Airway & Respiratory

• Expiratory wheezing (polyphonic, diffuse)
• Prolonged expiratory phase
• Accessory muscle use (sternocleidomastoid, intercostal retractions)
• Dyspnea — inability to complete a sentence without stopping
• Tachycardia and diaphoresis with severe attacks
• Tripod positioning; hunched forward

vs. COPD: Asthma typically occurs in younger patients with episodic attacks and reversible bronchospasm. COPD presents in older smokers with a chronic baseline. Both wheeze — age, history, and reversibility are the differentiators.

Silent chest (no wheezing audible) = severe air trapping with minimal airflow. This is near-respiratory failure, not improvement. Immediate aggressive management.

• Barrel chest (chronic air trapping, increased AP diameter)
• Pursed-lip breathing (applies PEEP-like back-pressure to prevent small airway collapse)
• Prolonged expiration; diminished breath sounds throughout
• Tripod positioning; use of accessory muscles
• Chronic productive cough; cyanosis in severe exacerbation
• History of smoking; baseline dyspnea worse than normal

vs. Asthma: COPD patients are typically older with irreversible obstruction and chronic baseline symptoms. Asthma patients present with episodic attacks between which they may be completely symptom-free.

Hypoxic drive concern: target SpO2 88–92% in confirmed COPD patients. High-flow O2 may blunt hypoxic drive and cause hypoventilation. Titrate O2 — do not withhold it if the patient is critically hypoxic.

• Productive cough (yellow, green, or rust-colored sputum)
• Fever and chills (often high-grade)
• Pleuritic chest pain (sharp, worse with inspiration)
• Crackles (rales) over the affected lobe; dullness to percussion
• Tachypnea; decreased breath sounds over consolidated area
• Fatigue, malaise; confusion in elderly ("altered pneumonia")

vs. Pulmonary edema: Pneumonia has fever, productive cough, and typically unilateral/lobar findings. Pulmonary edema has bilateral crackles, frothy sputum, cardiac history, and orthopnea — no fever.

SpO2 <90% with fever in elderly = high-acuity presentation. Suspect septic shock if hypotension develops. Pneumonia is the leading infectious cause of sepsis.

• Sudden-onset dyspnea (most consistent finding)
• Pleuritic chest pain (sharp, worse with breathing)
• Tachycardia and tachypnea
• Hypoxia with a clear chest (no crackles, no wheezes)
• Hemoptysis (blood-tinged sputum)
• Unilateral leg swelling/pain (DVT source clue)

vs. Acute MI: PE pain is pleuritic (worse with breathing). MI pain is pressure/squeezing. PE classically presents with a clear lung exam despite severe dyspnea — MI may show crackles if heart failure develops. Ask about DVT risk factors (long travel, surgery, immobility, cancer).

Massive PE causes sudden hemodynamic collapse (obstructive shock) with profound hypotension and hypoxia. S1Q3T3 pattern on ECG (right heart strain) suggests significant clot burden.

• Unilateral absent/decreased breath sounds
• Pleuritic chest pain (sharp, unilateral)
• Dyspnea; increased work of breathing
• Tension adds: JVD, tracheal deviation (toward unaffected side — late sign), severe hypotension, tachycardia
• Tension: hypoxia refractory to oxygen; cyanosis
• Tension: patient deteriorating despite ventilatory support

Simple vs. Tension: Hemodynamic instability (hypotension + JVD) defines tension. Simple pneumothorax does not cause shock. Tracheal deviation is a late sign — do not wait for it to treat a clinically deteriorating patient.

Tension pneumothorax causes obstructive shock and is immediately life-threatening. Decompress with needle decompression (2nd ICS, MCL) before transport if hemodynamically unstable — do not wait for imaging.

• Severe dyspnea; orthopnea (can't lie flat) and PND
• Bilateral basilar crackles (rales) — wet lung sounds
• Pink frothy sputum (severe alveolar flooding)
• Diaphoresis; pallor; tachycardia
• JVD and peripheral edema (3+ pitting)
• Hypertension (hypertensive CHF) or hypotension (cardiogenic shock)

vs. Pneumonia: CHF has bilateral crackles, cardiac history, orthopnea, and responds rapidly to CPAP and nitroglycerin. Pneumonia has fever, productive cough, and typically unilateral/lobar presentation.

Flash pulmonary edema deteriorates rapidly. Apply CPAP early — do not wait for the patient to "try" oxygen first. RSI/intubation if mental status deteriorates despite CPAP.

• Stridor (upper airway angioedema) and/or wheezing (bronchospasm)
• Urticaria (hives) and skin flushing
• Angioedema (swelling of lips, tongue, uvula, glottis)
• Dysphagia and muffled voice (impending airway loss)
• Hypotension and tachycardia (distributive shock)
• Known exposure: foods, medications, venom, latex

vs. Acute asthma: Anaphylaxis has systemic allergic features — urticaria, flushing, angioedema, and hypotension. Asthma lacks skin findings and hemodynamic compromise. Recent exposure to a known allergen is a critical history finding.

Airway compromise can develop within minutes of exposure. Epinephrine IM (0.3 mg of 1:1000 solution) is the only definitive treatment — do not delay for an IV or for antihistamines alone.