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

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

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.