ACUTE RESPIRATORY FAILURE

Definition - Pathophysiology - Clinical picture - Signs and Symptoms

- Diagnosis - Treatment - Croup - Asthma - COPD - ARDS

Definition

Acute respiratory failure (ARF) exists when the patient's breathing

apparatus fails in its ability to maintain arterial blood gases within the
normal range. By definition, ARF is present when the blood gases
demonstrate:

 An arterial oxygen tension (PaO2) of < 8 kPa (60 mmHg) with

normal or low PaCO2 (Type I or hypoxaemic respiratory
failure)

or

 An arterial carbon dioxide tension (PaCO2) of > 6.7 kPa

usually accompanied by a fall in pH (<7.3,H+ > 45 n mols l-1)
in addition to hypoxaemia (Type II or ventilatory respiratory
failure)

Hypoxaemia on its own does not always mean respiratory failure, for
example, if the subject is at altitude or has a right to left shunt due to
congenital heart disease.

We are concerned only with ARF, one of the most dramatic and life
threatening emergencies that the casualty officer and the house office
may have to deal with in the hospital setting.

Pathophysiology

Any part of the respiratory system may be involved in the causation of

a respiratory emergency, i.e.

 The respiratory centre in the CNS

 The respiratory apparatus (e.g. chest wall and lungs)
 The respiratory muscles including the diaphragm, the main
respiratory pump
 The gas exchanging units in the lung i.e. the respiratory
bronchioles and the alveoli

It is pertinent to remember that in assessing patient’s with ARF, most

attention is paid to what is happening at the alveolar level i.e. the
blood gases

Examples of conditions causing ARF are shown in Table 1

 

Clinical Picture

The clinical picture varies with the cause but any of those mentioned
in Table 1 leads to a deterioration in the patient's respiratory gas
exchange. The subsequent changes which occur in blood gases,
particularly carbon dioxide, cause stimulation of the medullary chemo-
receptor and compensatory mechanisms to be activated. The patient
becomes aware of the necessity to breathe, and as the precipitating
cause progresses, exhibits overt signs of distress, i.e. dyspnoea.
Eventually blood gases can no longer be kept in the normal range and
ARF supervenes.

ARF resulting from CNS depression as a result of drugs or injury does

not produce overt signs of respiratory distress. Accurate diagnosis is
dependent on a high index of suspicion and is confirmed by arterial
blood gas analysis.

TABLE 1 Causes of respiratory failure

Examples
Site
Respiratory centre Depressant drugs, opiates; traumatic and
(CNS) ischaemic lesions
Loss of respiratory sensitivity to CO2
Spinal cord and Spinal injury, Guillain Barre, poliomyelitis
peripheral nerves
Neuromuscular junction Myasthenia, neuromuscular blocking drugs
Muscle Myopathies, respiratory muscle fatigue in
COPD
Pleura and thoracic cage Flail chest, pneumothorax, haemothorax
Deformities, trauma (e.g. rib fractures),
loss of optimal shape due to chronic lung
hyperinflation
Airways Extrathoracic: foreign bodies, croup
Intrathoracic: asthma, bronchiolitis,
bronchitis
Gaseous exchange Emphysema, pulmonary oedema, ARDS,
pneumonia
Lung vasculature Pulmonary embolus, ARDS

ARDS refers to adult respiratory distress syndrome (see later)

 

Clinical signs and symptoms

Generally, the patient becoming anxious and completely preoccupied

with the necessity to concentrate every effort on ventilation heralds the
onset of ARF. The eyes are closed, the accessory muscles of
ventilation are fully used; often a characteristic position is adopted,
such as sitting forward with drooling secretions, as in the child with
acute epiglottitis. Hypoxia and hypercarbia produce characteristic
effects on the CNS and cardiovascular system (CVS), for example:

1 Hypoxia:

CNS - Uncooperative, confused, drunken-like state

CVS - Bradycardia, variable blood pressure, cyanosis

2 Hypercarbia:

CNS - Tremor and overt flap

CVS - Raised pulse rate, peripheral vasodilation with pink peripheries,

blood pressure changes are variable

Diagnosis

Diagnosis depends on history, clinical examination and special

investigations such as chest X-ray, peak expiratory flow rate and
arterial blood gas analysis. It is important to establish the causative site
(Table 1).

For example, the history gives a clue to pre-existing disease such as

chronic bronchitis and asthma, or may distinguish between acute
epiglottitis (sudden onset) and laryngo-tracheobronchitis (slower onset
over 24 hours), when the clinical signs are equivocal. On clinical
examination, expiratory wheeze suggests intrathoracic airway
obstruction whilst inspiratory wheeze suggests that it is extrathoracic.
Chest X-ray will reveal parenchymal causes such as pneumonia,
airway obstruction due to foreign bodies (ipsilateral hyperinflation of
lung), pleural and thoracic cage causes, such as effusion,
pneumothorax and fractured ribs. Raised bicarbonate levels in the
blood gases suggest chronic pre-existing disease, and a combination of
hypoxia, hypocarbia and an initial metabolic alkalosis followed by
acidosis is a common accompaniment of ARDS.
 

Treatment

Whatever the cause, four important principles of treatment apply:

(a) Establish an airway

This applies particularly to the unconscious patient, e.g. due to

overdose, general anaesthesia, CNS trauma and so on. The patient is
placed on the side with the head down, and lower jaw pulled forward
to prevent the tongue falling back and obstructing the upper airway. At
this stage it may become obvious that the obstruction is due primarily
to foreign bodies or vomit, so this must be cleared, if possible.

Indications for artificial airways

(1) Oropharyngeal: this is useful where it is expected that the patient

will soon recover consciousness, e.g. post-operatively, or where there
is lack of expertise in endotracheal intubation. A laryngeal mask may
be used as an alternative in this situation

(2) Endotracheal tube (ETt): If unconsciousness is expected to last

for more than a matter of minutes, as in drug overdose, then an ETT
must be used both to ensure and to protect the airway (e.g. from
aspiration of gastric contents). If ventilation is depressed or inadequate
due to trauma or disease, than mechanical ventilation will be required.

(3) Cricothyrotomy and tracheostomy obstruction above the cords due

to disease or infection may make intubation impossible.
Cricothyrotomy or tracheostomy is then necessary to restore the
airway.

(4) Bronchoscopy may also be required for bronchial toilet, removing

viscid mucous and obtaining specimens for microscopy and culture

(b) Administer oxygen to ensure adequate tissue oxygenation

(see this link)

It is of paramount importance to maintain a PaO2 sufficient to give an

arterial Hb saturation of at least 85% (i.e. 8-9 kPa or 60-70 mmHg).
Hyperoxia should be avoided, particularly in the bronchitic who is a
CO2 retainer and dependent on hypoxic ventilatory drive.

(c) Maintain alveolar ventilation and treat underlying cause

These two are inextricably linked. The causes of ARF are many and
varied as are the requisite therapies. If treatment of the underlying
cause is not successful (i.e. steroids, bronchodilators in asthma;
physiotherapy, antibiotics, mucolytics, bronchodilators in acute or
chronic bronchitis), then the carbon dioxide tension will begin to rise,
necessitating intermittent positive pressure ventilation (IPPV). There is
little place for respiratory stimulants, except perhaps narcotic
antagonists in opiate overdose. NB Infection is a cause of exacerbation
of ARF in bronchitics in less than 50% of cases. Other causes such as
heart failure, dysrthymias and pneumothorax must be excluded and
treated where necessary.

In ARF due to chronic obstructive pulmonary disease (COPD), muscle

fatigue is a major contributory factor to continuing hypoxia and
hypercarbia. Non-invasive methods of ventilation (e.g. nasal mask) as
well as endotracheal intubation and IPPV may be needed.

SPECIAL PROBLEMS ENCOUNTERED IN THE INTENSIVE

CARE UNIT (ICU)

Despite the fact that there are many causes of ARF, anaesthetists in
ICU are faced with a relatively small number of problems, which
occur frequently.

(a) The croup syndrome

Upper airway obstruction in the small child represents one of the most
life-threatening situations in clinical medicine. Croup means literally
'noisy breathing' and is due to upper airway obstruction,
conventionally delineated into supra-and subglottic. The most
common causes are infectious and traumatic.

(1) Infectious

Supraglottic obstruction is usually due to epiglottitis. The main

features of the disease are rapid onset of severe respiratory obstruction
and a high temperature with the patient adopting the classical sitting
position with drooling secretions.

The diagnosis is made on the history and clinical findings, and as the
child (usually 3 to 7 years old) may completely obstruct at any time,
he or she must be taken immediately to the operating theatre with an
experienced anaesthetist and surgeon prepared for endotracheal
intubation (ETI) or tracheotomy. This is usually performed under
general anaesthesia as attempted manipulations to visualise the
epiglottis in the awake patient often results in total obstruction and
death. Following preferably nasotracheal intubation, the child is
sedated and treated for Haemophilus influenzae infection with
ampicillin and other appropriate antibiotics together with
humidification of inspired gases.

Subglottic obstruction is usually due to laryngotracheobronchitis, with

a much more slowly progressive course, lower temperature and fewer
signs of respiratory obstruction. Intubation is required more rarely, and
less often in a hurry. However, the clinical course is often more
protracted and, once instituted, ETI is needed for longer periods than
with epiglottitis.

The incidence of both has decreased markedly in the last decade.

(2) Trauma

This may be due to instrumentation (eg post-extubation), inhalation of

a foreign body, external trauma or aspiration of noxious substances
such as acid or alkali. The history will usually confirm the diagnosis.
Treatment will depend on the cause, but usually requires intubation
and steroid administration, and in the case of foreign body, operative
removal with bronchoscopy.

(b) Acute (status) asthma

By the time the patient with an acute asthmatic attack reaches the ICU,
the anaesthetist is faced with one of the most difficult management
problems. The patient is often exhausted, tachycardic, hypoxic,
hypercarbic, acidotic and dehydrated, yet needs intubation and
ventilation to restore reasonable blood gases. Attempting to intubate
the patient 'awake' may precipitate cardiovascular collapse. Following
intubation, ventilation is usually extremely difficult necessitating high
inflation pressures which can only be lowered by prolonging
inspiration, and yet air trapping requires that expiration is also
prolonged. This conundrum requires considerable compromise with
ventilator settings and can often only be accommodated by accepting
relatively high PaCO2 levels.

(c) The chronic bronchitic patient requiring ventilation

In a previous section it was mentioned that the chronic bronchitic who

presents in ARF may proceed, despite optimal therapy, to the point
where nasal mask and non invasive ventilation or endotracheal
intubation and mechanical ventilation (IPPV) is required. In such cases
it is paramount that the patient is assessed as to the suitability of this
form of treatment. This involves a thorough history from the patient
(or relatives) with particular regard to:

 Previous hospital admissions, with lung function tests and

blood gases
 Previous requirements for IPPV or tracheostomy
 Exercise tolerance

Only guidelines can be given, but in cases where the patient has had
frequent previous admissions with IPPV treatment, progressive lung
damage can be anticipated so that further periods of IPPV may be
unwarranted. This is also applicable to cases where the patient is
housebound and/or breathless at rest. However, recent studies suggest
that the patient with ARF due to COPD has as good a chance of
weaning from mechanical ventilation s a patient who needs IPPV from
an acute attack of asthma.

(d) Adult Respiratory Distress Syndrome (ARDS)

In recent years, it has become evident that the lung can be injured
primarily (as in aspiration pneumonitis) as well as by a secondary
process in severe illness or trauma. Generally speaking it is the
vascular endothelium (either bronchial venular or capillary) which is
affected. Damage from any of the causes below results in loss of
membrane integrity and thus increased permeability to fluid and
protein. This leaks into the interstitial space and lymphatics, producing
an exudative 'non' cardiogenic pulmonary oedema', with a
characteristic 'fluffy' appearance on chest X-ray. It is distinguished
from 'cardiogenic pulmonary oedema', by demonstration of a normal
or low pulmonary capillary wedge pressure, and from oedema due to a
low colloid oncotic pressure by demonstration of a serum albumin of
>30 g l-1. A pronounced decrease in functional residual capacity
(FRC) and compliance occurs, with a resulting increased work of
breathing and dyspnoea. This together with the associated vascular
damage results in an imbalance of ventilation and perfusion, with
hypoxia and increase in dead space. A pronounced inflammatory and
fibrotic stage may supervene and lead to permanent lung damage.

ARDS may result from:

1. ischaemia (following major trauma and hypotension),

2. complement and neutrophil activation (as in sepsis, or prolonged

hypovolaemia)

3. disseminated intravascular coagulation (DIC) with vascular

microthrombosis and ischaemia

4. fat embolus syndrome

5. acid aspiration causes primarily alveolar epithelial damage, but

vascular endothelial damage follows leading to ARDS

6. inhalation injury, e.g. noxious fumes

The symptoms are those of severe ARF with dyspnoea being

prominent. The 'clinical' condition of the patient may not immediately
give cause for concern, e.g. in early 'fat embolism'. However, sampling
of the arterial blood gases reveals profound hypoxaemia (PaO2 < 5
kPa or 35 mmHg) and secondary hyperventilation with a low PaCO2
(< 4 kPa or 30 mmHg). If left untreated, CO2 retention and metabolic
acidosis develop. The profound hypoxia is often unresponsive to
additional oxygen by mask, in which case ETI with IPPV and positive
end expiratory pressure (PEEP) is required. The latter works by
increasing FRC by backward distending pressure thus reducing V/Q
mis-match and improving compliance at the same time.

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