COPD, asthma, cystic fibrosis, ILD, pneumonia, pulmonary embolism, and lung cancer.
95 min estimated
COPD is an irreversible obstructive lung disease, predominantly caused by tobacco smoke (90% of cases). Encompasses emphysema and chronic bronchitis.
Emphysema: destruction of alveolar walls → loss of elastic recoil → air trapping. 'Pink puffer' (Type A COPD): thin, tachypneic, pursed-lip breathing, barrel chest, minimal hypoxemia until advanced.
Chronic bronchitis: productive cough ≥3 months/year for ≥2 consecutive years. Mucus hypersecretion, airway inflammation. 'Blue bloater' (Type B COPD): hypoxic, hypercapnic, polycythemic, edematous, frequent exacerbations.
GOLD staging by post-bronchodilator FEV1: GOLD 1 (mild ≥80%), GOLD 2 (moderate 50–79%), GOLD 3 (severe 30–49%), GOLD 4 (very severe <30%).
Clinical Tip
Oxygen therapy for COPD: target SpO2 88–92%. Avoid excessive O2 — can worsen hypercapnia by releasing hypoxic vasoconstriction and Haldane effect.
Asthma is reversible airway hyperresponsiveness and inflammation with intermittent episodes of bronchospasm. Classified by frequency and severity per GINA guidelines:
Intermittent: symptoms ≤2 days/week, no nighttime symptoms, FEV1 ≥80%. Step 1: SABA PRN. Mild persistent: >2 days/week, ≤1 nighttime/month. Step 2: low-dose ICS. Moderate persistent: daily symptoms, nighttime 1×/week. Step 3–4: medium-dose ICS + LABA. Severe persistent: continuous symptoms, frequent nighttime. Step 5–6: high-dose ICS + LABA + biologics/oral steroids.
Status asthmaticus: severe acute asthma not responding to initial treatment — risk of respiratory arrest. Management: aggressive bronchodilators, IV magnesium, possible intubation (avoid if possible — very difficult to ventilate).
Clinical Tip
Venting an asthmatic: use long expiratory times (I:E 1:3 to 1:4), low RR (10–12), and be prepared for high pressures and auto-PEEP. Accept permissive hypercapnia.
Pulmonary embolism (PE) is a thrombus obstructing the pulmonary arterial circulation. PE is on the differential for any unexplained tachycardia, hypoxemia, or pleuritic chest pain.
Risk factors (Virchow's triad): venous stasis (prolonged immobility, surgery), endothelial injury, hypercoagulability (malignancy, genetic thrombophilia, OCP).
Classification: massive PE (hemodynamic instability, SBP <90 or 40 mmHg drop) → systemic thrombolytics or catheter-directed therapy; submassive PE (RV dysfunction but hemostable) → anticoagulation ± catheter therapy; low-risk PE → anticoagulation.
Respiratory findings: tachypnea, pleuritic chest pain, hemoptysis, sudden-onset dyspnea. ABG: respiratory alkalosis + elevated A-a gradient. ECG: S1Q3T3, sinus tachycardia.
Clinical Tip
In PE, the A-a gradient is elevated (V/Q mismatch/dead space) but the PaCO2 is low (hyperventilation). Unlike pneumonia where you'd expect high PaCO2 with severe disease.
COPD Exacerbation with Hypercapnia
A 66-year-old smoker with COPD presents with dyspnea and increased sputum. SpO2 82% on RA. You apply 100% NRB mask. After 20 min SpO2 is 99% but he becomes increasingly somnolent.
What happened and what should you do?
Hypercapnic respiratory failure worsened by excessive O2. Remove NRB, titrate O2 to SpO2 88–92%, consider NIV (BiPAP).
COPD patients with chronic CO2 retention can develop worsening hypercapnia with high-flow O2 (Haldane effect: O2 displaces CO2 from hemoglobin; loss of hypoxic ventilatory drive). Target SpO2 88–92%. BiPAP is first-line for COPD exacerbation with hypercapnia — reduces need for intubation and mortality.
Mechanical Ventilation
Master ventilator modes, initial settings, troubleshooting, weaning, and complications.
Respiratory Pharmacology
Master every drug an RT uses — bronchodilators, steroids, mucolytics, surfactants, and more.
Arterial Blood Gas Interpretation
Master systematic ABG interpretation including primary disorders, compensation, and mixed disturbances.
Oxygen Therapy
Delivery systems, FiO2 calculations, indications, complications, and oxygen toxicity.