Aortic stenosis is the narrowing of the outflow tract of the left ventricle due to calcification of the aortic valve.
Asymptomatic aortic stenosis may be initially detected on physical exam. Peripheral pulses may be weak and late (sometimes called pulsus parvus et tardus). A harsh systolic crescendo-decrescendo murmur may also be present, which is best heard at the right upper sternal border at the 2nd intercostal space. This murmur may also radiate to the carotid arteries.
Patients with suspected aortic stenosis should undergo Transthoracic echocardiogram to confirm the diagnosis and evaluate the severity of the disease. For severe disease, valve replacement therapy should be considered prior to proceeding with elective surgery.
- For severe disease, a pre-induction arterial line should be placed to rapidly detect hemodynamic changes.
- Advanced monitoring such as a pulmonary artery catheter or transesophageal echocardiography can be considered.
- Consider placement of defibrillation pads as chest compressions can be ineffective with severe stenosis.
- Hypotension should be avoided to preserve afterload (i.e. coronary perfusion pressure). Treat with afterload-increasing agents such as phenylephrine.
- Bradycardia should be avoided as these patients are often heart rate dependent to preserve adequate cardiac output. A heart rate of 60-90 bpm is optimal.
- Tachycardia and hypertension should be avoided to preserve left ventricular diastolic filling and reduce myocardial oxygen demand. Treat with increasing anesthetic depth or short-acting beta-blockade with esmolol.
Neuraxial anesthesia is contraindicated in all but mild disease due to the risk of decreased systemic vascular resistance leading to decreased diastolic blood pressure and reduced myocardial perfusion
Patients with significant disease may require close postoperative monitoring to quickly identify and manage any hemodynamic instability.
Related surgical procedures
In aortic stenosis, the opening of the aortic valve is narrowed, typically due to calcification from tissue damage over time. The most common cause is valve degeneration in older patients, though stenosis may develop in younger patients with a bicuspid aortic valve. It is thought that stenosis results from inflammation due to endothelial cell damage from increased mechanical stress.
As aortic stenosis progresses, higher pressures must be generated by the left ventricle to maintain cardiac output. This initially leads to the development of concentric left ventricular hypertrophy, thereby increasing myocardial oxygen requirement. In later stages of the disease, the left ventricle dilates and the ventricular walls thin, resulting in reduced systolic function.
Signs and symptoms
- Slow/late peripheral pulses (pulsus parvus et tardus)
- Harsh systolic crescendo-decrescendo murmur
- Best auscultated at the right upper sternal border at the 2nd intercostal space
- May radiate to both carotids
- Decreased intensity of the second heart sound (A2)
- Decreased exercise tolerance
- Symptoms of congestive heart failure
|Severity of aortic stenosis|
|Aortic valve area|
|Moderate||25 - 40||1.0 - 1.5|
|Very severe||>70||< 0.6|
Aortic stenosis may be initially suspected from the physical exam findings described above. Definitive diagnosis and classification of disease severity can be determined using echocardiography or heart catheterization.
In general, medication has poor efficacy in the treatment of aortic stenosis. However, medical therapy is important to manage concomitant cardiac diseases such as heart failure, hypertension and symptoms such as angina.
Severe symptomatic aortic stenosis is typically treated with aortic valve replacement. For patients who are poor candidates for surgical valve replacement, transcatheter aortic valve replacement is an alternative. Balloon valvuloplasty is can be effective in infants and children, but has limited efficacy in adults since the valve generally returns to a stenosed state.
Untreated severe symptomatic aortic stenosis has a poor prognosis, with a 2-year survival rate of 50-60%. For patients who undergo valve replacement, life expectancy is about 5 years less than the general population for patients under 65, and similar to patients without aortic stenosis for patients over 65.