIRS/sepsis or AKI

Question 19

Give examples of natural colloids?

Answer 19

Plasma fresh or frozen

Packed red blood cells

Albumin

Question 20

What are the indications for fluid therapy? Hi

Answer 20

Correct hypovolaemia and therefore perfusion

Correct dehydration

Correct electrolyte and acid-base derangements

Meet ongoing losses

Question 21

How do fluid correct hypovolaemia?

Answer 21

Maintain adequate delivery of oxygen to tissues

Prevent shock, MODS, death

Question 22

What is the dose rate for a synthetic colloid?

Answer 22

3-5ml/kg over 15-30 mins

Question 23

What physical examination findings indicate an improvement in perfusion status following fluid therapy?

Answer 23

An improved mentation

A decrease in heart rate (dogs)

Return of/stronger peripheral pulses

Return to normal mms and CRT

An increase in urine production

Question 24

What is a normal urinalysis output?

Answer 24

1-2ml/kg/hr

Question 25

What can be assessed to assess the results of a resuscitation ?

Answer 25

Arterial blood pressure

Central venous pressure

Mixed/central venous oxygen levels

Quantification of urine output

Lactate measurements

Question 26

If a patient is hypotensive, what should the central venous pressure be greater than before stopping fluid therapy?

Answer 26

8mmHg (10.5 cmH2O)

Question 27

What time period should correction of dehydration be done over?

Answer 27

24 hours dogs and cats

Labs such as PCV/TP and urine SG can help to assess

Question 28

How signs estimate that a patient is 5/6% dehydrated?

Answer 28

Tacky mms

History fluid loss/no drinking

Question 29

How signs estimate that a patient is 6/8% dehydrated?

Answer 29

Slow return of skin tent

Dry mms

Question 30

How signs estimate that a patient is 8/10% dehydrated?

Answer 30

Slow return of mms

Dry mms

Sunken eyes

Question 31

How signs estimate that a patient is 10/12 % dehydrated?

Answer 31

Slow return of skin tent or stays tented

Sunken eyes (protruding third eyelid for cat)

Dry mms

Decreased mentation/ unresponsive

Dull desiccating corneas

Cold extremities

Question 32

What is the calculation for volume of replacement fluids needed to correct dehydration?

Answer 32

Deficit (ml) = BW (KG) x 10 x % dehydrated

Question 33

How do you calculate maintenance fluids?

Answer 33

40-60ml/kg/day

Or

Same as RER
30x BW +70

Question 34

What rate of potassium administration should not be exceeded?

Answer 34

0.5 mmol/kg/hour

As cardiac arrhythmias may occur

Question 35

Generally how much fluid is lost each episode of vomiting or diarrhoea?

Answer 35

4-5ml/kg

Question 36

What is aerobic respiration?

Answer 36

The process of producing cellular energy involving oxygen

Question 37

What is anaerobic respiration?

Answer 37

The process of producing cell energy when there is not
enough oxygen for aerobic respiration. Glucose → lactic
acid (+ energy released)

Question 38

What is metabolic acidosis?

Answer 38

A pH imbalance where too much acid has accumulated in
the body or too much alkali (bicarbonate) has been lost from
the body.

Question 39

What is respiratory acidosis?

Answer 39

The result of hypoventilation and accumulation of CO2.

Question 40

what is stroke volume?

Answer 40

The volume of blood pumped out of the left ventricle with

every heart beat.

Question 41

What is blood pressure?

Answer 41

The force exerted on the walls of arteries as blood is pumped
from the left ventricle.

Question 42

What is shock?

Answer 42

Situation where oxygen delivery to cells/ tissues is
insufficient for demand
inadequate cellular energy
production or decreased cellular oxygen utilization related to decreased blood flow
that leads to cell death and organ failure
Whilst, there are many definitions for shock it is considered to be failure of the
circulatory system to adequately perfuse vital organs. This means the basic metabolic
requirements for cells are not delivered which can quickly lead to cell death

Question 43

What is SIRS?

Answer 43

Systemic Inflammatory Response Syndrome
SIRS represents the body’s excessive response to an inciting event/insult e.g. tissue
damage (septic or non-septic), in certain circumstances. Normally, following an inciting event/insult e.g. injury/infection which causes tissue damage, there is a localised proinflammatory response, associated with the release of pro-inflammatory mediators
and acute phase proteins (Lewis, 2014). In an individual patient, if the inciting
event/insult is severe enough, a systemic pro-inflammatory response develops i.e. the
localized inflammatory response becomes systemic (generalised). N.B. remember
that inflammation is the response if living tissue to injury- the normal inflammatory
response is the body’s first line of defense following injury. It is usually a localised,
acute response intended to be short-lived and to only work on damaged cells and
tissues.

Question 44

What is bacteraemia?

Answer 44

The presence of viable bacteria in the blood

Question 45

What is sepsis?

Answer 45

Clinical manifestations of SIRS secondary to an infectious

cause

Question 46

What is severe sepsis?

Answer 46

Sepsis with evidence of dysfunction of at least one organ

Question 47

What is septic shock?

Answer 47

Severe sepsis associated with hypotension; that is
unresponsive to appropriate fluid resuscitation
Septic shock- is defined as sepsis with refractory hypotension that does not respond
to normal interventions or fluid therapy.

Question 48

What is multiple organ dysfunction (MODS)?

Answer 48

Dysfunction of the endothelial, cardiopulmonary, renal,
nervous, endocrine and gastrointestinal systems associated
with the progression of systemic inflammation

Question 49

What is DIC?

Answer 49

Disseminated Intravascular Coagulation

Question 50

What is a crystalloid?

Answer 50

Solutions of electrolytes and / or glucose in water

Question 51

What is a colloid?

Answer 51

Colloids are macromolecules in solution: they are retained

intravascularly and exert colloid osmotic pressure

Question 52

What are most cases of shock caused by? What happens in the body?

Answer 52

Most cases of shock are caused by decreased blood supply to tissues meaning
decreased delivery of oxygen to tissues.

Question 53

Why is oxygen essential for normal cell energy? What happens in shock?

Answer 53

Oxygen is essential for normal cell energy
production and function (Thomovsky and Johnson, 2013). Shock is a syndrome
resulting from inadequate cellular energy production. This arises due to an imbalance
between oxygen delivery (DO2) and oxygen consumption (VO2)

Question 54

What happens to cell respiration in shock?

Answer 54

As well as having a
reduced DO2, many patients in shock, have an increased metabolic requirement for
oxygen which worsens the imbalance. In the absence of oxygen, cell respiration
changes from aerobic, which is efficient, to anaerobic cellular metabolism which is
inefficient.

Question 55

What role does anaerobic metabolism play?

Answer 55

Anaerobic metabolism provides a temporary fix for the inadequate cellular
energy production but results in lactic acid/ lactate accumulation and metabolic
acidosis.

Question 56

Why does anaerobic cellular respiration lead to abnormal cell function and cell death?

Answer 56

Because anaerobic metabolism is less efficient than aerobic, insufficient
energy is produced to allow the cells to perform their normal functions leading to
abnormal cell function and cell death.

Question 57

What harmful substances can be produced as a result of cellular respiration?

Answer 57

ongoing anaerobic respiration
results in harmful substances being produced (e.g. cytokines, lactate and nitric oxide)
which also causes cell damage and cell death (Thomovsky and Johnson, 2013).

Question 58

What are the four main categories of shock recognised in small animals?

Answer 58

There are four main categories of shock recognised in small animals.

1) Hypovolaemic
2) Cardiogenic
3) Distributive
4) Obstructive

Question 59

How does hypovolaemic shock result in an alteration in tissue perfusion?

Answer 59

Shock most commonly results from alterations in tissue perfusion- this could be due
to loss of intravascular volume which leads to decreased venous cardiac return/
cardiac preload (very common) (hypovolaemic shock);

Question 60

How does cardiogenic shock result in an alteration in tissue perfusion?

Answer 60

cardiac dysfunction (cardiogenic shock)

Question 61

How does distributive shock result in an alteration in tissue perfusion?

Answer 61

maldistribution of blood flow

distributive or septic shock

Question 62

How does obstructive shock result in an alteration in tissue perfusion?

Answer 62

obstruction

to normal blood flow (obstructive shock)

Question 63

What type of shock may be treated differently to other types of shock?

Answer 63

All the types of shock
cause similar clinical signs which are associated with reduction in cardiac output and
poor perfusion; the treatment, however, differs for cardiogenic shock which is normally
an issue with maintaining systolic function rather than a loss of circulating volume.

Question 64

What are the two most common types of shock seen in practice?

Answer 64

Hypovolaemic shock and septic shock are the two most common causes of
shock in veterinary practice

Question 65

What are the common causes of hypovolaemic shock?

Answer 65

Common causes of hypovolaemic shock include
o Haemorrhage (trauma, surgical, coagulopathy etc.)
o Gastrointestinal losses (e.g. vomiting secondary to gastrointestinal
foreign body).

Question 66

What are common causes of septic shock?

Answer 66

Common causes of septic shock include septic peritonitis, pyometra and
pyothorax.

Question 67

What are common causes of obstructive shock?

Answer 67

Causes of obstructive shock include pericardial effusion, gastric dilation and
volvulus and pulmonary thromboembolism (some sources consider obstructive
shock to be a type of hypovolaemic shock). Any type of condition that leads to
an obstruction of blood flow to, through or out of the heart could be considered
an obstructive syndrome in that the obstruction needs to be alleviated to restore
normal perfusion.
Other causes of obstructive shock can include gastric dilation and volvulus, pulmonary
thromboembolism and heartworm disease

Question 68

What are common causes of cardiogenic shock?

Answer 68

End-stage dilated cardiomyopathy and severe arrhythmias are examples of
cardiogenic shock.

Question 69

What is oxygen delivery to tissues dependent on?

Answer 69

Oxygen delivery (DO2) is dependent on cardiac output and local tissue blood flow
(perfusion)

Question 70

How do you calculate cardiac output?

Answer 70

Cardiac output= stroke volume x heart rate.

Question 71

What is blood pressure affected by?

Answer 71

Blood pressure is affected by -
• Cardiac output
• Total peripheral resistance -the resistance the blood encounters as it travels in the blood
vessels (vasodilation- low resistance; vasoconstriction/ arterial occlusion- high resistance)
• (Blood viscosity)

Question 72

How does cardiac output affect tissue perfusion?

Answer 72

decreased cardiac output could lead to decreased blood pressure
(hypotension). Hypotension will lead to decreased tissue perfusion.

Question 73

Consider the effect of a garden hose (blood vessel) watering the flowers (cells) if the
water supply is significantly decreased (cardiac output) …….

Answer 73

Consider again, the garden hose trying to unsuccessfully water the flowers. One way of
increasing the amount of water going to the flowers is to increase the output from the hose i.e.
turn the tap on more (equivalent to ↑ cardiac output); another option is to pinch the hose to
make the stream of water narrower (↑ blood vessel tone/ peripheral vasoconstriction) so that,
temporarily, only the flowers in the centre (the most important ones) are watered effectively;
the less important flowers on the periphery are temporarily deprived of a water supply until the
problem can be fixed…..
➢ What happens to the flowers on the periphery if they remain deprived of water?
➢ What will ultimately happen to the water supply to all the flowers if the water supply cannot be
restored?
➢ Now consider what happens in a patient that has lost/ is losing blood volume….

Question 74

How does hypovolaemia affect stroke volume?

Answer 74

Hypovolaemic shock
Hypovolaemic shock arises from depleted, effective intravascular volume. The
hypovolaemia leads to decreased venous return/cardiac preload (end-diastolic
volume) and a subsequent reduction in stroke volume as demonstrated below -

Question 75

How can hypovolaemia arise?

Answer 75

1. Internal or external blood loss (haemorrhagic shock)
2. Excessive loss of other body fluids (through vomiting, diarrhoea, burns,
   polyuria) resulting in progressive dehydration and eventual loss of intravascular
   volume N.B. It is important to appreciate that dehydration and hypovolaemia
   are NOT the same however
3. Obstruction to venous return, as in gastric dilatation and volvulus (obstructive
   shock.

Question 76

What is the aim of compensatory mechanisms following any drop in cardiac output?

Answer 76

Following any drop in cardiac output and decreased cell oxygenation, compensatory
mechanisms are activated aimed at maintaining normal blood pressure and thus
tissue perfusion, with delivery of oxygen.
These compensatory mechanisms aim to increase cardiac output and blood vessel
tone and so increase cell perfusion.

Question 77

What are the compensatory mechanisms mediated by?

Answer 77

These compensatory mechanisms are both
neural and hormonal – neuroendocrine responses; and are mediated by the
hypothalamo- pituitary- adrenal (HPA) axis - the sympatho-adrenal response.

Question 78

How are the compensatory mechanisms categorized?

Answer 78

Compensatory Mechanisms
Based on how rapidly they are activated and start to have an effect, the compensatory
mechanisms are considered–
• Acute (immediate onset; response within minutes)
• Moderate (response within 10- 60 minutes)
• Chronic (response within 1-48 hours)

Question 79

Within what time frame could acute compensatory mechanisms arise?

Answer 79

Acute (immediate onset; response within minutes)

Question 80

Within what time frame could moderate compensatory mechanisms arise?

Answer 80

Moderate (response within 10- 60 minutes)

Question 81

Within what time frame could chronic compensatory mechanisms arise?

Answer 81

Chronic (response within 1-48 hours)

Question 82

What are the acute compensatory mechanisms focused on in shock?

Answer 82

Acute- these are focused on increasing venous return to the heart and increasing the
blood supply to the myocardium to enable it to function effectively under increased
demands. They are temporary steps triggered by the sympathetic nervous system to
keep the animal alive. However, if treatment is not instigated rapidly these
compensatory measures are likely to fail, leading to decompensated shock.

Question 83

What stimulates the sympathetic nervous system in shock and what effects does this have on the body?

Answer 83

Decreasing blood volume leads to decreased baroreceptor impulses (less pressure if
less blood in blood vessels). This stimulates the sympathetic nervous system leading
to increased sympathetic activity and catecholamine release (nor-adrenaline/ norepinephrine)- resulting in peripheral vasoconstriction, tachycardia and an increase in
cardiac contractility

Question 84

What effect does nor-adrenaline/nor-epinephrine have on the body in acute shock?

Answer 84

Nor-adrenaline/ nor-epinephrine binds to α receptors on blood
vessels to cause vasoconstriction and β-1 receptors in the heart to cause increased
heart rate and force of contraction. Peripheral vasoconstriction diverts blood to
essential organs and the positive inotropic and chronotropic effects increase cardiac
output

Question 85

What detects hypoxaemia and results in increased sympathetic nervous system activity?

Answer 85

Hypoxaemia, which is detected by chemoreceptors in the aorta and carotid artery, also
results in increased sympathetic nervous system activity and catecholamine release

Question 86

What is the main functions of cortisol release during shock?

Answer 86

Cortisol release from the adrenal cortex is also an acute response to hypovolaemia.
Whilst it is not clear what all the roles of cortisol are in a hypovolaemic patient, one
main function is to provide an immediate glucose energy source. Cortisol plays a vital
role in the normal maintenance of vascular tone and endothelial integrity; and
regulation of fluid within extravascular compartments. It also potentiates the impact of
catecholamines on vasoconstriction

Question 87

What is activated in moderate compensatory mechanisms in shock?

Answer 87

Neurohormonal mechanisms are also activated aiming to return vascular volume to
normal e.g. activation of the renin angiotensin aldosterone system (RAAS).

Question 88

What does RAAS stand for?

Answer 88

renin angiotensin aldosterone system (RAAS).

Question 89

What compensatory stage in shock is renin angiotensin aldosterone system activated?

Answer 89

Moderate

Question 90

What are the 4 steps from decrease renal perfusion to the angiotensin II response?

Answer 90

Decreased renal perfusion results stimulates baroreceptors in the kidney.

This stimulates RENIN release which converts ANGIOTENSINOGEN
to Angiotensin I then Angiotensin II

Immediate response of Angiotensin II - peripheral vasoconstriction ( and
reabsorbs some salt and water)

Delayed response Angiotensin II - ALDOSTERONE release from adrenal
cortex. Increased sodium, chloride and water reabsorption from distal
convoluted tubules in kidney → increased blood volume

Question 91

What does decreased renal perfusion stimulate and what conversions take place?

Answer 91

Decreased renal perfusion results stimulates baroreceptors in the kidney.

This stimulates RENIN release which converts ANGIOTENSINOGEN
to Angiotensin I then Angiotensin II

Question 92

What immediate effects does the release of renin following reduced renal perfusion have on the body?

Answer 92

Immediate response of Angiotensin II - peripheral vasoconstriction ( and
reabsorbs some salt and water)

Question 93

What delayed effects does the release of renin following reduced renal perfusion have on the body?

Answer 93

Delayed response Angiotensin II - ALDOSTERONE release from adrenal
cortex. Increased sodium, chloride and water reabsorption from distal
convoluted tubules in kidney → increased blood volume

Question 94

What is the net result from reduced renal perfusion stimulating the release of renin?

Answer 94

The net result of these neurohormonal responses is to retain more fluid at the kidney
aiming to restore normal intravascular volume and increase cardiac preload/ venous
return.

Question 95

Is vasoconstriction as a result of compensatory mechanisms in shock sustainable?

Answer 95

Whilst the short-term compensatory response of vasoconstriction can be
lifesaving, it is not sustainable. If it continues for any length of time, cellular hypoxia
and death will occur due to decreased perfusion.

Question 96

What large organ is affected by the reduced perfusion in shock?

Answer 96

The gastrointestinal tract (GIT) is
especially of concern in cases of reduced perfusion. Whilst it is a large system within
the body, during times of poor perfusion and “shock” blood flow to the GIT is reduced
by up to 70%, as it is not essential to keeping the animal alive.

Question 97

How much is the blood flow to the GI tract reduced by in shock?

Answer 97

Whilst it is a large system within
the body, during times of poor perfusion and “shock” blood flow to the GIT is reduced
by up to 70%, as it is not essential to keeping the animal alive.

Question 98

What GI symptoms can occur in shock and why?

Answer 98

The gastrointestinal tract (GIT) is
especially of concern in cases of reduced perfusion. Whilst it is a large system within
the body, during times of poor perfusion and “shock” blood flow to the GIT is reduced
by up to 70%, as it is not essential to keeping the animal alive. This decreased
perfusion commonly leads to gastrointestinal complications, such as vomiting and
diarrhoea, which can worsen hypovolaemia

Question 99

Where is vasopressin released from and what effects does it have in the moderate stage of compensatory shock?

Answer 99

Vasopressin/ antidiuretic hormone (ADH) is released from the posterior pituitary gland
when the osmolarity of blood increases and the volume of blood decreases. An
immediate effect of vasopressin, when there is hypovolaemia, is to bind to V1
receptors on peripheral arterioles (N.B. NOT α receptors) causing peripheral
vasoconstriction (as angiotensin II and catecholamines also do).

Question 100

What is the net effect of the chronic stage of compensatory mechanisms in shock?

Answer 100

Chronic
These are responses to hypovolaemia, after the immediate, acute life-saving
responses, that take slightly longer to have an effect and are aimed at increasing/
restoring blood volume.
Aldosterone and ADH/ vasopressin act on nephrons to reabsorb sodium, chloride and
water (aldosterone) and water (ADH). ADH binds to V2 receptors in the distal
convoluted tubules to reabsorb water.
The net effect of this is to restore blood volume (if no ongoing loss).
➢ Consider what effect these compensatory mechanisms will have on urine
output

Question 101

What effect do aldosterone, ADH and vasopressin have on the body in chronic stage of compensatory mechanisms?

Answer 101

Aldosterone and ADH/ vasopressin act on nephrons to reabsorb sodium, chloride and
water (aldosterone) and water (ADH). ADH binds to V2 receptors in the distal
convoluted tubules to reabsorb water.
The net effect of this is to restore blood volume (if no ongoing loss).

Question 102

Explain what happens in cardiogenic shock?

Answer 102

Cardiogenic Shock
This, as its name suggests, is when the heart suffers major failure of forward flow such
that the cardiac output is insufficient to allow perfusion of the whole body. This is not
common but can occur due to severe, dilated cardiomyopathy, for example in dogs,
where the thin myocardial walls are unable to develop sufficient contractile strength to
produce an adequate stroke volume.

Question 103

In feline patients what is cardiogenic shock more commonly associated with?

Answer 103

In feline patients, cardiogenic shock is more

commonly associated with hypertrophic cardiomyopathy and aortic thromboembolism.

Question 104

What causes the abnormal distribution of blood in distributive/septic shock?

Answer 104

Distributive / Septic Shock
With distributive shock, there is abnormal distribution of blood caused by peripheral
vasodilation

Question 105

How does distributive shock lead to an inadequate supply of blood to tissues?

Answer 105

With distributive shock, there is abnormal distribution of blood caused by peripheral
vasodilation. This causes in blood to pool in peripheral blood vessels and capillaries
meaning there is decreased volume of circulating blood. This results in inadequate
supply of blood to the body’s tissues and organs.

Question 106

Why can distributive shock present similar to hypovolaemic shock?

Answer 106

With distributive shock, there is abnormal distribution of blood caused by peripheral
vasodilation. This causes in blood to pool in peripheral blood vessels and capillaries
meaning there is decreased volume of circulating blood.
There is a different underlying cause
and slight variation in clinical signs, initially, but the effect in the patient is like
hypovolaemic shock e.g. there is less blood circulating than is required. It can be
difficult to immediately identify hypovolaemic shock versus distributive shock based
on clinical signs – it is very important is to monitor the patient’s response to treatment.

Question 107

How can you tell the difference in hypovolaemic shock compared to distributive shock after initial treatment and why?

Answer 107

Patient’s with hypovolaemic shock will usually respond to (improve) bolus IVFT where
patient’s with distributive shock often do not.

This causes in blood to pool in peripheral blood vessels and capillaries
meaning there is decreased volume of circulating blood.

When a patient has
septic shock, it remains hypotensive despite adequate fluid resuscitation and
administration of sympathomimetics (which would normally cause peripheral
vasoconstriction).

Question 108

What is the underlying abnormality in distributive shock?

Answer 108

The underlying abnormality with distributive shock is vasoplegia- which literally means
paralysis of blood vessels. The peripheral blood vessels cannot vasoconstrict which causes low systemic vascular resistance and pooling of blood. With this condition,
there is hypotension despite normal or raised cardiac output.

Question 109

What causes widespread vasodilation in distributive shock?

Answer 109

Inflammatory mediators (produced in response to a serious cause e.g. major burns,
septic focus) cause widespread vasodilation and vasoplegia of blood vessels. This
means there is low vascular resistance due to failure of peripheral vasoconstriction

Question 110

What is the difference between SIRS and sepsis?

Answer 110

Systemic inflammatory response syndrome (SIRS) – is vasodilation and poor
perfusion, without infection. It is possible for SIRS to occur on its own in cases such
as pancreatitis.
Sepsis – is defined as SIRS with an identifiable infectious cause

Question 111

What is the most common cause of sepsis?

Answer 111

Septic causes are frequently obvious and are associated with bacterial, fungal, viral
and parasitic causes
Bacteria are perhaps the most common culprits, with the E. coli
families that release endotoxins, highly represented. Examples include pyothorax,
septic peritonitis and parvoviral enteritis.

Question 112

How can anaphylaxis cause distributive shock?

Answer 112

Distributive shock may also be caused by anaphylaxis. Anaphylactic causes are
associated with an inappropriate immune system response to an otherwise innocuous substance. If a previously healthy patient presents with acute, sudden onset collapse, the cause could be anaphylaxis

Question 113

How can you detect anaphylaxis on ultrasound?

Answer 113

The presence of oedema in the wall of the gall bladder
of the dog (halo sign), on ultrasound examination, is highly suggestive of anaphylaxis
(Lisciandro, 2015). However, whilst this is helpful in trying to establish a diagnosis,
there are other reasons for oedema of the gall bladder being present. Rarely,
distributive shock can have a neurogenic cause.

Question 114

What main effects does SIRS/SEPSIS have on the body?

Answer 114

With SIRS and sepsis, inflammatory chemicals are released into the blood stream
which cause vasodilation, decreased perfusion of organs and hypotension leading to
shock.

Question 115

What early distinguishing signs may there be in distributive shock in dogs?

Answer 115

Early clinical signs include pyrexia, brick-red red mucous
membranes, bounding pulses and rapid CRT < 1 second.
Due to the vasoplegia, peripheral vasodilation and an initial hyperdynamic
response (in dogs) (Koenig, 2011), the early signs of distributive shock differ from
hypovolaemic shock

Question 116

How does sepsis in dogs and cats differ and what clinical signs can be seen in a cat?

Answer 116

A cat with sepsis is not likely to have a hyperdynamic response
marked lethargy, pale mucous membranes, tachypnoea, weak
pulses, hypotension, hypothermia, icterus, and diffuse abdominal pain (Koenig, 2011).
Cats may progress through compensated responses without the owner noticing that
too much is wrong and so they often present when decompensated. Depending on
how advanced the condition is there may be tachycardia or bradycardia- bradycardia
is a very serious sign as it indicates severe sepsis /worsening of the condition.

Question 117

How can pericardial effusion be considered as obstructive shock?

Answer 117

Obstructive shock is not included in all classifications of shock- some consider it to be
a type of hypovolaemic shock but with a different aetiology. An example is a
pericardial effusion. Due to fluid within the pericardial sac, insufficient blood can return
to the right atrium (pre-load) resulting in reduced cardiac output- this is called
‘tamponade’. In this situation, there is not actually decreased blood volume but there
is decreased venous return due to obstruction. Removing this obstruction (e.g. by performing pericardiocentesis) will cause resolution of the clinical signs of shock.
Pericardial effusions will sometimes be classified under cardiogenic shock.

Question 118

What group of patients can develop shock in hospital

Answer 118

There are certain groups of veterinary patients at risk of developing shock
syndromes even if they do not present for those. For example, patients that have
ongoing inflammation or infectious processes can develop SIRS +/- sepsis during the
hospitalisation period for the initial complaint. A patient with pancreatitis often has
ongoing inflammation for several days and may develop SIRS as a result of this. A
patient with parvovirus may develop sepsis on day two/ three as the body is
overwhelmed by inflammatory mediators

Question 119

What is compensated shock?

Answer 119

• Compensated shock- this is the early phase of shock where the
body’s compensatory mechanisms can maintain adequate perfusion of the
brain and vital organs. The patient is likely to have a normal blood pressure at
this stage as cardiac output is being maintained.

Question 120

What is decompensated shock?

Answer 120

Decompensated shock- this is when the compensatory mechanisms are not
able to fix the underlying problem. With ongoing lack of perfusion and
increasing cell death, progressive peripheral vasodilation starts to occur with
pooling of blood. This means the circulation is even less effective and less
blood is delivered to vital organs. The patient becomes increasingly stuporous
or comatose; mucous membranes become grey/ brown in colour and there is
increasing hypotension. The patient may become bradycardic or develop
ventricular arrhythmias (Butler, 2011). At this stage prompt, effective treatment
may still help the patient although there is a risk of further decompensation.

Question 121

What is irreversible shock?

Answer 121

Irreversible shock – There has been too much cell damage- due to the initial
insult and the effects of circulating inflammatory mediators and free radicals
from ongoing tissue hypoperfusion and damage. This can lead to systemic
inflammatory response syndrome (SIRS), disseminated intravascular
coagulation (DIC), multi-organ dysfunction (MOD) and death (Butler, 2011).
Patients become increasingly comatose, bradycardic and hypotensive with
prolonged CRT and discoloured mucous membranes; respiratory rate and
effort decreases leading to decreased PaO2 and increased PaCO2.

Question 122

What is AKI?

Answer 122

acute kidney injury

Question 123

What is ALI?

Answer 123

Acute lung injury?

Question 124

What sis ARDS?

Answer 124

Acute respiratory distress syndrome

Question 125

How does peripheral vasoconstriction affect the mucous membranes in shock?

Answer 125

peripheral vasoconstriction leads to decreased perfusion of the mucous
membranes therefore they appear pale with prolonged CRT; decreased blood volume
results in catecholamine release which causes tachycardia…

Question 126

How does catecholamine release in shock affect the heart?

Answer 126

decreased blood volume

results in catecholamine release which causes tachycardia…

Question 127

What clinical signs does hypovolaemia, cardiogenic, obstructive or advanced distributive shock all share?

Answer 127

Clinical signs in patients with hypovolaemic, cardiogenic, obstructive or advanced
distributive/ septic shock include1) Impaired mentation- decreased oxygen delivery to neurons
2) Tachycardia (cats may be bradycardic or have a normal heart rate N.B a normal
heart rate in a ‘very sick’ cat is likely to be significant- why?)
3) Tachypnoea
4) Pale mucous membranes
5) Prolonged capillary refill time
6) Weak/ absent peripheral pulses (N.B. central pulses will often be normal
strength initially. Weak central pulses suggest that the compensatory
mechanisms are failing, and the patient is progressing to irreversible shock)
7) Cold extremities
8) Decreased peripheral temperature
9) Decreased rectal/core temperature

Question 128

What different clinical signs would a dog in early septic shock display compared to other types of shock?

Answer 128

Dogs with early septic shock will have similar findings except for:
1) Red mucous membranes due to vasoplegia and pooling of red blood cells in
the capillaries
2) Rapid CRT
3) Normal to increased body temp.

Question 129

What biochemical changes will occur in a patient with anaerobic respiration.

Answer 129

Therefore, it is likely that a patient
with shock will have increased blood lactate levels which will result in metabolic
acidosis.

Question 130

What would happen to a patients lactate levels if they were improving or deteriorating?

Answer 130

Increasing blood lactate levels would suggest that the patient’s condition is
deteriorating whereas decreasing lactate levels would indicate a return to aerobic
respiration due to improved perfusion

Question 131

Can a one-off lactate reading give you an idea on patient prognosis or response to treatment?

Answer 131

Whilst lactate is a useful parameter when considering perfusion, it is important to
monitor the trend rather than evaluating a one-off value. One reading shows what the
lactate level is at the precise moment the sample is taken – an increased lactate level
is associated with poor perfusion. The elevated lactate, however, does not show what
the underlying issue is and how that patient will respond to treatment interventions.
What is more significant is what happens to the lactate level once treatment starts- I it
lowers the patient would appear to be responding; if it remains high/ increases, the
patient is not responding and the prognosis becomes poorer.

Question 132

What blood gases would indicate a deterioration in acidosis?

Answer 132

Increasing PaCO2 and decreasing PaO2/ SpO2 indicate deterioration and worsening
of acidosis

Question 133

What test is useful to do in an animal suspected to have disseminated intravascular coagulopathy

Answer 133

The platelet count is
often the first haematological parameter to change in DIC, with the count dropping as
consumption increases. Therefore, regular reviews of fresh blood smears, performing
a manual platelet count each time, can be useful in these patients.

Question 134

What can be the signs of dehydration?

Answer 134

Loss of interstitial fluid leads to a loss of tissue pliability and lubrication. Dehydration
can often be first detected on examination of the mucous membranes, although
assessment may be confounded by nausea-induced hypersalivation. Findings on
physical examination may include depression, dry/tacky mucous membranes and a
prolonged skin tent. Body condition score and age should be considered when
assessing skin tent. Subcutaneous fat provides greater lubrication than lean tissue
and the amount of subcutaneous fat decreases with advancing age. As a result, the
cranium and axillary region may provide more information about hydration status than
the more commonly assessed scruff. Following retropulsion of the eye of a wellhydrated cat, the nictitating membrane/ third eyelid should immediately return to the
normal position; in a dehydrated cat the nictitating membrane is more likely to stick to
the globe and slowly slide back.

Question 135

What the PCV be up to in sighthounds and why?

Answer 135

Several sources agree that the normal PCV can be up to 60-65% in
sighthounds and greyhounds
Some variations in
“normal” PCV need to be considered such as in sighthounds and greyhounds. Due to
the large muscle mass and low body fat normally present in these patients, the PCV
is usually higher

Question 136

Aside from a physical examination what else can be done to assess hydration levels?

Answer 136

Depending on the clinical signs that are present, an approximate estimation of the
patient’s degree of dehydration may be made. Assessment of PCV and total protein
(TP) can also be used to assess the degree of dehydration (Aldridge and O’Dwyer,
2013). In patients that are dehydrated the PCV and total proteins will be elevated due
to overall loss of free water leading to haemoconcentration

Question 137

How will the PCV /TP read in an animal that is dehydrated?

Answer 137

Assessment of PCV and total protein
(TP) can also be used to assess the degree of dehydration (Aldridge and O’Dwyer,
2013). In patients that are dehydrated the PCV and total proteins will be elevated due
to overall loss of free water leading to haemoconcentration.

Question 138

How would a PCV/TP usually read in a young animal under 6 months?

Answer 138

Because of the larger amount of free water present in
young animals (<6 months), they are likely to have lower than normal PCV and total
protein

Question 139

How can a dehydrated patient become hypovolaemic?

Answer 139

In serious or ongoing patients with dehydration, as cells and interstitial fluid become
progressively dehydrated, fluid will start to be drawn from the intravascular space due
to osmosis- eventually leading to hypovolaemia.

Question 140

Are hypovolaemic patients always dehydrated? What cases might they be one and not the other?

Answer 140

These animals will present with signs
consistent with hypovolaemic shock and dehydration. However, an animal that has
acute blood loss or is suffering from e.g. GDV will be hypovolaemic but not dehydrated.
Dehydration normally occurs over a longer time period and is associated with reduced
intake or increased losses. Not all hypovolaemic animals are dehydrated and not
all dehydrated animals are hypovolaemic.

Question 141

What are the most common infectious causes of sepsis?

Answer 141

The most common infectious causes of sepsis in veterinary medicine include:
o Septic abdomen
o Bite wounds
o PyNon-infectious causes include:
o Trauma
o Burns
o Pancreatitis
o Surgery
o Immune-mediated disease
o Neoplasia othorax
o Pyometra
o Parvoviral enteritis.

Question 142

Is SIRS caused by infectious or non infectious causes?

Answer 142

SIRS is the systemic inflammatory response syndrome: where ‘injury to one organ
system might cause damage in others’ (Lewis, 2014). It is a complex condition which
can occur secondary to infectious (septic/sepsis) or non-infectious causes. Both
Gram-negative and Gram-positive bacteria can initiate the inflammatory response and
cause sepsis.

Question 143

What are the non-infectious causes of SIRS?

Answer 143

Non-infectious causes include:
o Trauma
o Burns
o Pancreatitis
o Surgery
o Immune-mediated disease
o Neoplasia

Question 144

What is the purpose of inflammation?

Answer 144

It is characterised by changes in the microcirculation to the affected area intended to
try to limit the damage-
• Increased blood supply to the area
• Increased capillary permeability
• Fluid exudate
• Leucocyte delivery

Question 145

What is the result of a patient with SIRS with what should be localised inflammation?

Answer 145

In a patient who develops SIRS, the result of, what should be a localised, inflammatory
response becoming systemic is:
• Loss of effective circulating volume (due to increased capillary permeability)
and vasoplegia caused by inflammatory mediators
• Decreased tissue perfusion (due to loss of circulating blood volume)
• Interference with cell energy production by mitochondria

Question 146

What are the main problems with SIRS development? What two other life threatening conditions could develop as a result?

Answer 146

Whilst the compensatory anti-inflammatory response could limit the progression of
SIRS, in many cases this is also excessive - leading to excessive immunosuppression
and immunoparalysis. This predisposes to cell death and further perpetuates the
systemic inflammatory response ultimately leading to serious conditions
e.g. DIC and multiple organ dysfunction (MOD) and, ultimately, death

Question 147

What is the gram negative key component and potent initiator of the septic inflammatory cascade?

Answer 147

Lipopolysaccharide (LPS) is a key component of the cell wall of Gram-negative
bacteria and is a potent initiator of the septic inflammatory cascade

Question 148

What organs are the most common source of leakage of gram negative bacteria?

Answer 148

The
gastrointestinal (GI) and urogenital (UG) systems are the most common sources of
Gram-negative bacteria which can lead to sepsis in veterinary patients Leakage of
GI contents into the abdomen can occur secondary to ingestion of foreign bodies,
enterotomy/biopsy dehiscence, GI neoplasia and perforated ulcers. The leakage of
GI contents will result in an extensive inflammatory response and clinical signs
resulting from, and associated, with systemic inflammation.

Question 149

What is the gram positive key component and can also initiate of the septic inflammatory cascade?

Answer 149

The cell wall of Gram-positive bacteria contains peptidoglycan and lipoteichoic acid
that can also activate the inflammatory cascade

Question 150

What organs are the most common source of leakage of gram positive bacteria?

Answer 150

Sources of Gram-positive sepsis in

the surgical patient can include wounds and intravenous catheters.

Question 151

What serious conditions can streptococcus canis result in?

Answer 151

Streptococcus

canis infection can result in toxic shock syndrome and necrotizing fasciitis in the dog

Question 152

What is septic shock characterised by?

Answer 152

It is characterised by
cardiovascular decompensation secondary to widespread vasodilation with inefficient
oxygen delivery and resultant cellular dysfunction

Question 153

What vascular abnormalities cdoes SIRS/Sepsis lead to?

Answer 153

o Vasodilation
▪ Leads to hypotension and decreased organ perfusion
o Vasoplegia
▪ Loss of vasoconstrictor response to catecholamines/
sympathomimetics
o Increased vascular permeability
▪ Leads to interstitial oedema (loss of fluid and albumin into the
interstitium) and decreased plasma volume and
hypoalbuminaemia
Feline patients which develop MOF, often have pulmonary
oedema or acute lung injuries which become unresponsive to
normal interventions.

Question 154

What clinical findings are there relating to vasodilation in a dog with SIRS/Sepsis?

Answer 154

Leads to hypotension and decreased organ perfusion

Question 155

What clinical findings are there relating to vasoplegia in a dog with SIRS/Sepsis?

Answer 155

Vasoplegia
▪ Loss of vasoconstrictor response to catecholamines/
sympathomimetics

Question 156

What clinical findings are there relating to increased vascular permeability in a dog with SIRS/Sepsis?

Answer 156

Increased vascular permeability
▪ Leads to interstitial oedema (loss of fluid and albumin into the
interstitium) and decreased plasma volume and
hypoalbuminaemia

Question 157

What are the haemostatic abnormalities associated with SIRS/sepsis?

Answer 157

disseminated intravascular coagulation
Activation of primary (platelets) and secondary (coagulation factors)
haemostasis leads to formation of micro-thrombi in organs
Consumption of coagulation factors and platelets follows- this results in
the development of a hypocoagulable state leading to bleeding
tendencies (overt DIC)
All patients with SIRS (systemic inflammation) have activation of
coagulation and hence DIC to some extent

Question 158

How can SIRS/sepsis lead to DIC?

Answer 158

Inflammation leads to
activation of haemostatic mechanisms inducing a prothrombotic state
(covert DIC).

Question 159

Why may a patient with SIRS/sepsis have a reduced blood flow to organs?

Answer 159

Activation of primary (platelets) and secondary (coagulation factors)
haemostasis leads to formation of micro-thrombi in organs
(hypercoagulable) e.g. widespread clot formation- with resultant organ
ischaemia due to blood flow being reduced and affected by the presence
of clots

Question 160

Why may a patient with SIRS/sepsis develop hypocoagulation?

Answer 160

o Consumption of coagulation factors and platelets follows- this results in
the development of a hypocoagulable state leading to bleeding
tendencies (overt DIC) i.e. the clotting factors have been used up and
there are none left so the patient will bleed readily.

Question 161

How can SIRS/sepsis affect renal function?

Answer 161

Renal Dysfunction
o Prolonged hypotension may result in renal failure
o Dogs in MOF commonly develop acute kidney injuries and azotaemia
which worsen over a short timescale.

Question 162

How can SIRS/sepsis affect pulmonary function?

Answer 162

Pulmonary dysfunction
o Both dogs and cats can develop life-threatening pathology of the lungs
secondary to SIRS. This is termed acute lung injury (ALI) or acute
respiratory distress syndrome (ARDS)
o ALI and ARDS occur secondary to the systemic inflammation. This leads
to loss of normal pulmonary surfactant and accumulation of protein-rich
fluids in the lungs.

Question 163

How can SIRS/sepsis affect cardiac function?

Answer 163

Cardiac dysfunction
o Septic animals have altered/decreased cardiac contractility and are
predisposed to arrhythmias.

Question 164

What might cause an alteration in blood flow to the GI tract in SIRS/Sepsis?

Answer 164

Hypotension, micro thrombi and deregulation of regional blood flow can
all lead to alterations in gastrointestinal (GI) perfusion.

Question 165

What can cause a bacterial translocation in to the lymphatics and blood stream in SIRS/sepsis?

Answer 165

Increased epithelial permeability, secondary to GI hypoperfusion, can
result in bacterial translocation into the lymphatics and blood stream.

Question 166

What can cause bowel oedmea in SIRS/sepsis?

Answer 166

Hypoalbuminaemia can result in bowel oedema.

Question 167

What are the clinical signs associated with sepsis in dogs?

Answer 167

Clinical signs associated with sepsis (or other types of SIRS) include:
• Depression
• Fever (> 104 F/ 40  C in dogs)
o Will become hypothermic in later sepsis
• Red mucous membranes and rapid capillary refill time (in dogs)
o Later in the disease process the mucous membranes will become pale with a prolonged CRT
• Bounding pulse (dogs only)
o Late sepsis the pulse will become weak
• Tachycardia in dogs
• Tachypnoea (RR >40bpm in dogs and cats)
• Gastrointestinal signs:
o Vomiting
Diarrhoea

Question 168

What are the clinical signs associated with sepsis in cats?

Answer 168

Clinical signs associated with sepsis (or other types of SIRS) include:
• Depression
o Septic cats will commonly be hypothermic
o Later in the disease process the mucous membranes will become pale with a prolonged CRT
o In cats icteric mucous membranes are quite common
o Late sepsis the pulse will become weak
• Bradycardia in cats
• Tachypnoea (RR >40bpm in dogs and cats)
• Gastrointestinal signs:
o Vomiting
Diarrhoea

Question 169

How much of the proposed criteria for diagnosis of SIRS in dogs should be present?

Answer 169

2/4

Question 170

How much of the proposed criteria for diagnosis of SIRS in cats should be present?

Answer 170

3/4

Question 171

What 4 clinical parameters are assessed for the diagnosis of SIRS/sepsis?

Answer 171

Heart rate
Respiratory rate
Temperature
Leukogram

Question 172

What will a dogs heart rate be that might indicate sepsis on the proposed criteria for diagnosis?

Answer 172

> 120

Question 173

What will a dogs heart rate be that might indicate sepsis on the proposed criteria for diagnosis?

Answer 173

<140 OR >225

Question 174

What will a dogs respiratory rate be that might indicate sepsis on the proposed criteria for diagnosis?

Answer 174

> 20 OR

PaCO2<30 mmHg

Question 175

What will a cats respiratory rate be that might indicate sepsis on the proposed criteria for diagnosis?

Answer 175

> 40

Question 176

What will a dogs temperature be that might indicate sepsis on the proposed criteria for diagnosis?

Answer 176

< 38.1˚C OR >39.2˚ C

Question 177

What will a cats temperature be that might indicate sepsis on the proposed criteria for diagnosis?

Answer 177

<37.8˚C OR > 40.0 ˚ C

Question 178

What will a dogs Leukogram be that might indicate sepsis on the proposed criteria for diagnosis?

Answer 178

> 16-18,000 WBCs / μl

OR <5-6000 / μl

Question 179

What will a cats leukogram be that might indicate sepsis on the proposed criteria for diagnosis?

Answer 179

> 19,000 WBCs / μl OR
<5000 / μl

Septic animals may have a leucocytosis (characterised by a ‘left shift’) or
leucopaenia.

Question 180

What test can help to measure inflammation?

Answer 180

Currently C-reactive proteins (CRP) can be measured in dogs as a marker for systemic
inflammation. C-reactive proteins are released by hepatocytes in response to tissue
injury. The concentration of CRP is monitored to identify improving or worsening
systemic inflammation. Whilst CRP does indicate the underlying cause of
inflammation, it can be a very helpful diagnostic (when SIRS is suspected) and
prognostic aid (IDEXX, 2017). Further blood biomarkers may also be developed and
used clinically/diagnostically in the future

Question 181

What is the main aim of the compensatory mechanisms in shock?

Answer 181

The compensatory mechanisms (mediated via the HPA and SNS)
e.g. increased heart rate and peripheral vasoconstriction are intended to try to
maintain circulation to the vital organs; however, the remainder of the body, including
the periphery and gastrointestinal tract, will be under perfused

Question 182

What happens if the underlying cause of compensated shock is not managed and identified?

Answer 182

Whilst an adequate
circulation to the vital organs is maintained the shock is compensated. If the underlying
cause is not identified and managed, the condition will progress with decreasing
perfusion of all tissues – decompensated shock
As this progresses to late-stage
irreversible/ decompensated shock, the prognosis for the patient becomes very poor
as increasing cell death and multiple organ dysfunction and failure arise

Question 183

Is shock a primary or secondary condition?

Answer 183

It is important to remember that shock is a syndrome or condition and NOT a
diagnosis. Shock is always a result of a disease or traumatic process (e.g. foreign
body obstruction). As such, the bloodwork may reflect the underlying disease process.

Question 184

Is SIRS/Sepsis a primary or secondary condition?

Answer 184

The same is true of SIRS and Sepsis. They are complications of another underlying
condition. SIRS for example does not occur as a stand-alone condition. There must
be an inciting cause.

Question 185

What is the normal lactate level?

Answer 185

normal <2.5 mmol/L

Question 186

If a patient has increased lactate levels and responds to intravenous fluids what should happen to cellular metabolism?

Answer 186

Increased lactate leads to metabolic acidosis- i.e. the bloodstream become more acidic (lowered pH). If the patient responds to shock treatment (e.g. IVFT) and tissue perfusion increases, the lactate levels should return to normal; and the metabolic acidosis will resolve as aerobic cellular metabolism is restored.

Question 187

Why are septic patients commonly hypoglycaemic?

Answer 187

Septic patients are commonly hypoglycaemic due to increased glucose utilisation and reduced response to cortisol and catecholamines (Chan, 2012).
Blood glucose level should be measured in all critically ill patients. In septic patients, glucose will often be low and need to be supplemented so levels should be monitored frequently

Question 188

What might blood glucose levels and lactate parameters might raise suspicion of sepsis?

Answer 188

Therefore, low blood glucose and increased blood lactate in a patient should highlight suspicion of sepsis - appropriate examination and diagnostics should be
carried out to confirm or rule out sepsis

Question 189

What might happen to an animals protein levels with SIRS/sepsis and why?

Answer 189

These animals are also commonly hypoalbuminaemic as the vasculitis,
which develops with SIRS, leads to protein loss from the vasculature.

Question 190

What might a cats bilirubin levels be with SIRS/sepsis and how may this present clinically?

Answer 190

Finally, cats will
often become mildly to moderated hyperbilirubinaemic (and clinically icteric) when
septic.

Question 191

What monitoring should a patient recieve if they have SIRS or sepsis?

Answer 191

Frequent patient assessment focusing especially on perfusion parameters e.g.
CRT, heart rate, pulse quality, mucous membrane colour, temperature,
demeanour, urine output etc.
• Frequent assessment for complications e.g. petechiation, prolonged bleeding
• Serial blood pressure monitoring is very important (direct or indirect) with
appropriate knowledge of what is normal and abnormal
• Monitoring delivery of and response to intravenous fluid therapy
• Collecting samples appropriately and aseptically for laboratory assessment e.g.
blood gases, electrolytes, PCV, WBC, platelets, lactate, clotting times,
urinalysis etc.
• Monitor ECG tracing for any evidence of abnormalities e.g. arrythmias
• Monitoring urine output- due to hypoperfusion the patient may be initially
oliguric/ anuric. If it responds to treatment, a normal urine output of 1-2 ml/kg/hr.
should return; ongoing oliguria/ anuria would be significant
• Pain scoring and monitoring should be carried out in all patients; and repeated
as required to monitor the need for analgesia or the response to administered
analgesia
• Pulse oximetry
• Shock index

Question 192

What specific care needs to be provided to a recumbent patient?

Answer 192

• Bladder/ urinary catheter/ collection bag care.
• Regular turning to prevent decubitus ulcers (every 2-4 hours)
• Prevention of aspiration pneumonia
• Oral care
• Ocular care
• Prevention of faecal soiling/ management of rectal foley systems
• Passive range of movement techniques
• Massage/ coupage/ physiotherapy as appropriate
All other nursing needs should be met, and nursing care provided as appropriate to
the patient’s condition

Question 193

What are intravenous catheters placed for?

Answer 193

Intravenous catheters can be placed for
1. Infusion of fluids (including blood products, as required)
2. Blood sampling
3. Administration of drugs
4. Parenteral nutrition N.B. due to the high osmolarity of what is being
administered, this should always be administered through a central line.

Question 194

What are the different types of catheters available for IV access?

Answer 194

There are many different types of catheter available for intravenous access (Battaglia
and Hirsch-Fitzpatrick, 2016)-
➢ Over-the needle
➢ Through-the-needle
➢ Butterfly/ winged
➢ Peel-away
➢ Over- the- wire/ guide wire

Question 195

Can butterfly catheters be kept in place?

Answer 195

Butterfly catheters are useful if patient movement is a potential issue due to the
connecting line attached to the catheter. A butterfly catheter is, however, just a needle
attached to a piece of extension tubing and port and so can traumatise the blood
vessel when in place- consequently, it is not appropriate for long-term use e.g. IVFT

Question 196

How many drops per ml does a standard giving set give?

Answer 196

20 drops per millilitre

Question 197

How many drops per ml does a paediatric giving set give?

Answer 197

40-60 drops per millilitre (paediatric).

Question 198

What vein should parenteral nutrition be administered through?

Answer 198

Product to be administered e.g. total parenteral nutrition should be administered
through a central vein

Question 199

What are the various considerations when placing an IV catheter?

Answer 199

Veins and access points
Vein selection- there are various considerations including
➢ Reason for placing the catheter
➢ Anticipated/ likely duration of use
➢ Product to be administered e.g. total parenteral nutrition should be administered
through a central vein
➢ Patient factors e.g. central catheter contra-indicated if patient has
coagulopathy; ease of access for maintenance etc. Aggressive patients may do
better with a catheter placed in the lateral or medial saphenous veins.
➢ Disease process e.g. a hind limb vein is not appropriate in a cat with paraplegia
due to aortic thromboembolism; or a patient with gastric dilation and volvulus
(GDV) due to the obstructive effect of the enlarged stomach. N.B. Hind limb
veins are not recommended in patients in CPA as discussed in Unit 1, Outcome

Question 200

What is the protocol for placing a peripheral IV catheter?

Answer 200

Standard peripheral venous access is via the cephalic and medial (cats) and lateral
(dogs) saphenous veins; the accessory cephalic, auricular vein and dorsal common
digital vein are other peripheral veins that could be used as appropriate (Adamantos,
2018).
Following appropriate hand hygiene, a large area of hair should be clipped around the
vein- especially if a central catheter is being placed; the skin should be aseptically
prepared and an aseptic technique used for placement. N.B. sterile gloves are not
required for peripheral vein cannulation but should be used for central vein
catheterisation. Placement should be as distal in the peripheral vein as possible. Once
in the vein, a T port/ Y port and extension set should be attached. Any organic material
(e.g. blood) should be cleaned away to reduce risk of infection prior to securing the
catheter. A clear sterile film can be used over the insertion site initially as this allows
for monitoring of the insertion site for infection and inflammation without removal. The
catheter should then be secured with non-elastic adhesive tape/ sterile swabs and
then bandaged in place to prevent contamination

Question 201

What are the reasons for placing a central venous catheter?

Answer 201

A central venous catheter might be placed into a large vein which lies within the thorax
or abdomen for various reasons-
➢ Longer term administration of fluids ( > 5 days)
➢ Administration of hypertonic medications/ fluids e.g. > 5% glucose, hypertonic
saline
➢ Administration of multiple medications
➢ Requirement for multiple/ serial blood sampling
➢ Administration of total parenteral nutrition
➢ Measuring central venous pressure

Question 202

Where are central lines placed in dogs and cats?

Answer 202

The lateral (dog) or medial (cat) saphenous vein can be used to introduce a
peripherally inserted central catheter, PICC, into the caudal vena cava (Adamantos,
2018). This can be useful if jugular vein access is limited.

Question 203

What tests should be run before placing a central line?

Answer 203

the patient’s
clotting and platelet should be checked prior to placement; a buccal mucosal bleeding
time should be performed in patients at risk of Von Willebrand’s disease (

Question 204

How long should a central line be?

Answer 204

The catheter should be long enough to reach the
thoracic inlet so that it will sit just outside the right atrium, in the cranial vena cava.
Should be measured to the 4th intercostal space

Question 205

What is the protocol for placing a guidewire inserted catheter central line?

Answer 205

With the patient in lateral recumbency, the hair is widely clipped over the jugular
vein and the skin is surgically prepared.
➢ Sterile gloves should be worn, the site should be draped and a strict aseptic
technique adhered to.
➢ A small incision should be made in the skin over the jugular vein.
➢ An assistant raises the jugular vein by applying pressure level with the thoracic
inlet.
➢ A standard peripheral intravenous catheter (as the needle is covered by sheath
this is the modified technique) (or hypodermic needle) is inserted into the
jugular vein. Ensure the needle or catheter is wide enough for the guide wire to
thread through
➢ The sterile guide wire provided with the Seldinger kit is inserted through the IV
catheter
➢ The IV catheter needle is then withdrawn from the jugular vein, leaving only the
guide-wire in place. The guide wire should be held carefully throughout to
prevent it disappearing into the vein. At this point, direct digital pressure using
a sterile swab will control any haemorrhage.
➢ A dilator (within the kit) is then placed over the guide wire, inserted through the
skin and rotated to dilate the subcutaneous tunnel created by the needle. Using
the dilator reduces tissue drag as the jugular/ central catheter is introduced into
the jugular vein.
➢ The dilator is removed again with the guide wire kept in place.
➢ The jugular/ central catheter is then inserted over the guide wire into the jugular
vein.
➢ The guide wire is then removed.
➢ Heparinised saline flushes should be introduced to each port of the catheter
and suction applied to remove air from the catheter.
➢ The ports should then be flushed with heparinised saline
➢ The catheter should be sutured in place at the ‘anchor points’, in the wings of
the catheter hub.
➢ It should be covered by a sterile dressing. Due to the catheter being sutured to
the skin, a very light bandage is needed to cover and protect it. The bandage
is not needed to hold the catheter in place.
➢ Following placement, the catheter should be managed aseptically.
Ultrasound guided placement of central catheters can be also be performed

Question 206

What are the contraindications for placing a central line?

Answer 206

Contraindications to placement include coagulopathy, raised intracranial pressure and
a prothrombotic state that will predispose to catheter clot formation

Question 207

What is the protocol for placing a peel away shath central line?

Answer 207

The hair is clipped over the jugular (or saphenous) vein with the patient in lateral
recumbency.
➢ The skin is aseptically prepared and a small incision is made through the skin
over the jugular.
➢ A peel-away, over the needle sheath is placed into the jugular vein and the
needle removed leaving the sheath in the vein.
➢ The catheter is then inserted, through the sheath into the vein, and the peel
away sheath is grasped and peeled up and out of the jugular leaving the
catheter in place.
➢ Care must be taken not to dislodge the catheter during this procedure.
➢ The catheter should be flushed with heparinised saline, if not immediately
connected to a drip set, and capped.
➢ The catheter should be sutured in place at the ‘anchor points’, in the wings of
the catheter hub. Following placement, the catheter should be managed
aseptically, a dressing applied and covered by a bandage.

Question 208

How often should catheter sites be cheked?

Answer 208

Dressings around the
catheter should be changed every 24 hours or sooner should they become soaked
with fluids or soiled, and the catheter site should be checked every 24 hours to identify
possible infection or thrombosis

Question 209

How often should a catheter be flushed to maintain patency?

Answer 209

Catheter patency should be maintained by the fluid running throughout – some
sources advocate flushing 3-4 times daily (every 6-8 hours). Flushing is required
whenever the drip/infusion is halted or if it used intermittently.

Question 210

How often should an intravenous catheter be changed?

Answer 210

A catheter should be removed as soon as it is no longer needed (Adamantos, 2018);
however, with excellent maintenance, an intravenous catheter should be able to be
kept in place for several days. Removal of a well-managed, functioning, complicationfree intravenous catheter, to minimise the risk of infection, is now NOT recommended
after a set period of time (e.g. 3 days)

Question 211

What should be checked/observed when doing catheter care?

Answer 211

The catheter site should be checked regularly for any signs of complications e.g.
phlebitis with pyrexia, reddening, swelling, pain, discharge or discomfort at the
catheter site. N.B. If the patient has pyrexia but no obvious signs of infection at the
catheter site, the IV catheter is unlikely to be removed. If there is evidence of phlebitis/
thrombophlebitis or indication of infection, the intravenous catheter may need to be
removed, to limit the chance of septicaemia (Adamantos, 2018), so veterinary
attention should immediately be sought. If the catheter is removed because of
suspected complications, the catheter tip should be retained and stored appropriately
in case a culture and sensitivity is indicated.

Question 212

What are the possible complications with intravenous catheter placement?

Answer 212

Other possible complications are-
➢ Thrombosis/ thromboembolism
➢ Infection
➢ Dislodgement of catheter
➢ Catheter embolism – great care should be taken when placing and removing
catheters. Scissors should be used with caution near to the catheter.
➢ Air embolism- great care to avoid this with correct set-up, injection technique
and use of injection ports
➢ Haemorrhage- the amount of blood loss could be significant depending on the
vessel used e.g. a central catheter or an arterial catheter (not discussed in this
section. Bruising around the catheter insertion site or excessive blood loss may
indicate coagulopathy and should be reported to the veterinary surgeon.
➢ Bandage issues
➢ Pyrexia – this could indicate infection

Question 213

What can be administered through an intraosseous catheter?

Answer 213

Fluids, drugs and blood products can all be given via the intraosseous route- although
hypertonic fluids and alkaline fluids can cause discomfort

Question 214

What are the sites for intraosseous catheter placement in dogs and cats?

Answer 214

Possible sites for intraosseous catheter placement in the cat or dog are the femur
(trochanteric fossa), tibia (medial surface of proximal tibia), humerus (cranial aspect
of the greater tubercle) and the wing of the ilium

Question 215

What are the contraindications for intraosseous catheter placement?

Answer 215

Skin wound or infection over proposed catheter site, fracture of the bone to be
used, pneumatic bones, sepsis and metabolic bone disease

Question 216

How do you prep an area for intraosseous catheterization? What should you do after placement?

Answer 216

Sterility is of the utmost importance when placing an intraosseous catheter and the skin should be clipped and surgically prepared. The site may be anaesthetised with lidocaine, due to the sensitivity of the periosteum, and a small incision made in the skin. The catheter can then be inserted into the bone and flushed with heparinised saline before connecting T- connector or infusion set. As with intravenous catheters the cannula will need to be secured with sutures or tape and the site covered with a
sterile dressing to prevent the cannula from being dislodged. Once in place an X-ray
should ideally be taken to ensure that the cannula is present within the marrow cavity.

Question 217

What type of patients usually require intraosseous catheters?

Answer 217

Intraosseous catheters are typically used in
collapsed, hypothermic, hypotensive and hypoglycaemic neonates. The
kittens/puppies can then be resuscitated with dextrose and fluids. Usually, within a
couple of hours it is possible to attain intravenous access (peripheral or central) and
the intraosseous catheter can be removed

Question 218

How should an intraosseous catheter be handled post insertion?

Answer 218

Post insertion, the catheter should be managed aseptically and covered with a sterile
dressing. Cushioning with a piece of sterile gauze can minimise discomfort before
bandaging in place. All handling of the catheter site and flushing should be performed
aseptically. Some patients may need the limb to be completely immobilised, using a
splint or similar.

Question 219

What are isotonic fluids commonly used for in veterinary practices?

Answer 219

Isotonic fluids are very versatile and are commonly used in veterinary practice- for
hypovolaemia, dehydration, replacing ongoing losses and maintenance and
replacement of electrolytes

Question 220

What are the different types of isotonic fluids?

Answer 220

Examples include 0.9%

saline, lactated Ringer’s (Hartmann’s) and Ringer’s solution.

Question 221

Why might 0.9% saline be used in a patient with hypercalcaemia?

Answer 221

0.9% saline might be chosen if a

patient has hypercalcaemia as it increases calcium excretion via the kidney

Question 222

Why might lactated ringers be the fluid of choice with a patient with metabolic acidosis?

Answer 222

Lactated Ringer’s is likely to be selected when there is a metabolic acidosis as it contains a
bicarbonate precursor(common).

Question 223

What electrolyte imbalance can be the result of prolonged isotonic crystalloid use?

Answer 223

As they are
all relatively/ actually low in potassium, prolonged use can lead to hypokalaemia. None
of the isotonic solutions available contain enough potassium to meet maintenance
requirements - so most patients will require some potassium supplementation
especially if they remain anorexic.

Question 224

How does isotonic fluid move when administered in to the body?

Answer 224

The electrolyte composition of isotonic fluids is similar to extracellular fluid (ECF) -
especially lactated ringers which has more potassium than 0.9% saline
Because there is no concentration gradient, there is no net movement from or into the
vascular space when isotonic fluids are administered

Question 225

What is the initial choice of fluids in most hypovolaemic patients and why?

Answer 225

Isotonic crystalloids are the initial replacement fluid choice in most hypovolaemic
patients. Isotonic crystalloids will increase intravascular volume and replace interstitial
deficits; though the effect is temporary due to capillary fluid shifts. A buffered isotonic
crystalloid solution (e.g. lactated Ringer’s solution) may be a more physiologically
appropriate resuscitation fluid than normal saline

Question 226

what is the blood volume in dogs considered to be?

Answer 226

90ml/kg in dogs

Question 227

what is the blood volume in cats considered to be?

Answer 227

60ml/kg in cats

Question 228

How much fluid bolus would a mildly hypovolaemic dog need need in an emergency?

Answer 228

A mildly hypovolaemic dogs may only require 10-20 ml/kg of isotonic crystalloid

Question 229

How much fluid bolus would a severely hypovolaemic dog need in an emergency?

Answer 229

a dog with evidence of severe hypoperfusion i.e. ongoing severe haemorrhage, may rarely require administration of the full 70-90 ml/kg of isotonic
crystalloids and, possibly, the addition of colloids

Question 230

What is the bolus rate of isotonic fluid for a cat with hypovolemia?

Answer 230

A hypovolaemic cat may respond to a single 10-20 ml/kg bolus of an isotonic
crystalloid solution, or may require repeated isotonic crystalloid boluses and,
potentially, the addition of a colloid.

Question 231

What are the potential issues when administering isotonic crystalloid therapy?

Answer 231

Potential issues with administering isotonic crystalloid therapy include prolonging
coagulation by dilution; theoretical compounding of acidosis (e.g. 0.9% NaCl is acidic)
and causing hypothermia (if using large volume of room temperature fluids). N.B.
ongoing blood loss leads to consumption of coagulation factors and platelets that is
made worse by the fluid therapy.

Question 232

Can a hypovolaemic patient with metabolic acidosis receive 0.9% saline for treatment?

Answer 232

A hypovolaemic patient, with decreased peripheral perfusion, will develop
metabolic acidosis because of build-up of lactic acid secondary to anaerobic
respiration. Administering 0.9% saline could in theory make the acidosis worse as it is
an acidic fluid BUT because it increases the blood volume, improves cardiac output
and renal glomerular filtration rate (GFR) so perfusion will improve. This means the
cells will return to aerobic respiration and should be able to function more effectivelythe lactate levels will decrease and the acidosis should resolve.

Question 233

What is the fluid maintenance value for small mammals?

Answer 233

80-100ml/kg/day

Question 234

What is the fluid maintenance value for birds?

Answer 234

50ml/kg/day

Question 235

What is the fluid maintenance value for reptiles?

Answer 235

15-30

ml/kg/day

Question 236

What organ is used to metabolise alkalising fluids?

Answer 236

These contain bicarbonate precursors, such as lactate, and are used in cases of
metabolic acidosis. Within 1-2 hours of administration, the lactate is metabolised into
bicarbonate by the liver. The bicarbonate ‘mops up’ hydrogen ions, thus raising the pH
and decreasing the acidity of blood.

Question 237

How do alkalising fluids raise the PH of blood?

Answer 237

These contain bicarbonate precursors, such as lactate, and are used in cases of
metabolic acidosis. Within 1-2 hours of administration, the lactate is metabolised into
bicarbonate by the liver. The bicarbonate ‘mops up’ hydrogen ions, thus raising the pH
and decreasing the acidity of blood.

Question 238

What type of alkalising fluids should not be given to animals in liver failure and why?

Answer 238

lactate is metabolised into
bicarbonate by the liver. The bicarbonate ‘mops up’ hydrogen ions, thus raising the pH
and decreasing the acidity of blood. Fluids requiring hepatic metabolism of lactate (e.g.
LRS/ Hartmann’s) should not, however, be administered, to animals in liver failure

Question 239

Why should sodium bicarbonate not be administered to animals as the first line of treatment for metabolic acidosis?

Answer 239

Sodium bicarbonate will theoretically correct metabolic acidosis but should not be used
as a first line treatment to correct the lactic acidosis caused by anaerobic metabolism,
seen in animals with hypoperfusion. As a result of fluid administration, perfusion
should improve leading to correction of metabolic acidosis. If bicarbonate has been
administered additionally, there is a risk the patient will become alkalaemic following
fluid therapy. Bicarbonate administration should only be considered if it is possible to
perform blood gas analysis; it is only likely to be considered in a patient with acidosis
which is non-responsive to other interventions such as appropriate aggressive fluid
therapy.

Question 240

What can be the cause of hypokalaemia in cats?

Answer 240

cats- chronic
renal failure, prolonged anorexia, muscle wastage and gastro-intestinal losses are
potential causes

Question 241

What are the main signs see with hypokalemia?

Answer 241

Hypokalaemia causes muscle weakness, especially obvious in cats, with plantigrade
stance and ventroflexion of the neck- it can also cause cardiac arrhythmias.

Question 242

How can fluid therapy and fluid loss affect potassium levels?

Answer 242

Hypokalaemia may arise with the increased urine
output associated with IVFT, especially if the fluid administered has no potassium e.g.
0.9% NaCL. There may also be reduced serum potassium levels associated with
dilution of electrolytes and fluid therapy administration.

Question 243

What can develop if potassium supplementation is administered too quickly?

Answer 243

The rate of administration should not exceed 0.5 mmol/kg/hour
otherwise a cardiac arrhythmia may develop

Question 244

What monitoring will a hypokalaemic cat require?

Answer 244

Monitoring of these patients will focus on ensuring cardiovascular stability (ECG) and
adequate tissue perfusion. Heart rate, rhythm, mucous membrane colour, CRT and
pulse quality will have to be frequently assessed; as well as temperature checks.
Blood pressure and blood work (including PCV/TS and lactate) may have to be
frequently monitored, particularly if the patient is haemodynamically unstable e.g. early
in the fluid plan, when still hypovolaemic and receiving bolus therapy. Blood gases,
acid, base, glucose and electrolyte assessments may also be performed. Patients
should have their urine output closely monitored

Question 245

What nursing care should be provided to a patient in septic shock?

Answer 245

A variety of treatments will be required when nursing these patients including fluid
therapy, analgesia, specific medication and treatment of underlying problems; in
addition to monitoring and recording of clinical parameters.
The key to treating a patient in septic shock is:
• Haemodynamic support
o Ensure adequate tissue perfusion and urine output
• Remove the septic focus
o Surgery for source control
o Appropriate antibiosis
• Metabolic support
o Correct hypoglycaemia
o Correct acid-base/electrolyte derrangements

Question 246

What effect does the Alpha-1 adrenergic (α-1) receptor of a vasopressor have?

Answer 246

Alpha-1 adrenergic (α-1)
Blood Vessel
Vasoconstriction

Question 247

What effect does the Beta- 1 adrenergic (β-1) receptor of a vasopressor have?

Answer 247

Beta- 1 adrenergic (β-1)
Heart Positive inotrope (increased strength)
Positive chronotrope (increased rate)

Question 248

What effect does the Beta- 2 adrenergic (β-2) receptor of a vasopressor have?

Answer 248

Beta- 2 adrenergic (β-2) Blood Vessels Vasodilation

Question 249

What effect does the Dopamine) receptor of a vasopressor have?

Answer 249

Dopamine
Blood vessels e.g.kidney

Vasodilation (other effects elsewhere)
(low dose)
Vasoconstriction (high dose)

Question 250

Why would vasopressor agents be used in dogs with septic shock?

Answer 250

Vasopressor agents (Silverstein, 2006) are commonly needed to maintain normal
blood pressure in the septic patient due to vasoplegia. They should not be used at
the expense of fluids and normovolaemia must be achieved. The aim of administering
vasopressors is to cause vasoconstriction and increase arterial blood pressure.

Question 251

What effects can occur as a result of excessive vasoconstriction from too many vasopressors? What can be done to avoid this?

Answer 251

However, they may also result in excessive vasoconstriction particularly of the
splanchnic circulation. This may lead to gastrointestinal ischaemia and dysfunction.
It is therefore important to use vasopressors at the lowest dose necessary to maintain
arterial blood pressure; and ensure that the animal is normovolaemic. The use of
vasopressors will also increase the work of the heart. This added workload, in
combination with septic-induced myocardial depression, may require the use of a
positive inotrope such as dobutamine.

Question 252

How should vasopressors be administered?

Answer 252

Many vasopressors need to be administered as
a constant rate infusion so small up or down dose adjustments can be made based on the patient’s response. As such it is important to have a reliable method of delivery such as a syringe driver.

Question 253

What receptors are present in noradrenaline? What effect does this have and what is the dose range?

Answer 253

Noradrenaline is a catecholamine with potent α-adrenergic but little β-adrenergic activity
It has pronounced vasoconstrictive effects
on the blood vessels at typical dosages of 0.1-0.3 μg/kg/min

Question 254

Why might noradrenaline doses need to be increased in sepsis?

Answer 254

However, due to sepsis induced vasoplegia, doses often have to be increased. In a number of open-label
trials, noradrenaline has been shown to increase mean arterial pressure (MAP) in
patients who remained hypotensive after fluid resuscitation and dopamine. Access to
noradrenaline can be limited in the UK but it can be obtained from certain veterinary
wholesalers and accident and emergency, if needed.

Question 255

What effect does a low dose of dopamine have on the body?

Answer 255

At low doses of between 5 and 10 μg/kg/min,
dopamine exerts predominantly β-adrenergic effects with resultant positive inotropic
and chronotropic effects. There is vasodilation of coronary blood vessels, increased force of contraction and increased heart rate. This results in increased cardiac outputand organ perfusion

Question 256

What effect does a high dose of dopamine have on the body?

Answer 256

The α-adrenergic effects of peripheral vasoconstriction (with resultant increase in
systemic vascular resistance) occur at doses greater than 10 μg/kg/min: although
there is considerable dose overlap particularly with sepsis-induced vasoplegia.

Question 257

How does a high dose of dopamine increase mean arterial pressure?

Answer 257

Dopamine therefore increases mean arterial pressure (MAP) by increasing cardiac
output and/or systemic vascular resistance.

Question 258

What is it important to carefully monitor when an animal is receiving a dopamine CRI?

Answer 258

It is important to carefully monitor blood
pressure in patients receiving dopamine. It is also sensible to use an ECG as
arrhythmias may develop. It is administered as a CRI with dose being titrated
according to effect. The dose is often limited by tachyarrhythmia in dogs- these
typically respond to a dose reduction.

Question 259

What is dobutamine and what effects does it have on the body?

Answer 259

Dobutamine is a direct- acting synthetic catecholamine. It has direct β-1 adrenergic
agonist effects and mild β-2 adrenergic and mild/ no α- 1 adrenergic effects. This
results in increased heart rate (so increased output) but with little effect on peripheral
blood vessels.

Question 260

How is dobutamine administered and what should be monitored carefully?

Answer 260

It is a potent and short-acting drug so needs to be titrated to effect with
careful patient monitoring- especially blood pressure and heart rhythm. As with all
sympathomimetics, it may cause tachyarrhythmias

Question 261

What receptor does vasopressin cause vasoconstriction through?

Answer 261

Vasopressin causes vasoconstriction through V1 receptors that are present on
vascular smooth muscle

Question 262

When should vasopressin be used in septic patients?

Answer 262

Vasopressin has started to
be used in veterinary medicine but should only be used if a septic patient has failed to
respond to noradrenaline and/or dopamine

Question 263

What is inhibited to avoid vasodilation when vasopressin is administered?

Answer 263

In addition to the direct vasoactive effects of vasopressin, it
also increases the responsiveness of the vasculature to catecholamines and inhibits
nitric oxide production: nitric oxide causes vasodilation.

Question 264

How soon should antibiotics be started when septic shock is suspected?

Answer 264

Intravenous antibiotic therapy
should be administered as early as possible and within the first hour of recognition of
septic shock.

Question 265

What antibiotics should be used in septic patients when the type of bacteria is unknown?

Answer 265

Empiric antibiotics should be started in a septic patient, whilst waiting for the culture
results and susceptibility testing. The choice of initial antibiotic should be made based
on the likely infectious agent and the local patterns of antibiotic susceptibility.
Changes can be made to the protocol following identification of the organism and the
antimicrobial susceptibility. Recent human studies have demonstrated that patient
survival is increased if early antibiosis is instigated- ideally this should be within an
hour of recognising septic shock

Question 266

How can sepsis affect the blood glucose levels?

Answer 266

Septic patients are commonly hypoglycaemic and will typically require dextrose
supplementation

Question 267

What dose can dextrose be administered in a septic patient?

Answer 267

An intravenous bolus of 0.5g/kg of dextrose can be administered
over 5-10 minutes. Supplementation of maintenance fluids with 2.5% or 5% dextrose
may then be necessary.

Question 268

can corticosteroids be used in patients with septic shock?

Answer 268

High-dose corticosteroids were historically administered to patients with sepsis or
septic shock due to their anti-inflammatory effects, and reports of an ability to stabilise
membranes. The use of high-dose corticosteroids remains controversial in veterinary
patients but there is currently insufficient evidence to recommend their use in patients
with severe sepsis or septic shock.

Question 269

Is nutritional support important in septic patients and why?

Answer 269

Nutritional support is important in all critically ill animals. Approach to nutrition should
be proactive in septic animals, and “waiting to see if a patient eats” is not acceptable
practice. Benefits of enteral over parenteral nutrition are well documented in people,
although many septic patients will not tolerate enteral feeding. Enteral nutrition via a
nasoenteric (oesophageal, gastric or jejunal) or surgically placed feeding tube
(oesophagostomy) should be considered in all septic patients that can tolerate enteral
feeding, have no contra-indication to placement of a feeding tube and are not meeting
their resting energy requirements (RER). Use of the GI tract should be avoided in
those patients that are hypotensive or require vasopressors so total parenteral
nutrition (TPN) may become a possibility

Question 270

Can you use NSAIDS in septic patients for analgesia?

Answer 270

non-steroidal antiinflammatory drugs (NSAID) compromise renal perfusion and can result in GI
ulceration and as such should be avoided in septic patients.

Question 271

Why may omeprazole be used in patients with sepsis?

Answer 271

Ulcer prophylaxis with an H2 receptor antagonist (e.g. ranitidine) or proton pump
inhibitor (e.g. omeprazole) may be administered to a patient with severe sepsis to
prevent upper GI bleeding. The 2018 ACVIM consensus statement (Marks et al., 2018)
reviews the use of gastro-intestinal protectants. The evidence base for some gastrointestinal protectants is very poor with no proven benefit shown for some. Proton pump
inhibitors seem to be more effective than H2 receptor antagonist for ulcer prophylaxis however long-term use of PPIs in people and animals can be harmful.

Question 272

Supplemental oxygen should be administered if a patient’s pulse oximeter reading is less than

( N.B. Please ensure you are aware of what a pulse oximeter measures and the factors that might influence the readings. Ensure you know the definition of hypoxia and hypoxaemia)

Select one:

a. 96%
b. 98%
c. 100%
d. 94%

Answer 272

The correct answer is: 94%

Question 273

Capnography is used to measure

Select one:

a. Total amount of CO2 in inhaled air
b. End tidal O2
c. End tidal CO2
d. Total amount of O2 in exhaled air

Answer 273

The correct answer is: End tidal CO2

Question 274

The normal physiological pH of cat and dog blood is

Select one:

a. 7.15-7.25
b. 7.45-7.55
c. 7.35-7.45
d. 7.25-7.35

Answer 274

The correct answer is: 7.35-7.45

Question 275

Oliguria is defined as
Select one:
a. Urine output > 2ml/kg/hr
b. Urine output 1-2 ml/kg/hr
c. Urine output < 5mL/kg/hr
d. Urine output < 1mL/kg/hr

Answer 275

The correct answer is: Urine output < 1mL/kg/hr

Question 276

The normal Arterial-alveolar (A-a) gradient is

Select one:

a. <40 mmHg
b. >30 mmHg
c. <50 mmHg
d. < 15 mmHg

Answer 276

(This estimates the effectiveness of gas transfer from the alveoli to the circulation- it indicates the difference in oxygen levels between the alveoli and the blood leaving the left ventricle - assumed to be the same as blood in the pulmonary capillaries. The Arterial- alveolar gradient indicates the effectiveness of oxygenation rather than the effectiveness of ventilation. N.B. ensure you understand the difference between oxygenation and ventilation. )

The correct answer is: < 15 mmHg

Question 277

Normal central venous pressure (CVP) in the dog is
Select one:
a. 10-20 cm H2O
b. 110-160 cm H2O
c. 0-5 cm H2O
d. 80-120 cm H2O

Answer 277

( N.B. Please ensure you are know the technique for performing CVP measurement; and understand what CVP results indicate in veterinary patients.

Please review indications and contraindications for placement of a central venous/ jugular catheter.

Review best practice nursing care of a central venous/ jugular catheter.)

The correct answer is: 0-5 cm H2O

Question 278

Which of the following is unlikely to influence a dog’s systolic blood pressure

Select one:

a. Peripheral vasoconstriction
b. Circulating blood volume
c. Total protein/ total solids in blood
d. Force of cardiac contractions

Answer 278

(N.B. Please ensure you consider factors that can affect the blood pressure readings in patients.
Ensure you know and understand the methods for recording blood pressure in veterinary patients and consider the advantages and disadvantages of each method.)

The correct answer is: Total protein/ total solids in blood