Pulmonary Emergencies · Rapid Reference for Medical Students

🚨 Pulmonary Emergencies A Rapid Reference for Medical Students · High‑Stakes Management

1. Tension Pneumothorax

Definition: One‑way valve mechanism → progressive air accumulation in pleural space → ↑ intrathoracic pressure → impaired venous return → obstructive shock.

Clinical Recognition

Hypotension, tachycardia, respiratory distress
Tracheal deviation away from affected side
Absent breath sounds, hyperresonance to percussion
Jugular venous distension (unless hypovolemic)

Immediate Management

Do not wait for CXR. Clinical diagnosis is sufficient.
Needle Decompression: 14‑16 gauge angiocatheter, 2nd intercostal space, midclavicular line (or 5th ICS anterior axillary line). Insert just above the rib.
Gush of air confirms diagnosis. Leave catheter in place.
Tube Thoracostomy (Chest Tube): Place immediately after needle decompression (usually 5th ICS, anterior axillary line).

⚠️ Needle decompression is a temporizing measure. Definitive management is chest tube. If no rush of air with needle, consider other causes of shock/arrest.

2. Massive Hemoptysis

Definition: Expectoration of >300–600 mL blood in 24 hours, or any amount causing hemodynamic compromise or gas exchange abnormality.

Most common source: Bronchial arteries (90%), not pulmonary arteries.

Etiologies

TB, bronchiectasis, lung cancer, aspergilloma, pulmonary embolism, coagulopathy

Management Algorithm

Airway Protection: Place patient in lateral decubitus position, bleeding side down to protect contralateral lung.
Intubate with large ETT (≥8.0) if unable to protect airway or severe hypoxemia. Consider mainstem intubation of unaffected lung.
Reverse Coagulopathy: FFP, platelets, vitamin K, TXA (inhaled or IV).
Localization: CXR, then CT angiography (bronchial artery mapping).
Definitive Control: Bronchial Artery Embolization (BAE) — first‑line interventional therapy. Bronchoscopy may be used for localization/tamponade but BAE is more definitive.
Surgery (lobectomy/pneumonectomy) reserved for failed BAE or specific lesions (e.g., Rasmussen aneurysm).

💡 "Bleed Down" — Position patient with bleeding lung dependent to prevent aspiration into healthy lung.

3. Acute Upper Airway Obstruction

Causes & Presentation

Foreign body aspiration: Sudden onset, choking, stridor. Incomplete obstruction: "café coronary" in elderly.
Angioedema: ACE inhibitor‑related, allergic reaction. Lip/tongue swelling, stridor.
Epiglottitis: Sore throat, drooling, "tripod" position. Do NOT examine oropharynx or lay patient flat.
Anaphylaxis: Stridor, wheezing, urticaria, hypotension.
Post‑extubation stridor: Laryngeal edema.

Immediate Interventions

Intervention	Indication	Notes
Heliox (70% Helium / 30% O₂)	Temporizing measure for partial obstruction	Lower density gas reduces turbulent flow; requires FiO₂ ≤0.4 to maintain helium fraction
Racemic Epinephrine (nebulized)	Post‑extubation stridor, croup	α‑adrenergic vasoconstriction reduces mucosal edema
IM Epinephrine	Anaphylaxis / angioedema	0.3‑0.5 mg IM (lateral thigh)
Awake Fiberoptic Intubation	Anticipated difficult airway	Preserves spontaneous ventilation; requires expertise
Cricothyroidotomy	"Can't intubate, can't ventilate"	Surgical airway of last resort

🚫 Avoid sedation/paralysis in upper airway obstruction — loss of airway tone can convert partial to complete obstruction.

4. Status Asthmaticus (Severe Asthma Exacerbation)

Definition: Severe asthma attack unresponsive to initial bronchodilator therapy; risk of respiratory failure.

Signs of Impending Respiratory Arrest

Altered mental status, exhaustion
Silent chest (no wheezing — airflow too low to generate sound)
Paradoxical thoracoabdominal movement
Normal or elevated PaCO₂ (should be low due to hyperventilation; "normal" PaCO₂ is a warning sign)
Pulsus paradoxus >25 mmHg

Management Algorithm

Oxygen: Target SpO₂ 94‑98% (do not restrict O₂ for fear of CO₂ retention — not a concern in acute asthma).
Continuous Nebulized Bronchodilators: Albuterol + Ipratropium.
Systemic Corticosteroids: Methylprednisolone 60‑125 mg IV or Prednisone PO. Give early; takes hours to work.
Magnesium Sulfate: 2 g IV over 20 min. Smooth muscle relaxant. Monitor for hypotension.
Consider NIPPV (BiPAP): May reduce work of breathing and avoid intubation. Use caution — risk of gastric insufflation.
Intubation & Mechanical Ventilation (if indicated):
- Use largest ETT possible to reduce resistance.
- Permissive Hypercapnia: Low Vᴛ (6‑8 mL/kg), low RR (8‑12), long expiratory time (I:E 1:4 or 1:5) to prevent auto‑PEEP.
- Ketamine is ideal induction agent (bronchodilator properties).
Rescue Therapies: Heliox, IV Terbutaline, Inhaled anesthetics (ICU), ECMO.

5. Massive Pulmonary Embolism (PE)

Definition: Acute PE with sustained hypotension (SBP <90 mmHg for >15 min) or requiring vasopressors, or cardiac arrest.

Recognition

Sudden dyspnea, chest pain, syncope
Hypotension, tachycardia, ↑ JVP
ECG: S1Q3T3, RBBB, RV strain
POCUS: RV dilation, McConnell's sign (RV free wall akinesis with apical sparing), D‑shaped septum

Management Algorithm (ESC Guidelines)

Anticoagulation: Heparin bolus (80 units/kg) + infusion unless cardiac arrest or extreme hemodynamic instability (then go directly to lytics).
Assess for Thrombolytics:
- Indicated: Massive PE with hypotension or cardiac arrest.
- Consider in submassive PE: RV dysfunction + elevated troponin + signs of deterioration (no hypotension).
- Contraindications: Recent surgery, bleeding diathesis, prior hemorrhagic stroke.
Thrombolytic Regimen: tPA (Alteplase) 100 mg IV over 2 hours (or accelerated 0.6 mg/kg over 15 min in cardiac arrest).
If Thrombolytics Contraindicated or Failed:
- Surgical Embolectomy
- Catheter‑Directed Thrombolysis or Thrombectomy
Cardiac Arrest: Continue CPR for at least 60‑90 min after lytics (thrombolysis takes time to work). Consider ECMO (ECPR).

💡 In cardiac arrest with suspected PE: Administer thrombolytics immediately (if no absolute contraindications) — this is one of the few reversible causes of PEA arrest.

6. Acute COPD Exacerbation with Hypercapnic Failure

Key ABG Findings

pH <7.35, PaCO₂ >45, HCO₃⁻ elevated (acute‑on‑chronic)
Severe acidosis (pH <7.25) indicates need for ventilatory support

Management

Controlled Oxygen: Target SpO₂ 88‑92%. Start with Venturi mask 24‑28%.
Bronchodilators: Nebulized SABA + SAMA (albuterol + ipratropium).
Corticosteroids: Prednisone 40 mg daily or Methylprednisolone IV.
Antibiotics: If increased sputum purulence or infiltrate.
Non‑Invasive Ventilation (NIV / BiPAP): First‑line for acute hypercapnic respiratory failure (pH <7.35). Reduces need for intubation and mortality.
- Start IPAP 10‑12, EPAP 4‑5 cm H₂O.
- Titrate IPAP to improve pH/PaCO₂, EPAP to improve oxygenation.
Intubation if: NIV failure, altered mental status, hemodynamic instability, severe acidosis (pH <7.15) despite NIV.

7. Rapid Deterioration in Mechanically Ventilated Patient (DOPES Mnemonic)

Letter	Cause	Immediate Action
D	Displacement of ETT	Check depth, listen for breath sounds, EtCO₂
O	Obstruction of ETT (mucus plug, kink, biting)	Suction, pass suction catheter, bite block
P	Pneumothorax (tension)	Needle decompression if suspected
E	Equipment failure (ventilator, circuit leak)	Disconnect from vent, bag with 100% O₂
S	Stacked breaths (Auto‑PEEP)	Disconnect circuit briefly to allow exhalation, then adjust settings

8. Other Urgent Pulmonary Scenarios

Inhalational Injury / Smoke Inhalation

Consider cyanide toxicity (elevated lactate, normal PaO₂). Treat with hydroxocobalamin (Cyanokit).
Carboxyhemoglobin levels; treat CO poisoning with 100% O₂ or hyperbaric O₂.
Early intubation for airway edema.

Tracheobronchial Injury

Blunt trauma → tear at carina or proximal bronchi.
Signs: subcutaneous emphysema, pneumomediastinum, persistent air leak despite chest tube.
Bronchoscopy for diagnosis; surgical repair.

Acute Chest Syndrome (Sickle Cell)

New infiltrate + fever + respiratory symptoms in sickle cell patient.
Treat with O₂, hydration, pain control, antibiotics (cephalosporin + macrolide), transfusion (simple or exchange).

Severe Pulmonary Hypertension Crisis

Acute RV failure. Avoid hypoxemia, acidosis, hypothermia, high PEEP.
Inhaled nitric oxide or IV prostacyclin (epoprostenol).
Vasopressors: Vasopressin or Norepinephrine (maintain RV perfusion).

9. Top 10 Pulmonary Emergency Pearls

Tension pneumothorax is a clinical diagnosis — do not delay for imaging.
In massive hemoptysis, protect the good lung first (bleeding side down).
A "normal" PaCO₂ in status asthmaticus is a pre‑arrest sign.
NIV (BiPAP) reduces mortality in COPD exacerbation with acute hypercapnic failure.
In cardiac arrest with known or suspected PE, give thrombolytics.
Always check blood glucose in any patient with altered mental status and respiratory distress (DKA can mimic pneumonia/ARDS).
Angioedema from ACE inhibitors can occur years after starting the drug.
When in doubt, bag the patient — DOPES covers most vent emergencies.
Ketamine is the ideal induction agent for intubating severe asthma.
If needle decompression yields no air but suspicion remains high, place a chest tube — the needle may be too short.

🚨 Pulmonary Emergencies Rapid Reference · High‑yield for medical students, wards, and ICU.
Actionable algorithms for tension pneumothorax, massive hemoptysis, upper airway obstruction, status asthmaticus, massive PE, COPD exacerbation, and ventilator emergencies.