Choosing an induction agent

Why examiners ask this

Almost every stem reaches the moment of induction, and "what will you induce with, and why?" is the cheapest way for an examiner to see whether you match pharmacology to physiology. A rote "propofol 2 mg/kg" in a hypovolemic or preload-dependent patient fails the question. It tests application of knowledge and judgment, and the follow-up ("the pressure is now 60/30") tests adaptability.

The 60-second answer

Decision points and the "why"

• Propofol as default — vasodilation and myocardial depression drop the pressure 20–30% in a healthy patient; that is acceptable when the patient has reserve and costs too much when they do not. The label halves the dose for the elderly, debilitated and ASA III–IV patient, given in 20 mg aliquots every 10 seconds,¹ because their central compartment is smaller and circulation time is slower.
• Etomidate for hemodynamic instability — it preserves sympathetic tone and contractility. The cost is a dose-dependent inhibition of 11-beta-hydroxylase lasting 6–12 hours after a single bolus and detectable in most patients at 12 hours; I accept it for one dose and never run an infusion.² Its use in sepsis remains debated without proof of harm,² so in septic shock I give it if it is the safest option and treat refractory hypotension with stress-dose hydrocortisone.
• Ketamine for shock and bronchospasm — its cardiovascular effects are indirect, through sympathomimetic activity and catecholamine reuptake inhibition, and it bronchodilates. It is a direct myocardial depressant, so in a catecholamine-depleted patient (prolonged sepsis, end-stage heart failure) it can still drop the pressure; the label lists cardiac decompensation in exactly that patient.³ I avoid it in uncontrolled coronary disease where tachycardia raises oxygen demand.
• Ketamine and intracranial pressure — the label still reports ICP rises and asks for a monitored setting;³ with controlled ventilation the rise is minimal, and preserving cerebral perfusion pressure matters more. I use it in the hypotensive head-injured trauma patient.
• Midazolam and opioids as co-induction — they reduce the hypnotic dose and blunt the response to laryngoscopy; in tamponade or severe stenosis I avoid a large opioid bolus because the loss of sympathetic tone is what drops the pressure.
• Methohexital for ECT — it does not raise the seizure threshold as propofol does; I choose it when the psychiatrist needs an adequate seizure duration.
• Inhalational induction — for the child without an IV and for the adult with a critical airway where I want spontaneous breathing preserved, I use sevoflurane, which is non-pungent.

The complication they will inject

After 120 mg of propofol in an 80-year-old with aortic stenosis, the pressure drops to 65/35 with a heart rate of 95. I recognize this as vasodilation in a fixed-output lesion, which is a coronary perfusion emergency. I tell the room, give phenylephrine 100–200 mcg and start an infusion, because pure alpha agonism raises diastolic pressure without increasing heart rate. I give a 250 mL fluid bolus, lighten the anesthetic and hold surgery until the pressure is back within 20% of baseline. If it does not respond I give epinephrine 10–20 mcg, check the ECG for ST changes, and ask for TEE. Then I tell the examiner what I would change: an arterial line before induction and etomidate titrated with phenylephrine already running.

Pitfalls that cost points

• Naming a drug without stating the dose for this patient.
• Saying "etomidate because it is cardiac-stable" without acknowledging adrenal suppression.
• Assuming ketamine always raises blood pressure.
• Treating the induction drug as the only variable while ignoring the vasopressor, the arterial line and the preload.
• Forgetting that a rapid-sequence induction fixes the dose in advance; titration is limited, so I choose the agent more carefully.

Rapid-why

Q: Why does propofol drop the pressure more in the elderly? A: Reduced volume of distribution, slower circulation and stiffer vasculature mean a higher peak concentration and less compensatory vasoconstriction.

Q: Why not etomidate in every sick patient? A: It suppresses cortisol synthesis, gives no bronchodilation, causes myoclonus in about a third of patients,² adds to PONV, and blunts the response to laryngoscopy less than propofol.

Q: Which agent would you choose for a patient with porphyria? A: Propofol, which the label reports has been used safely in porphyria, or ketamine;¹ barbiturates are a classic trigger and etomidate is best avoided.

Q: Why give less propofol in tamponade? A: The patient survives on high sympathetic tone and tachycardia; anything that vasodilates or slows the heart collapses cardiac output.

Numbers to know

Links

• Rapid sequence induction and full stomach, Dexmedetomidine and ketamine (coming), Intraoperative hypotension: differential and management, Aortic stenosis, Cardiac tamponade, including post-cardiac surgery, ect
• Surviving Sepsis Campaign guidelines (2021)