RespiratoryTier 1Disease (DEADMAN)

Respiratory failure - acute

Description

Failure of the respiratory system to achieve adequate gas exchange, developing over minutes to hours

	Type 1 (hypoxaemic)	Type 2 (hypercapnic/ventilatory)
Definition	PaO2 <60 mmHg on room air	PaCO2 >45 mmHg with pH <7.35
Problem	Oxygenation - V/Q mismatch, shunt	Ventilation - the pump has failed
A-a gradient	Raised	Normal if pure hypoventilation; raised if lung disease too
Prototype	Pneumonia, ARDS, pulmonary oedema, PE	COPD exacerbation, opioid overdose, neuromuscular disease

Expected A-a gradient = (Age/4) + 4 (on room air)
*A hypercapnic patient with a raised A-a gradient has both a lung problem and a pump problem*

Acute vs acute-on-chronic - decided by pH and bicarbonate

	pH	HCO3-	Base excess
Acute	Low	Normal	Normal
Chronic (compensated)	Normal	High	High
Acute-on-chronic	Low	High	High

Rule of thumb: acute CO2 rise increases HCO3- by ~1 mmol/L per 10 mmHg; chronic by ~4 mmol/L per 10 mmHg

Epidemiology

The commonest reason for ICU admission and for medical emergency team activation
COPD exacerbation is the commonest cause of acute hypercapnic failure in Australian practice
Pneumonia and cardiogenic pulmonary oedema dominate hypoxaemic failure
In-hospital mortality of acidotic hypercapnic COPD failure ~10%; ~25-40% at 1 year
ARDS mortality ~35-45% despite lung-protective ventilation

Aetiopathogenesis

Five mechanisms of hypoxaemia - and how to tell them apart

Mechanism	A-a gradient	Responds to O2?	Example
Hypoventilation	Normal	Yes	Opioids, neuromuscular, obesity
V/Q mismatch	Raised	Yes	COPD, asthma, PE, pneumonia - commonest
Shunt	Raised	*No/poorly*	Consolidation, ARDS, pulmonary oedema, PFO, AVM
Diffusion limitation	Raised	Yes	ILD, emphysema (mainly on exertion)
Low inspired PO2	Normal	Yes	Altitude

*Hypoxaemia that does not correct with high-flow oxygen = shunt*
Low mixed venous O2 (shock, anaemia, low output) amplifies all of the above

Causes of type 2 failure - localise the failure along the pump

Won't breathe (central drive) - opioids, benzodiazepines, sedatives, brainstem stroke, raised ICP, encephalitis, central hypoventilation, excess O2 in chronic CO2 retention
Can't breathe (neuromuscular) - Guillain-Barre, myasthenic crisis, motor neurone disease, muscular dystrophy, phrenic palsy, high cervical injury, botulism, critical illness neuromyopathy
- Electrolytes: hypokalaemia, hypophosphataemia, hypomagnesaemia
Chest wall / pleura - kyphoscoliosis, obesity hypoventilation, flail chest, circumferential burns, massive effusion, tension pneumothorax, abdominal compartment syndrome
Airway/lung (increased load) - COPD, severe asthma, bronchiectasis, upper airway obstruction

Why oxygen causes hypercapnia in COPD

1. Loss of hypoxic pulmonary vasoconstriction -> worsened V/Q matching -> inc dead space (the dominant mechanism)

2. Haldane effect - oxygenated Hb binds less CO2, releasing it into plasma

3. Small reduction in hypoxic respiratory drive

Hence target SpO2 88-92% in anyone at risk of hypercapnia

What kills

Type 1: tissue hypoxia -> lactic acidosis, arrhythmia, multi-organ failure
Type 2: respiratory acidosis -> CO2 narcosis, arrhythmia; and respiratory muscle fatigue -> apnoea
- *Exhaustion, not the number on the gas, is the reason to intubate*

Diagnosis

Recognise before the gas

Respiratory rate is the earliest and most neglected vital sign - tachypnoea precedes deterioration by hours
Work of breathing: accessory muscles, tracheal tug, intercostal recession, abdominal paradox (diaphragm fatigue), inability to speak in sentences, tripod position
Hypoxaemia: agitation, confusion, cyanosis (needs >50 g/L deoxygenated Hb - unreliable in anaemia), tachycardia
Hypercapnia: flapping tremor, bounding pulse, warm peripheries, headache, confusion, drowsiness, papilloedema
*A falling respiratory rate with a rising CO2 in a distressed patient is peri-arrest*

ABG - do it, and interpret in order

1. pH - acidaemic or alkalaemic?

2. PaCO2 - respiratory contribution

3. HCO3-/base excess - metabolic contribution and chronicity

4. PaO2 and the A-a gradient (interpreted against the FiO2)

5. Anion gap and lactate

P/F ratio (PaO2/FiO2) - severity of hypoxaemic failure; <300 mild, <200 moderate, <100 severe ARDS
Venous gas: pH and HCO3- track arterial well; PvCO2 is a good screen (normal excludes hypercapnia); venous PO2 is useless**

Establish the cause

CXR - consolidation, oedema, pneumothorax, effusion, hyperinflation
ECG, troponin, BNP - cardiac cause
Bedside ultrasound - B-lines (oedema), consolidation, effusion, pneumothorax (absent lung sliding), RV dilatation (PE)
FBC, UEC, CRP, cultures, CTPA if PE suspected
Toxicology, drug chart - opioids, benzodiazepines
Neuromuscular: FVC (not spirometry ratio), SNIP, bulbar assessment

Neuromuscular respiratory failure - do not wait for the ABG

*The ABG stays normal until immediately before arrest*
Serial FVC is the monitoring test
- FVC <20 mL/kg, MIP <30 cmH2O, MEP <40 cmH2O = "20/30/40 rule" -> ICU and likely intubation
- A fall in FVC >30% from supine to erect indicates diaphragmatic weakness
Bulbar involvement, weak cough, secretion retention -> NIV is often inappropriate; intubate

ARDS - Berlin criteria

Within 1 week of a known insult
Bilateral opacities not fully explained by effusion, collapse or nodules
Not fully explained by cardiac failure or fluid overload
P/F <=300 with PEEP/CPAP >=5

Management

1. Oxygen - a drug with a dose and a target

Population	Target SpO2
Most acutely unwell adults	92-96%
At risk of hypercapnia - COPD, OHS, neuromuscular, kyphoscoliosis, CF, bronchiectasis	88-92%

Escalate: nasal prongs -> Hudson -> Venturi (for controlled FiO2 in COPD) -> non-rebreather -> HFNO -> NIV -> intubation
*Never withhold oxygen from a hypoxaemic patient for fear of CO2 retention - treat the hypoxia and monitor the gas*
High-flow nasal oxygen (HFNO) - heated, humidified, up to 60 L/min
- Provides washout of nasopharyngeal dead space, modest PEEP, precise FiO2, better comfort and secretion clearance
- First-line for acute hypoxaemic (type 1) failure - reduced intubation vs conventional O2 (FLORALI)
- Monitor the ROX index (SpO2/FiO2 divided by RR); a low or falling value predicts HFNO failure - do not let it delay intubation**

2. Treat the cause in parallel

Antibiotics for pneumonia, bronchodilators + steroid for COPD/asthma, diuretic + nitrate for pulmonary oedema, anticoagulation for PE, naloxone for opioids, decompression for pneumothorax, drainage for effusion, correct electrolytes

3. Non-invasive ventilation

### Indications - the evidence is not equal

Indication	Strength
Acute hypercapnic COPD exacerbation with pH <7.35 and PaCO2 >45	*Strongest evidence* - dec mortality, dec intubation, dec length of stay, dec nosocomial infection
Cardiogenic pulmonary oedema (CPAP or bilevel)	Strong - dec intubation, dec dyspnoea
Acute-on-chronic hypercapnia in OHS, neuromuscular, chest wall disease	Strong
Post-extubation failure prevention in high-risk patients	Moderate
Immunocompromised with hypoxaemic failure	Moderate - avoids intubation-associated infection
De novo hypoxaemic failure / pneumonia	*Weak - high failure rate; HFNO usually preferred*

Start NIV early - within the first hour of a persisting acidosis after optimal medical therapy
*NIV is appropriate even at pH 7.20-7.25 in an alert, cooperative COPD patient*, in an area able to escalate
Assess response at 1-2 h: pH, PaCO2, RR, conscious state. Failure to improve = escalate, do not persist
Set a ceiling of care decision before starting - is NIV the ceiling, or a bridge?

### Contraindications

Absolute: respiratory or cardiac arrest, inability to protect the airway, inability to fit a mask, facial trauma/burns/recent upper airway or facial surgery, untreated pneumothorax, fixed upper airway obstruction
Relative: haemodynamic instability or uncontrolled ischaemia/arrhythmia, agitation or non-cooperation, copious secretions or high aspiration risk, life-threatening hypoxaemia (PaO2 <60 on FiO2 1.0), uncontrolled upper GI bleeding, bowel obstruction, vomiting

### How the pressures work

IPAP - augments tidal volume -> clears CO2
EPAP/PEEP - recruits alveoli, offsets intrinsic PEEP -> improves oxygenation
Typical COPD start: IPAP 12-15, EPAP 4-5, titrating IPAP upward by gas response

### In cardiogenic pulmonary oedema, positive pressure works haemodynamically

inc intrathoracic pressure -> dec venous return (preload)
-> dec LV transmural pressure (afterload) -> inc LV performance and cardiac output
Alveolar recruitment -> inc FRC -> dec intrapulmonary shunt -> better oxygenation, less work of breathing

4. Invasive ventilation - when NIV is not appropriate or has failed

Indications: apnoea or arrest, GCS depression with unprotected airway, haemodynamic instability, failure of NIV, exhaustion, copious secretions, need for airway protection
Lung-protective ventilation (mandatory in ARDS, sensible in most)
- Tidal volume 6 mL/kg predicted body weight, plateau pressure <30 cmH2O, driving pressure <15
- Permissive hypercapnia - tolerate pH >=7.20
ARDS: higher PEEP strategy, prone positioning >=16 h/day (PROSEVA - mortality benefit), neuromuscular blockade in severe, conservative fluids, VV-ECMO in refractory cases
Severe asthma/COPD: low rate, long expiratory time, low tidal volume, permissive hypercapnia
- Watch for dynamic hyperinflation/breath-stacking -> hypotension. If BP drops, disconnect and let the chest deflate**

5. Decide the ceiling of care early

Frailty, premorbid function, patient wishes, reversibility
*Have this conversation before the crisis, not during intubation*
Palliative approach where escalation is inappropriate: opioids and benzodiazepines for dyspnoea, fan therapy, secretion management

Associations

COPD, asthma, bronchiectasis, ILD, OSA, obesity hypoventilation
Heart failure - cardiogenic pulmonary oedema; and cardiac disease worsens tolerance of any respiratory insult
Neuromuscular disease - Guillain-Barre, myasthenia gravis, motor neurone disease, muscular dystrophy
Obesity - dec FRC, dec compliance, inc work of breathing, OHS
Sepsis and pneumonia - the commonest precipitant of ARDS
Opioid and sedative use - iatrogenic and illicit
Kyphoscoliosis and chest wall disease
Malnutrition and critical illness myopathy - respiratory muscle weakness prolongs ventilation
Electrolyte disturbance - hypophosphataemia, hypokalaemia, hypomagnesaemia
Frailty, delirium, malnutrition - all worsen outcome independently

Natural history & complications

Outcome is determined by the reversibility of the precipitant and the premorbid reserve, not by the initial gas
NIV for acidotic COPD failure reduces mortality, intubation, nosocomial infection and length of stay and is one of the highest-yield interventions in acute medicine
*A hypercapnic COPD admission is a prognostic milestone* - ~25-40% 1-year mortality; it should trigger:
- Review of therapy and inhaler technique, pulmonary rehabilitation
- Assessment for home NIV if hypercapnia persists
- Advance care planning

Complications

Of the failure: hypoxic brain injury, arrhythmia, myocardial ischaemia, multi-organ failure, death
Of NIV: pressure injury to the nasal bridge, dryness, aerophagia and gastric distension, aspiration, claustrophobia, delayed intubation
Of invasive ventilation: VAP, barotrauma/pneumothorax, ventilator-induced lung injury, ICU-acquired weakness, delirium, tracheal stenosis, difficulty weaning
Of prolonged critical illness: PTSD, cognitive impairment, deconditioning, malnutrition

After the event

Establish the cause and prevent recurrence
Review sedating drugs and oxygen prescriptions
Repeat ABG when stable to define the chronic baseline - determines home oxygen and home NIV eligibility
Pulmonary rehabilitation, vaccination, smoking cessation, action plan

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