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EVALUATION OF PULMONARY HEMODYNAMICS AND ALTERATION IN DISEASE STATES
1. EVALUATION OF PULMONARY
HEMODYNAMICS AND ALTERATION
IN DISEASE STATES
DR. SOUMEN PRASAD BEHERA
DM RESIDENT,CARDIOLOGY
S.C.B MEDICAL COLLEGE AND HOSPITAL,
CUTTACK
2. PULMONARY VALVE
• It is a semilunar valve with 3 cusps, and it is located anterior,
superior, and slightly to the left of the aortic valve.
• Like the aortic valve, the pulmonic valve is formed by 3 cusps, each
with a fibrous node at the midpoint of the free edges (similar to the
nodes of Aranti in the aortic valve) as well as lunulae, which are the
thin, crescent-shaped portions of the cusps that serve as the coaptive
surfaces of the valve.
• In contrast with the aortic valve, the cusps of the pulmonic valve are
supported by freestanding musculature with no direct relationship with
the muscular septum; its cusps are much thinner and lack a fibrous
continuity with the anterior leaflet of the right atrioventricular (AV)
valve (tricuspid valve).
3. • The cusps of the pulmonic valve are defined by their relationship to the
aortic valve and are thus termed anterior or nonseptal, right and left
cusps.
• They can also be defined by their relationship to a commissure found in
the pulmonic and aortic valves and hence termed right adjacent (right
facing), left adjacent (left facing), and opposite (nonfacing).
• The pulmonic valve, like the other 3 cardiac valves, is formed by
endocardial folds that are supported by internal plates of dense
collagenous and elastic connective tissue and are continuous with the
cardiac skeleton.
8. M MODE
• The only cusp recorded by M mode
scanning from the PSAX view is the
posterior(left) cusp.
• The anterior and the right cusps are
infrequently visualised due to obliquity of
the valve to the ultrasound beam.
9. The excursion of posterior pulmonary leaflet can be
divided into following slopes:
• B-C SLOPE : systolic opening motion
• C-D SLOPE : open valve during systole.
• D-E SLOPE : systolic closing motion.
• E-F SLOPE : diastolic posterior motion.
10. • e Point: Pulmonary valve in closed position
• f Point: Posterior excursion of valve apparatus with right ventricular diastolic
filling
• a Point: Additional blood flow into the right ventricle after right atrial
contraction results in a slight increase in right ventricular end-diastolic
pressure, causing momentary excursion of the valve
• b Point: Ventricular systole results in a mild anterior excursion of the valve
apparatus
• c Point: Right ventricular contraction and blood flow through the right
ventricular outflow tract causes rapid posterior deflection of the right cusp
• d Point: Gradual closure of the pulmonary valve with progression of right
ventricular systole
11.
12. PULMONARY HEMODYNAMICS
• Pulmonary hemodynamics are involved in many
clinical situations, not only because of the strict
relationship between left-heart and right-heart
hemodynamics, but also because the pulmonary
vascular tree is a potential target of every disease
that damages arterial vessels.
13. • The gold-standard method for evaluating pulmonary
hemodynamics is invasive right-heart catheterization, but
its use cannot be justified for many conditions.
• Ultrasound imaging has continuously developed over recent
years, leading to the development of several novel
echocardiographic indexes that allow the evaluation of
pulmonary pressures (systolic, mean, and diastolic) and the
estimation of other pulmonary hemodynamic parameters,
such as pulmonary vascular resistance (PVR), pulmonary
capillary wedge pressure (PCWP), and pulmonary
capacitance and impedance.
• Therefore, it is now possible to obtain a complete and
accurate description of pulmonary hemodynamics using
noninvasive imaging.
14. • Pulmonary hypertension (PH) is a complex
disease that can be idiopathic, familial, or
associated with a wide range of disease processes.
• According to the most recent guidelines,
15. MPAP > 25 mm of Hg.
PVR > 3 Wood Units.
PCWP, LEFT ATRIAL PRESSURE or LEFT VENTRICULAR
END DIASTOLIC PRESSURE =< 15 mm Hg
16.
17.
18. • In the context of PH, many echocardiographic signs can be
present, many involving the right ventricle (hypertrophy,
dilation, or reduction of systolic function).
• Another sign is the systolic position of the interventricular
septum, which can appear flat or can bow toward the right
ventricle because of a decreased interventricular pressure
gradient when pulmonary pressure becomes near systemic.
• Over the past few years, many indexes have been proposed
to improve, replace, or complete the standard basic
echocardiographic evaluation of pulmonary pressures.
22. SYSTOLIC PULMONARY ARTERY PRESSURE
Systolic pulmonary artery pressure (sPAP) is considered equal to
right ventricular (RV) systolic pressure in the absence of
pulmonary valve stenosis or outflow tract obstruction.
• RV systolic pressure can be determined by addition of right
atrial (RA) pressure (RAP) to the pressure gradient between
the right chambers.
• Many methods can be used to estimate RAP, while the
pressure gradient between the right chambers can be
calculated using the modified Bernoulli equation:
where v is the tricuspid regurgitant velocity (TRv).
In the 1980s, several key studies were performed to validate this
technique versus RV catheterization, and it was subsequently used to
estimate sPAP in patients with various diseases.
.
23. Although the application of this technique to estimate
sPAP has been widely validated, its precision is
debatable:
• In studies that have compared echocardiographically
estimated values and true values measured by right-
heart catheterization, the mean difference ranged
from 3 to 38 mm Hg, and Spap was underestimated
with the echocardiographic method by >20 mm Hg in
31% of all patients studied.
• In a more recent study, in 48% of 63 patients
studied, echocardiography-derived sPAP differed
more than +-10 mm Hg from invasively measured
sPAP; the magnitude of pressure underestimation
was greater than that of its overestimation.
24. • For this reason, sPAP evaluation with Doppler methods
should not be used to decide when to treat patients or
to monitor therapy efficacy.
• Although the accuracy of Doppler sPAP measurements
has been questioned, thus limiting its utility as a
diagnostic tool in asymptomatic PH, sPAP estimation
by TRv measurement remains the most feasible and
reliable screening method for suspected PH and in
patients with associated conditions or risk factors for
the development of PH (such as family history,
connective tissue diseases, coronary heart disease,
human immunodeficiency virus infection, portal
hypertension, congenital heart diseases, and chronic
hemolytic anemia, as well as use of fenfluramine
derivatives, amphetamines, and other agents).
25.
26. TRv > 2.8 m/s (corresponding to a right
atrioventricular pressure gradient > 31 mm Hg)
is considered a reasonable cutoff to define
elevated pulmonary pressures, except in elderly
and in very obese patients, in which physiologic
sPAP tends to be more elevated.
30. • Because of its importance as a screening test, the
major concern in the noninvasive evaluation of sPAP
(and of mPAP and diastolic PAP [dPAP]) is to reduce as
much as possible false-negative results (ie, to
minimize the risk for sPAP underestimation).
• The underestimation of sPAP with echocardiography is
probably due to the frequent underestimation of RAP
and of TRv.
• To minimize error, TRv should be measured in multiple
views, seeking the maximal TRv; the use of color flow
Doppler is recommended to obtain the best alignment
between regurgitant flow and the Doppler signal.
31. • Many studies have also demonstrated that
inadequate TRv signals can be enhanced with the use
of contrast.
• An easier and less expensive solution, a simple air-
blood-saline mixture, can dramatically improve the
correlation between Doppler-measured and catheter
measured Spap.
• Care must be taken in using contrast to avoid the
possible overestimation of Doppler velocities because
of contrast artifacts.
• If atrial fibrillation is present, taking the mean of 5
TRv measurements is required.
35. 1) PEAK PRV
• When present, the PRv pattern is characterized by a rapid
rise in flow velocity immediately after the closure of the
pulmonary valve (peak PRv) and a gradual deceleration until
the next pulmonary valve opening (end-diastolic PRv).
PDG + RAP = MPAP
• Peak PRv represents the diastolic pressure gradient between
the pulmonary artery and the right ventricle.
• Masuyama et al demonstrated that the application of the
Bernoulli equation to peak PRv would provide an estimate of
mPAP.
• More recently, Abbas et al validated this method and
demonstrated that adding RAP improves the accuracy of the
mPAP estimate.
37. 2) MEAN RV-RA SYSTOLIC GRADIENT
• Aduen et al proposed a novel and simple method to
estimate mPAP on the basis of the addition of RAP to
the RV-RA mean systolic gradient obtained by tracing
the TRv profile.
• This method was validated in 102 patients,
comparing it with simultaneous right-heart
catheterization; it showed great reliability and
accuracy in diagnosing PH.
• The addition of saline contrast did not improve
accuracy.
• This method appears straightforward and could easily
be incorporated into a standard echocardiographic
exam, allowing a reliable estimation of mPAP.
38.
39. DIASTOLIC PULMONARY ARTERY PRESSURE (DPAP)
1)END-DIASTOLIC PRV
2)RV PRESSURE ASSESSMENT AT THE TIME OF
PULMONARY VALVE OPENING.
40. DIASTOLIC PULMONARY ARTERY PRESSURE
1)END-DIASTOLIC PRV.
• The DPAP is equivalent to the LA and LV end-diastolic pressure
(LVEDP) when evaluated in individuals without moderate or severe
PH.
• Normal range is between 6 and 12 mm Hg.
• In patients with a PVR of >200 dynes/s/cm–or a MPAP > 40 mm
Hg, the DPAP is higher (>5 mm Hg difference) than the mean
pulmonary capillary wedge pressure(PCWP).
• As demonstrated in Figure below, Doppler echocardiography can
be used to estimate DPAP by using the simplified Bernoulli
equation with the velocity of the pulmonic regurgitation (PR) jet at
end diastole providing the end-diastolic PA –RV gradient.
• The pulmonary artery diastolic pressure ( PADP) can be estimated
by adding the end-diastolic PA –RV to the RAP.
EDG + RAP = DPAP
41. • This measurement correlates well with invasive measurements.
• The most common errors in DPAP estimation have been
attributed to inaccurate estimation of RAP.
• However, the PR jet is not always detected (even with the use of
saline).
• Ristow et al demonstrated that a >5 mmHg end-diastolic
pulmonary regurgitant gradient seems to be correlated with
cardiac dysfunction, in particular with decreased functional
status, elevated serum B-type natriuretic peptide, elevated LV
mass index, and systolic and diastolic dysfunction.
• As with tricuspid regurgitation, weak pulmonary regurgitant
Doppler signals can be enhanced with the use of contrast, with
increased reliability of the dPAP estimate.
42. • Evaluation of diastolic and mean pulmonary artery pressure ( DPAP and MPAP) using
Doppler imaging of the pulmonic regurgitation ( PR) jet.
• The maximal velocity ( Vmax) is 281 cm/s (asterisk), and the velocity at end diastole is
195 cm/s (arrow).
• Using the Bernoulli equation: P = 4 × V2, the maximal pressure gradient of 32 mm Hg
between the pulmonary artery ( PA) and the right ventricle ( RV) during diastole is
calculated and corresponds with the MPAP. When added to the right atrial pressure (
RAP), this improves accuracy.
• The gradient at end diastole between the PA and the RV is also calculated and is 15
mm Hg. When added to the RAP, the DPAP is given.
43. 2)RV PRESSURE ASSESSMENT AT THE TIME OF
PULMONARY VALVE OPENING.
• It has been demonstrated that dPAP can be estimated
by measuring RV pressure at the time of pulmonary
valve opening, because RV and pulmonary pressures
are balanced at this point of the cardiac cycle.
• As discussed above, the gradient between the right
chambers can be estimated by the TRv.
• Therefore, the application of the simplified Bernoulli
equation to the TRv measured at the time of
pulmonary valve opening and the sum of this value
with RAP allows an estimation of dPAP.
44. • The TRv at the time of pulmonary valve opening is
measured by superimposing the time from the QRS
complex to the onset of pulmonary flow on the
regurgitation velocity envelope (Figure).
• This method has demonstrated a high correlation
with invasively measured dPAP.
• However, because the measurement is made on the
steep portion of the TRv slope, any small error in
timing measurement (or small differences in timings
between different cardiac cycles) could lead to large
errors in dPAP estimates.
45. RV pressure assessment
at the time of pulmonary
valve opening.
Transpulmonary flow (top)
and tricuspid regurgitant
flow (bottom).
Red lines: time between Q
wave and pulmonary valve
opening.
Blue line: TRv at the time
of pulmonary valve
opening.
46. RIGHT ATRIAL PRESSURE (RAP)
• Inferior vena cava size and collapsibility.
• Systolic filling fraction of hepatic venous flow.
• Ratio of tricuspid peak early inflow velocity to peak
early diastolic velocity of the lateral tricuspid annulus.
47. 1)INFERIOR VENA CAVA SIZE AND COLLAPSIBILITY.
• Because RAP is strictly correlated with central venous
pressure, the most frequently used technique for its
estimation is the observation of the diameter and
collapsibility of the inferior vena cava (IVC; Figure ).
• The IVC should be visualized in the subcostal view.
• The patient should be in the supine position, because IVC size
is significantly larger in the right lateral position and
significantly smaller in the left lateral position.
48. • IVC diameter should be measured within 2 cm of
the right atrium at end-expiration and end-diastole
and at end-inspiration or during a ‘‘sniff’’
maneuver; the decrease of its diameter with
inspiration (or the sniff maneuver) is a measure of
IVC collapsibility.
• It is important to remember that the IVC can be
dilated (>2 cm) in younger subjects despite normal
RAPs; IVC size should also be considered with
caution in patients who are mechanically
ventilated.
49. Echocardiographic evaluation of RAP using IVC dimension and collapsibility.
Subcostal 2DE during expiration (A) and inspiration(B) and M-mode echocardiography
(C) demonstrating good inspiratory collapse (asterisk) of the IVC (arrow) in a patient with
normal RAP and
2DE during expiration (D) and inspiration (E) and M-mode echocardiography (F)
demonstrating no inspiratory collapse of the IVC in a patient with elevated RAP.
50.
51.
52. 2)SYSTOLIC FILLING FRACTION OF HEPATIC VENOUS
FLOW.
Like the IVC, the hepatic veins are strictly associated with
central venous pressure and RAP, but unlike the IVC, it is
possible to easily analyze their flow using Doppler in
transthoracic echocardiography, because of their orientation.
Hepatic venous flow: how to obtain ?
• Optimize the subcostal view to obtain a clear view of the
IVC displayed in its long axis.
• Use color Doppler to identify and maximize hepatic vein
view; align the cursor as parallel as possible to the hepatic
vein.
• Use pulsed Doppler; place the sample volume (size, 5-7 mm)
1 to 2 cm into the hepatic vein; correct Doppler gain,
baseline, scale, and velocity to maximize curve view.
53. Normal hepatic venous flow consists of :
• 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.
54. Hepatic vein flow recorded from the subcostal view
with pulsed Doppler imaging.
55. • 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.
• For example, increased right atrial pressure has been
associated with a decrease in the systolic filling fraction of
hepatic vein flow.
• Thus, as right atrial pressure increases, antegrade systolic
hepatic vein flow decreases.
56. • In patients with severe tricuspid regurgitation, flow
reversal during ventricular systole is characteristic.
• As the tricuspid regurgitant jet is transmitted retrograde
into the right atrium, the normal antegrade systolic flow is
replaced by a prominent retrograde wave.
• In the setting of atrial fibrillation, retrograde flow during
atrial systole and the velocity of systolic antegrade flow are
diminished.
• In contrast, pulmonary hypertension typically results in
prominent flow reversal during atrial systole.
• Analysis of right atrial filling plays an important role in the
evaluation of patients with restrictive physiology and
constrictive pericarditis.
57. DOPPLER RECORDINGS OF HEPATIC VEIN FLOW.
A: Color flow imaging of hepatic vein flow (arrows).
B: A prominent systolic (sys) retrograde wave is consistent with significant tricuspid
regurgitation.
C: Variable flow patterns and significant respiratory variation are recorded from a patient
with atrial fibrillation. dias, diastole; sys, systole.
58. The sHVF is directly associated with the pressure gradient
between the hepatic veins and the right atrium; when RAP
increases, the gradient decreases along with sHVF.
In a study by Nagueh et al, the index showing the best
correlation with RAP was the
systolic filling fraction, calculated as the ratio between the
time-velocity integral (TVI) of sHVF and the sHVF TVI added
to the diastolic forward flow TVI (Figure).
sHVF TVI
sHVF TVI + dHVF TVI.
IF RATIO IS <55%,RAP > 8 mm Hg
59. 3)RATIO OF TRICUSPID PEAK EARLY INFLOW VELOCITY
TO PEAK EARLY DIASTOLIC VELOCITY OF THE LATERAL
TRICUSPID ANNULUS.
• Nageh et al evaluated the ratio of the tricuspid peak early
inflow velocity (Etr) to the peak early diastolic velocity of the
tricuspid annulus (E’tr) as an index of RV filling pressures,
paralleling the use of the ratio of the mitral peak early inflow
velocity to the peak early diastolic velocity of the lateral
mitral annulus as an index of LV filling pressures.
• Nageh et al showed a strong relation between Etr/E’tr and
RAP, also in patients on mechanical ventilation and with or
without RV systolic dysfunction:
• An Etr/E’tr ratio > 6 had 79% sensitivity and 73% specificity
for mean RAP >= 10 mm Hg.
• However, a recent study by Michaux et al demonstrated that
Etr/E’tr failed to predict RAP in anesthetized, paralyzed, and
mechanically ventilated patients.
60. PULMONARY FLOW MORPHOLOGY AND
ACCELERATION TIME. (PVAT)
• Under normal conditions, the Doppler pulmonary flow
velocity curve has, a dome like contour with a maximum
velocity in the middle of systole.
• In PH, it acquires a more triangular contour, with a peak
velocity in early systole, and in some cases a slower rise
during deceleration can be observed, resulting in midsystolic
notching.
• The PVAT, defined as the time interval from the onset of
forward flow in the pulmonary artery to the peak velocity of
this flow (Figure), has been demonstrated to be inversely
related to sPAP and mPAP.
• AcT is a highly feasible index.
61. • In a study by Lanzarini et al, an AcT< 93 ms
identified 67.4% of patients with PAH.
• In combination with other indexes of pulmonary
pressures, AcT can be a very powerful tool in PAH
diagnosis.
• In normal individuals, acceleration time exceeds
140 milliseconds and progressively shortens with
increasing degrees of pulmonary hypertension.
• Most have suggested that at an acceleration time of
less than 70 to 90 milliseconds, pulmonary artery
systolic pressures will exceed 70 mm Hg.
64. SPECTRAL FLOW PROFILES
RECORDED IN A NORMAL
INDIVIDUAL
(A)with an acceleration
time (AT) of 190
milliseconds and
(B) a patient with
significant pulmonary
hypertension in whom
the acceleration time is
80 milliseconds AT,
acceleration time.
65.
66.
67. RV MYOCARDIAL PERFORMANCE INDEX
• The myocardial performance index (MPI), or Tei index, is
defined as the ratio of isovolumic contraction time(IVCT)
plus isovolumetric relaxation time (IVRT) to systolic
ejection time.
IVCT + IVRT/ET
• This index is important in the assessment of RV
performance, as the active energy cycles of contraction
and relaxation occur during isovolumic contraction and
relaxation periods.
68. • In a recent study in a pediatric population with
idiopathic PAH, Dyer et al demonstrated that the RV
MPI is strictly related with invasive mPAP, independent
of TRv, and can be used to monitor mPAP after medical
therapy.
• In a small population with connective tissue disease,
Vonk et al demonstrated that an MPI > 0.36 combined
with sPAP threshold >= 35 mmHg might increase the
accuracy of echocardiography in predicting PAH.
• Further studies on larger and adult populations are
required to validate the role of the RV MPI in pulmonary
pressure evaluation.
69. PULMONARY VASCULAR RESISTANCE
• The PVR is directly proportional to the pressure gradient across
the entire lungs from the PAP to the left atrial pressure (LAP).
• PVR equals: [( MPAP – mean PCWP) × 80]/ CO and is a
hemodynamic variable, which contributes to the management of
patients with advanced cardiovascular and pulmonary disease.
• Normal values :
20 and 130 dynes/s/m/ cm–5, which equals
0.25 – 1.6 woods units ( WU).
• While increased SPAP may be secondary to increased backflow
from the heart, it can also be the cause of pulmonary vascular
disease.
• An elevated PVR is used to define PH, and it is also an essential
component in the evaluation of patients awaiting heart and lung
transplantation as well as in the determination of which patients
should have closure of their intracardiac shunt.
70. • Elevated values of PVR correlate with worse clinical outcomes and
prognosis in many different patient populations.
• Initial studies evaluating PVR noninvasively found only weak
correlations with invasive monitoring.
• However, using the maximal TR velocity and the RVOT VTI has
recently been shown to correlate well with the transpulmonary
pressure gradient and transpulmonary flow, respectively (which
are the parameters used for invasive estimation of PVR).
PVR ( WU) = 10 × TR velocity/ RVOT VTI + 0.16
• In patients with PVR < 2 WU, excludes pulmonary vascular
disease.
• This ratio has been validated in several studies, but in patients
with a very high PVR (>8 WU), its reliability as a quantitative
measurement is poor. .
71. PCWP
• PCWP is an invasively measured parameter used to quantify LV
filling pressures;
• This parameter is helpful in discriminating between PAH and
pulmonary venous hypertension (ie, secondary to LV disease;
the cutoff used is 15 mm Hg.
• Patients with PAH typically have Doppler mitral inflow patterns
of impaired relaxation (grade I diastolic dysfunction), with
normal E’ waves on DTI and E/E’ septal ratios < 10, despite high
sPAP.
• Gurudevan et al demonstrated that these findings are due
predominantly to low LV preload and underfilling rather than RV
hypertrophy, enlargement, and LV compression.
• In contrast, patients with high sPAP secondary to elevated left
atrial pressures and left-heart disease tend to have pulsed-wave
Doppler mitral inflow patterns of grade II or III, with increased
E/E’ ratios.
72. • e', the early diastolic velocity of mitral annulus as
obtained by tissue Doppler imaging (TDI) of the septal
and lateral sides of the mitral annulus behaves as a
pre-load-independent index of LV relaxation.
• Mitral inflow E velocity as obtained by pulsed-wave
(PW) Doppler when corrected for the influence of
relaxation by using E/e' ratio correlates well to the
mean pulmonary capillary wedge pressure (PCWP) as
obtained by simultaneous catheter measurements.
73. • It is preferable to use the average e' velocity obtained
from the septal and lateral sides of the mitral annulus
for the prediction of LV filling pressures.
• Because septal e' is usually lower than lateral e'
velocity, the E/e’ ratio using septal signals is usually
higher than the ratio derived by lateral e', and different
cutoff values should be applied on the basis of LV EF,
as well as e' location.
74. • E/e' ratio < 8 is usually associated with normal LV
filling pressures (PCWP < 15 mmHg),
• E/e’ ratio > 15 is associated with increased filling
pressures (PCWP > 15mmHg).
• Between 8 and 15, there is a gray zone with
overlapping of values for filling pressures.
e' = (e'lateral + e'septal) / 2
PCWP = 1.24 * (E/e') + 1.9
75.
76. PULMONARY ARTERIAL CAPACITANCE.
• Pulmonary arterial capacitance (PAC) measures
how much the aggregate pulmonary arteriolar tree will
dilate with each contraction of the right ventricle.
it reflects the ability of the pulmonary vessels to dilate
during systole and recoil during diastole.
• The capacitance index is a measure of right-heart load and lung
parenchyma status.
• It is a strong survival predictor in idiopathic PH: the lower the
PAC, the higher the mortality.
• In the past, a mathematical method to evaluate PAC was
elaborated and then validated in vivo in systemic and splanchnic
circulation; this method calculates PAC through stroke volume
(SV) and pulse pressure ratio.
77. • Recently, two studies validated the PAC calculation through
invasive and noninvasive SV and pulmonary pulse pressure
determination.
• In a study by Mahapatra et al, RVSV was assumed equal to LV SV
and thus determined by the product of LV outflow area (derived
from the diameter of the LV outflow tract from a parasternal
long-axis view) and the TVI of the LV outflow velocity obtained
from pulsed-wave Doppler.
• The sPAP was calculated using peak systolic TRv and dPAP from
end-diastolic PRv through the simplified Bernoulli equation and
adding estimated RAP.
• The final formula used to calculate PAC was thus
SV/4* TRv2 - PRv2
78. • In a study by Friedberg et al, the RV SV was calculated using the
pulmonary valve diameter measured in the parasternal short-
axis view or subcostal coronal or sagittal views and the RV
Doppler flow TVI.
• The sPAP was estimated using peak systolic TRv, while dPAP was
calculated as 0.49 *sPAP ; RAP was not added.
• Both studies demonstrated a high correlation between PAC
calculated from noninvasive and invasive parameters.
79. • Both studies have limitations connected to the accuracy and
feasibility of the measured parameters.
• LIMITATIONS
1. direct RV SV quantification requires clear visualization of the
pulmonary artery and pulmonary valve;
2. LV SV evaluation is more accurate, so the latter parameter
should be used unless more than mild aortic regurgitation is
present.
3. Finally, mathematical formulas should be avoided when
calculating dPAP, with direct Doppler assessment being
preferred.
80. PULMONARY ARTERIAL IMPEDANCE.
The pulmonary arterial impedance spectrum, defined as
the ratio of harmonic pressure to flow, reflects
a) proximal arterial stiffness,
b) distal vascular resistance,
c) wave transmission properties.
81. • Although pulmonary artery impedance could give a complete
description of the components of RV afterload and thus be
useful in the evaluation of patients with PH, its evaluation
requires pulmonary artery flow velocities measured by pulsed
Doppler echocardiography and instantaneous pressure
measurement evaluated by right-heart catheterization at the
same time.
• Therefore, it is a very difficult parameter to obtain, and at
present only a few clinical studies measuring pulmonary artery
impedance are available.
82. What Indexes Must Be Used:
• There are many parameters to evaluate pulmonary
hemodynamics.
• Clearly, it is not possible to calculate them all during a
standard echocardiographic exam; moreover, some
parameters, such as pulmonary compliance and pulmonary
impedance, are very challenging and time consuming to
obtain, so their use is limited mainly to a research setting.
• A basic but exhaustive evaluation of pulmonary
hemodynamics can be provided through the combination of 3
parameters.
84. When to Use These Indexes
When pulmonary pressures are increased, a complete
description of pulmonary hemodynamics with
pulmonary wedge pressure and PVR should be
performed.
86. PAH.
• PAH is characterized by highly increased pulmonary pressures
and PVR, while the pulmonary wedge pressure, in the absence
of primary LV dysfunction, is generally normal or mildly
increased.
• Among the various conditions that can lead to PAH, it is
important to remember congenital heart diseases, especially
those with relevant systemic-to-pulmonary shunts.
• The most advanced form of PAH associated with congenital
heart disease is Eisenmenger syndrome, in which an initial large
systemic-to-pulmonary shunt induces progressive pulmonary
vascular disease and PAH, with resultant reversal of the shunt
and central cyanosis.
87. PH DUE TO LEFT-HEART DISEASE.
• This condition is characterized by mild to moderate increases
in pulmonary pressures, with a notable increase in pulmonary
wedge pressure (so that the transpulmonary gradient is
low);PVR is generally normal.
• Although this is the usual presentation, in some cases, PAP is
notably elevated, and therefore PVR is increased.
• Any impairment of the left heart (systolic dysfunction, diastolic
dysfunction, valvular diseases) could lead to PH.
88. PH DUE TO LUNG DISEASES.
• When obstructive or restrictive lung involvement is
present, PH is generally modest, and PVR may be
mildly or moderately increased.
• PCWP, in the absence of concomitant left heart
disease, is normal or mildly elevated.
• A similar pattern is present in all conditions that
determine chronic hypoxia, including residence at
high altitude.
89. ACUTE PULMONARY EMBOLISM.
In the acute setting, pulmonary embolism causes only mild to moderate
increases in pulmonary pressures and PVR, and PCWP is generally normal in
the absence of concomitant left-heart disease;
the increases in PAP and PVR are correlated with the degree of pulmonary
vascular obstruction.
There are other echocardiographic findings, such as
• The McConnell sign (normal wall motion of the apex of the right ventricle
and abnormal wall motion in the mid free wall),
• The 60/60 sign (pulmonary flowAcT < 60 ms in the presence of right
atrioventricular pressure gradient =<60 mmHg), and
• The RV overload criteria (at least one of right-sided cardiac thrombus, RV
diastolic dimension in the parasternal view > 30 mm or RV/LV ratio > 1,
systolic flattening of the interventricular septum, and pulmonary flow AcT <
60 ms or right atrioventricular pressure gradient > 30 mm Hg in the absence
of RV hypertrophy),
which could greatly increase the diagnostic power of
echocardiography to identify an acute pulmonary embolism, especially when
concomitant lung disease is not present.
90. CHRONIC THROMBOEMBOLIC PULMONARY EMBOLISM.
• This condition occurs in up to 4% to 5% of patients after acute
pulmonary embolism.
• The hemodynamic pulmonary pattern is virtually
indistinguishable from that of PAH; again, PAP and PVR are
markedly increased, while PCWP is generally normal.
• The treatment of choice is surgical pulmonary endarterectomy.
91. CHANGES IN PAP, PCWP, AND PVR IN SEVERAL CLINICAL
CONDITIONS
92. APPARENTLY INCREASED PULMONARY PRESSURES IN HEALTHY
SUBJECTS
• Echocardiography can underestimate but also overestimate
pulmonary pressures.
• This is due to the overestimation of TRv (or PRv) (usually when
contrast is used to enhance the Doppler signal) but can also be
due to the overestimation of RAP (eg, in young patients when IVC
diameter is often >2 cm while RAP is normal.
• It should be noted that older and obese patients have
physiologic PAPs higher than younger and thinner subjects; in
these patients, a higher cutoff of PAP should be used before
reporting increased PAP to avoid false-positive results.
93. NOT INCREASED PULMONARY PRESSURES.
A complete description of pulmonary hemodynamics is
appropriate in some specific clinical conditions, even
when the PAP estimate is (or appears) within the normal
range.
94. DISEASES WITH THE POTENTIAL INVOLVEMENT OF PULMONARY
HEMODYNAMICS.
• It has been demonstrated that in chronic lung involvement, PVR
can also be increased in the absence of PH, especially in the
early phase of the disease.
• Because of its important role as a prognostic parameter in the
various pulmonary or systemic diseases that could determine
pulmonary vascular remodeling, PVR estimation could be
appropriate and potentially useful also in monitoring the course
of the disease.
• For this reason, it is important for complete evaluation of
pulmonary hemodynamics in the case of chronic obstructive
pulmonary disease, interstitial lung disease, collagen vascular
diseases, and cirrhosis.
95. APPARENTLY NORMAL PULMONARY PRESSURES.
A clinical condition in which the estimation of PAP by
echocardiography could be falsely normal is when
severe tricuspid regurgitation is present, in which RAP
could exceed the value of 20 mm Hg that is, generally,
the maximum value used in the noninvasive estimation
of RAP.
In this case, it is important to associate surrogate
indexes with a conventional PAP estimation to avoid
false-negative results.
96.
97. The study of pulmonary hemodynamics is of great
importance in many diseases directly or indirectly
involving the cardiopulmonary apparatus.
Therefore estimation of each and every parameter of
pulmonary hemodynamics to be done in suspected
cases of pulmonary disease.
CONCLUSION
