Respiratory Failure — Types, Causes and Management

Respiratory Failure — Types, Causes and Management 15 marks Pathy's addresses respiratory failure within the chapters on ageing of the respiratory system, COPD and pneumonia rather than as a stand-alone chapter; the answer below builds on that material and standard ERS/ATS and ESICM guidance.

Definition: failure of the respiratory system to maintain adequate gas exchange, defined on arterial blood gas as PaO2 <60 mmHg (8 kPa) breathing room air, with or without PaCO2 >50 mmHg (6.7 kPa).

Acute vs chronic vs acute-on-chronic. Acute develops over minutes to hours with an uncompensated respiratory acidosis (low pH, normal bicarbonate). Chronic develops over days to years with renal compensation — raised bicarbonate and near-normal pH. Acute-on-chronic shows a raised bicarbonate with an acidotic pH and is the commonest pattern seen in an elderly COPD patient in the emergency room.

Structural: loss of elastic recoil, alveolar enlargement, air trapping and hyperinflation; kyphosis and rib-cage stiffening reduce chest wall compliance and total lung capacity; loss of diaphragm curvature and respiratory muscle mass.

Physiological: higher respiratory rate with lower tidal volume → increased work of breathing → reduced exercise tolerance; closing volume encroaches on tidal breathing, worsening V/Q mismatch; blunted ventilatory response to hypoxia and hypercapnia means the older patient decompensates suddenly and without warning.

Clinical: lung "inflammageing", impaired cough and mucociliary clearance, sarcopenia of respiratory muscles, malnutrition, polypharmacy (sedatives, opioids, antipsychotics) and multimorbidity.

Hypoxaemia: dyspnoea, tachypnoea, tachycardia, restlessness, confusion, central cyanosis (appears only when reduced haemoglobin >5 g/dL, so it is unreliable in anaemia), arrhythmias, and in chronic hypoxaemia — polycythaemia, pulmonary hypertension and cor pulmonale.

Hypercapnia: headache (worse in the morning), warm peripheries with a bounding pulse, flapping tremor (asterixis), papilloedema, drowsiness progressing to CO2 narcosis and coma. In the elderly, delirium may be the only sign.

Signs of exhaustion demanding urgent escalation: inability to speak in sentences, use of accessory muscles, paradoxical abdominal movement, a falling respiratory rate with worsening gases, and a deteriorating conscious level.

Arterial blood gas is mandatory — pulse oximetry cannot detect hypercapnia and is unreliable in poor perfusion, anaemia and darker skin pigmentation. Calculate the alveolar–arterial gradient to separate hypoventilation (normal gradient) from V/Q mismatch or shunt (widened gradient).

Add chest radiograph, ECG, full blood count, urea and electrolytes, blood glucose, CRP, cultures, and where relevant D-dimer or CTPA, BNP, echocardiography, spirometry, sleep study, and drug levels or toxicology.

Treat the underlying cause — antibiotics for pneumonia, bronchodilators and steroids for COPD, diuretics for pulmonary oedema, anticoagulation for PE, naloxone for opioid toxicity, drainage of pneumothorax.

Oxygen therapy is a drug and must be prescribed with a target range. Target SpO2 94–98% in most acutely ill patients, but 88–92% in those at risk of hypercapnic respiratory failure (COPD, obesity hypoventilation, kyphoscoliosis, neuromuscular disease). Pathy's warns of "a small but definite risk in giving too much oxygen to a patient with long-standing CO2 retention", causing depressed hypoxic drive, increased coronary and cerebral arterial resistance, and worsened acidosis. Delivery: nasal prongs 1–6 L/min, simple face mask 6–10 L/min, Venturi mask for controlled FiO2, non-rebreather reservoir mask at ≥15 L/min in emergencies.

Non-invasive ventilation (NIV/BiPAP) is the treatment of choice for acute hypercapnic respiratory failure. Start when pH <7.35 with PaCO2 >45 mmHg despite maximal medical therapy. It reduces mortality, need for intubation and length of stay, and is strongly evidence-based in COPD exacerbation and cardiogenic pulmonary oedema (where CPAP is equally effective). Typical settings: IPAP 10–16 cmH2O, EPAP 4–6 cmH2O, titrated by gases at 1 and 4 hours. Contraindications: respiratory arrest, facial trauma or surgery, vomiting, inability to protect the airway, haemodynamic instability, undrained pneumothorax, agitation or a low GCS.

High-flow nasal oxygen (HFNO) delivers heated humidified gas up to 60 L/min with an FiO2 of 0.21–1.0. It washes out nasopharyngeal dead space, generates a small PEEP effect, improves secretion clearance and is far better tolerated than a mask. The ERS 2022 guideline suggests HFNO over conventional oxygen and over NIV in hypoxaemic ARF, HFNO over conventional oxygen during breaks from NIV, and — importantly — NIV should be tried first in COPD with hypercapnic ARF. Pathy's already notes HFNO as "safe and effective in exacerbated COPD patients with both normocapnic and hypercapnic insufficiency", and specifically valuable where there is a do-not-intubate order or where intermediate care is needed outside the ICU.

Invasive mechanical ventilation when non-invasive support fails or is contraindicated: for ARDS use lung-protective ventilation — tidal volume 6 mL/kg predicted body weight, plateau pressure <30 cmH2O, appropriate PEEP, and prone positioning for severe ARDS. Permissive hypercapnia is acceptable provided pH stays above about 7.20.

Adjuncts: chest physiotherapy and secretion clearance, cautious fluid balance (restrictive in ARDS without shock), nutrition, VTE prophylaxis, treatment of anaemia, avoidance of sedatives, delirium prevention and early mobilisation to prevent ICU-acquired weakness.

Chronic respiratory failure: long-term oxygen therapy for chronic hypoxaemia; domiciliary NIV for persistent daytime hypercapnia after a COPD admission, obesity hypoventilation syndrome, kyphoscoliosis and neuromuscular disease; pulmonary rehabilitation and nutritional support.

Decide the ceiling of care early and explicitly. Base it on premorbid functional status, frailty (Clinical Frailty Scale), cognition, comorbidity and the patient's own wishes — never on chronological age alone. Document whether NIV is being used as a bridge to recovery or as the ceiling of treatment, and record any advance directive.

Prognosis and palliation: outcomes in the elderly are driven by the underlying diagnosis and premorbid function rather than age. Where reversal is not achievable, provide opioids and benzodiazepines for refractory breathlessness, a fan to the face, positioning, and early palliative care involvement.