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CONTEMPORARY TOPIC
Year : 2018  |  Volume : 2  |  Issue : 2  |  Page : 95-105

Echocardiographic evaluation of pulmonary hypertension


Shri Krishna Hospital, Aurangabad, Maharashtra, India

Date of Web Publication6-Sep-2018

Correspondence Address:
Dr. Rajesh Krishnachandra Shah
Shri Krishna Hospital, Aurangabad - 431 001, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jiae.jiae_6_18

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  Abstract 

Pulmonary hypertension (PH) is the end result of nearly all cardiac and some noncardiac conditions. It is an important marker of mortality and morbidity. It is also the deciding factor in the management of the etiological conditions, such as the timing of surgery in valvular heart disease, follow-up of pulmonary arterial hypertension, diuretic therapy for diastolic dysfunction, and so on. To add to the problems, early signs and symptoms are nonspecific, and so the diagnosis is attained at a later and advanced stage. Although clinical evaluation is always essential, echocardiography is now the main tool for the evaluation of PH. The aims of echocardiography in PH are: (1) to identify the etiology, (2) assess the effects of PH on the right ventricle, (3) estimation of the severity of the PH, (4) monitoring the progression and therapeutic response in PH, and finally (5) predicting the prognosis. It is hence very important that one measures the pulmonary pressures accurately for proper patient management. The aim of this article is to provide a detailed information of the different parameters of PH in the different echocardiographic views and the technique of measuring these parameters.

Keywords: Mean pulmonary artery pressure, pulmonary artery diastolic pressure, pulmonary artery systolic pressure, pulmonary hypertension, pulmonary vascular resistance


How to cite this article:
Shah RK. Echocardiographic evaluation of pulmonary hypertension. J Indian Acad Echocardiogr Cardiovasc Imaging 2018;2:95-105

How to cite this URL:
Shah RK. Echocardiographic evaluation of pulmonary hypertension. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2018 [cited 2018 Oct 23];2:95-105. Available from: http://www.jiaecho.org/text.asp?2018/2/2/95/240640


  Introduction Top


Pulmonary hypertension (PH) is defined as a condition where there are hemodynamic and pathophysiologic changes, with increased mean pulmonary artery pressure (MPAP) of ≥25 mmHg at rest, at sea level, as measured by right heart catheterization (RHC).[1] The normal or increased pulmonary capillary wedge pressure (PCWP) decides whether it is precapillary, where the PCWP is ≤15 mmHg. or postcapillary, where in the PCWP is >15 mmHg. The increase in the pulmonary vascular resistance (PVR) is seen in precapillary PH, the cut-off value being >2 wood units.[2] Shortly, combining various echo techniques, may make echocardiography the gold standard for the evaluation of PH, having a high sensitivity and accuracy. This will reduce the need for repeated invasive assessments in these patients.[3]

RHC is considered the “gold standard” for the measurement of the systolic pulmonary artery pressure (SPAP). However, as it is invasive in nature, and sometimes has fatal complications,[4] it is utilized less frequently. RHC may be required for measurement of cardiac output, evaluation of intracardiac shunts, valve dysfunction, and finally in conditions where the cause of the PH is uncertain.[5]

Transthoracic echocardiography is a promising method for the evaluation of PH, the right-sided heart structure, and right ventricular function.[6],[7] It provides us with direct and indirect signs of elevated pulmonary pressures. Thus, echocardiography has become a more preferred investigation for evaluation of SPAP and detecting the cause of PH.[1] Echocardiography is highly utilized as it is noninvasive, economical, convenient, bedside procedure, giving an instant diagnosis and can be repeated as many times as required. It has been demonstrated that SPAP and MPAP measured during RHC are similar to measurements obtained by echocardiography.[8] In some studies, it is observed that the SPAP by echo correlates well with SPAP by RHC, in patients with left-sided heart diseases, while the correlation is not as accurate in right-sided heart diseases.[9]


  Causes and Classification of Pulmonary Hypertension Top


PH is a hemodynamic condition caused by various diseases of the lungs, various congenital, valvular and left heart conditions, and certain systemic diseases.[10],[11] One of the conditions that can be overlooked as a cause of PH is the left ventricular (LV) diastolic dysfunction. One should keep in mind that grade I diastolic dysfunction of the LV is commonly seen in precapillary PH and it should not be considered as a cause of pulmonary venous hypertension leading to PH.[12] The most recent WHO clinical classification of PH is the Dana Point 2008, which is based on the etiology of PH. It is classified into five groups [Figure 1].
Figure 1: The Dana point classification of pulmonary hypertension. CTD: Connective tissue disorders, CHD: Congenital heart disease, PAH:Pulmonary arterial hypertension, PVOD: Pulmonary veno occlusive disease, PCH:Pulmonary capillary haemangiomatosis, PH:Pulmonary hypertension, COPD:Chronic obstructive pulmonary disease, ILD:Interstitial lung disease, CTEPH:Chronic thromboembolism pulmonary hypertension

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  Echocardiographic Evaluation of Pulmonary Hypertension Top


No single echocardiographic parameter is pathognomonic of PH, and as PH is such an important entity, the echocardiographic evaluation has to be meticulous and all the parameters systematically evaluated for its diagnosis. A thorough assessment of the PH should include three main entities, namely,

  1. Estimation of pulmonary arterial hypertension (PAH) (pulmonary artery systolic pressure, MPAP and diastolic pulmonary artery pressure [DPAP])
  2. Evaluation of the right ventricle (RV) function (systolic and diastolic)
  3. The measurement of the PVR.


The RV systolic function could be global or regional [Table 1]. The different parameters for their evaluation are as shown in [Table 1]. Another peculiarity of the RV is that it has only two layers of muscle the longitudinal and the circumferential; hence the wringing motion is not present in RV contraction. Here also, the longitudinal action is dominant. This is opposed to the three types of contractions seen in LV, namely longitudinal, circumferential and rotational. In healthy individuals, as opposed to the LV and the systemic circulation, the pulmonary circulation is a low-resistance system, accommodating the whole cardiac output.[13] The RV is more compliant than the LV and adapts better to volume loading than to pressure loading. Another change seen in the RV in PH is ventricular remodeling, which is a result of chronic progressive pressure loading. This is initially in the form of hypertrophy and later as dilation.[14]
Table 1: Parameters of RV Systolic Dysfunction

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The different parameters to be evaluated in accordance with the different views are systematically discussed:

Parasternal long axis view

We all start our echocardiographic examination with this view, and the moment the probe is kept on the chest a fair idea as to the condition of the RV can be inferred. The following parameters can be evaluated from this view [Table 2].
Table 2: Summary of parameters evaluated in PLAX view

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  1. The proximal right ventricular outflow tract (RVOT) dimension can be measured. The normal value is 25 ± 2 mm.[15] The RV wall thickness can also be measured in this view, the normal value is 3 ± 1 mm [15] [Figure 2]
  2. With increasing PH, the RV pushes the ventricular septum into the LV cavity, thereby reducing the size of LV. This paradoxical motion of the inter ventricular septum (IVS) can be studied in this view. The LV systolic function remains preserved [16] [Video 1] and [Table 2]
  3. Due to the impaired lymphatic drainage as a result of increased right atrial pressure (RAP) pericardial effusion can occur in PH and can be seen in this view [17] [Video 1]
  4. As a result of a decrease in the size of the LV, mitral valve prolapse can occur with PH and can be seen in this view [17] [Video 1]
  5. Very often in PH, a dilated coronary sinus can be observed in this view [Figure 2], [Video 1] and [Table 2].
Figure 2: Parameters of pulmonary hypertension in parasternal long-axis view. IVS: Inter ventricular septum, LVPW: Left ventricular posterior wall, LV:Left ventricle, LA:Left atrium, RV:Right ventricle, AO:Aorta

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Parasternal short axis view at aorta/left atrium level

  1. This view allows us to measure the proximal and distal RVOT. The cut off for the proximal RVOT is 28 mm ± 3.5 mm and distal RVOT is 22 mm ± 2.5 mm [15] [Figure 3]
  2. The size of the pulmonary artery which is usually less than the aortic diameter can also be measured in this view. Although there are no data to suggest that as an isolated parameter the dilatation of the pulmonary artery has any significance for the measurement of PH [16] [Table 3]
  3. MPAP and PADP can be measured in this view from the early and end diastolic pulmonary regurgitant (PR) velocities. It is discussed in detail in continuous wave (CW) Doppler evaluation [Figure 3] and [Table 3]
  4. Interatrial septum (IAS), which bulges into the left atrium (LA), is an indirect indicator of PH and is seen in this view. This view also helps to identify the presence of any echo dropouts for the diagnosis of atrial septal defect (ASD). The diagnosis can be confirmed by colour flow imaging
  5. LV eccentricity index: Under normal circumstances, the higher pressures in the LV cavity Pushes the IVS into the lower pressure RV cavity. In patients with PH, initially the septum is pushed toward the LV, causing the IVS to flatten, but as the pulmonary pressure increases the septum may even bulge into the LV cavity in systole.[14] These changes in the motion of the IVS are evaluated by the LV eccentricity index. It is measured in the parasternal short axis (PSAX) view at the papillary muscle level and is equal to the ratio of the anteroposterior to septolateral LV diameter. The ratio is considered abnormal when it is >1 [Figure 4]. It also helps to differentiate between volume and pressure overload. If the RV is dilated and pushes the septum into the LV only in diastole, it indicates volume overload, but if the IVS is shifted into the LV both in systole and diastole, it will indicate RV pressure overload [16] [Video 2].
Figure 3: Parameters of pulmonary hypertension in parasternal short axis view

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Figure 4: Right ventricle special views. RV: Right ventricle

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Table 3: Summary of parameters evaluated in PSAX view

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Right ventricle inflow view

This view is obtained by a medial and inferior angulation of the probe in the parasternal long-axis (PLAX) view toward the Tricuspid Valve [Figure 4].

  1. The RV anterior and posterior wall can be evaluated to give a qualitative idea of the RV function. [Video 3]
  2. The anterior and posterior tricuspid leaflets are seen so that any primary valvular pathology can be ruled out
  3. The tricuspid regurgitation (TR) jet if it is eccentric can be interrogated in this view [Table 4].
Table 4: Summary of parameters evaluated in RV Inflow view

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Right ventricle outflow view

This view is obtained by the lateral and superior tilt of the probe towards the left shoulder in the PLAX view [Figure 4].

  1. In this view, the distal outflow tract can be fully evaluated with the pulmonary valve and the pulmonary artery
  2. The PR can also be addressed in a parallel fashion in this view
  3. The pulsed wave (PW) Doppler pulmonary flow can also be evaluated in this view [Video 4].





Right ventricle focused view

This view is obtained by the lateral placement of the probe in the apical four chamber view, so as to see the complete RV, with its free walls and the apex still being formed by the left ventricle [Figure 4] and [Video 5].




  1. It allows us to visualize the RV free wall, and the basic three measurements are taken in this view: (a) basal (<42 mm), (b) mid-RV (<34 mm) and (c) the longitudinal (<86 mm)[15] [Figure 5]. One thing that should be kept in mind is that sometimes the RV is obviously equal to or larger than the LV on visual appearance in the apical four chamber view, but the dimensions are normal. In this case, the RV should be reported to be visually dilated [15] [Table 5]
  2. RV fractional area change is another important parameter which is recommended by the American Society of Echocardiography (ASE) for the evaluation of the RV systolic function. It is shown to be an indicator of prognosis, and the response to treatment [1] and survival [18] in PH. The main limitation is the endocardial delineation [Figure 5] and [Table 5].
Figure 5: Right ventricle measurements (top images) and fractional area change (bottom images)

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Table 5: Summary of parameters evaluated in RV special views

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The cut off for the normal value is >35% [Table 6].[15]
Table 6: RA dimensions

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Right ventricle modified apical view

In this view, the probe is shifted medially in the apical four chamber view so that the apex is formed by the RV [Figure 4] and [Video 6]. It is a useful view to evaluate the following parameters:

  1. The RV dilation and hypertrophy in PH can be evaluated in this view [Video 6]. One of the earliest structure to become hypertrophied is the moderator band [12] [Video 6]. In PH, it is also observed that the apex is frequently hypertrophied and akinetic, thereby favoring thrombus formation which has to be excluded in this view, by using the zoom and focus modalities [17]
  2. Sphericity index: it is the ratio of the short axis at the mid-ventricular level of the RV divided by the RV long axis in end-diastole, in the apical 4 chamber view. It is an indicator of RV remodeling and dilatation. The upper limit being 0.4 (35/86). The ratio is increased in RV remodeling. In patients with PAH, dilation of the RV is related to adverse clinical outcomes and also to the mortality [19] [Figure 5]
  3. The IAS can also be evaluated in this view as regards the direction of the bulging and for any echo dropouts in the ASD [Video 6]. In PH the IAS will bulge into the LA, and color flow imaging will help to diagnose ASD [Video 6]
  4. Right atrial linear dimensions can be measured in this view in end systole. These include the RA major and minor diameters. The cut off was >54 and >44, respectively [Figure 6]
  5. Right atrial volume index is usually recommended rather than the linear dimensions and can also calculated from this view. It is measured at end-systole. The single plane area8211; length method recommended by the ASE is used and right atrial volume is measured using the area and the long-axis dimension [Table 6].[15]
Figure 6: Right atrial measurements

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Right atrium volume index = (0.85 A 2/L)/BSA

Where A is the right atrial area (cm 2), L is the long-axis RV dimension (cm) and BSA is body surface area [Figure 6].

The normal range of the dimensions and volume as shown in [Table 5].[15] Due to the paucity of the standard RA volume data by two dimensional (2D) echocardiography, it is recommended to be done by three dimensional (3D) echocardiography.[15]

Right ventricle subcostal view

It is a very useful view in patients with a poor transthoracic view, such as in patients with corpulmonale, as the heart becomes vertical. Even in pediatric practice, it is the preferred view. The following parameters are evaluated in this view [Figure 7] and [Table 7].
Figure 7: Subcostal view right ventricular hypertrophy. RV: Right ventricle

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Table 7: Summary of parameters evaluated in Sub-costal view

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  1. The subcostal view allows the measurement of the RV free wall thickness and the RV systolic function. The recommended method of measurement of the RV wall thickness is at end diastole at the level of the tip of the tricuspid leaflet. The upper limit of thickness being 5 mm [Figure 7] and [Video 7]
  2. .It is also the best window for diagnosis of ASD [Video 8]
  3. This is also the best view for the evaluation of the inferior vena cava (IVC) for the estimation of the right atrial (RA) pressures. It is described in detail in the M-Mode evaluation of the IVC [Video 9]
  4. In acute pulmonary thromboembolism (PTE), there is a peculiar type of RV dysfunction wherein there is akinesia of the free wall and sparing of the apical function known as the McConnell's sign. McConnell's sign is said to be highly suggestive of massive PTE [18] [Video 10].














M-Mode utility in the evaluation of pulmonary hypertension

Due to the high-frame rate and temporal resolution, M-Mode is highly useful for the different measurements required for evaluation of the indirect signs of PH [Table 8].
Table 8: Summary of parameters evaluated by M mode

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  1. In the PLAX view the RV wall thickness and the proximal RVOT can be measured accurately utilizing the M-Mode [Figure 8]
  2. In the PLAX view, the IVS motion can also be studied showing paradoxical IVS motion, the exact timing of the events can be done by M-Mode examination [Figure 8]
  3. In the PSAX view, the pulmonary leaflet motion can be studied, showing the absence of the “a” wave and mid systolic anterior motion, corresponding to the mid-systolic notching (closure) of the RVOT flow [Figure 8] and [Video 11]
  4. The predominant muscles in the RV are the longitudinal one. Moreover, their function can be evaluated in the apical view. For this the M-Mode can be used to record the movement of the lateral tricuspid annulus, known as the tricuspid annular plane excursion (TAPSE), The normal range is >17 mm, and reduced value indicates RV systolic dysfunction.[15] When measuring TAPSE, it is important to be parallel to the RV free wall and to see that that the entire RV is included in the view [Figure 8] and [Video 12]. TAPSE is recommended as it is simple, reproducible and has prognostic value [Table 9]
  5. In the sub-costal view (SCV), M-Mode can be used to measure the RV free wall thickness
  6. Most important is the evaluation of the size and degree of collapsibility of the IVC with respiration [Figure 9] which will estimate the RA pressure for SPAP calculation. The IVC is used for the estimation of the RA pressure for several reasons.
  7. Figure 8: Utility of M-Mode in pulmonary hypertension

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    Figure 9: Size and collapsibility of inferior vena cava

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    Figure 10: Tricuspid regurgitant spectrum

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    1. The IVC is in direct communication with the RA
    2. It is highly compliant, so the RA pressure changes are reflected back into the IVC
    3. We can interrogate the IVC at right angles for exact measurement [Figure 10].


If the IVC is dilated and noncollapsing, it is mandatory to check the collapsibility after a sniff, to rule out occasional noncompliant IVC. However, it should be kept in mind that the accuracy of the evaluation of the IVC diameter and the degree of collapse with inspiration is limited in conditions such as in athletes, patients on ventilators and in patients who are dyspnoeic [Table 9].[19]
Table 9: IVC size, collapse and RA pressure

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Continuous wave Doppler evaluation of pulmonary hypertension

The CW Doppler is one of the important echocardiographic modality for the evaluation of certain parameters of PH [Table 10].
Table 10: Parameters of PH evaluated by CW Doppler

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  1. The intensity of the CW Doppler signal is a guide to the severity of the TR, and an intense signal indicates severe TR, while a faint, incomplete signals indicates mild TR [15] [Figure 10]
  2. The shape of the TR envelope is also guide to the severity. It is parabolic in mild PH and in severe TR there is an early equalization of the RA and RV pressures. Hence, the spectrum is triangular with an early systolic peaking. This is known as the “cut-off” sign [15] [Figure 10]
  3. The severity of PH is evaluated by the tricuspid regurgitant velocity (TRV), according to the European Society of Cardiology (ESC) guidelines, as shown in [Table 11]. One very important fact that should be kept in mind while measuring the TR velocity is that the gain settings should be optimal, or we may underestimate the velocity, and the terminal hazy part should not be the end point, it should in the dark area (nodal velocity) up to which it should be measured. It is commonly referred to as measure “up to the chin, not the beard.”
  4. The calculation of the SPAP by CW Doppler was first reported by Yock and Popp 30 years ago.[20] Right ventricular systolic pressure (RVSP) is calculated from the maximal TRV which indicates the pressure difference between the RA and RV and adding the RA pressure to this. The RVSP is the same as the SPAP, provided there is no RVOT obstruction. The velocities are converted to gradients using the modified Bernoulli equation


ΔP = 4 × V 2max
Table 11: TR velocity & severity of PH

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Thus, we see that it is necessary to measure the TR jet accurately, as any mistake will be “squared.” The velocity has to be measured at end expiration otherwise it will be underestimated. Hence, to accurately measure the TR jet velocity it is necessary that we have adequate signals. If the signals are inadequate, they can be enhanced by injection of agitated saline, sonicated albumin or air-blood saline mixture [21],[22]

It has to be kept in mind that the normal resting range of SPAP varies as per the age and the body mass index (BMI) and can be as high as 40 mmHg in the elderly, i.e. >50 years of age or obese, with a BMI of >30 kg/m 2.[23]

  1. The PR flow velocities are higher in patients with PH. As the PR spectrum can be easily recorded, and so the MPAP and the PADP can be easily calculated. The MPAP can be calculated from the initial peak velocity of the PR spectrum,[24] and adding the RA pressure to it [Figure 11]
  2. While if we add the RA pressure to the end diastolic velocity, we will get the value of the PADP [Figure 11]. The normal value of the PR end-diastolic pressure gradient is usually <5 mmHg. The rise in the PR end-diastolic gradient has been shown to indicate systolic dysfunction, diastolic dysfunction, increased brain natriuretic peptide and decreased functional status [25]
  3. One other method of calculation of the MPAP is by measuring the mean TR velocity by tracing the spectrum and adding the RA pressure [Figure 12]
  4. In shunts, such as ventricular septal defect (VSD) and patent ductus arteriosus (PDA), the SPAP can be estimated by the CW Doppler and the systolic blood pressure (BP). The gradient is calculated by the peak systolic velocity across the shunt and is subtracted from the systolic BP to give the RV systolic pressure, in VSD, which is equal to the SPAP in the absence of RVOT obstruction. In PDA, we directly get the SPAP [Figure 13]
  5. By similar method we can get the PADP, utilising the peak end diastolic velocity across the shunt and diastolic blood pressure [Figure 13]
  6. PVR may be estimated by dividing TRV (in meters per se cond) by the time-velocity integral of the RV outflow tract (in centimeters).[13],[24] The PVR helps us also to differentiate the PH due to high pulmonary flow, seen in anemia, hyperthyroidism, and obesity (normal PVR) from the PH seen in PAH (high PVR). The estimation of the PVR also helps us to identify the terminal patients with low MPAP, which is due to failing RV and not due to basically low PH [Table 11].
Figure 11: Mean pulmonary artery pressure and diastolic pulmonary artery pressure. PAEDP: Pulmonary artery end diastolic pressure, MPAP: Mean pulmonary artery pressure, V: Velocity, PR: Pulmonary regurgitation, RAP: Right atrial pressure

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Figure 12: Mean pulmonary artery pressure by mean tricuspid regurgitant velocity. PH: Pulmonary hypertension, PAP: Pulmonary artery pressure, TR: Tricuspid regurgitation, PAP: Pulmonary artery pressure, RAP: Right atrial pressure

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Figure 13: Systolic pulmonary artery pressure in shunts. VSD: Ventricular septal defect, PASP: Pulmonary artery systolic pressure, SBP: Systolic blood pressure, PS: Pulmonary stenosis

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Pulsed wave Doppler evaluation of pulmonary hypertension

1. Pulmonary acceleration time (PAT) is another entity that is useful for the evaluation of PH. The PAT is measured on the PW spectrum of the RVOT flow obtained, by placing the sample volume at the center of the pulmonary annulus, in the short-axis view. PAT is the time from the start to the peak of the pulmonary flow [Figure 14]. PAT can be very useful in the absence of recordable TR jet. The normal value being >120 m.seconds.[26] The time progressively shortens with rising in the pulmonary pressure [Table 12]. It is shown in many studies that PAT <708211;90 m.sec. indicates pulmonary pressure of >70 mmHg.[15] PAT is the rate dependant parameter and has to be corrected for heart rate when it is either >100 or <70/min. This is done by multiplying the observed PAT by 75 and dividing the result by the heart rate [12]
Figure 14: Pulmonary acceleration time and pulsed wave right ventricular outflow tract spectrum. PH:Pulmonary hypertension, PAT:Pulmonary acceleration time

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Table 12: Acceleration time and severity of PH

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Although this is not usually used in routine practice.[15] It should be kept in mind that PAT is also flow dependant and if the right-sided flow is more as in ASD the PAT can be normal even with raised pulmonary pressure

The MPAP can be derived from PAT. This is possible by using the Mahan's equation

Mahan's equation - MPAP = 90 − (0.62 × PAT)

But the use of the TR jet velocity, for measuring the MPAP is said to be more reliable than PAT. For PW evaluation of the PH the position of the sample volume is very important. The velocity of the flow varies from the inner to the outer edge being higher on the inner edge of the pulmonary artery. Hence, it is recommended to put the sample volume in the center, just prior to the pulmonary valve leaflets. This will also avoid the turbulence in the spectrum, if the sample volume is placed beyond the valve [Table 13][26]
Table 13: Parameters evaluated by PW Doppler

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2. Pattern of pulmonary flow spectrum can also be a guide as to the level of PH. In normal individuals, pulmonary flow tracing has a symmetric counter with a peak velocity occurring at mid systole. As the pulmonary pressure increases, peak velocity occurs earlier in systole, the velocity time integral (VTI) decreases and a late systolic notching is often present [Figure 14]. This notch is analogous to the mid-systolic notch seen in M-Mode examination of the pulmonary valve [15] [Figure 8] and [Video 13]. The Doppler pattern of the mid-systolic notch is highly specific for PH.[27] It has been observed that a notched pattern of the RVOT flow spectrum is seen in 100% of the patients with raised PVR as in PAH. The absence of the notch pattern strongly suggests presence of pulmonary venous hypertension [28]

3. PVR may be estimated by dividing TRV (in meters per se cond) by the time-velocity integral of the RV outflow tract (in centimeters)[13],[24]



The PVR helps us to differentiate the PH due to high pulmonary flow as is seen in anaemia, hyperthyroidism and obesity, where the PVR will be normal, as against PH in PAH, where the PVR will be high. The PVR also helps us to identify the terminal patients with low MPAP, which is due to failing RV and not due to low normal pulmonary pressure [24]

4. The evaluation of hepatic vein (HV) flow constitutes the cornerstone of Doppler assessment of RAP. The normal HV flow has two main components, a larger systolic “S” wave and a slightly smaller diastolic “D” wave. The HV flow is dependent on the respiratory cycle with an increased flow in inspiration and decrease flow in expiration. Sometimes, at the end systole, a small retrograde flow may be seen, the systolic reversal 'SR' wave. With bradycardia we see a diastolic reversal “DR” wave also Thus, it is quite obvious that any condition that affects the RA pressure or filling will affect the HV flow. With increase in the RA pressure the gradient between the HV and the RA decreases thereby reducing the forward flow. Thus, the main findings in PH are the blunting or absence of the “D” wave with a large right atrial reversal. If the “A” wave is more than the forward systolic “S” wave it predicts increase RAP [29],[30] [Figure 15]
Figure 15: Hepatic vein flow in pulmonary hypertension

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If there is RV systolic dysfunction, there will be decrease in the “S” velocity and increase in the “D” velocity

5. The SVC can also be used for the evaluation of the flow patterns. It is visualized from the suprasternal notch as a blue colored flow just to the right of the aortic arch. It is more readily evaluated using transoesophageal echocardiography [15]

6. The tissue Doppler imaging (TDI) is another modality to evaluate the RV systolic function and the RAP by a single step method. It involves the PW Doppler evaluation of the lateral TV annulus in the TDI mode. The three waves studied are the systolic “S” wave, and the Diastolic E' and A' waves. The “S” wave provides the idea as to the RV function. The normal value being 14.1 ± 2.3 cm/sec. the cut off for poor RV function being <9.5 cm/s [15] [Figure 16]
Figure 16: E/e' for right atrial pressure

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7. The Tei Index or the myocardial performance index (MPI) is another parameter which helps us to evaluate the RV function. MPI is a unit less entity calculated by the ratio of the sum of the iso-volumic contraction time (ICT) and iso-volumic relaxation time to the ejection time. It is obtained by the PW interrogation of the TV flow and the RVOT flow. The calculation is as shown.



TC: Tricuspid closure, TO: Tricuspid opening time, ET: Ejection time of PV

The normal value is 0.28 ± 0.04,[15] An increase in the Tei or MPI is suggestive of RV dysfunction. An increased RV MPI is a sensitive and specific marker of PH.[15]

8. The MPI can be calculated by the TDI as well. TDI is proposed to be less preload dependent compared to the traditional PW technique. PW TDI is simpler and more robust to use, with high temporal resolution.[15] It is recommended that the MPI should not be used as a sole criterion and also in patients with irregular heart rhythm

9. The RAP can be estimated by the ratio of the early tricuspid inflow velocity to the tissue Doppler early tricuspid annular velocity (E/E'). The normal ratio being <6. A ratio of >6 indicated a RAP of >10 mmHg.[30] It provides information independent of RV function and is still useful in mechanically ventilated patients [15] [Figure 16].




Colour flow imaging

A qualitative estimate of the PH can be made from the colour flow patterns of the severity of the TR and PR jets and the flow reversal in the HV [Figure 17].
Figure 17: Color flow mapping (CFM) in pulmonary hypertension

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Transoesophageal echocardiography

There are very few indications for transoesophageal echocardiography in patients who have PH, & they are namely (1) to confirm and assess congenital intracardiac shunts, (2) to assess the severity and contribution of left-sided heart disease, (3) rarely in right-sided masses and finally (4) to guide the invasive procedures like inter atrial septostomy.

Strain imaging

These days speckle tracking is used very frequently for the noninvasive evaluation of the global and regional RV function. Though the machines still do not have dedicated right sided speckle tracking software, one can measure the global longitudinal strain (GLS) of the RV by tracing the RV free wall in place of the LV, in the apical four chamber view as shown in [Figure 18] and [Video 14]. It is easy, angle independent and less load dependent. In PH, the RV strain is reduced due to the increase in the afterload. This can be with or without RV dysfunction. Some echo cardiographers exclude the IVS from the speckle tracking to remove the LV component in its measurement [Figure 18]. With speckle tracking the segmental strain can also be inferred [Figure 18]. The normal GLS is - 29 %+ 4.5 %” (> - 20 %).[15] These values are after excluding the IVS. Strain imaging is useful to identify the response to treatment, and also helps to detect early signs of RV dysfunction in PH.[31] The main disadvantage is the necessity of a good 2D image.
Figure 18: Speckle-tracking echocardiography of right ventricle. RV GLS: Right ventricular global longitudinal strain

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Real-time three-dimensional echocardiography

Due to the complex shape of the RV, real-time three-dimensional echocardiography (RT3D) is the ideal modality of investigation for the measurement of the RV function and volumes. This allows the measurements without geometric assumptions, and foreshortened views. Good correlation was seen in the volumes and ejection fraction measured by RT3D echocardiography and other imaging modalities.[32]


  Conclusion Top


Thus, we see that echocardiography is a convenient, portable, accurate, economical, and noninvasive method of evaluation of PH, which is an integral part of the echocardiographic examination of the heart. Doppler echocardiography provides a complementary, comprehensive method to assess the right-sided hemodynamics in PH. It is recommended to use multiple parameters for the comprehensive evaluation of PH, to avoid common pitfalls and we should never forget to integrate the findings in a clinical context. Thus, combining various techniques may make echocardiography the standard for the evaluation of PH, having a high sensitivity and accuracy. This will reduce the need for repeated invasive assessments in these patients.[33]

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17], [Figure 18]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11], [Table 12], [Table 13]



 

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