Up to 70% to 90% of patients have trace to mild tricuspid regurgitation on echocardiography; the regurgitant volume in these cases is almost always insignificant. Clinically significant tricuspid regurgi-tation, however, is most commonly due to dilatation of the right ventricle from pulmonary hypertension that is associated with chronic left ventricular fail-ure. Tricuspid regurgitation can also follow infec-tive endocarditis (usually in injecting drug abusers), rheumatic fever, carcinoid syndrome, or chest trauma or may be due to Ebstein’s anomaly (down-ward displacement of the valve because of abnormal attachment of the valve leaflets).
Chronic left ventricular failure often leads to sus-tained increases in pulmonary vascular pressures. The chronic increase in afterload causes progressive dila-tation of the thin-walled right ventricle, and exces-sive dilatation of the tricuspid annulus eventually results in regurgitation. An increase in end-diastolic volume allows the right ventricle to compensate for the regurgitant volume and maintain an effective forward flow. Because the right atrium and the vena cava are compliant and can usually accommodate the volume overload, mean right atrial and central venous pressures are generally only slightly elevated. Acute or marked elevations in pulmonary artery pressures increase the regurgitant volume and are reflected by an increase in central venous pressure. Moreover, sudden marked increases in right ven-tricular afterload sharply reduce the effective right ventricular output, reduce left ventricular preload, and can precipitate systemic hypotension.
Chronic venous hypertension leads to pas-sive congestion of the liver and progressive hepatic dysfunction. Severe right ventricular failure with underloading of the left heart may also produce right-to-left shunting through a patent foramen ovale, which can result in marked hypoxemia.
The normal right ventricle does not extend to the apex of the heart when visualized using echocardiog-raphy. As the right heart dilates, it acquires a more spherical shape, the right ventricle extends to the apex of the heart, and the interventricular septum is flat-tened. These changes can impair left heart function.
With severe tricuspid regurgitation, the normal sys-tolic inflow into the right atrium is reversed, and the reversal of flow is also observed in the hepatic veins.
Systolic pulmonary artery pressure (PAS) can be estimated from the peak velocity of the regurgitant jet:
∆P = 4 × V2
where ∆P is the systolic pressure gradient (mm Hg) between the right ventricle and right atrium, and V is peak blood flow velocity (m/s) of the regurgitant jet. If the central venous pressure (CVP) is known or assumed, then
PAS = CVP + ∆P
Tricuspid regurgitation is generally well tolerated by most patients. Because the underlying disorder is generally more important than the tricuspid regur-gitation itself, treatment is aimed at the underlying disease process. With moderate to severe regurgi-tation, tricuspid annuloplasty may be performed in conjunction with replacement of another valve. Recent studies suggest that correction of significant tricuspid regurgitation is beneficial when patients are brought to surgery for replacement of another valve.
Hemodynamic goals should be directed primar-ily toward the underlying disorder. Hypovolemia and factors that increase right ventricular afterload, such as hypoxia and acidosis, should be avoided to maintain effective right ventricular SV and left ven-tricular preload. Positive end-expiratory pressure and high mean airway pressures may also be undesirable during mechanical ventilation because they reduce venous return and increase right ventricular afterload.
In these patients, invasive monitoring may be use-ful. Pulmonary artery catheterization is not always possible; rarely a large regurgitant flow may make passage of a pulmonary artery catheter across the tri-cuspid valve difficult. Increasing CVP implies wors-ening right ventricular dysfunction. The x descent is absent, and a prominent cv wave is usually present on the CVP waveform. Thermodilution cardiac out-put measurements are falsely elevated because of the tricuspid regurgitation. Color-flow Doppler TEE is useful in evaluating the severity of the regurgitation and other associated abnormalities.
The selection of anesthetic agents should be based on the underlying disorder. Most patients tolerate spinal and epidural anesthesia well. Coagulopathy second-ary to hepatic dysfunction should be excluded prior to any regional technique. During general anesthesia, nitrous oxide may exacerbate pulmonary hyperten-sion and should be administered cautiously, if at all.
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