Respiratory Failure — Symptoms, Causes & Treatment | MyMedicPlus

Respiratory failure is a life-threatening condition where the lungs fail to maintain adequate gas exchange — either oxygenation (Type I), ventilation (Type II), or both. Type I (hypoxemic): PaO2 below 60 mmHg on room air — caused by ventilation-perfusion mismatch, shunt, or diffusion impairment (pneumonia, ARDS, pulmonary oedema, pulmonary embolism). Type II (hypercapnic): PaCO2 above 45 mmHg with respiratory acidosis — caused by ventilatory failure from COPD, neuromuscular disease, drug-induced respiratory depression, or chest wall abnormality; also called 'pump failure'. Acute respiratory failure develops over hours to days and is immediately life-threatening, requiring ICU management. Chronic respiratory failure (COPD, interstitial lung disease, neuromuscular disease) develops over months to years and may be managed with long-term oxygen therapy (LTOT) or home non-invasive ventilation (NIV). ARDS (acute respiratory distress syndrome) is the most severe form of Type I failure — caused by bilateral inflammatory lung injury from sepsis, pneumonia, aspiration, trauma, or pancreatitis; carries 30–40% hospital mortality. P/F ratio (PaO2/FiO2): below 300 is mild ARDS, below 200 moderate, below 100 severe.

Common causes of Type I (hypoxemic) failure: community-acquired and hospital-acquired pneumonia, ARDS (sepsis, aspiration, trauma, transfusion-related — TRALI), acute pulmonary oedema (cardiac failure), pulmonary embolism with large shunt, COVID-19 pneumonitis, interstitial lung disease exacerbations, and endobronchial obstruction. Common causes of Type II (hypercapnic) failure: COPD exacerbation (the most common cause of hypercapnic failure in UK practice — triggered by respiratory infection in 70%), status asthmaticus, opioid and benzodiazepine overdose causing central hypoventilation, neuromuscular disease (Guillain-Barré syndrome — ascending weakness causing diaphragm failure; myasthenia gravis crisis; ALS/MND), chest wall trauma (flail chest, multiple rib fractures), obesity-hypoventilation syndrome, and kyphoscoliosis. Risk factors for respiratory failure: COPD, obesity, immunosuppression, advanced age, frailty, heart failure, and sepsis-induced multi-organ dysfunction. Sepsis is both a cause and a consequence of respiratory failure — the two are closely interrelated in critical illness.

Severe dyspnea (described as 'inability to breathe in enough'), tachypnea (respiratory rate above 30 breaths per minute), use of accessory muscles (sternocleidomastoid, scalenes, and intercostal muscles), cyanosis of lips and fingertips (a late sign — appears when SaO2 falls below 85%), paradoxical breathing (abdominal paradox — the abdomen moves in on inspiration, indicating diaphragm fatigue in neuromuscular failure), and SpO2 below 90% on pulse oximetry. Altered consciousness — agitation, confusion, or drowsiness — is a critical sign of cerebral hypoxia and indicates impending respiratory arrest. Hypercapnic failure signs: somnolence, early morning headache (from CO2 retention during sleep), bounding pulse, warm extremities (peripheral vasodilation from CO2), asterixis (liver flap — a sign of CO2 narcosis), and progressive drowsiness progressing to coma if untreated. Pursed-lip breathing, tripod positioning (leaning forward on arms), and inability to complete sentences in one breath are important clinical signs of severe respiratory failure.

Arterial blood gas (ABG) is the definitive investigation — identifies type (hypoxemic vs. hypercapnic), severity of gas exchange impairment, and acid-base status (respiratory acidosis in Type II; respiratory alkalosis in early hypoxia as patients hyperventilate). P/F ratio (PaO2 mmHg/FiO2 as a fraction): below 300 is mild ARDS, below 200 moderate ARDS, below 100 severe ARDS (Berlin Definition 2012). Chest X-ray: bilateral fluffy infiltrates in ARDS; unilateral consolidation in pneumonia; hyperinflation and flattened diaphragms in COPD. CT thorax for uncertain cases (pulmonary embolism — CT pulmonary angiography; interstitial lung disease). Echocardiography: distinguishes cardiogenic pulmonary oedema (elevated BNP, dilated left ventricle, high PCWP) from non-cardiogenic ARDS (normal PCWP). Bronchoscopy with bronchoalveolar lavage (BAL): identifies pathogen in ICU-acquired pneumonia and immunocompromised patients with atypical infections. Blood cultures, procalcitonin, and urinary antigens (Legionella, pneumococcal) assess for bacterial cause. SOFA and NEWS2 scoring guide deterioration recognition and escalation.

Supplemental oxygen (target SpO2 94–98%; 88–92% in COPD with known hypercapnia — to avoid hypercapnic respiratory failure from oxygen-induced loss of hypoxic drive). High-flow nasal cannula (HFNC — 30–60 L/min humidified oxygen): superior to standard facemask for moderate-severe hypoxemia — reduces intubation rates in non-hypercapnic respiratory failure (FLORALI trial). Non-invasive ventilation (NIV/BiPAP): first-line for Type II (hypercapnic) failure in COPD and cardiogenic pulmonary oedema — IPAP 14–20 cmH2O, EPAP 4–8 cmH2O; reduces mortality and intubation rates significantly vs standard oxygen. Invasive mechanical ventilation (intubation): when NIV fails or consciousness is impaired; lung-protective ventilation (tidal volume 6 mL/kg ideal body weight, PEEP 5–10 cmH2O, plateau pressure below 30 cmH2O) for ARDS — reduces mortality versus high-volume ventilation (ARMA trial). Prone positioning for moderate-severe ARDS (P/F below 150) for 16+ hours daily reduces 28-day mortality from 33% to 16% (PROSEVA trial). Neuromuscular blockade (cisatracurium 48 hours) for severe ARDS improves synchrony and reduces ventilator-induced lung injury (ACURASYS/ROSE trials). Treat the underlying cause urgently: antibiotics for pneumonia/sepsis, diuresis and CPAP for cardiogenic pulmonary oedema, thrombolysis for massive PE. Inhaled nitric oxide and extracorporeal membrane oxygenation (ECMO) for refractory severe ARDS in specialist centres.

ARDS (bilateral pulmonary infiltrates, non-cardiogenic pulmonary oedema — develops in 10–15% of ICU patients); ventilator-associated pneumonia (VAP — incidence 10–20% after 5 days of mechanical ventilation, caused by biofilm formation on endotracheal tube); barotrauma (pneumothorax from high ventilation pressures — occurs in 5–10% of mechanically ventilated patients and can be rapidly fatal if not immediately treated); ICU-acquired weakness (intensive care unit-acquired neuromuscular dysfunction — affects 25–50% of critically ill patients, causing prolonged ventilator dependence and rehabilitation needs); oxygen toxicity (free radical damage from FiO2 above 0.60 for more than 24 hours — injures lung epithelium); post-ICU syndrome (PICS — cognitive impairment, PTSD, depression, and physical deconditioning persisting for months to years after ICU discharge — recognised in approximately 30–50% of survivors of prolonged mechanical ventilation); pulmonary fibrosis following ARDS (occurs in a proportion of survivors — causes persistent exertional dyspnoea). Hospital mortality: ARDS 30–40%; septic shock-associated respiratory failure 40–50%.

Prevention: influenza and pneumococcal vaccinations reduce pneumonia-related respiratory failure in high-risk groups (elderly, COPD, heart failure, diabetes, immunosuppression); smoking cessation is the single most important intervention to prevent COPD progression and respiratory failure; optimal COPD management (LAMA + LABA combination inhalers, rehabilitation, pulmonary rehabilitation — reduces hospitalisation by 30%). In hospital: VTE prophylaxis (LMWH and compression stockings) prevents PE-related respiratory failure; aspiration precautions (30-degree head-of-bed elevation, swallowing assessment before feeding, PPI for high-risk patients); VAP prevention bundle (hand hygiene, oral chlorhexidine 0.12%, subglottic secretion drainage, daily sedation holds, spontaneous breathing trials to minimise intubation duration). Lung-protective ventilation strategies from intubation onset prevent VILI. Early recognition of deteriorating patients using NEWS2 (National Early Warning Score 2) triggers rapid response team review at score above 5. Early goal-directed therapy in sepsis prevents progression to respiratory failure requiring intubation.

Call emergency services (999/911) or attend Emergency Department immediately for any of the following — these are signs of acute respiratory failure and can be rapidly fatal without emergency treatment: severe breathlessness — unable to complete sentences in one breath, or breathing at rest is laboured; lips or fingernails turning blue or grey (cyanosis) — indicates critical hypoxaemia (oxygen saturation below 85%); rapidly increasing respiratory rate (above 30 breaths per minute) with visible use of accessory muscles (neck, between ribs); altered consciousness, confusion, or loss of consciousness with breathlessness — indicates hypercapnic or hypoxic encephalopathy; SpO2 below 92% on a home pulse oximeter — especially in a person with known COPD, asthma, heart failure, or following recent pneumonia; a person with COPD becoming drowsy or difficult to rouse — may indicate dangerous hypercapnia (CO2 retention requiring controlled-oxygen therapy, not high-flow); inability to cough effectively, especially after stroke, brain injury, or in neuromuscular disease — risk of aspiration and type 2 respiratory failure. If someone is already on home CPAP/BiPAP (non-invasive ventilation) and stops tolerating or responding to it — immediate Emergency Department attendance is required.