Download Doppler Flow Patterns in the Evaluation of Pulmonary Hypertension

Doppler Flow Patterns in the Evaluation of Pulmonary Hypertension
CARMEN GINGHINĂ, DENISA MURARU, AURORA VLĂDAIA,
RUXANDRA JURCUŢ, B.A. POPESCU, ANDREEA CĂLIN, S. GIUŞCĂ
“Prof. Dr. C.C. Iliescu” Institute of Cardiovascular Diseases, Bucharest, Romania
Pulmonary arterial hypertension is defined as a group of diseases characterised by a
progressive increase in pulmonary vascular load, leading to marked increase in pulmonary artery
pressure, right ventricular failure and premature death.
Given the nonspecific nature of its early symptoms and signs, pulmonary arterial hypertension
(PAH) is often diagnosed in its advanced stages. Although clinical assessment is essential when
initially evaluating patients with suspected PAH, echocardiography is a key screening tool in the
diagnostic algorithm, because, in comparison with invasive measurements, it has the advantages of
being safe, portable, and repeatable.
Therefore, Doppler echo is the modality most frequently used in pulmonary hypertension
patients. Several echocardiographic techniques centered on the Doppler principle (both conventional
Doppler parameters and tissue Doppler imaging) used in the assessment of PAH magnitude and its
cardiac effects are presented in this paper. They provide important data on the severity, possible
causes and consequences of pulmonary hypertension, both initially and during follow-up, therefore
having the ability to estimate disease progression, prognosis, or to monitor therapeutic response.
Doppler echocardiography allows to noninvasively estimate systolic pulmonary arterial pressure
(SPAP), mean and end-diastolic pulmonary arterial pressure, as well as the quantification of right
ventricular (RV) function and the evaluation of pulmonary vascular resistance (PVR).
Key words: pulmonary arterial hypertension, right arterial pressure, tissue Doppler imaging.
Pulmonary arterial hypertension is defined as
a group of diseases characterised by a progressive
increase in pulmonary vascular load, leading to
marked increase in pulmonary artery pressure, right
ventricular failure and premature death [1].
The evaluation of pulmonary artery pressure is
a routine part of an echocardiography examination.
Although certain two-dimensional (2D) echocardiographic features can suggest pulmonary hypertension,
Doppler echocardiography is the primary method for
determining actual pulmonary pressures [2].
However, in certain cases it can be challenging
or even impossible to make a definite diagnosis
based solely on Doppler findings, because there is
no single parameter to discriminate the presence of
pulmonary hypertension or a specific cutoff value to
work in any conditions. There are rather frequent
false positive/false negative results and the influence
of age, rhythm, preload or the technical pitfalls
which render Doppler parameters more or less
reproducible must be taken into account. To increase
the accuracy of diagnosis, it is highly recommended
to do a comprehensive evaluation by a multiple
parameter approach, to avoid the most frequent
pitfalls and to finally integrate the findings in
clinical context.
ROM. J. INTERN. MED., 2009, 47, 2, 109–121
A thorough Doppler assessment in pulmonary
hypertension must cover 3 main objectives: estimation
of pulmonary arterial pressure, evaluation of
pulmonary vascular resistance and right ventricular
function.
DOPPLER ECHOCARDIOGRAPHY FOR ESTIMATION
OF PULMONARY ARTERIAL PRESSURE
Doppler echocardiography allows to noninvasively estimate systolic pulmonary arterial
pressure (SPAP), as well as mean and enddiastolic pulmonary arterial pressure.
SPAP is equivalent to right ventricular (RV)
systolic pressure assuming there is no gradient in
systole between the RV and pulmonary artery (PA)
(such as infundibular or valvular pulmonary stenosis).
The most common approach is to measure the peak
velocity of a tricuspid regurgitant jet (TRVmax) and
apply the modified Bernoulli equation (4TRVmax2 +
estimated RAP). This method has a good correlation
with invasive pressure measurements.
However, the assessment of tricuspid regurgitation
(TR) is thought to be problematic in 20% of healthy
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subjects and up to 70% of patients suffering from
chronic obstructive pulmonary disease (COPD).
Contrast agents can be used to enhance the TR
signal, but require venous catheterization [3].
Tricuspid regurgitation can be evaluated from
multiple echocardiographic windows, including the
parasternal inflow tract view, short-axis view at the
base of the heart, and apical four-chamber view.
From the apical position, the transducer needs to be
angled more medially and inferiorly from the mitral
valve signal. It should be emphasized that in the
normal disease-free state, the tricuspid valve,
because of its complex closure pattern, often
exhibits mild degrees of valvular regurgitation,
which may be confined to early systole. The
2
prevalence of regurgitation increases with patient
age. The normal tricuspid regurgitation velocity is
1.7 to 2.3 m/s at rest. A higher velocity indicates
pulmonary hypertension, right ventricular outflow
tract (RVOT) obstruction, or pulmonic stenosis.
When noted, the normal physiologic degrees
of regurgitation are typically associated with
relatively low tricuspid regurgitation velocities,
implying right ventricular systolic pressures in the
normal range.
When the continuous wave Doppler spectrum
of the tricuspid regurgitation jet is suboptimal,
injection of agitated saline solution into an arm
vein enhances the tricuspid regurgitation velocity
signal (Fig. 1A,B).
A
B
Fig. 1. – Transthoracic echocardiography, apical four-chamber view,continuous wave Doppler recording of tricuspid regurgitation
velocity: A) suboptimal spectrum; B) enhanced signal after injection of agitated saline solution.
Probably the most common cause of tricuspid
regurgitation is functional valvular regurgitation
secondary to annular dilation, altered RV geometry
with apical displacement of tricuspid leaflets
[4], which in turn may be the result of pulmonary
hypertension of any cause. The severity of
functional tricuspid regurgitation can range from
mild to severe.
The examiner should make sure that the
maximum TR jet envelope is obtained, as any
underestimation of the TR jet velocity will result in
an underestimation of the pressure by a “squared”
factor. The best approach is to position the
transducer over the RV apex, medial to the 4-chamber
view apical position. The subcostal approach may
confer additional diagnostic power in patients with
hyperexpanded lungs. Use of color flow Doppler
helps in optimal alignment of the cursor with the
regurgitant jet (Fig. 2A,B).
Moreover, the velocity may be also underestimated if not measured at end expiration (Fig. 3A,B).
An intense continuous wave Doppler signal
usually indicates at least moderate TR. A duration of
longer than 100 ms is usually considered significant.
Marked TR is associated with an increased forward
tricuspid flow velocity (but usually <1 m/s) and a
rapid tricuspid inflow deceleration time. An early
peaking TR jet by CW with a TR “cut-off” sign
(similar to that seen with acute severe MR) is
consistent with severe TR and is associated with early
equalization of RA and RV pressures (Fig. 4).
As stated before, for assessing the SPAP the
best validated method is the modified Bernoulli
equation. The tricuspid regurgitation jet can be
used to determine right ventricular systolic
pressure, by calculating the right ventricle to right
atrial pressure gradient and then adding estimated
right atrial pressure.
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Doppler flow patterns and pulmonary hypertension
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A
B
Fig. 2. – Transthoracic echocardiography, CW Doppler recording of TR from: A) apical 4-chamber view which would signify that
PAP is normal (25mmHg) in the presence of mean RAP of 5 mmHg; B) subcostal approach, which allows better alignment with a
more accurate estimation of increased PAP of approximately 46 mmHg.
B
A
Fig. 3. – Transthoracic echocardiography CW Doppler recording of TR from apical 4-chamber view: A) a marked respiratory variation
with a decreased TR velocity with inspiration; B) the optimal recording in held expiration with no variability of peak TR velocity.
Fig. 4. – Transthoracic echocardiography CW Doppler recording
of TR from apical 4-chamber view: note the features of severe
tricuspid regurgitation (see text).
A major variable in determining the right
ventricular systolic pressure is the method by
which a right atrial pressure (RAP) is either
assumed or calculated. Multiple algorithms have
been proposed, each of which has provided a
relatively good correlation over a broad range of
pulmonary artery pressures. Many laboratories use
a floating constant of 5, 10, or 15 mm Hg, based on
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the size of the right atrium and the severity of
tricuspid regurgitation. Using this qualitative
approach, when tricuspid regurgitation is mild and
the right atrial size is normal, an assumed right
atrial pressure of 5 mm Hg is used. For moderate
degrees of tricuspid regurgitation with mild or no
right atrial enlargement, an assumed constant of 10
mm Hg can be used. If tricuspid regurgitation is
severe and noted in the presence of a dilated right
atrium, an assumed constant of 15 mm Hg can be
used. Instead, for a more precise estimation,
several parameters have been proposed, such as:
caval respiratory variability, flow recordings in
hepatic or superior vena cava veins, tricuspid
inflow or tissue Doppler recordings of RV free
wall. The accuracy of RAP estimation is of key
importance especially for intermediate TR jet
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velocities, because it may discriminate between
normal and abnormal PAP.
A highly compliant vessel, the inferior vena
cava changes shape and dimensions with changes
in central venous pressure and the respiratory
cycle. The size and respiratory variation of the
inferior vena cava have been used to predict right
atrial pressure. Dilation of the inferior vena cava
suggests increased central venous pressure and may
accompany volume overload states. The diameter
of the inferior vena cava normally decreases more
than 50% during inspiration. A blunted or absent
inspiratory decrease in the inferior vena cava
diameter suggests increased right atrial pressure.
The most common estimation of RAP is based on
caval respiratory index: if less than 50% then RAP
is at least 10 mmHg (Fig. 5A,B).
A
B
Fig. 5. – Transthoracic echocardiography subcostal view: A) two-dimensional image of a moderate dilated inferior vena cava; B) in
the same patient, M-mode cursor placed at the inferior vena cava to assess the caval respiratory index.
However, the significance of inferior vena
cava (IVC) diameter and collapse with inspiration
is limited in several categories: athletes,
mechanically ventilated or dyspneic patients [5].
From the subcostal transducer location,
alignment of the Doppler beam with inferior vena
caval flow is difficult, and it has become customary
to substitute hepatic vein flow for this purpose.
Because hepatic vein flow and inferior vena caval
flow are similar and because it is generally easier
to align the Doppler signal with a hepatic vein, this
is both useful and practical. Antegrade flow
(toward the right atrium) has two main
components: a larger systolic wave and a slightly
smaller diastolic wave. Between these two
antegrade flow patterns, at end-systole, a small
retrograde flow pattern may be recorded. Likewise,
during atrial systole, some retrograde flow is also
present. Hepatic vein flow is respiratory cycle
dependent with increased flow velocity during
inspiration and decreased flow velocity (and a greater
degree of retrograde flow) during expiration. Several
disease states result in characteristic abnormalities of
hepatic vein flow. As a surrogate for inferior vena
caval flow, any condition that affects either right
atrial pressure or filling will alter hepatic vein flow
velocity. The evaluation of hepatic venous flow
constitutes the cornerstone of Doppler assessment of
RAP. As RAP increases, the pressure gradient
between the hepatic veins and the RA decreases, thus
lowering the forward systolic flow (Fig. 6A,B). The
hepatic venous systolic filling fraction (calculated as
the ratio between the time-velocity integral [TVI]
of the systolic forward flow (PVS-wave), PVS and
5
Doppler flow patterns and pulmonary hypertension
A
113
B
Fig. 6. – Transthoracic echocardiography subcostal view hepatic venous Doppler flow in: A) healthy patient-normal hepatic vein
inflow consists of flow reversal with atrial systole (A), systolic forward flow (S), forward flow nadir or reversal at end systole (atrial
V wave), and diastolic forward flow (D). Note that systolic filling fraction is greater than 55% (68%) and that S velocity is higher
than A velocity, both of which predict normal mean right atrial pressure. TVI, Time-velocity integral; B) PAH patient: systolic filling
fraction is less than 55% (33%) and A wave is larger compared to systolic S wave.
sum of PVS and diastolic forward flow pulse
(PVD) TVIs) has been shown to be a predictor of
RAP with dichotomous separation of RAP greater
than 8 mm Hg by a hepatic vein systolic filling
fraction of less than 55% with a sensitivity of 86%
and a specificity of 90% [6]. Moreover, a larger A
wave after atrial contraction compared to forward
systolic S wave also predicts increased RAP [7][8].
The superior vena cava can be visualized from
the suprasternal notch as a vertical structure just to
the right of the aortic arch but it is more readily
evaluated using transesophageal echocardiography.
Both long- and short-axis views of the vessel are
possible. Occlusion or external compression of the
superior vena cava is a common clinical problem
that can be assessed using echocardiography.
Doppler interrogation of flow velocities into the
superior vena cava is easy to obtain in all patients
with congestive heart failure and makes it possible to
estimate the severity of the impairment of the right
circulatory function using simple categoric classes.
The venous flow velocity pattern was considered
normal when the systolic/diastolic ratio was ≥1 and
≤2, the flow pattern was categorized as “predominant
systolic wave” when the ratio was >2, and as
“predominant diastolic wave” when the ratio was
<1 (Fig. 7A,B). The differentiation among normal,
“predominant systolic wave,” and “predominant
diastolic wave” central venous flow velocity patterns
not only distinguished patients with normal from
congestive heart failure patients with high right atrial
pressure, but also differentiated patients with normal
right heart hemodynamics from those in whom a
normal right atrial pressure was associated with an
impaired right ventricular function [9].
An advantage of tissue Doppler imaging
(TDI) in assessing RAP is that it does not require
subcostal imaging and allows 1-step method for
assessment. It provides information independent of
RV function and is still useful in mechanically
ventilated patients. Two TDI techniques have been
described for estimation of mean RAP. Both methods
allow for dichotomous differentiation of mean RAP.
To apply the technique, pulse wave TDI is performed
at the lateral tricuspid annulus in the apical 4-chamber
view. Tricuspid E/E’ ratio allows dichotomous
differentiation of the mean RAP. An early tricuspid
inflow velocity/early tricuspid annular motion (E/E’)
ratio greater than 6 predicts a mean RAP greater than
10 mm Hg with a sensitivity of 79% and a specificity
of 73% (Fig. 8A,B). The ratio of tricuspid peak early
inflow velocity (E) obtained by Doppler to the
tricuspid annular early diastolic velocity (E’) obtained
by TDI was also studied and showed to have a weak
correlation with RAP, but requires two Doppler
measurements [6].
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A
6
B
Fig. 7. – Superior vena cava Doppler flow with systolic wave (S) and diastolic wave (D): A) normal flow with S wave> D wave;
B) abnormal flow S<D.
A
B
Fig. 8. – Transthoracic echocardiography PW Doppler in apical 4-chamber view: A) tricuspid E/A ratio (1.1) measured with
traditional PW Doppler; B) tissue Doppler imaging performed at the lateral tricuspid annulus E/E’ ratio (6) measured in a patient with
elevated RAP and severe PH.
Another method involves measuring the time
interval between the end of the systolic annular
motion to the onset of the E’ wave (RV regional
isovolumic relaxation time [rIVRT]). RV rIVRT
exhibits an inverse relation with mean RAP
independent of the effect of RV end-diastolic or PA
pressure (Fig. 9A,B).
A RV rIVRT less than 59 milliseconds has a
sensitivity of 80% and a specificity of 87.7% to
determine mean RAP greater than 8 mm Hg. RV
rIVRT inversely correlates with mean RAP with a
correlation coefficient of 0.92 (95% confidence
interval 0.82-0.97, P <0.001) [10].
The RV IVRT exhibits an inverse relationship
to heart rate, and increases proportionately with
PA systolic pressure when RAP is normal. However,
when the RA fails or is volume overloaded, RAP
is increased with an earlier tricuspid valve opening,
so that RV IVRT shortens. Consequently, RV IVRT
was found useful in the stable pediatric congenital
heart disease population to predict PA systolic
pressure, where compensatory RA hypertrophy
would keep mean RA pressure normal, as compared
to patients who are older or acutely ill, who
tend to have more RV failure and higher RAP
[10]. RAP reflects both left- and right-sided cardiac
7
Doppler flow patterns and pulmonary hypertension
115
A
B
Fig. 9. – Tissue Doppler imaging performed at the lateral tricuspid annulus in the apical 4-chamber view for measuring the RV
rIVRT: A) in a patient with normal RAP; B) in a patient with elevated RAP.
function and chamber volumes, and thus carries
diagnostic, therapeutic, and prognostic values
for patients with cardiac and/or pulmonary
diseases. In addition to guiding the management of
the fluid status in patients with heart failure,
elevated mean RAP is a marker for increased
mortality in patients with primary pulmonary
hypertension, likely because it reflects decompensation
of atrial systolic function after a long period of
compensatory hypertrophy. The advantage of
measuring RV rIVRT using TDI lies in the fact
that it identifies mean RAP for patients with
suboptimal subcostal views and thus may assist
in treatment of these patients when their fluid status
is in question.
A practical way to assess SPAP in patients
with cardiac shunts with optimal recording and
alignment with Doppler flow (e.g. patients with
patent ductus arteriosus or ventricular septal
defects), may be the calculation of PASP using the
difference between systolic blood pressure and
peak systolic shunt gradient (Fig. 10A,B).
A
B
Fig. 10. – Transthoracic echocardiography CW Doppler in a patient with patent ductus arteriosus: A) recording of tricuspid
regurgitation velocity in apical 4-chamber view; B) recording peak systolic Ao-PA gradient (based on a simultaneously measured
systolic systemic blood pressure of 125 mmHg, SPAP can be derived as SPAP=125–100=25 mmHg).
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As we said before, Doppler echocardiography
allows to noninvasively estimate systolic PAP, as
well as mean and end-diastolic PAP.
Doppler imaging is very useful to assess right
ventricular pressure overload. Both pulmonary
valve flow and tricuspid regurgitation velocity
should be evaluated.
In normal individuals, pulmonary artery
flow has a symmetric contour with a peak velocity
occurring in midsystole. As pulmonary pressure
increases, peak velocity occurs earlier in systole
and late systolic notching is often present. With
increased pulmonary pressure, the right ventricular
ejection pattern approximates more a leftsided
ejection pattern. The acceleration time (time from
onset to peak flow velocity) (AcT) can be
measured and provides a rough estimate of the
degree of increase in pulmonary artery pressure. In
normal individuals, AcT exceeds 140 milliseconds
and progressively shortens with increasing degrees of
pulmonary hypertension. The shorter the acceleration
time, the higher the pulmonary artery pressure. Most
studies have suggested that at an AcT of less than
70 to 90 milliseconds, pulmonary artery systolic
pressures will exceed 70 mm Hg. This assessment has
been largely replaced by the more direct Doppler
assessment of right ventricular systolic pressure from
the tricuspid regurgitation signal. On occasion, in a
patient without a measurable tricuspid regurgitation
velocity, shortening of the pulmonary acceleration
time may be the only evidence of pulmonary
hypertension. The pulmonary artery acceleration time
is easily measured in most patients, including those
with chronic lung disease. Reliability of the method
is less than when using the tricuspid regurgitant
jet velocity, however. Mahan’s equation is simplest
and preferred for estimating MPAP: MPAP = 79–
0.45 × (AcT).
It should be noted that AcT is dependent on
cardiac output and heart rate. With increased output
through the cardiac chambers on the right side (as in
atrial septal defect), AcT may be normal even when
pulmonary artery pressure is increased. If the heart
rate is slower than 60 beats per minute or more than
100 beats per minute, AcT needs to be corrected for
heart rate. This method is rarely used in our practice.
There is heavy dependence on the position of
the Doppler sample volume because acceleration and
velocities are higher along the inner edge of curvature
of the pulmonary artery. Because the curvature is
three-dimensional, positioning of the sample volume
in the middle of the vessel in the imaged plane may
8
not avoid overestimation of velocity by sampling
adjacent to the vessel wall in the orthogonal
nonimaged plane. Furthermore, the short absolute
time interval of AcT lends itself to high measurement
error and lower reproducibility.
Right ventricular ejection time shortens with
increasing pulmonary hypertension. In contrast, the
right ventricular pre-ejection time lengthens with
increasing pulmonary arterial pressure. Although
neither time is useful alone, the ratio of pulmonary
acceleration time to total right ventricular ejection
time or pre-ejection time can be used to estimate
mean pulmonary artery pressure with correlation to
mean pulmonary pressure similar or better than
acceleration time alone. Again, the short values of
these time intervals render them impractical for
general clinical use.
With severe pulmonary hypertension, a midsystolic notch may be present in the deceleration
slope of the pulmonary artery Doppler flow profile
(Fig. 11A,B). This notch is analogous to the midsystolic notch seen in M-mode examination of the
pulmonary valve. The notch may be secondary to
transient elevation of pulmonary artery pressure
above right ventricular pressure due to a decrease
in pulmonary artery compliance and an increase
in main pulmonary artery size, impedance, and
transmission time of the velocity wave. The
presence of a mid-systolic notch in the pulmonary
outflow Doppler profile is highly specific for
pulmonary hypertension [11].
Data in the literature show that the pulmonary
flow systolic notch (mid-systolic deceleration in
pulmonary flow, as assessed using Doppler
echocardiography) may distinguish proximally located
obstructions in the pulmonary arterial vasculature
from distal obstructions. This notch occurs
significantly later in systole in patients with IPAH
than in those with proximal pulmonary embolism.
A novel and easily applicable echocardiographic sign with prognostic significance has been
described, estimating the timing of pulmonary flow
systolic notch as the ratio t1/t2: the time interval from
the onset of pulmonary artery systolic flow to the
maximal systolic flow deceleration (t1) is divided by
the time interval from the maximal systolic flow
deceleration to the end of pulmonary artery systolic
flow (t2). This parameter seems to distinguish
proximally located obstructions in the pulmonary
arterial vasculature from distal obstructions in PPH;
9
Doppler flow patterns and pulmonary hypertension
A
117
B
Fig. 11. – Right ventricular outflow tract flow velocity recordings by pulsed wave Doppler echocardiography. The sample volume is
placed in the region of the pulmonary valve annulus: A) normal flow pattern; B) flow velocity in pulmonary hypertension
(note midsystolic cessation of flow – notching [arrow]).
in the latter this notching appears significantly later
than in patients with proximal pulmonary embolism.
Thus, patients with pulmonary embolism with a
t1/t2 ratio more than 1.0 may have an increased inhospital mortality risk and a limited haemodynamic
improvement after pulmonary endarterectomy,
because of distally located obstruction [12–14].
The position of the dicrotic notch on the PA
pressure waveform approximates the mean PA
pressure. Peak diastolic pressure gradient between
the PA and the RV approximates mean PA pressure
and, therefore, application of the modified Bernoulli
equation to the peak.
The pulmonary regurgitant (PR) flow velocity
patterns in patients with pulmonary hypertension
display significantly higher velocities than in
patients with normal pulmonary pressures. The
higher detection rate of PR flow in PH makes
easier to estimate mean PAP and end-diastolic PAP
using Bernoulli equation. Mean PA pressure can be
calculated with the following formula: MPAP = 4
(PR peak velocity)² [15] (Fig. 12).
Fig. 12. – Continuous wave Doppler interrogation of pulmonary
regurgitation from the left parasternal window; note the peak
diastolic pulmonary regurgitation velocity RV (1) and enddiastolic pulmonary regurgitation velocity (2).
The continuous wave Doppler profile of
pulmonary regurgitation velocity in a patient with
normal pulmonary artery pressure may display a dip
after atrial contraction, because the pressure
difference between the pulmonary artery and right
ventricle is small during diastole (Fig. 13). Conversely,
when pulmonary pressure is high, right atrial
contraction usually does not make a notable change
in the pressure gradient, with no dip in the signal
of pulmonary regurgitation [2]. Normally, the
pulmonary regurgitation end-diastolic pressure
gradient is less than 5 mmHg. An increase in this
pressure gradient (> 5mmHg) has been found to
correlate with systolic dysfunction, diastolic dysfunction, increased brain natriuretic peptide, and
decreased functional status [16].
PA end-diastolic pressure is frequently used as
an estimate of pulmonary capillary wedge pressure.
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The presence of pulmonary regurgitation (PR) can be
exploited to estimate PA end-diastolic pressure. The
application of the modified Bernoulli equation to the
end-diastolic PR velocity, adding to this an estimate
10
of RAP, provides an estimation of PA diastolic
pressure (Fig. 12). The diastolic PA pressure can be
estimated using the following formula: Diastolic PA
pressure = 4(end PR V)² + estimated RAP [17].
Fig. 13. – Continuous wave Doppler spectrum of pulmonary
regurgitation velocity in a patient with normal pulmonary artery
pressure (note the dip in pulmonary velocity – red arrows).
DOPPLER ECHOCARDIOGRAPHY FOR
DETERMINATION OF PULMONARY VASCULAR
RESISTANCE
Doppler echocardiography has significantly
impacted clinical medicine by its ability to determine
intracardiac hemodynamics noninvasively. Pulmonary
vascular resistance (PVR) is a hemodynamic variable
that contributes to the management of patients with
advanced cardiovascular and pulmonary conditions.
Pulmonary vascular resistance is calculated invasively
by the ratio of transpulmonary pressure gradient to
transpulmonary flow (Qp)[18]. Therefore, noninvasive
determination of PVR is possible using variables that
are routinely obtained by Doppler echocardiography.
Increased SPAP may be secondary to increased
transpulmonary flow or abnormal PVR. Peak tricuspid
regurgitant velocity (TRV) and right ventricular
outflow time-velocity integral (TVI RVOT) can be
used to estimate PVR. The ratio of TRV: RVOT TVI
has been shown to correlate with PVR with a
correlation coefficient of r=0.93 (95% confidence
interval 0.87–0.96) [19]. Patients with TRV/ RVOT
TVI <0.2 are likely to have low PVR values
(<2 WU), and pulmonary vascular disease may
be excluded despite increased SPAP by Doppler
[19]. A value higher than 0.2 demands further
invasive workup. In conclusion, a “normal” SPAP
combined with a small flow but high PVR could be
abnormal in fact.
There are some reasons for which right heart
catheterization, although invasive, remains the gold
standard for accurately assessing PAP. Despite
many advantages, Doppler echo is limited by load
dependency and reproducibility or by the fact that it
is not reliable enough to reflect minor therapeutic
improvement. As a rule, Doppler echo overestimates
PASP and mean PAP, which may lead to unnecessary
catheterizations. A useful approach to keep invasive
procedures to a minimum is to noninvasively assess
RV function.
DOPPLER ECHOCARDIOGRAPHY FOR RIGHT
VENTRICULAR FUNCTION EVALUATION
Quantifying right ventricular systolic function
is not always easy to do and several approaches have
been suggested, including the Doppler derived
Tei index or myocardial performance index (MPI)
[20]. This index is defined as the isovolumic
contraction time (ICT) and isovolumic relaxation
time (IRT) divided by the ejection time (ET). An
increased right ventricular myocardial performance
index is a sensitive and specific marker of pulmonary
hypertension. MPI may be of value in patients in
whom TR is either not present or cannot be quantified
to assess for pulmonary hypertension. Normal value
of Tei index is 0.28 ± 0.04, increased Tei index being
correlated with RV dysfunction. The MPI also
appears to provide powerful prognostic information.
However, the short absolute values of the times used
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Doppler flow patterns and pulmonary hypertension
in the index confer a high degree of measurement
error and elevated RAP may limit its accuracy [21].
The estimation of the Tei index is based on
separate PW recordings from tricuspid (with tissue
Doppler) and RV outflow (with conventional PW
Doppler) (Fig. 14A,B) at different HR.
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Tissue Doppler imaging (TDI) is a relatively
new echocardiographic tool in the assessment of
myocardial function. The method is available in most
modern ultrasound systems and can provide accurate
information on myocardial motion throughout the
cardiac cycle. In contrast to traditional pulsed Doppler
B
A
Fig. 14. – The estimation of Tei index based on separate PW recordings from tricuspid with traditional Doppler on different cardiac
cycles (A) and from RV outflow with tissue Doppler velocity on the same cardiac cycle (B). In both cases, MPI is calculated as the
ratio (a–b)/b.
echocardiography, which detects high velocity with
low amplitudes, offline TDI detects low velocity with
high amplitudes. Tissue velocities can be displayed
with spectral pulsed or colour-encoded Doppler
visualized with 2D, M-mode or Doppler signals.
TDI is proposed to be less preload dependent
compared to the traditional pulsed Doppler
technique. Pulsed TDI is simpler and more robust
to use, with high temporal resolution. The major
disadvantages of pulsed TDI are poor spatial
resolution due to movement of the heart, while the
sample volume is fixed and apical velocities from
the apical long axis projection are difficult to
measure [22]. TDI determines the timing, direction,
and velocity of RV wall motion. The PW approach
measures online peak velocities. Colour DTI is an
alternative approach to measuring myocardial
motion and can be used off-line, therefore is
favoured for simultaneous wall motion analysis,
exercise and stress echocardiography. It is
important to note that offline TDI analysis provides
mean values compared to pulsed TDI which
provides peak velocities. Thus, it is important to
emphasize that the velocities measured by color
TDI are lower (approximately by 25%) than maximal
velocities measured online [23].
Other proposed measures of RV systolic and
diastolic functions that have been explored include
right ventricular fractional area change (RV FAC)
and RV wall stress, tricuspid annular plane systolic
excursion (TAPSE; a measurement of systolic
elevation of tricuspid annular plane), tricuspid
deceleration duration, E/E’ ratio. In some of these
cases, the amount of data built to date is small and
one cannot make any conclusion on their potential
value in the future [24].
CONCLUSIONS
In conclusion, Doppler echocardiography
provides several complementary methods and indices
to assess RV hemodynamics for a comprehensive
evaluation of PH. Doppler echocardiography may
noninvasively characterize each component of flowpressure-resistance interactions both at rest and
during exercise. The development of new ultrasound
imaging equipment has decreased the number of
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technically inadequate studies and has simultaneously
increased the accuracy of echo PAP estimation in
everyday clinical practice.
12
Acknowledgements. This work was partially supported
by the Romanian National Research Programme II of the
UEFISCSU, grant ID_246/2008.
Hipertensiunea arterială pulmonară este definită ca un grup de boli,
caracterizate prin creşterea progresivă a presiunii în circulaţia pulmonară, ceea
ce conduce la creşterea presiunii în artera pulmonară, la apariţia fenomenelor de
insuficienţă cardiacă dreaptă şi riscul de moarte prematură.
Dată fiind lipsa de specificitate a simptomelor şi semnelor iniţiale,
hipertensiunea arterială pulmonară este adesea diagnosticată în stadiile avansate.
Astfel, deşi evaluarea clinică este esenţială în cazul pacienţilor suspectaţi de
hipertensiune pulmonară, ecocardiografia este instrumentul cheie de screening în
cadrul algoritmului de diagnostic, deoarece, în comparaţie cu metodele invazive,
are avantajul de a fi sigură, portabilă şi reproductibilă. De aceea, evaluarea
ecocardiografică Doppler este metoda cea mai utilizată la pacienţii cu
hipertensiune pulmonară. Ea aduce date importante despre severitatea, etiologia
posibilă şi consecinţele hipertensiunii pulmonare, atât în faza iniţială, cât şi
ulterior, în perioada de urmărire în vederea estimării progresiei, prognosticului şi
pentru monitorizarea răspunsului terapeutic. Ecocardiografia Doppler permite
estimarea noninvazivă a presiunii arteriale pulmonare sistolice (PAPS), medii şi
diastolice, cuantificarea funcţiei ventriculului drept (VD) precum şi evaluarea
rezistenţelor vasculare pulmonare (RVP).
Corresponding author: Carmen Ginghina, MD, PhD, FESC, FACC
100, V. Lascar Str.
020506 Bucharest, Romania
E-mail: [email protected]
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Received March 10, 2009
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