Breathing

Respiratory failure

Respiratory failure occurs when air transfer in and out of the lungs is reduced, or when gas exchange within the lungs fails (due to shunt, VQ mismatch, or poor gas diffusion), resulting in either:

Type I respiratory failure—causing hypoxia.
Type II respiratory failure—causing hypoxia and hypercapnia.

Type I respiratory failure typically has parenchymal causes. Type II respiratory failure occurs with mechanical/obstructive causes, or as a result of fatigue/↓consciousness alongside respiratory failure.

Causes

Upper airway obstruction (see p.18).
Lower airway obstruction:
- Acute bronchoconstriction, asthma, anaphylaxis
- COPD
- Foreign body, mucous plugging, atelectasis
Lung tissue damage/gas exchange failure:
- Pneumonia
- Lung contusion
- ARDS
- Pulmonary haemorrhage
- Cardiogenic pulmonary oedema
- Lung fibrosis
Pulmonary circulatory compromise:
- Pulmonary embolus
- Pulmonary vascular disease
- Heart failure
- Excessively raised cardiac output
Neuromuscular damage:
- ↓level of consciousness (e.g. intracranial catastrophe or sedative agents)
- Paralysis/weakness (e.g. spinal damage, tetanus, Guillain-Barré, myasthenia gravis)
Mechanical compromise of lung tissue (e.g. pneumothorax, haemothorax, pleural effusion, flail chest, kyphoscoliosis, obesity or ascites).
Inadequate mechanical ventilation.

Presentation and assessment

Respiratory failure may present with respiratory or cardiac arrest (

p.98).

Evidence of respiratory distress that may precede or accompany respiratory failure includes:

Agitation, sense of impending doom.
Sense of ‘tight chest’ or breathlessness in conscious patients.
Inability to talk normally or in full sentences.
Sweating, clamminess.
Tachypnoea >25 breaths/minute.
Dyspnoea, or laboured breathing, with use of accessory muscles.
Gasping or ‘pursed-lip’ breathing.
Sitting, or hunched posture.
Cyanosis.
Hypoxia, as evidenced by ABG or SpO₂ <92%.
Hypercapnia: flapping tremor, warm peripheries and bounding pulse.
Tachycardia (> 110 beats/minute).

Pre-terminal signs include:

Bradycardia, arrhythmia, or hypotension.
Silent chest on auscultation.
Bradypnoea or exhaustion.
Confusion or ↓level of consciousness.

In mechanically ventilated patients, evidence of respiratory failure may also be accompanied by:

High, or low, ventilator pressure alarms.
Low delivered tidal volume alarm, or low minute-volume alarm.
Audible leak from ventilator circuit, or leak alarm.
Inability to ventilate using self-inflating bag.
Lack of chest movement.
Lack of respiratory sounds on auscultation.

Other features associated with respiratory failure depend upon the cause, but may include:

Cough.
Pleuritic chest pain.
Haemoptysis.
Evidence of sepsis (pyrexia, rigors, purulent sputum).
Reduced air-entry or altered percussion note associated with pneumothorax, consolidation, or effusion.
Audible wheeze on external examination; or wheeze, rub, or bronchial breathing on auscultation.
Reduced peak flow.
Mediastinal deviation (tracheal deviation, altered apex).
Raised JVP; evidence of cardiac failure (peripheral oedema, hepatic engorgement, cardiomegaly).

Investigations

In most cases clinical assessment will reveal evidence of respiratory distress. Investigations which may aid in assessing severity or establishing a diagnosis include:

ABGs:
- The PaO₂/FiO₂ ratio may be calculated to give a measure of the degree of respiratory failure (see p.90)¹
FBC (↑ Hb in chronic hypoxia, ↓Hb in acute anaemia).
U+Es (hyponatraemia in pneumonia, raised urea/creatinine in pneumonia, pulmonary-renal syndrome, heart failure).
LFTs (deranged in heart failure, malignancy).
Peak flow measurements, where appropriate (restrictive: lung fibrosis, obstructive: asthma, COPD).
ECG (RV strain pattern in PE, severe lung disease).
CXR (consolidation, collapse, alveolar/interstitial shadowing, pneumothorax).
Chest ultrasound (pleural fluid, pneumothorax).

Further investigations may be required depending on cause or clinical progress:

Coagulation studies (DIC in sepsis/trauma).
CRP (↑ in sepsis/inflammation).
D-dimers (↑ in PE, but of limited use in ICU as also ↑ by inflammation).
Culture (blood, sputum).
Atypical serology.
Urine for legionella and pneumococcal antigen.
Bronchoscopy or non-directed BAL (see p.548).
Echocardiogram (acute RV strain in PE; chronic RV strain in severe chronic lung disease; LV impairment in IHD).
CT chest.
CT pulmonary angiogram.

Differential diagnoses

Patients may appear to be in respiratory distress despite having adequately saturated arterial blood, in these cases it is important to consider:

Anaemia (severe).
Cytotoxic hypoxia (e.g. cyanide or carbon monoxide poisoning).
Metabolic acidosis (with compensatory respiratory alkalosis: Kussmaul breathing).
Hyperventilation, either hysterical or associated with disease (e.g. thyrotoxicosis or pain).

Also consider:

Upper airway obstruction (see p.18).
Endotracheal tube/breathing system obstruction (see pp.38 and 42).

Immediate management

If the patient is spontaneously breathing without ventilatory support:

Ensure that the airway is patent (use adjuncts if necessary).
Increase FiO₂ to maintain SpO₂ at 94-98% for most acutely ill patients, or 88-92% for those at risk of hypercapnic respiratory failure.
Assist breathing with bag and mask if required.
Consider escalating respiratory support in a stepwise progression (non-invasive CPAP or BIPAP may be indicated p.53).
Endotracheal intubation and mechanical ventilation may be required (see pp.12 and 52).

If patient is already intubated and/or receiving ventilatory support (noninvasive or invasive) the following may be necessary:

Increase FiO₂ to 100%.
Check that the airway is patent; in intubated patients check the patency and position of the endotracheal or tracheostomy tube (check with a suction catheter if in doubt, see pp.38 and 42).
If already on a ventilator, ensure ventilation is possible; check equipment is working and not disconnected.
If in doubt switch to self-inflating ambu-bag and manually ventilate.

Establish a probable diagnosis as soon as possible and treat as appropriate, especially any reversible causes such as: endobronchial intubation, pneumothorax, pulmonary oedema, secretions and mucous plugs, bronchospasm, and pleural effusions

Once Airway and Breathing are stabilized, continue ABC approach:

Patients may require aggressive circulatory support.

Further management

Titrate oxygen therapy and respiratory support to keep PaO₂ >8 kPa and PaCO₂ <6.3 kPa (and respiratory rate <30 breaths/minute if spontaneously breathing) where possible.
If basic ventilatory support is not enough, consider additional manoeuvres for hypoxia ( p.58) or hypercapnia ( p.56).
Consider invasive monitoring with serial ABG analysis.
If mechanical ventilation is necessary, sedation (with or without muscle relaxation) will be required, at least initially ( p.13).
Follow a lung-protective ventilation strategy ( p.53).

Pitfalls/difficult situations

Double-check equipment as it may be faulty or not be delivering high enough O₂; switch to alternative equipment if in doubt.
Cold limbs or poor skin perfusion may make SpO₂ readings unreliable or difficult to maintain.
Chest X-ray interpretation can be difficult in supine patients; certain conditions such as anterior pneumothoraces or pleural effusions may require additional imaging (CT or US).
The presence of a metabolic acidosis increases dyspnoea; do not ignore circulatory support and correction of acidosis.

Oxygen delivery devices

Devices which deliver variable concentrations (and estimated FiO₂):

Nasal cannulae:¹
- At 2 L/minute O₂ flow: maximum FiO₂ = 28%
- At 4 L/minute O₂ flow: maximum FiO₂ = 35%
- At 6 L/minute O₂ flow: maximum FiO₂ = 45%
Non-Venturi masks (e.g. Hudson mask):
- At 5 L/minute O₂ flow: maximum FiO₂ = 35%
- At 8 L/minute O₂ flow: maximum FiO₂ = 55%
- At 12 L/minute O₂ flow: maximum FiO₂ = 65%
Reservoir bag masks (non-rebreathing masks, trauma masks):
- At 15 L/minute O₂ flow: maximum FiO₂ = 80-90%

Devices which deliver fixed O₂ concentrations:

All Venturi masks: 24-60% if O₂ flow rate is set according to instructions written on adapter (to change FiO₂, change adapter).
Ventilator circuits: up to100% O₂ as set.
Oxylog portable ventilators:
- Modern machines up to100% O₂ as set
- Older machines: if set to ‘Airmix’ 50-60%, if set to ‘No airmix’ 100%

Indications for ventilatory support

Invasive ventilatory support should be considered where:

Endotracheal intubation is required:
- Airway protection
- Secretion clearance
Respiratory failure is present, or likely to occur:
- Respiratory rate >30 breaths/minute, or apnoea/bradypnoea
- Vital capacity <10-15 ml/kg
- Hypercapnia with pH <7.35
- PaO₂ <11 kPa on FiO₂ <40%
- Fatigue, exhaustion, inadequate respiratory effort
- ↓level of consciousness
- Acute pulmonary oedema
Cardiopulmonary support is required:
- Following cardiac arrest
- Postoperative support of certain high-risk patients
- Severe shock or LVF
Sedation, anaesthesia, and/or paralysis is required to:
- Control intracranial pressure
- Transfer critically ill patients
- Control muscle spasms (e.g. tetanus)
- Allow assessment or treatment, particularly in agitated or combative patients

Also see indications for endotracheal intubation (

p.12).

Respiratory failure, actual or incipient, as outlined here may also be considered as an indication for non-invasive ventilation, but it should be borne in mind that this will not provide any degree of airway protection (see

‘Non-invasive respiratory support’, p.53.).

Lung protective mechanical ventilation¹

Lung protective ventilation strategies help to reduce the development of ALI/ARDS by attempting to avoid barotrauma, volutrauma, and shearing forces in the ventilated lungs:

Use tidal volumes of ˜6 ml/kg ideal body weight (IBW).
Keep maximum ventilatory pressure at <30 cmH₂O.
Use adequate level of PEEP.
Keep I:E ratio >1:1 where possible.
Use assist-controlled ventilation where possible.
Use the minimum required FiO2 to keep SpO₂ above 90% (or PaO₂ above 8 kPa).
Allow CO₂ to rise if necessary (permissive hypercapnia).

Ideal body weight calculation

In morbidly obese patients IBW should be used to calculate appropriate tidal volumes.

Male: IBW (kg) = 50 + 2.3 × (height (inches) − 60)

Female: IBW (kg) = 45.5 + 2.3 × (height (inches) − 60)

Alternative means of estimating height are also available, see Fig. 17.29 on

p.579.

Non-invasive respiratory support

Potential advantages

↓incidence of ventilator-associated pneumonia (VAP).
No endotracheal intubation or tracheostomy required:
- No risk of failure to intubate
- No risk of long-term tracheal damage
No sedation required:
- Patient can communicate
- Patients can often eat and drink

Indications

Acute pulmonary oedema:
- (Use CPAP or BIPAP ¹ with PEEP of 10-15 cmH₂O)
Obstructive sleep apnoea:
- (Use CPAP or BIPAP with PEEP and inspiratory pressure adjusted to alleviate obstruction)
COPD:
- (Use CPAP or BIPAP with inspiratory pressure adjusted to ease work of breathing or avoid hypercapnic acidosis and PEEP adjusted to ˜80% of intrinsic PEEP)
Weaning from mechanical ventilation.
Respiratory failure in immunocompromised patients at high risk of VAP (e.g. neutropaenic patients).
Other causes of acute respiratory failure where there are no contraindications.

Contraindications²

Risk of airway obstruction or inability to protect the airway.
Facial abnormalities, trauma, or burns; or recent facial/airway surgery.
Upper airway obstruction.
Excessive secretions or vomiting; bowel obstruction.
Very high oxygen requirement/life-threatening hypoxia.
Severe acidaemia.
Haemodynamic instability, arrhythmias, or severe comorbidity.
Confusion, agitation, or patient refusal.
Pneumothoraces (an intercostal drain should be inserted first).
Upper GI surgery is a relative contraindication.

¹Alternatively the alveolar arterial (A-a) O₂ gradient may be calculated: A-a difference = (FiO₂ × 94.8) − (PaCO₂ + PaO₂)

¹High-flow O₂ (at rates of >20 L/minute) can be delivered by some delivery devices which obtain near 100% humidification (e.g. Vapotherm^TM).

¹From The New England Journal of Medicine, The Acute Respiratory Distress Syndrome Network, ‘Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome’, 342, 18, pp. 1301-1308. Copyright © 2000 Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society.

¹Evidence supporting the efficacy of NIV is variable, as is the evidence for which mode to use (CPAP or BIPAP), see

Further reading

Baudouin S, et al. BTS Guidelines: Non-invasive ventilation in acute respiratory failure. Thorax 2002; 57: 192-211.

O’Driscoll BR, et al. BTS guideline for emergency oxygen use in adult patients. Thorax 2008; 63(SVI): vi1-vi68.

Levy MM. Pathophysiology of oxygen delivery in respiratory failure. Chest 2005; 128(5 S2): 547S-553S.

Malarkkan N, et al. New aspects of ventilation in acute lung injury. Anaesthesia 2003; 58: 647-67.

Riley B. Strategies for ventilatory support. Br Med Bull 1999; 55(4): 806-20.

The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301-8.

Severe hypercapnia

Hypercapnia is defined as a PaCO₂ >6.3 kPa. It can occur as a result of ↓clearance of CO₂ or, less commonly, as a result of ↑production.

Causes

↓ventilation—all causes of type II respiratory failure (see

p.48), including:

Acute severe bronchospasm.
COPD—acute exacerbation.
Airway obstruction—partial/chronic.
Inadequate respiratory rate (e.g. head injury or overdose).
Inadequate ventilation (e.g. neuromuscular disease or traumatic damage).
Impaired gas exchange (e.g. ALI, ARDS, or infection).
Inadequate mechanical ventilation.

↑production of CO₂:

Severe sepsis/SIRS (e.g. major burn injury).
Thyroid storm.
Reperfusion event (e.g. following release from crush injury).
Hyperpyrexias (e.g. malignant hyperpyrexia, neuroleptic malignant syndrome).
Drug reaction (e.g. serotonin syndrome, ecstasy (MDMA) poisoning).

Equipment failure may also cause re-breathing of expired CO₂; this is associated with breathing circuits in anaesthetic rather than ICU practice.

Presentation and assessment

Most commonly revealed by ABG analysis:
- Hypercapnia results in a respiratory acidosis, which may be compensated for metabolically by retention of bicarbonate ions in chronic conditions (e.g. COPD)
Where end-tidal CO₂ measurements are available these will be raised.
Symptoms of hypercapnia include:
- Agitation, sweating, flapping tremor
- Respiratory distress: tachypnoea, dyspnoea
- Tachycardia, bounding pulse, hypertension, vasodilatation
- ↓consciousness level, narcosis

Investigations

ABGs (to confirm diagnosis and estimate whether acute, acute-on-chronic, or chronic on basis of pH and bicarbonate (‘Boston rules’) see p.207).
FBC, coagulation studies (possible raised WCC; DIC).
U&Es (hyperkalaemia 2° to acidosis; AKI 2° to underlying cause, e.g. rhabdomyolysis).
TFTs (↑ T4,T3 in thyroid storm).
CK and urine myoglobin (where MH or reperfusion injury suspected).
ECG (for signs of hyperkalaemia).

Immediate management

Titrate FiO₂ to maintain SpO₂ 94-98%—via reservoir mask if spontaneously breathing or ventilator if receiving respiratory support:
- If spontaneously breathing and suspected of having hypercapnic respiratory failure caused by COPD then aim for 88-92%
Treat any underlying cause of type II respiratory failure:
- If hyperpyrexia is suspected (MH, neuroleptic malignant syndrome, serotonin syndrome, MDMA poisoning) see p.246
- If thyroid storm is suspected see p.238.

If the patient is spontaneously breathing without ventilatory support:

Secure airway and support ventilation if required.
Consider NIV or endotracheal intubation and mechanical ventilation if the patient is tiring, or hypercapnia/oxygenation are worsening.

If patient is already intubated and/or receiving ventilatory support (noninvasive or invasive) the following may be necessary:

Tolerate moderate hypercapnia (PaCO₂ <8 kPa) if it is not obviously compromising the patient.
Alter ventilation parameters:¹
- Increase inspiratory pressure, inspiratory time, or tidal volume if ventilatory volumes are inadequate
- Increase respiratory rate if minute volumes are inadequate despite good tidal volumes
- Increase PEEP to maintain lung recruitment
Progress to intubation/ventilation if NIV is ineffective; if intubated:
- Try increasing sedation or use short-term muscle relaxation to allow greater tolerance of hypercapnia and to reduce CO₂ produced by the work of breathing
- Consider advanced airway manoeuvres or oxygenation techniques (e.g. alveolar recruitment measures ( p.65); patient positioning: either positioning bad lung uppermost if lung pathology is unilateral, or prone position)

Once Airway and Breathing are stabilized, continue ABC approach.

Further management

If acidaemia is severe with mixed metabolic/respiratory components consider starting renal replacement therapy or bicarbonate infusions.
Aggressively treat hyperpyrexia with antipyretics and/or cooling measures (non-invasive or invasive).
High-frequency oscillatory ventilation may aid CO₂ clearance, as may tracheal gas insufflation (TGI).
Extracorporeal CO₂ removal (ECCO₂R) may be possible.

Pitfalls/difficult situations

Avoid hypercapnia where possible in patients with head injuries.
Where hypercapnia has been tolerated for a prolonged period, and metabolic compensation has occurred, avoid rapid correction as the relative hypocapnia may result in cerebral vasoconstriction.

Complications of mechanical ventilation

Complications of mechanical ventilation that may require emergency treatment include:

Failure to ventilate.
Failure to oxygenate.
Haemodynamic instability.
Pneumothorax.
Mucous plugging.

Other complications covered in more detail in other sections include:

Hypercapnia ( p.56).
Air trapping ( p.78).
Ventilator-associated pneumonia ( pp.62 and 334).

Causes

Complications are more likely in:

Agitated, undersedated, or very mobile patients.
Patients with abnormal anatomy.
Patients with severe respiratory diseases, especially severe pneumonia, ARDS, bronchospasm, trauma, and contusions.
Patients with underlying chronic chest conditions.
Patients requiring airway pressures >35 cmH₂O, or patients receiving high tidal volumes via mechanical ventilation.

Haemodynamic instability:

May result from ↓venous return/cardiac output.
Is made worse by coexisting dehydration, hypovolaemia, sepsis, cardiac ischaemia or failure.

Presentation and assessment

Difficulty in ventilating/oxygenating may present with:

Hypoxia (SpO₂ <92%, or PaO₂ <8kPa), cyanosis.
Increasing airway pressures.¹
High, or low-pressure, ventilator alarms.
Evidence of low delivered tidal volume, or low minute-volume alarm.
Audible leak from ventilator circuit, or leak alarm.
Inability to ventilate using self-inflating ambu-bag.
Lack of chest movement or respiratory sounds on auscultation.
Hypercapnia.
Dynamic hyperinflation (next inspiratory cycle starts before last expiratory cycle finished), see p.78.

Where the patient is conscious and/or spontaneously breathing alongside mechanical ventilatory support complications of ventilation may result in:

Agitation, sweating, clamminess.
Increasing respiratory distress, tachypnoea, dyspnoea.

Cardiovascular abnormalities may include:

Cardiac arrest.
Tachycardia, bradycardia, or arrhythmia.
Hypotension.

Evidence of pneumothorax may include:

Tracheal deviation away from affected side.
Absent/diminished breath sounds on affected side.
Hyper-resonant percussion note on affected side.
Subcutaneous emphysema.
Pneumothorax or pneumomediastinum on CXR.

Investigations

ABGs (hypoxia, hypercapnia).
FBC (↑WCC in infection).
CXR (collapse, consolidation, pneumothorax, effusion).
Bronchoscopy (ETT or bronchial obstruction: mucous plug, blood clot, foreign body, extrinsic compression, tumour).
ECG if CVS instability (ischaemia, RV strain).
Chest US (pneumothorax, effusion).
CT chest (if considering anterior/loculated pneumothorax, effusion).

Differential diagnoses

Where there is difficulty in ventilating always consider the possibility of an occluded or semi-occluded airway (see pp.38 and 42).

Indications for fibreoptic bronchoscopy in ventilated patients

To obtain microbiological samples via suction or lavage, particularly if patients are immunocompromised or suspected of having atypical infections.
To localize and control haemoptysis.
Removal of secretions, blood clots, or foreign bodies allowing lung re-expansion.
To examine for strictures, tumours, or tracheobronchial trauma
To assess patency or position of ETT.
To evaluate degree of tracheobronchial trauma following airway burns or smoke inhalation.

Relative contraindications include:

Moderate/severe hypoxia or hypercapnia.
Coagulopathy, SVC obstruction, or other risk of bleeding.
Near-complete tracheal obstruction.
Myocardial ischaemia, arrhythmias, or hypotension.

Immediate management

If there is difficulty in ventilating the patient:

Increase FiO₂ to 100%, pulse oximetry, and capnography.
Airway: check ETT or tracheostomy for position, patency, and presence of cuff leak; exchange of ETT/tracheostomy or re-intubation may be required (see pp.38 and 42).
Check for equipment failure and disconnection; if in doubt switch to self-inflating bag and manually ventilate.
Consider the possibility of the following (treat as appropriate):
- Bronchospasm (bronchodilator therapy, reduce RR and lengthen I:E ratio; p.79)
- Breathing against (‘fighting’) the ventilator (increase sedation/anxiolysis and consider instituting neuromuscular blockade)
- Foreign body, mucous plugs, retained chest secretions, or major collapse of the lung tissue ( pp.34 and 65)
- Pneumothorax (tension or non-tension), tension haemothorax, massive effusion ( pp.80 and 82)
- ARDS ( p.90)
Ventilation parameters may need adjusting:¹
- Increase inspiratory pressure, inspiratory time, or tidal volume if ventilatory volumes are inadequate
- Increase respiratory rate if minute volumes are inadequate despite good tidal volumes
- A trial of ↑ PEEP to find best lung compliance/maintain lung recruitment
- Reduce rate and increase expiratory time if bronchospasm

Where there is haemodynamic instability:

Treat hypotension using fluid and/or inotropes where required
Consider the possibility of the following (treat as appropriate):
- Hypovolaemia ( p.112)
- Sepsis ( p.332)
- Tension pneumothorax ( p.80)
- Cardiac ischaemia, failure, or arrhythmia ( p.122).

Where there is hypoxia despite adequate ventilation:

Increase FiO₂ to 100%; double check this value and switch to alternative supply if concerned.
Consider the possibility of the following—treat as appropriate:
- Endobronchial intubation ( p.26)
- Pneumothorax ( p.80)
- Pleural effusions ( p.82)
- Mucous plugs or retained chest secretions ( p.65)
- Acute pulmonary oedema ( p.86)
- Pulmonary embolism ( p.92)
- ARDS ( p.90)
- Cardiac shunting/ASD
Ventilation parameters may be altered as outlined earlier in box:¹
- Decreasing I:E ratios to 1:1.5, 1:1 (or even less, 2:1) may maximize inspiration and allow gas redistribution with lower pressures
- Tolerate moderate hypercapnia
Consider advanced airway manoeuvres or oxygenation techniques:
- Alveolar recruitment measures ( p.65)
- Bronchoscopy to aid diagnosis or remove secretions
- If lung pathology is unilateral try positioning bad lung uppermost
- Start a neuromuscular blocking agent infusion (e.g. atracurium)
- Prone positioning
- Inhaled nitric oxide or nebulized epoprostenol
- High-frequency oscillatory ventilation (HFOV)
- Extra corporeal membrane oxygenation (ECMO)

Further management

Identify and treat any coexisting/exacerbating infections.
Where possible use assist-controlled or pressure-support ventilation.

Pitfalls/difficult situations

Have a high index of suspicion for tension pneumothorax in patients with cardiovascular collapse.
CXR interpretation can be difficult in supine patients; certain conditions such as anterior pneumothorax or pleural effusion may require additional imaging (CT or US).
Obese patients may require much higher inspiratory pressures and levels of PEEP than expected.
Insert prophylactic chest drains in patients with severe chest trauma who require ventilation.
Minimize intravenous volume replacement in patients who have had major lung surgery.

Complications associated with HFOV

Hypotension: very common at initiation of HFOV (may need aggressive fluid therapy and/or vasopressor support), can also be caused by pneumothorax/air-trapping.
Blocked ETT or secretions (fall in PaO₂, reduced ‘wiggle’, rise in amplitude, rise in PaCO₂); may need suction, bronchoscopy and/or re-intubation.
Pneumothorax (fall in PaO₂, unilateral ‘wiggle’, fall in amplitude, hypotension); will need intercostal drainage ( p.532).
Air trapping/dynamic hyperinflation (gradual fall in PaO₂, hypotension and rise in CVP); try temporary disconnection, or reduce frequency and/or cycle volume.

¹Follow a lung-protective strategy in intubated/ventilated patients where possible (

p.53).

¹Increasing airway pressures will occur if using volume-controlled ventilation; decreasing tidal volumes will occur with pressure-controlled ventilation.

¹Follow a lung-protective strategy where possible (

p.53).