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Second-generation SGAs (e.g., i-gel, LMA Supreme) improve seal at higher pressures and include gastric drain channels that reduce insufflation and aspiration risk. Correct sizing and depth are critical; reinsertion with proper technique often resolves leaks. Simply tightening straps (A) doesn’t fix an internal seal issue. Forcing pressures (C) increases gastric insufflation and aspiration risk. Blind nasal intubation (D) is low-success and traumatic. If ventilation remains inadequate, transition to definitive airway (ETT via flexible bronchoscope through SGA or surgical airway) per failed-airway algorithm. Continuous waveform capnography, chest rise, and auscultation guide adequacy while preparing the next step.

Persistent leak compromises ventilation and risks aspiration. Excess cuff inflation injures mucosa without fixing an undersized/malpositioned tube. Uncuffed trachs are inappropriate for positive pressure ventilation. Confirm depth and orientation; an undersized or partially extraluminal tube is common. Exchange to correct size/length, then keep cuff pressure 20–30 cm H₂O with a manometer. Re-secure ties, verify with capnography and auscultation, and reassess exhaled VT. Have contingency equipment ready (BVM with trach adapter, SGA/ETT) in case of accidental decannulation during exchange—critical in transport where rescue options must be immediate.

Hydrostatic error alters invasive pressures by ~0.74–0.77 mmHg per cm. Twelve centimeters below adds ≈9 mmHg to systolic, diastolic, and MAP—masking hypotension and risking undertreatment. Reposition the transducer at the phlebostatic axis (4th ICS, mid-axillary line), re-zero, and confirm fidelity with a square-wave test. Correlate with cuff readings and the clinical picture before vasoactive adjustments. In transport, re-level after any position change and keep tubing free of dependent loops to avoid damping artifacts—fundamental to safe vasoactive titration in CCP-C practice.

HFNC offers heated, humidified high flow that washes out nasopharyngeal dead space, provides mild distending pressure, and reduces work of breathing—first-line escalation after low-flow failure in bronchiolitis. Properly sized cannula (not occluding nares) and careful titration of flow/FiO₂ are essential. Immediate intubation (A) is reserved for refractory hypoxemia, apnea, or exhaustion; premature intubation increases complications in a transport environment. A non-humidified NRB (C) is uncomfortable, poorly tolerated, and does not address airway obstruction/mucus plugging. Opioids (D) risk respiratory depression. CCP-C priorities: frequent suctioning, thermoregulation, hydration management, continuous SpO₂ monitoring, and readiness to escalate to CPAP or invasive ventilation if SpO₂ or CO₂ deteriorate. Communicate early with the receiving pediatric facility and ensure equipment compatibility en route.

For septic shock with persistent hypotension after adequate fluid resuscitation, first-line vasopressor therapy is norepinephrine. It primarily stimulates α1 receptors with some β1 activity, improving vascular tone and MAP with less tachyarrhythmia than dopamine. While central venous administration is preferred, evidence supports initiating norepinephrine through a well-placed large-bore peripheral IV in a proximal vein (forearm/antecubital) with frequent site checks during transport. Initial dosing commonly starts at 0.05–0.1 mcg/kg/min (or 2–5 mcg/min titrated to MAP ≥65 mmHg), titrating to effect. Phenylephrine (A) is pure α-agonist and can decrease stroke volume; it’s reserved for specific scenarios (e.g., catecholamine-induced tachyarrhythmias). Dopamine (C) at 10–20 mcg/kg/min increases tachyarrhythmia risk and is no longer favored. Epinephrine (D) is acceptable as an alternative pressor, but its β-effects increase lactate and tachycardia; it’s typically second-line in septic shock. Monitor for extravasation and have phentolamine available if permitted by protocol.