Acute respiratory failure is the sudden inability of the respiratory system to maintain adequate oxygenation, carbon dioxide removal, or both. It is a syndrome, not a disease — the cause must always be found and treated.
| Type | ABG definition (breathing room air) | Main mechanisms | Examples |
|---|
| Type 1 — hypoxemic | PaO₂ < 60 mmHg (8 kPa) or SaO₂ < 90%, PaCO₂ normal or low | V/Q mismatch, shunt, diffusion limitation | Pneumonia, ARDS, pulmonary edema, pulmonary embolism, atelectasis |
| Type 2 — hypercapnic (ventilatory) | PaCO₂ > 50 mmHg (6.7 kPa) with pH < 7.35 | Alveolar hypoventilation — weak "pump," depressed drive, or airway obstruction | COPD exacerbation, severe asthma, opioid or sedative overdose, neuromuscular disease (Guillain-Barré, myasthenia gravis), chest wall injury, obesity hypoventilation |
Many clients have both. Acute-on-chronic failure (e.g., in COPD) is recognized by a low pH: chronic CO₂ retention is buffered by high bicarbonate, so pH is near normal until an acute rise in PaCO₂ outpaces renal compensation.
P/F ratio (PaO₂ ÷ FiO₂) expresses oxygenation relative to the oxygen given. FiO₂ is written as a decimal. Example: PaO₂ 60 mmHg on FiO₂ 0.50 → 60 ÷ 0.5 = 120. A normal value is about 400–500; ≤ 300 indicates significant impairment and is one of the oxygenation criteria for ARDS.
Hypoxemia and hypercapnia first activate the sympathetic system; later the brain and heart fail.
| Stage | Hypoxemia | Hypercapnia |
|---|
| Early | Restlessness, anxiety, tachycardia, tachypnea, hypertension, dyspnea | Headache, flushed warm skin, tachycardia |
| Late | Confusion, lethargy, cyanosis (late and unreliable), bradycardia, hypotension, dysrhythmias | Drowsiness, confusion, asterixis, coma (CO₂ narcosis) |
Other findings:
- Increased work of breathing: accessory muscle use, nasal flaring, retractions, tripod position, inability to speak full sentences
- Paradoxical (abdominal) breathing or a slowing rate in an exhausted client — ominous signs of respiratory muscle fatigue, not improvement
- Diaphoresis, decreased SpO₂
- Findings of the cause: crackles (pneumonia, edema), wheezes (asthma, COPD), absent breath sounds (pneumothorax), pinpoint pupils (opioids)
Anxiety increases respiratory rate and oxygen demand. Assess it, and respond with calm presence and clear explanations while treating the physiologic cause.
| Test | Key finding |
|---|
| Arterial blood gas | Confirms and classifies failure; shows acid–base status; used to track response |
| Pulse oximetry | Continuous trend; may be inaccurate with poor perfusion, dark skin pigmentation (tends to overestimate), carbon monoxide poisoning |
| Capnography (ETCO₂) | Trends ventilation; confirms endotracheal tube placement |
| Chest X-ray / CT, lung ultrasound | Identify pneumonia, edema, effusion, pneumothorax, ARDS |
| CBC, electrolytes, lactate, cultures, BNP, troponin, drug screen | Find the cause |
| ECG, echocardiogram | Cardiac causes, right heart strain |
| CT pulmonary angiography | Suspected pulmonary embolism |
ABG example: pH 7.28, PaCO₂ 62 mmHg, PaO₂ 55 mmHg, HCO₃⁻ 26 mEq/L → acute respiratory acidosis with hypoxemia = type 2 (with type 1) failure.
Goals: correct hypoxemia, correct acidosis/hypercapnia, treat the cause, prevent complications.
Oxygen delivery (titrate to target SpO₂ — generally 92–96%, or 88–92% when there is risk of hypercapnia)
| Device | Flow | Approximate FiO₂ | Notes |
|---|
| Nasal cannula | 1–6 L/min | 0.24–0.44 | Comfortable; FiO₂ varies with breathing pattern |
| Simple face mask | 5–10 L/min | 0.40–0.60 | At least 5 L/min to flush exhaled CO₂ |
| Venturi mask | Set per adapter | 0.24–0.60, precise | Useful in COPD and hypercapnic risk |
| Non-rebreather mask | 10–15 L/min | 0.60–0.90 | Reservoir bag must stay inflated; short-term for severe hypoxemia |
| High-flow nasal cannula (HFNC) | Up to 60 L/min | Up to 1.0 | Heated, humidified; small PEEP effect; reduces work of breathing |
Noninvasive ventilation (NIV — BiPAP/CPAP)
- Strongest evidence: COPD exacerbation with acute respiratory acidosis (pH ≤ 7.35, PaCO₂ > 45 mmHg) and cardiogenic pulmonary edema. (Guidelines start NIV at PaCO₂ > 45 mmHg; textbooks often define type 2 failure as PaCO₂ > 50 mmHg — both describe the same process)
- Contraindications: cardiac or respiratory arrest, inability to protect the airway or clear secretions, vomiting or upper GI bleeding, facial trauma or surgery, hemodynamic instability, severe agitation
- Reassess clinical status and ABG within about 1–2 hours; failure to improve → intubation without delay
Intubation and invasive mechanical ventilation — for failure or contraindication to NIV, decreasing level of consciousness, inability to protect the airway, severe acidosis, refractory hypoxemia, or exhaustion.
- Common modes: assist-control (AC) — full support, every breath delivers the set volume or pressure; SIMV; pressure support (PSV) — client-triggered breaths supported by pressure, used in weaning; CPAP
- As the client improves, move from full support to partial support and daily spontaneous breathing trials; prolonged full support without reassessment contributes to respiratory muscle weakness
Treat the cause: bronchodilators and corticosteroids (asthma, COPD), antibiotics (pneumonia), diuretics (pulmonary edema — monitor potassium and blood pressure), naloxone (opioid overdose — watch for recurrent sedation as it wears off), anticoagulation (PE).
Drug safety for ventilated clients
- Propofol: hypotension, bradycardia, hypertriglyceridemia, propofol infusion syndrome (acidosis, rhabdomyolysis); strict aseptic handling of the lipid emulsion
- Dexmedetomidine: bradycardia, hypotension; allows lighter, cooperative sedation
- Opioids (fentanyl): respiratory depression, hypotension, constipation
- Benzodiazepines: increase delirium — avoid routine continuous use
- Stress ulcer prophylaxis (PPI or H₂ blocker) for high-risk clients — associated with C. difficile and pneumonia; stop when no longer indicated
Listed in priority order.
- Recognize and respond immediately
- A confused, tachypneic client with low SpO₂ needs oxygen now and immediate notification of the provider/rapid response team — history, imaging, and routine tasks come later
- Prepare for NIV when ABG shows acidosis and the client can protect the airway, or for intubation when consciousness is decreasing
- Airway and breathing
- Position upright (high-Fowler's) unless contraindicated
- Deliver oxygen and titrate to target; evaluate the client's response (rate, effort, SpO₂, mental status) — equipment checks matter, but the client's response is what defines success
- Encourage deep breathing and effective coughing, adequate fluids to thin secretions, suction as needed
- NIV care
- Stay with the client during initial application, explain, coach the client to breathe with the machine
- Fit the mask snugly but not tightly — a small leak is acceptable; protect the nasal bridge with a dressing and check skin regularly
- Watch for gastric distension, aspiration, and claustrophobia
- Mechanical ventilation care
- Confirm and document tube position (waveform capnography, bilateral breath sounds, chest X-ray, depth at teeth/lips)
- Keep cuff pressure about 20–30 cmH₂O
- Respond to alarms: high-pressure (secretions, coughing, biting, kinked tube, bronchospasm, pneumothorax); low-pressure (disconnection, cuff leak, extubation). If the cause cannot be found quickly, disconnect and ventilate with a bag-valve device and call for help
- Suction only when needed; hyperoxygenate first; each pass ≤ 10–15 seconds
- Prevent ventilator-associated complications (see section 7)
- Head of bed 30–45°
- Daily sedation interruption paired with a spontaneous breathing trial
- Oral care with toothbrushing; routine chlorhexidine oral rinse is no longer recommended
- Aseptic suctioning and closed-circuit care; turn at least every 2 hours
- DVT prophylaxis (anticoagulant and/or mechanical devices), early mobilization
- Early enteral nutrition when feasible
- Weaning
- Readiness: cause improving, awake, hemodynamically stable, adequate oxygenation on low FiO₂ (about ≤ 0.40–0.50) and low PEEP (≤ 5–8 cmH₂O)
- During the trial, sit the client upright, stay nearby, reassure
- Stop the trial and notify for RR > 35/min, SpO₂ < 90%, heart rate or blood pressure change > 20%, diaphoresis, agitation, or dysrhythmias
- Psychosocial — use communication boards, orient frequently, include family
- Before weaning: rest and good nutrition improve muscle strength; practice relaxation; report breathlessness immediately; sitting upright makes breathing easier
- After recovery: deep breathing, coughing, incentive spirometry, gradual activity
- Prevention of recurrence: smoking cessation, vaccination, adherence to COPD/asthma action plans, safe opioid use (avoid combining with alcohol or sedatives; naloxone at home if prescribed)
- Home oxygen or home NIV: correct use, cleaning, fire safety
- Family: signs of worsening (confusion, drowsiness, blue lips, rapid breathing) require emergency care
| Complication | Prevention / what to watch |
|---|
| Ventilator-associated pneumonia | Head of bed elevation, oral care, aseptic suctioning, turning, shortest ventilation time |
| Ventilator-induced lung injury, barotrauma, pneumothorax | Sudden high-pressure alarm, falling SpO₂, absent breath sounds, tracheal shift |
| Hypotension | Positive pressure reduces venous return, especially with sedation or hypovolemia |
| Stress-related GI bleeding | Coffee-ground aspirate, melena; prophylaxis in high-risk clients |
| DVT / PE | Prophylaxis and mobility — prolonged bed rest increases risk |
| Pressure injury | Reposition at least every 2 hours; device-related injury under masks and tubes |
| Delirium, ICU-acquired weakness | Minimize sedation, early mobility, sleep hygiene |
| Unplanned extubation | Secure tube, assess sedation and restraint need per policy |
Red flags: falling respiratory rate in an exhausted client, decreasing consciousness, SpO₂ not reaching target on high FiO₂, rising PaCO₂ with falling pH.
- Type 1: PaO₂ < 60 mmHg; Type 2: PaCO₂ > 50 mmHg with pH < 7.35
- Early sign of hypoxemia = restlessness/anxiety and tachycardia; cyanosis is late
- P/F ratio = PaO₂ ÷ FiO₂ (e.g., 60 ÷ 0.5 = 120); ≤ 300 = significant impairment
- Priority: oxygen and immediate notification, not history or imaging
- The key monitoring point during oxygen therapy is the client's response (RR, effort, SpO₂, mentation)
- NIV best for COPD hypercapnic acidosis and cardiogenic pulmonary edema; stay with the client at first; avoid overtightening the mask
- Decreasing consciousness with acidosis → prepare for intubation and mechanical ventilation (NIV is contraindicated if the airway cannot be protected)
- VAP prevention: HOB 30–45°, oral care, aseptic suctioning, daily sedation interruption and breathing trials
- Prolonged full assist-control ventilation weakens respiratory muscles — move to partial support as able
- Wean in an upright position; stop for RR > 35, SpO₂ < 90%, distress
- Cuff pressure 20–30 cmH₂O; suction ≤ 10–15 seconds per pass
Country Notes
United States
- Respiratory therapists typically manage ventilator settings and NIV in collaboration with nurses; nurses remain responsible for continuous assessment and alarm response.
- The FDA issued draft guidance (2025) on pulse oximeter accuracy across skin pigmentation; confirm low or unexpected readings with an ABG.
Philippines
- In facilities with limited ICU beds or ventilators, early recognition on the ward and timely NIV or HFNC where available are especially important.