Calculating Aortic Valve Area & Transvalvular Gradient

CALCULATING AORTIC VALVE AREA & TRANSVALVULAR GRADIENT

As with mitral stenosis, the pressure gradient across the aortic valve can be determined noninvasively using continuous wave Doppler echocardiography:

∆P =4V²

where ∆P is the peak pressure gradient (mm Hg) and V is peak blood flow velocity (m/s) distal to the obstruction. Peak velocities greater than 4.5 m/sec are usually indicative of severe stenosis. Moreover, if the area proximal to the stenosis (LVOT) can be measured, the continuity equation can then be applied to estimate valve area. Either TVIs or maxi-mum velocities can be used:

where A₂ is valve area, A₁ is the cross-sectional area of the LVOT, V₁ is maximum blood flow velocity in LVOT, and V₂ is maximum flow velocity through the aortic valve.

Treatment

Once symptoms develop, most patients, with-out surgical treatment, will die within 2–5 years. Percutaneous balloon valvuloplasty is generally used in younger patients with congenital aortic stenosis; it can also be used in elderly patients with calcific aor-tic stenosis who are poor candidates for aortic valve replacement. Its efficacy for the latter group is short-lived, however, and restenosis usually occurs within 6–12 months. Catheter-delivered aortic valves are increasingly being perfected and deployed in the treatment of aortic valve disease. Surgical replace-ment of the stenotic aortic valve remains the main-stay of therapy.

Anesthetic Management

A. Objectives

Maintenance of normal sinus rhythm, heart rate, vascular resistance, and intravascularvolume is critical in patients with aortic stenosis. Loss of a normally timed atrial systole often leads to rapid deterioration, particularly when associated with tachycardia. The combination of the two (AF with rapid ventricular response) seriously impairs ventricular filling and necessitates immediate car-dioversion. The reduced ventricular compliance also makes the patient very sensitive to abrupt changes in intravascular volume. Many patients behave as though they have a fixed SV in spite of adequate hydration; under these conditions, car-diac output becomes very rate dependent. Extreme bradycardia (<50 beats/min) is therefore poorly tolerated. Heart rates between 60 and 90 beats/min are optimal in most patients.

B. Monitoring

Close monitoring of the ECG and blood pressure is crucial. Monitoring for ischemia is complicated by baseline ST-segment and T-wave abnormali-ties. Intraarterial pressure monitoring is desir-able in patients with severe aortic stenosis, as many of these patients do not tolerate even brief episodes of hypotension. Pulmonary artery cath-eterization data should be interpreted carefully; a higher than normal pulmonary capillary wedge pressure is often required to maintain adequate left ventricular end-diastolic volume and car-diac output. Prominent a waves are often visible on the pulmonary artery wedge pressure wave-form. Vasodilators should generally be used cau-tiously because patients are often very sensitive to these agents. TEE can be useful in these patients for monitoring ischemia, ventricular preload, contractility, valvular function, and the effects of therapeutic interventions.

C. Choice of Agents

Patients with mild to moderate aortic stenosis (gen-erally asymptomatic) may tolerate spinal or epidural anesthesia. These techniques should be employed very cautiously, however, because hypotension readily occurs as a result of reductions in preload, afterload, or both. Epidural anesthesia may be pref-erable to single-shot spinal anesthesia in many situ-ations because of its slower onset of hypotension, which allows more timely correction. Continuous spinal catheters can similarly be used to gradually increase the level of regional anesthesia and limit the possibility of blood pressure collapse. Spinal and epidural anesthesia are relatively contraindicated in patients with severe aortic stenosis.

In the patient with severe aortic stenosis the choice of general anesthetic agents is less impor-tant than managing their hemodynamic effects. Most general anesthetics can produce both vaso-dilation and hypotension, which require treatment post induction. If a volatile agent is used, the con-centration should be controlled to avoid excessive vasodilatation, myocardial depression, or loss of normal atrial systole. Significant tachycardia and severe hypertension, which can precipitate isch-emia, should be treated immediately by increasing anesthetic depth or administration of a β-adrenergic blocking agent. Most patients with aortic stenosis tolerate moderate hypertension and are sensitive to vasodilators. Moreover, because of an already precarious myocardial oxygen demand–supply bal-ance, they tolerate even mild degrees of hypotension poorly. Hypotension should generally be promptly treated with escalating doses (25–100 mcg) of phen-ylephrine. Intraoperative supraventricular tachy-cardias with hemodynamic compromise should be treated with immediate synchronized cardioversion. Frequent ventricular ectopy (which often reflects ischemia) is usually poorly tolerated hemodynami-cally and should be treated. Amiodarone is generally effective for both supraventricular and ventricular arrhythmias.