ACUTE RESPIRATORY FAILURE 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)


An arterial carbon dioxide tension (PaCO2) of > 6.7 kPa usually accompanied by a fall in pH (<7.3,H+ > 45 nmols/l) 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

ARDS. bronchiolitis. variable blood pressure. The eyes are closed. the accessory muscles of ventilation are fully used. rib fractures). pneumothorax. pulmonary oedema. pneumonia Pulmonary embolus. Hypoxia and hypercarbia produce characteristic effects on the CNS and cardiovascular system (CVS).Raised pulse rate. opiates. often a characteristic position is adopted. peripheral vasodilation with pink peripheries. as in the child with acute epiglottitis. such as sitting forward with drooling secretions.g. traumatic and ischaemic lesions Loss of respiratory sensitivity to CO2 Spinal cord and peripheral nerves Neuromuscular junction Muscle Pleura and thoracic cage Spinal injury.Tremor and overt flap CVS . neuromuscular blocking drugs Myopathies.Uncooperative. the patient becoming anxious and completely preoccupied with the necessity to concentrate every effort on ventilation heralds the onset of ARF.Bradycardia. haemothorax Deformities. trauma (e. blood pressure changes are variable Diagnosis . Guillain Barre. ARDS ARDS refers to adult respiratory distress syndrome (see later) Clinical signs and symptoms Generally. TABLE 1 Causes of respiratory failure Site Respiratory centre (CNS) Examples Depressant drugs. loss of optimal shape due to chronic lung hyperinflation Airways Extrathoracic: foreign bodies. cyanosis 2 Hypercarbia: CNS . croup Intrathoracic: asthma. confused. poliomyelitis Myasthenia. drunken-like state CVS . for example: 1 Hypoxia: CNS .arterial blood gas analysis. bronchitis Gaseous exchange Lung vasculature Emphysema. respiratory muscle fatigue in COPD Flail chest.

then an ETT must be used both to ensure and to protect the airway (e. On clinical examination. as in drug overdose. removing viscid mucous and obtaining specimens for microscopy and culture . If ventilation is depressed or inadequate due to trauma or disease. e. The patient is placed on the side with the head down. e. due to overdose. pleural and thoracic cage causes. (4) Bronchoscopy may also be required for bronchial toilet. hypocarbia and an initial metabolic alkalosis followed by acidosis is a common accompaniment of ARDS. so this must be cleared. from aspiration of gastric contents). and a combination of hypoxia. expiratory wheeze suggests intrathoracic airway obstruction whilst inspiratory wheeze suggests that it is extrathoracic. post-operatively. clinical examination and special investigations such as chest X-ray.g. or where there is lack of expertise in endotracheal intubation. when the clinical signs are equivocal. than mechanical ventilation will be required. and lower jaw pulled forward to prevent the tongue falling back and obstructing the upper airway. Chest X-ray will reveal parenchymal causes such as pneumonia. Treatment Whatever the cause. airway obstruction due to foreign bodies (ipsilateral hyperinflation of lung). Cricothyrotomy or tracheostomy is then necessary to restore the airway. the history gives a clue to pre-existing disease such as chronic bronchitis and asthma. pneumothorax and fractured ribs. Raised bicarbonate levels in the blood gases suggest chronic pre-existing disease.g. For example. It is important to establish the causative site (Table 1). (3) Cricothyrotomy and tracheostomy obstruction above the cords due to disease or infection may make intubation impossible. four important principles of treatment apply: (a) Establish an airway This applies particularly to the unconscious patient. 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. or may distinguish between acute epiglottitis (sudden onset) and laryngo-tracheobronchitis (slower onset over 24 hours). general anaesthesia. CNS trauma and so on. if possible. peak expiratory flow rate and arterial blood gas analysis.g. At this stage it may become obvious that the obstruction is due primarily to foreign bodies or vomit. such as effusion.Diagnosis depends on history. Indications for artificial airways (1) Oropharyngeal: this is useful where it is expected that the patient will soon recover consciousness.

conventionally delineated into supra-and subglottic. NB Infection is a cause of exacerbation of ARF in bronchitics in less than 50% of cases. bronchodilators in asthma. If treatment of the underlying cause is not successful (i. except perhaps narcotic antagonists in opiate overdose. antibiotics. particularly in the bronchitic who is a CO2 retainer and dependent on hypoxic ventilatory drive. The most common causes are infectious and traumatic. Croup means literally 'noisy breathing' and is due to upper airway obstruction. mucolytics. nasal mask) as well as endotracheal intubation and IPPV may be needed. physiotherapy. anaesthetists in ICU are faced with a relatively small number of problems.(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. SPECIAL PROBLEMS ENCOUNTERED IN THE INTENSIVE CARE UNIT (ICU) Despite the fact that there are many causes of ARF. The diagnosis is made on the history and clinical findings. then the carbon dioxide tension will begin to rise. steroids.e. (a) The croup syndrome Upper airway obstruction in the small child represents one of the most life-threatening situations in clinical medicine. (c) Maintain alveolar ventilation and treat underlying cause These two are inextricably linked. necessitating intermittent positive pressure ventilation (IPPV). Other causes such as heart failure. and as the child (usually 3 to 7 years old) may completely obstruct at any time. muscle fatigue is a major contributory factor to continuing hypoxia and hypercarbia. 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. bronchodilators in acute or chronic bronchitis). (1) Infectious Supraglottic obstruction is usually due to epiglottitis. The causes of ARF are many and varied as are the requisite therapies. There is little place for respiratory stimulants. which occur frequently. In ARF due to chronic obstructive pulmonary disease (COPD).e. Hyperoxia should be avoided.g. he or she must be taken immediately to the operating theatre with an experienced anaesthetist and surgeon prepared for endotracheal intubation (ETI) or . 8-9 kPa or 60-70 mmHg). Non-invasive methods of ventilation (e. dysrthymias and pneumothorax must be excluded and treated where necessary.

external trauma or aspiration of noxious substances such as acid or alkali. operative removal with bronchoscopy. and in the case of foreign body. hypercarbic. In such cases it is paramount that the patient is assessed as to the suitability of this form of treatment. with lung function tests and blood gases . the clinical course is often more protracted and. Following intubation. 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. despite optimal therapy. acidotic and dehydrated. yet needs intubation and ventilation to restore reasonable blood gases. Treatment will depend on the cause. The history will usually confirm the diagnosis. (c) The chronic bronchitic patient requiring ventilation In a previous section it was mentioned that the chronic bronchitic who presents in ARF may proceed. This conundrum requires considerable compromise with ventilator settings and can often only be accommodated by accepting relatively high PaCO2 levels. ventilation is usually extremely difficult necessitating high inflation pressures which can only be lowered by prolonging inspiration. However. Subglottic obstruction is usually due to laryngotracheobronchitis. This involves a thorough history from the patient (or relatives) with particular regard to:  Previous hospital admissions. tachycardic. to the point where nasal mask and non invasive ventilation or endotracheal intubation and mechanical ventilation (IPPV) is required. ETI is needed for longer periods than with epiglottitis. once instituted. The patient is often exhausted. inhalation of a foreign body. and yet air trapping requires that expiration is also prolonged. the anaesthetist is faced with one of the most difficult management problems. Attempting to intubate the patient 'awake' may precipitate cardiovascular collapse. Intubation is required more rarely. (b) Acute (status) asthma By the time the patient with an acute asthmatic attack reaches the ICU. and less often in a hurry. lower temperature and fewer signs of respiratory obstruction. but usually requires intubation and steroid administration.tracheotomy. Following preferably nasotracheal intubation. hypoxic. (2) Trauma This may be due to instrumentation (eg post-extubation). with a much more slowly progressive course. the child is sedated and treated for Haemophilus influenzae infection with ampicillin and other appropriate antibiotics together with humidification of inspired gases. The incidence of both has decreased markedly in the last decade.

but vascular endothelial damage follows leading to ARDS 6. fat embolus syndrome 5. However. progressive lung damage can be anticipated so that further periods of IPPV may be unwarranted. Damage from any of the causes below results in loss of membrane integrity and thus increased permeability to fluid and protein. acid aspiration causes primarily alveolar epithelial damage. inhalation injury. ischaemia (following major trauma and hypotension). with a resulting increased work of breathing and dyspnoea. (d) Adult Respiratory Distress Syndrome (ARDS) In recent years. by demonstration of a normal or low pulmonary capillary wedge pressure. complement and neutrophil activation (as in sepsis. sampling of the arterial blood gases reveals profound hypoxaemia (PaO2 < 5 kPa or 35 mmHg) and secondary . producing an exudative 'non' cardiogenic pulmonary oedema'. noxious fumes The symptoms are those of severe ARF with dyspnoea being prominent. Generally speaking it is the vascular endothelium (either bronchial venular or capillary) which is affected. The 'clinical' condition of the patient may not immediately give cause for concern. e. disseminated intravascular coagulation (DIC) with vascular microthrombosis and ischaemia 4. e. in early 'fat embolism'. This together with the associated vascular damage results in an imbalance of ventilation and perfusion. This leaks into the interstitial space and lymphatics. or prolonged hypovolaemia) 3. 2. However. It is distinguished from 'cardiogenic pulmonary oedema'. A pronounced decrease in functional residual capacity (FRC) and compliance occurs. with a characteristic 'fluffy' appearance on chest X-ray. with hypoxia and increase in dead space. ARDS may result from: 1. but in cases where the patient has had frequent previous admissions with IPPV treatment. This is also applicable to cases where the patient is housebound and/or breathless at rest.g.  Previous requirements for IPPV or tracheostomy Exercise tolerance Only guidelines can be given. and from oedema due to a low colloid oncotic pressure by demonstration of a serum albumin of >30 g/l. 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.g. 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. A pronounced inflammatory and fibrotic stage may supervene and lead to permanent lung damage.

The profound hypoxia is often unresponsive to additional oxygen by mask. CO2 retention and metabolic acidosis develop. If left untreated.hyperventilation with a low PaCO2 (< 4 kPa or 30 mmHg). 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. .