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Respiratory support 

Respiratory support
Respiratory support

Heather Baid

, Fiona Creed

, and Jessica Hargreaves

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date: 08 May 2021

Respiratory physiology

Lung volumes

  • Tidal volume (V T)—volume of gas that moves in and out of the lungs in one breath. Normal range is 5–9 mL/kg.

  • Minute volume (MV)—volume of gas that moves in and out of the lungs in 1 minute. Normal range is VT × respiratory rate = 5–9 mL/kg × 12 = 5–6 L.

  • Vital capacity (VC)—volume of gas exhaled after maximum inspiration. Normal range is 3–4.8 L.

  • Functional residual capacity (FRC)—volume of gas remaining in the lungs after normal exhalation. Normal range is 1.8–2.4 L.

  • Anatomical dead space—volume of gas that fills the conducting airways (from nose to lower airways, but not including the bronchioles), which is not available for gas exchange. Alveoli that are ventilated but not perfused can also be included as dead space. Normal value is 2 mL/kg.

Gas exchange in the lungs

An area of approximately 70m2 is provided for gas exchange in the adult lung.

Diffusion of gases across the alveolar–capillary membrane is dependent on the difference in the concentration of the gas (i.e. its partial pressure) in the alveolus and in the capillary. Movement of the gases is explained by Dalton’s law.

Dalton’s law

The pressure exerted by a mixture of gases in a space is equal to the sum of the pressure that each gas exerts if occupying the space alone.

Air is a mixture of predominantly three gases—79% nitrogen, 21% oxygen, and 0.03% carbon dioxide. Air at atmospheric pressure = 101 kPa. Therefore each gas exerts a proportional (i.e. partial) pressure:

79  kPa  N  +  21  kPa  O2  +  0.03  kPa  CO2  =  101  kPa.

Boyle’s law

For a fixed amount of gas kept at a fixed temperature, the pressure and volume are inversely proportional—that is, if the volume of a gas increases, the pressure that it exerts decreases, or if the volume of a gas decreases, the pressure that it exerts increases.

Partial pressure of alveolar oxygen (PAO2)

This is the oxygen level in the alveoli calculated using the alveolar gas equation. The normal range is 2.6–5.3 kPa.


where RQ is the respiratory quotient, estimated to be 0.8.

The partial pressure of alveolar oxygen is less than that of arterial oxygen because the partial pressure of oxygen is reduced by the addition of water vapour from the humidification of the air in the upper airways and the ongoing exchange of oxygen and carbon dioxide in the pulmonary capillaries and the alveoli.

A–a gradient

This is the alveolar (A)–arterial (a) oxygen gradient. The normal range is 2–3.3 kPa (the value increases with age).

Aa gradient=FiO2×94.8PaCO2/RQPaO2

PaO2/FiO2 ratio

This is the ratio of deoxygenated blood to oxygenated blood. The normal range is > 40 kPa (a ratio of < 26 kPa reflects intra-pulmonary shunting).

FiO2 is a fraction, not a percentage (i.e. 50% oxygen = 0.50 FiO2).

Work of breathing

This is the effort involved in moving air in and out of the lungs. Accessory muscles are used to assist breathing during exercise or when the work of breathing is increased.

It is affected by:

  • elasticity of the lung tissue

  • chest wall compliance

  • resistance to gas flow in the airways

  • obstruction to gas flow in the airways.

Elasticity of lung tissue

This is dependent on two factors:

  • Alveolar surface tension—surfactant is secreted to reduce surface tension and reduce resistance to expansion. Surfactant secretion can be impaired by acidosis, hypoxia, hyperoxia, atelectasis, pulmonary oedema, and acute respiratory distress syndrome (ARDS).

  • Elastic fibres of the lung—these contract and help to force air out of the lung.

Chest wall compliance

This is the change in volume of the lung divided by the amount of pressure required to produce the volume change.

Large volume changes produced by small pressure changes indicate a compliant lung. Table 5.1 lists the factors that affect lung compliance.

Table 5.1 Factors that affect lung compliance

Factors that decrease lung compliance

Factors that increase lung compliance

Pulmonary congestion

Pulmonary oligaemia (decreased blood volume)

Increased pulmonary smooth muscle tone

Decreased pulmonary smooth muscle tone

Increased alveolar surface tension

Augmented surfactant secretion

Pulmonary fibrosis, infiltration, or atelectasis

Destruction of lung tissue (e.g. emphysema)

Lung compliance has two components—static and dynamic compliance.

Static compliance

This is the compliance of the lung excluding resistance to gas flow. It is measured at the end of a known volume inspiration with the airway occluded for 2 s to achieve a plateau pressure.

Dynamic compliance

This is the compliance of the lung including resistance to gas flow. It refers to the change in pressure from end inspiration to end expiration.

In healthy lungs there is little difference between static and dynamic compliance. In patients with airway obstruction, dynamic compliance will decrease rapidly due to resistance to gas flow, without a significant change in static compliance.

Ventilation/perfusion match

Efficient gas exchange within the lung depends on the relationship between alveolar ventilation (V) and pulmonary capillary perfusion (Q).

  • When V/Q = 1, there is good ventilation and good perfusion.

  • When V/Q is > 1, there is good ventilation but poor perfusion (increased dead space).

  • When V/Q is < 1, there is poor ventilation but good perfusion (increased venous admixture or shunt).

In the normal lung there is a certain degree of variation in ventilation and perfusion, with up to 15% mismatch. The pathological causes of V/Q mismatch are summarized in Table 5.2.

Table 5.2 Causes of V/Q mismatch

V/Q > 1 (dead space)

V/Q < 1 (shunt)

Pulmonary embolus


Decreased cardiac output


Extrinsic pressure on pulmonary arteries (tumour, pneumothorax) Pulmonary oedema

Obstructive lung disease (emphysema, bronchitis, asthma)

Destruction of pulmonary vessels

Restrictive lung disease (ARDS, pulmonary and alveolar fibrosis, pneumonia)

Decreased cardiac output

Obstruction of the pulmonary microcirculation (ARDS)

The body has two homeostatic responses to allow it to adjust to variations in ventilation and perfusion:

Hypoxic pulmonary vasoconstriction

Capillaries in areas with low alveolar PO2 will vasoconstrict to reduce perfusion to the affected areas.

Hypocapnic bronchoconstriction

Bronchioles in areas with low capillary PCO2 will constrict to reduce ventilation to the affected areas.

Respiratory failure

The majority of patients who require ventilator support will have some degree of respiratory failure.

Type I respiratory failure

The patient is hypoxaemic, but has normal levels of carbon dioxide—that is, PO2 is < 11 kPa on FiO2 0.4, with PCO2 in the range 4.5–6.0 kPa.

Type II respiratory failure

The patient is both hypoxaemic and hypercapnic—that is, PO2 is < 11 kPa on FiO2 0.4, or < 8.0 kPa on air, with PCO2 > 6.5 kPa without a primary metabolic acidosis.

Patient indicators of respiratory failure

  • Respiratory rate > 25 breaths/min or < 8 breaths/min.

  • Deteriorating vital capacity.

Oxygen therapy

Oxygen is transported dissolved in plasma (3%) and bound to haemoglobin in the red blood cells (97%). The affinity of haemoglobin for oxygen is governed by the partial pressure of oxygen. At higher partial pressures (i.e. at the lungs) more oxygen binds to haemoglobin and it is 98–100% saturated. At lower partial pressures (i.e. at the tissues) only 75% of the haemoglobin remains saturated, to allow utilization of oxygen by the cells. In extreme circumstances more oxygen can be unbound, reducing saturation even further, to 20–30%.

When the partial pressure of oxygen is plotted against the haemoglobin saturation, an ‘S’-shaped curve is produced. This is known as the oxyhaemoglobin dissociation curve (see Figure 5.1).

Figure 5.1 The oxyhaemoglobin dissociation curve.

Figure 5.1 The oxyhaemoglobin dissociation curve.

(Reproduced with permission from James Munis, Just Enough Physiology (Oxford University Press, 2011) © Mayo Foundation for Medical Education and Research.)

Specific factors affect oxyhaemoglobin dissociation by shifting the position of the curve to the right or left, making more or less oxygen dissociate from haemoglobin (see Box 5.1).

2,3-DPG is 2,3-diphosphoglycerate, a chemical compound produced in the cell during anaerobic respiration (glycolysis).

Carbon dioxide is transported dissolved in plasma (7%), bound to haemoglobin in the red blood cells (23%), or converted to bicarbonate in the red blood cells (70%).

In the presence of deoxygenated blood more carbon dioxide will bind to the red blood cells.

Indications for administration of oxygen

  • Respiratory distress (respiratory rate > 25 or < 8 breaths/min).

  • Hypoxaemia (PO2 < 8 kPa on air).

  • Acute events, including:

    • acute coronary syndrome

    • major haemorrhage

    • pulmonary oedema

    • pulmonary embolus

    • seizures

    • low cardiac output

    • metabolic acidosis.

Oxygen is a drug, and should only be administered without a prescription in an emergency (see Table 5.3).

Table 5.3 Modes of oxygen delivery

Delivery mode


Associated problems

Safety priorities


Nasal cannulae

  • 2 L/min

  • 23–28%

  • 3 L/min

  • 28–30%

  • 4 L/min

  • 32–36%

  • Limited O2 (%)

  • Inaccurate O2 delivery with high minute volumes

  • Requires patent nasal passages

  • Avoid if patient is a mouth breather

  • Drying and discomfort of nasal passages

  • Regular monitoring of respiratory rate and pattern

  • Pulse oximetry

  • Check O2 flow rate

  • Position cannulae inside nares

  • Low-level O2 supplementation

  • Short to long term

  • Disposable delivery system

Variable- performance face mask

  • 5 L/min ~35%

  • 6 L/min ~50%

  • 8 L/min ~55%

  • 10 L/min ~60%

  • 15 L/min ~80%

  • Inaccurate O2 delivery with high minute volumes

  • Limits patient activities (e.g. eating and drinking)

  • Drying and discomfort of upper respiratory tract

  • Rebreathing

  • Regular monitoring of respiratory rate and pattern

  • Pulse oximetry

  • Check O2 flow rate

  • Check mask position

  • Low- to medium-level O2 supplementation

  • Short to medium term

  • Disposable delivery system

Fixed- performance face mask (Venturi)

  • 2 L/min 24%

  • 4 L/min 28%

  • 8 L/min 35%

  • 10 L/min 40

  • 15 L/min 60%

  • O2 percentage may still not be achieved with high flow

  • Limits patient activities (e.g. eating and drinking)

  • Drying and discomfort of upper respiratory tract

  • Regular monitoring of respiratory rate and pattern

  • Pulse oximetry

  • Check O2 flow rate

  • Check mask position

  • Medium- to high-level O2 supplementation

  • Short to medium term

  • Disposable delivery system

Humidified oxygen using nebulizer system

Varying rates of flow to deliver 28–60% O2

  • Inaccurate O2 delivery with high minute volumes

  • Limits patient activities (e.g. eating and drinking)

  • Regular monitoring of respiratory rate and pattern

  • Pulse oximetry

  • Check O2 flow rate, including on nebulizer circuit

  • Check mask position

  • Low- to medium-level O2 supplementation

  • Medium to long term

  • Disposable delivery system

Non- rebreathing mask with reservoir bag

80–85%, depending on respiratory rate and flow rate 15 L/min O2

Reservoir bag should be partially inflated at all times

Ensure that reservoir bag is fully inflated before placing on patient

Emergency situations and short-term use only

Target oxygen saturation should be > 92%.

Risks of oxygen therapy

A small proportion (approximately 12%) of patients with acute or chronic pulmonary disease, in type II respiratory failure, are dependent on the hypoxic drive. They may require lower target oxygen saturation in order to maintain adequate respiration. These patients should be closely monitored during oxygen delivery for signs of increasing drowsiness and decreased respiratory effort (respiratory rate < 10 breaths/min and shallow depth).

Oxygen is a dry gas, so will adversely affect cilia function and sputum clearance. This risk increases with duration of use and high flow rates. In any patient who requires oxygen for more than 24 h, humidification is required.

Use of high percentage oxygen (> 80%) is associated with nitrogen washout and alveolar collapse, as diffusion of most of the gas through to the capillary can occur and little nitrogen is left to maintain intra-alveolar pressure. When it is appropriate to do so, oxygen delivery should be at the lowest level possible to maintain normal PO2.

Further reading

British Thoracic Society (BTS). Emergency Oxygen Use in Adults. BTS: London, 2008.Find this resource:

Non-invasive ventilation (NIV)

Non-invasive ventilation (NIV) allows support of respiratory function without the requirement for intubation. Therefore the patient must be spontaneously breathing and have a level of consciousness to comply with the treatment. NIV can be delivered via a tight-fitting face mask, a nasal cannula, or a helmet. This is to ensure that there is no gas leak in order to maintain the positive pressure. There are two forms of NIV:

  • continuous positive airway pressure (CPAP)

  • bi-level positive airway pressure (BPAP).

Continuous positive airway pressure (CPAP)

CPAP maintains a positive pressure throughout inspiration and expiration; this is equivalent to positive end expiratory pressure (PEEP). The pressure level is set and adjusted according to patient response. It is used to increase or maintain functional residual capacity (FRC) (see Respiratory support p. [link]). An increased FRC is associated with reduced work of breathing, improved oxygenation, and improved lung compliance.

Bi-level positive airway pressure (BPAP)

BPAP cycles between two positive pressure settings—inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP). The pressure levels are set and adjusted according to patient response. Respiratory rate is usually determined by the patient’s spontaneous rate, but may be time cycled (i.e. the machine will cycle between IPAP and EPAP at set intervals). It is used to augment tidal volume (VT) (see Respiratory support p. [link]). An increased VT is associated with a reduction in PaCO2, reduced work of breathing, and improved oxygenation.


  • Acute exacerbation of COPD.

  • Acute pulmonary oedema.

  • Specific groups of patients with acute respiratory failure in whom intubation is associated with poor outcomes (e.g. immunocompromised patients, and those with neuromuscular disease or end-stage COPD).

  • Facilitation of weaning.

  • Post-operative respiratory failure.

  • Obstructive sleep apnoea.


  • Inability to protect the airway and/or high risk of aspiration.

  • Facial surgery or trauma.

  • Poor patient tolerance or compliance.

  • Claustrophobia.

Before starting NIV, establish a clear management plan and document the settings. Agreement on the escalation and/or discontinuation of treatment should be reached with the patient. A successful outcome should be evident within 4 h, and evidence shows that it is dependent on nursing care. NIV is supportive, and therefore the cause of the respiratory difficulty should be managed and treated. Often the key to successful NIV is developing the patient’s trust and confidence. It is worth spending time explaining, reassuring, and trialling different set-ups so that the patient will tolerate the equipment, overcome their initial anxiety, and allow continuation of NIV. Nurse the patient in a highly visible area and ensure that the call bell is within easy reach of the patient. The use of NIV is highly dependent on patient monitoring and nursing support. In addition, effective NIV is improved by correct positioning of the patient to optimize respiratory expansion. Table 5.4 provides further information on nursing care.

Table 5.4 Nursing support for patients with NIV

Setting up

Provide patient explanation

Set up machine and/or attach correct PEEP valve for agreed level of support (usually 5–10 cmH2O)

Choose the correct size of mask (use sizing guide)

Connect the mask to the machine

Allow the patient to try the mask without fixing the straps. Once the patient is confident, attach the straps and continue to offer support and reassurance until the patient can tolerate the secured mask


  • Gas flow, PEEP valve, and O2 levels

  • Ongoing respiratory assessment—ABG, saturations, and respiratory rate

  • Vital signs—haemodynamic changes due to reduced venous return resulting from raised intra-thoracic pressure may decrease blood pressure and cardiac filling pressures

Patient problems

Pressure damage:

  • Check fitting of mask and straps

  • Protect bridge of nose, ears, and chin with hydrocolloid dressing

Drying of eyes:

  • Check mask fitting for leaks

Gastric distension:

  • Insert nasogastric tube on free drainage

Difficulty eating or drinking:

  • Support fluid and nutrition delivery by alternative routes

Feelings of claustrophobia:

  • Offer a supportive presence

  • Allow the patient opportunities to remove the mask

  • Consider use of earplugs to reduce the noise of high-flow gas

Further reading

Esquinas Rodriguez AM et al. Clinical review: helmet and non-invasive mechanical ventilation in critically ill patients. Critical Care 2013; 17: 223–35.Find this resource:

Nava S and Hill N. Noninvasive ventilation in acute respiratory failure. Lancet 2009; 374: 250–59.Find this resource:

Intubation and extubation

A secure airway is the primary goal of airway management. There are a number of different airway adjuncts that can be used for this purpose, including a nasal or oral endotracheal tube or a tracheostomy tube. The tubes are most often made of polyvinyl chloride with an inflatable cuff to seal the trachea to prevent air leakage and aspiration of oropharyngeal and gastric secretions. The cuff pressure should be in the range 20–30 cmH2O in order to maintain a seal and reduce the risk of capillary occlusion in the mucosa of the trachea, which could lead to tracheal erosion. Endotracheal tubes may also have a subglottic port for suctioning above the cuff to remove secretions (see Figure 5.2), and to aid extubation. An ‘armoured’ tube will be wire-reinforced and can be used for long-term intubation or for patients with compressible tracheas (e.g. flexed neck position in surgery). Tracheostomy tubes can have a single or double lumen with a replaceable inner tube to maintain tube patency, and can be fenestrated to allow the patient to vocalize and communicate. The tube must be secured in order to avoid unintended extubation.

Figure 5.2 Endotracheal tube with subglottic port.

Figure 5.2 Endotracheal tube with subglottic port.

(Reproduced with permission from Eelco Wijdicks, The Practice of Emergency and Critical Care Neurology (Oxford University Press, 2010). © Mayo Foundation for Medical Education and Research.)

Process of endotracheal intubation

Intubation requires the following equipment:

  • laryngoscope

  • stylet (guidewire)

  • Magill’s forceps

  • endotracheal tube (internal diameter, range 6.0–10.5 mm), cut to length and lubricated (if indicated)

  • 10-mL syringe

  • suctioning equipment

  • oxygen and bag-valve mask

  • tapes to secure tube

  • scissors

  • stethoscope

  • intravenous cannula

  • capnography

  • monitoring equipment (e.g. heart rate, saturations, blood pressure)

  • nasogastric tube (this can be inserted at the same time, or if already present can be aspirated to empty the stomach contents; ensure that feed is stopped)

  • catheter mount, ventilation tubing, and mechanical ventilator.

The patient should be prepared for the procedure by informing them of what will be happening, positioned supine with their neck slightly flexed and their head extended ‘sniffing the air’, and then pre-oxygenated for 3 min. Intubation should take no longer than 30 s (i.e. from loss of airway protection to secured airway and ventilation).

Rapid sequence induction (RSI) is indicated in patients who are at risk of aspiration of gastric contents into the lungs (e.g. in emergencies when the patient will not have been starved in advance of anaesthesia). Cricoid pressure is applied, to prevent gastric reflux, by compressing the cricoid cartilage against the cervical vertebrae. Once applied it should only be removed once, when indicated by the person intubating (i.e. once the trachea is intubated, the cuff is inflated, and both of the lungs are ventilating) (see Figure 5.3).

The nurse’s role is to inform the person intubating of the vital signs and observe for complications. Once the tube is inserted, the cuff should be inflated and the patient’s chest observed and auscultated for bilateral expansion. The tube must then be secured and the patient attached to the ventilator and a check X-ray performed. Arterial blood gas sampling should also be performed to confirm the initial ventilation settings and inform any changes that are required.

Drugs used during intubation

Safe intubation of a patient outside of a cardiac arrest situation will require the administration of drugs to enable insertion of the tube. The drugs used are subdivided into sedatives, neuromuscular blocking agents (NMBAs), and sympathomimetics (pp. [link] and [link]):

  • sedatives (e.g. propofol, etomidate, midazolam, ketamine)

  • NMBAs (e.g. suxamethonium, which is a depolarizing muscle relaxant, or atracurium, pancuronium, and vecuronium, which are non-depolarizing muscle relaxants)

  • sympathomimetics (e.g. metaraminol, ephedrine, adrenaline).

Process of endotracheal extubation

Extubation requires the following equipment and two individuals:

  • 10-mL syringe

  • suctioning equipment

  • oxygen and oxygen mask/non-invasive ventilation

  • scissors

  • stethoscope

  • monitoring equipment (e.g. heart rate, saturations, blood pressure)

  • emergency reintubation equipment.

The decision to extubate the patient should be multidisciplinary and follow a period of weaning from mechanical ventilatory support. For further details on weaning, see Respiratory support p. [link]. The reason for the intubation must be resolved and the patient must be able to maintain adequate gas exchange.

Reassess the patient’s spontaneous respiratory rate, tidal volume, oxygen saturations, and arterial blood gas. Ensure that they are able to cough and clear secretions, that they have cardiovascular stability, and that they are able to obey commands. Aspirate the nasogastric tube.

The patient should be prepared for the procedure by informing them of what will be happening. Then position the patient upright in a seated position in the bed, suction the oropharynx and down the tube, and then cut the tapes. Simultaneously applying suctioning, deflate the cuff and withdraw the tube in a single rapid movement. Encourage the patient to cough, and suction secretions in the oropharynx. Apply the face mask to the patient and provide reassurance. Once the tube has been removed continue to monitor the patient for signs of respiratory distress.

Factors that can result in failed extubation

  • Obstruction of airway.

  • Inability to clear secretions, or the presence of copious secretions.

  • Aspiration of gastric contents.

  • Fatigue or poor respiratory effort.

  • Poor gas exchange.

The process of tracheostomy placement

A tracheostomy can be sited surgically or percutaneously. The percutaneous method is generally used for intubated patients in the critical care setting (i.e. as a bedside intervention).

The following equipment is required for percutaneous insertion:

  • sterile field and cleaning fluid

  • lubricant

  • local anaesthetic

  • bronchoscope with catheter mount

  • percutaneous tracheostomy kit (with tracheostomy, dilators and 10-mL syringe)

  • suctioning equipment

  • oxygen and bag-valve mask

  • tapes to secure the tube

  • stethoscope

  • intravenous cannula

  • monitoring equipment (e.g. heart rate, saturations, blood pressure)

  • catheter mount, ventilation tubing, and mechanical ventilator.

The procedure is ideally performed under bronchoscopy guidance.

Local anaesthetic is infiltrated subcutaneously and a 1 cm incision is made in the skin midline above the trachea. The introducer needle and syringe are advanced at 45° until air is aspirated from the trachea. The guidewire is passed through the needle, and dilators of increasing diameter are used to extend the hole for insertion of the tracheostomy tube.

The nurse’s role is to inform the person performing the tracheostomy of the vital signs and observe for complications. Once the tube has been inserted, the cuff should be inflated and the patient’s chest observed and auscultated for bilateral expansion. The endotracheal tube can be removed. The tube must then be secured and the patient attached to the ventilator, and a check X-ray may be performed. Arterial blood gas sampling is also necessary, to confirm the initial ventilation settings and inform any changes that may be required.

Process of tracheostomy decannulation

The following equipment is required for decannulation:

  • suctioning equipment

  • gauze

  • clear semi-permeable dressing

  • stethoscope

  • monitoring equipment (e.g. heart rate, saturations, blood pressure)

  • emergency reintubation equipment.

The decision to decannulate the patient should be multidisciplinary and follow a period of weaning from mechanical ventilatory support (for further details about weaning, see Respiratory support p. [link]). The reason for the tracheostomy insertion must be resolved, and the patient must be able to maintain adequate gas exchange.

Reassess the patient’s spontaneous respiratory rate, tidal volume, oxygen saturations, and arterial blood gas. Ensure that they are able to cough and clear secretions, that they have cardiovascular stability, and that they are able to obey commands. Aspirate the nasogastric tube.

The patient should be prepared for the procedure by informing them of what will be happening. Position the patient upright in a seated position in the bed. Generally the patient will have had the cuff deflated for a period of time before the decannulation. Suction the oropharynx and down the tube, and then loosen the tapes. Withdraw the tube in a single rapid movement. Encourage the patient to cough, and suction secretions in the oropharynx. Apply the gauze dressing over the stoma and provide reassurance. Once the tube has been removed, continue to monitor the patient for signs of respiratory distress. Advise the patient to support the stoma when speaking or coughing. Inspect the stoma site daily. Once skin closure has occurred the site can remain exposed for ongoing healing.

Factors that can result in failed decannulation

  • Obstruction of the airway.

  • Inability to clear secretions, or the presence of copious secretions.

  • Aspiration of gastric contents.

  • Fatigue or poor respiratory effort.

  • Poor gas exchange.

Management of the patient with an endotracheal tube or tracheostomy

The nurse is responsible for the ongoing management of patients with an endotracheal tube or a tracheostomy. Considerations with regard to the care of the patient include infection prevention and control, suctioning, humidification, analgesia and/or sedation, and communication.

Checks to be completed at the start of a shift

  • Tube patency.

  • Tube position—lip level.

  • Cuff pressure (20–30 cmH2O).

  • Tube security (change the tapes only if they are soiled or loose, observe for ulceration, and ensure that venous drainage is unimpeded).

  • Emergency ventilation equipment (bag-valve-mask, suction equipment and catheters, oxygen).

  • Tracheostomy emergency equipment (one tube of the same size and one tube of a smaller size, obturator, disposable inner cannulas, 10-mL syringe, tracheostomy ties, tracheostomy dressing, dilator forceps, disconnection wedge).

Checks to be completed routinely during a shift

  • Inner cannula patency (inspect and replace).

Infection prevention and control

The intubated patient is at high risk of infection, particularly ventilator-associated pneumonia (see Respiratory support p. [link]). Measures to minimize contamination, colonization, and infection must be adhered to at all times and with each patient (e.g. hand hygiene, patient hygiene, single-use or sterilized equipment and fluid, patient screening, and environmental cleaning). Tubes should remain in situ for as long as indicated in the manufacturer’s guidance (which ranges from 7 days up to 60 days).

The tracheostomy stoma should be assessed 4- to 8-hourly and the stoma cleaned and dressed as required.


  • Use closed suction to minimize cross-contamination.

  • Suction catheter size—multiply inner diameter by 3, and divide by 2.

  • Suction catheter length—caution is needed when suctioning via tracheostomy.

  • Suction only as needed—presence of secretions, flow loop changes, hypoxaemia.

  • Consider pre-oxygenation prior to suctioning.

  • Limit suction pressure to < 120 mmHg.

  • Ensure that non-fenestrated inner tube is in situ in tracheostomy.

  • Apply suction for a maximum of 10 s with each pass of the catheter.

  • Undertake a maximum of three passes in a single episode.

  • Note the colour, consistency, and quantity of the secretions.

Hypoxaemia may result from suctioning due to entrainment of alveolar air rather than air around the catheter. This can be minimized by using the correct catheter diameter, pre-oxygenation, minimal negative pressure, minimal time suctioning, and minimal number of catheter passes.

Mucosal irritation can be minimized by minimal negative pressure, rotation of the catheter, and withdrawal of the catheter from the carina before applying negative pressure.


All patients with an artificial airway should receive continuous humidification. As the upper airway is bypassed during mechanical ventilation, humidification is necessary in order to avoid damage to the airway mucosa, atelectasis, thickened secretions, and airway obstruction. Humidification can be active, via a heated humidifier, or passive, via a heat and moisture exchanger (HME). Heated humidifiers increase the heat and water content (water vapour) of inspired gas. Set temperatures are in the range 37–41°C. Excess fluid will condense and should be collected in a water trap. HMEs trap exhaled heat and water vapour in order to warm and moisten the subsequently inspired gas. HMEs will increase dead space and should be used with caution in lung-protective ventilation strategies with low tidal volumes. Both forms of humidification can increase work of breathing, aerosol contaminants if disconnected, and may not adequately humidify inspired gas.


Communication with the patient while they are intubated is vital irrespective of the patient’s level of sedation. The patient will be unable to vocalize, so the nurse must continue to observe and assess non-verbal signs of pain, anxiety, delirium, and discomfort (Respiratory support p. [link]). The inability to communicate can in itself contribute to the patient’s anxiety. The patient’s family will need to be educated about the care and communication of their relative, with ongoing explanations and reassurance.

Key considerations include the following:

  • Introduce yourself to the patient.

  • Orientate the patient.

  • Explain the interventions to the patient.

  • Allow the patient time to respond.

  • Provide reassurance to the patient.

With a tracheostomy it is possible to trial cuff deflation to allow air to pass through the vocal cords. This can be achieved using a one-way valve once the patient is able to clear secretions and is spontaneously breathing.

In the conscious patient, alternative means of communication include devices such as tablets and alphabet, picture, or writing boards. Support from a speech and language therapist is also recommended.

Further reading

Restrepo R and Walsh B. Humidification during invasive and non-invasive mechanical ventilation. Respiratory Care 2012; 57: 782–8.Find this resource:

Dawson D. Essential principles: tracheostomy care in the adult patient. Nursing in Critical Care 2014; 19: 63–72.Find this resource:

Khalaila R et al. Communication difficulties and psychoemotional distress in patients receiving mechanical ventilation. American Journal of Critical Care 2011; 20: 470–79.Find this resource:

Morris L et al. Tracheostomy care and complications in the Intensive Care Unit. Critical Care Nurse 2013; 33: 18–30.Find this resource:

Ortega R et al. Endotracheal extubation. New England Journal of Medicine 2014; 370: e4(1)–(4).Find this resource:

Stollings J et al. Rapid-sequence intubation: a review of the process and considerations when choosing medications. Annals of Pharmacotherapy 2014; 48: 62–75.Find this resource:

Mechanical ventilation

Although it is a life-saving intervention, mechanical ventilation or intermittent positive pressure ventilation (IPPV) exposes the patient to a large number of potential risks and complications. These include the effects of positive intra-thoracic and intra-pulmonary pressure (barotrauma, decreased venous return) and the increased risks associated with endotracheal intubation. Nurses must be fully aware of these risks and understand how to reduce them in order to protect the patient.

Indications for mechanical ventilation

  • To support acute ventilatory failure.

  • To reverse life-threatening hypoxaemia.

  • To decrease the work of breathing.

Causes of acute ventilatory failure

  • Respiratory centre depression—decreased conscious level, intra-cerebral events, sedative or opiate drugs.

  • Mechanical disruption—flail chest (multiple rib fractures resulting in a free segment of chest wall), diaphragmatic trauma, pneumothorax, pleural effusion.

  • Neuromuscular disorders—acute polyneuropathy, myasthenia gravis, spinal cord trauma or pathology, Guillain-Barré syndrome, critical illness.

  • Reduced alveolar ventilation—airway obstruction (foreign body, bronchoconstriction, inflammation, tumour), atelectasis, pneumonia, pulmonary oedema (cardiac failure and ARDS), obesity, fibrotic lung disease.

  • Pulmonary vascular disruption—pulmonary embolus, ARDS, cardiac failure.

Causes of hypoxaemia

  • V/Q mismatch—pulmonary embolus, obstruction of the pulmonary microcirculation, ARDS.

  • Shunt—pulmonary oedema, pneumonia, atelectasis, consolidation.

  • Diffusion (gas exchange) limitation—pulmonary fibrosis, ARDS, pulmonary oedema.

Causes of increased work of breathing

  • Airway obstruction.

  • Reduced respiratory compliance.

  • High CO2 production (e.g. due to burns, sepsis, overfeeding).

  • Obesity.

Physiological effects of mechanical ventilation

IPPV has significant effects on the respiratory, cardiac, and renal systems. These are principally related to increased intra-thoracic pressure and its effect on normal physiological responses.

Decreased cardiac output and venous return

Increased intra-thoracic pressure reduces venous return (the passive flow of blood from central veins to the right atrium) and increases right ventricular afterload (the resistance to blood flow out of the ventricle by the pulmonary circulation). This reduces right ventricular output and consequently left ventricular filling and ultimately output. The use of PEEP means that this occurs throughout the respiratory cycle.

  • Effects—hypotension, tachycardia, hypovolaemia, decreased urine output.

  • Management—fluid loading to optimize stroke volume and cardiac output. Inotropes may be necessary if cardiac function is compromised.

Increased incidence of barotrauma

The pressure required to deliver gas to the alveoli through airways which may be resistant to gas flow can cause damage to more compliant areas through over-distension. Greater damage is caused at higher tidal volumes, causing gas to escape into the pleura and interstitial tissues. Up to 15% of patients develop barotrauma. The risk is particularly high in conditions with increased airway resistance due to bronchoconstriction, such as asthma.

  • Effects—pneumothorax, pneumomediastinum, subcutaneous emphysema.

  • Management—tidal volumes that are close to physiological values (e.g. 6–8 mL/kg). Avoid high airway pressures, if necessary by manipulating the inspiratory:expiratory (I:E) ratio. Chest drain management of pneumothorax is required.

Decreased urine output

The response to reduced cardiac output includes release of antidiuretic hormone, activation of the renin–angiotensin–aldosterone (RAA) response, and increased salt and water retention.

  • Effects—oliguria, increased interstitial fluid, and generalized peripheral oedema.

  • Management—fluid filling to optimize stroke volume and cardiac output, and careful fluid monitoring.

Ventilator-associated pneumonia

Ventilator-associated pneumonia (VAP) develops 48 h or later after commencement of mechanical ventilation via endotracheal tube or tracheostomy. It develops as a result of colonization of the lower respiratory tract and lung tissue by pathogens. Intubation compromises the integrity of the oropharynx and trachea, allowing oral and gastric secretions to enter the airways.

VAP is the most frequent post-admission infection in critical care patients, and significantly increases the number of mechanical ventilation days, the length of critical care stay, and the length of hospital stay overall.1 Patients at increased risk include those who are immunocompromised, the elderly, and those with chronic illnesses (e.g. lung disease, malnutrition, obesity).

Diagnosis of VAP is difficult due to the number of differential diagnoses that present with the same signs and symptoms (e.g. sepsis, ARDS, cardiac failure, lung atelectasis). Radiological changes include consolidation and new or progressive infiltrates. Clinical signs include pyrexia > 38°C, raised or reduced white blood cell (WBC) count, new-onset purulent sputum, increased respiratory secretions/suctioning requirements, and worsening gas exchange. Microbiology criteria include a positive blood culture growth not related to any other source, and positive cultures from bronchoalveolar lavage.

Use of a care bundle approach has been demonstrated to be an effective preventive strategy. The Department of Health has established a care bundle1 with six elements for the prevention of ventilator-associated pneumonia, which should be reviewed daily:

  1. 1. Elevation of the head of the bed—the head of the bed is elevated to 30–45° (unless contraindicated).

  2. 2. Sedation level assessment—unless the patient is awake and comfortable, sedation is reduced or held for assessment at least daily (unless contraindicated).

  3. 3. Oral hygiene—the mouth is cleaned with chlorhexidine gluconate (≥ 1–2% gel or liquid) 6-hourly. Teeth are brushed 12-hourly with standard toothpaste.

  4. 4. Subglottic aspiration—a tracheal tube (endotracheal or tracheostomy) that has a subglottic secretion drainage port is used if the patient is expected to be intubated for > 72 h. Secretions are aspirated via the subglottic secretion port 1- to 2-hourly.

  5. 5. Tube cuff pressure—cuff pressure is measured 4-hourly, and maintained in the range 20–30 cmH2O (or 2 cmH2O above peak inspiratory pressure).

  6. 6. Stress ulcer prophylaxis—stress ulcer prophylaxis is prescribed only for high-risk patients, according to locally developed guidelines.

Modes of mechanical ventilation

There are no generic terms for modes of ventilation and therefore the principles of mechanical ventilation and common terminology/abbreviations are discussed here. Refer to individual ventilator specifications for comprehensive information on the modes and settings available.

Controlled mechanical ventilation (CMV)

There is a set frequency of patient breaths delivered as either pressure controlled (with a set inspiratory pressure) or volume controlled (with a set tidal volume).

Synchronized intermittent mandatory ventilation (SIMV)

There is a set frequency of patient breaths, but this mode of ventilation allows spontaneous breaths to be taken in between. Ventilator breaths are synchronized to these spontaneous breaths, and can be pressure controlled (SIMV-PC) or volume controlled (SIMV-VC). The current trend is for pressure-controlled ventilation in order to control pressure and limit potential barotrauma.

Volume-controlled ventilation

The set tidal volume is delivered at a constant flow rate, resulting in changes to airway pressure through inspiration. The set tidal volume remains constant as lung compliance and resistance change. A high inspiratory flow rate delivers the set tidal volume more quickly. Therefore if ventilation is time cycled and the set tidal volume has been reached before the end of inspiration, there will be a pause before expiration and the airway pressure will drop. High inspiratory flow rates will also elevate the peak airway pressure. Therefore low inspiratory flow rates are recommended to keep the peak airway pressure as low as possible. Pressure-limited, volume-controlled ventilation ensures that the tidal volume delivered is as close as possible to the set tidal volume for the set pressure limit (e.g. 30–35 cmH2O).

Pressure-controlled ventilation

Set pressures throughout the inspiratory and expiratory cycle are delivered at a decelerating flow rate, resulting in a tidal volume that varies with lung compliance and resistance. For example, an increase in resistance or a reduction in lung compliance will decrease the tidal volume delivered, resulting in hypoventilation. Common pressure controlled modes which also allow for pressure supported spontaneous breaths (see Respiratory support p. [link]) include BIPAP, PCV+, DuoPAP, BiLevel and Bi-vent (terms and abbreviations depend on the Trademark name of the specific ventilator being used).

Airway pressure release ventilation (APRV)

This is a pressure-regulated mode of ventilation, with set inspiratory pressure and PEEP. The settings produce an inverse ratio in ventilation, with the time at the higher pressure exceeding the time at the lower pressure. A combination of patient spontaneous and mandatory set breaths is allowed.

Pressure support ventilation/assist (PSV/assist)

A set level of inspiratory pressure support or tidal volume is delivered when the patient triggers a breath. The tidal volume of each breath is dependent on lung compliance and respiratory rate. In addition, a back-up rate of breaths will occur if the patient does not initiate (trigger) breaths at the required rate. PSV is used to provide ventilator support (e.g. when the patient’s own respiratory efforts are diminished). This mode reduces the requirement for sedation, allows ongoing use of respiratory muscles, and provides the opportunity to gradually reduce the level of support to facilitate weaning. Pressure supported breaths can also be added into other modes which allow for spontaneous breaths over and above the set mandatory controlled breaths (e.g. SIMV, BIPAP).

Mechanical ventilator settings

Respiratory rate (f) (breaths/min)

Typically the respiratory rate is 10–15 breaths/min, but it may be altered in order to optimize minute volume and/or PCO2.

Tidal volume (VT) (mL/kg)

Typically this is in the range 6–8 mL/kg, but it may be altered to optimize minute volume and/or PCO2.

Minute volume (MV or VE) (L/min)

Typically this is in the range 3–10 L/min. It is derived from tidal volume and respiratory rate

Flow rate (V) (L/min)

Typically this is in the range 40–80 L/min, and adjusted to ensure that tidal volume is achieved within inspiratory time. A decelerating flow pattern is always seen in pressure support modes.

Positive end expiratory pressure (PEEP) (cmH2O)

Typically this is in the range 5–10 cmH2O.

Airway pressure (cmH2O)

Typically plateau pressure is limited to < 30 cmH2O in order to reduce barotrauma.

Pressure support/assist (cmH2O)

Typically this is in the range 5–20 cmH2O, set according to patient requirements for assistance.

Inspiratory:expiratory (I:E) ratio

Typically this is 1:2 (i.e. expiratory time is twice as long as inspiratory time). It may vary with extended or inverted ratios in order to increase time for inspiration in patients with severe airflow limitation (e.g. due to asthma), or to assist expiration by lengthening expiratory time and avoid air trapping.


This can be flow based, pressure based, volume based, or time based, and is vital for reducing the delay between the initiation of a breath and the ventilator response and thus the patient’s work of breathing.

  • Flow-based triggers require the patient to produce a minimum flow rate of 1 L/min to initiate a breath.

  • Pressure-based triggers require the patient to generate a negative pressure of –1 to –10 cmH2O to initiate a breath.

  • Volume-based triggers require the patient to inhale a certain volume of gas to initiate a breath.

  • Time-based triggers are independent of the patient effort, with preset frequency and delivered at regular intervals of time.

The ventilator settings are summarized in Table 5.5.

Table 5.5 Ventilator settings


Initial setting for ventilator

Respiratory rate

10–15 breaths/min

Tidal volume

6–8 mL/kg

Positive end expiratory pressure

3–10 cmH2O

Peak airway pressure

≤ 35 cmH2O

Inspiratory: expiratory ratio


Oxygen (adjusted to blood gas results)

0.4–0.6 FiO2

Pressure–volume relationships

Pressure–volume loops can be viewed graphically on most modern ventilators, and the information obtained can be used to inform ventilator settings, such as PEEP and upper airway pressure limits.

The pressure–volume relationship in a ventilator breath consists of three stages:

  • initial increase in pressure with little change in volume

  • linear increase in volume as pressure increases

  • pressure increase with no further volume increase.

The inflection points represent the change between the different stages of the ventilator breath (see Figure 5.4).

Figure 5.4 Pressure–volume loop showing inflection points and hysteresis.

Figure 5.4 Pressure–volume loop showing inflection points and hysteresis.

Lower inflection point

This occurs between stages 1 and 2, and is the point at which airway resistance is overcome, allowing alveolar opening. In a patient who is fully ventilated and making little or no respiratory effort, the lower inflection point is the point at which lower airways would close on expiration. PEEP should therefore be set at this level to avoid gas trapping.

Upper inflection point

This occurs between stages 2 and 3, and is the point at which lung capacity for the breath has been reached. It can be used to adjust settings for maximum inspiratory pressure.

Protective lung ventilation

Protective lung ventilation is the current standard of care for mechanical ventilation for both ARDS and non-ARDS patients. Features include permissive hypercapnia, lower plateau pressures, and low tidal volume ventilation (4–8 mL/kg) (ideal body weight, not actual body weight).

Ideal body weight

Male patients: 50 kg + 2.3 kg for each inch over 5 feet.

Female patients: 45.5 kg + 2.3 kg for each inch over 5 feet.

Mechanical ventilation: troubleshooting

The patient is highly vulnerable to a number of problems while dependent on a mechanical ventilator. The critical care nurse is responsible for the patient’s safety, and it is his or her responsibility to ensure that any problems are recognized as soon as possible and dealt with in an effective and timely manner.

A guide to recognition and management of the more common problems is provided in Table 5.6. If there is any doubt about the functioning of the ventilator, and the patient is deteriorating, the nurse should immediately:

  • call for help

  • manually ventilate the patient using a manual ventilation bag with high-flow oxygen

  • review the patient for indicators of what is causing the problem.

Table 5.6 Troubleshooting problems in the ventilated patient

High airway pressure: airway pressure alarm sounds, persistent rise in peak airway pressure, evidence of patient distress, haemodynamic instability

Life-threatening causes

  • Endotracheal tube (ETT) and/or ventilator tubing obstruction

  • Pneumothorax

  • Severe bronchospasm

Other causes

  • Build-up of airway secretions

  • Asynchrony with mechanical ventilation (tidal volume too high)

  • Patient coughing

  • ETT displacement


  • Ascertain cause of high airway pressure and treat accordingly

  • Consider manual ventilation if patient is in respiratory distress

  • Emergency re-intubation

  • Review ventilator settings

  • Check tubing and filter integrity

  • Auscultate lungs for abnormal breath sounds

  • Perform suction

  • Check arterial blood gas and treat accordingly

  • Review sedation if an increase with or without paralysis is indicated

Low airway pressure: airway pressure alarm sounds, audible air leak, decreased minute volume, evidence of patient distress, haemodynamic instability

Life-threatening causes

  • ETT and/or ventilator tubing disconnection or leak


  • Ascertain cause of low airway pressure and treat accordingly

  • Consider manual ventilation if patient is in respiratory distress

  • Emergency re-intubation

  • Check connections

  • Check tubing integrity

  • Check cuff pressure

  • Review ventilator settings

  • Auscultate lungs for abnormal breath sounds

  • Perform suction

  • Check arterial blood gas and treat accordingly

  • Review sedation if an increase with or without paralysis is indicated

Low minute volume: low MV alarm sounds, audible air leak, evidence of patient distress, haemodynamic instability

Life-threatening causes

  • Disconnection from the ventilator,

  • Asynchrony with mechanical ventilation (i.e. flow rate may be too low to allow set volume in time allocated by set respiratory rate)

  • Air leak via chest drain


  • Ascertain cause of low minute volume and treat accordingly

  • Consider manual ventilation if patient is in respiratory distress

  • Emergency re-intubation

  • Check connections and tubing integrity

  • Check cuff pressure

  • Review ventilator settings (increase to compensate for chest drain)

  • Auscultate lungs for abnormal breath sounds

  • Check arterial blood gas and treat accordingly

  • Review sedation if an increase with or without paralysis is indicated

High minute volume: high MV alarm sounds, evidence of patient making respiratory effort


  • Ventilator malfunction

  • Asynchrony with mechanical ventilation (patient making respiratory effort)


  • Check causes of patient’s tachypnoea (e.g. pain, hypoxia, hypercapnia)

  • Review ventilator settings

Auto-PEEP (intrinsic PEEP, air-trapping): failure of alveolar pressure to return to zero at the end of exhalation, causing increased resistance to airflow and increased work of breathing


  • Incomplete or impeded exhalation, as a result of either high MV (> 10 L/min) or airway resistance (due to chronic pulmonary disease)


  • Ensure low-compressible-volume ventilator tubing is used

  • Review ventilator settings to reduce MV by decreasing respiratory rate or altering inspiratory flow rate to decrease inspiratory time and increase expiratory time

  • Reduce metabolic workload to reduce respiratory demand

Improving oxygenation in the ventilated patient

In patients with severe acute lung pathology (e.g. ARDS), simply increasing the FiO2 may not be sufficient to support the patient’s oxygen requirements. Alternative interventions may also be needed, including the following.

Positive end expiratory pressure

  • PEEP will increase FRC by improving V/Q match and will prevent collapse of recruited alveoli.

  • Increase by increments of 1–2 cmH2O.

  • Response to any alteration in PEEP should be monitored using blood gas analysis.

  • Pressure–volume loops can be used to identify the lower inflexion point to determine the optimal PEEP setting.

  • suggests higher PEEP to lower FiO2 ratios. For example:

    • PEEP 8–14 cmH2O with 0.3 FiO2

    • PEEP 14–16 cmH2O with 0.4 FiO2

    • PEEP 16–20 cmH2O with 0.5 FiO2

    • PEEP 22–24 cmH2O with 0.5–1.0 FiO2.

Prone positioning

Placing the patient in the prone position improves oxygenation which is likely due to the increased expansion of the dorsal aspect of the lungs which then optimises alveolar recruitment2.

Prone positioning has been shown to reduce mortality of patients who have severe acute respiratory distress syndrome although the timing, duration and frequency of proning has not been established3,4,5. Not all patients can be turned prone, and the risk–benefit of this manoeuvre must be evaluated before commencing it. Sufficient people should be available while turning the patient onto their front and during regular head/arm repositioning. Other nursing responsibilities of the proned patient include frequent mouth care, eye care, pressure area care and suctioning. Vigilant attention should be taken to ensure the airway is protected at all times and the patient is adequately sedated.

Nitric oxide (NO)

Inhaled NO crosses the alveolar membrane, acting locally on the pulmonary vasculature by dilating vessels and increasing blood flow. This improves V/Q match and therefore gas exchange. As soon as it enters the blood, NO is bound to haemoglobin and has no further systemic (i.e. hypotensive) effect.

NO gas is added to the gas delivery of the ventilator or in the inspiratory limb of the ventilation circuit. Optimal delivery is titrated according to PO2 at least once a shift. Withdrawal of NO should be slow, as there may be rebound pulmonary hypertension and hypoxaemia. Significant increases in oxygenation are seen in up to 60% of patients. However, this has not been associated with an improvement in overall mortality.

The safe use of nitric oxide is summarized in Box 5.2.

Extracorporeal membrane oxygenation (ECMO)

ECMO uses an artificial lung (the membrane) to oxygenate the blood outside the body (hence ‘extracorporeal’) in a similar way to heart and lung bypass. By providing oxygenation outside the body the lungs can be rested (i.e. not exposed to high ventilator pressures or high oxygen levels), and the use of a blood pump can provide support for reversible heart disorders. ECMO can be either veno-venous or veno-arterial.

The main risk associated with ECMO is bleeding due to anticoagulant use.

There are ECMO centres throughout the UK for adult and paediatric patients, with referral and acceptance criteria. Specialist retrieval teams from these centres will transfer the patient, and in extreme circumstances ECMO may be started prior to transfer of the patient.

Managing hypercapnia in severe pulmonary disease

In patients with severe pulmonary disease, such as ARDS, where there is a risk of further lung damage being caused by the high airway pressures necessary to reduce PCO2, it may be preferable to tolerate high levels of CO2 provided that acidosis is adequately compensated for. This is termed ‘permissive hypercapnia.’ Rather than increasing the likelihood of barotrauma by increasing the volume of the breath, the patient’s PCO2 is allowed to rise to 10 kPa or more, provided that the pH can be maintained at ≥ 7.2. As a high CO2 level is a very strong respiratory stimulant, permissive hypercapnia can only be tolerated if the patient is well sedated.

High-frequency ventilation (HFV)

This incorporates techniques using ventilation frequencies greater than 60–2000 breaths/min and tidal volumes of 1–5 mL/kg. This is useful when the lungs are non-compliant or there is a bronchopleural fistula causing large leaks of gas (and subsequent loss of tidal volume) during normal mechanical ventilation.

High-frequency oscillation

A rapidly oscillating gas flow is created by a device that acts like a woofer on a loudspeaker, producing a high-frequency rapid change in direction of gas flow. Most of the experience that has been gained with this approach has been in the paediatric population, but recent research in adults with severe ARDS suggests that it may be beneficial. Oscillation can be applied externally or via the endotracheal tube.

High-frequency jet ventilation

High-pressure air and oxygen are blended and then supplied through a non-compliant injection (jet) system to the patient via an open (uncuffed) circuit. The driving pressure of this gas can be adjusted to alter the rate of flow from the maximum (2.5 atm) down to zero. Added (warmed and humidified) gas is entrained from an additional circuit via a T-piece attached to the endotracheal tube. The entrainment circuit should provide at least 30 L/min of flow. Highly efficient humidification (usually via a hot-plate vaporizer humidifier) is necessary due to the high flows of otherwise dry gas. The usual frequency set is 100–200 breaths/min delivering tidal volumes of 2–5 mL/kg.

In an entrainment system, the tidal volume delivered by the ventilator increases with driving pressure and decreases with respiratory frequency. It remains the same with alterations in I:E ratio.


1 Department of Health. High Impact Intervention No.5: care bundle to reduce ventilation-associated pneumonia. Department of Health: London, 2010.Find this resource:

2 Gattinoni L et al. Prone position in acute respiratory distress syndrome: rationale, indications, and limits. American Journal of Respiratory and Critical Care Medicine 2013; 188: 1286–1293.Find this resource:

3 Guérin C et al. (PROSEVA Study Group). Prone positioning in severe acute respiratory distress syndrome. New England Journal of Medicine 2013; 368: 2159–2168.Find this resource:

4 Lee JM et al. The efficacy and safety of prone positional ventilation in acute respiratory distress syndrome: updated study-level meta-analysis of 11 randomized control trials. Critical Care Medicine 2014; 14: 1252–1262.Find this resource:

5 Sud S et al. Effect of prone positioning during mechanical ventilation on mortality among patients with acute respiratory distress syndrome: a systematic review and meta-analysis. Canadian Medical Association Journal 2014; 186: E381–E390.Find this resource:

Further reading

de Beer J and Gould T. Principles of artificial ventilation. Anaesthesia and Intensive Care Medicine 2013; 14: 83–93.Find this resource:

Grossbach I et al. Overview of mechanical ventilatory support and management of patient- and ventilator-related responses. Critical Care Nurse 2011; 31: 30–44.Find this resource:

Henzler D. What on earth is APRV? Critical Care 2011; 15: 115.Find this resource:

Lambert M-L et al. Prevention of VAP: an international online survey. Antimicrobial Resistance and Infection Control 2013; 2: 1–8.Find this resource:

Mireles-Cabodevila E et al. A rational framework for selecting modes of ventilation. Respiratory Care 2013; 58: 348–66.Find this resource:

National Heart, Lung, and Blood Institute (NHLBI) ARDS Network. Respiratory

National Institute for Health and Care Excellence (NICE). Technical Patient Safety Solutions for Ventilator-Associated Pneumonia in Adults. PSG002. NICE: London, 2008. Respiratory this resource:

Singer M and Webb AR. Oxford Handbook of Critical Care, 3rd edn. Oxford University Press: Oxford, 2009.Find this resource:

Tobin M. Principles and Practice of Mechanical Ventilation, 3rd edn. McGraw-Hill: London, 2013.Find this resource:


With the growing awareness of the hazards of prolonged mechanical ventilation there is an increasing emphasis on effective weaning strategies. Weaning can be defined as a gradual reduction in ventilatory support so that the patient either requires no assistance with their breathing or no further reduction in support is possible. Protocol-directed weaning has shown positive outcomes, with shorter duration of mechanical ventilation and decreased critical care stay. It also counters the under-estimation by physicians of the patient’s ability to be successfully weaned. A current trend in protocol use is nurse-led weaning.

Weaning often consists of a succession of stages rather than a single transition from full ventilatory support to independent breathing. The implication is that in order for progress to be made the patient only has to be fit enough to achieve each stage.

Weaning must take place alongside other care activities, and therefore consideration should be given to time of day, nursing interventions, medical treatments, and patient response.

The decision to wean

The decision to wean can be informed by the Rapid Shallow Breathing Index (RSBI). The use of the RSBI as a weaning predictor was first reported in the early 1990s.6 It is the ratio of respiratory rate to tidal volume (f/VT), and is measured as follows:

  • Perform a 1-min trial of unassisted breathing with a T-piece.

  • Measure the respiratory rate and tidal volume with a spirometer.

  • Divide the respiratory rate by the tidal volume to calculate the RSBI.

For example, 25 (breaths/min)/450 (mL/breath)  25/0.45 L   = 55 (breaths/min/L).

An RSBI of ≤ 105 breaths/min/L, indicating a relatively low respiratory rate to tidal volume, is used as an indication of readiness to wean or extubate. RSBI is most accurate when used to predict failure to wean, rather than readiness to wean.

Additional parameters include the following:

  • PaO2/FiO2 < 200 mmHg

  • PEEP < 5 cmH2O.

The decision to wean will also be based on an assessment of patient improvement—that is, whether the cause of respiratory failure requiring mechanical ventilation has been resolved, and whether the patient is stable (see Box 5.3).

Weaning methods

The initial process of weaning involves changing the mode of ventilation or support to assess the patient’s ability to maintain their own work of breathing. A spontaneous breathing trial (SBT) for 30 min is used. The SBT may be coupled with a sedation hold (See Respiratory support p. [link]). SBT can be achieved by using a T-piece, pressure support plus PEEP, CPAP or flow-by. If the patient shows no signs of fatigue (i.e. they display no cardiovascular or respiratory distress) this can then be followed by a pressure support or external CPAP trial prior to extubation. If respiratory distress is identified, no further attempt to wean should be undertaken until the following day (see Box 5.4). The exception to this practice is in patients ventilated on APRV, as this is a spontaneous breathing mode. The aim of weaning from this mode is to adjust gas flow to the level of CPAP, with progressively fewer releases occurring per minute.

Non-invasive ventilation has been utilized in the weaning process in the following ways:

  • as an alternative weaning method for patients who are unsuccessful in initial weaning trials

  • for patients who are extubated but develop acute respiratory failure within 48 h

  • as prophylaxis after extubation for patients who are at high risk for reintubation.

Weaning classification8

  • Simple weaning—patients who proceed from initiation of weaning to successful extubation on the first attempt without difficulty.

  • Difficult weaning—patients who fail initial weaning and require up to three SBTs or as long as 7 days from the first SBT to achieve successful weaning.

  • Prolonged weaning—patients who fail at least three weaning attempts or require > 7 days weaning after the first SBT.

Prolonged weaning

Prolonged weaning is often a direct consequence of the complexities of critical illness. Patients who survive the acute phase of their admission will experience a range of physical and psychological disturbances (including neuromyopathy, weakness, sleep deprivation, and delirium). These can all have a negative impact both on the patient’s readiness to wean and on the weaning process itself.

Measures to support the patient with prolonged weaning include rehabilitation, tracheostomy insertion, and specialized weaning units.


6 Crocker C. Weaning from ventilation—current state of the science and art. Nursing in Critical Care 2009; 14: 185–90.Find this resource:

7 Kaplan L and Toevs C. Weaning from mechanical ventilation. Current Problems in Surgery 2013; 50: 489–94.Find this resource:

8 Boles J-M et al. Weaning from mechanical ventilation. European Respiratory Journal 2007; 29: 1033–56.Find this resource:

Further reading

Blackwood B et al. Protocolized versus non-protocolized weaning for reducing the duration of mechanical ventilation in critically ill adult patients. Cochrane Database of Systematic Reviews 2010; Issue 5: CD006904.Find this resource:

Burns K et al. Non-invasive positive-pressure ventilation as a weaning strategy for intubated adults with respiratory failure. Cochrane Database of Systematic Reviews 2013; Issue 12: CD004127.Find this resource:

Intensive Care Society. Weaning Guidelines. Intensive Care Society: London, 2007.Find this resource: