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336
S. Bain and B. Ohlson
racic pressure promotes systemic venous return,
and RV lling is enhanced. Conversely, pulmonary venous (PV) ow to the left atrium is
reduced in inspiration (largely due to the intrathoracic/extrapericardial location of the pulmonary veins), with a subsequent reduction in LV
end-diastolic volume. In expiration, changes to
lling pressures are reversed with enhanced LV
lling and reduced RV lling. A normally compliant pericardium allows for a septal shift, ventricular distensibility, and minimal impact on
hemodynamics.
The fundamental pathway leading to the ndings of CP results from inammation leading to
the formation of a non-compliant pericardial scar
[5]. As brinous changes encase the heart and
obliterate the normal pericardial space, diastolic
function is impaired. Rather than acting as a reservoir and structural support for ventricular lling,
the brotic and calcied pericardium forms a rigid
complex with the ventricle. The rigidity of the ventricular/pericardial structure leads to an early
increase in diastolic lling pressures and minimal
distensibility. With this progressive impairment in
ventricular relaxation, lling pressures across the
cardiac chambers increase and equalize, cardiac
output decreases, and venous pressure rises.
The underlying lack of ventricular compliance
drives the hemodynamic changes seen with constrictive pericarditis. In general, exaggerations of
ventricular interdependence and respirophasic
changes in ventricular lling occur with constriction [6, 7]. During inspiration, intrapleural pressure is reduced with the expected decrease in PV
inow pressure. However, the constrictive
encasement of the heart functionally limits the
transmission of intrathoracic pressure changes to
the heart so that left atrial pressure is less reduced
than expected, resulting in a decreased pressure
gradient and decreased left-sided lling. This,
coupled with limited pericardial compliance,
forces septal shifting from right to left (as the
right-sided chambers are favored). As left-sided
lling falls with inspiration, a pronounced
(>10 mmHg) drop in systolic blood pressure
occurs—the classic nding of pulsus paradoxus.
During expiration, the reversal occurs with
increased intrapleural pressure and restoration of
the pressure gradient from the PVs to the left
atrium. This allows left heart lling but at the
expense of right heart lling due to septal shift in
a xed space.
Signs and symptoms of constrictive pericarditis are reective of right-sided failure in the setting of normal-appearing ventricular function.
Typical patients present with evidence of peripheral edema, fatigue, and dyspnea on exertion [8].
Signs of constriction include pulsus paradoxus,
Kussmaul’s sign (increased jugular venous distention with inspiration), a pericardial “knock”
on auscultation, and a congested abdomen.
Echocardiographic Diagnosis
Clinical identication of constrictive pericarditis
can be challenging (and frequently missed) as it
can manifest with general symptoms of heart failure [9]. Two-dimensional and Doppler echocardiography should be utilized as an initial
diagnostic tool to identify and differentiate constrictive pericarditis from other causes of heart
failure, specically restrictive cardiomyopathy,
severe tricuspid regurgitation (TR), and tamponade. While some cases might require computerized tomography, MRI, cardiac catheterization,
or surgical visualization for denitive diagnosis,
transthoracic echocardiography is effective and
noninvasive in the evaluation of patients with
suspected CP.
The echocardiographic ndings of CP are due
to increased ventricular interdependence (or
enhanced ventricular interaction) in a xed space
and the
intracardiac pressures [9]. There is usually
some level of ventricular dependence with a normal pericardium, but this is enhanced with a
thickened sac. This noncompliant pericardial sac
also insulates cardiac chambers from changes in
intrathoracic pressures [9].
dissociation of intrathoracic-
26 Pericarditis andConstriction
337
Evolving Evidence
In the largest, blinded study to date, 130 patients
with surgically conrmed constrictive pericarditis in comparison to 36 patients with restrictive
disease or severe TR was conducted by the Mayo
Clinic group that evaluated the test performance
of ve principal echocardiographic ndings in
the diagnosis of CP, including (1) respirationrelated ventricular septal shift, (2) variation in
mitral inow E velocity, (3) medial mitral annular
velocity, (4) ratio of medial mitral annular e’ to
lateral e’, and (5) hepatic vein expiratory diastolic reversal ratio [10].
All ve varied signicantly between the
groups, and all but mitral inow velocity
remained signicantly different in patients with
atrial brillation or utter.
Three of the variables were independently
associated with CP: (1) ventricular septal shift,
(2) medial mitral e’, and (3) hepatic vein diastolic
reversal ratio. The presence of septal shift in
combination with either medial mitral e’≥9cm/s
or hepatic vein diastolic reversal ratio≥0.79 was
sensitive (87%) and specic (91%) for a diagnosis of constrictive pericarditis [6, 10].
When pericardial disease is suspected, an
echocardiographic examination should include
the 2D appearance of septal motion and the
IVC and Doppler interrogation of mitral
inow, the medial and lateral mitral annulus,
and the hepatic veins (9), with specic attention
to ventricular septal shift, medial mitral e’ velocity, and hepatic vein reversal ratio; otherwise,
constrictive physiology could be overlooked. [6]
Two-Dimensional Evaluation
Septal Motion
Analysis of septal wall motion reveals two main
abnormalities in patients with CP physiology,
including a septal bounce and a respirophasic
septal shift [9]. The septal bounce is essentially a
shuddering or oscillatory motion [10] of the septal wall during diastole and is due to the difference in the diastolic pressures of the right (RV)
and left ventricle (LV) (Video 26.1). It should be
noted that this can look like postoperative pacing
[9]. A more specic observation is the bulging of
the septum towards the LV during inspiration and
then towards the RV in expiration [9]. LV lling
decreases during inspiration (secondary to the
decreased gradient between the PVs and LV) and
the septum shifts towards the LV as the RV has
increased lling. The opposite then occurs during
expiration. This phenomenon is due to both the
dissociation of intrathoracic-intracardiac pressures and the ventricular interdependence in the
xed space caused by the noncompliant pericardium [10]. It can be observed in multiple views
using 2D and M-mode.
Imaging oftheIVC
Plethora or dilatation of the inferior vena cava is
a common nding in CP given the expected
increased venous pressure but alone does not differentiate from restrictive physiology [6].
Other 2D Findings
Assessment of the pericardial thickness can
assist in making a diagnosis but 2D transthoracic
echocardiography and M-mode have shown poor
sensitivity and correlation to anatomic specimens. Transesophageal echocardiography has a
higher specicity and sensitivity to detect thickened pericardium, but note that one in ve
patients with CP will have a normal pericardium,
and an isolated thickened pericardium should not
conrm the diagnosis [11].
Tethering of the RV free wall to the liver
rather than the normal sliding motion has been
observed in CP as has the distortion in the
appearance of the contour of the RV and LV
[6, 10].
338
S. Bain and B. Ohlson
Doppler Evaluation
Mitral Inow Pulse-Wave Doppler
The dissociation of intrathoracic and intracardiac
pressures that is a hallmark of CP physiology is
demonstrated with pulse wave Doppler interrogation of the mitral inow as an inspiratory
decrease in mitral E velocity [10]. This is due to
the decreased gradient between the PVs and LV
during inspiration with the opposite occurring
during expiration. This respiratory variation
should not be observed in restrictive physiology
or severe TR, as there should not be a dissociation
of pressures [10]. The percent change of mitral E
velocity during respiration can be calculated as
follows: [(expiratory velocity − inspiratory
velocity)/expiratory velocity×100] and ranges
from 15%–35% in constrictive physiology [6]
(Fig. 26.1). While this variation can be compromised in the setting of high left atrial pressures
and atrial arrhythmias [6], it can still be appreciated by utilizing extended recording clips [11].
Hepatic Vein Pulse-Wave Doppler
The phenomena of both intrathoracic and intracardiac pressure dissociation and interventricular
dependence in CP are further demonstrated by
the assessment of the hepatic vein ow velocities
during respiration. As LV lling is increased during expiration, the septum shifts towards the
right, and right-sided chamber lling decreases.
Subsequently, hepatic vein forward ow is
decreased with a pronounced reversal of ow
during diastole. During inspiration, right heart
lling increases, and the diastolic hepatic vein
ow reversal becomes less prominent [6, 9, 10].
The expiratory diastolic reversal ratio (expi-
ratory diastolic reversal velocity/diastolic forward velocity) can be used to quantify the
respirophasic hepatic vein velocities with higher
values expected in CP (Fig. 26.2). The Mayo
Clinic Criteria identied that a reversal ratio of
≥0.79 was the most specic (88%) for CP (and
the most specic of the ve variables studied)
[10].
Fig. 26.1 Pulse-wave
Doppler mitral inow
velocities during
inspiration and
expiration utilizing a
respirometer. The yellow
marker is the E velocity
during inspiration, and
the blue marker is the
expiratory E velocity.
There is a percent
change of approximately
25% [(expiratory
velocity−inspiratory
velocity)/expiratory
velocity × 100]
26 Pericarditis andConstriction
Fig. 26.2 Pulse-wave
Doppler hepatic vein
velocities. The red
marker is the expiratory
diastolic reversal
velocity, and the blue
marker is the diastolic
forward velocity. The
ratio (expiratory
diastolic reversal
velocity/diastolic
forward velocity) is
approximately 1
339
Tissue Doppler oftheMitral Annulus
Doppler echocardiography of the diastolic mitral
annular tissue velocity (e’) allows evaluation of
myocardial relaxation [10]. In constrictive pericarditis (vs. restrictive myocardial disease), the
myocardium is usually spared and exhibits normal to supranormal motion [6] so higher e’
velocities in patients with heart failure should be
a sign of constriction. It should be noted that e’
velocities would be higher in primary CP vs postoperative or radiation-related cases of CP and
that lateral annular e’ velocities might be lower
than medial e’ velocities given the possibility that
the lateral myocardium can be tethered to the
pericardium (annulus reversus) [6, 9].
The Mayo Clinic study demonstrated that a
medial e’>9.0cm/s (Fig. 26.3) was the optimal
cutoff for constrictive physiology in a patient
with heart failure with a sensitivity of 83% and
specicity of 81% [6, 9, 10]. Note other
publications and texts refer to e’>8.0cm/s as the
limit to identify CP [12, 13].
Given that the e’ velocity is preserved (or
higher) in these patients, the E/e’ velocity ratio
will be lower than expected in the setting of
higher left-sided lling pressures (annulus paradoxus) [6, 10].
340
Fig. 26.3 This is an
example of a pulse-wave
tissue Doppler of the
medial mitral annular
velocity (e’). The yellow
marker denotes an e’ of
15.5cm/s
S. Bain and B. Ohlson
Summary Points
• Previously, tuberculosis was the most common etiology of constrictive pericarditis. Now
the most dominant causes are idiopathic, postsurgical, and post-radiation.
• Constrictive pericarditis is a type of diastolic
heart failure with preserved systolic function
in patients presenting with common rightsided heart failure symptoms like peripheral
edema, fatigue, and dyspnea on exertion.
• The pathophysiology is unique from other etiologies due to the dissociation of intracardiac
and intrathoracic pressures and enhanced ventricular dependence secondary to a stiff, noncompliant pericardial sac but preserved
myocardial function.
• Utilization of 2D and Doppler echocardiography facilitates successful identication and
diagnosis of constrictive pericarditis from
other forms of diastolic heart failure.
• In patients with diastolic heart failure or suspected pericardial disease, the echocardiography exam should include specic attention to
ventricular septal shift, mitral inow velocities, mitral annular tissue velocities, hepatic
vein diastolic ow reversal, and IVC
appearance.
• Current evidence suggests that 3 variables
(ventricular septal shift, medial mitral e’, and
hepatic vein expiratory diastolic reversal ratio)
are independently associated with the diagnosis of constrictive pericarditis.
Questions
1. All of the following hemodynamic changes
are true EXCEPT:
A. Early, elevated diastolic lling pressures
result from brous thickening of the
pericardial- ventricular complex in constrictive pericarditis.
B. Pulmonary venous drainage shows intra-
thoracic pressure dissociation in constrictive pericarditis.
C. Septal bowing from right to left results in
exaggerated systemic blood pressure
decreases in constrictive pericarditis.
D. Signs and symptoms of constrictive peri-
carditis are non-specic and show signicant overlap with other causes of cardiac
dysfunction.
E. Patients with restrictive cardiomyopathy
maintain normal intrathoracic/intracardiac pressure variability.
Answer/Explanation: B.
26 Pericarditis andConstriction
341
The pulmonary venous system (and thus
left atrial occlusion pressure) is primarily
extrapericardial and remains signicantly
inuenced by intrathoracic pressure changes
while the remainder of the heart shows intrathoracic/intracardiac pressure dissociation in
constrictive pericarditis. This dissociation is
the result of the brous complex formed
between the heart/pericardium. Similarly, the
rigid complex causes impaired relaxation of
the ventricles and early, elevated diastolic lling pressures. The right-to-left septal bowing
is evidence of exaggerated interventricular
dependence and reduced left-sided lling
pressures, leading to a decrease in blood pressure. Constrictive pericarditis often appears as
non-specic RV failure and a hallmark nding to help differentiate it from restrictive cardiomyopathy is the response to intrathoracic
pressure changes.
2. Which of the following echocardiographic
ndings is FALSE when differentiating
between constrictive pericarditis (CP)and
restrictive cardiomyopathy (RCM)?
A. There are usually enlarged right and left
atria in RCM whereas patients with CP
have smaller atrial size.
B. CP is characterized by respirophasic sep-
tal bowing while there is little septal shift
in RCM.
C. Medial mitral annular tissue velocities
(e’) are preserved in both CP and RCM.
D. There is minimal respiratory variation in
mitral and pulmonary vein inow in
patients with RCM.
Answer/Explanation: C.
In restrictive myocardial disease, mitral
annular motion will be inhibited (decreased
e’) both medially and laterally. In constrictive
pericarditis (without concurrent restrictive
disease), the medial mitral annular motion
should be preserved or exaggerated. Lateral
annular motion might be reduced due to pericardial tethering.
References
1. Mori M, Mullan CW, Bin Mahmood SU, etal. Us
national trends in the management and outcomes of
constrictive pericarditis: 2005-2014. Can J Cardiol.
2019;35(10):1394–9.
2. Robertson R, Arnold CR. Constrictive pericarditis
with particular reference to etiology. Circulation.
1962;26:525–9.
3. George TJ, Arnaoutakis GJ, Beaty CA, Kilic A,
Baumgartner WA, Conte JV. Contemporary etiologies, risk factors, and outcomes after pericardiectomy.
Ann Thorac Surg. 2012;94(2):445–51.
4. Hoit BD. Anatomy and physiology of the pericardium. Cardiol Clin. 2017;35(4):481–90.
5. Kumar V, Abbas AK, Aster JC, Perkins JA, Ramzi
S, Robbins, Stanley L.Robbins & Cotran pathologic
basis of disease; 2021.
6. Welch TD, Oh JK.Constrictive pericarditis. Cardiol
Clin. 2017;35(4):539–49.
7. Geske JB, Anavekar NS, Nishimura RA, Oh JK,
Gersh BJ.Differentiation of constriction and restriction: complex cardiovascular hemodynamics. J Am
Coll Cardiol. 2016;68(21):2329–47.
8. Adler Y, Charron P, Imazio M, etal. 2015 ESC guidelines for the diagnosis and management of pericardial
diseases: the task force for the diagnosis and management of pericardial diseases of the European Society
of Cardiology (ESC) endorsed by: the European
Association for Cardio-thoracic Surgery(Eacts). Eur
Heart J. 2015;36(42):2921–64.
9. Miranda WR, Oh JK. Constrictive pericarditis: a
practical clinical approach. Prog Cardiovasc Dis.
2017;59(4):369–79.
10. Welch TD, Ling LH, Espinosa RE, Anavekar NS, Wiste
HJ, Lahr BD, Schaff HV, Oh JK.Echocardiographic
diagnosis of constrictive pericarditis: Mayo clinic criteria. Circ Cardiovasc Imaging. 2014;7(3):526–34.
11. Dal-Bianco JP, Sengupta PP, Mookadam F,
Chandrasekaran K, Tajik AJ, Khandheria BK.Role
of echocardiography in the diagnosis of constrictive
pericarditis. J Am Soc Echocardiogr 2009;22(1):2433; quiz 103-4.
12. Chiabrando JG, Bonaventura A, Vecchié A, Wohlford
GF, Mauro AG, Jordan JH, Grizzard JD, Montecucco
F, Berrocal DH, Brucato A, Imazio M, Abbate
A. Management of acute and recurrent pericarditis:
JACC state-of-the-art review. J Am Coll Cardiol.
2020;75(1):76–92.
13. Mathew J, Swaminathan M, Ayoub C.Clinical manual and review of transesophageal echocardiography.
2nd ed. McGraw-Hill; 2010.
Benign Masses, Normal Anatomic
Variants, andArtifacts
TaraBrakke andStephenBrannan
27
Learning Objectives
1. Assess some of the common normal anatomical variants, benign cardiac masses, and artifacts that can frequently be misinterpreted as
masses or objects.
2. Describe common benign cardiac masses
seen on echocardiography.
3. Review common ultrasound artifacts appearing as masses.
Introduction
Point-of-care ultrasound (POCUS), and particularly bedside echocardiographic cardiac assessment, is increasingly employed in the critical
care setting to evaluate, diagnose, and guide
treatment in an expanding array of hemodynamic
and physiologic situations. With increasing numbers of physicians and specialties utilizing ultrasound, it is crucial to recognize and distinguish
normal anatomic variants from cardiac masses,
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 80038- 2_27.
T. Brakke (*) · S. Brannan
Department of Anesthesiology, University of
Nebraska Medical Center, Omaha, NE, USA
e-mail: tbrakke@unmc.edu;
stephen.brannan@unmc.edu
artifacts, and pathological ndings. This chapter
explores some of the common normal anatomical
variants and benign cardiac masses and reviews
some artifacts that can frequently be misinterpreted as masses or objects. We encourage the
reader to verify ndings in multiple windows,
views, and modalities (that is, two-dimensional
ultrasound, color ow Doppler, and spectral
Doppler) when concerned about possible abnormalities. Wherever possible, we have included
transthoracic images that reect POCUS images,
but unfortunately, some of these variants are
best—or only—visualized with transesophageal
echocardiography and are shown thusly herein.
Normal Anatomical Variants
Right Atrium
Crista Terminalis
The Crista Terminalis (Fig. 27.1) is a smooth,
crescent-shaped ridge of myocardium located at
the cavo-atrial junctions, although most often
identied via imaging along the superior vena
cava and right atrial junction. Anatomically this
delineates the smooth right atrial muscle from the
trabeculated right atrial appendage muscle. Due
to its high density of adrenergic bers, it can be
an origin for atrial tachyarrhythmias and thus a
target in ablation procedures.
© 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_27
343
344
Fig. 27.1
Transesophageal
midesophageal bicaval
view showing the crista
terminalis (red arrow)
along the superior vena
cava-right atrial junction
and separating the
trabeculated right atrial
appendage wall from the
smooth right atrial wall.
RA right atrium, LA left
atrium, SVC superior
vena cava, IVC inferior
vena cava
T. Brakke and S. Brannan
Eustachian Valve
The Eustachian Valve (Fig. 27.2) functions in
utero to shunt oxygenated blood entering the right
atrium from the inferior vena cava across the interatrial septum’s fossa ovalis into the left atrium. In
this way, oxygenated blood bypasses the pulmonary circulation, which at that point does not participate in gas exchange, and goes to the systemic
circulation to deliver oxygen to organs and tissues.
This valve does not completely regress in approximately 25% [1] of adults and appears posteriorly
along the inferior vena cava as a prominent strand
of tissue projecting into the right atrium. The
Eustachian Valve does not cause signicant blood
ow disturbances when viewed with color ow
Doppler. This distinguishes it from the triatriatum
dexter, which is a similar-appearing thin band of
tissue that traverses the entirety of the right atrium
and causes ow disturbance.
Thebesian Valve
The Thebesian Valve is a thin ap of tissue covering the entrance to the coronary sinus in up to
80% of patients [2]. It can appear semilunar,
fenestrated, biconcave, or bandlike and inhibit
cannulation of the coronary sinus for retrograde
cardioplegia or placement of a biventricular pacing wire.
Chiari Network
A Chiari Network is a remnant of sinus venosusderived embryologic structures that appears as a
thin, fenestrated, mobile, and membranous structure within the right atrium. It is distinguished
from thrombus or vegetation by being visualized
moving in multiple right atrial views. It is often
associated with a patent foramen ovale, interatrial septal aneurysms, and paradoxical emboli.
Coronary Sinus
The coronary sinus arises from the left-sided sinus
venosus, with contributory veins regressing in most
adults. It runs approximately 3 cm posteriorly
along the atrioventricular groove superior to the
mitral valve annulus. Although it is typically less
than 1 cm wide, dilation can occur due to atrial
hypertension, tricuspid regurgitation, or the presence of a persistent left-sided superior vena cava.
Persistent Left Superior Vena Cava (PLSVC)
PLSVC occurs when the embryologic left-sided
superior vena cava does not regress. Typically, it
drains into the coronary sinus, causing the coronary sinus to dilate above 1.1cm. It cannot be
identied directly via POCUS; however, indirect
suggestions are seen, such as a dilated coronary
27 Benign Masses, Normal Anatomic Variants, andArtifacts
345
a
b
c
Fig. 27.2 A eustachian valve (red arrow) is noted (a) in a
transthoracic apical four chamber view with the tricuspid
valve noted by the white arrow, (b) in a transesophageal
midesophageal bicaval view, and (c) in a transesophageal
midesophageal right ventricle inow and outow view
with a color ow doppler box in the right portion of the
sinus. A conrmatory bubble study administered
via a left upper extremity peripheral IV with
opacication emanating from the coronary sinus
rather than the right-sided superior vena cava is
conrmatory for its presence. Ineffective myocardial protection from a retrograde coronary
perfusion cannula during an on-cardiopulmonary
bypass open-heart procedure resulting in postoperative cardiogenic shock is also a consequence
sometimes encountered in the critical care unit.
image (color ow doppler scale not pictured, tricuspid
valve denoted by the white arrow). RA right atrium, RV
right ventricle, LA left atrium, LV left ventricle, TV tricuspid valve, IVC inferior vena cava, SVC superior vena
cava, AV aortic valve
Patent Foramen Ovale (PFO)
The foramen ovale occurs in utero to shunt oxygenated blood from the highly pressurized right
heart to the lower pressured left heart via a connection between the atria through the septum primum and septum secundum. With the rst breaths
ex utero, the left heart pressures increase above
the right heart pressure from a drastic reduction in
pulmonary vascular resistance as the alveoli are
lled with air for the rst time, causing the sep-
346
ab
cd
T. Brakke and S. Brannan
Fig. 27.3 Transesophageal midesophageal bicaval views
with lowered Nyquist limits (red arrows). (a) Patent foramen ovale with color ow doppler showing ow parallel
to the fossa ovalis (green interrupted arrow for emphasis).
The fossa ovalis is the thinnest portion of the interatrial
septum located between the superior and inferior limbs of
the septum. This indicates ow between the two incompletely fused septae that comprise the fossa. (b)
Representative photo from a bubble study conducted
through the left upper extremity. The bubbles entered
through the superior vena cava ruling out a persistent left
sided superior vena cava, which in this view would enter
from the coronary sinus at the left side of the screen if a
persistent left sided superior vena cava was present. No
bubbles appear in the left atrium within six cardiac cycles
tum primum to close against the septum secundum. Over time the septae fuse. In up to 25% of
adults, this connection remains patent (Fig.27.3)
due to incomplete closure or incomplete fusion
[3] and can increase the risk of stroke. Right-toleft shunting (Eisenmenger’s physiology) can
occur when the right atrial pressure exceeds the
left atrial pressure, resulting in a hypoxemic
shunt. One example occurs following implantation of a durable left ventricular assist device
(LVAD) when right heart pressures increase sec-
demonstrating the absence of a PFO.Importantly, note the
interatrial septum (blue arrow) bowing into the left atrium
with a Valsalva maneuver via the ventilator, indicating a
true negative PFO test as it signies even when the right
atrial pressure is higher than left atrial pressure there is no
ow across the atrial septum. (c) Iatrogenic PFO with left
to right sided ow following placement of a left atrial
appendage exclusion device. Note the ow is perpendicular to the fossa ovalis, which is characteristic for a lesion
classied as an atrial septal defect, and is owing into the
right atrium (green interrupted arrow for emphasis). (d)
Iatrogenic PFO with right to left sided ow following
placement of a left atrial appendage exclusion device
(green interrupted arrow for emphasis). RA right atrium,
LA left atrium, SVC superior vena cava
ondary to pulmonary hypertension and/or right
ventricular dysfunction, resulting in profound and
refractory hypoxemia. Identifying and xing a
PFO is a critical component of successful durable
LVAD implantation. The interatrial septum should
always be evaluated by 2D and color ow Doppler.
Because of the lower ow velocity in the atria, the
Nyquist limit must be reduced (ideally to
<30cm/s) to help identify a PFO.Additionally, a
bubble study with a Valsalva maneuver and 3D
imaging provides more denitive evaluations.