Acute Respiratory Failure

Acute respiratory failure is a sudden failure of the respiratory system to maintain gas exchange. Type 1 (hypoxaemic) is defined as PaO2 under 8 kPa (60 mmHg) with a normal or low PaCO2, and type 2 (hypercapnic, ventilatory) as PaCO2 over 6.0 kPa (45 mmHg) with a pH under 7.35. Some patients have both.

Type 1 causes are pneumonia, acute respiratory distress syndrome, pulmonary oedema, pulmonary embolism, pneumothorax, aspiration and asthma. Type 2 causes are acute exacerbation of COPD, severe asthma, obesity hypoventilation, neuromuscular disease (Guillain-Barre syndrome, myasthenic crisis), chest wall disease (flail chest), sedative or opioid overdose, and head injury.

Pathophysiology. Hypoxaemia arises from ventilation perfusion mismatch, shunt, diffusion limitation and hypoventilation. Hypercapnia arises from alveolar hypoventilation, from reduced central drive, neuromuscular weakness, increased work of breathing (airway obstruction, reduced compliance) or increased dead space. Respiratory acidosis follows hypercapnia, and exhaustion progresses to apnoea.

Breathlessness, tachypnoea (respiratory rate over 25 per minute), use of accessory muscles, central cyanosis, tachycardia, sweating, agitation, confusion, drowsiness, and in hypercapnia flapping tremor, bounding pulse and headache. A quiet chest, exhaustion, bradycardia and a falling level of consciousness are late and ominous. The cause is sought from history and signs (wheeze, crackles, absent breath sounds, leg swelling, fever, trauma).

Respiratory rate over 30, saturation under 90% on oxygen, pH under 7.25, confusion or exhaustion needs immediate senior and intensive care help.

• Clinical assessment of airway, breathing and circulation with oxygen saturation, respiratory rate, heart rate, blood pressure and consciousness. Early warning score.
• Arterial blood gas on a known inspired oxygen fraction: PaO2, PaCO2, pH, bicarbonate (a high bicarbonate indicates chronic retention), lactate, and the PaO2/FiO2 ratio (under 300 mmHg indicates acute lung injury, under 200 moderate and under 100 severe ARDS).
• Chest radiograph, point-of-care lung and cardiac ultrasound (B-lines, pleural effusion, pneumothorax, ventricular function, inferior vena cava), electrocardiogram, and CT chest or CT pulmonary angiography when the cause is unclear.
• Laboratory tests: full blood count, urea and electrolytes, glucose, C-reactive protein, procalcitonin, troponin, NT-proBNP, D-dimer, blood and sputum cultures, respiratory viral PCR, and toxicology.
• Spirometry or peak flow if safe, and bedside neuromuscular tests (forced vital capacity, maximal inspiratory pressure) in neuromuscular disease: intubation is considered when forced vital capacity is under 20 mL/kg, or falls by over 30%.

Differential diagnosis.

• Cardiogenic pulmonary oedema
• Pulmonary embolism
• Metabolic acidosis with compensatory tachypnoea
• Panic attack and hyperventilation
• Upper airway obstruction
• Sepsis with acute respiratory distress syndrome

• Immediate resuscitation: airway opening and suction, oxygen by mask (15 L/min non-rebreather) while preparing definitive support, intravenous access, and monitoring.
• Oxygen targets: saturation 94 to 98% in most patients, and 88 to 92% (PaO2 8 to 10 kPa) in COPD and others at risk of hypercapnia, using a controlled mask (24 to 28% Venturi), with repeat blood gas at 30 to 60 minutes.
• High flow nasal oxygen (flow 40 to 60 L/min, FiO2 0.4 to 1.0, temperature 37 degrees Celsius) for type 1 failure, which reduces intubation compared with conventional oxygen.
• Non-invasive ventilation: continuous positive airway pressure (5 to 10 cmH2O) for cardiogenic pulmonary oedema; bilevel (inspiratory 10 to 20 cmH2O, expiratory 4 to 5 cmH2O, rate 12 to 16, titrated) for hypercapnic COPD exacerbation with pH 7.25 to 7.35, with blood gas at 1 hour and failure defined as no improvement at 1 to 2 hours. It reduces intubation and mortality in COPD.
• Intubation and invasive ventilation for: failure of non-invasive support, pH under 7.25 with deterioration, exhaustion, loss of airway protection, severe hypoxaemia (PaO2/FiO2 under 100 despite high flow oxygen or CPAP), or shock. Use rapid sequence induction with preoxygenation.
• Lung protective ventilation for ARDS: tidal volume 6 mL/kg predicted body weight, plateau pressure 30 cmH2O or less, driving pressure under 15 cmH2O, positive end expiratory pressure titrated to oxygenation (10 to 15 cmH2O), and permissive hypercapnia (pH over 7.2). Conservative fluid strategy once off vasopressors.
• Severe ARDS (PaO2/FiO2 under 150): prone position for at least 16 hours daily, neuromuscular blockade (cisatracurium 15 mg bolus then 37.5 mg/hour) for the first 48 hours in selected patients, and extracorporeal membrane oxygenation for refractory hypoxaemia at a centre.
• Treat the cause: antibiotics for pneumonia within 1 hour in sepsis (ceftriaxone 2 g and clarithromycin 500 mg twice daily in community acquired pneumonia), nebulised salbutamol 5 mg and ipratropium 500 micrograms with prednisolone 30 to 40 mg for 5 days in COPD (with doxycycline 200 mg then 100 mg daily if purulent sputum), diuretic (furosemide 40 to 80 mg intravenously) and nitrate in pulmonary oedema, anticoagulation or thrombolysis in pulmonary embolism, chest drain for pneumothorax, and naloxone 0.4 to 2 mg for opioid overdose.
• Dexamethasone 6 mg daily for 10 days for severe COVID-19 requiring oxygen, and dexamethasone 20 mg daily for 5 days then 10 mg for 5 days in selected ARDS.
• Supportive care: enoxaparin 40 mg daily for thromboprophylaxis, proton pump inhibitor, early enteral nutrition, glycaemic control, sedation holidays and early mobilisation, and avoidance of fluid overload.
• Doxapram is used only when non-invasive ventilation is not available, as a short term measure.
• Palliative approach and treatment ceilings agreed with the patient and family when appropriate.

Complications and prognosis. Ventilator associated pneumonia, barotrauma, ARDS, multi-organ failure, delirium, critical illness neuromyopathy, and post-intensive care syndrome. Hospital mortality is about 10 to 15% in COPD exacerbation with hypercapnic failure and 35 to 45% in ARDS.

Monitoring. Continuous saturation and cardiac monitoring, repeat blood gases at 30 to 60 minutes after any change and at least every 4 to 6 hours, and daily chest radiograph, electrolytes and fluid balance.

Referral and escalation. Refer early to intensive care or high dependency care for failure of first line support, pH under 7.25, PaO2/FiO2 under 150, or exhaustion, and to a respiratory physician for ventilation planning.