Overview of Aortic Stenosis
Aortic stenosis is the most common cause of LV outflow obstruction (less common causes include HOCM, subvalvular stenosis, or, rarely, supravalvular stenosis).
AS can be divided into congenital (bicuspid), rheumatic, or degenerative (calcific). If in concert with rheumatic fever, is almost always associated with mitral pathology. These patients have an increased incidence of sudden death as compared to the general population. Most will not become symptomatic (valve area < 0.9 cm2) until 30 years after onset.
Valve Dimensions / Measurements
Normal valve area is 2.5–3.5 cm2 (2-4 cm2 in Barash). “Hemodynamically significant stenosis” occurs when area < 1.2 cm2 but these patients are not necessarily symptomatic. “Symptomatic stenosis” usually occurs when area falls below 0.8-0.9 cm2. Symptoms include angina (heart), dyspnea on exertion (lungs), and orthostatic or exertional syncope (brain). Non-surgical survival is 2-5 years after symptom onset. Treatment options at this point include medical therapy (digoxin, Na restriction, diuretics), valvuloplasty (ideal for younger patients, effectiveness is usually only transient in elderly patients), or surgical repair/replacement.
“Critical aortic stenosis” occurs when the valve area is < 0.7 cm2, at which point the transvalvular gradient will be 50 mm Hg at rest (ie with a normal cardiac output) – at 0.7 cm2/50 mm Hg, patients cannot appreciably increase their cardiac output.
Effect on cardiac anatomy
Left ventricle becomes concentrically thickened due to increased afterload, which has the dual effects of increasing myocardial demand and reducing ventricular compliance (thus, sinus rhythm and atrial kick are CRITICAL, providing 30-40% of LVEDV). Increased systolic pressures further increase demand. Early in the disease, LVEDP will increase (leading to pulmonary symptoms), although LVEDV (preload) does not increase until late in the disease. Myocardial contractility deteriorates over time, further compromising left ventricular function.
Aortic Stenosis in Non-Cardiac Surgery
An arterial catheter shortens the detection time for hemodynamic abnormalities and is mandatory in severe cases of AS. EKG findings are often obscured by the LVH, making myocardial infarction difficult to detect. Pulmonary artery catheters are often used, however keep in mind that the wedge pressure is not a good indicator of ventricular filling, as ventricular compliance is greatly reduced. Vasodilators should be avoided unless a PA catheter is in place. TEE can be a useful adjunct as well. Always have a defibrillator available because external compressions are essentially useless with significant stenosis.
Patients with AS are best thought of based on their hemodynamic derangements – they have increased myocardial oxygen demands, reduced left ventricular filling, and, with time, reduced contractility. With regards to myocardial perfusion, diastolic volume must be maintained. Normal sinus is critical in order to fill the LV, with HR 60-90 being optimal (these patients often behave HR-dependent, thus bradycardia can be devastating).
Afterload (and thus perfusion pressure) must be maintained, AVOID hypotension. Volatile or intravenous general anesthesia can be used, although volatile anesthetics may reduce sinus automaticity, leading to a junctional rhythm, as well as produce myocardial depression, thus an opiate-based anesthetic is preferred. Induction can be safely accomplished with opiates/benzodiazepines, etomidate, or benzodiazepines/ketamine. If a volatile agent is used, it should be titrated carefully to avoid myocardial depression, vasodilation, or loss of NSR.
Tachycardia and hypertension, which are poorly tolerated, should be treated by increasing anesthetic depth. If an adrenergic blocking agent is used, esmolol is preferable. Hypotension should generally be treated with small doses (25–50 ucg) of phenylephrine. Amiodarone is effective for both supraventricular and ventricular arrhythmias, although if hemodynamic instability is present, immediate cardioversion is indicated. Frequent ventricular ectopy (which often reflects ischemia) is poorly tolerated hemodynamically and should be treated with IV lidocaine.
Central neuraxial analgesia can be used (with extreme caution) in mild cases, but is otherwise to be avoided as it may lead to excessive decreases in SVR and consequently DBP/myocardial perfusion. If used, epidural analgesia is preferable to spinal analgesia.
Aortic Stenosis in Cardiac Surgery
Post-Repair / Bypass
Keep systolic pressures < ~ 100 mm Hg in order to protect the aortic suture line. Remember that while the valve has been replaced, the LV is still dysfunctional (ex. decreased compliance) and these patients may need relatively high LVEDP (i.e., they can be preload dependent).
Echocardiographic Assessment of Aortic Stenosis
For quantitative assessment of AS, the ASE recommends measuring jet velocity, mean pressure gradient, and valve area (using the Continuity Equation). If additional information is needed, the “dimensionless index” (VTI_LVOT/VTI_valve, severe if < 0.25) and valve area via 2D planimetry can be assessed.
ASE Recommendations for AS Quantification 1. Jet Velocity ( > 4 m/s is severe) 2. Mean Pressure Gradient (> 40 mm Hg is severe) 3. Valve Area (by Continuity Equation, < 1.0 cm2 is severe)
For complete recommendations and commentary, see the ASE Guidelines.