Recommended Induction Strategy for Severe Critical Aortic Stenosis Undergoing Aortic Valve Replacement
For patients with severe critical aortic stenosis undergoing aortic valve replacement, maintain hemodynamic stability through careful volume optimization, avoidance of hypotension and tachycardia, and consideration of prophylactic low-dose noradrenaline infusion (0.1 μg/kg/min) starting at induction to prevent the profound hypotension that commonly occurs in this population. 1, 2
Pre-Induction Preparation
Volume Status Optimization
- Optimize intravascular volume before induction, as elderly patients are typically volume depleted, but avoid both extremes—severely underfilled ventricles pose problems for guidewire insertion in hypertrophied ventricles, while volume overload is equally problematic. 1
- Use a combination of pulmonary artery pressures, central venous pressure, and echocardiographic evaluation to guide tailored volume therapy rather than empiric fluid administration. 1
- Patients with severe concentric LV hypertrophy and intravascular volume depletion may exhibit rapid and sustained hemodynamic deterioration during induction. 1
Monitoring Setup
- Establish arterial pressure monitoring via radial artery before induction (plan for contralateral radial or femoral access if ipsilateral axillary bypass is present). 1
- Consider pulmonary artery catheter placement in patients with poor LV function or severe pulmonary hypertension. 1
- Obtain at least one large-volume intravenous line peripherally or centrally. 1
- Apply defibrillator pads connected to defibrillator before starting, as ventricular fibrillation can occur with catheter manipulation or rapid ventricular pacing. 1
Additional Preparations
- Ensure immediate availability of inhaled nitric oxide or inhaled epoprostenol for treatment of severe pulmonary hypertension and right ventricular failure. 1
- Implement hypothermia prevention: appropriate ambient room temperature, fluid warmers, and forced air or fluid underbody heating systems. 1
- Administer routine surgical antibiotic prophylaxis prior to surgical incision or vascular access. 1
Induction Technique
Prophylactic Vasopressor Strategy
Consider continuous prophylactic noradrenaline infusion at 0.1 μg/kg/min starting at the time of anesthesia induction, as this significantly prevents hypotension during induction (lowest mean blood pressure 63 vs 47 mmHg without prophylaxis, P<0.01). 2
- This approach maintains mean blood pressure immediately before intubation significantly higher (75 vs 57 mmHg, P<0.01) compared to reactive vasopressor administration. 2
- Postoperative complications are negligible between prophylactic and reactive approaches, making prevention preferable. 2
Anesthetic Agent Selection and Dosing
Use significantly reduced doses of induction agents—patients over 60 years with severe systemic disease require 50-70% less midazolam and other sedatives than healthy young patients. 3
For sedation/induction with midazolam in elderly patients with severe systemic disease:
- Start with no more than 1.5 mg given over at least 2 minutes (compared to 5 mg in healthy adults). 3
- Wait an additional 2 or more minutes to fully evaluate sedative effect before additional dosing. 3
- If additional titration necessary, give no more than 1 mg over 2 minutes, waiting 2+ minutes each time. 3
- Total doses greater than 3.5 mg are not usually necessary in this population. 3
- If concomitant CNS depressant premedications used, these patients require at least 50% less midazolam. 3
For induction of general anesthesia in elderly patients with severe systemic disease:
- Unpremedicated patients over 55 years: initial dose 0.2-0.3 mg/kg (compared to 0.3-0.35 mg/kg in younger patients). 3
- Patients with severe systemic disease or debilitation: 0.15-0.25 mg/kg will usually suffice. 3
- Premedicated patients over 55 years: 0.2 mg/kg recommended. 3
- Patients with severe systemic disease: as little as 0.15 mg/kg may suffice. 3
Critical Hemodynamic Goals During Induction
Avoid Three Key Triggers of Decompensation
Maintain strict avoidance of hypotension, excessive hypertension, and tachycardia—these three factors precipitate acute decompensation in severe AS patients. 1
- Hypotension is particularly dangerous: The fixed cardiac output from severe stenosis prevents compensatory increases in stroke volume, leading to critical coronary and cerebral hypoperfusion. 1, 2
- Tachycardia reduces diastolic filling time: This is catastrophic in hypertrophied, non-compliant ventricles that depend on atrial contribution and adequate filling time. 1
- Excessive hypertension increases afterload: This further stresses the already pressure-overloaded left ventricle. 1
Specific Hemodynamic Targets
- Maintain mean arterial pressure within 10-20% of baseline values throughout induction. 1, 2
- Keep heart rate at or slightly below baseline—avoid increases above patient's intrinsic rate. 1
- Titrate slowly to desired effect (e.g., initiation of slurred speech) rather than targeting specific depth endpoints. 3
Common Pitfalls and How to Avoid Them
Pitfall 1: Reactive Rather Than Prophylactic Vasopressor Use
- The traditional approach of waiting for hypotension before treating it results in mean blood pressures dropping to 47 mmHg, whereas prophylactic noradrenaline maintains pressures at 63 mmHg. 2
- Once hypotension develops in severe AS, it may be difficult to reverse due to fixed cardiac output and coronary hypoperfusion creating a downward spiral. 1, 2
Pitfall 2: Standard Induction Doses in Elderly Patients
- Using standard adult doses in elderly patients with severe AS causes excessive cardiovascular depression. 3
- The danger of hypoventilation, airway obstruction, or apnea is greater in elderly patients with chronic disease states. 3
- Peak effect takes longer in these patients, requiring slower titration and smaller increments. 3
Pitfall 3: Inadequate Volume Assessment
- Empiric fluid boluses without hemodynamic assessment can cause either volume overload (worsening pulmonary hypertension) or persistent depletion (worsening hypotension with induction). 1
- Severely underfilled ventricles create additional problems for guidewire/applicator device insertion in hypertrophied ventricles during TAVR. 1
Pitfall 4: Failure to Anticipate Rapid Deterioration
- Patients with severe concentric LV hypertrophy and volume depletion may exhibit rapid and sustained deterioration in response to induction agents, rapid ventricular pacing, or catheter manipulations. 1
- Have inotropic support and mechanical circulatory support immediately available for shock or hemodynamic collapse. 1
Special Considerations for Concomitant Coronary Artery Disease
In patients with both severe AS and coronary artery disease (a common combination due to shared pathophysiology), maintain particular vigilance regarding coronary perfusion pressure during induction. 4, 5
- These patients have increased vulnerability to myocardial ischemia from hypotension due to both fixed coronary stenoses and increased myocardial oxygen demand from LV hypertrophy. 4, 5
- Ensure coronary perfusion pressure remains adequate by maintaining diastolic blood pressure and avoiding tachycardia that shortens diastolic time. 4, 5
Algorithm Summary
- Pre-induction: Optimize volume status using PA pressures/CVP/echo guidance, establish arterial line and large-bore IV access, apply defibrillator pads, ensure vasopressors/inotropes immediately available
- At induction: Start prophylactic noradrenaline 0.1 μg/kg/min infusion
- Agent dosing: Use 50-70% of standard doses in elderly patients with severe disease, titrate slowly over 2+ minutes with 2+ minute evaluation periods
- Hemodynamic targets: Maintain MAP within 10-20% of baseline, avoid tachycardia, keep HR at or below baseline
- Monitoring: Continuous arterial pressure, consider PA catheter if poor LV function or severe pulmonary hypertension
- Rescue: Have inotropes, mechanical circulatory support, and inhaled pulmonary vasodilators immediately available