Hemodynamic findings in severe tricuspid regurgitation

Abstract

Tricuspid regurgitation (TR) most commonly occurs in response to right ventricular (RV) dilation with structural abnormalities in the tricuspid valve being rarer. In addition to RV size and valvular integrity, the amount of TR is influenced by RV preload and afterload, the respiratory cycle, left heart function and atrial fibrillation. Hemodynamic changes in right atrial (RA) pressures in severe TR include elevated mean pressures, a large systolic wave called an “s” wave, a prominent ‘Y’ descent and a blunted ‘X’ descent. In addition, RV end diastolic pressure is elevated and cardiac output is reduced, especially with exercise. “Ventricularization” of the RA pressure tracing, in which the contour of the RA pressure is similar to, but of lower amplitude than, the contour of the RV pressure is the most specific finding but is found in a minority of patients with severe TR. In summary, alterations in the RA pressure tracing are common in patients with severe TR but specific hemodynamic findings lack sensitivity, which may in part be due to the large effects of RV preload, RV afterload and RA compliance on the amount of TR. © 2012 Wiley Periodicals, Inc.

INTRODUCTION

Tricuspid regurgitation (TR) is a common abnormality but clinical sequelae are rare since the right atrium and the vena cavae are relatively compliant structures. Hemodynamic changes in patients with mild or moderate TR are minor with patients frequently asymptomatic and TR diagnosed by physical examination or echocardiography [1]. Severe TR, however, is a different story with resultant volume overload and increases in right atrial (RA) and right ventricular (RV) diastolic pressures leading to characteristic hemodynamic changes and clinical findings of right heart failure.

CASE PRESENTATION

A 61-year-old female with hypertension, diabetes and coronary artery disease (status-post coronary artery bypass grafting one year previously) was admitted to an outside hospital with a several month history of progressive dyspnea. Physical examination was remarkable for a prominent “cv” wave on jugular venous examination, a holosystolic murmur at the left lower sternal border that increased with inspiration, a pulsatile liver and pedal edema. An echocardiogram showed normal left ventricular (LV) size and function, dilated RV, dilated RA and severe TR. Angiography showed that her bypass grafts were patent. Pulmonary artery pressure was 30/19 mm Hg, RV pressure was 27/15 mm Hg, and mean RA pressure was 18 mm Hg. LV filling pressures were normal with a mean pulmonary capillary wedge pressure (PCWP) of 14 mm Hg and LV end diastolic pressure of 14 mm Hg. A ventilation perfusion scan was unremarkable. The patient refused transesophageal echocardiography and was transferred to our hospital for further management.

Cardiac magnetic resonance imaging confirmed normal LV systolic function, dilation of the RV and RA, and severe TR. The tricuspid valve was redundant, and there appeared to be two jets of regurgitant flow (Supporting Information video loop S1). The integrity of the valve apparatus could not be assessed. Imaging of her tricuspid valve with intracardiac echocardiography (ICE) showed a flail septal leaflet. Right heart catheterization at the time of ICE showed that RA pressure was elevated throughout the cardiac cycle with a marked increase in RA pressure at the onset of systole producing a tall “V” wave (Fig. 1A). An “A” wave and “X” descent were obscure while the “Y” descent was prominent. Comparison of RA and RV pressures (recorded with a six F dual lumen pigtail catheter) showed that the RA tracing had a similar contour to the RV tracing with a lower peak pressure during ventricular systole and higher pressures during early diastole (Fig. 1B). PA and PCWP were normal (Fig. 1C and D).

Figure 1. Pressure tracings from a patient with severe TR Pressures were recorded using a fluid filled, end-hole catheter (A, C, and D) or a dual lumen pigtail catheter (B). All pressures were recorded on a 50 mm Hg scale. (A) RA pressure during spontaneous respiration; (B) simultaneous recording of RA and RV pressures during cessation of respiration; (C) PA pressure; (D) PCWP pressure.

A flail septal leaflet of the tricuspid valve was confirmed at surgery and a 31-mm stented tissue valve was implanted.

DISCUSSION

The tricuspid valve apparatus includes three leaflets (anterior, posterior, and septal), the chordae tendinae, two discrete papillary muscles and the fibrous tricuspid annulus. The tricuspid valve has the largest orifice of the intracardiac valves and during diastole, excursion of the leaflets and expansion of the annulus results in a tricuspid orifice area of 7–9 cm². The average tricuspid annular diameter is 21 ± 2 mm/m² of body surface area [2] and the average tricuspid annular circumference is 78 ± 7 mm/m² of body surface area [3], in normal individuals. The tricuspid annulus is the most dynamic of the intracardiac valves and a reduction in annular size of approximately 20% occurs with atrial systole [3, 4].

TR most commonly occurs in response to RV dilation with structural abnormalities in the tricuspid valve being rarer [5]. “Functional” TR results from leaflet malcoaptation and can be associated with any condition that causes dilation of the tricuspid valve annulus. The septal leaflet is fairly fixed, limiting the ability of the valve to adapt to dilation of the annulus as the distance between the RV free wall and septum increases [6, 7] Structural damage to the tricuspid valve can result from infective endocarditis, rheumatic heart disease, carcinoid syndrome, myxomatous degeneration of the tricuspid valve, marantic endocarditis in systemic lupus erythematosus, pacemaker, or implantable cardioverter-defibrillator leads and repeated biopsies in patients with orthotopic heart transplants. Certain pharmaceutical agents have been linked to damage of the tricuspid valve including drugs used to treat migraines (e.g., ergotamine), obesity (e.g., fenfluramine), and Parkinson's disease (e.g., pergolide) [8]. Congenital heart disease involving the tricuspid valve is rare with Ebstein's anomaly being the most common congenital condition resulting in TR.

NONVALVULAR FACTORS INFLUENCING THE DEGREE OF TR

RV preload and afterload can dramatically influence the amount of TR. This was demonstrated in a pig model in which TR produced by direct injury to the chordae and papillary muscles could be varied between mild and severe by manipulating preload and afterload [9]. Moderate TR resulted in an increase in RA and RV volumes whereas a further increase in the amount of TR was associated with abolishment of RA pump function and ventricularization of the RA pressure. Mild TR could be changed to severe TR by increasing RV afterload with pulmonary artery constriction or infusion of methoxamine. This change was reversible with TR going from severe to mild with removal of the afterload enhancement. Similarly, severe TR could be reduced to mild TR by decreasing preload via constriction of the inferior vena cava or infusion of nitroprusside.

Under normal conditions, RV afterload is low since the RV is coupled with a low-pressure, high capacitance pulmonary vascular system [10]. The effects of increasing pulmonary artery pressures on the amount of TR were evaluated in a study of 2139 subjects with either mild (<50 mm Hg), moderate (50 to 69 mm Hg), or severe (70 mm Hg) elevations in pulmonary artery systolic pressure [11]. PA pressures were independently associated with greater degrees of TR however the correlation was limited and many patients with severe pulmonary hypertension had only mild TR.

In addition to RV size, valvular function, preload and afterload, other factors influencing the degree of TR include the respiratory cycle, left heart function, and atrial fibrillation. Inspiration is associated with a large increase in effective regurgitant orifice, a decline in regurgitant gradient, and an increase in regurgitant volume [12]. A decline in the pressure gradient between RV and RA (i.e., the regurgitant gradient) during spontaneous respiration in our patient is shown in Figure 2. Elevated left atrial pressures will indirectly influence TR by increasing RV afterload, and thus, conditions which increase LV filling pressures can also increase TR. LV function may also have a direct influence on TR as animals models have shown that 20–40% of RV systolic pressure and volume outflow results from LV contraction [13]. Atrial fibrillation has been associated with increased TR [11]

Figure 2. Pressure tracings from a patient with severe TR during spontaneous respiration. Pressures were recorded during spontaneous respiration using a dual lumen pigtail catheter. All pressures were recorded on a 50 mm Hg scale. Simultaneous RA and RV pressures (A) and simultaneous RA and PA pressures (B) are shown. Note that the “ventricularization” of RA pressure and Y descent increase during inspiration.

There is very little information on how invasively measured hemodynamic parameters change over time in patients with severe TR. There are also limited data on whether hemodynamics can be used to determine which patients benefit from surgical repair and/or on hemodynamic changes after surgical treatment of severe TR. Studies using noninvasive imaging have shown that corrective surgery for isolated severe TR in patients with a prior history of aortic or mitral valve surgery results in reductions in RV end-diastolic volume index [14, 15] but effects on hemodynamic parameters are largely unknown.

HEMODYNAMIC CHANGES OF TR OBSERVED DURING RIGHT HEART CATHETERIZATION

Echocardiography is currently the primary diagnostic tool used to evaluate TR. In addition to being noninvasive, echocardiography is better able to quantify the amount of TR and is more useful in distinguishing between structural and functional TR. Patients with severe TR however will undergo invasive diagnostic procedures for other indications, and thus, it is important to recognize and to be able to interpret the hemodynamic changes associated with TR.

RA pressures are generally elevated in patients with severe TR, include a large systolic wave called an “s” wave, and have a prominent Y descent. The magnitude of the systolic wave (also called a “cv” wave as it reflects a merger of the normally independent “c” and “v” waves) is determined both by the severity of the regurgitation and the compliance of the RA. As the amount of TR increases, the “s” wave increases in both magnitude and width as RA pressures more closely approximate RV pressures. In cases of severe TR, the contour of the RA pressure is similar to, but of lower amplitude than, the contour of the RV pressure; this has been labeled as “ventricularization” of the RA pressure (Fig. 3).

Figure 3. “Ventricularization” of RA pressure. Simultaneous RA and RV pressures from a 67-year-old male who had undergone heart transplantation 9 years previously (A) and from a 55-year-old female with a history of aortic and mitral valve surgery 5 years previously (B).

Because of elevated RA pressures at the end of systole, early diastolic filling is accentuated leading to a pronounced Y descent in the RA pressure tracing. Further exaggeration of the Y descent during inspiration can also be found in some patients with severe TR (Fig. 2A). This accentuated early diastolic filling of the RV is due to the decrease in early diastolic pressures in the RV during inspiration. In their study of 59 patients with TR, Cha et al. describe a pattern of pressures in the RA in which the mean pressure was elevated or normal and there were prominent V waves with rapid Y descents which were further accentuated during inspiration. This pattern was present in 21 patients (37%) [16]. The “X” descent is often obscured because the usual decrease in atrial pressures following atrial systole is absent due to the regurgitant flow during ventricular systole.

Specific hemodynamic findings lack sensitivity in the diagnosis of severe TR although RA pressure abnormalities are common. The lack of sensitivity may in part be due to the effects of RA compliance on pressures and the effects of changing preload and afterload conditions on the amount of TR. Ventricularization of the RA pressure tracing is the most specific finding but is found in a minority of patients with severe TR. In a study of 60 patients who had right ventriculography, Lingamneni et al found that ventricularization of the RA pressure contour was present in only 40% of patients with severe TR [17]. Cha et al. in their study of 59 patients with severe TR diagnosed on right ventriculography and/or at the time of surgery, found that a “ventricularization” pattern was present in 31%, and that prominent V waves (not further defined in the paper) and steep Y descents were present in an additional 37%, of the patients. In the remaining patients, the RA pressure contour was normal during expiration but prominent V waves and rapid Y descents were observed with deep inspiration [16].

In another study, the sensitivity and positive predictive value of prominent V waves or an elevated mean RA pressure to identify moderate or severe TR was poor, whereas, the absence of these two hemodynamic findings was relatively specific for the absence of moderate or severe TR [18]. In a group of 174 patients who had echocardiography within 30 days of right heart catheterization, mean RA pressure >12 mm Hg was found in 55% of patients with moderate or severe TR and in only 8% of patients with no, trivial or mild TR. Similarly, large “V” waves in the RA tracing (defined as >15 mm Hg) were present in 48% of patients with moderate or severe TR and in only 7% of patients with no, trivial or mild TR. Echocardiography was not concurrent with right heart catheterization, and thus, potential changes in preload or afterload may have influenced the results.

RV hemodynamic findings that have been reported with significant TR are elevations in RV end diastolic pressure (RVEDP) and a “dip and plateau” pattern in RV diastolic pressures with equalization of RVEDP and LVEDP. Hansing and Rowe studied 28 patients with TR diagnosed by the indicator-dilution method and found that all patients had elevated RVEDP with an average of 10, 13, and 16 mm Hg in patients with mild, moderate and severe TR, respectively. The average RVEDP was 7 mm Hg in the control group [19] In a study of seven patients who had surgical removal of the tricuspid valve as treatment of pseudomonas endocarditis, there was a 43% increase in RVEDP although the change was not statistically significant. In this study, the average RA pressure increased from 4.3 to 11.9 mm Hg (P < 0.001) with no change in pulmonary artery pressures or LV end diastolic pressure [20].

A “dip and plateau” pattern in RV diastolic pressures and equalization of RVEDP and LVEDP have also been reported in patients with severe TR. Studley et al. reported the case of a 72-year-old female with severe TR who had a “dip and plateau” configuration in the RV diastolic pressures as well as equalization of RV and LV end-diastolic pressures. Other hemodynamic findings were similar to those seen in constrictive pericarditis and included prominent X and Y descents on the RA and PCWP tracings and lack of a decrease in RA pressure with respiration [21]. Jaber et al. reported 14 patients with severe TR who had a “dip and plateau” configuration in the RV diastolic pressures and elevation and equalization of LVEDP and RVEDP [22] Many of the hemodynamic findings in these patients were similar to those found in a control group of 14 patients with constrictive pericarditis, however, differences in RVEDP and LVEDP increased during inspiration in patients with TR (RVEDP exceeded LVEDP in a majority of patients) whereas differences in RVEDP and LVEDP were more apparent during expiration (and RVEDP never exceeded LVEDP) in patients with constrictive pericarditis.

Other hemodynamic findings that have been reported with significant TR are a decrease in cardiac output and phasic waveforms in central venous pressures. Hansing and Rowe found that cardiac index was 2.5, 2.5, and 1.9 L/min/m² in patients with mild, moderate and severe TR, respectively, compared to an average of 3.0 L/min/m² in the control group [19] Cardiac output under basal conditions was unchanged but did not increase as much in response to bicycle exercise after surgical removal of the tricuspid valve [20]. Kern and Deligonul reported a case in which femoral vein pressure was elevated and had a marked “s” wave in a patient with severe TR [23].

Significant TR has been associated with underestimation of cardiac output by the thermodilution technique. A study of 30 patients found that thermodilution cardiac outputs were consistently lower (by approximately 20%) than those obtained with the Fick or indocyanine green dye methods in patients with TR whereas there was excellent agreement between the different methods of measuring cardiac output in patients without TR [24]. Balik et al. found that thermodilution underestimated cardiac output in 27 ventilated patients (using transesophageal echocardiographic cardiac output as the gold standard) and that inaccuracies increased proportional to the amount of TR [25]. A theoretical explanation for these results is that TR prolongs the time versus temperature curve because of recirculation which results in an underestimation of cardiac output. Results have not been consistent across all patient subgroups as TR had no effect on the accuracy of thermodilution cardiac output in patients with chronic pulmonary hypertension [26] or in patients with severe congestive heart failure [27].

Acute TR has been reported with chest trauma, endocarditis, PA catheter removal, RV infarction and other causes. Moderate acute TR is associated with increased atrial contraction, possibly due to the Starling mechanism. Severe acute TR is associated with increased RV diastolic pressures, RV and RA dilation, loss of atrial pump function and a large “s” wave in the RA pressure tracing [9].

It is important to avoid artifactual pitfalls when evaluating TR on the basis of hemodynamics. Measurement of RA pressure with a balloon tipped end-hole catheter can sometimes lead to confusion as the tip of the catheter crosses the tricuspid valve during inspiration (Fig. 4). Conversely, dual lumen catheters can interfere with the valvular apparatus, and thus, cause TR with resulting changes in hemodynamics. Careful attention to the phasic waveforms, catheter placement throughout the cardiac cycle, and correlation of the various tracings allows one to discriminate artifact from true waveforms.

Figure 4. Pressure artifact mimicking TR A balloon-tipped catheter was inserted into the RA. Whereas pressures were being recorded, the catheter moved so that the end-hole was partially across the tricuspid valve leading to a narrow wave coincident with the T wave on the ECG (A). True RA and RV pressures are shown in B and C.

CONCLUSIONS

Hemodynamic alterations are common in severe TR. Changes in RA pressures include elevated mean pressures, a large “s” wave, a prominent “Y” descent and a blunted “X” descent. “Ventricularization” of the RA pressure tracing, in which the contour of the RA pressure is similar to, but of lower amplitude than, the contour of the RV pressure is the most specific finding but is found in a minority of patients with severe TR. RVEDP is often elevated and cardiac output is reduced, especially with exercise.