module9 Respiratory emergencies Flashcards
Discuss respiratory physiology in terms of hypoxaemia and hypoxia, and their causes
HYPOXAEMIA=low O2 in blood.(PaO2 of<80mmHg.)
To get O2 into blood need air to go via resp tract, through lungs alveoli and into arteriolar system.
Causes of hypoxaemia:
1.Hypoventilation. Hypoventilation causes decrease in Alveolar Minute Ventilation and results in high PaCO2. The Alveolar Minute Ventilation can be improved with O2 supplementation, but this has not addressed the cause of hypoventilation.
As there is continuous transfer of oxygen from the alveoli to the blood stream and transfer of carbon dioxide from blood stream to alveoli, with reduced ventilation the partial pressure of CO2 in the alveoli will increase and the partial pressure of O2in the alveoli will decrease.
Normal pressures in (21% oxygen and 79% nitrogen at sea level) in the alveoli is constant and it is divided into the following:
Water vapour 50mm Hg
CO2 40mm Hg
Oxygen 105mm Hg
Nitrogen 560mm Hg
Nitrogen and water not used by body and stay same (with 100% will gradually get the nitrogen to diffuse away though) so because total pressure same, if CO2 partial pressure changes by 20, O2 partial pressure changes by 20 also (in the opposite direction).
2. Venous admixture (not just shunts, but any way blood gets from right to left without being properly oxygenated).i.e. if a patient is hypoxaemic in room air and has a normal or low PaCO2, you can
infer that venous admixture is occurring and is likely parenchymal disease.
Parenchymal lung dz (pus, water, haemorrhage in lung)
Diffusion defect (thickened diffusion barrier eg chronic smoking, acute resp distress. smoke inhalation etc)
Right to left shunt.
(sometimes have hypoventilation and venous admixture)
Consider the following cases:
1. A patient has SPO2 90% in room air and CO2 of 60mmHg. The SPO2 improves to 100% with supplemental oxygen.
a. What is the likely cause of the hypoxaemia?
i. Hypoventilation
2. A patient has SPO2 90% in room air and CO2 40mmHg. The patient responds to oxygen
– SPO2 improves to 98%.
a. What is the likely cause of the hypoxaemia?
i. Hypoventilation is not the cause of the hypoxaemia
ii. Likely venous admixture
3. A patient has SPO2 90% in room air and CO2 of 60mmHg. The SPO2 only improves to
92% with supplemental oxygen.
a. What is the likely cause of the hypoxaemia?
i. Both hypoventilation and venous admixture
The 120 rule;
HYPOXIA= inadequate oxygen content in the tissues, which can be due to hypoxaemia but may occur in a normoxaemic patient with poor perfusion - and therefore reduced oxygen delivery to the tissues. Surrogate markers of perfusion such as lactate, ScvO2, urine output and blood pressure are useful as cannot directly measure tissue perfusion.The body’s oxygen content is determined by three variables;
i.concentration of haemoglobin saturated with oxygen (SaO2) (pulse oximetry)
ii.concentration of the haemoglobin itself (Hb) (i.e.
how many RBCs)
iii.dissolved oxygen in the blood (PaO2 from an arterial blood gas).Dissolved oxygen content contributes very little to the overall oxygen in arterial blood, but it is an indirect measure of the ability of the lungs to exchange oxygen.
Together,
Oxygen content = (1.34 x Hb x SaO2) + 0.003 x PaO2 (in mL/dL. For SI , do mL/dL x 10).
The BIGGEST contributor to oxygenation by far is Haemoglobin concentration and when very anaemic, O2 therapy is negligible cf oxygenation improvements from transfusion.
Describe the difference between ventilation and oxygenation measures and V/Q mismatch
VENTILATION;Movement of air through lungs, with the aim of reducing CO2. (increasing inspired oxygen content does not decrease paCO2-need mechanical or manual ventilation to do this).Arterial or venous CO2.Persistent elevation in CO2 will lead to acidosis and subsequent cardiac and neurological damage.
OXYGENATION;ability of lungs to oxygenate the blood.PaO2. SpO2 can be used but may not always be accurate.
V/Q MISMATCH;V=ventilation and Q=perfusion. There are really considering the amount of ventilation in an alveolarcapillary unit cf the amount of perfusion of the same alveolarcapillary unit.When there is VQ mismatch, there are areas of high VQ and areas of low VQ. Because the lower areas of lung have greater perfusion (due to gravity and lower bp of pulmonary artery system), whenever there is VQ mismatch, there is much greater volume of blood receiving inadequate oxygenation and so a total result of hypoxaemia.
VQ mismatch does respond to 100% inspired oxygen with a correction of hypoxaemia (but if have a shunt, the response is only partial).
VQ mismatch is the most common reason for hypoxaemia and specific causes include: COPD, fibrosis,asthma, pulmonary embolism, pulmonary hypertension and pneumonia.
Note that in pulmonary embolism, that area of lung has less perfusion, but as a result, everywhere else has increased perfusion and so results in total decreased VQ.
Explain the oxyhaemoglobin dissociation curve
The oxyhaemoglobin dissociation curve illustrates how the binding affinity of oxygen
with haemoglobin differs at different partial pressures of oxygen.At low partial pressures, the gradient of the curve is almost flat as the first oxygen molecule has difficulty binding to the haemoglobin molecule. After the first O2 molecule is bound, the subsequent molecules bind more easily,resulting in the curve becoming steeper. At the top of the graph, almost all the oxygen binding
sites are occupied, and the curve flattens out again. Clinically, it is important to recognise that
small changes in SaO2 correlates to large changes in PaO2.
There are several physiological factors that influence the affinity of haemoglobin to oxygen.
1. Partial pressure of CO2
* Increase in CO2 shifts the curve to the right
* Hyperventilation and hypocapnia shifts the curve to the left
2. pH, independent of CO2
* Decreasing pH (acidosis) shifts the curve to the right
* Alkalosis shifts the curve to the left
3. The concentration of 2,3 DPG inside the red blood cells
* Increase 2,3 DPG (e.g. in response to hypoxia) shifts the curve to the right
* Decrease 2,3 DPG (e.g. in red cell storage lesion) shifts the curve to the left
4. Presence of unusual haemoglobin species
* Methaemoglobin, carboxyhaemoglobin shift the curve to the left
5. Temperature
* Hyperthermia shifts the curve to the right
* Hypothermia shifts the curve to the left
An oxyhaemoglobin curve to the right indicates that there is a decreased affinity of
haemoglobin for oxygen, hence an increased tendency to give up oxygen to the tissue. This is
a useful adaption when there is an increase in CO2, acidosis, hypoxia and hyperthermia.
An oxyhaemoglobin curve to the left indicates that there is an increased tendency for
haemoglobin to take up oxygen. This can be clearly seen in patients with carbon monoxide
toxicity, with oxygen therapy as the mainstay treatment for carbon monoxide toxicity.
Explain lung function assessment in terms of the PF ratio
This can only be used when inspired oxygen (FiO2) (which is F)is over 40%. Then P is PaO2.
Then use P:F ratio to grade lung function severity (more severe = worse prognosis and requires far more intensive tx). So when P:F is
<300 Mild Acute Lung Injury
<200 Moderate Acute Lung Injury
<100 Severe Acute Lung Injury.
Detail a diagnostic plan for patients with respiratory distress
First, categorise as upper resp(obstructions, laryngeal paralysis, etc), parenchymal (primary lung disease vs cardiac disease), or pleural space dz (pneumothorax, pleural effusions, diaphragmatic hernia).
UPPER AIRWAY DZ
Present with increased inspiratory effort and audible upper airway noise e.g. upper airway obstruction from foreign bodies, soft tissue swelling or laryngeal paralysis. Breathing is
termed “obstructive pattern” characterised by prolonged inspiratory respiratory phase with
increased effort and generally noise from airway turbulence. The patients are stabilised with oxygen and sedation while examinations are performed to determine the cause of the obstruction.
Acepromazine should be used with caution and avoided in animals with perfusion deficits or
with underlying cardiac disease. Butorphanol given IM of IV is a safer choice in these
patients. It should always be a consideration in these cases if intubation is required to bypass
the upper airway pathology and in some cases a tracheostomy tube may be performed. The
priority in these cases is to establish and maintain an airway while further investigations are
performed.
PARENCHYMAL DZ
Identified by a restrictive breathing pattern (short,
shallow breaths with effort on both inspiration and expiration) with no audible respiratory noise. Think of breathing with a tight strap around your chest that limits the expansion of
your lungs. These patients will often have adventitious lung sounds as a result of fluid within
the lower airways and alveoli. This fluid can be blood, pus, oedema etc. They generally
require a combination of Vet-BLUE and/or radiographs to fully define the pathology and
progressive assessments, especially repeat Vet-BLUE, can be valuable as a monitoring tool.
Initially stabilisation is with oxygen and sedation as well as initiating treatment for the
underlying cause(s). In cases where pulmonary pathology is severe, stabilisation may require
mechanical ventilation and this should be considered if initial efforts at stabilisation fail.
PLEURAL SPACE DZ
Patients with pleural space disease have a characteristic breathing pattern with marked
inspiratory effort, with generally but not always a rapid rate but without audible respiratory
noise. The lack of noises is what differentiates this from upper airway disease that also
presented with inspiratory effort. Again Vet-BLUE assessment is invaluable in differentiating
between fluid, gas or tissue (organs) within the pleural space. In the event of fluid or air,
rapid thoracocentesis is recommended to help stabilise the patient.
DIAGNOSTIC TOOLS;
Pulse Ox-arterial oxygen saturation.
Thoracic xrays-aspiration pneumonia often affects right middle lung lobe (can see better on v/d)
T-Fast/Vet blue-view 4 sites per side (caudodorsal. perihilar, middle lung lobe and cranial lung lobe).
Glide sign - The lung ‘gliding’ over the pleural lining during the respiratory cycle. This is a normal finding and rules out a pneumothorax at that site.
o A-lines - White lines that run perpendicular to the lung interface. They are artefactual reverberations and are present air. In combination with glide sign this means there is normal ‘dry’ lung tissue, but in the absence of glide sign this
indicates a pneumothorax.
o B-Lines - Also known as lung rockets, these are perpendicular white lines that
arise from the lung interface and are an indication of ‘wet’ lungs.
Blood gas
Step 1: What is the pH? A normal pH is 7.35-7.45.
* <7.35 = acidaemia
* >7.45 = alkalaemia
Step 2: What is the cause of the acid-base disturbance?
* Assess the respiratory component (pCO2)
o Normal pC02 = 35-45mmHg
o <35 = respiratory alkalosis
o >45 = respiratory acidosis
* Assess the metabolic component (Base excess)
o Normal base excess = -2 - +2 mmol/L
o <-2 = Metabolic acidosis
o >+2 = Metabolic alkalosis
o The most common causes of a metabolic acidosis are hyperlactataemia,
azotaemia, ketonaemia, toxins etc
Step 3: Is there compensation?
* When a disease (e.g. vomiting causing a loss of acids) leads to a metabolic alkalosis,
the body will attempt to maintain neutrality by retaining acids (hypoventilation will
retain pCO2 and a compensatory respiratory acidosis).
* Remember that respiratory compensation occurs quickly (within hours), while
metabolic compensation takes several days.
Detail a treatment plan for patients with respiratory distress
OXYGEN THERAPY
1.Flow by oxygen
Administered by directing the fresh gas flow in front of the patient’s airway. It is noninvasive and well tolerated but cannot be provided long term (unless patients are severely obtunded). Typically achieves an FiO2 of approx 30%.
2.Mask
A tight-fitting mask can achieve inspired oxygen levels of ~90%. It is important to have high
flow rates (>200 ml/kg/min) to avoid rebreathing. Disadvantages of this method are that it is
generally not well tolerated.
3.Intranasal oxygen catheters
Nasal oxygen catheters provide a more long-term option for oxygen supplementation. They
are tubes that are placed into the nose via the ventral meatus as far caudal as the medial
canthus of the eye. They can be placed in conscious patients with a local infusion of
lignocaine into the nose. Nasal oxygen lines are often used for large patients where an
oxygen cage is not practical. They can be unilateral or bilateral and achieve an FiO2 of 40-
60%. It is important to only administer humidified oxygen via this route.
4.Oxygen Cage
Oxygen cages are an effective way of delivering high levels of inspired oxygen (60% with
high flow) to patients with minimal stress, generally considered the least invasive and
stressful of all oxygen therapy options.
Small animal cages with Perspex fronts and a seal around the edges/ clear plastic curtain that
has enough of a flange to seal around the edges can be used reasonably effectively. Both
options allow the patients to be monitored visually without opening the door. The oxygen
level rapidly drops when the cage door is opened so this should be kept to a minimum.
Temperatures can get very high in these systems; ice bricks can be placed in the cage.
Hood/Elizabethan-collar
In large breed dogs where an oxygen cage is not practical, and intranasal lines are not
tolerated, a hard plastic e-collar with plastic wrap over the top and high flow oxygen lines
directed into the cone can be an effective alternative. Again, heat can build up quickly as well
as CO2.
5.Transtracheal Oxygen
Transtracheal oxygen involves placing an over the needle catheter into the tracheal lumen. It
must be placed aseptically, with the ventral cervical area clipped and aseptically prepared. It is
most used in cases of upper airway obstruction prior to temporary tracheostomy. It can achieve
a higher FiO2 than nasal oxygen and can be used for patients that remain hypoxaemic with
nasal oxygen but do not require mechanical ventilation.
6.Intubation
Indications for intubation
It is important to be able to recognise when a patient requires endotracheal intubation. This
decision needs to be made quickly and is a life-saving procedure. Indications include:
* To relieve airway obstruction
* To protect the airway from aspiration
* To administer oxygen (for hypoxaemia), allow positive pressure ventilation (for
hypercapnoea) or to deliver inhalational anaesthesia
* In the event of a cardiopulmonary arrest
7.Mechanical ventilation
Mechanical ventilation involves using a machine to take over the work of breathing for the
patient. The machine pushes air into the lungs to inflate them, which is different from
normal breathing, where the chest wall and diaphragm move to create a negative pressure
within the lungs, which draws air in.
Indications
There are three indications for initiating mechanical ventilation:
1. Hypoxaemia PaO2 <60mmHg
2. Severe hypoventilation PaCO2 >60mmHg
3. An unsustainable effort of breathing
Animals that require mechanical ventilation can have primary lung disease, suffer from
neurological or muscular dysfunction or a combination of these. Mechanical ventilation has
the potential to cause serious damage to lung tissue. To reduce the risk of ventilatorassociated complications, the least aggressive settings should be used to maintain adequate
oxygenation and ventilation.
SEDATION AND ANXIOLYSIS
Reducing stress and anxiety in hospitalised patients is an important part of their management.
This becomes more important in patients in respiratory distress, with the goal of reducing
their oxygen demand. Options available include:
* Benzodiazepines (diazepam, midazolam)
o Cause minimal cardiovascular and respiratory depression and is a safe choice
in critical patients
o Sedative effects can be variable, often mild
* Opioids (methadone, butorphanol, buprenorphine)
o Of the opioids, butorphanol has the greatest sedative effect.
o Opioids have good cardiovascular stability, but can cause some respiratory
depression. Respiratory depression can be clinically significant in patient with
upper airway obstruction.
* Phenothiazine derivatives(acepromazine)
o Causes peripheral vasodilation and therefore should not be used if the
cardiovascular system is compromised.
o Minimal respiratory depression.
o No anxiolytic effects
* Alpha 2 Agonists(medetomidine)
o Even low doses can cause profound decreases in cardiac output and heart rate.
o Micro-dose CRIs (0.5-3mcg/kg/hr) can be useful to reduce anxiety in
hospitalised patients.
* SARI (Trazadone)
o Not well studied but can be used to control anxiety in hospitalised patients.
o Do not use concurrently with other serotonin potentiating drugs (eg. tramadol)
o Oral only
INDUCTION AGENTS
* Alfaxalone
o Associated with dose dependent respiratory depression (less of a concern
when you can manually ventilate).
o Safe to use as an induction agent in both cats and dogs.
o Unfortunately prolonged CRI’s of alfaxalone in large dogs becomes
prohibitively expensive for owners.
* Propofol
o Dose dependent hypotension and capable of causing cardiac arrhythmias.
o Should not be used in cats for prolonged periods (cats have a limited ability to
metabolise the preservative used in propofol).
List common disease states that present as respiratory emergencies
PULMONARY PARENCHYMAL DISEASE
1.Pulmonary Oedema;fluid accumulation in the alveoli. It can develop as a resultof increased hydrostatic pressure or increased vascular
permeability, or combination of.
Cardiogenic pulmonary oedema is the most common type of increased hydrostatic pressure
oedema. It develops as a result of left sided congestive heart failure. A failure of forward
flow into the systemic circulation results in a backup of pressure into the pulmonary
circulation, resulting in fluid extravasation into the alveolus.
Increased vascular permeability occurs when there is direct damage to the respiratory
capillary endothelium, the alveolar epithelium or both. More commonly seen in
systemic diseases such as acute respiratory distress syndrome (ARDS), systemic
inflammatory response syndrome (SIRS) or sepsis, where circulation of proinflammatory
cytokines upregulate the inflammatory response.
Noncardiogenic pulmonary oedema is a broad term that encapsulates all noncardiac causes of
pulmonary oedema. This can include high pressure oedema (e.g. fluid overload), increased
permeability oedema or a combination of the two. The more common causes of
noncardiogenic pulmonary oedema include neurogenic pulmonary oedema (head trauma,
strangulation, electrocution), ARDS, aspiration pneumonia, pulmonary contusions.
Management is Oxygen supplementation.
Fluid therapy is withheld in patients with cardiogenic pulmonary oedema
and diuretics are used instead (see cardiovascular module). Low-rate fluid therapy is required
in oedema secondary to increase in vascular permeability if the patient is not drinking.
Anxiolytic should be considered for this patient.
2.Pulmonary Contusions;usually occur following blunt force trauma. There is bruising/bleeding
of both the alveolar and interstitial spaces. Contusions can continue to worsen for 24 to 48
hours following the initial insult.
Management
is Oxygen supplementation. Fluid therapy should not be withheld but used with caution,
as overzealous fluids can result in further extravasation of fluid into the interstitial space.
There is a low incidence of bacterial pneumonia after contusions so routine antibiotics are not
recommended. Appropriate pain relief should be given after considering any concurrent
injuries.
3.Pneumonia; develops because of the natural defence mechanisms being overwhelmed with
large numbers of organisms (in the case of aspiration) or highly virulent organisms. In most
cases of infectious pneumonia in dogs, an underlying cause is present. Bacterial pneumonia
left untreated can rapidly progress from mild signs (soft cough) to acute lung injury/acute
respiratory distress syndrome (ALI/ARDS) (severe dyspnoea, hypoxaemia). ALI/ARDS is the
common end point of many disease processes. It is beyond the scope of this document to
describe acute lung injury and acute respiratory distress syndrome.
Treatment of pneumonia depends on disease severity. Mild cases can be treated with
appropriate antimicrobials as outpatients. Any patient with dyspnoea or hypoxaemia should
be given oxygen supplementation to maintain a Pa02 of >80mmHg. Antibiotic choice should
be based on culture results of fluid recovered from the respiratory track (e.g. bronchoalveolar
lavage/trans tracheal wash, endotracheal wash). Radiographs should be performed in all
patients. The distribution of the lesion can aid in a diagnosis (e.g. Aspiration of fluid more
commonly affects the right middle lobe –therefore a left lateral and VD view will be most
likely to yield a diagnosis. Three view radiographs should be taken in all cases of suspect
pneumonia.
BRONCHIAL DISEASE
eg Feline asthma; usually an allergic condition where exposure to a trigger causes inflammation
and narrowing of the airways, as well as airway hypersensitivity. Some cats may have chronic
bronchitis with airway inflammation and excessive mucous production.
These cats can present acutely due to an environmental change, causing severe respiratory
distress. They can present with dyspnoea, tachypnoea, coughing, open mouth breathing and
wheezing may be heard. The lung sound may be harsh and crackles can be heard. They can
have a prolonged expiratory phase or decreased lung sounds with barrel-shaped chest.
Management
Acute severe feline asthma patient needs to be treated with anti-inflammatory and
bronchodilator therapy. The most commonly used anti-inflammatory in acute severe feline
asthma patient is injectable corticosteroids (Dexamethasone 2mg/kg IV). This is usually
combined with injectable bronchodilator (Terbutaline 0.01mg/kg IM or SC) to relax the airway smooth muscle and to help them dilate.
PLEURAL SPACE DISEASE
1.Pneumothorax; defined as:
● Open - The thoracic wall is compromised and the pleural cavity has the same pressure as the atmosphere
● Closed - The air originates from the trachea, bronchus or alveoli
● Tension - A one-way valve results in air pressure in the pleural space that exceeds the
atmospheric pressure
The most common cause is trauma (secondary to motor vehicle accidents, dog bite wounds or
penetrating wounds). Iatrogenic wounds are also possible (FNA, surgical (eg gastropexy),
chest drain placement). They can also occur spontaneously, usually because of underlying
lung pathology (bullous emphysema).
Mild pneumothoraces can be managed conservatively, as the air will eventually diffuse out of the pleural space. If the patient is in respiratory distress and ventilation is compromised,
immediate therapeutic thoracentesis is indicated. Most patients will require drainage of the
air only once or twice. If a thoracocentesis needs to be performed more than twice in a 12-
hour period, a thoracostomy tube should be placed. The tube can be suctioned intermittently
(every 4-6 hours as required) or they can be attached to two or three bottle system which
provides constant low pressure suction. Tension pneumothorax will require continuous
suction. Surgical exploration is indicated if the leak persists beyond 3-5 days.
2.Pleural effusion;refers to any fluid accumulation in the pleural space. Fluid types can include
purulent exudate (pyothorax), blood (haemothorax), chyle (chylothorax), neoplastic effusions
or pure/modified transudates. Any fluid recovered from the chest should be classified as one
of the following:
1. Pure transudate
○ These fluids are typically clear, with low protein and cell counts. They
develop secondary to low oncotic pressure (e.g. hypoalbuminaemia) or high
hydrostatic pressure or vascular permeability (e.g. congestive heart failure)
○ Total protein: <2.5 g/dl
○ Total nucleated cell count: <1500/ul
2. Modified Transudate
○ These fluids are moderately cellular and usually result from either increased
vascular permeability or increased hydrostatic pressure (e.g. neoplastic
effusions, congestive heart failure, lung lobe torsion, etc)
○ Total protein: 2.5-7.5 g/dl
○ Total nucleated cell count: 1000-7000/ul
3. Exudate
○ These fluids are highly cellular and can be septic (pyothorax) or aseptic
(neoplastic). They develop as a result in increased vascular permeability.
○ Total protein: >3.0 g/dl
○ Total nucleated cell count: >7000/ul
Management
The treatment of pleural effusion depends on the type of effusion present. A diagnostic
thoracentesis should be performed on any patient presenting with a pleural effusion. Inhouse
analysis of the fluid should include cytology, glucose/lactate concentration (compare these to
peripheral glucose taken at the same time). The goal here is to quantify the fluid as
neoplastic, infectious or inflammatory. Any fluid that is suspicious for a neoplastic or
infectious process should be sent for culture and cytology. Always repeat imaging following
drainage to confirm that sufficient fluid has been drained (especially if draining
therapeutically) and to assess pulmonary pathology.
3.Pyothorax;an accumulation of purulent material (neutrophilic exudate) within the pleural
space. It is most commonly seen in cats but can occur in dogs. The route of infection is
thought to be via the respiratory tract, possibly secondary to aspiration pneumonia, lung
abscesses, tracheal perforation etc. In dogs it more commonly develops secondary to
penetrating trauma/foreign bodies migrating through the thoracic wall. Diagnosis is made via
diagnostic thoracocentesis. In-house cytology usually reveals a purulent effusion with
intracellular bacteria. All samples should be sent for culture to guide antimicrobial therapy.
Treatment involves empirical antibiotic therapy targeting the four quadrants therapy, for
example enrofloxacin, ampicillin and metronidazole. Antibiotic should be de-escalated once microbial culture and sensitivity result is available. Placement of bilateral chest drains is
required if there is a complete mediastinum separation. These will typically stay in place for
4-6 days. Saline can be infused into the drains to facilitate drainage of thick exudates,
10ml/kg lavage and then suction. When doing this, it is important to monitor fluid balance
closely as fluid overload can occur if residual saline is absorbed across the pleural lining. The
survival rate of these cats with pyothorax is very good (up to 95%) but they can require
intensive monitoring/treatment in the early stages, especially if septic shock develops.
Occasionally surgical exploration will be required.
CHEST WALL DISEASE
1.Rib fractures
Most often because of trauma, the pain from rib fractures can result in significant hypoventilation. This can lead to hypoxaemia and hypercapnia. The presence of rib fractures
should always alert the clinician to the possibility of lung damage (pulmonary contusions,
pneumothorax or haemothorax etc).
Pain relief is paramount – breathing with rib fractures can be very painful – pure opioids,
local anaesthetic blocks are required to help prevent hypoventilation from causing
hypoxaemia. Ensure there are not wounds that penetrate the pleural space that would
necessitate surgical exploration. Otherwise, apart from pain management, surgical
stabilisation is rarely indicated.
2.Respiratory muscle paralysis
The two most common causes of respiratory muscle paralysis are snake envenomation and
tick paralysis. However, acute idiopathic polyradiculoneuritis, botulism, tetrodotoxin and
myasthenia gravis should also be considered in patients presenting with a diffuse lower motor
neuron paralysis.
Respiratory muscle paralysis can result in hypoventilation causing hypercapnia and is a
common reason for mechanical ventilation
It is important to be aware that animals can die from severe hypercapnia despite having a
normal SpO2 (>95%).
Oxygen therapy should be given to any dyspnoeic or hypoxaemic patients. Following
treatment of the underlying disease, anxiolytic and sedative medication should be used to
reduce the work of breathing. However, they should be used with care as some medications
can cause respiratory depression and worsen the hypoventilation. Monitoring PaCO2 in these
patients is very important and is often used to guide decision making when considering if an
animal requires mechanical ventilation. If PaCO2 is >60mmHg or there is an unsustainable
work of breathing, mechanical ventilation should be considered.
