Severe Aortic Stenosis and a Fractured Hip: Resisting the Reflex Spinal

I explain the physiology, then negotiate the technique.

In severe AS the left ventricle is a thick, stiff, small-cavity pump ejecting through a fixed obstruction. Stroke volume is essentially fixed and cannot increase on demand; cardiac output therefore depends heavily on heart rate and on venous return, and systemic pressure depends on systemic vascular resistance (MAP ≈ CO × SVR). Consequences:

• She is preload-dependent - filling is what generates the gradient that fills a noncompliant ventricle.
• She is afterload-critical - if SVR falls, CO cannot rise to compensate, and pressure falls.
• She is intolerant of tachycardia - a short diastole reduces coronary filling in a ventricle with massive oxygen demand from hypertrophy, and reduces the time available to fill.

A standard spinal produces a sympathectomy: venodilation (preload down) plus arteriolodilation (SVR down), often with a reflex tachycardia. That is a near-perfect storm for this patient, and the resulting hypotension is notoriously difficult to reverse once it occurs.

The "spinels are safer" premise: The REGAIN trial found no significant difference in mortality or major complications between spinal and general anesthesia for hip fracture. The claim of a mortality benefit is not supported, so the decision should be made on hemodynamic grounds - which favor neither a high spinal nor an uncontrolled one.

My proposal: general anesthesia with a controlled, titrated induction, an arterial line, and a vasopressor infusion running before induction. If the patient or surgeon strongly prefers neuraxial, I would use a low-dose, unilateral, incremental technique with an arterial line and a phenylephrine infusion started beforehand - never a full-dose single-shot spinal with sedation.

Preparation (in the room before the patient arrives):

• Arterial line placed pre-induction under local, with the patient awake; a reliable pressure trace is the whole plan.
• Phenylephrine drawn up and running as a low-dose infusion before induction; norepinephrine available as a backup on a second pump.
• Defibrillator pads on, suctions, difficult-airway trolley; standard monitors plus a cautiously placed large-bore IV (do not over-resuscitate a stiff ventricle).
• Continue the beta-blocker (avoid withdrawal tachycardia); keep her warm.

Induction:

• Etomidate 0.2–0.3 mg/kg, titrated slowly; avoid propofol boluses and avoid a high-dose volatile-only induction.
• Opioid in small aliquots (fentanyl 1–2 mcg/kg) - avoid histamine-releasing or vagolytic large doses.
• Rocuronium for intubation; gentle, brief laryngoscopy; maintain a normal PaCO2 (hypercarbia raises pulmonary vascular resistance and can drop preload; hypocarbia reduces venous return).
• Maintain sinus rhythm at 60–80 bpm. Treat bradycardia promptly with anticholinergics or a β-agonist, and treat tachycardia by deepening anesthesia rather than by vasodilating.

The hypotensive episode (MAP 55, HR 95):

• The tachycardia tells me something is off: light anesthesia, hypovolemia, or a falling SVR. A MAP of 55 in severe AS is a coronary-perfusion emergency - treat now, diagnose in parallel.
• Phenylephrine 50–100 mcg boluses, escalate, and increase the infusion. Raising SVR is the correct lever when stroke volume is fixed; a β-agonist that primarily raises heart rate would worsen ischemia.
• If there is no response to α-agonists plus a small fluid challenge (250 mL), add norepinephrine for combined α and modest β1 support, and reassess contractility with echocardiography before considering an inotrope.
• Reduce volatile concentration or lighten the plane; check for surgical bleeding; verify the arterial line is not damped.
• Do not give vasodilators or large fluid boluses - the first risks a collapse in coronary perfusion, and the second risks pulmonary edema in a stiff ventricle.

Key teaching point: in severe AS, hypotension should be prevented rather than chased, and the correct first drug is almost always a pure α-agonist given early and generously.

This is a real tradeoff, and I would present it as one.

The case for operating: hip fracture surgery delayed beyond 24–48 hours is associated with increased mortality, pressure injuries, delirium, and pneumonia. A patient immobilized with a fracture that is not fixed is at risk of dying of immobility. The anesthetic techniques available (titrated general or a low-dose neuraxial technique with invasive monitoring and vasopressors) are not intrinsically prohibitive in severe asymptomatic AS.

The case for caution: symptomatic severe AS - angina, syncope, or heart failure - carries a very high perioperative risk, and if the patient has symptoms, valve intervention should be considered. This patient has none of the three classic symptoms, which materially changes the risk estimate. Her EF is preserved, and she is not in heart failure.

What I would tell the family:

• Guideline position is that hip fracture surgery generally should not be postponed for a full cardiac workup; the delay carries its own mortality. Severe AS alone is not a reason to wait for a valve.
• If she develops symptoms, or if the fracture can be stabilized while awaiting a definitive workup, a hybrid plan with cardiology and structural heart intervention (TAVR) can be discussed. That is a multidisciplinary decision, not one made in the corridor.
• I would request a formal cardiology and echocardiography consult postoperatively regardless, and document that the risk, the alternatives, and the reasoning (including the absence of symptoms) were discussed.

Professionalism point: I do not tell the family "the right thing was done" as if it were a certainty. I tell them the tradeoff that was weighed, who weighed it, and what we are doing now.