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32 Diagnosing Acute Aortic Syndromes withUltrasound
Image 32.5 Transverse
view, distal abdominal
aorta, branching of the
common iliac arteries.
LCIA left common iliac
artery, RCIA right
common iliac artery
Image 32.6 Abdominal
aortic aneurysm.
Courtesy Dr. Kristin
Dwyer
399
TEE artifacts are discussed extensively in
Chap. 10, Artifacts and Pitfalls in TEE.Thoracic
aortic dissection can be well visualized with TEE
(Videos 32.8, 32.9, and 32.11).
Specic POCUS ndings for the diagnosis of
acute aortic syndromes include the visualization
of an intraluminal aortic ap (Videos 32.4 and
32.9), an intramural aortic clot (video 32.6), and
a visible aortic ulcer. Indirect ndings may
include aortic dilatation at any level >4 cm
(Image 32.6, Videos 32.5 and 32.6), pericardial
effusion and/or tamponade, and aortic regurgitation [2, 10].
400
M. Snuckel and A. T. Levinson
Pitfalls
The aorta is visualized deep into the IVC.If there
is any confusion about whether the IVC or aorta
is being visualized, compression and the use of
Doppler signaling may be helpful.
The TEE often provides very limited visualization of the aortic arch and cannot diagnose
pathology there. Suprasternal TTE can be performed in addition to TEE to possibly better evaluate aortic arch pathology.
Some ultrasound artifacts can mimic aortic
dissection. For example, on TTE, a side-lobe artifact from a central venous catheter in the innominate vein and/or SVC can mimic dissection.
Evidence fortheUse ofPOCUS
intheRapid Diagnosis ofAortic
Syndromes
Diagnostic accuracy of POCUS for acute aortic
processes can be useful but cannot exclude the
absence of pathology in symptomatic patients.
For patients with a high pretest probability of an
acute aortic process but a negative POCUS exam,
formal imaging is suggested, such as CTA.
TTE has been estimated to have a sensitivity
of 88–91%, but CTA, MRA, and TEE all have
sensitivities >95% for both types of aortic dissection. Formal cardiology-performed TTE has a
sensitivity >95% for type A aortic dissection.
POCUS in the literature has a sensitivity between
80% and 90% for type A aortic dissection and
70% for type B aortic dissection [5].
One recent point-of-care ultrasound (POCUS)
protocol prospective study combining transthoracic echocardiography (TTE) and ultrasound
imaging of the abdominal aorta found a sensitivity of 93.2% (95% CI 81.3–98.6), specicity of
90.9 (95% CI 89.2–92.5), positive predictive values of 26.3%, and a negative predictive value of
99.7% [5]. The prospective multicenter study
enrolled 1324 patients who presented to emergency departments and compared the protocolized TTE and abdominal aorta scans to the
ndings from a CT angiogram utilizing a dissection protocol [6].
Regarding abdominal aortic pathology, transesophageal echocardiography (TEE) has been
well described for some time in the critical care
literature as a very rapid and sensitive tool for
diagnosing aortic injury. Diagnostic accuracy is
quite high in diagnosing acute dissection, compared to the gold standard of angiography, MRI,
or CT angiography [11–13].
With basic training, both physicians and students have been shown to have high diagnostic
accuracy at measuring the aorta and detecting
aortic dissection rapidly using trans-thoracic and
trans-abdominal ultrasound [14–16].
Specically for thoracic acute aortic syndromes, it is not recommended by most experts
as a stand-alone test. If acute ndings are noted,
they can be extremely helpful given ease of use,
cost, lack of radiation, and timeliness. However,
if they are not diagnostic and there is a moderate
to high pre-test probability, additional tests that
have higher diagnostic accuracy, especially for
descending thoracic aortic processes, should be
performed, such as computed tomography (CT),
magnetic resonance imaging (MRI), and/or transesophageal echocardiography (TEE) [2].
TTE has not been recognized as a useful
modality for the assessment and/or diagnosis of
diseases of the descending thoracic aorta. This is
because standard TTE windows usually do not
offer good visualization due to the larger distance
from the anterior chest to the descending thoracic
aorta and because of lung artifacts. One recent
small single-center study, however, suggested
that, compared to contrast-enhanced CT as the
gold standard, a posterior para-vertebral approach
for TTE with the patient in a lateral decubitus
position has signicantly increased sensitivity
(compared to standard anterior TTE views) for
detecting acute aortic pathology in the descending thoracic aorta [17].
Summary Points
• Transesophageal echocardiography (TEE) has
been well described for some time in the criti-
cal care literature as a very rapid and sensitive
tool for diagnosing aortic injury.
• TTE and Transabdominal point-of-care ultra-
sound have been shown to have high diagnos-
32 Diagnosing Acute Aortic Syndromes withUltrasound
401
tic accuracy in measuring the aorta and
detecting aortic dissection rapidly using transthoracic and transabdominal ultrasound.
• TTE should not be used as a stand-alone test
for acute thoracic aortic pathology. If acute
ndings are noted, they can be extremely
helpful given timeliness and ease of use while
waiting for a gold-standard test; however, if
they are not diagnostic, additional tests that
have higher diagnostic accuracy, especially
for descending thoracic aortic processes,
should be performed.
References
1. Azhar B, Patel SR, Holt PJ, Hinchliffe RJ, Thompson
MM, Karthikesalingam A.Misdiagnosis of ruptured
abdominal aortic aneurysm: systematic review and
meta-analysis. J Endovasc Ther. 2014;21:568–75.
2. Morello F, Santoro M, Fargion AT, Grifoni S,
Nazerian P.Diagnosis and management of acute aortic syndromes in the emergency department. Intern
Emerg Med. 2021;16:171–81.
3. Chinthamuneedi M.Diseases of the aorta in the critically ill. Crit Care Resusc. 2000;2:117–24.
4. Abdominal aortic aneurysm: diagnosis and management. NICE; 2020. Accessed 3 Jan 2024.
5. Gibbons RC, Smith D, Feig R, Mulur M, Costantino
TG.The sonographic protocol for the emergent evaluation of aortic dissections (SPEED protocol): a multicenter, prospective, observational study. Acad Emerg
Med. 2024;31:112–8.
6. Gibbons RC, Singh G, Donuru A, Young
M.Abdominal Aortic Aneurysm Imaging. StatPearls.
Treasure Island (FL) ineligible companies. Disclosure:
Gagandeep Singh declares no relevant nancial relationships with ineligible companies. Disclosure:
Achala Donuru declares no relevant nancial relation-
ships with ineligible companies. Disclosure: Michael
Young declares no relevant nancial relationships
with ineligible companies. 2024.
7. Boivin Z, Mensel E, She T. Role of POCUS in
assessing an acute aortic thrombus. POCUS J.
2023;8:129–31.
8. Barbry T, Bouhemad B, Leleu K, de Castro V,
Remerand F, Rouby JJ. Transthoracic ultrasound
approach of thoracic aorta in critically ill patients with
lung consolidation. J Crit Care. 2006;21:203–8.
9. Hartrich M, Eilbert W.An approach to point-of-care
ultrasound evaluation of the abdominal aorta. J Vis
Exp. 2023.
10. Hansen MS, Nogareda GJ, Hutchison SJ.Frequency
of and inappropriate treatment of misdiagnosis of
acute aortic dissection. Am J Cardiol. 2007;99:852–6.
11. Khalil A, Helmy T, Porembka DT.Aortic pathology:
aortic trauma, debris, dissection, and aneurysm. Crit
Care Med. 2007;35:S392–400.
12. Porembka DT.Importance of transesophageal echocardiography in the critically ill and injured patient.
Crit Care Med. 2007;35:S414–30.
13. Shiga T, Wajima Z, Apfel CC, Inoue T, Ohe
Y. Diagnostic accuracy of transesophageal echocardiography, helical computed tomography, and magnetic resonance imaging for suspected thoracic aortic
dissection: systematic review and meta-analysis. Arch
Intern Med. 2006;166:1350–6.
14. Jaynstein D, Baeten R, Bafuma P, etal. Point-of-care
ultrasound assessment of the abdominal aorta by physician assistant students: a pilot study. Emerg Radiol.
2021;28:245–50.
15. Pare JR, Liu R, Moore CL, etal. Emergency physician focused cardiac ultrasound improves diagnosis
of ascending aortic dissection. Am J Emerg Med.
2016;34:486–92.
16. Nazerian P, Vanni S, Morello F, etal. Diagnostic performance of focused cardiac ultrasound performed by
emergency physicians for the assessment of ascending aorta dilation and aneurysm. Acad Emerg Med.
2015;22:536–41.
17. Yamaguchi S, Murakami H, Kudo T, etal. Usefulness
of the echocardiographic paravertebral approach for
the diagnosis of descending thoracic aortic dissection.
J Echocardiogr. 2017;15:127–34.
Adult Congenital Heart Disease
ErikSu andSaulFlores
33
Learning Objectives
1. Understand the most common congenital
heart defects
2. Recognize diagnostic echocardiographic targets for patients with suspected congenital
heart defects
3. Correlate congenital lesions with echocardiographic ndings
Summary Points
• Identication of congenital heart defects
requires an excellent working knowledge of
normal cardiac anatomy and function, as well
as advanced qualitative and quantitative skills
in echocardiography.
• As point-of-care ultrasound (POCUS)
becomes increasingly used in initial hemodynamic assessment, the recognition of congenital abnormalities and their physiological
sequelae is important for optimal evaluation
and management of critically ill patients.
This chapter is intended for clinicians experienced in focused cardiac ultrasound or critical
care echocardiography optimally with a level of
veried and mentored experience examining
E. Su (*) · S. Flores
Adult Congenital Heart Disease ICU, Division of
Critical Care Medicine in the Department of
Pediatrics, Baylor College of Medicine at Texas
Children’s Hospital, Houston, TX, USA
e-mail: saul.ores2@bcm.edu
patients in acute hemodynamic instability with
structurally normal hearts. A necessary skill in
assessing patients with cardiac morphology skills
is sweeping (also fanning or tilting) the beam of
an ultrasound toward and away from the operator
along a direction perpendicular to the plane of the
view. As an operator performs this while visualizing the heart, different sections of the heart are
visible and a slow sweep can identify structures
outside of traditional view planes. This is instrumental for identifying structures such as coronary arteries in the parasternal short axis view at
the aortic valve level, and the coronary sinus in
the apical four-chamber view. With color
Doppler, it may be used to survey for atrial and
septal defects from the subcostal four-chamber
window.
The exhaustive views used to comprehensively phenotype a heart with dysmorphology
often exceed 100 images in echocardiography
labs and are unfortunately too extensive for this
discussion. Rather traditional views used in critical care echocardiography are mentioned with
accompanying caveats for assisting readers in
discussing these patients for timely cardiac referral and consultation.
Within congenital heart disease, defects are
often classied into three, sometimes four categories based on physiology in infancy:
1. Problems causing increased pulmonary blood
ow (Qp>Qs)
© 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_33
403
404
E. Su and S. Flores
(a) Septal defects, Patent Ductus Arteriosus,
Anomalous Pulmonary Veins
2. Problems causing too little pulmonary blood
ow (Qp<Qs)
(a) Tetralogy of Fallot with Major Aorto-
Pulmonary Collateral Arteries (MAPCAs),
Ebstein’s Malformation, Pulmonary
Stenosis
3. Obstruction to systemic blood ow
(a) Aortic Stenosis, Coarctation of the Aorta
4. Cardiomyopathy (discussed in Chapter IIc)
(a) Congenitally Corrected Transposition of
the Great Arteries (L-TGA)
Recognizing the long-term sequelae of CHD
as clues that will help you seek timely consultation is crucial when a patient with known or
unknown CHD presents to your care.
Within this chapter, unless otherwise noted,
apical and subcostal views appear in the pediatric
convention where the probe is at the bottom of
the screen and structures distal to it appear at the
top of the screen.
Problems Causing Increased Pulmonary Blood Flow
These lesions proceed toward Eisenmenger’s
syndrome, due to a left to right shunt. Depending
on location of the shunt, the excess volume load
to the heart initially leads to left heart dilatation
and insufciency, and increased left atrial (LA)
pressure. Increasing pulmonary vascular pressures lead to progressive right heart dilatation
and insufciency. Increasing pulmonary vascular
pressures over time can reverse shunt physiology
as well. In congenital heart disease of this type
that persists into adult ages, patients may manifest progressive left heart failure and potential
biventricular failure with pulmonary
hypertension.
Patent Ductus Arteriosus (PDA)
PDA occurs in 1 per 2000 live infant births and
occurs when the ductus arteriosus, which serves a
left-to-right shunt in the normal fetal circulation,
fails to close more than 48h after birth [1].
In terms of physiology and presentation, PDA
is a risk factor for endarteritis and a major cause
of morbidity and mortality in untreated PDA.This
is irrespective of the size of the shunt. Vegetations
appear on the pulmonary side of the PDA, and
embolization typically travels to the lungs as
opposed to the systemic vasculature. Patients
with a large shunt will demonstrate a wide pulse
pressure. The majority of patients may be asymptomatic with a machine-like continuous murmur
in the left upper chest, others may have signicant congestive heart failure in the case of
increasing longstanding shunt. Pathological PDA
is usually diagnosed in childhood and if untreated
over a lifetime, the persistent left to right shunt
causes volume overload of the heart. Variability
in the degree of the shunt leads to heterogeneous
presentations along a spectrum congestive heart
failure (CHF) as well as secondary pulmonary
hypertension (PHTN). Patients may present with
impaired exercise tolerance, syncope, and palpitations depending on the degree of heart failure.
Findings on the image of the patient may demonstrate dilation of the left heart chambers with
some level of compromised function, and potentially mitral valve regurgitation (Fig.33.1). ECG
may demonstrate left atrial dilatation and left
ventricular strain depending on the degree of
CHF. Targets of diagnostic echocardiography
include identifying the location of the PDA and
its ow direction, and a detailed functional
assessment of the right and left heart. The PDA is
visualized using dedicated ductal views modied
from parasternal long and short axis views at the
level of the pulmonary arteries. The pressure gradient across the PDA is used for determining
right ventricular systolic pressure. Architecture
and size of the PDA is relevant in its procedural
management. Diastolic runoff through the PDA
can result in reversal of aortic ow in the descending abdominal aorta during diastole.
In critical care echocardiography, recognizing
left heart dilatation and function, and valvular
competence are essential. Assessing right heart
dilatation and function, and right ventricular systolic pressures are also important. The PDA
33 Adult Congenital Heart Disease
Fig. 33.1 Apical four-Chamber view of 6-month-old
with untreated PDA and subsequent left heart failure.
Image is shown in traditional echocardiography convention with probe at the top of the screen and objects distal
to the probe at the bottom of the screen. LV: left ventricle
views are challenging in adults and difcult to
render even if the windows are obtainable due to
thoracic ossication and air artifact.
Atrial Septal Defect (ASD)/Patent Foramen Ovale (PFO) (Unrepaired/ Repaired)
ASDs arise from various causes but comprise
roughly 1–2 per 1000 of live births. ASDs appear
in a variety of forms:
• Primum ASDs appear immediately above the
atrioventricular (AV) valves due to a failure of
the septum primum in fetal embryology. They
may be associated with other ventricular septal and AV valve malformation issues
• Secundum ASDs arise from failure of the septum secundum and occur in the middle of the
septum
405
• Coronary sinus ASDs occur in the vicinity of
the coronary sinus when the sinus is unroofed
and exposed to the left atrium
• Sinus venosus ASDs occur at the posterior
margin of the atrial septum where either the
superior or inferior vena cava insert in a way
that overrides the septum and are commonly
associated with anomalous pulmonary venous
return
• Iatrogenic leakage around prior instrumentation
The degree of pathology imaged is inuenced
by the size of the defect and evolves from complications left-to-right shunting physiology.
Closure is indicated in many situations given the
risk of paradoxical emboli causing a cerebrovascular accident, though ASDs may also aid in
decompressing the right heart as a “pop-off” in
pulmonary hypertension.
Diagnostic imaging targets include a detailed
functional assessment of the left and right heart
comparing function and size. A defect may or
may not be visible. Defects of the atrial septum
are not readily assessed in apical views where
the septum can be parallel to the beam and dropout of signal in the fossa ovalis, where a secundum ASD would appear. Subcostal (Fig. 33.2)
and parasternal (Fig. 33.3) views are helpful
sweeping through the entire septum. Defects are
sometimes associated with anomalous pulmonary vein return though the sites where the veins
connect can vary greatly. Targets for critical
care echocardiography include assessment of
left and right heart function, with right heart
failure a possibility. A cardiology consultation
is recommended for identication of an ASD,
but techniques that may identify them include
performing:
• A subcostal sweep through the septum in the long
and short axis with and without color Doppler.
• A parasternal sweep in the short axis with and
without color Doppler.
• Agitated saline (Bubble) study.
• An evaluation of left and right heart function.
• Areas around ASD device closures, presence
of patch repair and noteworthy artifacts.
406
Fig. 33.2 Subcostal
long axis view of
17-year-old male with
previously undiagnosed
secundum ASD. LA
(Left Atrium), RA
(Right Atrium), and
ASD (Atrial Septal
Defect)
E. Su and S. Flores
Fig. 33.3 Parasternal short axis view of 17-year-old male
with previously undiagnosed secundum ASD. LA (Left
Atrium), RA (Right Atrium), and ASD (Atrial Septal
Defect)
Targets to note include that partial anomalous
pulmonary vein return (PAPVR) can result in a
continuous right-to-left shunt across an ASD
independent of pulmonary hypertension.
Additionally, a large coronary sinus seen in an
apical view can also reect PAPVR, as well as a
left-sided SVC.
Ventricular Septal Defects (VSDs)
andAtrioventricular Septal Defect
(AVSD)
Ventricular septal defects (VSDs) are common in
children but only comprise 10% of CHD in adults
as some close through development.
There are multiple types of VSDs (Fig.33.4),
due to the conformation of the interventricular
septum as a delta shaped structure curved to the
contour of the left ventricle (LV) comprised of
differing tissue types. Consequently defects can
occur each of the ve areas of the septum
• Infundibular Type 1 VSDs occur just beneath
the semilunar valves and can cause prolapse of
the left aortic valve cusp, resulting in aortic
insufciency.
• Membranous Type 2 VSDs are the most com-
mon VSDs in adults and occur inferior to the
crista supraventricular is adjacent to the infun-
dibular septum and therefore, are less proxi-
mate to the aortic valve but border the septal
leaet of the tricuspid valve.
• Inlet Type 3 VSDs (also known as AV canal
type) are located below the AV valves but are
Perimembranous
Supraventricularis
33 Adult Congenital Heart Disease
Fig. 33.4 Types of
ventricular septal defects
(VSDs)
SVC
407
PV
Ao
Supracristal
Crista
RV
Muscular
TV
Inlet
not typically associated with valvular
insufciency unless the defect is an atrioventricular septal defect.
• Muscular Type 4 VSDs may appear in multiples in the muscular septum closer to the papillary muscle level of the septum.
• A Gerbode defect is a rare VSD of the atrioventricular septum that occurs in the small
area of ventricular septum above the tricuspid
valve and base of the right ventricle (RV)
where a defect permits blood ow directly
from the left ventricle to the right atria.
• VSDs can also occur as a complication
of cardiac injury and/or complications of
instrumentation.
Given the variety of VSD types, presentation,
and imaging ndings can vary signicantly. In
the setting of a symptomatic VSD, left to right
shunting will vary based on the size of defect as
well as the pressure gradient between the ventricles as pulmonary arterial hypertension may
develop from increased ows. Ventricular size
may not provide insights particularly in VSDs
occurring in the outow tract. Most membranous
Type 2 and muscular Type 4 VSDs close in childhood with cardiac growth. Endocarditis is a possible presenting diagnosis in patients with small
restrictive VSDs. With increased left to right
shunting, left heart enlargement from volume
overload can occur and in the progression of pulmonary hypertension right heart failure can
ensue. In moderate defects, where Qp:Qs exceeds
1.5:1, left heart overload and pulmonary hypertension can develop. In severe defects where the
area of the defect exceeds 75%, these patients
often require surgery while infants and untreated
will progress to pulmonary hypertension and
Eisemenger complex more rapidly.
Typical complete echocardiogram targets
include a detailed functional assessment of the
left and right heart comparing function and size.
The defect again may or may not be visible due to
size, windows, and location. An agitated saline
(bubble) study may help identify a VSD.
• Infundibular Type 1 VSDs are differentiable
from perimembranous Type 2 VSDs in the
parasternal short axis view at the level of the
aortic valve. If looking at the aortic valve en
face as a clock face, an infundibular VSD will
appear on Doppler imaging as a jet from the
aorta into the right ventricular outow tract
(RVOT) in the 11 o’clock to 3 o’clock range.
A perimembranous VSD will appear as a jet
from the aorta into the RV near the tricuspid
valve at the 9 o’clock to 11 o’clock position. A
sweeping motion up and down the Left
Ventricular Outow Tract (LVOT) in this view
will be necessary to identify the VSD.
408
E. Su and S. Flores
• Muscular Type 4 VSDs may be identiable in
apical, parasternal, or subcostal sweeps of the
long-axis view anterior and posterior through
the ventricular septum with color Doppler on
and optimized.
• Inlet Type 3 VSDs and Gerbode defects can
also be identied using apical sweeps with
color Doppler.
It is important that indices of LV and/or RV
dysfunction are assessed in critical care echocardiography, as well as the presence of pulmonary
hypertension.
Problems Causing Decreased Pulmonary Blood Flow
A decrease in pulmonary blood ow is a consequence of obstruction of right heart outow with
a right-to-left diversion of blood ow to the systemic circulation. Examples including those
below can include pulmonary stenosis. This
results in early manifestations of cyanotic heart
disease, and patients with untreated CHD in this
category may see exercise intolerance and growth
restriction over their lifespan potentially resulting in chronic end organ hypoxemia. A patient
may experience renal and hepatic insufciency as
well clubbing.
Ebstein’s Malformation (Unrepaired)
An Ebstein’s Malformation occurs rarely in 1in
20,000 births. It may be associated with intrapartum exposure to lithium. In this defect, the septal
and posterior leaets of the tricuspid valve are
displaced toward the apex of the RV and the
degree of this is variable, and the upper RV chamber is “atrialized” as the tricuspid valve (TV) orice appears lower in the ventricle. This results in
variable amounts of TV regurgitation. An ASD is
commonly associated with Ebstein’s malformation and commonly a source for right-to-left
shunting.
In pursuing complete diagnostic echocardiography, the following are assessed. The tricuspid
valve orice descends toward the apex as can be
seen in multiple views and the RV cavity may not
be visible in apical views in severe cases
(Figs.33.5 and 33.6). Due to its smaller size, the
appearance of RV movement may overestimate
its function. In critical care echocardiography, an
operator should assess tricuspid valve regurgitation, and also right atrial enlargement, which may
increase the chance of arrhythmias. Flow-related
ASD enlargement and right-to-left shunting may
predispose to paradoxical embolic event.
Tetralogy ofFallot (TOF)
Tetralogy of Fallot occurs in 7% of CHD and the
most common cyanotic heart disease to reach
adulthood without repair. It is dened as four anatomic components consisting of pulmonary stenosis, VSD (Fig. 33.7), overriding aorta over the
muscular interventricular septum, and RV hypertrophy. Methods for repair in childhood can
include a transannular patch to widen the RV outow, resection of obstructive trabecular structures,
replacement of the outow tract with a valved conduit, monocusp revision of the valve. Repairs may
also require shunts or stenting for preservation of
pulmonary blood ow pending complete repair.
Later in life, pulmonary stenosis and/or insufciency can develop with negative effects on RV
function. In adults, repair is possible though pulmonary valve repair is often required. Symptoms
early in life relate to inadequate pulmonary blood
ow with right-to-left shunting and cyanosis. Later
in life, RV failure can develop.
Typical full diagnostic echocardiography targets include a detailed functional assessment of
the right heart evaluating the RV outow tract
and pulmonary arteries. Identication of the VSD
in parasternal and apical views as mentioned
above encompasses the membranous septum and
passes under an overriding aortic orice.
Coronary artery position and aortic arch position
is identied as these can be abnormal. It is also
33 Adult Congenital Heart Disease
Fig. 33.5 Apical
four-Chamber view of
17-year-old female with
Ebstein’s malformation.
Note apical
displacement of the
tricuspid valve and large
atrialized portion of the
RV. Right atrium (RA),
tricuspid valve (TV),
and left ventricle (LV)
409
Fig. 33.6 Parasternal
short axis view of
17-year-old female with
Ebstein’s malformation.
Right atrium (RA),
tricuspid valve (TV),
right ventricle (RV), and
left ventricle (LV)