Ultrasound imaging has continuously developed over recent years, leading to the development of several novel echocardiographic indexes. Among these, of particular interest are those that focus on pulmonary hemodynamics, because they not only improve both sensitivity and specificity in the echocardiographic evaluation of pulmonary pressures (systolic, mean, and diastolic), but can also be used to estimate other pulmonary hemodynamic parameters, such as pulmonary vascular resistance, pulmonary capillary wedge pressure, and pulmonary capacitance and impedance. Such parameters can provide important diagnostic and prognostic information in patients with heart failure, chronic obstructive pulmonary disease, and pulmonary arterial hypertension and in every patient with suspected pulmonary impairment. In this review, the authors present a comprehensive overview of the echocardiographic indexes involved in pulmonary hemodynamic evaluation and discuss the applications of these indexes in the clinical setting.
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Target Audience
This activity is designed for all cardiovascular physicians and cardiac sonographers with a primary interest and knowledge base in the field of echocardiography: in addition, residents, researchers, clinicians, intensivists, and other medical professionals with a specific interest in cardiac ultrasound will find this activity beneficial.
Target Audience
This activity is designed for all cardiovascular physicians and cardiac sonographers with a primary interest and knowledge base in the field of echocardiography: in addition, residents, researchers, clinicians, intensivists, and other medical professionals with a specific interest in cardiac ultrasound will find this activity beneficial.
Objectives
Upon completing the reading of this article, the participants will better be able to:
- 1.
Name the hemodynamic criteria that define pulmonary hypertension.
- 2.
Identify various echocardiographic methods for estimating systolic, mean and diastolic pulmonary artery pressures.
- 3.
Recognize formulas for calculating pulmonary vascular resistance.
- 4.
List other echocardiographic (2D and Doppler) signs of pulmonary hypertension.
- 5.
Describe the components of a full pulmonary vascular hemodynamic assessment and how this assessment can help distinguish various clinical scenarios.
Echocardiographic Indexes
Estimation of Pulmonary Pressures
Pulmonary hypertension (PH) is a complex disease that can be idiopathic, familial, or associated with a wide range of disease processes. Although a new and simplified definition has been proposed, according to the most recent guidelines, PH is still defined as mean pulmonary artery pressure (mPAP) > 25 mm Hg at rest; a diagnosis of pulmonary arterial hypertension (PAH) requires PVR ≥ 3 mm Hg/L/min (Wood units [WU]) and PCWP, left atrial pressure, or left ventricular (LV) end-diastolic pressure ≤ 15 mm Hg.
In the context of PH, many echocardiographic signs can be present, many involving the right ventricle (hypertrophy, dilation, or reduction of systolic function). Another sign is the systolic position of the interventricular septum, which can appear flat or can bow toward the right ventricle because of a decreased interventricular pressure gradient when pulmonary pressure becomes near systemic. Echocardiographic techniques for the evaluation of the right ventricle and its morphologic and functional modifications during PH have been reviewed elsewhere.
It has been known for many years that Doppler echocardiography can be used to estimate systolic pulmonary pressure, but because of its limited accuracy and reproducibility, invasive cardiac catheterization remains the gold standard for the correct assessment of right-heart hemodynamics. Over the past few years, many indexes have been proposed to improve, replace, or complete the standard basic echocardiographic evaluation of pulmonary pressures. Table 1 summarizes all indexes cited in this review. Technical tips are summarized in Table 2 .
| Index | Measures required | Formula | Cutoff | Sensitivity (%) | Specificity (%) |
|---|---|---|---|---|---|
| sPAP | |||||
| TRv | • Continuous Doppler of tricuspid regurgitation • RAP | 4 × V 2 + RAP | |||
| RV rIVRT′ on DTI | • Tricuspid DTI | <40 ms: normal PAPs | |||
| RV rIVRT′/HR | • Tricuspid DTI • HR | >10%: sPAP > 30 mm Hg | 86 | 75 | |
| >65 ms: sPAP > 40 mm Hg | 96 | 93 | |||
| Pulmonary flow AcT | • Pulsed Doppler of pulmonary forward flow | <93 ms: elevated sPAP | 71 | 56 | |
| RV diameter and tricuspid annular DTI velocity ratio | • 4-chamber view optimized for RV measurement • Tricuspid DTI | RV diameter/T peak | >22 cm/s: elevated sPAP | 80 | 83 |
| Tricuspid annular DTI systolic velocity | • Tricuspid DTI | ≤12 cm/s: sPAP > 40 mm Hg | 85 | 93.3 | |
| Tricuspid annular DTI systolic TVI | • Tricuspid DTI | ≤2.5 cm: sPAP > 40 mm Hg | 85.7 | 90 | |
| mPAP | |||||
| Peak PRv | • Continuous or pulsed Doppler of pulmonary regurgitation • RAP | 4 × V 2 + RAP | |||
| Mean RV-RA systolic gradient | • Continuous Doppler of tricuspid regurgitation • RAP | Mean RV-RA systolic gradient + RAP | |||
| RV MPI (Tei index) | • Pulsed Doppler of tricuspid inflow • Pulsed Doppler of pulmonary regurgitation • Tricuspid DTI | (IVRT + IVCT)/RVET | >0.36: elevated mPAP | NR | NR |
| dPAP | |||||
| End-diastolic PRv | • Continuous or pulsed Doppler of pulmonary regurgitation • RAP | 4 × V 2 + RAP | |||
| RV pressure assessment at the time of pulmonary valve opening | • Pulsed Doppler of pulmonary forward flow • Continuous Doppler of tricuspid regurgitation • RAP | 4 × V 2 + RAP | |||
| RAP | |||||
| IVC size and collapsibility | • Subcostal view of the IVC | See text and Table 2 | |||
| sHVF | • Pulsed Doppler of hepatic venous flow | sHVF TVI/(sHVF TVI + dHVF TVI) | <55%: RAP > 8 mm Hg | 86 | 92 |
| Systolic flow velocity and atrial reversal sum | • Pulsed Doppler of hepatic venous flow | sHVF + rHVF | • <0 and IVC size < 15 mm: RAP = 5 mm Hg • >0 and IVC size > 20 mm: RAP = 25 mm Hg • Any value and IVC size 15-19 mm: RAP = 14 mm | NR | NR |
| RV rIVRT′ on DTI | • Tricuspid DTI | <59 ms: RAP > 8 mm Hg | 80 | 87.7 | |
| Etr/E′tr ratio | • Pulsed Doppler of tricuspid inflow • Tricuspid DTI | Etr/E′tr | >6: RAP ≥ 10 mm Hg | 79 | 73 |
| PVR | |||||
| PEP/AcT/RV total systolic time | • Continuous Doppler of tricuspid regurgitation • Pulsed Doppler of pulmonary forward flow | (PEP/AcT)/(PEP + RVET) | >2.6: elevated PVR (>2.5 WU) | NR | NR |
| Ratio of TRv to TVI of RV outflow tract | • Continuous Doppler of tricuspid regurgitation • Pulsed Doppler of pulmonary forward flow | TRv/TVIrvot | >0.2: PVR > 2 WU | 70 | 94 |
| >0.38: PVR > 8 WU | 75 | 100 | |||
| >0.12: PVR > 1.5 WU | 100 | 86 | |||
| sPAP and TVIrvot/HR | • Continuous Doppler of tricuspid regurgitation • Pulsed Doppler of pulmonary forward flow • RAP • HR | sPAP/(HR × TVIrvot) | >0.076: PVR indexed > 15 resistance units | 86 | 82 |
| Peak velocity of tricuspid annular systolic movement | • Tricuspid DTI | <10 cm/s: PVR > 1000 dyne/s/cm 5 (∼12.5 WU) | 80 | 100 | |
| RV MPI (Tei index) | • Pulsed Doppler of tricuspid inflow • Pulsed Doppler of pulmonary regurgitation • Tricuspid DTI | (IVRT + IVCT)/RVET | NR | NR | |
| PAC | |||||
| PAC | • LV or RV SV • Continuous Doppler of tricuspid regurgitation • Continuous or pulsed Doppler of pulmonary regurgitation | SV/4(TRv 2 − PRv 2 ) |
| Parameter | Technical tips |
|---|---|
| TRv | • Measure in multiple views (including the subcostal view) looking for the best curve and the maximal velocity; in atrial fibrillation, consider a mean of 5 TRv measurements • Use color flow Doppler and, when necessary, off-axis view to obtain the best alignment between regurgitant flow and Doppler signal • Use continuous Doppler; correct continuous Doppler gain, baseline, scale, and velocity to maximize curve view • Use contrast with air-saline or air-blood-saline to enhance inadequate tricuspid regurgitation signals; pay attention to potential overestimation |
| PRv | • Measure in parasternal long-axis view modified for the RV outflow tract and in short-axis view looking for the best curve and maximal velocity • Use color flow Doppler and, when necessary, off-axis view to obtain the best alignment between regurgitant flow and Doppler signal • Use continuous or pulsed Doppler; when pulsed Doppler is used, place sample volume (size, 5-7 mm) as proximal as possible to the start of pulmonary regurgitation near to the pulmonary valve; pay attention to avoid aliasing; correct Doppler gain, baseline, scale, and velocity to maximize curve view • Use contrast with air-saline or air-blood-saline to enhance inadequate pulmonary regurgitation signals; pay attention to potential overestimation |
| Pulmonary forward flow | • Sample in parasternal long-axis view modified for the RV outflow tract and in short-axis view looking for the best velocity profile and maximal velocity • Use color flow Doppler and, when necessary, off-axis view to obtain the best alignment between forward flow and Doppler signal • Use pulsed Doppler; place the sample volume (size, 5-7 mm) in the RV outflow tract just proximal to the pulmonary valve; correct Doppler gain, baseline, scale, and velocity to maximize curve view |
| Tricuspid DTI | • Optimize the 4-chamber view to obtain a clear view of the tricuspid annulus; reduce the sector to increase frame rate; try to make the RV free wall as parallel as possible with the Doppler cursor using, if necessary, off-axis view • Place the sample volume (size, 3-8 mm) on the lateral tricuspid annulus • Correct tissue Doppler gain, baseline, scale, and velocity to optimize the signal. |
| IVC | • Optimize the subcostal view to obtain a clear view of the right atrium and of the IVC displayed in its long axis • Measure IVC diameter at end-diastole and end-expiration or after deep inspiration or “sniff” maneuver; measurement can be made in 2-dimensional view approximately 2 cm before right atrium or using M-mode on subcostal short-axis view |
| Hepatic venous flow | • Optimize the subcostal view to obtain a clear view of the IVC displayed in its long axis • Use color Doppler to identify and maximize hepatic vein view; align the cursor as parallel as possible to the hepatic vein • Use pulsed Doppler; place the sample volume (size, 5-7 mm) 1 to 2 cm into the hepatic vein; correct Doppler gain, baseline, scale, and velocity to maximize curve view |
Systolic Pulmonary Artery Pressure
Systolic pulmonary artery pressure (sPAP) is considered equal to right ventricular (RV) systolic pressure in the absence of pulmonary valve stenosis or outflow tract obstruction. RV systolic pressure can be determined by addition of right atrial (RA) pressure (RAP) to the pressure gradient between the right chambers. Many methods can be used to estimate RAP (see below), while the pressure gradient between the right chambers can be calculated using the modified Bernoulli equation:
where v is the tricuspid regurgitant velocity (TRv). In the 1980s, several key studies were performed to validate this technique versus RV catheterization, and it was subsequently used to estimate sPAP in patients with various diseases. Although the application of this technique to estimate sPAP has been widely validated, its precision is debatable: in studies that have compared echocardiographically estimated values and true values measured by right-heart catheterization, the mean difference ranged from 3 to 38 mm Hg, and sPAP was underestimated with the echocardiographic method by >20 mm Hg in 31% of all patients studied. In a more recent study, in 48% of 63 patients studied, echocardiography-derived sPAP differed more than ±10 mm Hg from invasively measured sPAP; the magnitude of pressure underestimation was greater than that of its overestimation. For this reason, sPAP evaluation with Doppler methods should not be used to decide when to treat patients or to monitor therapy efficacy. Although the accuracy of Doppler sPAP measurements has been questioned, thus limiting its utility as a diagnostic tool in asymptomatic PH, sPAP estimation by TRv measurement remains the most feasible and reliable screening method for suspected PH and in patients with associated conditions or risk factors for the development of PH (such as family history, connective tissue diseases, coronary heart disease, human immunodeficiency virus infection, portal hypertension, congenital heart diseases, and chronic hemolytic anemia, as well as use of fenfluramine derivatives, amphetamines, and other agents ). TRv > 2.8 m/s (corresponding to a right atrioventricular pressure gradient > 31 mm Hg) is considered a reasonable cutoff to define elevated pulmonary pressures, except in elderly and in very obese patients, in which physiologic sPAP tends to be more elevated. The European guidelines for the diagnosis and treatment of PH consider the echocardiographic diagnosis of PH “likely” when TRv is >3.4 m/s (or sPAP is >50 mm Hg) and “possible” when TRv is between 2.9 and 3.4 m/s (or sPAP is between 37 and 50 mm Hg), with or without additional echocardiographic signs suggestive of PH, or when TRv is ≤2.8 m/s (or sPAP is ≤36 mm Hg) with additional variables suggestive of PH (RV hypertrophy or dilation, increased pulmonary regurgitant velocity [PRv], etc).
Because of its importance as a screening test, the major concern in the noninvasive evaluation of sPAP (and of mPAP and diastolic PAP [dPAP]) is to reduce as much as possible false-negative results (ie, to minimize the risk for sPAP underestimation). The underestimation of sPAP with echocardiography is probably due to the frequent underestimation of RAP (see below) and of TRv. To minimize error, TRv should be measured in multiple views, seeking the maximal TRv; the use of color flow Doppler is recommended to obtain the best alignment between regurgitant flow and the Doppler signal. Many studies have also demonstrated that inadequate TRv signals can be enhanced with the use of contrast. An easier and less expensive solution, a simple air-blood-saline mixture, can dramatically improve the correlation between Doppler-measured and catheter-measured sPAP (from r = 0.64 to r = 0.92 in a study by Jeon et al ). Care must be taken in using contrast to avoid the possible overestimation of Doppler velocities because of contrast artifacts. If atrial fibrillation is present, we suggest taking the mean of 5 TRv measurements.
mPAP
Peak PRv
When present, the PRv pattern is characterized by a rapid rise in flow velocity immediately after the closure of the pulmonary valve (peak PRv; Figure 1 ) and a gradual deceleration until the next pulmonary valve opening (end-diastolic PRv). Peak PRv represents the diastolic pressure gradient between the pulmonary artery and the right ventricle. Masuyama et al demonstrated that the application of the Bernoulli equation to peak PRv would provide an estimate of mPAP. More recently, Abbas et al validated this method and demonstrated that adding RAP improves the accuracy of the mPAP estimate.
Mean RV-RA Systolic Gradient
Aduen et al recently proposed a novel and simple method to estimate mPAP on the basis of the addition of RAP to the RV-RA mean systolic gradient obtained by tracing the TRv profile. This method was validated in 102 patients, comparing it with simultaneous right-heart catheterization; it showed great reliability (mean difference with invasively obtained pressures, −1.6 mm Hg; median absolute percentage difference, 18%) and accuracy in diagnosing PH (area under the curve, 0.92; 95% confidence interval, 0.87-0.97). The addition of saline contrast did not improve accuracy. This method appears straightforward and could easily be incorporated into a standard echocardiographic exam, allowing a reliable estimation of mPAP.
Empirical Formulas
The relationships among sPAP, dPAP, and mPAP have been found to be constant under many conditions. Many empirical formulas derived from invasive studies have been proposed to estimate mPAP from sPAP and/or dPAP; specific descriptions of these formulas lie outside the scope of the present review. However, it must be remembered that the use of these formulas applied to echocardiographic data has not been validated. We suggest limiting when possible the use of empirical formulas and trying to estimate mPAP and dPAP using different echocardiographic methods to increase the accuracy of their estimation.
dPAP
End-Diastolic PRv
The application of the simplified Bernoulli equation to end-diastolic PRv ( Figure 1 ) enables the calculation of the pressure gradient between the right ventricle and the pulmonary artery in end-diastole; the pressure gradient added to RAP estimates dPAP, with a high correlation with invasive dPAP measurements. Recently Ristow et al demonstrated that a >5 mmHg end-diastolic pulmonary regurgitant gradient seems to be correlated with cardiac dysfunction, in particular with decreased functional status, elevated serum B-type natriuretic peptide, elevated LV mass index, and systolic and diastolic dysfunction. As with tricuspid regurgitation, weak pulmonary regurgitant Doppler signals can be enhanced with the use of contrast, with increased reliability of the dPAP estimate.
RV Pressure Assessment at the Time of Pulmonary Valve Opening
It has been demonstrated that dPAP can be estimated by measuring RV pressure at the time of pulmonary valve opening, because RV and pulmonary pressures are balanced at this point of the cardiac cycle. As discussed above, the gradient between the right chambers can be estimated by the TRv. Therefore, the application of the simplified Bernoulli equation to the TRv measured at the time of pulmonary valve opening and the sum of this value with RAP allows an estimation of dPAP. The TRv at the time of pulmonary valve opening is measured by superimposing the time from the QRS complex to the onset of pulmonary flow on the regurgitation velocity envelope ( Figure 2 ). This method has demonstrated a high correlation with invasively measured dPAP. However, because the measurement is made on the steep portion of the TRv slope, any small error in timing measurement (or small differences in timings between different cardiac cycles) could lead to large errors in dPAP estimates.
Stress Echocardiography
Exercise-induced PH has been recognized as an early phase of the PH spectrum, especially in high-risk patients. In the past, stress echocardiography was widely used to unmask and assess PH; however, its validity is debated. Recently Kovacs et al published a systematic review based on 1187 individuals from 47 studies, and they concluded that exercise mPAP is age related and frequently exceeds 30 mm Hg also in healthy people, especially in elderly individuals. For these reasons, the 4th World Symposium on Pulmonary Hypertension stated that the exercise criteria for the diagnosis of PH should be eliminated, and so they were in the recent European guidelines. Moreover, because of the difficulty in performing and interpreting exercise echocardiography, no treatment decisions can be made on the basis of exercise-induced PH alone, and in general, exercise echocardiography is not recommended for the assessment of patients with PH.
RAP
An accurate estimation of RAP is of paramount importance to obtain more reliable noninvasive evaluations of pulmonary pressures.
Inferior Vena Cava Size and Collapsibility
Because RAP is strictly correlated with central venous pressure, the most frequently used technique for its estimation is the observation of the diameter and collapsibility of the inferior vena cava (IVC; Figure 3 ). The IVC should be visualized in the subcostal view; the patient should be in the supine position, because IVC size is significantly larger in the right lateral position and significantly smaller in the left lateral position. IVC diameter should be measured within 2 cm of the right atrium at end-expiration and end-diastole and at end-inspiration or during a “sniff” maneuver; the decrease of its diameter with inspiration (or the sniff maneuver) is a measure of IVC collapsibility. It is important to remember that the IVC can be dilated (>2 cm) in younger subjects despite normal RAPs ; IVC size should also be considered with caution in patients who are mechanically ventilated.
Several algorithms have been proposed to estimate RAP through a combination of IVC size and collapsibility ( Table 2 ). The first, proposed by Kircher et al, estimates RAP on the basis of percentage collapsibility alone (full collapse, 5 mmHg; >50% collapse, 10 mm Hg; <50% collapse, 15 mm Hg; no collapse, 20 mm Hg), regardless of the IVC’s absolute size. A modified algorithm, proposed by Pepi et al, considers 3 groups only (collapsibility > 45%, 6 mm Hg; collapsibility between 35% and 45%, 9 mm Hg; collapsibility < 35%, 16 mm Hg).
| Collapsibility index | |||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Dimension (cm) | Full collapse | >50% | 35%-50% | <35% | No collapse | ||||||||||
| Source ∗ | 49 | 56 | 57 | 49 | 56 | 57 | 49 | 56 | 57 | 49 | 56 | 57 | 49 | 56 | 57 |
| <1.7 | 5 | 0-5 | 0-5 | 10 | 0-5 | 0-5 | 15 | NR † | 0-10 | 15 | NR † | I ‡ | 20 | NR † | I ‡ |
| 1.7-2.1 | 5 | 6-10 | 0-5 | 10 | 6-10 | 0-5 | 15 | 10-15 | 0-10 | 15 | 10-15 | I ‡ | 20 | > 15 | I ‡ |
| >2.1 | 5 | 6-10 | 0-10 | 10 | 6-10 | 0-10 | 15 | 10-15 | 10-15 | 15 | 10-15 | 10-20 | 20 | > 15 | 10-20 |
∗ Kircher et al, Lang et al, or Brennan et al.
† This scheme does not take into account the possibility of an IVC < 1.7 cm with a collapsibility index < 50%.
‡ In these conditions, invasively measured RAP assumes values with a high range of variability, so it is not possible to estimate RAP through IVC measurement.
A second algorithm is reported in the American Society of Echocardiography’s guidelines. In this scheme, RAP is estimated on the basis of a cutoff of 50% of collapsibility and on a cutoff of 1.7 cm of absolute IVC diameter measured in the left lateral decubitus position. This scheme was discussed in a recent study performed by Brennan et al, in which the traditional classification of RAP into 5 mm Hg ranges performed poorly (43% accuracy) compared to invasive RAP measurements. Brennan et al proposed a new classification, dividing both size and collapsibility (evaluated in supine position) into 3 categories, thereby enhancing the accuracy of RAP estimations. Interestingly, in that study, it was noted that with a nondilated IVC (<2.1 cm) and collapsibility < 35%, it is not possible to estimate RAP, because of the high range of variability that invasively measured RAP can assume in this condition.
Systolic Filling Fraction of Hepatic Venous Flow
Like the IVC, the hepatic veins are strictly associated with central venous pressure and RAP, but unlike the IVC, it is possible to easily analyze their flow using Doppler in transthoracic echocardiography, thanks to their orientation. Normal hepatic venous flow consists of systolic forward flow (sHVF), reverse flow at end-systole, diastolic forward flow, and a diastolic flow reversal wave with atrial systole. The sHVF is directly associated with the pressure gradient between the hepatic veins and the right atrium; when RAP increases, the gradient decreases along with sHVF. In a study by Nagueh et al, the index showing the best correlation with RAP was the systolic filling fraction ( r = 0.86), calculated as the ratio between the time-velocity integral (TVI) of sHVF and the sHVF TVI added to the diastolic forward flow TVI ( Figure 4 ). However, another study performed by Ommen et al demonstrated that the systolic filling fraction correlates poorly ( r = 0.25) with RAP; moreover, sHVF is dependent not only on RAP but also on several other factors, such as atrial compliance and relaxation, severe tricuspid regurgitation, tricuspid annular descent, and increases in left atrial and ventricular preload. This group subsequently proposed estimating RAP combining a new index derived from hepatic venous flow (the sum of the velocities of sHVF and the diastolic flow reversal wave with atrial systole) with the evaluation of IVC diameter; with this new scheme, patients could be divided into those with normal RAP (5 mm Hg), mildly increased RAP (14 mm Hg), and severely increased RAP (25 mm Hg).
RV Regional Isovolumic Relaxation Time
The evaluation of both IVC and hepatic venous flow requires subcostal views that in some patients, especially in the postoperative period, can be difficult to achieve. Abbas et al proposed using RV regional isovolumic relaxation time (rIVRT; Figure 5 ) as an index of RAP. RV rIVRT is the regional measurement on Doppler tissue imaging (DTI) of the duration of the tricuspid annular motion between systolic and diastolic annular movements. Abbas et al demonstrated an inverse relationship between RV rIVRT and RAP, with 80% sensitivity and 87.7% specificity for RV rIVRT < 59 ms to predict RAP > 8 mm Hg.
Ratio of Tricuspid Peak Early Inflow Velocity to Peak Early Diastolic Velocity of the Lateral Tricuspid Annulus
Nageh et al evaluated the ratio of the tricuspid peak early inflow velocity (Etr) to the peak early diastolic velocity of the tricuspid annulus (E′tr) as an index of RV filling pressures, paralleling the use of the ratio of the mitral peak early inflow velocity to the peak early diastolic velocity of the lateral mitral annulus as an index of LV filling pressures. Nageh et al showed a strong relation between Etr/E′tr and RAP, also in patients on mechanical ventilation and with or without RV systolic dysfunction: an Etr/E′tr ratio > 6 had 79% sensitivity and 73% specificity for mean RAP ≥ 10 mm Hg. As for the RV rIVRT method, the authors suggested the use of this method in patients without subcostal windows or in mechanically ventilated patients in which the IVC index is inaccurate. However, a recent study by Michaux et al demonstrated that Etr/E′tr failed to predict RAP in anesthetized, paralyzed, and mechanically ventilated patients.
Complementary Indexes
A good tricuspid regurgitation jet is fundamental for the estimation of sPAP and in some methods of dPAP estimation. However, tricuspid regurgitation jets are not clearly evaluated in about 15% of patients, so many authors have tried to find alternative indexes.
RV Rivrt
RV rIVRT ( Figure 5 ) measured by DTI is associated with sPAP and could help in its estimation when TRv is not present. In particular, RV rIVRT seems to have high sensitivity in detecting PAH: RV rIVRT < 40 ms excludes PAH with a negative predictive value of 100%. Because the IVRT is a diastolic parameter and the duration of diastole is influenced by heart rate, it is recommended to correct for RV IVRT′ to RR interval. In a study by Elnoamany and Dawood, RV IVRT corrected for heart rate > 65 ms displayed 96% sensitivity and 93% specificity to predict sPAP > 40 mm Hg. RV rIVRT evaluation at the mid cavity segment seems to better correlate with sPAP than when evaluated at basal segment. The correlation between RV rIVRT and sPAP seems to fail in patients with significantly reduced RV systolic function.
RV rIVRT lengthening is probably a direct expression of myocardial diastolic relaxation impairment that parallels increasing afterload and reflects impairment of intracellular calcium transport as a result of myocyte hypoxia. However, a prolonged RV rIVRT is not specific for PAH and is strictly associated with preload and RAP: when RAP is normal, RV rIVRT increases proportionately with sPAP, but when the right atrium fails or is volume overloaded, RAP is increased with an earlier tricuspid valve opening, so that RV rIVRT shortens. Therefore, a prolonged RV rIVRT is in favor of but cannot be used alone to make a diagnosis of elevated sPAP.
Pulmonary Flow Morphology and Acceleration Time
The Doppler pulmonary flow velocity curve has, under normal conditions, a domelike contour with a maximum velocity in the middle of systole. In PH, it acquires a more triangular contour, with a peak velocity in early systole, and in some cases a slower rise during deceleration can be observed, resulting in midsystolic notching.
The pulmonary flow acceleration time (AcT), defined as the time interval from the onset of forward flow in the pulmonary artery to the peak velocity of this flow ( Figure 6 ), has been demonstrated to be inversely related to sPAP and mPAP. AcT is a highly feasible index; in a study by Lanzarini et al, an AcT < 93 ms identified 67.4% of patients with PAH. In combination with other indexes of pulmonary pressures, AcT can be a very powerful tool in PAH diagnosis.
