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When face mask seal is impossible, a second-generation SGA provides rapid, effective oxygenation/ventilation while protecting the c-spine with MILS. It serves as a bridge to definitive airway (ETT or surgical airway) and allows apneic oxygenation if transitioning to RSI. Low-flow nasal cannula (A) is inadequate. Blind nasal intubation (C) is low-success and hazardous in facial trauma. Cricothyrotomy (D) is reserved for “can’t oxygenate, can’t ventilate” when SGA fails or is contraindicated. Confirm SGA placement with waveform capnography, secure the device, and prepare equipment for definitive intubation or surgical airway as needed.

A sluggish square-wave response without oscillations indicates overdamping—air, clot, or compliant tubing blunting the signal and falsely elevating MAP. Troubleshoot the system: vigorous flush, purge bubbles, check for kinks/clots, ensure stiff tubing, re-level at the phlebostatic axis, and re-zero. Correlate with NIBP and clinical exam before vasoactive changes. Replacing the catheter (C) may be necessary if damping persists but is not the first step. Blindly titrating to a faulty MAP (A) risks undertreating hypotension; discarding all invasive data (D) ignores the value of a corrected waveform. Reliable hemodynamic data is essential for safe transport titration of pressors and fluids.

Refractory pediatric anaphylaxis warrants IV epinephrine infusion when IM doses and fluids are inadequate. Epinephrine addresses bronchospasm and vasoplegia simultaneously via β and α effects. Propranolol (B) is contraindicated; β-blockers can worsen anaphylaxis and blunt epinephrine response. Furosemide (C) has no role in acute anaphylaxis. Nicardipine (D) lowers blood pressure and is harmful. Alongside epinephrine infusion, provide aggressive isotonic fluids, H1/H2 blockers, corticosteroids, and inhaled β-agonists. Prepare for airway deterioration; consider early advanced airway if edema progresses. Continuous monitoring for arrhythmias and extravasation is essential; secure proximal IV or IO access and titrate carefully to perfusion targets while expediting transport.

Inhaled pulmonary vasodilators (epoprostenol, nitric oxide) preferentially dilate vessels in ventilated lung regions, improving V/Q matching and oxygenation without systemic hypotension. They are rescue adjuncts for refractory hypoxemia or RV strain but have not shown consistent mortality benefit (D). They do not act as mucolytics (C) and don’t meaningfully increase systemic cardiac output (A). In transport, ensure nebulizer/ventilator compatibility, monitor for rebound hypoxemia if interrupted, and continue core ARDS therapy: low VT, adequate PEEP, prone positioning when feasible, and hemodynamic optimization. Communicate dosing and delivery method to the receiving team to maintain continuity of care.

Analgesia-first (treat pain before deep sedation) improves comfort and synchrony with fewer hemodynamic hits. Fentanyl provides potent analgesia with relative stability; adding low-dose dexmedetomidine offers cooperative sedation and sympatholysis without respiratory depression. High-dose propofol (A) risks hypotension. Benzodiazepine boluses (C) lack analgesia and increase delirium/hypotension. NSAID monotherapy (D) is inadequate and potentially harmful in trauma/renal hypoperfusion. Titrate to pain/sedation goals, reassess frequently, and maintain MAP with balanced resuscitation; consider ketamine as a supplemental analgesic if opioid-tolerant.