Transport Pharmacology: Drugs That Matter in the Aircraft

Transport pharmacology is different from bedside pharmacology in ways that matter clinically. The drugs are the same, but the context changes everything: limited formulary, finite supply, weight-based dosing calculated under time pressure, no pharmacy backup, altitude effects on nebulized medications, and the reality that if you pick the wrong agent or the wrong dose, the next pharmacy is 30 minutes away at a minimum.

This is not a comprehensive drug reference. It is the framework for thinking about the drugs that matter most in the transport environment — organized by the problems they solve and the reasoning behind each choice.

Vasopressors: choosing the right agent for the right mechanism.

Vasopressor selection in transport is not formulaic. It depends on the hemodynamic mechanism, the patient’s underlying pathophysiology, and what is available in the formulary. Understanding the receptor pharmacology is what allows correct selection when the clinical picture does not match a textbook protocol.

Norepinephrine is the first-line vasopressor for distributive shock (septic, anaphylactic after epinephrine, neurogenic). It acts primarily on alpha-1 receptors (vasoconstriction) with moderate beta-1 effect (inotropy). It raises SVR and MAP without producing the tachycardia that dopamine does at vasopressor doses. Starting dose 0.1–0.2 mcg/kg/min, titrated to MAP ≥65 mmHg. Requires central access ideally, though peripheral administration for brief periods with careful monitoring is practiced in some transport programs pending central access.

Epinephrine is the drug for anaphylaxis (IM 0.3–0.5 mg) and the vasopressor of choice when norepinephrine has failed to maintain perfusion or when cardiac arrest is imminent. Its combined alpha and beta effects produce vasoconstriction plus inotropy plus chronotropy. In cardiac arrest: 1 mg IV/IO every 3–5 minutes. As an infusion for refractory shock: 0.05–0.5 mcg/kg/min.

Vasopressin (0.03–0.04 units/min) acts on V1 receptors in vascular smooth muscle, producing vasoconstriction independent of the catecholamine system. It is added as a second agent in septic shock to allow reduction of norepinephrine dose (norepinephrine-sparing) and may be particularly useful when norepinephrine is failing. It does not increase heart rate and has no direct cardiac effect at standard doses.

Dopamine has dose-dependent effects: at low doses, dopaminergic; at moderate doses, beta-1 (inotropy, chronotropy); at high doses, alpha-1 (vasoconstriction). It is associated with higher rates of arrhythmia than norepinephrine and is no longer first-line in septic shock or most vasopressor indications. Its primary role in current practice is in bradycardia (dopamine 2–20 mcg/kg/min) when atropine has failed and pacing is not yet available.

Sedation and analgesia in the transport intubated patient.

The transport intubated patient requires analgesia-first sedation: address pain before adding sedation to avoid over-sedation from stacking pharmacologic layers. The CPOT (Critical Care Pain Observation Tool) or BPS are used for mechanically ventilated patients who cannot self-report.

Fentanyl is the preferred opioid in most transport programs: rapid onset, titratable, hemodynamically stable in euvolemic patients, no active metabolites. Dose for infusion: 25–100 mcg/hour. Bolus for procedures or pain control: 1–2 mcg/kg IV. Caution in hemodynamically unstable patients — it can cause hypotension through histamine release (less common than morphine) and sympatholytic effects.

Midazolam is the most commonly used benzodiazepine for procedural sedation and short-term transport sedation. Dose: 0.01–0.1 mg/kg IV. Avoid in hypotension — benzodiazepines produce vasodilation and can precipitate cardiovascular collapse in volume-depleted patients.

Ketamine is particularly valuable in transport for hemodynamically unstable or borderline patients requiring sedation. It produces dissociative anesthesia while preserving airway reflexes and sympathetic tone, maintaining blood pressure in most patients. Dose for sedation: 1–2 mg/kg IV. Historically taught as a contraindication in elevated ICP, though current evidence in mechanically ventilated patients does not reliably support significant ICP elevation from ketamine — use clinical judgment and follow program protocol. Use with caution in ischemic cardiac disease at high doses (tachycardia increases myocardial oxygen demand).

RSI medications in transport.

Rapid sequence intubation (RSI) in transport requires a paralytic and an induction agent. Selection is patient-specific.

Succinylcholine (1.5 mg/kg IV) is a depolarizing agent with onset of 45–60 seconds and duration of 8–12 minutes. Absolute contraindications: crush injury, burns >72 hours old, denervation injuries, prolonged immobility, pre-existing hyperkalemia — all because succinylcholine causes transient potassium release from cells that can produce fatal dysrhythmia in patients with already elevated potassium.

Rocuronium (1.2 mg/kg IV for RSI, 0.6 mg/kg for routine intubation) is the non-depolarizing alternative with comparable onset at RSI doses and without the contraindications of succinylcholine. Duration is 60–90 minutes at RSI dosing. Sugammadex (16 mg/kg IV) provides rapid reversal of rocuronium, which is critical in a “cannot intubate, cannot oxygenate” scenario where rocuronium was used instead of succinylcholine.

Induction agents: Ketamine (1–2 mg/kg) for hemodynamically unstable patients. Etomidate (0.3 mg/kg) for hemodynamically stable patients or RSI where cardiovascular preservation is desired (it does cause adrenal suppression with a single dose, which is noted but generally not a contraindication for single-use induction). Propofol (1–2 mg/kg) for hemodynamically stable patients, causes significant hypotension — not first-line in the transport patient with any cardiovascular instability.

Altitude effects on pharmacology.

Nebulized medication delivery is impaired at altitude. Decreased barometric pressure changes the particle size distribution from jet nebulizers, potentially reducing pulmonary deposition efficiency. For critically bronchospastic patients in flight, consider MDI with spacer as an alternative to nebulization. This is a nuanced point that appears on CFRN examinations and reflects the depth of transport-specific pharmacologic knowledge expected of flight nurses.

The exam relevance.

CFRN pharmacology questions are mechanism-based. They ask why one agent is preferred over another, what contraindications change the choice, and what the correct response is when the expected drug effect is not what occurs. Knowing that dopamine causes more arrhythmia than norepinephrine is the answer to a question, but understanding why — because of its dose-dependent chronotropic effects mediated through beta-1 receptors — is what makes the answer retrievable when the question is framed differently than you expect.