U1 O2 - Shock, vascular access and fluid therapy Flashcards
Shock, Vascular access and fluid therapy
Give an example of a hypertonic crystalloid?
7.2-7.5% NaCl
Hypertonic saline
What does hypertonic crystalloids do when entering the body?
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
In what cases can hypertonic saline be used?
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
What does hypertonic saline rely on for its effect?
Because of this what cases would it not be recommended?
It relies on interstitial fluid for effect so not recommend in patients with dehydration
Hypernatraemia
Due to the rapid rise in blood pressure hypertonic saline would give in what situation would you not use it?
Worsen any bleeding so should be used cautiously with ongoing haemorrhage
How can hypertonic saline effect the heart?
It can cause dysarrhthmias, ECG should be used whilst administering
How long do the effects of hypertonic saline last?
30 mins
Useful when rapid intravascular volume expansion needed
What are the hypertonic crystalloid bolus rates for dogs and cats?
What is this equivalent to?
Dogs- 4-7ml/kg
Cats- 2-4mg/kg
Over 2-5 minutes
Equivalent to 60-90ml/kg of isotonic crystalloid
Is hypertonic saline administered alone?
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
What do hypotonic fluids do when entering the body?
Net movement of fluid from vascular space to the interstitial and extracellular space
In what cases are hypotonic fluids not suitable for?
Hypovolaemia
What are the benefits of hypotonic fluids?
Primary water replacement
Dehydration
Carriers for medicine
Give some examples of hypotonic fluids?
5% dextrose in water
4% dextrose/0.18% NaCl
0.45% saline
(Dextrose rapidly metabolised so patient only really getting the water)
What are the potential hazards associated with hypotonic fluids?
Overhydration
Cerebral/pulmonary oedema
Electrolyte derangements
NOT TO BE USED WITH HYPOVOLAEMIA
What are colloids and what do they do?
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
In what cases are colloids suitable?
Volume expansion
Haemorrhage
Burns
Severe GI disease
What are the three types of synthetic colours used?
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
What are the contraindications and side effects of synthetic colloids
Hypocoaguable state
Potential for anaphylaxis
Not advised for patients with vascular leaks SIRS/sepsis or AKI
Give examples of natural colloids?
Plasma fresh or frozen
Packed red blood cells
Albumin
What are the indications for fluid therapy? Hi
Correct hypovolaemia and therefore perfusion
Correct dehydration
Correct electrolyte and acid-base derangements
Meet ongoing losses
How do fluid correct hypovolaemia?
Maintain adequate delivery of oxygen to tissues
Prevent shock, MODS, death
What is the dose rate for a synthetic colloid?
3-5ml/kg over 15-30 mins
What physical examination findings indicate an improvement in perfusion status following fluid therapy?
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
What is a normal urinalysis output?
1-2ml/kg/hr
What can be assessed to assess the results of a resuscitation ?
Arterial blood pressure
Central venous pressure
Mixed/central venous oxygen levels
Quantification of urine output
Lactate measurements
If a patient is hypotensive, what should the central venous pressure be greater than before stopping fluid therapy?
8mmHg (10.5 cmH2O)
What time period should correction of dehydration be done over?
24 hours dogs and cats
Labs such as PCV/TP and urine SG can help to assess
How signs estimate that a patient is 5/6% dehydrated?
Tacky mms
History fluid loss/no drinking
How signs estimate that a patient is 6/8% dehydrated?
Slow return of skin tent
Dry mms
How signs estimate that a patient is 8/10% dehydrated?
Slow return of mms
Dry mms
Sunken eyes
How signs estimate that a patient is 10/12 % dehydrated?
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
What is the calculation for volume of replacement fluids needed to correct dehydration?
Deficit (ml) = BW (KG) x 10 x % dehydrated
How do you calculate maintenance fluids?
40-60ml/kg/day
Or
Same as RER
30x BW +70
What rate of potassium administration should not be exceeded?
0.5 mmol/kg/hour
As cardiac arrhythmias may occur
Generally how much fluid is lost each episode of vomiting or diarrhoea?
4-5ml/kg
What is aerobic respiration?
The process of producing cellular energy involving oxygen
What is anaerobic respiration?
The process of producing cell energy when there is not
enough oxygen for aerobic respiration. Glucose → lactic
acid (+ energy released)
What is metabolic acidosis?
A pH imbalance where too much acid has accumulated in
the body or too much alkali (bicarbonate) has been lost from
the body.
What is respiratory acidosis?
The result of hypoventilation and accumulation of CO2.
what is stroke volume?
The volume of blood pumped out of the left ventricle with
every heart beat.
What is blood pressure?
The force exerted on the walls of arteries as blood is pumped
from the left ventricle.
What is shock?
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
What is SIRS?
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.
What is bacteraemia?
The presence of viable bacteria in the blood
What is sepsis?
Clinical manifestations of SIRS secondary to an infectious
cause
What is severe sepsis?
Sepsis with evidence of dysfunction of at least one organ
What is septic shock?
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.
What is multiple organ dysfunction (MODS)?
Dysfunction of the endothelial, cardiopulmonary, renal,
nervous, endocrine and gastrointestinal systems associated
with the progression of systemic inflammation
What is DIC?
Disseminated Intravascular Coagulation
What is a crystalloid?
Solutions of electrolytes and / or glucose in water
What is a colloid?
Colloids are macromolecules in solution: they are retained
intravascularly and exert colloid osmotic pressure
What are most cases of shock caused by? What happens in the body?
Most cases of shock are caused by decreased blood supply to tissues meaning
decreased delivery of oxygen to tissues.
Why is oxygen essential for normal cell energy? What happens in shock?
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)
What happens to cell respiration in shock?
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.
What role does anaerobic metabolism play?
Anaerobic metabolism provides a temporary fix for the inadequate cellular
energy production but results in lactic acid/ lactate accumulation and metabolic
acidosis.
Why does anaerobic cellular respiration lead to abnormal cell function and cell death?
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.
What harmful substances can be produced as a result of cellular respiration?
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).
What are the four main categories of shock recognised in small animals?
There are four main categories of shock recognised in small animals.
1) Hypovolaemic
2) Cardiogenic
3) Distributive
4) Obstructive
How does hypovolaemic shock result in an alteration in tissue perfusion?
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);
How does cardiogenic shock result in an alteration in tissue perfusion?
cardiac dysfunction (cardiogenic shock)
How does distributive shock result in an alteration in tissue perfusion?
maldistribution of blood flow
distributive or septic shock
How does obstructive shock result in an alteration in tissue perfusion?
obstruction
to normal blood flow (obstructive shock)
What type of shock may be treated differently to other types of shock?
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.
What are the two most common types of shock seen in practice?
Hypovolaemic shock and septic shock are the two most common causes of
shock in veterinary practice
What are the common causes of hypovolaemic shock?
Common causes of hypovolaemic shock include
o Haemorrhage (trauma, surgical, coagulopathy etc.)
o Gastrointestinal losses (e.g. vomiting secondary to gastrointestinal
foreign body).
What are common causes of septic shock?
Common causes of septic shock include septic peritonitis, pyometra and
pyothorax.
What are common causes of obstructive shock?
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
What are common causes of cardiogenic shock?
End-stage dilated cardiomyopathy and severe arrhythmias are examples of
cardiogenic shock.
What is oxygen delivery to tissues dependent on?
Oxygen delivery (DO2) is dependent on cardiac output and local tissue blood flow (perfusion)
How do you calculate cardiac output?
Cardiac output= stroke volume x heart rate.
What is blood pressure affected by?
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)
How does cardiac output affect tissue perfusion?
decreased cardiac output could lead to decreased blood pressure
(hypotension). Hypotension will lead to decreased tissue perfusion.
Consider the effect of a garden hose (blood vessel) watering the flowers (cells) if the
water supply is significantly decreased (cardiac output) …….
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….
How does hypovolaemia affect stroke volume?
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 -
How can hypovolaemia arise?
- Internal or external blood loss (haemorrhagic shock)
- 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 - Obstruction to venous return, as in gastric dilatation and volvulus (obstructive
shock.
What is the aim of compensatory mechanisms following any drop in cardiac output?
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.
What are the compensatory mechanisms mediated by?
These compensatory mechanisms are both
neural and hormonal – neuroendocrine responses; and are mediated by the
hypothalamo- pituitary- adrenal (HPA) axis - the sympatho-adrenal response.
How are the compensatory mechanisms categorized?
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)
Within what time frame could acute compensatory mechanisms arise?
Acute (immediate onset; response within minutes)
Within what time frame could moderate compensatory mechanisms arise?
Moderate (response within 10- 60 minutes)
Within what time frame could chronic compensatory mechanisms arise?
Chronic (response within 1-48 hours)
What are the acute compensatory mechanisms focused on in shock?
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.
What stimulates the sympathetic nervous system in shock and what effects does this have on the body?
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
What effect does nor-adrenaline/nor-epinephrine have on the body in acute shock?
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
What detects hypoxaemia and results in increased sympathetic nervous system activity?
Hypoxaemia, which is detected by chemoreceptors in the aorta and carotid artery, also
results in increased sympathetic nervous system activity and catecholamine release
What is the main functions of cortisol release during shock?
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
What is activated in moderate compensatory mechanisms in shock?
Neurohormonal mechanisms are also activated aiming to return vascular volume to
normal e.g. activation of the renin angiotensin aldosterone system (RAAS).
What does RAAS stand for?
renin angiotensin aldosterone system (RAAS).
What compensatory stage in shock is renin angiotensin aldosterone system activated?
Moderate
What are the 4 steps from decrease renal perfusion to the angiotensin II response?
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
What does decreased renal perfusion stimulate and what conversions take place?
Decreased renal perfusion results stimulates baroreceptors in the kidney.
This stimulates RENIN release which converts ANGIOTENSINOGEN
to Angiotensin I then Angiotensin II
What immediate effects does the release of renin following reduced renal perfusion have on the body?
Immediate response of Angiotensin II - peripheral vasoconstriction ( and
reabsorbs some salt and water)
What delayed effects does the release of renin following reduced renal perfusion have on the body?
Delayed response Angiotensin II - ALDOSTERONE release from adrenal
cortex. Increased sodium, chloride and water reabsorption from distal
convoluted tubules in kidney → increased blood volume
What is the net result from reduced renal perfusion stimulating the release of renin?
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.
Is vasoconstriction as a result of compensatory mechanisms in shock sustainable?
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.
What large organ is affected by the reduced perfusion in shock?
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.
How much is the blood flow to the GI tract reduced by in shock?
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.
What GI symptoms can occur in shock and why?
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
Where is vasopressin released from and what effects does it have in the moderate stage of compensatory shock?
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).
What is the net effect of the chronic stage of compensatory mechanisms in shock?
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
What effect do aldosterone, ADH and vasopressin have on the body in chronic stage of compensatory mechanisms?
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).
Explain what happens in cardiogenic shock?
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.
In feline patients what is cardiogenic shock more commonly associated with?
In feline patients, cardiogenic shock is more
commonly associated with hypertrophic cardiomyopathy and aortic thromboembolism.
What causes the abnormal distribution of blood in distributive/septic shock?
Distributive / Septic Shock
With distributive shock, there is abnormal distribution of blood caused by peripheral
vasodilation
How does distributive shock lead to an inadequate supply of blood to tissues?
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.
Why can distributive shock present similar to hypovolaemic shock?
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.
How can you tell the difference in hypovolaemic shock compared to distributive shock after initial treatment and why?
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).
What is the underlying abnormality in distributive shock?
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.
What causes widespread vasodilation in distributive shock?
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
What is the difference between SIRS and sepsis?
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
What is the most common cause of sepsis?
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.
How can anaphylaxis cause distributive shock?
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
How can you detect anaphylaxis on ultrasound?
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.
What main effects does SIRS/SEPSIS have on the body?
With SIRS and sepsis, inflammatory chemicals are released into the blood stream
which cause vasodilation, decreased perfusion of organs and hypotension leading to
shock.
What early distinguishing signs may there be in distributive shock in dogs?
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
How does sepsis in dogs and cats differ and what clinical signs can be seen in a cat?
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.
How can pericardial effusion be considered as obstructive shock?
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.
What group of patients can develop shock in hospital
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
What is compensated shock?
• 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.
What is decompensated shock?
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.
What is irreversible shock?
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.
What is AKI?
acute kidney injury
What is ALI?
Acute lung injury?
What sis ARDS?
Acute respiratory distress syndrome
How does peripheral vasoconstriction affect the mucous membranes in shock?
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…
How does catecholamine release in shock affect the heart?
decreased blood volume
results in catecholamine release which causes tachycardia…
What clinical signs does hypovolaemia, cardiogenic, obstructive or advanced distributive shock all share?
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
What different clinical signs would a dog in early septic shock display compared to other types of shock?
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.
What biochemical changes will occur in a patient with anaerobic respiration.
Therefore, it is likely that a patient
with shock will have increased blood lactate levels which will result in metabolic
acidosis.
What would happen to a patients lactate levels if they were improving or deteriorating?
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
Can a one-off lactate reading give you an idea on patient prognosis or response to treatment?
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.
What blood gases would indicate a deterioration in acidosis?
Increasing PaCO2 and decreasing PaO2/ SpO2 indicate deterioration and worsening
of acidosis
What test is useful to do in an animal suspected to have disseminated intravascular coagulopathy
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.
What can be the signs of dehydration?
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.
What the PCV be up to in sighthounds and why?
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
Aside from a physical examination what else can be done to assess hydration levels?
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
How will the PCV /TP read in an animal that is dehydrated?
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.
How would a PCV/TP usually read in a young animal under 6 months?
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
How can a dehydrated patient become hypovolaemic?
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.
Are hypovolaemic patients always dehydrated? What cases might they be one and not the other?
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.
What are the most common infectious causes of sepsis?
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.
Is SIRS caused by infectious or non infectious causes?
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.
What are the non-infectious causes of SIRS?
Non-infectious causes include: o Trauma o Burns o Pancreatitis o Surgery o Immune-mediated disease o Neoplasia
What is the purpose of inflammation?
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
What is the result of a patient with SIRS with what should be localised inflammation?
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
What are the main problems with SIRS development? What two other life threatening conditions could develop as a result?
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
What is the gram negative key component and potent initiator of the septic inflammatory cascade?
Lipopolysaccharide (LPS) is a key component of the cell wall of Gram-negative
bacteria and is a potent initiator of the septic inflammatory cascade
What organs are the most common source of leakage of gram negative bacteria?
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.
What is the gram positive key component and can also initiate of the septic inflammatory cascade?
The cell wall of Gram-positive bacteria contains peptidoglycan and lipoteichoic acid
that can also activate the inflammatory cascade
What organs are the most common source of leakage of gram positive bacteria?
Sources of Gram-positive sepsis in
the surgical patient can include wounds and intravenous catheters.
What serious conditions can streptococcus canis result in?
Streptococcus
canis infection can result in toxic shock syndrome and necrotizing fasciitis in the dog
What is septic shock characterised by?
It is characterised by
cardiovascular decompensation secondary to widespread vasodilation with inefficient
oxygen delivery and resultant cellular dysfunction
What vascular abnormalities cdoes SIRS/Sepsis lead to?
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.
What clinical findings are there relating to vasodilation in a dog with SIRS/Sepsis?
Leads to hypotension and decreased organ perfusion
What clinical findings are there relating to vasoplegia in a dog with SIRS/Sepsis?
Vasoplegia
▪ Loss of vasoconstrictor response to catecholamines/
sympathomimetics
What clinical findings are there relating to increased vascular permeability in a dog with SIRS/Sepsis?
Increased vascular permeability
▪ Leads to interstitial oedema (loss of fluid and albumin into the
interstitium) and decreased plasma volume and
hypoalbuminaemia
What are the haemostatic abnormalities associated with SIRS/sepsis?
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
How can SIRS/sepsis lead to DIC?
Inflammation leads to
activation of haemostatic mechanisms inducing a prothrombotic state
(covert DIC).
Why may a patient with SIRS/sepsis have a reduced blood flow to organs?
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
Why may a patient with SIRS/sepsis develop hypocoagulation?
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.
How can SIRS/sepsis affect renal function?
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.
How can SIRS/sepsis affect pulmonary function?
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.
How can SIRS/sepsis affect cardiac function?
Cardiac dysfunction
o Septic animals have altered/decreased cardiac contractility and are
predisposed to arrhythmias.
What might cause an alteration in blood flow to the GI tract in SIRS/Sepsis?
Hypotension, micro thrombi and deregulation of regional blood flow can
all lead to alterations in gastrointestinal (GI) perfusion.
What can cause a bacterial translocation in to the lymphatics and blood stream in SIRS/sepsis?
Increased epithelial permeability, secondary to GI hypoperfusion, can
result in bacterial translocation into the lymphatics and blood stream.
What can cause bowel oedmea in SIRS/sepsis?
Hypoalbuminaemia can result in bowel oedema.
What are the clinical signs associated with sepsis in dogs?
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
What are the clinical signs associated with sepsis in cats?
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
How much of the proposed criteria for diagnosis of SIRS in dogs should be present?
2/4
How much of the proposed criteria for diagnosis of SIRS in cats should be present?
3/4
What 4 clinical parameters are assessed for the diagnosis of SIRS/sepsis?
Heart rate
Respiratory rate
Temperature
Leukogram
What will a dogs heart rate be that might indicate sepsis on the proposed criteria for diagnosis?
> 120
What will a dogs heart rate be that might indicate sepsis on the proposed criteria for diagnosis?
<140 OR >225
What will a dogs respiratory rate be that might indicate sepsis on the proposed criteria for diagnosis?
> 20 OR
PaCO2<30 mmHg
What will a cats respiratory rate be that might indicate sepsis on the proposed criteria for diagnosis?
> 40
What will a dogs temperature be that might indicate sepsis on the proposed criteria for diagnosis?
< 38.1˚C OR >39.2˚ C
What will a cats temperature be that might indicate sepsis on the proposed criteria for diagnosis?
<37.8˚C OR > 40.0 ˚ C
What will a dogs Leukogram be that might indicate sepsis on the proposed criteria for diagnosis?
> 16-18,000 WBCs / μl
OR <5-6000 / μl
What will a cats leukogram be that might indicate sepsis on the proposed criteria for diagnosis?
> 19,000 WBCs / μl OR
<5000 / μl
Septic animals may have a leucocytosis (characterised by a ‘left shift’) or
leucopaenia.
What test can help to measure inflammation?
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
What is the main aim of the compensatory mechanisms in shock?
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
What happens if the underlying cause of compensated shock is not managed and identified?
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
Is shock a primary or secondary condition?
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.
Is SIRS/Sepsis a primary or secondary condition?
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.
What is the normal lactate level?
normal <2.5 mmol/L
If a patient has increased lactate levels and responds to intravenous fluids what should happen to cellular metabolism?
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.
Why are septic patients commonly hypoglycaemic?
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
What might blood glucose levels and lactate parameters might raise suspicion of sepsis?
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
What might happen to an animals protein levels with SIRS/sepsis and why?
These animals are also commonly hypoalbuminaemic as the vasculitis,
which develops with SIRS, leads to protein loss from the vasculature.
What might a cats bilirubin levels be with SIRS/sepsis and how may this present clinically?
Finally, cats will
often become mildly to moderated hyperbilirubinaemic (and clinically icteric) when
septic.
What monitoring should a patient recieve if they have SIRS or sepsis?
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
What specific care needs to be provided to a recumbent patient?
• 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
What are intravenous catheters placed for?
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.
What are the different types of catheters available for IV access?
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
Can butterfly catheters be kept in place?
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
How many drops per ml does a standard giving set give?
20 drops per millilitre
How many drops per ml does a paediatric giving set give?
40-60 drops per millilitre (paediatric).
What vein should parenteral nutrition be administered through?
Product to be administered e.g. total parenteral nutrition should be administered
through a central vein
What are the various considerations when placing an IV catheter?
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
What is the protocol for placing a peripheral IV catheter?
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
What are the reasons for placing a central venous catheter?
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
Where are central lines placed in dogs and cats?
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.
What tests should be run before placing a central line?
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 (
How long should a central line be?
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
What is the protocol for placing a guidewire inserted catheter central line?
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
What are the contraindications for placing a central line?
Contraindications to placement include coagulopathy, raised intracranial pressure and
a prothrombotic state that will predispose to catheter clot formation
What is the protocol for placing a peel away shath central line?
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.
How often should catheter sites be cheked?
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
How often should a catheter be flushed to maintain patency?
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.
How often should an intravenous catheter be changed?
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)
What should be checked/observed when doing catheter care?
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.
What are the possible complications with intravenous catheter placement?
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
What can be administered through an intraosseous catheter?
Fluids, drugs and blood products can all be given via the intraosseous route- although
hypertonic fluids and alkaline fluids can cause discomfort
What are the sites for intraosseous catheter placement in dogs and cats?
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
What are the contraindications for intraosseous catheter placement?
Skin wound or infection over proposed catheter site, fracture of the bone to be
used, pneumatic bones, sepsis and metabolic bone disease
How do you prep an area for intraosseous catheterization? What should you do after placement?
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.
What type of patients usually require intraosseous catheters?
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
How should an intraosseous catheter be handled post insertion?
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.
What are isotonic fluids commonly used for in veterinary practices?
Isotonic fluids are very versatile and are commonly used in veterinary practice- for
hypovolaemia, dehydration, replacing ongoing losses and maintenance and
replacement of electrolytes
What are the different types of isotonic fluids?
Examples include 0.9%
saline, lactated Ringer’s (Hartmann’s) and Ringer’s solution.
Why might 0.9% saline be used in a patient with hypercalcaemia?
0.9% saline might be chosen if a
patient has hypercalcaemia as it increases calcium excretion via the kidney
Why might lactated ringers be the fluid of choice with a patient with metabolic acidosis?
Lactated Ringer’s is likely to be selected when there is a metabolic acidosis as it contains a bicarbonate precursor(common).
What electrolyte imbalance can be the result of prolonged isotonic crystalloid use?
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.
How does isotonic fluid move when administered in to the body?
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
What is the initial choice of fluids in most hypovolaemic patients and why?
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
what is the blood volume in dogs considered to be?
90ml/kg in dogs
what is the blood volume in cats considered to be?
60ml/kg in cats
How much fluid bolus would a mildly hypovolaemic dog need need in an emergency?
A mildly hypovolaemic dogs may only require 10-20 ml/kg of isotonic crystalloid
How much fluid bolus would a severely hypovolaemic dog need in an emergency?
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
What is the bolus rate of isotonic fluid for a cat with hypovolemia?
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.
What are the potential issues when administering isotonic crystalloid therapy?
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.
Can a hypovolaemic patient with metabolic acidosis receive 0.9% saline for treatment?
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.
What is the fluid maintenance value for small mammals?
80-100ml/kg/day
What is the fluid maintenance value for birds?
50ml/kg/day
What is the fluid maintenance value for reptiles?
15-30
ml/kg/day
What organ is used to metabolise alkalising fluids?
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.
How do alkalising fluids raise the PH of blood?
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.
What type of alkalising fluids should not be given to animals in liver failure and why?
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
Why should sodium bicarbonate not be administered to animals as the first line of treatment for metabolic acidosis?
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.
What can be the cause of hypokalaemia in cats?
cats- chronic
renal failure, prolonged anorexia, muscle wastage and gastro-intestinal losses are
potential causes
What are the main signs see with hypokalemia?
Hypokalaemia causes muscle weakness, especially obvious in cats, with plantigrade
stance and ventroflexion of the neck- it can also cause cardiac arrhythmias.
How can fluid therapy and fluid loss affect potassium levels?
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.
What can develop if potassium supplementation is administered too quickly?
The rate of administration should not exceed 0.5 mmol/kg/hour
otherwise a cardiac arrhythmia may develop
What monitoring will a hypokalaemic cat require?
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
What nursing care should be provided to a patient in septic shock?
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
What effect does the Alpha-1 adrenergic (α-1) receptor of a vasopressor have?
Alpha-1 adrenergic (α-1)
Blood Vessel
Vasoconstriction
What effect does the Beta- 1 adrenergic (β-1) receptor of a vasopressor have?
Beta- 1 adrenergic (β-1)
Heart Positive inotrope (increased strength)
Positive chronotrope (increased rate)
What effect does the Beta- 2 adrenergic (β-2) receptor of a vasopressor have?
Beta- 2 adrenergic (β-2) Blood Vessels Vasodilation
What effect does the Dopamine) receptor of a vasopressor have?
Dopamine
Blood vessels e.g.kidney
Vasodilation (other effects elsewhere)
(low dose)
Vasoconstriction (high dose)
Why would vasopressor agents be used in dogs with septic shock?
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.
What effects can occur as a result of excessive vasoconstriction from too many vasopressors? What can be done to avoid this?
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.
How should vasopressors be administered?
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.
What receptors are present in noradrenaline? What effect does this have and what is the dose range?
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
Why might noradrenaline doses need to be increased in sepsis?
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.
What effect does a low dose of dopamine have on the body?
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
What effect does a high dose of dopamine have on the body?
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.
How does a high dose of dopamine increase mean arterial pressure?
Dopamine therefore increases mean arterial pressure (MAP) by increasing cardiac
output and/or systemic vascular resistance.
What is it important to carefully monitor when an animal is receiving a dopamine CRI?
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.
What is dobutamine and what effects does it have on the body?
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.
How is dobutamine administered and what should be monitored carefully?
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
What receptor does vasopressin cause vasoconstriction through?
Vasopressin causes vasoconstriction through V1 receptors that are present on
vascular smooth muscle
When should vasopressin be used in septic patients?
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
What is inhibited to avoid vasodilation when vasopressin is administered?
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.
How soon should antibiotics be started when septic shock is suspected?
Intravenous antibiotic therapy
should be administered as early as possible and within the first hour of recognition of
septic shock.
What antibiotics should be used in septic patients when the type of bacteria is unknown?
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
How can sepsis affect the blood glucose levels?
Septic patients are commonly hypoglycaemic and will typically require dextrose
supplementation
What dose can dextrose be administered in a septic patient?
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.
can corticosteroids be used in patients with septic shock?
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.
Is nutritional support important in septic patients and why?
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
Can you use NSAIDS in septic patients for analgesia?
non-steroidal antiinflammatory drugs (NSAID) compromise renal perfusion and can result in GI
ulceration and as such should be avoided in septic patients.
Why may omeprazole be used in patients with sepsis?
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.
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%
The correct answer is: 94%
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
The correct answer is: End tidal CO2
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
The correct answer is: 7.35-7.45
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
The correct answer is: Urine output < 1mL/kg/hr
The normal Arterial-alveolar (A-a) gradient is
Select one:
a. <40 mmHg
b. >30 mmHg
c. <50 mmHg
d. < 15 mmHg
(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
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
( 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
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
(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
