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Acute respiratory failure 

Acute respiratory failure

Acute respiratory failure

Susannah Leaver

and Timothy Evans



Management—new protocol for management of patients with acute respiratory distress syndrome (according to Berlin definitions); discussion of new data relating to effects of PEEP and prone positioning on outcome.

Updated on 29 May 2014. The previous version of this content can be found here.
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date: 28 April 2017

Acute respiratory failure

Acute respiratory failure is defined clinically by hypoxaemia (PaO2 <8 kPa, normal range 10–13.3 kPa) with (type 2) or without (type 1) hypercapnia (PaCO2 >6.5 kPa). It is one of the most common problems afflicting the severely ill patient and often necessitates intensive care unit admission.

Clinical context—critical illness may be manifest solely as respiratory insufficiency, especially in patients with covert infection. Acute respiratory failure frequently coexists with other organ system failures in the critically ill, and delayed recognition of the condition has been shown to affect outcome adversely.

Clinical features—the signs of critical illness tend to be similar whatever the precipitating cause and are manifest in failure of the respiratory, cardiovascular, and neurological systems. The airway, breathing, circulation, disability, and exposure (ABCDE) approach to clinical assessment is advocated. Respiratory rate should normally be 12 to 20 breaths per minute: a higher or increasing rate is a ‘hard’ sign of critical illness. Full and repeated physical examination may be required to elucidate the cause of acute respiratory failure.

Investigation—pulse oximetry allows the continuous noninvasive monitoring of arterial oxygen saturation and is useful in all clinical settings. Arterial blood gas (ABG) analysis confirms the type and severity of acute respiratory failure. A full range of imaging modalities, particularly including computed tomography and echocardiography, may be required for diagnosis.

Management—the main steps in treating acute respiratory failure are: (1) Establishing and securing the airway (if compromised)—this may require (1) endotracheal intubation—evaluating the need for this is a task that should be undertaken only by those experienced in the technique (usually an anaesthetist); the decision to intubate is based on a number of factors including (a) inability to maintain an airway, (b) exhaustion, (c) deteriorating physiological parameters despite the provision of adequate therapy, (d) reversibility of underlying condition; (2) tracheostomy—this may be indicated (and beneficial) early in the course of acute respiratory failure in patients likely to require prolonged ventilatory support, but respiratory arrest consequent upon tracheostomy blockage with sputum or blood, although rare, is well documented and preventable. (2) Increasing FiO2 to treat hypoxaemia—oxygen can be administered by a variety of different methods depending on the required oxygen concentration. (3) Instituting mechanical ventilation (invasive or noninvasive) as necessary to treat impaired oxygenation and hypercapnia—noninvasive positive pressure ventilation involves the delivery of mechanically generated breaths via a tight-fitting nasal or full face mask. In patients receiving mechanical ventilation, the optimum mode depends in part upon the nature of the underlying illness, particularly the presence or absence of pulmonary parenchymal or airway pathology, the phase of the illness (acute or chronic), and the aims of support at the time it is applied. (4) Identifying and managing the precipitating condition. (5) Discontinuing and withdrawing support in stages (‘weaning’) as the underlying condition improves.

Acute respiratory distress syndrome (ARDS)

ARDS is characterized by intense inflammatory reactions in the alveolar space. There are three identifiable phases: (1) exudative, characterized by increased pulmonary capillary permeability; (2) inflammatory, in which alveolar neutrophilia predominates; (3) fibroproliferative or reparative, during which inflammation gradually resolves, giving way to increased collagen deposition. This condition complicates a wide variety of serious medical and surgical conditions, not all of which involve the lung directly.

Diagnosis—this requires: (1) An appropriate clinical setting, with one or more recognized risk factors. (2) New, bilateral, diffuse, patchy, or homogenous pulmonary infiltrates on chest radiography. (3) No clinical evidence of heart failure, fluid overload, or chronic lung disease. (4) PaO2:FiO2 ratio of less than 40 kPa (<300mmHg) for mild ARDS, <26.6 kPa (<200mmHg) for moderate ARDS and <13.3kPa (100mmHg) for severe ARDS.

Investigations—these are aimed at defining the extent of lung injury and elucidating the precipitating cause. Computed tomography (CT), if practical, may be useful in guiding therapy and detecting complications.

Management and prognosis—aside from other standard supportive measures, low tidal volume (‘protective’) ventilation has been shown to improve outcome. Overall mortality of patients with ARDS is in the range 25 to 40%, but higher in some subgroups (e.g. sepsis) than others (e.g. trauma). Survivors of ARDS may have persistent functional disability and require long-term follow-up and support.

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