Abstract
TS is defined as a fixed obstruction to RV filling due to TV orifice narrowing. It is most commonly of rheumatic origin, and often combined with regurgitation. Rheumatic TS is invariably associated with left-sided valvular disease.
The Tricuspid Valve
The TV complex lies between the RA and RV in a slightly more apical position than the MV on the left side. Anatomy of the TV apparatus consists of:
Three unequal membranous leaflets – anterior (usually largest), septal and posterior
A saddle-shaped annulus
The chordae tendinae
The papillary muscles
Tricuspid Stenosis
TS is defined as a fixed obstruction to RV filling due to TV orifice narrowing. It is most commonly of rheumatic origin, and often combined with regurgitation. Rheumatic TS is invariably associated with left-sided valvular disease.
Non-rheumatic TS is rare. Causes include congenital atresia or stenosis, right heart tumours (e.g. RA myxoma), systemic lupus erythematosus, endomyocardial fibroelastosis, carcinoid syndrome, prosthetic-valve endocarditis and pacemaker lead infection or adhesions.
Clinical Presentation
Clinical features are often overshadowed by left-sided (particularly mitral) valve disease. The normal TV area is 7–9 cm2, making it the largest cardiac valve. Clinically significant TS only develops when the TV area reaches less than 2 cm2 and, hence, there can be a long asymptomatic period as stenosis develops.
Isolated TS presents with features of systemic venous hypertension and RV failure (dyspnoea, fatigue, peripheral oedema, hepatomegaly and ascites). An opening snap and high-pitched, mid-diastolic murmur are best heard at the left lower sternal edge, and a dominant a-wave and a slow y-descent can be seen on the CVP (Figure 11.1). A pansystolic murmur may indicate concomitant TR (Chapter 2).
Figure 11.1 RA and RV pressure waveforms in TS. The RA pressure tracing shows the prominent a-wave and a slow y-descent. At end diastole, there is a significant pressure gradient between the RA and RV due to the elevated RA pressure and a drop in RV end-diastolic pressure (RVEDP).
Investigations
ECG: This may show tall peaked P-waves in leads II, III and aVF indicative of RA enlargement. AF or flutter may be present.
Echocardiography: This is the most useful investigation and can be used to assess the anatomy, measure the severity and diagnose concomitant TR in addition to left-sided valve lesions. 2D and 3D assessment of the TV may reveal thickening or calcification of the leaflets, with restricted movement. Diastolic doming of the leaflets may be seen and RA and IVC enlargement is common. Quantification of the orifice area by 2D and 3D planimetry is difficult and currently not validated or recommended.
CWD: This technique may be of limited use for assessing the severity of TS. Tricuspid inflow velocities are affected by respiration, HR and rhythm and the presence of TR. The pressure half-time is less valid than in MS and the continuity equation (the SV can be derived from the LV or RV outflow) is unreliable in the presence of more than mild TR. Mean pressure gradients in a normal TV are usually less than 1 mmHg. Features indicative of significant TS are listed in Box 34.1.
Right heart catheterization: This is rarely used but may be useful in determining the contribution of TS to the patient’s symptoms. The relative changes in RA pressure and RV end-diastolic pressure mirror left heart pressure changes in MS (Figure 11.1).
Surgery
TV surgery is usually performed with other valve procedures. The need for isolated tricuspid surgery is determined by both the severity of symptoms and the degree of stenosis. Surgery is preferred to percutaneous balloon valvotomy due to the high incidence of concomitant TR, the risk of creating or worsening the TR and the lack of long-term outcome data.
Surgical options include repair by open commissurotomy and valve replacement. If the valve is replaced, biological prosthesis is preferred due to the higher risk of thrombosis with mechanical valves and the durability of bioprosthetic valves in the tricuspid position.
Anaesthetic Goals
These are summarized in Box 11.1.
Box 11.1 Anaesthetic considerations in TS
Preoperative medical management – includes diuretics for heart failure and hepatic congestion and treatment of atrial arrhythmias.
Attention to left-sided valvular disease.
RV filling – the need for adequate preload, to maintain forward flow, has to be balanced against the risk of worsening venous congestion.
Heart rate – AF and other SVTs may cause rapid cardiovascular collapse and should be treated promptly. Conversely, bradycardia can also be harmful and a sinus rhythm of 70–80 bpm should be targeted.
RV contractility – a sudden drop in RV contractility can cause a severe decrease in CO and increase in RA pressure. Adequate perfusion pressure and RV coronary blood flow should be maintained, and arterial hypotension avoided.
PA catheters – may be almost impossible to place and will have to be removed during surgery. Surgical assistance in placement is advised if required following CPB.
Tricuspid Regurgitation
TR is defined as retrograde blood flow from the RV into the RA during systole. Mild or ‘physiological’ TR is present in as many as 70% of asymptomatic, normal individuals. Clinically significant TR is usually functional in origin – occurring secondary to RV enlargement and dilatation of the tricuspid annulus. This is often seen in association with other cardiac disorders such as left-sided mitral and AV disease, PHT, congenital heart disease and cardiomyopathies.
Secondary TR carries a poor prognosis with a vicious cycle of disease whereby progressive dilatation and remodelling of the RV causes TV annular dilatation, papillary muscle displacement and leaflet tethering. This causes worsened TR with a further increase in RV and RA size and a further increase in the dimensions and flattening of the TV annulus. Furthermore, the increase in RV pressure can cause a leftwards shift of the interventricular septum with a decrease in the LV size, an increase in the LV diastolic pressures, an increase in PAPs and further worsening of RV function and TR.
Primary TR is rare; causes include Ebstein’s anomaly, infective endocarditis, rheumatic heart disease, carcinoid syndrome and iatrogenic damage from surgery, endocardial biopsies, catheter placements and pacemaker leads.
Clinical Presentation
Isolated TR may be tolerated for many years without symptoms. Like TS, patients with significant TR present with fatigue, dyspnoea, exercise intolerance and features of systemic venous hypertension. A pansystolic murmur is best heard at the left lower sternal edge and the CVP is characterized by a prominent cv-wave, an absent x-descent, and a sharp y-descent (Figure 11.2).
Figure 11.2 The RA pressure (RAP) waveform in TR shows a large cv-wave caused by the regurgitant jet, disappearance of the x–descent and a steep y–descent. The jugular vein pressure may feel pulsatile with a systolic thrill in patients with severe TR, and may be confused with the carotid pulse.
Investigations
ECG: This may reveal RV dysfunction, right-axis deviation, tall P-waves, RBBB and AF.
Echocardiography: An assessment of the TV can be difficult as it is challenging to visualize all three cusps simultaneously, and measurements are less robust than for the MV. Assessment should consider the 2D and 3D anatomy of the valve, right heart chambers, IVC and Doppler measures of severity. Endocarditis, catheter and pacemaker trauma can be well seen on TOE. Significant TR is identified on 2D echocardiography by significant leaflet tethering and annular dilatation. Tethering can be assessed by measuring the systolic tenting area (the area between the annulus and leaflet body in mid systole in the apical four-chamber view) or the tethering distance (the distance between the coaptation point and the annular plane). A tenting area of over 1 cm2 or tethering distance of over 0.8 cm indicates severe TR. The tricuspid annulus can be measured in diastole in the four-chamber view. The normal diameter is 28 ± 5 mm. A diameter of over 40 mm is considered dilated and an indication for surgery (it corresponds to intraoperative measurement from anterior–septal commissure to anterior–posterior commissure of over 70 mm).
CWD: An assessment of severity is less robust than for MR and has significant limitations due to eccentric jets, haemodynamics and equipment settings.
CFD: This Doppler technique, however, is commonly used and detection of a large eccentric jet extending to the posterior wall of the RA lies in favour of severe TR while thin central jets usually are mild. Although the geometry of the TV is complex and CFD measurements can be difficult, a vena contracta greater than 7 mm, an effective regurgitant orifice area of more than 75 mm2 and a proximal isovelocity surface area (PISA) of 9 mm at a Nyquist limit of 28 cm s–1 usually indicates severe TR. PA systolic pressure can be estimated using the modified Bernoulli equation. Estimated PA systolic pressure = 4 × (peak TR jet velocity)2 + RA pressure.
PWD: This can be used to look at the TV inflow and, in the absence of TS, a peak E-wave of greater than 1 m s–1 indicates severe TR, while the density of the CWD TR jet can also indicate severity. This is summarized in Table 34.5.
Other findings on TOE indicative of severe TR include PWD systolic flow reversal in the hepatic veins (specific to severe TR), a dilated and pulsatile IVC, a dilated coronary sinus, an enlarged RA with bowing of the interatrial septum towards the LA and RV dysfunction.
Surgery
Tricuspid surgery is indicated for severe TR and is usually undertaken at the time of surgery for left-sided valves. It should also be considered in patients with moderate primary TR and mild–moderate secondary TR with dilatation of the annulus greater than 40 mm. Isolated TV surgery should be considered in patients with severe primary TR who are symptomatic and those with progressive RV dilatation or early dysfunction.
Ring annuloplasty is usually all that is required for isolated annular dilatation, although repair may be indicated when the leaflets are deformed. Some utilize suture (DeVega) annuloplasty with excellent outcomes. If TV replacement is necessary, large bioprosthetic valves are generally preferred to mechanical valves as they are associated with a lower risk of thromboembolic complications.
Anaesthetic Goals
These are summaraized in Box 11.2.
Box 11.2 Anaesthetic considerations in TR
As TR is usually secondary, the anaesthetic management is generally dictated by the primary pathology.
RV preload – adequate filling must be achieved to maintain forward flow and limit TR. A drop in CVP can severely reduce CO. Airway pressures during mechanical ventilation should be minimized to avoid reduced RV filling.
HR – most patients are in chronic AF and are impossible to convert to NSR. A normal to high HR is preferred to maintain forward flow.
RV contractility – RV failure is usually the cause of severe clinical deterioration in these patients and inotropic support is often required.
PVR – hypercarbia, hypoxia, acidosis and other factors that increase PVR should be avoided and consideration given to the use of pulmonary vasodilators such as inhaled NO. If inotropic support is necessary, inodilators such as enoximone or dobutamine should be considered.
Immediately post TV surgery, the RV will be compromised as the entire SV is ejected forward without the pressure relief of blood into the RA through a leaking TV. This may require inotropic support to prevent RV failure.
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