Respiratory failure is one of the commonest reasons for which patients are admitted to the intensive care unit. It may be the primary reason for admission to intensive care (for example, in a patient suffering an exacerbation of chronic obstructive pulmonary disease or acute pneumonia). Alternatively, it may be a feature of a non-respiratory pathological process, for example severe sepsis from an intra-abdominal source, though it is often the respiratory failure rather than the intra-abdominal sepsis which triggers intensive care admission. Respiratory failure is conventionally classified either as ‘type 1’ or ‘type 2’ based on blood gas findings.

The interpretation of blood gases is fundamental to the management of patients requiring intensive care, not just those with respiratory failure. When drawing an arterial blood sample into a heparinized syringe, ensure that any liquid heparin is completely expelled from the syringe before use, as this will contaminate the sample and influence the results. Arterial blood is obtained either by direct puncture of an artery or from an indwelling arterial line. (See Practical procedures: Arterial cannulation, p. 372.)

Most ICUs now have a blood gas analyser for ‘point of care testing’ (POCT). These are expensive to maintain and repair. You will be unpopular if you damage it by, for example, blocking the sample channels with clotted blood. If you do not know how to use it, ask for help. Normal blood gas values are as shown in Table 5.1.

TABLE 5.1 ‘Normal’ blood gas values

Interpreting blood gas results will eventually become second nature. To begin with, it is helpful to follow a system, for example:

Look at the PaO₂. Is the patient hypoxaemic?

Note the inspired oxygen concentration (FiO₂). The higher the FiO₂ required to achieve any given PaO₂ the more significant the problem (see below).

Look at the PaCO₂. Is it low, normal or high?

Look at the pH. Is the patient acidotic (pH < 7.34) or alkalotic (pH > 7.45)?

If the patient has a disturbance of acid–base balance, then it is necessary to examine the blood gas further to determine the cause.

Look again at the PaCO₂. Is the PaCO₂ consistent with the change in pH, i.e. if the patient is acidotic, is the PaCO₂ raised? If the patient is alkalotic, is the PaCO₂ low? If so the primary abnormality is likely to be respiratory.

If the PaCO₂ is normal or does not explain the abnormality in pH, look at the base deficit / base excess.

The base deficit / base excess is a calculation of how much base (e.g. bicarbonate) would need to be added to or taken away (by titration) to normalize the pH of the sample. For example, in a metabolic acidosis, bicarbonate would need to be added to correct the pH because there is insufficient buffering capacity present, i.e. there is a base deficit. In metabolic alkalosis, bicarbonate would need to be taken away to correct the pH, because there is too much base (or insufficient hydrogen ions) present, i.e. there is a base excess.

If the base deficit / base excess is consistent with the abnormality in pH then the primary abnormality is metabolic.

If both the PaCO₂ and the base excess/base deficit are both altered in a way that is consistent with the abnormality in pH then a mixed picture is present.

If the PaCO₂ and base excess / deficit are both altered in such a way that one is consistent with the change in pH and the other is not, then it is likely that a compensated acidosis / alkalosis is present (see descriptions below).

This simple scheme for the interpretation of blood gases is practical and will suffice for most situations. More complex systems, such as that described by Stewart, which take account of other plasma constituents, are beyond the scope of this book, but for which good up-to-date reviews are readily available. If in doubt always seek senior help.

A number of patterns of disturbance of acid–base balance are recognized.

Respiratory failure occurs when pulmonary gas exchange becomes impaired such that normal arterial blood gas tensions are no longer maintained, and hypoxaemia is present with or without hypercapnia. Two patterns are described: types 1 and 2.

Common causes of respiratory failure are listed in Table 5.3.

TABLE 5.3 Common causes of respiratory failure

Blood gases are only one indicator of respiratory function. The primary assessment of a patient with respiratory failure is clinical:

Look at the patient.

Is the patient conscious? Is he or she able to talk and is lucid?

Is the patient using accessory muscles of respiration and making adequate respiratory effort, or exhausted with minimal respiratory effort? Is there an adequate cough?

If possible, take a history. If the patient is too short of breath to talk, the history may be obtained from the notes, staff or relatives. Try to obtain some idea of the patient’s normal respiratory reserve. How far can the patient walk? Are they oxygen dependent? Can they leave the house?

Examine the patient, particularly the cardiovascular and respiratory systems, bearing in mind the causes of respiratory failure. Note:

Pulse, BP, JVP, heart sounds, peripheral oedema. Is there any evidence of cardiac failure or of dehydration?

Increased or decreased respiratory rate, tracheal shift, percussion, bilateral air entry. Presence of crackles or wheeze. Is there any evidence of obstruction (stridor), collapse or consolidation, bronchospasm, pleural effusion?

If there is wheeze, peak flow measurement may help to document severity but is often unrecordable in the critically ill.

Look at the CXR, blood gases and other available investigations.

Management is based around correction of hypoxia, ventilatory support if required, and treatment of the underlying condition.

Hypoxaemia

Hypoxaemia is the primary concern and should be corrected:

If there is evidence of chronic CO₂ retention, (raised bicarbonate on blood gas) give controlled oxygen therapy 24–28%, via a Venturi system. While it may be appropriate to give higher oxygen concentrations this should only be done in a controlled environment where advanced respiratory support and close observation are available (see COPD, p. 152).

In all other cases, give high flow oxygen via a face mask, preferably via a humidified system. Higher inspired oxygen can be achieved with a reservoir mask (plastic bag attached to mask acts as an oxygen reservoir)

Consider facial CPAP or non-invasive ventilation (see Non-invasive ventilation, p. 122).

Hypercapnia

Exhausted patients with minimal respiratory effort will require immediate intubation and ventilation. In those patients that are not in extremis, non-invasive ventilation together with treatment of the underlying condition may lead to improvement (see Non-invasive ventilation, p. 122).

Oxygen, antibiotics, nebulizers, physiotherapy and non-invasive ventilation may prove highly effective. Continually reassess the response to treatment.

Treatment of the underlying condition

Bronchodilators. If there is wheeze, nebulized salbutamol may help. In more severe cases consider intravenous bronchodilators and steroids (see Asthma, p. 149).

Physiotherapy may help clear secretions and re-expand areas of collapse. If possible sit patients upright or in a chair.

Antibiotic therapy is best directed on the basis of Gram stains of sputum and on subsequent culture results. Seek microbiological advice. In the first instance broad-spectrum cover, e.g. with a cephalosporin is reasonable. A macrolide antibiotic such as clarithromycin should be added if there is a possibility of an atypical chest infection (see Pneumonia, p. 141).

Diuretics. If there is evidence of congestive cardiac failure and pulmonary oedema, then diuretics may help. Frusemide (furosemide) 40 mg or bumetanide 1–2 mg i.v.

Intravenous or nebulized steroids, nebulized adrenaline and helium oxygen mix may be of value in upper airway obstruction.

Continually reassess response to treatment. If there is no improvement or if the patient’s condition worsens, tracheal intubation and assisted ventilation may become necessary. Possible indications for intervention are shown in Box 5.1.

Box 5.1 Indications for ventilatory support in respiratory failure

Reduced conscious level

Exhaustion

Tachycardia / bradycardia

Hypotension

Increasing respiratory rate

Falling PaO₂ despite oxygen therapy

Rising PaCO₂ despite therapy

Worsening acidosis

Continuous positive airway pressure (CPAP) is a system for spontaneously breathing patients which is analogous to PEEP in ventilated patients (see p. 126). It may be provided either through a tight-fitting face mask or via connection to an endotracheal / tracheostomy tube. Newly developed full hood systems are useful for the claustrophobic / confused patient. A high gas flow (which must be greater than the patient’s peak inspiratory flow rate) is generated in the breathing system. A valve on the expiratory port ensures that pressure in the system, and the patient’s airways, never falls below the set level. This is usually +5 to +10 cm H₂O (Fig. 5.1).

Fig. 5.1 Typical CPAP system.

The application of CPAP has a number of effects:

Airways are splinted open, reducing alveolar collapse.

Alveolar recruitment leads to improved oxygenation.

Increased functional residual capacity (FRC) allows the lung to function on a more favourable part of the compliance curve and may therefore reduce the work of breathing.

CPAP is well tolerated by most patients even via a tight fitting face mask, although where it is required for a prolonged period there is a risk of skin necrosis over the bridge of the nose and this may be another indication for the use of a CPAP ‘hood’ rather than a face mask. Relative disadvantages of CPAP include noise, difficulties with humidification, distension of the stomach and increased risks of reflux and aspiration.

Over recent years, there has been increased use of non-invasive ventilation to manage acute respiratory failure. It may avoid the need for endotracheal intubation and conventional ventilation, so avoiding many of the associated complications. Patients with acute exacerbations of COPD have been demonstrated to have a better outcome where non-invasive positive pressure ventilation (NIPPV) has been used in place of conventional ventilation. Non-invasive ventilation techniques are also increasingly being used in the management of pulmonary oedema in congestive cardiac failure and to aid weaning from conventional ventilation (see COPD, p. 152, and Weaning from artificial ventilation, p. 135).

Most intensive care ventilators are now highly sophisticated, computer-controlled machines with complicated interfaces, a large number of different ventilatory modes, and inbuilt monitoring and alarm systems. Detailed descriptions and discussion are beyond the scope of this book.

One problem is that there is no uniformly agreed terminology in relation to ventilator modes and different manufacturers use different terms for similar functions. The following terms and modes are in common use but are by no means universal. Before using a ventilator you should familiarize yourself with it. If you have any difficulties seek advice.

Volume controlled ventilation

The simplest form of volume controlled ventilation is controlled mandatory ventilation (CMV) (Fig. 5.2).

Fig. 5.2 Controlled mandatory ventilation.

The patient is ventilated at a preset tidal volume and rate (for example, tidal volume 500 mL and rate 12 breaths/min). The tidal volume delivered is therefore predetermined and the peak pressure required to deliver this volume varies depending upon other ventilator settings and the patient’s pulmonary compliance. One disadvantage, therefore, of volume controlled modes of ventilation is that high peak airway pressures may result and this can lead to lung damage or barotrauma.

This is suitable for patients who are heavily sedated and/or paralysed and who are making no respiratory effort. It is not suitable for patients who are attempting spontaneous breaths. There is no pressure support for spontaneous breaths and ventilator valves may be closed during attempted inspiration or expiration. The ventilator may also deliver a breath immediately after the patient’s own inspiration, or as the patient tries to breathe out. This is uncomfortable and distressing, and may result in trauma to the lungs (see below).

Pressure controlled ventilation

To overcome some of the disadvantages of volume controlled ventilation, pressure controlled modes of ventilation are preferred in patients with poor pulmonary compliance. Instead of setting a predetermined tidal volume, a peak inspiratory pressure is set. The tidal volume delivered is a function of the peak pressure, the inspiratory time and the patient’s compliance. By using lower peak pressures and slightly longer inspiratory times the risks of barotrauma can be reduced. As the patient’s condition improves and lung compliance increases, the tidal volume achieved for the same settings will increase and the inspiratory pressure can therefore be reduced (see Acute lung injury p. 154).

It is important when using pressure controlled ventilation to understand the relationship between rate, inspiratory time and the I:E ratio (ratio of inspiratory time to expiratory time). Rate determines the total time period for each breath (60 s divided by rate = duration in seconds for each breath). The I:E ratio then determines how this time is apportioned between inspiration and expiration.

For example:

If respiratory rate is 10/min, total time for breath 60/10 s = 6 s.

If I:E ratio 1:2, then inspiratory time = 2 s and expiratory time = 4 s.

If the rate is reduced while the I:E ratio is fixed, inspiratory time becomes progressively longer, effectively holding the patient in sustained inspiration. To avoid this, the inspiratory time should be fixed whenever pressure controlled ventilation is used (e.g. 1.5–2 s), so that, as the respiratory rate is changed, it is only the length of expiration that alters.

Synchronized intermittent mandatory ventilation (SIMV)

Although historically a volume controlled mode of ventilation, the equivalent of SIMV is now available in both volume controlled and pressure controlled modes (Fig. 5.3). Immediately before each breath there is a small time window during which the ventilator can recognize a spontaneous breath and respond by delivering the set (SIMV) breath early.

Fig. 5.3 Synchronized intermittent mandatory ventilation.

SIMV modes improve patient synchrony with the ventilator and reduce the problems described with CMV above. SIMV modes are therefore potentially more comfortable for the patient.

Pressure support / assisted spontaneous breathing (ASB)

Breathing through a ventilator can be difficult because respiratory muscles may be weak and ventilator circuits and tracheal tubes provide significant resistance to breathing. These problems can be minimized by the provision of pressure support. The ventilator senses a spontaneous breath and augments it by addition of positive pressure. This reduces the patient’s work of breathing and helps to augment the tidal volume. Pressure support modes are available on all modern ventilators and can be used in conjunction with both volume and pressure controlled modes of ventilation.

Pressure support is usually set at 15–20 cm H₂O in the first instance and can be reduced as the patient’s condition improves. It is best not to remove pressure support completely, however, because of the resistance of the ventilator. (See Weaning from artificial ventilation, p. 135.)

Positive end expiratory pressure (PEEP)

Intubation, artificial ventilation and the effects of lung disease leads to a reduction in the functional residual capacity (FRC) of the lung. This results in the collapse of small airways, particularly in dependent lung zones, increasing ventilation–perfusion mismatch and worsening blood gases. To prevent this +5 to +10 cm H₂O of PEEP can be used to help maintain FRC and alveolar recruitment. Disadvantages of PEEP include reduced venous return to the heart and a subsequent reduction in CO and blood pressure. Unnecessarily high levels of PEEP are therefore best avoided.

Patients with severe expiratory airflow limitation, e.g. due to asthma or obstruction, may develop high levels of intrinsic PEEP, with the risk of progressive air trapping. Most modern ventilators include functions for displaying dynamic compliance curves and calculating intrinsic PEEP. If you are unsure how to use or interpret these functions, seek advice.

If a patient has high levels of intrinsic PEEP, evidence suggests that applying external PEEP up to, but not exceeding, the level of intrinsic PEEP, causes little cardiovascular compromise, does not increase air trapping and may improve gas exchange by facilitating recruitment in non-flow limited parts of the lung. Increasing external PEEP above the level of intrinsic PEEP may worsen hyperinflation and should be avoided. Seek advice.

PEEP is relatively contraindicated in asthmatics and in chronic emphysema. Although some patients benefit, there are also risks: seek senior help.

Triggering

Both SIMV and pressure support modes of ventilation require the ventilator to be able to detect the patient’s own respiratory effort in order to trigger the appropriate ventilator response. Historically triggering was achieved by detection of pressure changes in the circuit. There was no gas flow in the breathing circuit between ventilator delivered breaths and the patient’s inspiratory effort was detected as a drop in pressure in the breathing circuit. This was an inefficient method of triggering which was uncomfortable and exhausting for patients. Modern ventilators rely on flow triggering. There is a constant low level of gas flow in the circuit at all times. Flow sensors detect small changes in flow in the circuit in response to spontaneous respiratory effort by the patient, triggering the appropriate ventilator response. This is a more efficient and comfortable method of triggering.