INTRODUCTION
Assessment of right ventricular (RV) function is an important component of the comprehensive evaluation of cardiac function in patients with known or suspected heart disease. RV function may be normal when left ventricular (LV) function is depressed, and conversely, RV dysfunction may occur in the presence of normal LV function. Therefore, a careful evaluation of RV function is essential irrespective of LV functional status. In this chapter, we will discuss the assessment of RV diastolic function with echocardiographic and Doppler techniques.
PATHOPHYSIOLOGY
RV diastolic function is determined by a number of factors at the cellular, myocardial, and cardiac chamber levels. Therefore, RV filling patterns and RV filling pressures reflect the net balance of many variables. Active relaxation is among the important determinants of RV diastolic function and is dependent on calcium uptake by the sarcoplasmic reticulum, intrinsic contractility, uniformity of relaxation, and the load-dependent properties of relaxation. Ventricular suction and active myocardial relaxation in health lead to a small positive pressure gradient between the right atrium and the right ventricle, hence the predominant RV filling in early diastole. In addition, recent animal studies with three-dimensional real-time echocardiography have drawn attention to the presence of vortical motion during early diastolic RV filling, which is reduced with chamber dilatation. This vortical motion can facilitate RV filling by shunting kinetic energy that could otherwise lead to increased convective deceleration and therefore a reduced right atrial (RA) to RV pressure gradient.
With impaired RV relaxation, an increase in RA pressure is needed to maintain adequate RV filling and stroke volume. Myocardial stiffness, RV chamber geometry (dimensions and wall thickness), and RA systolic function determine RV filling later in diastole. In particular, RA systolic function appears to play an important compensatory role in preventing heart failure in the presence of pulmonary hypertension. In addition, factors extrinsic to the right ventricle determine RV filling, including pericardial properties, LV filling, and extrinsic compression by mediastinal masses or large pleural effusions. In turn, RV filling can affect LV diastolic volume and pressure.
It is possible to assess RV relaxation invasively by using high-fidelity pressure catheters to measure peak negative pressure/time change (dP/dt) and the time constant of pressure decay during isovolumic relaxation (τ). Both measurements, however, are load dependent, with an inverse linear relation to systolic load. There is a paucity of data with respect to human measurements that include small numbers of patients with coronary artery disease, pulmonary hypertension, and hypertrophic cardiomyopathy. RV chamber stiffness can also be quantified using the combination of RV diastolic pressures and volumes. In comparison with invasive measurements, echocardiography has the advantages of safety, versatility, and portability, and therefore is the modality that is most frequently utilized to gain insight into RV diastolic function and filling pressures ( Table 14-1 ).
|
Right Atrial and Ventricular Dimensions
The assessment of RV diastolic function should begin with the evaluation of RV dimensions and systolic function, as patients with reduced RV systolic performance have diastolic dysfunction. RV systolic function is usually assessed in a qualitative manner by paying attention to RV dimensions and fractional area change. This is done utilizing two-dimensional echocardiography, with images acquired from the parasternal, apical, and subcostal views. Likewise, the presence of RV hypertrophy is associated with diastolic dysfunction.
RA volume is another useful parameter obtained with two-dimensional echocardiography. It is usually increased in patients with RV diastolic dysfunction. RA volumes should be considered when drawing conclusions about RA pressure in patients with equivocal findings in Doppler parameters. Although RA volumes can be measured at any time during the cardiac cycle, maximal RA volumes ( Fig. 14-1 ) are most frequently measured before tricuspid valve opening at end systole; RA minimum volume is measured after tricuspid valve closure at end diastole. RA emptying fraction can be computed as the difference between RA maximum and minimum volumes/RA maximum volume. In patients with increased mean RA pressure, RA maximum and minimum volumes are increased, whereas RA emptying fraction is decreased. The correlation of RA volumes with RA pressure, however, is weak and is heavily modified by RA stiffness and contractility. In addition, RA volumes may be increased for reasons other than diastolic dysfunction, such as atrial fibrillation and tricuspid valve disorders.
Inferior Vena Cava Diameter and Respiratory Collapse
Inferior vena cava (IVC) diameter and its change during inspiration are useful indicators of RA pressure. Previous studies have noted that the segment within 2 cm of the RA-IVC junction is the region most responsive to changes in respiratory effort. In particular, IVC expiratory and inspiratory diameters as well as percent collapse were reported to have significant relations with RA pressure in patients with spontaneous respiration. Clinically, IVC imaging is acquired in the subcostal view at rest and with inspiratory effort, or a “sniff test.” The presence of at least 50% collapse is usually seen with an RA pressure less than 10 mmHg, whereas patients with RA pressure greater than 10 mmHg typically exhibit less than 50% IVC collapse. Figure 14-2 is from a patient with an increased RA mean pressure (>20 mmHg) who exhibits a dilated IVC and minimal change in IVC diameter with inspiration.
The limitations of this method occur in patients with dyspnea and those on mechanical ventilation. In patients on mechanical ventilation, IVC percent collapse relates poorly ( Fig. 14-3 ) to mean RA pressure, whereas IVC diameter at expiration has a somewhat better correlation ( r = .58). An IVC diameter no greater than 12 mm appears highly accurate in identifying patients with an RA pressure less than 10 mmHg, whereas a diameter greater than 12 mm has no predictive value in this population.
In addition, it is possible to image the left hepatic vein from the same window. In one study, the transverse diameter of this vein at expiration and inspiration, as well as end expiratory apnea, was shown to relate significantly to mean RA pressure in a group of 32 patients presenting with acute myocardial infarction. Assessment of the left hepatic vein diameter could be helpful in patients where the IVC is not well visualized. However, there is a paucity of data on the clinical application of this approach in patients on mechanical ventilation.
Tricuspid and Pulmonary Regurgitation Signals by Continuous Wave Doppler
The rate of rise and fall in tricuspid regurgitation (TR) jet velocity by continuous wave (CW) Doppler parallels the corresponding events in RV pressure, assuming minimal fluctuations of RA pressure throughout the cardiac cycle. Therefore, it is possible to calculate RV peak positive and peak negative dP/dt by using the TR jet and applying the modified Bernoulli equation to convert the TR velocity to RV pressure. In one study, a strong correlation was observed between the invasive measurement and the noninvasive estimate of peak negative dP/dt. The limitations of this approach include the need for a complete TR signal and the underestimation of peak negative dP/dt in patients with an RA “v” wave pressure of at least 10 mmHg. For clinical application, one depends more on the shape of the signal (slow decay of the peak velocity to baseline) than the actual measurement, as shown in Figure 14-4 .
A pulmonary regurgitation (PR) signal by CW Doppler can be recorded in many patients, particularly in the presence of pulmonary hypertension. In addition, it is possible to enhance the signal by using intravenous contrast. Once an adequate signal is recorded, its peak velocity can be used to estimate mean pulmonary artery pressure, whereas its end diastolic velocity in conjunction with mean RA pressure can be used to estimate pulmonary artery diastolic pressure. Discrepancies may occur if RV end diastolic pressure is significantly different than mean RA pressure.
In addition, in the absence of significant PR, the deceleration slope and the pressure half-time of the PR jet by CW Doppler can provide unique insight into RV diastolic function. Patients with increased RV stiffness and rapidly rising RV diastolic pressure have a rapid equalization of the pressure gradient between the pulmonary artery and the right ventricle and therefore a short pressure half-time ( Fig. 14-5 ). In one study, which used right heart catheterization, a pressure half-time of no greater than 150 ms was the best predictor of RV involvement in patients presenting with acute inferior wall myocardial infarction. The same investigators reported that this parameter was the only predictor of overall in-hospital clinical events in the same patient population.
Tricuspid Inflow
Pulsed-wave (PW) Doppler recording of tricuspid inflow is essential for the assessment of RV filling. Care should be exercised to obtain the best alignment with the direction of blood flow, which typically requires a medial movement of the transducer from the conventional apical position. The recording is obtained by placing a 1–2 mm sample volume at the valve annulus and tips with filter and gain adjustments to obtain a clear signal. Respiratory variability is an additional factor that needs to be considered with measurements taken at end expiratory apnea or as the average of five to seven consecutive cardiac cycles. The latter approach has been shown to yield identical results to those obtained at end expiratory apnea.
Similar to mitral inflow, tricuspid inflow ( Fig. 14-6 ) is analyzed for peak early (E) and late (A) diastolic velocity, deceleration time (DT) of E velocity, duration of A velocity, and the fraction of RA contribution to RV filling (the atrial filling fraction [AFF]). All measurements except for the A duration are obtained from the Doppler recordings at the level of the valve tips. The A duration is measured from the recording at the level of the tricuspid annulus. Because the tricuspid and pulmonary valves are in different planes, isovolumic relaxation time (IVRT) is measured by Doppler using two time intervals, as the difference between the duration from the QRS complex to onset of tricuspid inflow and the interval from the QRS complex to end of pulmonic flow. Alternatively, IVRT can be calculated by subtracting the time between the QRS complex and the end of pulmonic ejection from the duration of the TR jet.
Early diastolic RV filling is reduced with normal aging, which should be considered when drawing conclusions about RV diastolic function using tricuspid inflow velocities. In general, patients with impaired RV relaxation have a reduced E/A ratio, a prolonged IVRT and DT, and an increased AFF. As RA pressure increases, E/A ratio increases and DT shortens ( Fig. 14-7 ). However, the individual response is highly variable and dependent on the interplay between many hemodynamic parameters, such that the E/A ratio has a significant positive relation with mean RA pressure but with a wide scatter ( Fig. 14-8 ). Nevertheless, in patients with RV systolic dysfunction, a short DT is usually associated with increased filling pressures. In addition, diastolic TR, when present and in the absence of atrioventricular (AV) block, indicates the presence of increased RV stiffness and highly increased RV filling pressures.
