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Assessment of
Pulmonary Hypertension
Standard Operating Procedure
Table of Contents
Parasternal Long and Short Axis Views 17 Tissue Doppler imaging (TDI) 43
of the Right Ventricular Outflow Tract Right Ventricular Diastolic Dysfunction 43
Parasternal Short Axis View of Aorta and 19 Measures of Function 44
Left Atrium
Myocardial Performance Index of 44
Short Axis View at the Level of 20 the Right Ventricle (RV MPI)
Left Ventricular Papillary Muscles
S’ wave velocity 46
Apical Four-Chamber View 22
Isovolumic Relaxation Time (IVRT) 46
Apical Five-Chamber View 26
Tricuspid Annular Plane 47
Subcostal View 26 Systolic Excursion (TAPSE)
Supported by: Indexing for Heart Rate 28 Stroke volume, Cardiac Output and 48
Indexing for Body Surface Area 28 Pulmonary Vascular Resistance
Dr Antionette Kenny
Professor Dr Simon Gibbs Dr Luke Howard Consultant Cardiologist, Freeman Hospital
Petros Nihoyannopoulos
Consultant Cardiologist Consultant Chest Physician
Head of Echocardiography Dr David Kiely
Hammersmith Hospital Hammersmith Hospital Consultant Chest Physician, Lead Clinician, Pulmonary Vascular Unit, Royal Hallamshire Hospital
Dept of Echocardiography
Imperial College Healthcare Imperial College Healthcare
Imperial College Healthcare NHS Trust NHS Trust Dr Laurence O’Toole
NHS Trust Consultant Cardiologist, Royal Hallamshire Hospital
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› 1 at end-diastole indicates
volume-loading of the RV
LV eccentricity index 9, 24, 25
1
› 1 at end-systole indicates
pressure-loading of the RV
*Heart – rate indexed (when rate ‹ 70 or › 100 beats per minute): 75 x value / HR
Table 2. Normal values for the right ventricle and pulmonary circulation: RVSP: right ventricular systolic pressure, TR: tricuspid regurgitation,
RA: right atrium, RV: right ventricle, MPI: myocardial performance index, TAPSE: tricuspid annular plane systolic exertion, S’ wave : systolic
wave, RVOT: right ventricular outflow tract, AT: acceleration time, IVRT: isovolumic relaxation time, LV: left ventricle, PVR: pulmonary vascular
resistance.
Figure 2. Change from the normal (A) configuration of the right and left ventricles to that seen in pulmonary hypertension (B). Due to
the increase in wall stress and intraventricular pressure, the right ventricular walls hypertrophy, its cavity dilates and the interventricular
septum bows in to the left ventricle.
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1. PARASTERNAL WINDOW: 3. D
oppler examination in the Structures seen:
a. Parasternal long-axis of the left ventricle following sequence:
• Anterior right ventricular wall • Aortic valve
b. Parasternal long-axis of the right a. Colour Doppler in all apical projections (right and non coronary cusps)
• Moderator band
ventricular inflow tract
b. C
olour Doppler in parasternal • Mitral valve
• Interventricular septum
c. Parasternal long-axis of the right projections (long-axis/short-axis) (anterior and posterior leaflets)
ventricular outflow tract • Left ventricular posterior wall
c. P
ulsed-wave Doppler for transmitral • Posterior mitral annulus
d. P
arasternal short-axis of the left velocities • Right ventricular cavity
• Aortic root & ascending aorta
ventricle – aortic root level
d. P
ulsed-wave Doppler for left ventricular • Left ventricular cavity
e. Parasternal short-axis of the left outflow tract
• Left atrium
ventricle – mitral valve level
e. Pulsed-wave Doppler for the
f. Parasternal short-axis at mid-left tricuspid inflow
ventricular level – papillary muscles
f. P
ulsed-wave Doppler for the
Measurements Normal range (men) Normal range (women) Pulmonary Hypertension
g. Parasternal short-axis view at the right ventricular outflow tract
apex – no internal landmarks
g. C
ontinuous-wave Doppler across the
Left ventricle end-diastolic
left ventricular outflow-aortic valve diameter (cm)9, 36, 37
4.2 – 5.9 3.9 – 5.3
2. APICAL WINDOW h. C
ontinuous-wave Doppler across
the tricuspid valve (for tricuspid
a. Apical “four-chamber” view (include Left ventricle end-systolic
regurgitation) 2.1 – 4.0 2 -4
both atrio-ventricular valves) diameter (cm)9, 36, 37
i. C
ontinuous-wave Doppler across
b. Apical “five-chamber” view (include the
the pulmonary valve (for pulmonary Interventricular septum (cm)9, 36, 37 0.8 – 1.1 0.8 – 1.1 –
left ventricular outflow)
regurgitation)
j. T issue Doppler index of the right Posterior wall (cm)9, 36, 37 0.8 – 1.1 0.8 – 1.1 –
ventricular free wall
k. Tricuspid annular plane systolic exertion Aortic root diameter (cm)9, 36, 37 3.1 – 3.7 2.7 – 3.3 –
(M-mode)
Left atrial linear dimension (cm)9, 34, 36, 37 3.0 – 4.0 2.7 – 3.8 –
4. SUBCOSTAL VIEW
Table 3. Normal range of measurements.
a. Four-chamber view
b. Atrial septum
In normal subjects, the anterior right ventricular Structures seen: The right ventricular cavity is normally small in
wall is usually thin and its mass is less than one size and there is good apposition of the tricuspid
• Inferior portion of the right atrium
sixth of the left ventricle. The diameter of the leaflets with trivial or mild tricuspid regurgitation
right ventricle (figure 3a) is less than one third of • Right ventricular inflow tract (a normal echocardiographic finding in around
the left ventricle, in this view. 25% of the population) (figure 4a).
• T wo principal papillary muscles (anterior
In pulmonary hypertension (figure 3b), the and posterior) In pulmonary hypertension (figure 4b), dilatation
right ventricle will appear dilated and in the of the right ventricle and atrium will be visible
• A
smaller supracristal (or conus)
parasternal long axis view, the moderator band in this view. This may lead to a functional
papillary muscle
is usually seen traversing the right ventricle, dilatation of the tricuspid annulus and tricuspid
close to the interventricular septum. Care should • Tricuspid annulus regurgitation. When the tricuspid regurgitant jet
Figure 3a. Normal: parasternal long axis: note that the
be taken not to include the moderator band in right ventricle is less than one third of the size of the is eccentric, optimal alignment for estimation of
• Anterior and septal tricuspid leaflets
the measurements of the interventricular septal left ventricle. tricuspid regurgitant velocity may be obtained in
thickness. In significant pulmonary hypertension, this view.
the left ventricular cavity may be reduced in size
Since tricuspid regurgitation may not always be
in both systole and diastole, with deviation of
functional in origin, abnormalities of the leaflets
the septum towards the left ventricle.
and subvalvular apparatus should also be
assessed to exclude primary valvular pathology.
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Figure 4a. Parasternal long axis view of the right ventricular inflow tract
in a normal subject.
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• Right ventricular outflow tract The normal values for the measurements which
may be made in this view may be found in the
• Interatrial septum
sections describing the parasternal long axis of
• Left atrium the left ventricle and the parasternal long and
short axis views of the right ventricular outflow
• Right atrium
tract. This view demonstrates the aortic, tricuspid
• Right ventricle and pulmonary valves simultaneously, making
this a useful view for the assessment of structural
• T ricuspid valve : anterior and
valvular abnormalities (figure 6a). Furthermore,
Figure 5a. Parasternal long axis view of the right ventricular outflow tract in a septal leaflets
normal patient showing the main pulmonary trunk, branches of the pulmonary a zoom view of the interatrial septum with the
artery and the pulmonary valve. • Aortic valve : left , right and use colour Doppler may help to identify an atrial
non coronary cusps septal defect.
• Pulmonary valve As in the other views previously described,
• Main pulmonary artery trunk pulmonary hypertension will produce right
ventricular dilatation and hypertrophy, as well as
• Aorta dilatation of the pulmonary artery (figure 6b).
• Descending aorta
Figure 6a. Parasternal short axis view of the left atrium and Figure 6b. Pulmonary hypertension: right atrial and
aorta in a normal patient. ventricular dilatation.
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Structures seen: Normally, the right ventricle appears triangular in Two-dimensional echocardiography
The tricuspid annulus sits up to 1 cm nearer the Left ventricular outflow tract velocity (m/sec)41 0.7 – 1.1 –
• T ricuspid valve apex than the mitral annulus. The tricuspid leaflets Aortic flow (m/sec)41 1 – 1.7 –
(anterior and septal leaflets) demonstrate wide diastolic opening, which
Severe mitral regurgitation:
become less vigorous as pulmonary hypertension Pulmonary venous inflow40
systolic flow reversal
develops.
• Pulmonary venous drainage: assessment S velocity (cm/sec) › 50
of three of the four pulmonary veins The tricuspid valve septal leaflet is adjacent to the
D velocity (cm/sec) › 50
draining into the left atrium is usually septum, whereas the leaflet adjacent to the free
possible wall may be either the anterior (most commonly) or AR velocity (cm/sec) › 20
posterior leaflet, depending on the exact rotation
• Right upper pulmonary vein : drains into Tricuspid inflow (m/sec) (E and A waves)41 0.3 – 0.7 –
and angulation of the image plane. Tricuspid leaflets
the supero-medial aspect of the are uniformly echogenic, with normal coaptation in Deceleration time – tricuspid inflow (msec)41 144 – 244
left atrium systole. When significant tricuspid regurgitation
RV MPI (Tei index) 9, 20-22 * ‹ 0.28
• T he right lower pulmonary vein is not develops in pulmonary hypertension, careful
usually seen in this view identification of any structural abnormalities is TAPSE (mm) 9, 11-13, 28, 29 ≥ 20
needed ensure primary tricuspid incompetence is
TDI right ventricular free wall : IVRT (msec)9, 15-17 ‹ 75
differentiated from secondary incompetence due
to the annular dilatation. Table 6. Normal measurements in the apical four-chamber view.
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In the four chamber view, the interatrial septum Finally, the application of tissue Doppler imaging
and interventricular septum can be clearly to the septal and lateral left ventricular walls
delineated. As for the parasternal short axis of is essential for the exclusion of significant left
the interatrial septum, “drop-out” artefact is ventricular diastolic dysfunction. In patients
commonly seen in the region of fossa ovalis. This with significant, longstanding pulmonary
should not be mistaken for an atrial septal defect. hypertension, left ventricular diastolic filling may
The interventricular septum is more muscular and be impaired and there may often be type I or even
thicker than the interatrial septum, due to higher type II diastolic dysfunction, in very severe cases.
pressures within the left ventricle compared those
within the atria. When the right ventricle becomes
pressure-loaded, the septal motion appears
dyskinetic, with bowing into the left ventricle.
Figure 8a. Normal apical four chamber view.
Systolic wave
Measurements PH E’ (cm/sec) PH A’ (cm/sec) PH
(cm/sec)
Table 7. Normal range of measurements – Tissue Doppler Imaging and normal values
Figure 8b. Apical four chamber view in pulmonary hypertension showing marked
right ventricular dilatation and hypertrophy.
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• Hepatic veins
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Most indices of function are unaffected by heart When indexing measurements for body surface Right ventricular volume overload, resulting from relationship between right ventricular ejection
rate, yet some require correction when heart area (BSA), they should be divided by the BSA an atrial septal defect, tricuspid insufficiency or fraction and afterload develops (pulmonary artery
rate exceeds 100 or drops below 70. These are (Dupois & Dupois), where: pulmonary insufficiency, causes an increase in pressure or pulmonary vascular resistance).
right ventricular outflow tract acceleration time, right ventricular end-systolic and end-diastolic Right ventricular pressure overload therefore
BSA = 0.007184 X weight (kg)0.425
myocardial performance index, S’ wave velocity volumes with normal right ventricular ejection distorts both left ventricular systolic and diastolic
x height (cm)0.725
and isovolumic relaxation time. In order to fraction. Although with time remodelling takes geometry. The effect on the left ventricle is the
index to heart rate, the measurement should be For the normal man, BSA is 1.9 m2 and for the place and left ventricular function becomes reduction of left ventricular ejection fraction, stroke
multiplied by 75/heart rate, eg: normal woman, BSA is 1.6m2. affected through ventricular interdependence, left volume, end-diastolic and end-systolic volume,
ventricular systolic function is relatively spared. as well as prolongation of the left ventricular
RVOT AT (indexed to HR) = RVOT AT x 75/HR
isovolumic relaxation time. The different effects of
Right ventricular pressure overload loads the
right ventricular volume- versus pressure-loading
right ventricle predominantly in systole, but also
on the left ventricle are best illustrated by the left
in diastole as both right ventricular end-diastolic
ventricular eccentricity index.
and end-systolic volumes increase. An inverse
Pressure and
Measurements Volume loading Pressure loading
volume loading
Dilatation
Hypertrophy
Contractility or
TAPSE or or
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Normally the right ventricle is 1/3 of the size of ventricle can be assessed in the parasternal In the face of chronically elevated right ventricular normal subjects it is thin and sometimes difficult
the left ventricle in the parasternal long axis view. long axis, short axis and the apical four-chamber afterload, the right ventricular walls become to see. From the apical four chamber view, right
One of the first changes in the right ventricle in view. In the apical four chamber view, the hypertrophied. One of the first anatomical ventricular hypertrophy is defined by a free wall
response to the increased preload and afterload right ventricle can be seen to wrap around the elements to do so is the moderator band, which in thickness of more than 5 mm.
is dilatation, which progresses with worsening apex of the left ventricle as seen in figure 11b.
pulmonary hypertension. Dilatation of the right
Figure 11a. Apical four-chamber view. Normal right-sided Figure 11b. Apical four-chamber view. Pulmonary Figure 12a. Dilated and hypertrophied right ventricle seen in Figure 12b. The apical four-chamber view.
chambers: the right ventricle is less than one third of the hypertension: dilatation and hypertrophy of the left ventricular short axis view.
size of the left ventricle . right ventricle.
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Pressure Measurements
Contractility Right Atrial Pressure
In pulmonary hypertension, right ventricular On the basis of these three parameters (dilatation,
impairment is global: this is in contrast to other hypertrophy and contractility), an experienced
conditions affecting the right ventricle, such as Echocardiographer will be able to make a good
right ventricular infarction or arrhythmogenic qualitative assessment of right ventricular systolic
right ventricular cardiomyopathy, where there will function, divided in to:
be regional wall motion abnormalities.
• Mild impairment
• Moderate impairment
• Severe impairment
Figure 13a. Subcostal view of the inferior vena cava. Figure 13b. M-mode during sniff manoeuvre.
From the subcostal view, the inferior vena cava respiration and/or dilation of the inferior vena
lies perpendicular to the ultrasound beam and cava and hepatic veins is associated with higher
M-mode is applied. Measurement of the diameter right atrial pressures. When there is no response
of the inferior vena cava at end-expiration and with normal respiration, the patient is asked to
during an inspiratory manœuvre provides an “sniff ”. This generates a sudden decrease in
estimate of right atrial pressure. If the inferior intrathoracic pressure, normally resulting in a
vena cava diameter is normal (1.5 – 2.5 cm) and decrease in inferior vena cava diameter. Right
the segment adjacent to the right atrium collapses atrial pressure can be estimated therefore from
by at least 50% with respiration, then right atrial the size and respiratory motion of the inferior
pressure is normal. Failure to collapse with vena cava (Table 10)9.
Inferior vena cava and diameter Change with respiration Estimated right atrial pressure (mmHg)
Table 10. Estimation of right atrial pressure from the inferior vena cava.
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Tricuspid regurgitant velocity is derived from the The normal expected upper limit of PASP depends A number of studies have highlighted the regurgitation, whereas blunting of systolic
application of continuous wave (CW) Doppler on age and body mass index (BMI). In the largest problem of relying solely on estimates of PASP flow indicates moderate regurgitation. None of
mapping on the tricuspid regurgitant jet, from the study to date, the estimated upper 95% limit for from echocardiography to diagnose/exclude these measurements should be considered in
apical four chamber view or from the parasternal PASP was 37.2 mmHg in low-risk subjects (VTR 2.6 pulmonary hypertension42, 43. In patients with isolation and it should be re-emphasised that the
right ventricular inflow view, if the regurgitant jet is m/sec), whereas the estimated upper 95% limit scleroderma being screened for pulmonary severity of tricuspid regurgitation is distinct from
eccentric. The peak velocity is measured in m/sec. for subjects aged 60 and over was 43.6 mmHg (VTR hypertension, a cut-off VTR of 2.7 m/sec has a the velocity.
2.9 m/sec). In those with a BMI › 30 kg/m2 the sensitivity of 88% for the detection of pulmonary
The velocity reflects the right ventricular to
limit was 40 mmHg (VTR 2.8 m/sec). In all these hypertension42. Some of the patients “missed”
right atrial pressure difference, ΔP, and when
measurements, right atrial pressure was assumed using this cut-off had mean PAP › 40 mmHg.
pulmonary stenosis is absent, right ventricular
to be 10 mmHg.
systolic pressure (RVSP) is assumed to equal Note that in cases of severe free-flow tricuspid
pulmonary artery systolic pressure (PASP), and is regurgitation, the Bernoulli equation is not
calculated through the Bernoulli Equation: valid and the tricuspid regurgitant velocity
will underestimate the transtricuspid pressure
PASP = RVSP = 4 (VTR) 2 + RAP
gradient: however, the severity of the tricuspid
[VTR : tricuspid regurgitant velocity; RAP : right regurgitation is predictive of survival regardless
atrial pressure] of the PASP, irrespective of the underlying
disease44. Severity may be assessed by a number
of measurements, including assessment of the
structure of the valve, jet area (Table 11) and density
and hepatic vein flow45. Density is assessed using Figure 15. Severe tricuspid regurgitation.
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With two-dimensional echocardiography, the Another view which might help the imaging The pulmonary valvular motion can be determined Mean pulmonary artery pressure, may also be
pulmonary valve is imaged from the parasternal of the pulmonary valve is the parasternal with M-mode echocardiography and M-mode derived from the pulmonary regurgitant velocity:
short axis (at the level of the aortic valve). In projection of the right ventricular outflow tract can highlight potential pulmonary stenosis,
Mean PAP = 4(PR VBD)2
some patients with difficult acoustic views, and the pulmonary valve, with the rotation of the for example in children with Tetralogy of Fallot.
imaging of the pulmonary valve is difficult. transducer 90 degrees towards the right arm of Atypical pulmonary valvular motion was one [VBD, beginning of diastole pulmonary
The imaging of the cusps in particular, is best the patient. This view is difficult in patients with of the first abnormalities to be described in regurgitant velocity]
done from the parasternal short axis projection high body mass index, but it is feasible in young pulmonary hypertension, as an indirect sign of
because the same view helps the imaging of the people, especially children. Another transthoracic right ventricular failure.
pulmonary artery and its division into right and projection is the subcostal view, which, with Measurement of PEDP and mPAP is not
As with the tricuspid regurgitant jet, the Bernoulli
left pulmonary branches. anterior angulation, can include the whole right routinely used in the diagnosis or follow-up
Equation can be applied to calculate pulmonary
ventricular outflow tract and pulmonary valve. pulmonary hypertension, but may be useful in its
arterial end-diastolic pressure (PEDP)5, 6 :
identification when tricuspid regurgitant velocity
PEDP = 4(VED )2 + RAP cannot be used or relied upon.
Figure 16a. Pulmonary regurgitation: Figure 16b. Measurement of pulmonary regurgitant velocity
continuous wave Doppler. at beginning of diastole (VBD ) and end-diastole (VED ).
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Right ventricular outflow tract acceleration time but these are not commonly used to derive The measurement of right atrial (RA) volume An alternative method for measuring right atrial
(RVOT AT) is the time in milliseconds from the pressure in clinical practice as they have been index is usually performed from the apical four- volume index from the apical four-chamber is the
beginning of the pulmonary ejection until the superseded by tricuspid regurgitant velocity. chamber view or from the subcostal view. Atrial method of discs or Simpson’s rule. In this plane,
maximum of the systolic velocity. It is measured Nonetheless, acceleration time may be a useful volume is measured at end-systole, where the the disc diameters at various levels of the atria
by pulsed-wave Doppler with the sample volume measure when the tricuspid velocity cannot maximum atrial volume can be obtained. are used to determine the cross-sectional area.
positioned at the centre of the pulmonary artery, be measured, particularly at diagnosis. A
The single plane area-length method is used and The normal right atrial volume when indexed
ideally at the annulus, in the parasternal short value below 105 ms is suggestive of pulmonary
RA volume is measured using the area and the for body surface area is 34 ml/m2 for men and
axis view of the right ventricular outflow tract. hypertension.
long axis length of the atrium9, 18, 19: 27 ml/m2 for women.
In normal people, the acceleration time *RVOT AT should be indexed for heart rate.
RA volume index = (0.85 A2/ L) / BSA
exceeds 140 ms and it shortens in pulmonary
hypertension. There is an inverse relationship [A, area of atrium in any view (cm2); L, long axis
between AT and mean PAP and several equations length of atrium (cm); BSA, body surface area]
have been described:8-10
Figure 18a. Measurement of right atrial area for calculation Figure 18b. Measurement of right atrial long axis for
of right atrial volume. calculation of right atrial volume.
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Right ventricular fractional area change (FAC) is Eccentricity index is measured by the parasternal
calculated as follows: short-axis at the level of left ventricular papillary
muscles. It is measured as the ratio of the
RV FAC (%) = (AED – AES) / AED
minor axis of the left ventricle parallel to the
where AED is end-diastolic area and AES is end- septum (D2), divided by the minor axis
systolic area, measured from the apical four- perpendicular to the septum (D1) (Figure 19).
Figure 19a. Measurement of left ventricular eccentricity Figure 19b. Measurement of left ventricular eccentricity
chamber view9, 33, 34. It is a simple method for index in end-diastole (EIED ). index in end-systole (EIES ).
The index is measured in end-diastole and
assessment of right ventricular systolic function
end-systole. In a purely pressure-loaded right
which has been shown to correlate with ejection
ventricle, there is flattening of the interventricular
fraction measured using cardiac MRI34 and
septum in end-systole, which results in increased
prognosis in pulmonary hypertension. It also
end-systolic left ventricular eccentricity index. In
correlates with response to treatment46.
pure volume-loading, the eccentricity index will
be increased in end-diastole9, 24, 25.
Normal Abnormal
Figure 20. Examples of the effects of pressure-loading (top two panels) and volume-loading (bottom two panels) of the right ventricle
on the eccentricity index of the left ventricle.
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Pulsed Mode TDI: right ventricular filling and right atrial pressure
and the E wave velocity will be higher with high
Peak velocities and the acceleration and
right atrial pressure (ie, pre-load), and lower
deceleration of structures can be measured. A
with impaired right ventricular relaxation. In
pulsed-wave Doppler sampling gate of 2-4 mm
some circumstances these two physiological
and a sweep of 100-150 mm/sec are used.
parameters may therefore balance each
other out. TDI has been proposed as a way
Conventional Colour Doppler mapping:
of determining whether a ‘normal’ tricuspid
The advantages of this technique include the inflow is actually ‘pseudonormal’. With a
capacity for rapid assessment of movement, pseudonormal pattern (E/A › 1), restriction
the ability to measure velocity of structures in and impaired relaxation are balanced, and the
numerous myocardial segments at once and good E/A ratio is pseudonormal due to high right
spatial resolution with accurate discrimination atrial pressure. E’ wave velocity, representing
between subepicardial and subendocardial early diastolic movement of the tricuspid
myocardial layers. annulus, will still be abnormal as it is relatively
pre-load-independent.
Measurements are made from the apical four-
chamber view, with the patient holding their Diastolic function of the right ventricle can be
Figure 21. Measurements made during tissue Doppler imaging of the free right ventricular wall at the level of the tricuspid annulus breath in end-expiration. assessed with many parameters, and those
from the apical four-chamber view. A’, late (atrial systole) myocardial diastolic wave; E’, early myocardial diastolic wave; ET, ejection useful in pulmonary hypertension include:
time; IVCT, isovolumic contraction time; IVRT, isovolumic relaxation time, S’, systolic myocardial wave. Measurements are made in
held end-expiration. Isovolumic relaxation time (IVRT) When
Right Ventricular prolonged, it indicates poor myocardial
Diastolic Dysfunction relaxation. A normal IVRT is 75±12 ms. With
abnormal relaxation, the value is usually in
Diastolic dysfunction comprises: excess of 110ms. However, when restriction is
present with high right atrial pressures, IVRT will
• poor relaxation fall below normal to durations less than 60 ms.
• d
ecreased compliance IVRT is discussed further below.9, 15-17
(change in unit volume per unit pressure) Transtricuspid inflow (E wave deceleration)
TDI of the tricuspid apparatus is less pre-load- Deceleration of inflow of the E wave is measured
dependent than conventional Doppler. The by deceleration time (DT), which shortens with
E’ and A’ waves represent myocardial velocity decreasing right ventricular compliance. DT is
corresponding to the E and A waves on tricuspid complex, as higher right atrial pressures also
inflow measured by conventional colour Doppler, shorten it. A normal DT is 198 ± 23 ms; values
that is filling in early diastole and during atrial over 240 ms indicate impaired relaxation, and
systole respectively. The E wave is dependent on under 160 ms suggest restriction.41
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Measures of Function
Myocardial Performance Index of
the Right Ventricle (RV MPI)*
Myocardial Performance Index, also known as Tei The advantages of its use are good reproducibility,
Index21, combines a combination of systolic and quick calculation, no need for use of geometric
diastolic measurements. The normal range for RV models and appliance even in the presence of a
MPI is 0.28-0.329, 20-22. It is relatively unaffected by difficult acoustic window.
heart rate, loading conditions or the presence and
There are two different approaches for the
the severity of tricuspid regurgitation. In patients
measurement of MPI.
with idiopathic pulmonary arterial hypertension,
the index correlates with symptoms and values
above 0.88 predict poor survival.
Figure 23. Measurement of MPI using tissue Doppler imaging. See Figure 22.
Colour Doppler (Two views: apical tricuspid Tissue Doppler Imaging (One view: Pulsed-wave
inflow and parasternal right ventricular inflow) Doppler of the right ventricular free wall)
Two different views are needed for the TDI can also be used to derive the same
determination of MPI - the apical four-chamber parameters as colour Doppler, but only one view
view for the tricuspid inflow pattern and the is required (Figure 23).
parasternal short axis right ventricular outflow
*MPI should be indexed for heart rate.
tract view for the determination of ejection time
Figure 22. Tricuspid inflow from valve opening to closure (TVC-O) is the sum of isovolumic contraction time (IVCT), ejection time (ET)
and isovolumic relaxation time (IVRT). The ejection time – as measured from the short axis RVOT view - is subtracted from TVc-o and
(Figure 22).
the result is divided by ET to give MPI.
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The average of three TDI signals from different Isovolumic relaxation time of the right ventricle is TAPSE is the reflection of the movement the In a volume-loaded ventricle with preserved
cardiac cycles is employed for data analysis defined as the time from pulmonary valve closure base to apex shortening of the right ventricle in function, such as in the presence of an atrial septal
(Figure 21). The patient has to be in sinus rhythm to tricuspid valve opening and can be measured systole (longitudinal function). During ventricular defect, TAPSE may be very high, over 30mm. In
and the velocities are indexed to the heart rate. by conventional Doppler echocardiography systole, long axis shortening is created by motion a volume- and pressure-loaded right ventricle,
The S’ wave velocity is normally greater than 12 (pulsed-wave Doppler from tricuspid inflow) of both atrioventricular valve annulae toward the such as a dilated, hypertrophied right ventricle
cm/sec, and we consider a cut-off value of 11.5 or with tissue Doppler imaging on the right cardiac apex. Because the septal attachment with significant functional tricuspid regurgitation,
cm/sec, below which right ventricular myocardial ventricular free wall, provided that the patient of the tricuspid annulus is relatively fixed, the TAPSE may become pseudonormalised (Table 9:
function may be impaired.35 does not have an irregular heart rate. In majority of tricuspid annular motion occurs in its Difference in measurements between pressure
Figure 23, it is shown as the time between the lateral aspect. and volume loading).
*S’ wave velocity should be indexed for heart rate.
end of the S’ wave and beginning of the E’ wave.
The measurement of TAPSE is derived from the
Prolongation indicates poor myocardial apical four chamber view. Special care has to be
relaxation. The normal isovolumic relaxation taken for the whole right ventricle to be included
time is approximately 75±12 ms, and perhaps in the view with no dropout in the endocardial
about 10ms longer in those aged over forty. outline along the interventricular septum and
With abnormal relaxation, the value is usually RV free wall. The width of sector should be
in excess of 110ms, which is highly suggestive of limited onto the right ventricular free wall, and
pulmonary hypertension, which may be useful in the M-mode cursor should be positioned on
the absence of tricuspid regurgitation. It does the lateral portion of the tricuspid annulus,
not provide prognostic value. measuring in control sweep mode.
With restrictive filling and/or high filling Maximal TAPSE is defined by the total excursion
pressures, the interval may fall to below 60ms. of the tricuspid annulus from its highest position
after atrial ascent to the peak descent during
*IVRT should be indexed for heart rate.
ventricular systole. Earlier studies using 2D
echocardiography showed that in the normal Figure 24. Measurement of TAPSE.
right ventricle this value exceeds 16 mm12. Using
M-mode the normal range is higher (24.9 ± 3.5
mm28; 25.4 ± 4.9 mm29) and a value of 20.1 mm has
been shown to be a useful cut-off in identifying
pulmonary hypertension29.
46 47
Pulmonary Hypertension Echocardiographic Protocol Pulmonary Hypertension Echocardiographic Protocol
Echocardiography uses the combination of two- Care should be taken to ensure that Doppler A value of VTR/VTIRVOT less than 0.2 has a 94% When investigating potential cases of idiopathic
dimensional and pulsed-wave Doppler imaging cursor is in line with the axis of the right sensitivity for a PVR of less than 2 Wood Units at PAH at cardiac catheterisation, a vasodilator
to measure cardiac output. Stroke volume (SV) ventricular outflow tract, otherwise a significant catheterisation26. As the definition of pulmonary (inhaled nitric oxide, intravenous prostacyclin
can be derived from the product of the velocity- error will appear in the measurements. In order arterial hypertension (PAH) includes a PVR or adenosine) is given to identify a subgroup
time integral (VTI) of the Doppler profile and the to calculate pulmonary vascular resistance (PVR), greater than 3 Wood Units, a VTR/VTIRVOT less than which may respond to long-term treatment with
cross-sectional area (CSA) of the left ventricular continuous-wave Doppler is used to determine 0.2 will exclude most cases of PAH. calcium channel blockers. A positive vasodilator
outflow tract (LVOT). Cardiac output (CO) is the the peak tricuspid regurgitant velocity (VTR) as response is defined by a drop in mean pulmonary
While measures of SV, CO and PVR are readily
product of SV and heart rate (HR). described above: the highest velocity is used. arterial pressure by more than 10 mmHg to less
measurable at echocardiography and correlate
In patients with atrial fibrillation, the average of than 40 mmHg, with a stable or increasing cardiac
SV = VTI(LVOT) x CSA(LVOT) with right and left heart function and the
five measurements should be taken. output47. As yet, echocardiography has not been
underlying pulmonary vascular resistance,
CO = SV x HR validated to identify this subgroup and therefore
PVR (Wood units) = 10.(VTR/VTIRVOT) + 0.16 these measurements are not considered core
should not be used outside the research setting.
Similarly, right ventricular SV and CO can be to the protocol and are thus not mandatory
This measurement has been shown to correlate
measured from the proximal right ventricular measurements. The value of serial measurements
well with PVR measured at cardiac catheterisation
outflow tract (RVOT), just within the pulmonary in the follow-up of pulmonary hypertension has
over a range of right and left atrial pressures.
valve from the parasternal short-axis view. not been validated.
Figure 25. Measurement of PVR from VTR (left) and RVOT VTI (right).
48 49
Pulmonary Hypertension Echocardiographic Protocol Pulmonary Hypertension Echocardiographic Protocol
The primary abnormality in pulmonary In line with these measurements, Echocardiography therefore provides invaluable
hypertension is increased afterload on the echocardiographic follow-up studies have shown additional information when assessing
right ventricle due to elevated pulmonary increased right atrial size to be associated prognosis and the clinical course of disease.
vascular resistance caused by remodelling of with poor prognosis49. Persistently high right No clinical or physiological measure should
the resistance pulmonary arteries. It is possible atrial pressure may lead to the development be considered in isolation and often several
that the right ventricle itself is predisposed to of a pericardial effusion, which is a powerful modalities of assessment are required to reach a
abnormal remodelling due to the same genetic predictor of mortality49. conclusion about the status of a patient, so that
abnormalities underlying vascular remodelling, a physician or team may be able to determine a
Other echocardiographic features that have been
but this is highly speculative. Nonetheless, it is course of action. Equally, patients may report
shown to correlate with survival include markers
clear from many studies that it is cardiac function stability or improvement in symptoms, but
of myocardial function such as myocardial
which determines prognosis and exercise progressive or persistent concerning features
performance index (MPI), right ventricular
capacity. In particular, it is worth noting that on echocardiography may lead suggest the
fractional area change and tricuspid annular
pulmonary arterial pressure by itself does not need for continued escalation of treatment or
plane systolic excursion (TAPSE)50. A cut-off
correlate at all well with exercise capacity or more detailed assessment. How all of these
value of greater than 0.88 for MPI and less than
prognosis. This is made abundantly obvious from parameters are integrated in to a treatment
15 mm for TAPSE have been particularly
the fact that pulmonary arterial pressure will fall strategy is beyond the scope of this protocol.
associated with poor prognosis. Increases in left
with advancing right ventricular failure.
ventricular eccentricity index at end-diastole
As right ventricular failure progresses, cardiac have also been shown in several studies49, 50 to be
output falls and right atrial pressure rises. Values associated with worse outcomes, indicating the
from cardiac catheterisation associated with poor adverse impact of left ventricular compression.
prognosis are48: Patients with values above 1.7 have a significantly
higher risk of dying51.
• Cardiac index ‹ 2.1 l/min/m2
While it may be important to use cut-off values
• Right atrial pressure › 10 mmHg
from echocardiography to risk-stratify patients,
ixed venous oxygen saturation ‹ 63 %
• M there are many other powerful clinical indicators of
(low values indicate increased oxygen severity, such as functional class, haemodynamics
extraction due to lower cardiac output) and exercise capacity. Nonetheless, there are
problems with using these measures in following
the clinical course of patients or response to
therapy. Haemodynamics can only be obtained
by invasive means; functional class is a crude
assessment for only small to moderate change;
and exercise capacity can be influenced by many
other factors.
50 51
Pulmonary Hypertension Echocardiographic Protocol Pulmonary Hypertension Echocardiographic Protocol
Significant shunting For corrective surgery, PVR For corrective surgery, PVR For corrective surgery, PVR
lesions is low and presents no elevated, risk increased elevated, risk too high, not
problem but accepted operable
This very short overview takes advantage of
its position at the end of this booklet with the iPAH-like physiology Small unoperated lesion Small residual after
pathophysiology and basics of echocardiography (eg., PFO, ASD, VSD, PAD) corrective surgery of
not haemodynamically a shunting lesion, not
well set out before, and thus can afford to
related to PAH haemodynamically related
focus only on the differences in children. The to PAH
suggestions reflect most of the practice of the “UK
PAH due to past or Persisting PH despite PAH due to left ventricular
Service for Pulmonary Hypertension in Children”, present PVH corrective surgery of dysfunction with abnormal
a network set up in 2001, which spans the entire pulmonary venous wedge pressure and
stenosis or aortic/ increased PVR
country, with all types of pulmonary hypertension,
mitral valvar disease or
from infancy to young adulthood. Within this coarctation, with normal
young subject, the practice is still evolving. wedge pressure and left
ventricular function
Table 13. New proposed classification of pulmonary arterial hypertension in the setting of congenitally malformed hearts as based on
circulatory pathophysiology
Abbreviations: ASD, interatrial communication; (i)PAH, (idiopathic) pulmonary arterial hypertension; PVR, pulmonary vascular resistance; PA system,
pulmonary vascular system; A0, aorta; PAD, persistently patent arterial duct; POF, patent oval foramen; PVH, pulmonary venous hypertension; VSD,
Ventricular septal defect, PFO, patent foramen ovale; Sat%, oxygen saturation; MAPCA, Major Aortopulmonary Collateral Arteries.
52 53
Pulmonary Hypertension Echocardiographic Protocol Pulmonary Hypertension Echocardiographic Protocol
54 55
Pulmonary Hypertension Echocardiographic Protocol Pulmonary Hypertension Echocardiographic Protocol
32 - +3z
30 - +2z
28 -
26 - mean
24 -
22 - -2z
20 -
TAPSE (mm)
-3z
18 -
16 -
14 -
12 -
10 -
8-
6-
4-
0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8
BSA (sqm)
Figure 27. Normal values for children for tricuspid annular plane systolic excursion (TAPSE). z, standard deviation.
Schulze-Neick 2010, modified after Koestenberger JASE 2009 52
56 57
Pulmonary Hypertension Echocardiographic Protocol Pulmonary Hypertension Echocardiographic Protocol
Echocardiography Reporting
Regardless of the clinical indications for spectral profile was obtained the peak velocity pressure loading. Diastolic septal displacement, Any cut off value for measurements which are
performing an echocardiogram, the report should has been underestimated. In the presence of resulting in an increased diastolic eccentricity either diagnostic or prognostic have limited
include measurements, descriptions of all valves, severe (free-flow) tricuspid regurgitation, the index, with significant valvular regurgitation or sensitivity or specificity. No measurement should
the proximal great arteries, the heart chambers, Bernoulli equation is invalid and right ventricular left-to-right shunting at the atrial level, identifies be considered in isolation but in conjunction with
the pericardium and Doppler findings, as well as systolic pressure is underestimated. volume-loading. However, diastolic septal all findings when forming an overall impression.
conclusions. displacement with systolic ventricular dysfunction
Evaluation of right ventricular size should not be In the reporting of follow-up echocardiograms,
in the absence of left-to-right shunting at the
Where pulmonary hypertension is the referral based on only a single measurement of cavity emphasis should be placed on changes in right
atrial level or significant valvular regurgitation,
indication or the incidental echocardiogram dimension but in combination with a qualitative ventricular function as pulmonary pressures
indicates increased right ventricular diastolic
finding, particular emphasis should be placed assessment from all right ventricular views. Any correlate poorly with the functional capacity or
pressures which should be differentiated from
on not only pulmonary pressures but also on single linear measurement may be inadequate in survival of patients. Reduction in pulmonary
volume-loading.
right heart chamber size and function and any describing the ventricle as a whole due its eccentric pressure may be related to deterioration of
findings indicating any secondary cause (left geometry. Trabeculations of the myocardial Evaluation of ventricular function should be ventricular function, while increases in pressures
ventricular dysfunction, left heart valve disease or walls and indistinct endocardial definition of the based on the evidence provided by the TAPSE, may reflect improvement of ventricular function
congenital heart disease, etc). Where pulmonary lateral free wall may also limit the accuracy and tricuspid annular S’ wave velocity and the MPI in in response to therapy. Consequently, changes
hypertension is confirmed, the report should reproducibility of linear and area measurements conjunction with any qualitative impression from in pulmonary pressure should be interpreted
also include the various parameters, described made from the apical four chamber view. all right ventricular views. Any single parameter in relation to changes in ventricular function.
in the protocol, that provide important prognostic should be viewed critically, when it suggests Reports should always be based on comparisons
In the normal heart, the right ventricle is
information (right atrial volume index, inferior a degree of ventricular dysfunction which is with previous echocardiographic findings.
approximately one third the size of the left
vena cava diameter, eccentricity index, presence significantly different from other parameters and
when assessed from parasternal views. This can
of pericardial effusion, etc). from a qualitative impression.For example, TAPSE
be a useful ‘yard stick’ by which to judge right
may be ‘pseudonormalised’ in the presence of a
The primary indicator of raised pulmonary ventricular size in a qualitative assessment. While
pressure and volume-loaded ventricle. Ambiguity
pressure in echocardiography is the right qualitative expressions of mild, moderate or severe
in defining the onset or offset of spectral Doppler
ventricular systolic pressure derived from the ventricular dilatation are subjective, they are well
velocity components from the tricuspid inflow,
tricuspid regurgitant velocity. Measurement of established in echocardiography reporting and
outflow tract or from TDI of the RV will lead to
a low peak tricuspid regurgitant velocity in the may have some value in concluding.
errors in measurements of time, significantly
presence of a clearly pressure loaded ventricle or
Comments on pressure and or volume-loading affecting the calculation of the MPI.
reduced outflow tract acceleration time should be
of the ventricle are based on the identification
viewed critically. Consideration should be given
of septal displacement toward the left ventricle.
as to whether optimal alignment of the tricuspid
Systolic septal displacement, resulting in an
regurgitant jet was obtained or where an indistinct
increased systolic eccentricity index, identifies
58 59
Pulmonary Hypertension Echocardiographic Protocol Pulmonary Hypertension Echocardiographic Protocol
with normal cusp excursion. EId: 1.5, EIs: 2.4. LV systolic diameter base LX 1.6 cm 2.0 – 4.0 cm
Pulmonary artery and branches are dilated MPI with Tissue Doppler Imaging : 0.88 Fractional shortening base LX 0.56 0.29 – 0.37 cm
(main pulmonary trunk: 3.6 cm, right pulmonary
artery: 2.2 cm, left pulmonary artery: 1.8 m, Tissue Doppler Imaging: S’ wave: 8 cm/sec, IVS diastolic thickness 0.92 cm 0.8 – 1.1 cm
in diameter). Pulmonary valve is structurally E’: 8.3 cm/sec, A’: 16.3 cm/sec, IVRT: 110 msec.
LVPW diastolic thickness 0.84 cm 0.8 – 1.1 cm
normal. Right ventricular free wall is hypertrophied
(measured as 0.6 cm from subcostal view). LA systolic diameter LX 3.3 cm 2.7 – 3.8 cm
Right atrium is dilated (85 ml/m2 in volume).
Right ventricle is dilated (basal diameter: 5.9 cm) TAPSE with M-mode: 8 mm Aortic root diameter 2.8 cm 2.7 – 3.3 cm
and pressure loaded with moderate to severe
RVOT acceleration time: 75 msec Doppler
impairment of systolic function.
Left atrium is normal (28 ml/m2 in volume). Left PVR (estimated with Doppler echocardiography): AV peak velocity 103 cm/sec
60 61
Pulmonary Hypertension Echocardiographic Protocol Pulmonary Hypertension Echocardiographic Protocol
Doppler-Measurements Doppler-Measurements
PDA
Coarctation
62 63
Pulmonary Hypertension Echocardiographic Protocol Pulmonary Hypertension Echocardiographic Protocol
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66 67
National Pulmonary Hypertension Centres
of Britain and Ireland
Freeman Hospital
Northern Pulmonary Vascular Unit,
Regional Cardiothoracic Centre,
Newcastle-upon-Tyne, NE7 7DN
Tel: 0191 223 1084 or 0191 244 8608
Golden Jubilee National Hospital Fax: 0191 223 1691
Scottish Pulmonary Vascular Unit,
Beardmore Street, Clydebank,
West Dunbartonshire, G81 4HX
Tel: 0141 951 5497
www.spvu.co.uk Royal Hallamshire Hospital
Pulmonary Vascular Unit,
Glossop Road, Sheffield, S10 2JF
Tel: 0114 271 2590
Fax: 0114 271 1718
Hammersmith Hospital
Pulmonary Hypertension Service,
Du Cane Road, London, W12 0HS
Tel: 0208 383 2330
Fax: 0208 383 2331
www.pulmonary-hypertension.org.uk
Royal Brompton
Great Ormond Street Hospital
Pulmonary Hypertension and Adult
UK Service for Pulmonary Hypertension
Congenital Heart Centre, Sydney Street,
in Children. London, WC1N 3JH
London SW3 6NP
Tel: 0207 405 9200
Tel: 0207 351 8362
ext 1005, 1007, 8495
Fax: 0207 351 8629
www.sphch.co.uk
www.rbht.nhs.uk