Severe Aortic Stenosis and Hip Fracture: Choosing Anesthesia for a Fixed-Output Heart

The main concern is that severe aortic stenosis creates a fixed cardiac output: the ventricle cannot increase output across the stenotic valve, so hypotension from vasodilation or a fall in preload can cause severe ischemia and collapse. A single-shot spinal produces rapid sympathectomy and vasodilation, which is hazardous if given as a full dose. However, a low-dose spinal with careful titration can provide excellent analgesia and avoid the sympathetic response to laryngoscopy. I would choose a low-dose spinal with hyperbaric bupivacaine 5–7.5 mg, possibly combined with a continuous spinal catheter so I can titrate, plus a fascia iliaca block for postoperative pain. General anesthesia is an acceptable alternative if the airway or patient cooperation is unfavorable, using etomidate or ketamine induction and maintaining vasopressor support.

I would place an arterial line before induction and aim for a heart rate of 60–80/min, a normal sinus rhythm, and a mean arterial pressure within 20% of baseline. I would have phenylephrine boluses and an infusion ready, avoid tachycardia with continued metoprolol, avoid excessive fluid loading that could cause pulmonary edema, and treat hypotension promptly. The judgement is to provide anesthesia that minimizes sympathetic swings rather than to avoid regional anesthesia entirely.

I would first confirm the blood pressure and check the rhythm, oxygenation, and depth of block. A heart rate of 52/min with hypotension is dangerous in aortic stenosis because cardiac output depends on stroke volume and adequate filling time; bradycardia can reduce output, but vasodilation is the more likely primary cause after spinal anesthesia. I would give phenylephrine 50–100 µg IV and start an infusion at 0.5–1 µg/kg/min, because alpha-1 agonism restores systemic vascular resistance without causing tachycardia. If the heart rate remains below 55/min and blood pressure does not respond, I would give ephedrine 5 mg or atropine 0.5 mg to restore an adequate rate, accepting that ephedrine may cause some tachycardia.

I would give small crystalloid boluses of 250 mL and reassess, because excessive fluid in a hypertrophied ventricle can precipitate pulmonary edema. If hypotension persists despite phenylephrine and fluids, I would add vasopressin 0.5–1 unit, and consider converting to general anesthesia with careful induction if the block is too high. I would avoid pure beta-agonists and avoid drugs that cause tachycardia. The endpoint is a mean arterial pressure near baseline with a heart rate of 60–80/min, not simply a normal blood pressure number.

I would continue metoprolol without interruption to avoid rebound tachycardia and ischemia, and monitor for hypotension from residual spinal anesthesia. He is at high risk of delirium because of age, fracture, and aortic stenosis, so I would use multimodal analgesia, avoid benzodiazepines and anticholinergics, restore his glasses and hearing aids, and mobilize early. I would monitor renal function because of the mildly elevated creatinine and the risk of hypoperfusion. I would also watch for pulmonary edema if he received excessive fluid.

Definitive aortic valve replacement should be planned after recovery, but it should not delay the hip fracture repair, because delay increases mortality and complications. I would arrange cardiology follow-up and preoperative optimization for the valve procedure. The key judgement is that the fracture is the urgent problem and that the perioperative period must focus on preserving coronary perfusion while avoiding the complications of immobility.