Respiratory Emergencies

Upper airway (obstructive) causes

• Anatomic obstruction: foreign body aspiration, epiglottitis (now largely non-Hib organisms post-vaccination), retropharyngeal abscess, croup, post-extubation laryngeal edema, expanding neck hematoma.
• Angioedema: ACE inhibitor–induced (bradykinin-mediated, no urticaria, may occur years into therapy) or hereditary C1-esterase inhibitor deficiency; histaminergic angioedema accompanies anaphylaxis.

Lower airway (dynamic obstruction) causes

• Status asthmaticus: triggered by viral respiratory infection, allergen or smoke exposure, aspirin/NSAIDs in aspirin-exacerbated respiratory disease, and nonadherence to inhaled corticosteroids. NAEPP/GINA identify prior intubation or ICU admission, ≥2 hospitalizations in the past year, heavy short-acting beta-agonist canister use, no ICS controller, and food allergy as markers of near-fatal asthma risk.
• COPD exacerbation: bacterial or viral infection, air pollution, missed maintenance therapy.

Pleural causes

• Tension pneumothorax: penetrating or blunt trauma, positive-pressure ventilation (barotrauma), central line placement, and rupture of apical blebs. Primary spontaneous pneumothorax favors tall, thin young men and smokers; Marfan and Ehlers-Danlos syndromes are non-modifiable predispositions; secondary pneumothorax complicates emphysema, cystic fibrosis, and Pneumocystis pneumonia.

Vascular causes

• Pulmonary embolism: Virchow triad — stasis (immobility, long travel, casting), endothelial injury (surgery, trauma), hypercoagulability. Non-modifiable: inherited thrombophilias (factor V Leiden, prothrombin G20210A), malignancy, prior VTE, increasing age. Modifiable: estrogen-containing contraceptives, pregnancy/postpartum, obesity, smoking, immobility.

Parenchymal causes

• ARDS: sepsis is the single most common precipitant, followed by aspiration of gastric contents, pneumonia, severe trauma with massive transfusion, pancreatitis, near-drowning, and inhalational injury. Chronic alcohol use and smoking increase susceptibility.
• TRALI: a distinct, immune-mediated transfusion reaction (donor anti-HLA/anti-neutrophil antibodies) producing hypoxemia with bilateral infiltrates within 6 hours of transfusion; it is non-cardiogenic, so filling pressures are normal — the key discriminator from TACO (transfusion-associated circulatory overload, which is volume-driven and responds to diuresis).

Neuromuscular and CNS causes

• Hypoventilatory failure: opioid or benzodiazepine overdose, high cervical cord injury, Guillain-Barré syndrome, myasthenic crisis, botulism, organophosphate poisoning.

• Hypoxemia mechanisms: Develop through five primary pathways—(1) hypoventilation (reduced minute ventilation from CNS depression, neuromuscular weakness, or fatigue), (2) diffusion impairment (thickened alveolar-capillary membrane from pulmonary edema or fibrosis), (3) ventilation-perfusion (V/Q) mismatch (blood perfusing unventilated alveoli in pneumonia or atelectasis), (4) shunting (deoxygenated blood bypassing ventilated alveoli in severe ARDS or cardiac disease), and (5) low inspired oxygen (high altitude, anesthetic errors). Most respiratory emergencies involve multiple simultaneous mechanisms.

• Acute hypercapnia and respiratory acidosis: Occurs when ventilation cannot match CO₂ production, causing elevated PaCO₂ and decreased pH. The respiratory center's limited ability to increase minute ventilation (maximum ~60 L/min) means even moderate increases in CO₂ production (sepsis, fever, agitation) rapidly overwhelm compensatory mechanisms. Hypercapnia causes cerebral vasodilation, increased intracranial pressure, and depression of consciousness, creating a vicious cycle of worsening hypoventilation.

• Increased work of breathing and respiratory muscle fatigue: In obstructive diseases (asthma, COPD exacerbation, anaphylaxis), narrowed airways dramatically increase airflow resistance (inversely proportional to the fourth power of radius), exponentially increasing the muscular effort required. Accessory muscle recruitment (intercostals, scalenes, sternocleidomastoid) initially compensates but depletes energy stores within hours, leading to acute fatigue and rapid decompensation. Positive end-expiratory pressure (PEEP) and intrinsic PEEP in obstructive disease further increase the elastic work needed.

• Airway obstruction mechanics: Complete or near-complete occlusion prevents air entry and creates high negative intrathoracic pressures during inspiratory effort, pulling tissue inward (stridor or wheeze) and predisposing to complete airway closure. Partial obstruction converts laminar airflow to turbulent flow, increasing resistance. Foreign bodies, angioedema, epiglottitis, and laryngospasm cause anatomic obstruction; anaphylaxis and asthma cause dynamic obstruction from smooth muscle contraction and edema.

• Tension physiology in pleural emergencies: Tension pneumothorax and tension hemothorax create progressive positive intrathoracic pressure that compresses the ipsilateral lung, shifts the mediastinum contralaterally, kinks the great vessels, and impairs venous return. This leads to cardiovascular collapse even with moderate volume loss. In contrast, simple pneumothorax allows equilibration between pleural and atmospheric pressure, causing gradual lung collapse without hemodynamic compromise.

• Acute dyspnea with stridor: High-pitched, musical breathing sound indicates upper airway obstruction (at or above glottis). Classic associations include croup (barky "seal bark" cough in children), epiglottitis (tripod position, drooling, "hot potato" voice, rarely seen post-Hib vaccine), angioedema (urticaria, tongue/lip swelling), and anaphylaxis (rapid onset with other systemic symptoms). Stridor may be biphasic (both inspiratory and expiratory) in fixed obstruction or predominantly inspiratory in variable obstruction.

• Acute dyspnea with wheezing: Low-pitched, musical breath sounds reflecting turbulent airflow through narrowed lower airways indicates lower airway obstruction. Classic presentation in acute asthma includes sudden-onset dyspnea, chest tightness, cough, and diffuse expiratory wheeze; however, severely obstructed patients may have "silent chest" (absent wheeze from insufficient airflow). Status asthmaticus describes severe asthma unresponsive to standard therapy. COPD exacerbations present with gradually worsening dyspnea, increased sputum production, and change in sputum character.

• Acute dyspnea with hypoxemia and crackles: Fine, late-inspiratory crackles (formerly "rales") indicate pulmonary edema from cardiogenic causes (acute decompensated heart failure, acute coronary syndrome, hypertensive crisis) or non-cardiogenic causes (ARDS, sepsis, aspiration, pneumonia). Patients report orthopnea, paroxysmal nocturnal dyspnea, and present with pink frothy sputum in acute pulmonary edema. Absence of crackles does not exclude pulmonary edema in early disease.

• Acute dyspnea with pleuritic chest pain and unilateral findings: Suggests tension pneumothorax (sudden-onset unilateral pleuritic pain, dyspnea, hypotension, tracheal deviation, JVD, absent breath sounds and hyperresonance to percussion on affected side—treat immediately with needle decompression before imaging) or tension hemothorax (similar presentation but from hemorrhage). Simple pneumothorax presents with milder dyspnea and chest pain, normal vital signs, and absent breath sounds.

• Acute dyspnea with throat symptoms and systemic features: Anaphylaxis presents with dyspnea secondary to angioedema, bronchospasm, or both; associated symptoms include urticaria, pruritus, angioedema of lips/tongue, hypotension, syncope, GI symptoms (vomiting, diarrhea), and cardiovascular collapse. Symptoms typically begin within minutes to 2 hours of exposure (food, medications, insects, latex). Epiglottitis presents with severe sore throat, difficulty swallowing, drooling, "hot potato voice," fever, and rapid progression to respiratory obstruction.

• Acute dyspnea with altered mental status or neuromuscular findings: Indicates potential hypoventilatory respiratory failure from CNS depression (opioid overdose, benzodiazepines, head injury, seizure), neuromuscular disease (Guillain-Barré syndrome, myasthenia gravis, spinal cord injury), or muscle weakness (status epilepticus, tetanus). Patients often appear calm or somnolent, with reduced respiratory effort despite hypoxemia and hypercapnia—the absence of tachypnea in a hypoxic patient is a red flag.

• Acute dyspnea with signs of shock: Combination of hypoxemia with hypotension, tachycardia, altered mental status, and poor perfusion suggests massive pulmonary embolism, acute decompensated heart failure with cardiogenic shock, or sepsis-induced ARDS. Massive PE may present with syncope as the first symptom and minimal respiratory findings if there is minimal initial V/Q mismatch.

• Pulse oximetry and capnography: Pulse oximetry measures oxygen saturation (SpO₂) and detects hypoxemia; critical threshold is SpO₂ <90% or <94% in COPD patients accustomed to higher CO₂. Capnography (end-tidal CO₂, ETCO₂) is the gold standard for confirming endotracheal tube placement and detecting hypoventilation (ETCO₂ <35 mmHg suggests inadequate ventilation). In asthma/COPD, prolonged expiratory phase with elevated ETCO₂ suggests obstructive physiology; in pulmonary edema, biphasic capnography waveform may appear ("shark fin").

• Arterial blood gas (ABG) analysis: Essential for characterizing acid-base status and severity. Respiratory acidosis (pH <7.35, PaCO₂ >45) indicates hypoventilation and requires urgent intervention. Respiratory alkalosis (pH >7.45, PaCO₂ <35) indicates hyperventilation (pain, anxiety, hypoxemia driving increased ventilation). **Normal ABG in a dyspneic patient with stridor or severe obstruction

Immediate stabilisation (before imaging)

• Tension pneumothorax: clinical diagnosis — perform needle decompression immediately. ATLS (American College of Surgeons) now favors a large-bore angiocatheter in the 5th intercostal space at the anterior axillary line in adults (2nd ICS midclavicular line remains acceptable), followed obligatorily by tube thoracostomy, which is the definitive therapy. Do not delay for chest radiograph.
• Anaphylaxis: epinephrine 0.3–0.5 mg IM (0.01 mg/kg in children) into the anterolateral thigh, repeated every 5–15 minutes; per the AAAAI/ACAAI Joint Task Force practice parameter, epinephrine is first-line and antihistamines/glucocorticoids are adjuncts only — never substitutes.
• Airway: definitive airway for failure to oxygenate, ventilate, or protect. Anticipate the difficult airway in angioedema and epiglottitis; prepare for surgical cricothyrotomy.
• Noninvasive positive-pressure ventilation: BiPAP for COPD exacerbation with hypercapnic respiratory acidosis (GOLD) and CPAP/BiPAP for cardiogenic pulmonary edema reduce intubation rates and mortality. Contraindicated with depressed mental status or inability to protect the airway, vomiting, facial trauma, or hemodynamic instability — these patients need intubation.
• Naloxone: opioid antagonist for opioid-induced hypoventilation; titrate to an adequate respiratory rate, not to full arousal, to avoid precipitating withdrawal. Its duration is shorter than that of many opioids, so observe for re-sedation and consider an infusion.

Status asthmaticus (NAEPP/GINA)

• Inhaled short-acting beta-agonist: albuterol, continuous nebulization, plus ipratropium in the first hour.
• Systemic corticosteroids: prednisone orally or methylprednisolone IV — the intervention that prevents relapse; onset takes hours.
• Magnesium sulfate 2 g IV over ~20 minutes for severe/refractory obstruction; consider heliox, epinephrine IM, and ketamine-facilitated intubation as rescue.

Pulmonary embolism (CHEST and AHA statements)

• Anticoagulation: LMWH (enoxaparin) or unfractionated heparin; a DOAC (apixaban, rivaroxaban) for stable patients.
• Systemic thrombolysis: alteplase for hemodynamically unstable (massive) PE; catheter-directed therapy or surgical embolectomy when lysis is contraindicated or fails. IVC filter only when anticoagulation is absolutely contraindicated.

ARDS (ATS/ESICM/SCCM)

• Lung-protective ventilation: tidal volume 6 mL/kg predicted body weight, plateau pressure <30 cmH₂O, higher PEEP, permissive hypercapnia — one of the few interventions with a demonstrated mortality benefit.
• Prone positioning >12 hours daily for PaO₂/FiO₂ <150 also reduces mortality (PROSEVA); a conservative fluid strategy increases ventilator-free days; consider ECMO referral in refractory hypoxemia.

Contraindicated

• Routine high-dose corticosteroids and inhaled beta-agonists for ARDS; thrombolysis in any prior intracranial hemorrhage, ischemic stroke within 3 months, known intracranial neoplasm or vascular malformation, active bleeding, or recent intracranial/spinal surgery; sedation of a hypercapnic patient without airway control.

Disease-related — emergencies

• Obstructive shock and PEA arrest (tension pneumothorax): rising intrapleural pressure kinks the vena cavae and abolishes venous return; signaled by hypotension with distended neck veins, absent unilateral breath sounds, and loss of pulses. Immediate needle decompression, not intubation, is the answer.
• Acute cor pulmonale (massive PE): sudden rise in pulmonary vascular resistance dilates the RV, bows the septum leftward, and drops LV preload; signaled by hypotension, elevated troponin/BNP, and RV dilation with McConnell sign on bedside echo. Herald of imminent arrest.
• Respiratory muscle fatigue in status asthmaticus: signaled by a normalizing or rising PaCO₂, silent chest, and somnolence — impending arrest, not improvement.
• Hypoxic-ischemic brain injury from any delayed airway intervention.

Treatment-related

• Dynamic hyperinflation / breath stacking after intubating an asthmatic: insufficient expiratory time creates intrinsic PEEP; signaled by abrupt post-intubation hypotension. Disconnect the circuit and allow passive exhalation, then reduce respiratory rate and tidal volume.
• Barotrauma/volutrauma: high plateau pressures rupture alveoli, producing pneumothorax, pneumomediastinum, or subcutaneous emphysema — the rationale for the ARDSNet 6 mL/kg strategy endorsed by ATS/ESICM/SCCM.
• Re-expansion pulmonary edema: rapid evacuation of a large, chronic pneumothorax or effusion causes ipsilateral capillary leak with unilateral infiltrate and hypoxemia.
• Chest tube injury: intercostal artery laceration, lung or diaphragm perforation, malposition.
• Bleeding from thrombolysis: intracranial hemorrhage is the feared complication; new headache or focal deficit mandates stopping the infusion and emergent noncontrast head CT.
• Heparin-induced thrombocytopenia: platelet fall ~5–10 days after heparin exposure with new thrombosis; stop all heparin and use a non-heparin anticoagulant.
• Ventilator-associated pneumonia, ICU-acquired weakness, and post-ARDS pulmonary fibrosis from prolonged mechanical ventilation.

• Tension pneumothorax is a clinical diagnosis: hypotension + unilateral absent breath sounds + JVD. The single best next step is needle decompression, then chest tube — never "obtain chest x-ray." Tracheal deviation is a late and unreliable sign; do not require it.
• A "normal" PaCO₂ in a tachypneic asthmatic is a red flag: severe asthma should produce respiratory alkalosis. Normalization means the patient is tiring, and the silent chest is the physical-exam correlate. Contrast this with the reassuring distractor of "improved wheezing."
• Systemic corticosteroids change outcomes in asthma; beta-agonists only buy time. Give steroids early even though the effect is delayed several hours (NAEPP/GINA).
• Post-intubation hypotension in an asthmatic = breath stacking. Disconnect the ventilator and press on the chest; the reflex answer of "give fluids and pressors" is the distractor. Ventilate with a low rate, long expiratory time, and permissive hypercapnia.
• PE workup follows pretest probability: PERC to avoid testing in low-risk patients, D-dimer for low/intermediate risk, CT pulmonary angiography otherwise. S1Q3T3, Westermark sign, and Hampton hump are classic but insensitive; sinus tachycardia is the most common finding. In hemodynamic instability or renal failure, bedside echo showing RV strain justifies treatment.
• Anaphylaxis: epinephrine 0.3 mg IM in the anterolateral thigh is always the first action (AAAAI/ACAAI). Diphenhydramine and steroids are distractors as first-line; steroids do not reliably prevent the biphasic reaction.
• ACE-inhibitor angioedema is bradykinin-mediated: no urticaria, no pruritus, and it does not respond to epinephrine, antihistamines, or steroids the way histaminergic angioedema does — secure the airway and stop the drug permanently.
• ARDS by the Berlin definition requires acute onset within a week, bilateral opacities, PaO₂/FiO₂ ≤300 on ≥5 cmH₂O PEEP, and hypoxemia not fully explained by cardiogenic edema. Only low tidal volume ventilation and prone positioning for severe disease have shown mortality benefit.