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19 Mitral andTricuspid Stenosis
263
Table 19.2
American Society of Echocardiography Recommendations
on ndings indicative of hemodynamically signicant tricuspid stenosis [1]
Findings of severe tricuspid stenosis
Mean pressure gradient
Inow VTI >60cm
PHT
Valve area by continuity equation
European Association of Echocardiography/
≥5mmHg
≥190ms
2
≤1cm
measurements can be acquired across the tricuspid
valve. As the RV inow velocities are affected by
respiration, all measurements taken should be averaged across the respiration cycle or be recorded at
end-respiration. By utilizing continuous wave doppler, the pressure gradient is calculated by utilizing
the simplied Bernoulli equation as previously
described. A mean pressure gradient greater than
5mmHg is considered severe tricuspid stenosis.
Pressure Half-Time
Evolving Evidence
Similar to the mitral valve, CWD can be
used to measure a pressure half-time to
grade tricuspid valve area and stenosis.
However, given the difference between
right and left heart atrio-ventricular com-
pliance and also because of the often-
concurrent tricuspid valve regurgitation,
this method has signicantly more variabil-
ity and there are far fewer validation stud-
ies of the tricuspid valve compared to the
mitral valve. Current consensus has agreed
that the tricuspid valve area can be calcu-
lated by equation below:
VA cm PHTms
2
190
/
Consequences
As tricuspid stenosis becomes increasingly
severe, patients develop increasing right atrial
pressures and venous congestion. Other echocar-
diographic ndings supportive of this pathophysiology include an enlarged right atrium and
dilated inferior vena cava. Symptomology wise,
this often manifests as hepatic congestion with
ascites, peripheral edema, and elevated liver
enzymes as generally seen in right heart failure
patients [11]. As tricuspid valve stenosis usually
has concurrent left heart valvular disease, patients
often have respiratory symptoms, however, if isolated tricuspid pathology, there should be an
absence of respiratory complaints [12].
Summary Points
• The most common etiology of mitral stenosis
and tricuspid stenosis globally is rheumatic
valvular disease.
• There are several ways to obtain an estimated
mitral valve area including direct 2-D or 3-D
planimetry, continuity equation calculation, or
via pressure half-time/deceleration time.
• The severity of stenosis is based on valvular
area, mean pressure gradients, and pulmonary
artery pressures.
• Tricuspid stenosis is rarely an isolated
pathology.
• There are a few ways to obtain a tricuspid
valve area but these come with limitations and
decisions about interventions often include
the patient’s symptomology.
Questions
1. If you measure a PHT of 240ms across the
mitral valve, what is the calculated MVA and
what severity of the stenosis does the patient
have?
(A) 0.92cm2, severe
(B) 3.45cm2, moderate
(C) 0.64cm2, severe
(D) 0.92cm2, moderate
Answer: A. 0.92cm2, severe. Mitral valve
area is calculated by 220 (ms cm2)/Pressure
half-time (ms). 220/240=0.92cm2. A mitral
valve area<1cm2 is severe.
2. Which of the following is not a validated
approach to obtain the MVA?
(A) Planimetry
(B) Continuity Eq.
264
N. Levin and C. Kelly
(C) Pressure Half-Time
(D) Pressure Gradient
Answer: D. Pressure Gradient. Pressure
gradient can offer insights into the severity of
stenosis, but is insufcient to calculate mitral
valve area. The other choices all offer quantitative methods to calculate mitral valve area.
3. Which of the following measurements is consistent with severe tricuspid valve stenosis?
(A) PHT of 170ms
(B) Mean pressure gradient of 8mmHg
(C) Tricuspid valve area of 1.2cm
2
(D) Inow VTI of 40cm
Answer: B. Mean pressure gradient of
8 mmHg. A is incorrect because a pressure
half-time of 170 would result in a TV area of
1.24cm2, and the time is lower than the threshold for severe stenosis, 190ms. The threshold
for severe stenosis is TV area of 1cm2. The
inow VTI is consistent with severe tricuspid
stenosis when it equals or exceeds 60cm.
References
1. Baumgartner H, Hung J, Bermejo J, Chambers JB,
Evangelista A, Grifn BP, etal. Echocardiographic
assessment of valve stenosis: EAE/ASE recommendations for clinical practice. Eur J Echocardiogr.
2009;10(1):1–25.
2. Iung B, Baron G, Butchart EG, et al. A prospective survey of patients with valvular heart disease in
Europe: the Euro Heart Survey on valvular heart disease. Eur Heart J. 2003;24(13):1231–43. https://doi.
org/10.1016/S0195- 668X(03)00201- X.
3. Lang RM, Goldstein SA, Kronzon I, Khandheria
B, Saric M, Mor-Avi V. 108-Rheumatic mitral stenosis. In: ASE’s comprehensive echocardiography.
Philadelphia: Elsevier; 2022.
4. Harb SC, Grifn BP.Mitral valve disease: a comprehensive review. Curr Cardiol Rep. 2017;19(8):73.
5. Silbiger J. Advances in rheumatic mitral stenosis:
echocardiographic, pathophysiologic, and hemodynamic considerations. J Am Soc Echocardiogr.
2021;34(7):709–722.e1.
6. Lang R, Goldstein S, Kronzon I, Khandheria B, Saric
M, Mor-Avi V. 109-Quantication of mitral stenosis. In: ASE’s comprehensive echocardiography.
Philadelphia: Elsevier; 2022.
7. Libanoff AJ, Rodbard S. Atrioventricular pressure half-time. Measure of mitral valve orice
area. Circulation. 1968;38(1):144–50. https://doi.
org/10.1161/01.cir.38.1.144.
8. Hatle L, Angelsen B.Doppler ultrasound in cardiology: physical principles and clinical applications,
118. Philadelphia: Lea and Febiger; 1985.
9. Teirstein PS, Yock PG, Popp RL. The accuracy of
Doppler ultrasound measurement of pressure gradients across irregular, dual, and tunnel like obstructions to blood ow. Circulation. 1985;72(3):577–84.
https://doi.org/10.1161/01.CIR.72.3.577.
10. Roberts W, Ko J.Some observations on mitral and
aortic valve disease. Baylor Univ Med Center Proc.
2008;21(3):282–99.
11. Coffey S, Rayner J, Newton J, Prendergast
BD. Right-sided valve disease. Int J Clin Pract.
2014;68(10):1221–6. https://doi.org/10.1111/ijcp.
12485.
12. Stapleton JF.Natural history of chronic valvular disease. Cardiovasc Clin. 1986;16(2):105–47.
Mitral andTricuspid Regurgitation
MouradH.Senussi
20
Learning Objectives
1. Describe primary and secondary causes of
mitral and tricuspid regurgitations
2. Review the use of Doppler to detect regurgitant jets
3. Discuss echocardiographic tools to characterize regurgitant jets
4. Analyze quantitative methods to grade the
severity of regurgitant lesions
Causes
Mitral and tricuspid regurgitation are conditions
in which there is incomplete coaptation of the
valve leaets, leading to retrograde ow of blood
from the ventricle to the atrium. The clinical consequence of tricuspid regurgitation is reected by
venous congestion and the clinical consequence
of mitral regurgitation is pulmonary congestion.
Etiologies are classied into primary (organic) or
secondary (functional) causes [1, 2]. Primary
(organic) causes are etiologies which represent
defects of the leaets whereas secondary (functional) causes are etiologies which involve annular dilatation.
M. H. Senussi (*)
Section of Cardiology, Baylor College of Medicine,
Houston, TX, USA
e-mail: Mourad.Senussi@bcm.edu
Primary Causes
• Valve Prolapse:
– Mitral Valve Prolapse (MVP): In MVP, the
mitral valve leaets bulge back into the left
atrium during contraction. This can lead to
improper valve closure and regurgitation
[3].
– Tricuspid Valve Prolapse: Similar to MVP,
tricuspid valve prolapse involves the tricuspid valve leaets bulging back into the
right atrium during contraction [2, 4].
• Valve Degeneration: Over time, the valves of
the heart can degenerate due to aging, wear
and tear, or other factors such as broelastic
deciency and myxomatous degeneration
(Barlow’s disease). This degeneration can
affect the proper functioning of the valves and
result in regurgitation [4].
• Rheumatic Heart Disease: Long-term inam-
mation and scarring associated with rheumatic
disease can also lead to functional mitral and
tricuspid regurgitation.
• Infective Endocarditis: Bacterial or fungal
infections of the heart valves (endocarditis)
can damage the valves, leading to regurgitation [2].
• Congenital Heart Defects: Congenital malfor-
mations of the mitral or tricuspid valve apparatus such as isolated cleft of the anterior
mitral valve, mitral valve prolapse associated
with Marfan’s or Ehler-Danlos syndromes,
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. J. Lanspa, A. T. Levinson (eds.), Echocardiography and Ultrasonography in the ICU,
Respiratory Medicine, https://doi.org/10.1007/978-3-031-80038-2_20
265
266
M. H. Senussi
Table 20.1
Jet area >10cm
Vena contracta >0.7cm
Jet density Equal to inow component, early peak, triangular [8, 10]
Effective regurgitant orice area >0.4cm
Regurgitant volume >45mL [8]
Regurgitant fraction Not dened >0.5
Metrics for severe tricuspid and mitral valve regurgitation
Tricuspid regurgitation Mitral regurgitation
2
[8] >50% LA size [9]
2
double orice mitral valve, arcade mitral valve
(thickened or absent chordae), and Ebstein’s
anomaly of tricuspid valve can lead to regurgitation [5, 6].
≥60mL [11]
ventricle and result in mitral valve insufciency and pulmonary hypertension and elevated right ventricular pressures can similarly
lead to mitral regurgitation.
• Connective Tissue Disorders: Conditions that
affect connective tissues, such as Marfan syndrome or Ehlers-Danlos syndrome, can lead to
abnormalities in the heart valves [1, 2].
A summary of jet area metrics for mitral and
tricuspid valvular regurgitation is found in
Table20.1.
• Trauma: Physical trauma to the chest or heart
externally can cause either mitral or tricuspid
regurgitation [1, 2].
Jet Area
• Iatrogenesis: Procedures such as pulmonary
artery catheters and pacemaker leads can
cause damage or restrict the valve leaets
leading to tricuspid regurgitation.
• Tumors: Tumors within the heart such as left
atrial myomas and carcinoid tumors though
rare, affect valve function and can lead to both
stenosis and regurgitation.
Often the rst indication of the presence of valvular insufciency is an appreciable regurgitant
jet seen with color Doppler. When color Doppler
is applied over a valve with regurgitant ow, the
regurgitant jet will have the color spectrum
“opposite” that of antegrade ow. It should be
noted that the size of a jet area does not translate
into the severity of retrograde ow, rather, it simply highlights the distribution of regurgitant
Secondary Causes
velocities [10]. In other words, a generous jet
area does not imply a high regurgitant volume
• Ischemic heart disease: Ischemia can cause
papillary muscle rupture and/or ventricular
dysfunction leading to enlargement of the
ventricles, annular dilatation, and displacement of the valve leaets resulting in incomplete coaptation of the leaets during systole
causing regurgitation.
• Dilated Cardiomyopathy: Enlargement of the
heart chambers, often associated with dilated
cardiomyopathy, causes insufcient coaptation
of the valve leaets leading to regurgitation [7].
• Hypertension: Chronic hypertension can lead
to changes in the structure of the heart, including the valves, and contribute to regurgitation
[7]. Mitral annular dilation from chronic systemic hypertension and remodeling of the left
[10, 12]. Additionally, the area of a regurgitant jet
should be contextualized to the size of the chamber in which the regurgitation occurs. The denition of jet area is the area of the regurgitant jet
divided by the total chamber size. For example,
mitral regurgitation jet area=mitral regurgitation
jet size/left atrial size. An example of a jet area is
seen in Fig.20.1. Large atrial sizes likely indicate
chronic regurgitation.
Regurgitant jets can be categorized as either
central or eccentric depending on its relationship
to the valve annulus. Central jets are often from a
functional etiology, where the valve annulus is
dilated as opposed to organic etiologies which
create eccentric jets because of structural injury
to the leaets.
20 Mitral andTricuspid Regurgitation
Fig. 20.1 Right-hand panel: highlighted in yellow is the
LA area. Left-hand panel: arrow demonstrates the jet area
Several factors may accentuate a jet area.
First, high driving pressures from the left ventricle to the left atrium may increase the jet area.
Second, when multiple jets are present, the jet
area often overestimates regurgitant severity
[13]. Third, central, often high-velocity jets often
recruit blood (“entrain”) from the chamber which
may augment the jet area. Once a regurgitant jet
has been identied, the next step should be dening the regurgitation severity by quantitative
metrics.
Vena Contracta
The vena contracta (VC), seen in Fig. 20.2, is
dened as the narrowest point of the highest
velocity regurgitant jet at the ow convergence
region between the ventricle and atrium [1, 12,
14]. The width or diameter of the regurgitant jet
is measured at this narrowest point. Vena contracta measured by either transthoracic or transesophageal echocardiography is usually reliable
if the jet is symmetrical [1, 12]. A width greater
than 0.7cm is indicative of severe regurgitation.
However, the vena contracta width is not a reliable measure of severity with multiple jets and
may vary under dynamic changes and different
afterload conditions and additional parameters
are required to quantify the severity of the regurgitation [1, 12].
267
Fig. 20.2 Vena contracta measurement in mitral
regurgitation
Jet Density
When performing continuous wave Doppler
(CWD) through a valvular apparatus with regurgitant ow, there will be a regurgitant velocity jet
whose density is proportional to erythrocyte density and severity [14, 15]. To maximize the signal,
place the CWD through the VC as seen in Fig.20.3
[12]. The more severe the regurgitation, higher
velocities will occur in early systole, and as pressures between chambers equilibrate quickly, the
CWD morphology will appear more triangular
than parabolic. One caveat to the triangular
appearance of the CWD with severe regurgitation
is that prosthetic valves often have a similar morphology. For tricuspid valve regurgitation, jets
can be best appreciated in the parasternal long
right ventricular inow view or an apical 4-chamber view. For mitral valve regurgitation, jets are
best appreciated in the apical 4-chamber view.
While it is possible to identify mitral regurgitation
in parasternal views, the ultrasound beam is not
parallel to regurgitant ow.
Tricuspid CWD provides rapid insight regarding right-heart hemodynamics. By way of the
modied Bernoulli equation, right ventricular
268
RVSP
=+
V
max
Fig. 20.3 Continuous
wave Doppler (CWD)
through the mitral valve
M. H. Senussi
systolic pressure (RVSP), can be estimated by
adding the right atrial pressure to the tricuspid
valve gradient:
2
4
RAP
TR
.
Assuming there is no gradient across the pulmonic valve, RVSP equals pulmonary artery systolic pressure (PASP). Although values greater
than 60mmHg are more likely to reect chronic
pulmonary hypertension (PH), the relationship
between echocardiogram-derived PASP and right
heart catheterization PASP in known PH is often
unreliable [16].
Pressure Half-Time
Although originally studied in mitral stenosis,
pressure half-time is a marker of regurgitation
severity [17]. A pressure half-time (PHT) is
dened as the amount of takes that it takes for a
peak pressure gradient to decrease by 50%.
Commonly used in the assessment of mitral stenosis and aortic insufciency severity, PHT is
also used to estimate mitral valve area. PHT is
not commonly used in the assessment of tricuspid and/or mitral regurgitation.
Proximal Isovelocity Surface Area,
Eective Regurgitant Orice Area,
Regurgitant Volume,
andRegurgitant Fraction
The severity of clinical consequence is proportional to the degrees of regurgitant ow. Several
quantitative methods exist to grade the severity of
regurgitant lesions. The proximal isovelocity surface area (PISA) method is predicated on principles of uid dynamics which makes several
assumptions, most notably a constant, laminar
ow before entering the orice. PISA is used to
calculate volumetrics when quantifying regurgitation, such as effective regurgitant surface area
(EROA) and regurgitant fraction (RF). PISA also
assumes that as blood nears the orice, that there
is an acceleration of blood which peaks at the
narrowest portion of the orice [18]. Using color
20 Mitral andTricuspid Regurgitation
269
Doppler, speeds of blood cells can be mapped in
the immediate area around the valve.
Conceptually, this ow acceleration can be modeled by a series of concentric spheres of blood
moving at increasing velocities until reaching the
center.
PISA leverages one of the artifacts of color
Doppler, aliasing. Aliasing occurs when observed
velocities exceed that of the set Nyquist limit.
The rst step to measuring PISA is to identify the
aliasing velocity and to measure the PISA radius
on the ventricular side of the valve as seen in
Fig.20.4 [18]. The aliasing velocity can be identied in the regurgitant jet where there is an
abrupt reversal in velocities (turning from blue to
red, for example) near the VC.At the point where
the color transition is located is exactly the
Nyquist limit and therefore the velocity of the
blood at that radius [15]. It is understood that the
surface area of a sphere is 4πr2, and therefore, the
surface area of a hemisphere, excluding the at
base, is 2πr2. Therefore, the hemispheric area, the
PISA=2πr2.
In uid dynamics, ow is dened as an
amount of uid passing a particular point per
unit time. As such, ow can be expressed as the
cross- sectional area of the orice times the
velocity of the uid (Q=A×V). It is also understood that the continuity equation holds across a
valve: A1×V1=A2×V2. The continuity equation
yields insight into the area of the regurgitant orice, the EROA.If EROA is considered as A1, V1
then represents the maximum velocity of the
blood traversing the regurgitant orice. V1 can
be obtained by measuring the maximum regurgitant velocity on continuous wave Doppler
through the valve (Fig.20.3). Both A2 and V2 are
known: 2πr2 and the Nyquist limit, respectively.
Therefore, EROA = (2π r2 × Nyquist
Limit)÷V
. It should be noted that for non-
max
holosystolic MR, this method overestimates its
severity [19].
One of the assumptions of PISA is that the
regurgitant orice occurs on a at surface (i.e.,
180°). With progressive leaet distortion, a correction factor is applied to the EROA equation by
multiplying the EROA by the ventricular side
angle of the leaets divided by 180:
EROA×(∢/180).
The total volume of blood that regurgitates
through the valve is known as Regurgitant
Volume (RV) [11]. RV may be deduced by PISA
and velocity-time-integrals (VTI) techniques.
Analogous to calculation of LV stroke volume,
RV = EROA× VTI. Consequently, regurgitant
fraction (RF) is dened as the ratio of retrograde
ow to total valvular ow (antegrade plus retrograde ow). In other words, RF=RV/SV.
Fig. 20.4 Proximal isovelocity surface area (PISA)
radius in mitral valve regurgitation
Summary Points
• Primary (organic) causes are etiologies which
represent defects of the leaets whereas sec-
ondary (functional) causes are etiologies
which involve annular dilatation.
• When color Doppler is applied over a valve
with regurgitant ow, the size of a jet area
does not translate into the severity of retro-
grade ow but shows the distribution of regur-
gitant velocities.
270
M. H. Senussi
• Vena contracta width is a key parameter used
in the assessment of valvular regurgitation. It
represents the narrowest portion of the regurgitant jet and is measured by color Doppler
ow mapping
• The proximal isovelocity surface area (PISA)
is used to calculate volumetrics when quantifying regurgitation utilizing the color Doppler
artifact aliasing
Questions
1. A 62-year-old man presents with complaints
of exertional dyspnea and fatigue. Cardiac
examination reveals a holosystolic murmur
heard best at the apex, radiating to the axilla.
Echocardiography demonstrates a regurgitant
jet originating from the mitral valve. Which of
the following parameters is commonly used to
assess the severity of mitral regurgitation and
is measured at the narrowest point of the
regurgitant ow?
A. Vena contracta width
B. Ejection fraction
C. Aortic valve area
D. Left atrial size
Answer: A vena contracta width Explanation:
Vena contracta width is a key parameter used
in the assessment of valvular regurgitation. It
represents the narrowest portion of the regur-
gitant jet and is measured in the color Doppler
ow mapping. In the context of mitral regur-
gitation, a wider vena contracta is indicative
of more severe regurgitation. The other
options are not specically used to assess the
severity of mitral regurgitation based on vena
contracta.
2. Which of the following metrics is unable to
reliably indicate valvular severity?
A. EROA
B. RF
C. Jet area
D. Vena contracta
Answer: C Jet Area Explanation: Color
Doppler is able to identify presence or absence
of valvular regurgitation and identify the range
of velocities of the regurgitation, however, does
not indicate the severity of a regurgitant lesion.
3. Which of the following echocardiographic
artifacts is utilized to gauge severity of mitral
regurgitation?
A. Mirroring
B. Aliasing
C. Shadowing
D. Stitching
Answer: B Aliasing Explanation: Aliasing
occurs when observed velocities are outside
of the preset Nyquist limits. Identication of
the aliasing velocity is integral into the PISA
method to determine regurgitant lesion
severity.
References
1. Chan KMJ. Functional mitral and tricuspid regurgitation: pathophysiology, assessment and treatment.
Springer; 2016.
2. Dal-Bianco JP, Beaudoin J, Handschumacher MD,
Levine RA.Basic mechanisms of mitral regurgitation.
Can J Cardiol. 2014;30(9):971–81.
3. Spartalis M, Tzatzaki E, Spartalis E, etal. Mitral valve
prolapse: an underestimated cause of sudden cardiac
death—a current review of the literature. J Thorac
Dis. 2017;9(12):5390–8.
4. Apostolidou E, Maslow AD, Poppas A. Primary
mitral valve regurgitation: update and review. Glob
Cardiol Sci Pract. 2017;2017(1):e201703.
5. Nalawade D, Borikar N, Bawaskar P, Chaurasia
A. Anomalous papillary muscle insertion as
a cause of mitral regurgitation: multimodality
imaging- based diagnosis. Circ Cardiovasc Imaging.
2020;13(12):e010592.
6. Ginghină C, Vlădaia A, Ghiorghiu I, Serban M,
Popescu BA, Jurcuţ R.Echocardiography in congenital mitral valve regurgitation—the liaison between cardiologist and surgeon. J Med Life. 2009;2(4):407–13.
7. Asgar AW, Mack MJ, Stone GW. Secondary mitral
regurgitation in heart failure: pathophysiology, prognosis, and therapeutic considerations. J Am Coll
Cardiol. 2015;65(12):1231–48.
8. Hahn RT. State-of-the-Art review of echocardiographic imaging in the evaluation and treatment of functional tricuspid regurgitation. Circ
Cardiovasc Imaging. 2016;9(12):e005332. https://doi.
org/10.1161/CIRCIMAGING.116.005332.
9. Zoghbi WA, Adams D, Bonow RO, et al.
Recommendations for noninvasive evaluation of
native valvular regurgitation: a report from the
American Society of Echocardiography Developed
in Collaboration with the Society for Cardiovascular
Magnetic Resonance. J Am Soc Echocardiogr.
2017;30(4):303–71.
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271
10. Grayburn PA, Weissman NJ, Zamorano
JL.Quantitation of mitral regurgitation. Circulation.
2012;126(16):2005–17. https://doi.org/10.1161/
CIRCULATIONAHA.112.121590.
11. Otto CM. Textbook of clinical echocardiography.
Elsevier; 2018.
12. American Society of Echocardiography. ASE’s comprehensive echocardiography. Elsevier; 2021.
13. Lin BA, Forouhar AS, Pahlevan NM, et al. Color
Doppler jet area overestimates regurgitant volume when multiple jets are present. J Am Soc
Echocardiogr. 2010;23(9):993–1000.
14. Zoghbi WA, Enriquez-Sarano M, Foster E, et al.
American Society of Echocardiography: recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler
echocardiography: a report from the American
Society of Echocardiography’s Nomenclature and
Standards Committee and The Task Force on Valvular
Regurgitation, developed in conjunction with the
American College of Cardiology Echocardiography
Committee, The Cardiac Imaging Committee,
Council on Clinical Cardiology, The American Heart
Association, and the European Society of Cardiology
Working Group on Echocardiography, represented by.
Eur J Echocardiogr. 2003;4(4):237–61.
15. Armstrong WF, Ryan T, Feigenbaum H.Feigenbaum’s
echocardiography. Wolters Kluwer; 2019.
16. Fisher MR, Fora PR, Chamera E, et al. Accuracy
of Doppler echocardiography in the hemodynamic
assessment of pulmonary hypertension. Am J Respir
Crit Care Med. 2009;179(7):615–21.
17. Holen J, Simonsen S.Determination of pressure gradient in mitral stenosis with Doppler echocardiography. Heart. 1979;41(5):529–35.
18. Lambert AS.Proximal isovelocity surface area should
be routinely measured in evaluating mitral regurgitation: a core review. Anesth Analg. 2007;105(4):940–3.
19. Grayburn PA, Thomas JD. Basic principles of the
echocardiographic evaluation of mitral regurgitation.
JACC Cardiovasc Imaging. 2021;14(4):843–53.
Calculation ofIntracardiac
P
dv
dt
1
()
=
P Pv
42
−=
()
Pressures Using Doppler Flow
CourtneyBennett
21
Learning Objectives
1. Describe the principle of conservation of
energy and the Bernoulli equation.
2. Understand how the Bernoulli equation can
be simplied and applied to measure pressure
gradients between two chambers in the heart.
3. Understand the limitations of the Bernoulli
equation.
4. Know how to calculate intracardiac pressures
using the measured pressure gradient and a
known pressure of one cardiac chamber.
The Bernoulli Equation
The assessment of intracardiac pressures and
valve stenoses by echocardiography has been
validated using ultrasound Doppler signals and
applying the Bernoulli principle, which states
that in the streamline ow of uid, the sum of all
forms of energy along that path is equal
(Fig.21.1) [1–3]. This concept is also described
as the conservation of energy.
Bernoulli Equation
−= −
C. Bennett (*)
Mayo Clinic College of Medicine and Science,
Rochester, MN, USA
e-mail: Bennett.Courtney@mayo.edu
ρρ
21
()
2
1
Pvv
12
2
+×→+ →
∫
R
ds v
Pressure decreaseconvective acceleration
flow acceleratio
+ nnviscous friction+ .
The Bernoulli equation may be modied by
assuming that the contribution from both ow
acceleration and viscosity are negligible in clinical applications. The upstream velocity (v12) of
blood ow is also negligible and may be excluded
in most settings. Finally, the mass density of
blood (ρ) of convective acceleration is a constant
and equal to approximately 4. Applying these
assumptions, the simplied Bernoulli equation
can be used to estimate pressure gradients
between the chambers of the heart.
Simplied Bernoulli Equation
In the presence of valvular regurgitation or an
intracardiac shunt, the peak velocity of that blood
ow is proportional to the difference in pressure
between the two cardiac chambers (see Fig.21.2)
[4]. If the pressure of one chamber is known,
such as jugular venous pressure as right atrial
pressure or the systemic blood pressure, then
intracardiac pressures may be derived.
There are limitations to the application of the
Bernoulli equation that are important to recognize in clinical practice. For example, if there are
lesions in series, such as in the clinical scenario
of concomitant left ventricular outow tract
obstruction and aortic valve stenosis, then the
upstream velocity (v1
12
2
) is no longer negligible
2
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. J. Lanspa, A. T. Levinson (eds.), Echocardiography and Ultrasonography in the ICU,
Respiratory Medicine, https://doi.org/10.1007/978-3-031-80038-2_21
273