Respiratory Failure — Types, Causes, Diagnosis & Emergency Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Respiratory failure is defined as inadequate gas exchange by the respiratory system, characterised by: Type I (hypoxaemic) — arterial oxygen tension (PaO2) below 60 mmHg (8 kPa) on room air, with normal or low PaCO2 — failure of oxygenation; or Type II (hypercapnic/ventilatory) — PaCO2 above 45 mmHg (6 kPa) with respiratory acidosis (pH below 7.35) — failure of ventilation. Both types represent a critical impairment of pulmonary gas exchange that, without timely intervention, leads to multi-organ failure and death. Acute respiratory failure (ARF) develops over minutes to hours; acute-on-chronic respiratory failure occurs in patients with pre-existing lung disease (COPD, pulmonary fibrosis) decompensated by an acute insult. ARDS (Acute Respiratory Distress Syndrome) is the most severe form of hypoxaemic respiratory failure — defined by Berlin criteria: acute onset within 1 week, bilateral radiographic infiltrates, non-cardiogenic pulmonary oedema, and PaO2/FiO2 (P/F ratio) below 300 mmHg. ARDS mortality ranges from 30-40% for severe cases despite modern intensive care.

Type I (hypoxaemic — V/Q mismatch, shunt, diffusion impairment): pneumonia (most common — bacterial, viral, atypical); ARDS (direct: pneumonia, aspiration, pulmonary contusion; indirect: sepsis, pancreatitis, massive transfusion); pulmonary embolism (V/Q mismatch and haemodynamic compromise); cardiogenic pulmonary oedema (hydrostatic fluid overload — heart failure, fluid overload); pneumothorax; acute asthma (severe bronchospasm causing air trapping and V/Q mismatch); pulmonary haemorrhage; interstitial lung disease (alveolar damage and diffusion impairment). Type II (hypercapnic — hypoventilation, increased dead space): COPD exacerbation (most common cause of hypercapnic failure — loss of respiratory drive plus airflow obstruction and hyperinflation); severe asthma; neuromuscular disorders (Guillain-Barré syndrome, myasthenia gravis, motor neurone disease — failure of respiratory muscles); opioid overdose (central respiratory depression); chest wall deformity (kyphoscoliosis, thoracic cage abnormality); obesity hypoventilation syndrome (Pickwickian syndrome); high spinal cord injury. Sedative/benzodiazepine overdose causes mixed type I/II.

Respiratory failure presents as a medical emergency — recognise rapidly. Dyspnoea: severe breathlessness with subjective air hunger; tachypnoea (respiratory rate above 25 breaths/minute — a critical early warning sign). Use of accessory respiratory muscles: sternocleidomastoid, intercostal, and scalene muscle recruitment indicates increased work of breathing. Cyanosis: central cyanosis (bluish discolouration of lips and tongue) is a late and unreliable sign — SpO2 below 85% is typically required for clinical cyanosis to become apparent. Altered consciousness: agitation and restlessness (hypoxia — early); confusion, somnolence, and progressive loss of consciousness (hypercapnia — CO2 narcosis). Paradoxical breathing: inward movement of the abdomen during inspiration (diaphragm fatigue/paralysis). Hypercapnia-specific signs: asterixis (flapping tremor of hands), bounding pulse, peripheral vasodilation, headache (from cerebral vasodilation), and papilloedema in severe cases. SpO2 below 90% on pulse oximetry is a critical threshold requiring immediate intervention.

Arterial blood gas (ABG): the definitive test — measures PaO2, PaCO2, pH, bicarbonate, base excess. Defines type of failure (I vs. II), severity, and degree of metabolic compensation. P/F ratio (PaO2 mmHg / FiO2): P/F 200-300 = mild ARDS; 100-200 = moderate ARDS; below 100 = severe ARDS. SpO2 via pulse oximetry: non-invasive, continuous, but does not measure CO2 — cannot diagnose Type II failure; unreliable in peripheral vasoconstriction and carbon monoxide poisoning (SpO2 falsely normal). Chest X-ray: bilateral infiltrates (ARDS, pulmonary oedema); unilateral consolidation (pneumonia); pneumothorax; pulmonary effusion. CT thorax: superior characterisation of underlying cause (ARDS distribution, pneumonia extent, PE on CTPA, interstitial disease pattern). SOFA score: Sepsis-related Organ Failure Assessment — quantifies multi-organ dysfunction. Echocardiography: distinguishes cardiogenic from non-cardiogenic pulmonary oedema (LV function, filling pressures — BNP/NT-proBNP elevated in cardiac cause). Bronchoscopy with BAL: identifies pathogen in immunocompromised or unexplained respiratory failure. Blood cultures, sputum culture, respiratory PCR panel, procalcitonin, CRP.

Immediate: call for critical care team; continuous monitoring (SpO2, ETCO2, ABG, cardiac monitoring). Oxygen therapy: target SpO2 94-98% in most patients; SpO2 88-92% in known/suspected COPD to avoid hypercapnic drive suppression. High-flow nasal cannula (HFNC): heated, humidified oxygen at 40-60 L/min at FiO2 up to 1.0 — superior to conventional oxygen for mild-moderate hypoxaemic failure; reduces intubation rate in pneumonia. Non-invasive ventilation (NIV/BiPAP): first-line for COPD exacerbation with hypercapnia — reduces intubation and mortality by 65%; also effective in cardiogenic pulmonary oedema. Invasive mechanical ventilation (IMV): indicated when NIV fails, airway cannot be protected, haemodynamic instability, or respiratory arrest. Lung-protective ventilation strategy (ARDSNet protocol) for ARDS: tidal volume 6 mL/kg ideal body weight (IBW) — not actual weight; PEEP titration (initially 5-8 cmH2O, higher if severe hypoxia); plateau pressure below 30 cmH2O; driving pressure below 15 cmH2O; respiratory rate 12-20 breaths/minute; FiO2 titrated to SpO2 target. Prone positioning: 16+ hours per day for P/F below 150 — reduces ARDS mortality by 16% (PROSEVA trial). Paralysis (cisatracurium) in severe ARDS within first 48 hours. Conservative fluid strategy in ARDS (avoid fluid overload — FACTT trial). Treat underlying cause urgently: antibiotics for pneumonia; heparin for PE; diuresis for cardiogenic pulmonary oedema; naloxone for opioid toxicity. Extracorporeal membrane oxygenation (ECMO): for refractory severe ARDS or respiratory failure unresponsive to maximal conventional therapy — specialist ECMO centres.

Respiratory failure — particularly when requiring mechanical ventilation — is associated with numerous serious complications. Ventilator-associated pneumonia (VAP) occurs in 10-20% of mechanically ventilated patients and significantly increases ICU length of stay and mortality. Ventilator-induced lung injury (VILI) from high-pressure ventilation causes barotrauma (pneumothorax, pneumomediastinum from overdistension), volutrauma, atelectrauma, and biotrauma (inflammatory cytokine release worsening ARDS) — lung-protective ventilation strategies minimise VILI. ICU-acquired weakness (critical illness myopathy and polyneuropathy) from prolonged immobility, corticosteroids, and neuromuscular blocking agents causes severe generalised weakness, respiratory muscle atrophy, and difficulty weaning from ventilation. Delirium occurs in 50-80% of mechanically ventilated ICU patients, associated with longer ICU stay, worse long-term cognitive function, and PTSD. Barotrauma: pneumothorax occurs in 2-5% of ventilated patients — potentially life-threatening tension pneumothorax requires immediate chest drain. Oxygen toxicity from prolonged high FiO2 above 0.6 causes reactive oxygen species-mediated lung injury. Post-intensive care syndrome (PICS) — cognitive impairment, PTSD, depression, anxiety, and physical weakness — affects up to 50% of ARDS survivors, with significant disability persisting for years after ICU discharge.

Influenza and pneumococcal vaccination prevent common causes of pneumonia-induced respiratory failure — particularly important for elderly, immunocompromised, and those with chronic lung disease. Optimal management of underlying conditions: COPD (long-acting bronchodilators — LABA/LAMA; inhaled corticosteroids; pulmonary rehabilitation; smoking cessation); heart failure (diuretics, ACE inhibitors, beta-blockers); neuromuscular disease (NIV during sleep prevents nocturnal hypoventilation and acute decompensation). Hospital-based prevention: aspiration precautions (head elevation 30-45 degrees, swallowing assessment); ventilator-associated pneumonia (VAP) bundle (oral chlorhexidine, subglottic suction, daily sedation holidays, early mobility); VTE prophylaxis; judicious use of opioids; avoid fluid overload; lung-protective ventilation even in non-ARDS patients. Early warning scores (NEWS2) identify deteriorating patients before respiratory failure develops — enabling early intervention.

Call emergency services (999/911) immediately or go to Emergency Department for any of the following: severe breathlessness at rest (unable to complete full sentences); lips or face turning blue (cyanosis); respiratory rate above 25 breaths per minute; SpO2 below 90% on home pulse oximeter; confusion, agitation, or drowsiness in anyone with breathing difficulty; any person found unresponsive with abnormal or absent breathing. Do not wait for an appointment — respiratory failure can progress to cardiac arrest within minutes. Call 999 immediately and follow dispatcher instructions regarding positioning and CPR if the person stops breathing. For patients with known COPD or asthma: have a written COPD exacerbation action plan; start oral prednisolone and amoxicillin at agreed trigger point; if no improvement within 24 hours or SpO2 falls below 88-90% despite rescue medication, attend Emergency Department.