EM · Respiratory failure (type 1 & 2)
Respiratory failure (type 1 and type 2)
Also known as Type 1 respiratory failure · Type 2 respiratory failure · Hypoxaemic respiratory failure · Hypercapnic respiratory failure
Respiratory failure — the type 1 (hypoxaemic) and type 2 (hypercapnic) classification from the arterial blood gas, the oxygen targets (94 to 98 per cent for most, 88 to 92 per cent for the CO2 retainer), the oxygen device ladder with inspired fractions, the mechanism by which excess oxygen worsens the CO2 (the Haldane effect and the loss of hypoxic pulmonary vasoconstriction), and the escalation to non-invasive ventilation (BiPAP for type 2, CPAP for type 1 pulmonary oedema) and invasive ventilation. ACEM-primary, globally tagged.
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Respiratory failure is the end-point of most respiratory emergencies, and its classification into type 1 (hypoxaemic) and type 2 (hypercapnic) on the arterial blood gas is the single most important framework the Fellowship candidate applies at the bedside, because it decides the oxygen target, the device and the ventilatory strategy. The classification is not academic: giving 94 to 98 per cent oxygen to a CO₂ retainer can precipitate a CO₂ narcosis, and missing the transition from a type 1 to a type 2 in a fatiguing patient costs the life. The ABG is the test that makes the call.[1]
Definition and classification
Respiratory failure is the state in which the respiratory system cannot maintain an adequate gas exchange — enough oxygen in, enough carbon dioxide out. The arterial blood gas defines the two types. Type 1 is hypoxaemic: a PaO₂ below 8 kPa (60 mmHg) on room air, with a normal or a low PaCO₂. Type 2 is hypercapnic: a PaCO₂ above 6.5 kPa (50 mmHg), with or without a concurrent hypoxaemia. The distinction drives everything that follows: the oxygen target, the device and the ventilatory support.[1][2]
The type 1 failure arises from a mismatch between the ventilation and the perfusion (the commonest mechanism), from a right-to-left shunt, from a diffusion impairment, or from a low inspired oxygen. The type 2 failure arises from an alveolar hypoventilation — the lungs cannot move enough air to clear the carbon dioxide — from a chronic obstructive pulmonary disease, a neuromuscular weakness, a chest-wall failure, a central respiratory depression (the opioid overdose), or a fatigue that evolves from a severe type 1. [1]
Pathophysiology — why excess oxygen worsens the CO₂
The type 1 failure is, at its core, a ventilation–perfusion mismatch: the blood flows past alveoli that are poorly ventilated (consolidated, oedematous, atelectatic), so it leaves the lungs without picking up enough oxygen. The shunt is the extreme form — the blood bypasses ventilated alveoli entirely, and the hypoxaemia is refractory to the supplemental oxygen. The type 2 failure is a pump failure — the respiratory muscles, the chest wall, or the central drive cannot sustain the minute volume needed to clear the carbon dioxide, so it accumulates, and the bicarbonate rises over time to compensate (the chronic retainer). [1]
The critical mechanism the Fellowship candidate must explain is why excess oxygen worsens the hypercapnia in the retainer. Two effects combine. The Haldane effect: when oxygen binds to the haemoglobin in the lungs, it displaces carbon dioxide from the haemoglobin, increasing the free CO₂ in the blood and therefore the PaCO₂. The loss of the hypoxic pulmonary vasoconstriction: in the normal lung, the poorly ventilated alveoli constrict their local vessels to redirect the blood to the ventilated ones; giving high-flow oxygen relieves this vasoconstriction, so the blood flows back to the poorly ventilated alveoli and picks up more CO₂. A third factor — the loss of the hypoxic ventilatory drive in the chronic retainer — contributes in a minority. [1]
[1]Clinical presentation
The patient with a respiratory failure presents with a dyspnoea, a tachypnoea, an accessory-muscle use, and an inability to speak in full sentences. The hypoxia produces a cyanosis, an agitation, a confusion and an arrhythmia. The hypercapnia produces a headache, a warm flush, a drowsiness, a coarse tremor (the asterixis) and, in the severe case, a CO₂ narcosis and a coma. The exhaustion — a falling respiratory rate, a loss of the accessory-muscle effort, and a drowsiness — is the pre-arrest sign. The transition from a type 1 (hypoxaemic, hyperventilating) to a type 2 (hypercapnic, tiring) is the critical deterioration to recognise. [1]
Differential diagnosis — the causes by type
The causes of each type are distinguished at the bedside and on the ABG. [1]
Type 1 causes (hypoxaemic)
- Pneumonia, pulmonary oedema, PE, asthma, ARDS
- Pneumothorax, interstitial lung disease
- Normal or low CO2; high A-a gradient
- High-flow O2 to 94-98%; CPAP for oedema
Type 2 causes (hypercapnic)
- COPD (commonest), neuromuscular weakness (GBS, MG)
- Opioid overdose, obesity hypoventilation
- Chest wall (kyphoscoliosis), fatigue from severe type 1
- Controlled O2 88-92%; BiPAP for COPD acidosis
Type 1 becoming type 2
- The exhausted asthmatic or the ARDS patient tiring
- CO2 rises from low/normal — a danger sign
- Prepare for invasive ventilation
- The transition is pre-arrest
Opioid overdose (reversible)
- Pinpoint pupils, low RR, drowsy
- Naloxone 400 mcg IV — titrated, not a full reversal
- Reverses the type 2 immediately
- Check for co-ingestants
Investigations and the ABG
The arterial blood gas is the defining test. It provides the PaO₂, the PaCO₂, the pH, the bicarbonate and the base excess, and from these the type of the failure and the acid-base status. The A-a gradient (the difference between the alveolar and the arterial oxygen tension) distinguishes a lung problem (a high gradient — the V/Q mismatch, the shunt, the diffusion impairment) from a pump problem (a normal gradient — the hypoventilation from the brain, the neuromuscular weakness or the chest wall). The chest radiograph shows the cause (the consolidation, the oedema, the pneumothorax, the hyperinflation). The bloods (the full blood count, the urea and electrolytes, the troponin, the toxicology) and the lactate seek the precipitant and the sepsis. [1]
The oxygen targets and the ABG criteria
Immediate management — the framework
Assess the airway, the breathing and the circulation. Secure the airway with adjuncts if the patient is obtunded. Give the oxygen by the type: the type 1 gets a high-flow oxygen to a target of 94 to 98 per cent; the type 2 gets a controlled oxygen via a Venturi mask (24 to 28 per cent, titrated to 88 to 92 per cent).[1][9] Treat the cause in parallel — nebulised salbutamol 5 mg for the bronchospasm, furosemide 40 to 80 mg intravenously and a nitrate for the oedema, the antibiotics for the pneumonia, the naloxone for the opioid.
[1] [1]The oxygen devices deliver a graded inspired fraction: the nasal cannulae (2 to 4 L/min, ~24 to 35 per cent), the simple face mask (5 to 10 L/min, ~35 to 50 per cent), the non-rebreather reservoir mask (10 to 15 L/min, ~60 to 90 per cent — the highest concentration available in the emergency department), and the Venturi mask (colour-coded valves delivering a precise, fixed FiO₂ of 24 to 60 per cent — the device of choice for the CO₂ retainer, because the FiO₂ is controlled and repeatable).[1]
The escalation — NIV and invasive ventilation
The non-invasive ventilation is the bridge between the oxygen and the intubation, and the Fellowship candidate must know when to apply it. The BiPAP (bilevel positive airway pressure — an inspiratory pressure support plus an expiratory pressure) is the first-line ventilatory support for the type 2 respiratory failure from a COPD exacerbation with a respiratory acidosis (a pH under 7.35); the evidence is among the strongest in emergency medicine for its mortality reduction.[6][7] The CPAP (continuous positive airway pressure) is the first-line support for the type 1 respiratory failure from a cardiogenic pulmonary oedema — it recruits the alveoli and reduces the preload and the afterload. The patient who cannot tolerate the mask, who is obtunded (a CO₂ narcosis), who is failing the NIV, or who needs an airway protection is intubated and ventilated. The acute respiratory distress syndrome (ARDS) — the severe, refractory type 1 from a non-cardiogenic pulmonary oedema — needs a lung-protective invasive ventilation with a low tidal volume (6 mL per kilogram of the ideal body weight) and a permissive hypercapnia, and may need a prone positioning and an extracorporeal support.[2]
The opioid-induced type 2 — a special case
The opioid overdose produces a type 2 respiratory failure by a central respiratory depression — a slow, shallow breathing with a pinpoint pupil and a drowsiness. The naloxone 400 micrograms intravenously, titrated to the respiratory rate (not to the full consciousness — the goal is to reverse the hypoventilation, not to precipitate an acute withdrawal), is the treatment. A co-ingestant is sought, and the patient is observed for the re-sedation (the naloxone's half-life is shorter than most opioids, so an infusion or a repeat dosing may be needed). [1]
Complications and pitfalls
The complications are the cardiac arrest from the untreated hypoxia, the CO₂ narcosis from the excess oxygen, the pneumothorax from the positive-pressure ventilation, and the infection and the barotrauma of the invasive ventilation. The pitfalls are the inverse of the framework: giving 94 to 98 per cent oxygen to a known CO₂ retainer; not escalating to the NIV when the acidosis persists; missing the opioid cause of a type 2; not recognising the transition from a type 1 to a type 2 in the exhausted patient (the rising CO₂ is the alarm); and using a high FiO₂ device without a target saturation. [1]
Prognosis and disposition
The prognosis depends on the cause and the severity. The COPD exacerbation with a pH under 7.25 has a high mortality without the NIV; the ARDS carries a mortality of 30 to 40 per cent; the opioid overdose is fully reversible with the naloxone. The disposition follows the severity: the ward for the improving, the high-dependency for the NIV-dependent, the intensive care for the invasively ventilated. [1]
Special populations
The COPD patient is the classic type 2 retainer — the target is 88 to 92 per cent, and the BiPAP is the first-line ventilatory support for the acidotic exacerbation. The neuromuscular patient (the Guillain-Barré, the myasthenia) develops a type 2 from the weakness and may need an early NIV or an intubation, guided by the falling vital capacity and the rising CO₂. The obesity hypoventilation patient is a chronic type 2 retainer on a home BiPAP. The pregnant patient needs a higher baseline PaO₂ (the fetus is sensitive to the hypoxia) and the supine position is avoided. The elderly have less reserve and decompensate faster. [1]
Type 1 respiratory failure — the mechanisms in depth
The type 1 failure is a failure of oxygenation with a preserved or augmented ventilation, so the PaCO₂ is normal or low (the hyperventilation of the hypoxic drive keeps it down). Four physiological mechanisms produce the hypoxaemia, and the Fellowship candidate must be able to separate them at the bedside, because the response to the supplemental oxygen distinguishes them: [1]
V/Q mismatch
- The commonest mechanism — blood past underventilated alveoli
- Pneumonia, oedema, atelectasis, COPD, asthma
- Corrects with supplemental O₂ (high FiO₂)
- A-a gradient raised; PaCO₂ normal/low
Shunt
- The extreme — blood bypasses ventilated alveoli entirely
- ARDS, lobar pneumonia, pulmonary AV malformation, hepatopulmonary syndrome
- Refractory to O₂ — does NOT correct with 100% FiO₂
- The defining test: shunt = refractory hypoxaemia
Diffusion impairment
- Thickened alveolar-capillary membrane
- Interstitial lung disease, pulmonary fibrosis, pulmonary oedema
- Improves with O₂; worsens with exercise (low transit time)
- Less common as an isolated mechanism
Low inspired O₂ / hypoventilation
- Altitude, low ambient FiO₂, rebreathing
- Pure hypoventilation gives a NORMAL A-a gradient
- PaCO₂ rises proportionally
- Corrects by restoring the FiO₂ or the ventilation
Type 2 respiratory failure — the mechanisms in depth
The type 2 failure is a failure of ventilation — the pump cannot move enough air to clear the carbon dioxide, so the PaCO₂ climbs above 6.5 kPa (50 mmHg) and the pH falls (the respiratory acidosis), unless the kidney has had time to retain the bicarbonate (the chronic retainer with a compensated, near-normal pH). The mechanism is alveolar hypoventilation, and the causes divide into the lung (the airway obstruction — COPD, asthma), the pump (the chest wall — kyphoscoliosis, the flail chest, the obesity), the muscle (the neuromuscular weakness — Guillain-Barré, myasthenia, the motor neuron disease), and the controller (the central depression — the opioid, the benzodiazepine, the brainstem stroke). The A-a gradient is normal in the pure pump or controller failure — the lungs are fine, they are just not being ventilated. [1]
Airway obstruction
- COPD (the classic), severe asthma tiring
- V/Q mismatch coexists; A-a gradient often raised
- BiPAP first-line for the COPD with a pH under 7.35
- Bronchodilator + steroid + the antibiotic if Anthonisen-positive
Central depression
- Opioid, benzodiazepine, alcohol, brainstem stroke
- Pinpoint pupil, low RR, drowsy — a normal A-a gradient
- Reversible: naloxone 400 mcg IV, titrated
- Watch for re-sedation — the naloxone half-life is short
Neuromuscular weakness
- Guillain-Barré, myasthenic crisis, MND, poliomyelitis
- Falling vital capacity and the rising CO₂ are the triggers
- Early NIV; intubate when the VC under 15 mL/kg or the cough fails
- Check the FVC, not the SpO₂, to time the airway
Chest wall / obesity
- Kyphoscoliosis, flail chest, obesity hypoventilation
- A restrictive pattern; the work of breathing is high
- BiPAP, often long-term; treat the precipitant
- The obesity hypoventilation patient is a chronic BiPAP retainer
The oxygen device ladder — the FiO₂ by device
The oxygen is delivered by a graded ladder of devices, each with a characteristic inspired fraction and an indication. The Fellowship candidate must know the FiO₂ of each device, because the choice of the device is the first therapeutic decision in the respiratory failure, and the wrong device (the high-flow mask on a retainer) can kill. [1]
The oxygen escalation ladder for the type 1 (hypoxaemic) failure
Nasal cannulae (2–6 L/min)
~24–44 per cent FiO₂. Low-flow, variable, comfortable. Adds ~3–4 per cent FiO₂ per litre. Use for the mild hypoxaemia; useless for the mouth-breather and the severe failure.
Simple face mask (5–10 L/min)
~35–50 per cent FiO₂. Needs a minimum 5 L/min to clear the dead-space CO₂. Cannot control the FiO₂ precisely — never for the retainer.
Non-rebreather reservoir mask (10–15 L/min)
~60–90 per cent FiO₂ — the highest available in the ED. The reservoir bag must stay at least two-thirds full. The device for the severe type 1 and the pre-intubation bridge.
High-flow nasal cannula (30–60 L/min)
Delivers a precisely controlled FiO₂ (21–100 per cent) at up to 60 L/min with heated, humidified gas. Reduces the work of breathing, washes out the dead space, provides a small PEEP. The FLORALI evidence supports it in the hypoxaemic failure.
CPAP (continuous positive airway pressure)
A single positive pressure (5–10 cmH₂O) throughout the cycle. The first-line NIV for the cardiogenic pulmonary oedema (recruits the alveoli, drops the preload and the afterload). Not a ventilatory support — it adds no pressure support.
NIV / BiPAP (bilevel)
IPAP 10–20 + EPAP 4–6 cmH₂O. The pressure support augments the tidal volume, so it supports the ventilation (clears the CO₂). The first-line for the acidotic COPD type 2.
Invasive mechanical ventilation
The intubation with the RSI and the lung-protective ventilation (6 mL/kg ideal body weight, plateau pressure under 30 cmH₂O). The end-point for the failing, the obtunded (GCS under 8), and the patient who cannot protect the airway.
Controlled oxygen in the CO₂ retainer — the Austin evidence
The single most important lesson for the type 2 retainer is to give the controlled oxygen, never the high-flow. The high-flow oxygen worsens the hypercapnia by the Haldane effect, the loss of the hypoxic pulmonary vasoconstriction, and (in a minority) the loss of the hypoxic ventilatory drive — and this is not a theoretical risk. [1]
Austin 2010 (BMJ) — the prehospital titrated oxygen in COPD
BMJ
PMID 20959284
Key finding
A randomised controlled trial of 405 patients with the suspected acute COPD exacerbation in the prehospital setting, comparing the titrated oxygen (to a saturation of 88 to 92 per cent) against the standard high-flow oxygen. The titrated group had a lower mortality (a relative risk reduction of around 78 per cent for the death or the respiratory failure).
Practice change
Do NOT give the high-flow oxygen to the suspected COPD patient in the prehospital or the emergency setting — the titrated 88 to 92 per cent target from the first contact reduces the mortality. The controlled oxygen via the Venturi mask is the default.
NIV (BiPAP) for the type 2 — the protocol, the monitoring, the evidence
The BiPAP is the first-line ventilatory support for the acidotic COPD exacerbation (a pH 7.25 to 7.35, a PaCO₂ over 6.5 kPa). The evidence for its mortality reduction is among the strongest in the whole of the emergency and the respiratory medicine, and the Fellowship candidate must know the protocol, the settings, the monitoring and the failure criteria. [1]
The BiPAP protocol for the acidotic COPD exacerbation
1 — Start within 60 minutes of the acidotic ABG
The earlier the better — the Plant data showed the ward-based NIV started within the hour reduced the mortality. Do NOT wait for the ICU bed.
2 — The initial settings
EPAP 4 to 5 cmH₂O (the expiratory pressure, the PEEP equivalent); IPAP 10 to 15 cmH₂O (the inspiratory pressure support). The pressure support (IPAP minus EPAP) is the driving pressure for the tidal volume.
3 — Titrate up
Increase the IPAP by 2 to 5 cmH₂O increments every 10 to 15 minutes toward an IPAP of 15 to 20 (the target tidal volume 6 to 8 mL/kg, the target pH correction). The EPAP is left at 4 to 6 unless the oxygenation demands more.
4 — The controlled oxygen
Bleed the oxygen into the circuit at 1 to 2 L/min (or the integrated FiO₂ control), targeting the SpO₂ 88 to 92 per cent — NOT 94 to 98 per cent. The NIV delivers the ventilation; the oxygen is the adjunct.
5 — Recheck the ABG at 1, 2 and 4 hours
The pH should rise and the PaCO₂ should fall within the first hour. A persistently low pH at 1 to 4 hours predicts the failure and the need for the intubation.
6 — Wean as the patient recovers
Reduce the IPAP, then the hours on the mask (the daytime use first, then the nocturnal), over 24 to 72 hours. The acute COPD exacerbation usually needs 2 to 4 days.
Plant 2000 (Lancet) — the early ward NIV in the acidotic COPD
Lancet
PMID 10859037
Key finding
A multicentre randomised controlled trial of 236 patients with the COPD exacerbation and a pH 7.25 to 7.35, comparing the early NIV on the general respiratory ward against the standard care. The NIV reduced the need for the intubation (from 27 to 15 per cent), the in-hospital mortality (from 20 to 10 per cent) and the length of the stay, without the need for the ICU admission.
Practice change
The BiPAP started within 60 minutes of the acidotic ABG, on the ward or in the ED, is the standard of care for the acidotic COPD. It is the single best evidence-based use of the NIV.
Ram 2004 (Cochrane) — the NIV for the COPD exacerbation
Cochrane Database of Systematic Reviews
PMID 15266518
Key finding
A meta-analysis of 14 randomised trials of the NIV for the acidotic COPD exacerbation. The NIV reduced the mortality (the number-needed-to-treat around 10), the need for the intubation, the treatment failure and the length of the hospital stay, with a low rate of complications.
Practice change
The NIV is the most evidence-supported respiratory intervention of the last 30 years for the acidotic COPD — the mortality benefit is robust and the number-needed-to-treat is small.
Brochard 1995 (NEJM) — the NIV in the COPD exacerbation
New England Journal of Medicine
PMID 7651472
Key finding
A randomised controlled trial of 85 patients with the severe COPD exacerbation, comparing the NIV against the standard care. The NIV reduced the need for the intubation (from 74 to 26 per cent), the complications (from 48 to 16 per cent), the in-hospital mortality (from 29 to 9 per cent) and the length of the stay.
Practice change
The landmark trial that established the NIV as the first-line ventilatory support for the COPD exacerbation, reducing the intubation rate by two-thirds.
CPAP for the cardiogenic pulmonary oedema — the type 1 special case
The cardiogenic pulmonary oedema produces a type 1 (hypoxaemic) failure by the hydrostatic flooding of the alveoli. The CPAP is the first-line NIV: the continuous positive pressure recruits the flooded alveoli, increases the functional residual capacity, drops the left ventricular preload (by the increased intrathoracic pressure) and the afterload (by the reduced transmural pressure), and so improves both the oxygenation and the cardiac output. The BiPAP is an alternative but carries a theoretical concern of the increased intrathoracic pressure swings precipitating the myocardial ischaemia — the CPAP is the default. [1]
[1]The transition from type 1 to type 2 — recognising the fatiguing patient
The most dangerous deterioration in the emergency department is the transition from a type 1 to a type 2 failure — the patient who was hyperventilating (clearing the CO₂) to compensate for the hypoxia now fatigues, the minute volume falls, and the PaCO₂ begins to rise. A rising PaCO₂ in a previously type-1 patient is the pre-arrest sign — the respiratory muscles have failed and the next step is the ventilatory support, not the increased oxygen. [1]
[1] [1]The A-a gradient — the lung vs the pump
The alveolar-arterial (A-a) gradient is the calculation that separates the lung problem (a high gradient) from the pump or the controller problem (a normal gradient). The alveolar oxygen (PAO₂) is estimated from the alveolar gas equation, and the arterial oxygen (PaO₂) is measured on the ABG; the difference is the gradient. A normal A-a gradient with a hypoxaemia points to the pure hypoventilation (the opioid, the neuromuscular weakness, the chest wall), because the lungs are healthy — they are just not being ventilated. A high gradient points to the V/Q mismatch, the shunt, or the diffusion impairment (the lung pathology). [1]
High A-a gradient
- A lung problem — V/Q mismatch, shunt, diffusion
- Pneumonia, PE, ARDS, oedema, ILD, asthma
- The hypoxaemia with a normal or a low CO₂
- Treat the lung; the oxygen, the CPAP, the ventilation
Normal A-a gradient
- A pump or controller problem — pure hypoventilation
- Opioid, neuromuscular weakness, chest wall, obesity
- The hypoxaemia with a high CO₂ (the type 2)
- Corrects by restoring the ventilation or the FiO₂
The calculation
- PAO₂ = FiO₂ × (Patm − PH₂O) − PaCO₂/R
- On room air: PAO₂ ≈ 150 − PaCO₂/0.8 ≈ 100 mmHg
- A-a gradient = PAO₂ − PaO₂; normal under 15 mmHg (under 25 in the elderly)
- Rises with age: ~ (age/4) + 4 mmHg
ARDS — the severe, refractory type 1
The acute respiratory distress syndrome (ARDS) is the extreme of the type 1 failure — a diffuse, non-cardiogenic pulmonary oedema from an inflammatory injury (the sepsis, the pneumonia, the trauma, the aspiration) that produces a severe shunt refractory to the oxygen. The Berlin definition classifies it by the PaO₂/FiO₂ ratio (the mild 200 to 300, the moderate 100 to 200, the severe under 100, on the PEEP of 5 or more), and the 2024 global definition added the requirement of the chest imaging (the bilateral opacities) and the exclusion of the hydrostatic oedema. The management is the lung-protective invasive ventilation with the low tidal volume and the permissive hypercapnia, the prone positioning for the severe, and the extracorporeal support for the refractory. [1]
ARDSnet 2000 (NEJM) — the low tidal volume ventilation
New England Journal of Medicine
PMID 10793162
Key finding
A landmark randomised controlled trial of 861 patients with the ARDS, comparing the ventilation with the low tidal volume (6 mL/kg of the ideal body weight, the plateau pressure under 30 cmH₂O) against the traditional tidal volume (12 mL/kg). The low tidal volume reduced the mortality from 40 to 31 per cent and increased the days off the ventilator.
Practice change
The lung-protective ventilation (6 mL/kg IBW, plateau pressure under 30) is the single most evidence-supported intervention for the ARDS. The intubated respiratory failure patient with the ARDS must be ventilated this way from the first breath.
Guérin 2013 (NEJM) — the prone positioning in the severe ARDS
New England Journal of Medicine
PMID 23688302
Key finding
A multicentre randomised controlled trial of 466 patients with the severe ARDS (a PaO₂/FiO₂ under 150), comparing the early and the prolonged prone positioning (at least 16 hours per day) against the supine. The prone positioning reduced the 28-day and the 90-day mortality (from 32 to 16 per cent at 28 days).
Practice change
The prone positioning for at least 16 hours a day is the standard of care for the severe ARDS (PaO₂/FiO₂ under 150) within the first 24 to 48 hours of the invasive ventilation. It is labour-intensive but life-saving.
Bellani 2016 (JAMA) — the LUNG SAFE ARDS epidemiology
JAMA
PMID 26903337
Key finding
A prospective observational study of 29 144 patients across 459 ICUs in 50 countries (the LUNG SAFE study). The ARDS was present in 10 per cent of the ICU admissions and 23 per cent of the mechanically ventilated patients; the in-hospital mortality ranged from 34 per cent (the mild) to 46 per cent (the severe). The ARDS was under-recognised (the clinicians identified only 51 per cent of the cases) and the lung-protective ventilation was under-used.
Practice change
The ARDS is common, lethal (a third die) and under-recognised at the bedside. The Fellowship candidate must actively screen for it (the PaO₂/FiO₂ ratio) and apply the lung-protective ventilation early — the recognition gap is the killing gap.
The intubation checklist for the respiratory failure
When the NIV fails, the patient obtunds, or the airway is threatened, the intubation is the end-point. The Fellowship candidate must prepare in parallel, not in sequence — the respiratory arrest patient has minutes. [1]
The RSI for the respiratory failure — the parallel preparation
1 — Recognise the need
The GCS under 8, the failure of the NIV (a persistent pH under 7.25, a rising CO₂ at 1 to 4 hours), the exhaustion (a falling RR, a drowsiness), the refractory hypoxaemia (a SpO₂ under 90 on the high-flow), the inability to clear the secretions.
2 — The pre-oxygenation
15 L/min via the non-rebreather for 3 minutes (or 8 vital-capacity breaths), or the HFNC. The target is the denitrogenation of the functional residual capacity — the apnoeic oxygenation buys the time.
3 — The haemodynamics
The induction (the propofol, the fentanyl, the midazolam) drops the blood pressure; the positive pressure drops the venous return. Resuscitate first; have the vasopressor (the metaraminol, the noradrenaline) drawn up. The peri-intubation cardiac arrest is the most common serious complication.
4 — The drugs
The induction (the propofol 1 to 2 mg/kg, or the ketamine 1 to 2 mg/kg if the hypotensive), the paralytic (the suxamethonium 1.5 mg/kg, or the rocuronium 1 mg/kg). The ketamine is the safer choice in the hypotensive and the bronchospastic (asthma).
5 — The post-intubation
Confirm with the waveform capnography (the sustained CO₂). Set the lung-protective settings: the tidal volume 6 mL/kg IBW, the respiratory rate 12 to 20 (higher for the asthma to keep the permissive hypercapnia), the FiO₂ to the target, the PEEP 5 (higher for the ARDS). The sedation and the analgesia (the propofol or the midazolam + the fentanyl).
6 — The cause and the disposition
Treat the precipitant (the antibiotics, the bronchodilator, the diuretic, the naloxone infusion). Transfer to the ICU. Send the post-intubation ABG and the chest radiograph.
NIV failure predictors and the ROX score
For the high-flow nasal cannula in the type 1 failure, the ROX score (developed and validated by Roca and colleagues) predicts the success or the failure of the HFNC and guides the decision to intubate. The score combines the SpO₂/FiO₂ ratio, the respiratory rate, and the accessory-muscle use at 2, 6 and 12 hours; a low score predicts the intubation need and prompts the escalation rather than the prolonged, unsuccessful HFNC trial. The Fellowship candidate must recognise that the HFNC and the NIV are bridges, not destinations — the patient who is failing must be intubated without delay, and the failure-to-intubate delay is the most preventable cause of the death. [1]
[1]The precipitant-focused treatment — treat the cause
The oxygen and the ventilation buy the time; the treatment of the cause cures the failure. The precipitant must be sought and treated in parallel with the oxygen, from the first contact: [1]
Pneumonia (the type 1)
- The commonest cause of the infective type 1
- The CURB-65 or the PSI to grade the severity
- The antibiotics within the hour (the 3C: the ceftriaxone + the clarithromycin for the CAP)
- Oxygen 94 to 98%; HFNC or the CPAP if the severe
COPD exacerbation (the type 2)
- The controlled oxygen 88 to 92%; the BiPAP for the pH under 7.35
- The salbutamol 5 mg + the ipratropium 500 mcg nebs
- The prednisolone 30 to 40 mg for 5 days
- The antibiotic if the Anthonisen type 1 or the purulent type 2
Cardiogenic pulmonary oedema (the type 1)
- The CPAP 5 to 10 cmH₂O is the first-line NIV
- The furosemide 40 to 80 mg IV; the GTN infusion if the hypertensive
- The cause (the ischaemia, the AF, the valve, the renal) — investigate and treat
- The NIV wean as the diuresis works
Opioid overdose (the type 2)
- The pinpoint pupil, the low RR, the drowsiness
- The naloxone 400 mcg IV, titrated to the RR (not the wakefulness)
- The infusion if the long-acting opioid; the observation for the re-sedation
- The co-ingestant and the cause (the naloxone does not reverse the benzo)
PE (the type 1, occasionally type 2)
- The Wells score, the D-dimer, the CTPA
- The anticoagulation (the LMWH); the thrombolysis if the massive (the shock, the RV strain)
- The large PE may produce a type 2 from the dead-space increase
- TheABCDE + the oxygen 94 to 98%
Asthma (the type 1, becoming the type 2)
- The salbutamol 5 mg + the ipratropium 500 mcg, repeated
- The hydrocortisone 100 mg IV; the magnesium 2 g over 20 min
- A normal CO₂ in the severe asthma = the fatigue = the pre-arrest
- The ketamine-based RSI if the intubation is needed
The pitfalls revisited — the high-yield exam traps
[1] [1] [1] [1]Evidence and regional guidelines
The contemporary framework is the British Thoracic Society emergency oxygen guideline[1] and the global ARDS definition.[2] The oxygen targets (94 to 98 per cent for most, 88 to 92 per cent for the retainer) and the NIV indications follow the BTS, the ARC and the local respiratory pathways. The drug and the device choices are global; the exact FiO₂ delivery and the NIV escalation thresholds are local.
ANZ practice note. The oxygen targets and the NIV escalation follow the BTS framework via the ANZ/ARC and the local respiratory pathways; a COPD exacerbation with a pH under 7.35 receives a BiPAP, a pulmonary oedema receives a CPAP, and the CO₂ retainer is targeted to 88 to 92 per cent from the arrival, not 94 to 98 per cent. [1]
Exam pearls
- Type 1 = hypoxaemic (PaO₂ under 8 kPa); Type 2 = hypercapnic (PaCO₂ over 6.5 kPa).
- The CO₂ retainer target is 88 to 92 per cent, not 94 to 98 per cent — excess O₂ worsens the CO₂ by the Haldane effect and the loss of the hypoxic vasoconstriction.
- BiPAP for the COPD type 2 with a pH under 7.35 — the strongest NIV evidence.
- CPAP for the cardiogenic pulmonary oedema (type 1).
- Venturi mask for the precise FiO₂ in the retainer (24 to 60 per cent, colour-coded).
- A rising CO₂ in a type-1 patient = fatigue = pre-arrest = escalate to ventilation.
- Naloxone 400 micrograms IV, titrated, for the opioid-induced type 2.
- The A-a gradient distinguishes a lung problem (high gradient) from a pump problem (normal gradient). [1]
Exam practice
SAQ — Acute-on-chronic type 2 respiratory failure from a COPD exacerbation
10 minutes · 10 marks
A 68-year-old man with known COPD presents with worsening dyspnoea over three days, now with RR 32, SpO2 86 per cent on the high-flow oxygen given by the ambulance, GCS 14, using the accessory muscles. ABG: pH 7.28, PaCO2 8.2 kPa, PaO2 7.6 kPa, HCO3 32 mmol per litre.
SAQ — Severe acute asthma with the rising PaCO2 — the fatiguing patient
10 minutes · 10 marks
A 25-year-old woman with the severe acute asthma presents with RR 38, SpO2 90 per cent on 15 L oxygen, unable to speak in full sentences, with a silent chest. ABG: pH 7.25, PaCO2 6.8 kPa (rising from 4.2 kPa an hour ago), HCO3 22 mmol per litre.
Red flags
[1]References
- [1]O'Driscoll BR, Howard LS, Earis J, et al. BTS guideline for oxygen use in adults in healthcare and emergency settings Thorax, 2017.PMID 28507176
- [2]Matthay MA, Arabi YM, Siegel ER, et al. A New Global Definition of Acute Respiratory Distress Syndrome Am J Respir Crit Care Med, 2024.PMID 37487152
- [3]The Acute Respiratory Distress Syndrome Network, Brower RG, Matthay MA, et al. 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.PMID 10793162
- [4]Guérin C, Reignier J, Richard JC, et al. Prone positioning in severe acute respiratory distress syndrome N Engl J Med, 2013.PMID 23688302
- [5]Bellani G, Laffey JG, Pham T, et al. Epidemiology, Patterns of Care, and Mortality for Patients With Acute Respiratory Distress Syndrome in Intensive Care Units in 50 Countries JAMA, 2016.PMID 26903337
- [6]Brochard L, Mancebo J, Wysocki M, et al. Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease N Engl J Med, 1995.PMID 7651472
- [7]Plant PK, Owen JL, Elliott MW. Early use of non-invasive ventilation for acute exacerbations of chronic obstructive pulmonary disease on general respiratory wards: a multicentre randomised controlled trial Lancet, 2000.PMID 10859037
- [8]Ram FSF, Picot J, Lightowler J, Wedzicha JA. Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease Cochrane Database Syst Rev, 2004.PMID 15266518
- [9]Austin MA, Wills KE, Blizzard L, Walters EH, Wood-Baker R. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial BMJ, 2010.PMID 20959284
- [10]Frat JP, Thille AW, Mercat A, et al. High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure N Engl J Med, 2015.PMID 25981908