Respiratory failure

Inability of the respiratory system to maintain gas exchange, leading to inadequate oxygenation and/or carbon dioxide removal. Type I (hypoxemic) failure is defined by low oxygen (PaO₂ <60 mmHg) with normal/low CO₂, while Type II (hypercapnic) failure features elevated CO₂ (PaCO₂ >50 mmHg) with accompanying hypoxemia.

• If unrecognized, respiratory failure can quickly progress to respiratory arrest, coma, or death. It's a common ICU condition (e.g., in ARDS, COPD exacerbations, acute pulmonary edema, severe COVID-19) and a frequent exam topic linking ABG interpretation to emergency management.

• Patients in acute respiratory distress: labored breathing, tachypnea, accessory muscle use, possibly cyanosis (if hypoxemic) or altered mental status (if hypercapnic). Vital signs often show tachycardia and maybe hypertension early (from stress catecholamines).
• Hypoxemic (Type I) failure: presents with profound dyspnea and tachypnea; common causes are acute lung issues like pneumonia, ARDS, pulmonary edema (cardiogenic or noncardiogenic), pulmonary embolism, or severe asthma exacerbation. Patients may be agitated or anxious; oxygen saturation is low despite breathing fast.
• Hypercapnic (Type II) failure: presents with hypoventilation (inadequate breathing) and often confusion or somnolence (high CO₂ causes CO₂ narcosis). Causes include COPD exacerbation (most common), drug overdose or CNS depression, neuromuscular weakness (e.g., Guillain-Barré, myasthenia gravis), severe obesity hypoventilation, or end-stage asthma/COPD where the patient tires out. Patients may have a headache and even a flapping tremor (asterixis) due to high CO₂.

1. Confirm respiratory failure with an arterial blood gas (ABG): PaO₂ <60 mmHg signifies hypoxemia; PaCO₂ >50 mmHg with pH <7.35 indicates hypercapnia. Use the ABG to classify Type I vs II and assess severity (degree of acidosis).
2. Calculate the alveolar–arterial (A-a) O₂ gradient: a normal A-a gradient in a hypoxemic patient suggests pure alveolar hypoventilation (e.g., opioid overdose) as the cause. An elevated A-a gradient indicates V/Q mismatch or shunt (intrinsic lung pathology).
3. Apply the 100% O₂ test if hypoxemia is severe: if PaO₂ does not significantly improve even on 100% FiO₂, suspect a right-to-left shunt (e.g., ARDS with shunting or cardiac shunt), since V/Q mismatch will usually improve with supplemental O₂.
4. Differentiate acute vs chronic hypercapnia: in chronic CO₂ retention (e.g., COPD), the kidneys retain bicarbonate, so baseline HCO₃⁻ is elevated and pH is near normal. An acute rise in CO₂ causes a large drop in pH (acute respiratory acidosis)—so a high CO₂ with normal pH implies chronic compensation.
5. Monitor clinical signs: altered mental status (especially drowsiness, confusion) is a key clue to rising CO₂; cyanosis indicates severe hypoxemia. Also check for asterixis (a flapping tremor seen in CO₂ retention). These signs help gauge how urgent intubation is needed.

1. Oxygen therapy for hypoxemia: give supplemental O₂ (nasal cannula, face mask, or high-flow nasal oxygen) aiming for PaO₂ ≥60 mmHg (SaO₂ ~90%). Avoid overshooting O₂ (especially in CO₂ retainers) to prevent oxygen toxicity or CO₂ narcosis; in hypercapnic patients, target 88–92% SaO₂.
2. Ventilatory support for hypercapnia or fatigue: use noninvasive ventilation (BiPAP/CPAP) if the patient is conscious and cooperative. If mental status or oxygenation worsens, secure the airway with intubation and mechanical ventilation. Goals of ventilation: correct hypoxemia and acidosis, and rest the respiratory muscles.
3. Treat the underlying cause in parallel: e.g., bronchodilators ± steroids for asthma/COPD exacerbation, diuretics for acute heart failure, antibiotics for pneumonia or sepsis, anticoagulation for pulmonary embolism, antidotes (e.g., naloxone) for drug overdose, etc. This definitive therapy addresses the trigger while supportive care buys time.

• Mnemonic – 5 Causes of Hypoxemia: 1) Low FiO₂ (high altitude), 2) Hypoventilation, 3) Diffusion limitation (e.g., fibrosis), 4) V/Q mismatch (e.g., PE, pneumonia), 5) Shunt (e.g., ARDS).
• Remember "can't breathe" vs "won't breathe" for Type II: hypercapnia occurs either when the respiratory pump can't generate ventilation (neuromuscular failure, severe asthma/COPD, chest wall restriction) or the brain won't drive breathing (CNS depression from stroke, opiates).
• Use O₂ carefully in CO₂ retainers: In chronic hypercapnic COPD patients, giving excessive oxygen can worsen CO₂ retention (loss of hypoxic respiratory drive and V/Q changes). Target saturations ~88–92% rather than 100% in these patients.

• Altered mental status (confusion, extreme drowsiness, or loss of consciousness) in a patient with respiratory distress – signals impending respiratory arrest or inability to protect airway. This is an indication for immediate intubation.
• Refractory hypoxemia (PaO₂ remains <60 mmHg despite high FiO₂) or severe acidosis (pH <7.25 from rising CO₂) are danger signs. These criteria, or signs of respiratory muscle exhaustion (such as paradoxical breathing), mandate urgent escalation to invasive ventilation.

1. Recognize & stabilize: Identify patients with suspected respiratory failure (acute dyspnea, cyanosis, lethargy). Immediately ensure the airway is open, assist breathing if needed, and start supplemental O₂ if O₂ saturation is low.
2. Assess: Check vital signs and obtain an ABG early to confirm respiratory failure and classify type (hypoxemic vs hypercapnic). Monitor mental status closely; prepare for possible intubation if CO₂ is high or patient is tiring.
3. Diagnose cause: Perform focused exam and investigations (lung auscultation, chest X-ray, ± ECG, labs). Common scenarios: pneumonia (fever, infiltrate on CXR), heart failure (JVD, edema, pulmonary edema on CXR), COPD/asthma (wheezing, history), pulmonary embolism (acute dyspnea with clear lungs, risk factors). Treatable toxic/metabolic causes (opioid overdose, neuromuscular crisis) should be identified and addressed.
4. Escalate support: If hypoxemia is moderate, use higher-flow O₂ or consider CPAP; if hypercapnia or distress is worsening, start BiPAP. If the patient cannot maintain oxygenation or mental status declines, perform endotracheal intubation and mechanical ventilation. Involve critical care/ICU early.
5. Definitive management: Once stabilized on appropriate respiratory support, address the underlying cause (e.g., antibiotics, diuresis, thrombolysis for PE, corticosteroids for asthma/COPD). Continuously reassess ABGs and vitals, and wean respiratory support as the patient improves.

• An older man with severe COPD becomes confused and somnolent after an infection; ABG shows pH 7.25, PaCO₂ 70 mmHg, PaO₂ 55 mmHg on oxygen → acute hypercapnic (Type II) respiratory failure from a COPD exacerbation, requiring BiPAP or intubation.
• A patient with ARDS from pneumonia is on a nonrebreather mask but PaO₂ remains 50 mmHg, PaCO₂ 30 mmHg → classic Type I respiratory failure with refractory hypoxemia. Intubation with mechanical ventilation and high PEEP is indicated.