Respiratory

Acute pulmonary oedema (OPA)

Airway obstruction (foreign body)
Asthma
COPD
Croup/epiglottis
Dyspnoea
Hyperventilation

Clinical Practice Guidelines Respiratory

Clinical practice guidelines Acute pulmonary oedema
Version 1.0 September 2011 Page 1 of 4

Acute pulmonary oedema (APO) refers to the rapid buildup of fluid

Clinical features (continued)
in the alveoli and lung interstitium that has extravasated out of
the pulmonary circulation. As the fluid accumulates, it impairs gas Pink, frothy sputum may be present in patients
exchange and decreases lung compliance, producing dyspnoea and with severe disease.
hypoxia.[1] The pathophyisiological mechanisms are traditionally
Tachypnoea and tachycardia
categorised into two primary causes:
Hypertension is often present because of the
Cardiogenic hyperadrenergic state.
This form of APO occurs when cardiac output drops despite an Hypotension indicates severe LV dysfunction
increased systemic resistance, so that blood returning to the left and cardiogenic shock.
atrium exceeds that leaving the left ventricle (LV). As a result, Patients usually appear anxious and diaphoretic.
pulmonary venous pressure increases, causing the capillary
Cyanosis (late sign)
hydrostatic pressure in the lungs to exceed the oncotic pressure
of the blood, leading to a net filtration of fluid out of the capillaries.[2]

Non-cardiogenic Risk assessment

Pathological processes acting either directly or indirectly on the Precipitants of acute pulmonary oedema (APO)
pulmonary vascular permeability are thought to cause this form of
Primary cardiogenic causes:
APO. As a result, proteins leak from the capillaries, increasing the
interstitial oncotic pressure, so that it exceeds that of the blood and LV failure:
fluid is subsequently drawn from the capillaries.[2] -- ACS
-- Arrhythmia
Clinical features -- Pericarditis, myocarditis or endocarditis
-- Valve dysfunction (e.g. Aortic stenosis,
Sudden onset of extreme breathlessness, mitral regurgitation)
anxiety, and the feeling of drowning
Increased intravascular volume:
Profuse diaphoresis
-- Fluid overload
Crackles are usually heard at the bases first; as the
-- Non-compliance with fluid restriction or diuretics
condition worsens, they progress to the apices.
-- Renal failure
Cough is a frequent complaint that suggests
worsening pulmonary oedema in patients Pulmonary venous outflow obstruction:
with chronic LV dysfunction. -- mitral valve stenosis
Risk assessment (continued) Additional information
Cardiogenic pulmonary oedema patients often have a history
Non-cardiogenic causes: of cardiac hypertrophy/AMI/LVF.[3]
High output states: The primary goal in the treatment of cardiogenic pulmonary
-- Septicaemia oedema is reduction in preload and afterload with nitrates.
-- Anaemia All patients with APO should be given supplemental oxygen
-- Thyrotoxicosis to meet their physiological needs and reduce hypoxia.
Systemic increase vascular permeability APO patients who are hypotensive are in cardiogenic shock
-- Pancreatitis and require ICP support where available. These patients
-- Eclampsia may have a fluid deficit and therefore cautious fluid bolus
(250500 mL maximum) resuscitation should be titrated
-- DIC
against haemodynamics and clinical effect. Inotropic support
-- Burns may be required to increase cardiac output.
Toxins/environmental Non-cardiogenic APO requires respiratory support and treatment
-- Immersion/submersion of the underlying cause.
-- Toxic inhalation
-- High altitudes (HAPE) & decompression illness
Other
-- Head Injury/intracranial haemorrhage
-- Drugs (e.g. NSAIDs, calcium channel blockers
and naloxone)
-- Pulmonary embolus

Acute pulmonary oedema Page 2 of 4

Clinical practice guidelines Acute pulmonary oedema
Version 1.0 September 2011 Page 3 of 4

Standard Cares

Appropriate posturing

Determine cause
of oedema

Cardiogenic? Non-cardiogenic?

Consider: Consider:
Oxygen Oxygen
Aspirin 12-Lead ECG
GTN IPPV
12-Lead ECG PEEP
IPPV CPAP
PEEP
CPAP
 Manage as per CPG: Manage as per CPG:
Relevant dysrrhythmia Burns
Post submersion
ACS
Head injury
Spinal injury
Toxicology

Is the patient hypotensive?

Manage as per CPG: Transport to hospital

Cardiogenic shock Pre-notify as appropriate

Acute pulmonary oedema Page 4 of 4

Clinical practice guidelines Airway obstruction (foreign body)
Version 1.0 September 2011 Page 1 of 2

A foreign body airway obstruction is a life threatening emergency, An infant may be placed in a head down position before
most often occurring when eating.[1] delivering the back blows (i.e. across the lap).[2]
It is important paramedics recognise an airway obstruction as it
can be readily treated pre-hospital.

Clinical features
History:
-- sudden dyspnoea, gagging or coughing
Examination:
-- respiratory distress with stridor, accessory
muscle use and recession
-- restlessness and cyanosis
-- unconsciousness and bradycardia (periarrest)

Risk assessment
Not applicable Chest thrusts:
If back blows are unsuccessful, perform up to five
chest thrusts.
Additional information Check to see if each chest thrust has relieved the airway
obstruction. The aim is to relieve the obstruction with
Back blows: each chest thrust rather then give all five.
Perform up to five sharp back blows with the heel To perform chest thrusts, identify the same compression
of one hand in the middle of the back between the point for CPR and give up to five chest thrusts. They are
shoulder blades. similar to a chest compression, but sharper and delivered
Check to see if each back blow has relieved the airway at a slower rate.
obstruction. The aim is to relieve the obstruction with If the obstruction is not relieved, repeat the back blows
each back blow rather then give all five. and chest thrusts.
 Standard Cares

Mild airway obstruction

Effective cough? Encourage coughing
Provide ongoing reassurance
Provide supportive cares

Severe airway obstruction

Consider:
Up to five sharp back blows
Conscious? Up to five chest thrusts
Repeat if required
Ensure ongoing assessment
of airway and conscious state

Consider:
Removing obstruction under direct
visualisation
Oxygen
Gentle IPPV
LMA/ETT
Appropriate resuscitation CPG
Note: Officers are only to
perform procedures for which
they have received specific
training and authorisation
Transport to hospital by the QAS.
Pre-notify as appropriate

Airway obstruction (foreign body) Page 2 of 2

Clinical practice guidelines Asthma
Version 1.0 September 2011 Page 1 of 4

Asthma is a potentially life threatening condition. It is a chronic

inflammatory, obstructive disorder of the lower airways, characterised Clinical features (continued)
by episodes of reversible partial lower airway obstruction. Episodes

of asthma commonly cause wheezing, coughing, chest tightness and Mild Moderate Severe Life-threatening
breathlessness.[1] Alert Alert Agitated Confused/
drowsy
Obstruction of the lower airways results from a combination of: Nil accessory Mild Moderate Severe
bronchospasm muscle use accessory accessory accessory
muscle use muscle use muscle use or
inflammation and oedema of airways minimal due
to tiring
mucous plugging
No tachypnoea Mild Some physical Physical
airway smooth muscle hyperplasia and hypertrophy. tachypnoea exhaustion exhaustion
The above result in increased airway resistance, increased work No tachycardia Mild Marked Marked
of breathing, alterations in pulmonary blood flow and mismatches tachycardia tachypnoea tachypnoea
between ventilation and perfusion, eventually causing hypoxia.[2] Variable Variable Marked Hypotension/
wheeze wheeze tachycardia bradycardia
Treatment of asthma has two key concepts: Talks in Talks in Variable Often silent chest
sentences phrases wheeze
Relieving the bronchospasm (relievers)
Saturation Saturations Talks in words Unable to talk
Reducing the inflammation (steroids). Steroids take several > 94% room 9094%
hours to work and so earlier administration means earlier air room air
onset of action. No cyanosis No cyanosis Saturations Saturations
< 90% room air < 90% room air
Cyanosis/ Cyanosis/
Clinical features sweating sweating

Asthma can be classified as mild, moderate, severe Patient seated Patient seated
upright, unable upright, unable
or near-fatal (life-threatening). Near-fatal is acute to lie supine, to lie supine,
asthma associated with respiratory arrest or significant pursed lip pursed lip
hypercarbia.[2] There are two broad categories: breathing breathing
Gradual onset over days or weeks in patients Prolonged Prolonged
with poorly controlled asthma. This form is slow expiratory expiratory phase
phase
to respond to therapy. This is the most common
form, responsible for 8085% of all fatal events.[2] Hyperinflated Hyperinflated
thorax thorax
This pattern responds slowly to treatment.
Rapid onset and responds quickly to treatment.
Clinical features (continued)
Complications of asthma
Respiratory compromise
Gas trapping with increased work of breathing,
reduced ventilation
Hypoxia (late) due to ventilation-perfusion
mismatch
Hypercarbia associated with exhaustion,
altered level of consciousness (late)
Barotrauma particularly in ventilated patients[3]
-- pneumothorax/tension pneumothorax
-- pneumomediastinum/pneumopericardium.
Pneumonia
Additional information
Respiratory arrest
Haemodynamic instability
Bradycardia/cardiac arrest usually secondary
to hypoxia
Cardiac arrhythmias
Hypotension
Electrolyte abnormalities
Lactic acidosis, hypokalaemia, hypomagnesaemia
Risk assessment
Risk Factors for life-threatening disease
Prior ICU admissions and prior intubation
Three or more hospital admissions over
the last 12 months
Currently taking steroids for asthma or chronic
steroid use
Poor compliance with medications
Risk assessment (continued)
Wheezing is an unreliable sign of severity, as
severe asthma may be associated with an inability
to move air due to physical exhaustion, resulting
in a silent chest.[4]
Not all patients with wheeze have asthma
consider differential diagnoses (e.g. smoke
inhalation, COPD, foreign body, APO).[5]
Asthma attacks are not generally characterised by
hypoxia until late in the episode. Beware the patient
with normal SpO2.
Important points in patient history:
Previous asthma history age of onset, frequency and
severity of symptoms, number of hospital presentations
in last 12 months, ICU admissions, previous intubation
Co-existing medical conditions
Allergies
Asthma triggers if known
Cause of current episode if known
Duration of symptoms prolonged episodes increase
possibility of physical exhaustion
Medications. (reliever, preventer, steroids, compliance)
How they have been managing current episode
Asthma Page 2 of 4
Clinical practice guidelines Asthma
Version 1.0 September 2011 Page 3 of 4

Standard Cares

Assess severity and consider

differential diagnosis

Life-threatening
/imminent arrest
 Consider:
Salbutamol and
ipratropium Neb
Salbutamol IV
Consider: Severe
Adrenaline IV/IM
Adrenaline (early) IV/IM
IV fluid
IPPV with prolonged expiratory phase
Hydrocortisone
-- adult: 46 b/m
Magnesium sulphate
-- large child: 810 b/m
-- small child: 1015 b/m
-- infant: 1520 b/m
Monitor for barotrauma
Magnesium sulphate Consider:
Hydrocortisone Salbutamol and
Intubation Moderate/mild ipratropium Neb
IV access
Hydrocortisone

Transport to hospital
Pre-notify as appropriate

Asthma Page 4 of 4
Clinical practice guidelines Chronic 0bstructive pulmonary disease
Version 1.0 September 2011 Page 1 of 2

Chronic obstructive pulmonary disease (COPD) describes a number

of pulmonary diseases that are characterised by chronic airflow Clinical features
limitation that is not fully reversible. COPD includes: An acute exacerbation of COPD usually follows
Chronic bronchitis is defined as daily sputum production infection, although in some cases no clear precipitant
for at least three months over two or more consecutive years.[1] is apparent. Clinical features of an acute exacerbation
Classical presentation: include:
Cyanosed History:
Often overweight -- URTI symptoms
Oedematous -- Increased dyspnoea, difficulty in speaking,
Chronic cough reduced exercise tolerance, fatigue
-- Increased sputum volume and purulence
Chronic sputum production
-- Chest tightness and wheeze
Cor pulmonale (late sign)
-- Increased cough
Emphysema is characterised by dilatation and destruction of -- Anxiety
alveoli. The loss of elasticity and enlargement of these air spaces -- Increased medication use with minimal
leads to hyperinflation of the lungs and increased work or no effect
of breathing.[1] Classical presentation:
Examination:
Thin
-- Respiratory distress
Barrel chest
-- Intercostal or suprasternal recession
Dyspnoea
-- Accessory muscle use
Tachypnoea -- Fever/sepsis
Pursed lip while breathing -- Cyanosis
Intercostal or suprasternal recession -- Wheeze, crackle, reduced air entry
Tripod posture on auscultation
Both presentations can share symptoms of dyspnoea, cough and -- Tachycardia
sputum production, with chest tightness, airway irritability and
wheezes also common. The natural course of COPD is characterised
by episodes of acute exacerbation where the above symptoms
worsen.[2]
Note: COPD is a spectrum of disease and many patients have
features of both chronic bronchitis and emphysema.
 Risk assessment Standard Cares

COPD exacerbation may mask other pathology,

making diagnosis and management difficult.
The following conditions are common differential
Consider:
diagnoses:[2]
Severe respiratory Maintain SpO2 at 8892%
Cardiogenic APO/CCF/AMI
distress? Salbutamol Neb
Asthma Ipratropium bromide Neb
Pneumonia/pleural effusion Hydrocortisone
Upper airway obstruction
Pulmonary embolism
Pneumothorax
Lung cancer
Consider:
Salbutamol Neb
Additional information Ipratropium
bromide Neb
Hypoxic drive Salbutamol IV
The aim of oxygen therapy is to prevent life-threatening hypoxia; Hydrocortisone
attempts should be made to titrate supplemental oxygen to Adrenaline
achieve SpO2 readings between 88% and 92%.[2] Some COPD IPPV
patients rely on hypoxia to drive respiration rather than
hypercapnia due to chronically raised CO2 levels. Thus
uncontrolled oxygen therapy can result in suppression of
respiratory drive, carbon dioxide narcosis and ultimately
respiratory arrest.[3]
If the patient is hypoxic high dosages of oxygen therapy are Transport to hospital
indicated, with a view to de-escalate oxygen concentration Pre-notify as appropriate
where appropriate; the lowest dosage of O2 possible should
be used.

Chronic obstructive pulmonary disease Page 2 of 2

Clinical practice guidelines Croup or epiglottitis
Version 1.0 September 2011 Page 1 of 2

Croup
Croup (laryngotracheitis) is an illness of infants and younger children Clinical features (continued)
with a peak incidence between seven months and three years of age.[1] High fever, septicaemia
It is most commonly associated with a viral URTI in colder months May present in a tripod position, mouth breathing
and is often worse at night.[2] with tongue and jaw protrusion
Stridor or respiratory distress:
Epiglottitis
-- snoring or stridor
Epiglottitis is an acute inflammation involving the epiglottis, vallecula,
aryepiglottic folds, and arytenoids occurring in both adults and children. -- dyspnoea
It occurs most often in adults in their 40s and 50s and children between -- intercostal or suprasternal retractions
two to five years of age.[3] -- cyanosis

It is an uncommon (due to vaccination for HiB), but dangerous cause Distinguishing between croup and epiglottitis
of airway obstruction.[4] Age
Onset
Type of cough
Clinical features
Degree of respiratory distress
Croup Usually, croup occurs in younger children and
URTI symptoms is proceeded by a cold or other viral infection
Fever and the child rarely appears toxic.
Croupy (seal bark) cough
Stridor (this may be absent in severe croup)
Respiratory distress: Risk assessment
-- suprasternal, intercostal or subcostal retractions Not applicable
-- cyanosis, pale/dusky appearance
-- agitation/distress
Epiglottitis
Rapid onset
Muffled or hoarse voice
Sore throat, pain on swallowing and drooling
Additional information
Standard Cares
Avoid agitating patients with croup or epiglottitis.
Let the patient assume a position in which they
feel comfortable.
Direct visualisation of the epiglottis should not
be performed.
Calm patient
Allow patient to assume
Loudness of stridor is not a good indicator of severity.[1] a position of comfort
ETI will be extremely difficult due to inflamation Consider aetiology
of the airway.
Mist, humidified, or cold air has not been demonstrated
to be an effective treatment for croup.[1]
All croup or epiglottitis patients should be transported
to hospital, irrespective of patients condition post
initial management. Nebulised adrenaline for croup is a Patient presentation Patient presentation
temporising measure only and clinicians must be aware consistent with croup? consistent with epiglottitis?
that symptoms may return.

Manage symptomatically Manage symptomatically

Consider: Do not visualise the airway
Adrenaline Neb Monitor for deterioration
Oxygen (allow adequate
expiratory time)
Monitor for deterioration

Transport to hospital
Pre-notify as appropriate

Croup or epiglottitis Page 2 of 2

Clinical practice guidelines Dyspnoea
Version 1.0 September 2011 Page 1 of 2

Dyspnoea is a subjective feeling, described as shortness of breath,

but it also implies a sense of discomfort, with breathing having
Risk assessment
become a conscious effort.[1] Acute coronary syndrome (ACS) can manifest as
There are four main causes of dyspnoea: dyspnoea and may be the only indication of an
AMI, therefore the need for a 12-Lead ECG should
airway obstruction be considered.[1]
respiratory failure
cardiovascular failure Oedematous upper airway obstructions of rapid
onset and any airway obstruction due to neck trauma
thoracic musculoskeletal compromise. have a high potential to evolve into complete airway
Whenever possible, determine and treat the cause of the dypnoea. obstruction.[2] Neck trauma can cause rapid oedema
and complete airway obstruction, therefore rapid
transport to definitive care is essential.
Clinical features Partial upper airway obstruction may progress to
complete obstruction. Limit interventions to only
General
those essential to maintain adequate oxygenation,
Abnormal respiratory rate or pattern calm the patient and transport rapidly to more
Difficulty in speaking or a change in tone skilled care; always prepare for the management
Diminished air entry or abnormal respiratory sounds of a complete obstruction.
Flaring nostrils, accessory muscle use, tracheal tug,
intercostal or supraclavicular recession
Restlessness or postural changes (tripoding)
Obstruction
Inspiratory stridor (FB or tissue oedema)
Snoring due to soft tissue collapse
Gurgling due to fluids in upper airway
Drooling, or a difficulty/inability to swallow
due to soft tissue oedema
Signs
Expiratory (or inspiratory) wheeze, crackles
Pursing of lips
Hyperinflated chest
Silent chest
 Standard Cares

Airway obstruction?

Treat cause
Foreign body?
Cardiovascular: Neurological:
Acute coronary Head injury
syndrome Spinal injury
Acute pulmonary CVA/TIA
oedema Seizure
Pulmonary embolism Pain
Manage as per CPG: Manage as per CPG: Shock & sepsis Hyperventilation
Airway obstruction Croup/epiglotitis Dysrrhythmias Metabolic acidosis
(foreign body) Anaphylaxis Specific toxidromes Toxidromes
or allergies Respiratory: Musculoskeletal:
Inhalation injury
Asthma Chest injuries
Anaphylaxis or Spinal injury
allergies Burns
COPD
Inhalation injury
Specific toxidromes
Transport to hospital
Pre-notify as appropriate

Dyspnoea Page 2 of 2
Clinical practice guidelines Hyperventilation
Version 1.0 September 2011 Page 1 of 2

Hyperventilation is an extreme form of tachypnea resulting in

significant hypocapnia and subsequent respiratory alkalosis.[1] Clinical features
In the absence of blood levels, if a patient has a rapid respiratory
Respiratory rate will depend on age and
rate it is essential to rule out potentially life-threatening
underlying comorbidities.
conditions, such as:
Hypocapnia as a result of hyperventilation
Lung pathology: may lead to paraesthesia (pins and needles)
-- pulmonary embolism around the mouth, hands and feet, restlessness,
-- pneumothorax dyspnoea, pain, vertigo, carpopedal spasm and
-- asthma eventually unconsciousness.[3]
-- pneumonia Rapid breathing due to hypoxaemia will usually
be reflected in low SpO2 readings, with the
Brain pathology:
notable exception of carbon monoxide poisoning.
-- hypoxia
-- brain stem injury
Systemic illness: Risk assessment
-- heat stroke
Hyperventilation due to emotional stress is rare
-- anaphylaxis
in children and so the focus should be on finding
-- toxidromes (e.g. tricyclics or aspirin) a physical cause for any rapid respiratory rate.[4]
-- metabolic acidosis (e.g. diabetic ketoacidosis)
The use of a paper bag to treat hyperventilation
-- sepsis has been discouraged for some time. This is due
Hyperventilation syndrome (rapid breathing caused solely by to the technique failing to reverse hypocapnia and
emotional disturbance) should always be considered a diagnosis actually causing mild hypoxia, which has had fatal
of exclusion.[2] consequences when cases of respiratory disease,
PE and AMI have been misdiagnosed.[5]
An often effective method of breathing control is
encouraging the patient to read a passage of text
out loud. This distraction technique also forces
the patient to modulate their breathing in order
to speak.
 Standard Cares

Is there any evidence of Manage as per CPG:

lung or brain pathology
or systemic illness? specific to pathology

Is a psychological Reconsider other causes

cause likely?

Calm patient and encourage Transport to hospital

a decreased respiratory rate Pre-notify as appropriate

Hyperventilation Page 2 of 2