AKT · Respiratory/Respiratory failure & ARDS

Respiratory failure & ARDS

Failure of gas exchange — type 1 (hypoxic) vs type 2 (hypercapnic); ARDS = non-cardiogenic oedema

Overview

Failure of the respiratory system to oxygenate and/or clear CO2. Type 1 (hypoxaemic, low PaO2 with normal/low CO2 — V/Q mismatch: pneumonia, PE, oedema, ARDS). Type 2 (hypercapnic, high CO2 — alveolar hypoventilation: COPD, neuromuscular, opioids, chest-wall). ARDS is severe non-cardiogenic pulmonary oedema with refractory hypoxia and bilateral infiltrates. Respiratory arrest is the terminal endpoint (→ cross-ref acute_care).

Recognise

Breathlessness, hypoxia (cyanosis, low SpO2); type 2 adds CO2 retention — drowsiness, flap, headache, bounding pulse, confusion
ABG defines it: type 1 = PaO2 6 kPa
ARDS: acute refractory hypoxaemia + bilateral infiltrates not fully explained by cardiac failure, after a trigger (sepsis, pancreatitis, trauma, aspiration, transfusion)

Red flags

Exhaustion, rising CO2 with acidosis, or peri-arrest → urgent ventilatory support (NIV/intubation) and critical care
Type 2 respiratory failure with respiratory acidosis (COPD) → controlled oxygen (88–92%) + NIV (BiPAP)

Differentials & how to tell them apart

Type 1 vs type 2 respiratory failurethe CO2 splits them — normal/low (type 1) vs high (type 2); guides oxygen target and NIV

Cardiogenic pulmonary oedemaraised JVP/BNP, responds to diuretics — vs non-cardiogenic ARDS

Pulmonary embolismhypoxia with clear CXR, RV strain — type 1 cause

Atelectasis (post-operative)the classic cause of post-op day 1–2 fever + breathlessness/hypoxia with basal collapse — treat with chest physiotherapy, deep breathing and analgesia

Investigations

ABG (the defining test — type 1 vs type 2, pH/acidosis); SpO2; CXR (cause/ARDS infiltrates); identify and treat the cause; ARDS — echo to exclude cardiogenic oedema, P/F ratio for severity.

Management

Treat the cause + targeted O2 (type 1: 94–98%, type 2: 88–92%); NIV/ICU for failure; ARDS → lung-protective ventilation

1Take an ABG to define type 1 (hypoxic, normal/low CO2) vs type 2 (hypercapnic). Give oxygen to the right target and treat the cause: type 1 → high-flow O2 (94–98%); type 2 with chronic retention → controlled O2 (88–92%).Gate: Type 2 respiratory failure with persistent respiratory acidosis (e.g. COPD) → NIV (BiPAP); uncontrolled high-flow oxygen can worsen CO2 retention. Exhaustion/peri-arrest → intubation/ICU.
2ARDS → lung-protective ventilation (low tidal volume, prone positioning) in ICU plus treating the trigger; escalate to intubation for NIV failure; respiratory arrest → ALS (cross-ref acute_care).

Treat the underlying cause + oxygen to target — type 1 → high-flow oxygen (94–98%); type 2 with chronic CO2 retention → controlled oxygen 88–92%

Type 2 respiratory failure with persistent acidosis → NIV (BiPAP) — e.g. COPD exacerbation; CPAP for cardiogenic oedema/type 1

ARDS: lung-protective ventilation (low tidal volume) in ICU + treat the trigger — 6 mL/kg tidal volume, prone positioning; treat sepsis/pancreatitis/aspiration

Escalate to intubation/ICU; respiratory arrest → ALS — for failure of NIV or peri-arrest (cross-ref acute_care)

Key points

ABG defines it: type 1 (low O2, normal/low CO2 — V/Q mismatch) vs type 2 (high CO2 — hypoventilation). O2 target: 94–98% normally, 88–92% in CO2-retainers. Type 2 + acidosis (COPD) → NIV. ARDS = refractory hypoxia + bilateral infiltrates, non-cardiogenic → lung-protective ventilation + treat the trigger.

Monitor & prognosis

Serial ABG/pH, oxygenation, work of breathing, NIV response; ICU escalation.

Depends on the cause; ARDS carries high mortality; reversible causes do well with timely support.

Source: BTS oxygen; cross-ref acute_care (sepsis/arrest)