Respiratory Failure
Introduction
Respiratory failure occurs when the lungs fail to maintain adequate gas
exchange (oxygenation and/or CO₂ elimination), leading to life-
threatening hypoxia and/or hypercapnia.
Key Causes (Mnemonics: “DAMAGE”)
Decreased ventilatory drive (e.g., drug overdose, CNS injury)
Airway resistance (e.g., asthma, COPD)
Muscle weakness (e.g., myasthenia gravis, polio)
Alveolar damage (e.g., ARDS, pneumonia)
Gas exchange impairment (e.g., pulmonary edema)
Elasticity loss (e.g., fibrosis, pneumothorax)
Types of Respiratory Failure
Type I Type II
(Hypoxem (Hypercapni
ic) c)
PaO₂ < 60 PaCO₂ > 50
mmHg mmHg (with
(with hypoxemia)
normal/lo
w PaCO₂)
Causes: Causes:
ARDS, COPD, drug
pneumoni overdose,
a, neuromuscul
pulmonar ar disorders
y edema
(B) Based on Onset
Acute: Rapid onset (minutes-hours), pH <7.3 (respiratory
acidosis).
Chronic: Slow onset (days-weeks), pH near-normal (renal
compensation).
Pathophysiology
### Mechanisms of Hypoxemia (Mnemonics: “V-SHUNT”)
Ventilation-perfusion (V/Q) mismatch (e.g., COPD, PE)
Shunting (blood bypasses alveoli, e.g., atelectasis)
Hypoventilation (e.g., opioids, CNS depression)
Alveolar diffusion barrier (e.g., fibrosis)
Non-cardiac pulmonary edema (e.g., ARDS)
Tissue oxygen demand ↑ (e.g., sepsis, fever)
Key Pathways
Injury → Inflammation → Capillary leak → Alveolar flooding → Surfactant
loss → Atelectasis.
Hypercapnia from reduced alveolar ventilation (e.g., airway
obstruction, muscle fatigue).
Clinical Manifestations
Hypoxemia
Cyanosis, restlessness, tachycardia, confusion.
Late signs: Bradycardia, coma.
Hypercapnia
Headache, drowsiness, asterixis, papilledema.
CO₂ narcosis: Confusion → Coma.
Pulmonary vs. Extrapulmonary Symptoms
Pulmonar Extrapulmo
y nary
Dyspnea, Fatigue,
cough, weight loss,
wheeze edema
Hemopty Morning
sis, chest headaches,
pain snoring
Diagnosis
Investigations
ABG: Gold standard (PaO₂, PaCO₂, pH, HCO₃⁻).
CXR/CT: Pneumonia, ARDS, PE.
PFTs: Obstructive vs. Restrictive patterns.
ECG/Echo: Rule out cardiac causes (e.g., CHF).
Mnemonics for Etiology: “AIRWAYS”
Asthma/ARDS
Infection (pneumonia)
Restrictive disease (fibrosis)
Weakness (neuromuscular)
Aspiration/atelectasis
Yes (COPD)
Shock/sepsis
Management
General Principles
Secure airway: Intubation if GCS <8 or severe hypoxia.
Oxygen therapy: Target SpO₂ 88–92% (COPD) or >94% (others).
Treat underlying cause: Antibiotics for infection, diuretics for edema.
Ventilatory Support
Non-invasive (BiPAP): COPD exacerbation, cardiogenic pulmonary
edema.
Invasive (MV): ARDS, coma, refractory hypoxia.
Pharmacotherapy
Bronchodilators: β-agonists (salbutamol), anticholinergics
(ipratropium).
Steroids: For inflammation (e.g., asthma, COPD).
Diuretics: Pulmonary edema.
Surgical Options
Bullectomy (for giant bullae in COPD).
Lung transplant (end-stage disease).
Nursing & Monitoring
Positioning: “Good lung down” for unilateral disease.
Nutrition: High-protein, low-carb diet to reduce CO₂ production.
Complication watch: Barotrauma, VAP, PE.
Complications & Prognosis
ARDS mortality: ~40%.
Chronic RF: Poor prognosis if untreated (e.g., O₂-dependent
COPD).
Key Takeaways (Mnemonics: “FAILURE”)
Fix oxygenation first.
ABG is mandatory.
Intubate if unstable.
Look for underlying cause.
Use BiPAP for COPD.
Repeat assessments.
Early rehab improves outcomes.
Conclusion
Respiratory failure demands rapid diagnosis and tailored intervention.
Focus on oxygenation, ventilation, and treating the root cause to
improve survival and quality of life.
