This document provides an overview of right ventricle anatomy, physiology, and echocardiographic assessment. It describes the irregular shape and trabeculated structure of the right ventricle. The physiology section covers the RV's adaptation to volume overload through distensibility and compliance. Echocardiographic assessment techniques are outlined, including measurements of RV dimensions, fractional area change, TAPSE, tissue Doppler imaging, and the TEI index. The document provides a detailed but technical summary of right ventricular structure and function.

1. Right Ventricle Anatomy, Physiology
& ECHO Assessment
Dr. Vaibhav Yawalkar
MD, DM Cardiology

2. Anatomy
 The right ventricle forms largest part of the
anterior surface of the heart, a small part of the
diaphragmatic surface, and almost entire inferior
border of the heart
 Shape of right ventricle can not be described using
any known standard geometrical shapes. It is
irregularly wedge shaped and crescent shaped in
cross section.
 Superiorly it tapers into an arterial cone, the conus
arteriosus (infundibulum), which leads into the
pulmonary trunk

3. Some simplifications that have been used
to describe RV shape:
 Parallelepiped (or three-dimensional
parallelogram)
 A prism
 A pyramid with a triangular base

6. Anatomy
• Inlet Portion:
from the tricuspid annulus to the insertions of
the papillary muscles
• Outlet Portion (Conus):
smooth-walled muscular sub-pulmonary
channel
• Apical Trabecular Portion:
extends inferiorly beyond the attachments of
the papillary muscles toward the ventricular
apex

8. Anatomy
 The interior of the right ventricle has irregular
muscular elevations (trabeculae carneae).
 A thick muscular ridge, the supraventricular crest,
separates the ridged muscular wall of the inflow part
of the chamber from the smooth wall of the conus
arteriosus, or outflow part. It is made up of three
components (parietal band, infundibular septum,
and septal band)
 Tendinous cords (chordae tendineae) attach to the
free edges and ventricular surfaces of the anterior,
posterior, and septal cusps of tricuspid valve much like
the cords attaching to a parachute

9. Moderator Band

11. Anatomy
 The tendinous cords (around 75) arise from the apices of 3
papillary muscles, which are conical muscular projections
with bases attached to the ventricular wall.
 The anterior papillary muscle, the largest and most
prominent of the three, arises from the anterior wall of the
right ventricle; its tendinous cords attach to the anterior
and posterior cusps of the tricuspid valve.
 The posterior papillary muscle, smaller than the anterior
muscle, arises from the inferior wall of the right ventricle,
and its tendinous cords attach to the posterior and septal
cusps of the tricuspid valve

12. Anatomy
 The septal papillary muscle arises from the
interventricular septum, and its tendinous cords attach to
the anterior and septal cusps of the tricuspid valve.
 The interventricular septum (IVS), composed of muscular
and membranous parts, is a strong, obliquely placed
partition between the right and left ventricles
 Superiorly and posteriorly, a thin membrane, part of the
fibrous skeleton of the heart , forms the smaller
membranous part of the IVS, while large muscular part is
rather a part of LV wall.

13. Anatomy
 The septal cusp of the tricuspid valve is attached to the
middle of this membranous part of the fibrous skeleton.
 This means that inferior to the cusp, the membrane is an
interventricular septum, but superior to the cusp it is an
atrioventricular septum, separating the right atrium from
the left ventricle

14. Anatomy
 The septomarginal trabecula (moderator band) is a curved
muscular bundle that traverses the right ventricular
chamber from the inferior part of the IVS to the base of the
anterior papillary muscle. This trabecula is important
because it carries part of the right branch of the AV
bundle.
 This “shortcut” across the chamber seems to facilitate
conduction time, allowing coordinated contraction of the
anterior papillary muscle.
 Also it is considered as dependable anatomic feature of
the right ventricle & helps to identify the morphologic
right ventricle and is best appreciated from the apical four-
chamber view.

15. Anatomy
 The inflow of blood into the right ventricle (inflow tract)
enters posteriorly; and when the ventricle contracts, the
outflow of blood into the pulmonary trunk (outflow tract)
leaves superiorly and to the left
 Consequently, the blood takes a U-shaped path through
the right ventricle, changing direction about 140°.
 This change in direction is accommodated by the
supraventricular crest, which deflects the incoming flow
into the main cavity of the ventricle, and the outgoing flow
into the conus arteriosus

16. Anatomy
 The inflow (AV) orifice and outflow (pulmonary) orifice are
approximately 2 cm apart.
 The pulmonary valve at the apex of the conus arteriosus is
at the level of the left 3rd costal cartilage.
 The wall of the right ventricle is thinner than that of the left
ventricle in a ratio of 1:3

17. Left Ventricle Right Ventricle
Mitral – Aortic Continuity Tricuspid – Pulmonary Discontinuity
Muscular Valvular Outflow tract Muscular outflow tract
No moderator band Moderator Band
Small apical trabeculations Large apical trabeculations
Circular in cross section Crescentic in cross section
Thick free wall Thin free wall
2 Papillary Muscles 3 Papillary Muscles
Coronary Perfusion almost
exclusively in diastole
Coronary Perfusion both in systole
and diastole
Better adaption to pressure
states
Better adaption to volume overload
states , Higher compliance than LV
Relatively low proportion of Alpha
Myosin Heavy chain
Higher proportion of Alpha Myosin
Heavy chain

18. Physiology of Right Ventricle
• Filling of RV –
– RV filling normally starts before and finishes after LV
– RV isovolumic relaxation time is shorter
– RV filling velocities (E and A) and the E/A ratio are
lower.
• RV can accommodate varying degrees of preload while
maintaining a stable cardiac output and normal filling
pressures.
• Two characteristics of RV:
1. Distensibility of its free wall
2. Compliance-the ability to increase volume without
significant changes in the wall surface area.

19. Dilation of the RV caused by volume overload is
usually well tolerated.
However, two consequences lead to symptoms –
1. Functional tricuspid regurgitation.
2. Compression of LV by mechanism of ventricular
interdependence – decreased cardiac output

20. AFTER LOAD
 Normally afterload is minimal as it is Low impedance,
highly distensible pulmonary vascular system
 PVR is the most commonly used index of afterload, but
may not reflect the complex nature of ventricular afterload.
 Several factors modulate PVR, including hypoxia (Euler-
Liljestrand reflex), hypercarbia, cardiac output, pulmonary
volume and pressure, and specific molecular pathways.
The nitric oxide pathway (vasodilation)
The prostaglandin pathway (vasodilation)
The endothelin pathway (vasoconstriction).

22. Compared with the LV, the RV demonstrates a heightened
sensitivity to afterload change

23. RV CONTRACTION
 RV consists of
1. The superficial oblique myocardial fibers , in continuity
with
the LV fibers
2. Deeper layer of longitudinally arranged fibers
 LV has additional middle transverse fibers
 RV contraction begins at the inflow region and progresses
toward the outflow tract (likened to a bellows).In
distinction, the LV contracts in a squeezing motion
(likened to wringing a towel) from the LV apex to the
outflow tract.

24. Fireplace Bellow

26. RV PRESSURE VOLUME LOOP
• External mechanical work is substantially lower in the right ventricle
• Most notably, RV pressure begins to decline before closure of the
pulmonic Valve
• RV continues to eject blood because of high compliance and low
resistance of the pulmonary vasculature

27. Maximal RV elastance
better reflects RV
contractility than does
the end-systolic
elastance.
The normal maximal R
elastance is 1.3 ± 0.84
mm Hg/mL

28. RV PRESSURE
 Right-sided pressures are Significantly lower than left side.
 RV pressure shows an early peaking and a rapid decline in
contrast to the rounded contour of LV pressure tracing
 RV isovolumic contraction time is shorter because RV
systolic pressure rapidly exceeds the low pulmonary artery
diastolic pressure.
 A careful study of hemodynamic tracings and flow
dynamics also reveals that end-systolic flow may continue
in the presence of a negative ventricular-arterial pressure
gradient. This interval, which is referred to as the hangout
interval.

29. HANGOUT INTERVAL
 Measure of impedance in arterial system.
 It is the time interval from the crossover of pressures
to actual closure of semi lunar valves.
 Longer on pulmonary side due to greater distensibility
and less impedance (65 msec vs 10 msec for LV-
aorta)
 Accounts for the normal split S2
 In cases of PAH narrows down.

30. AV SYNCHRONY
 Maintenance of sinus rhythm and AV synchrony is
especially important in the presence of RV dysfunction.
 For example, atrial fibrillation or complete AV block are
poorly tolerated in
Acute RV myocardial infarction
Acute pulmonary emboli
Chronic RV failure

31. VENTRICULAR INTERDEPENDENCE
The size, shape, and compliance of one ventricle may affect
the size, shape, and pressure-volume relationship of other
ventricle through direct mechanical interactions.
Systolic – Mainly through the interventricular septum &
continuity
of muscle fibres
Diastolic – Mainly through the pericardium

33. Limitations of Echocardiography in
The
Evaluation of RV Function• Difficulties in the estimation of RV volume
• Crescentic shape of RV
• Separation between RV inflow and outflow
• No uniform geometric assumption for measuring volume
• Difficulties in the delineation of endocardial border owing to
well developed trabeculation
• Difficulties in the adequate image acquisition owing to the
location just behind the sternum

34. Echocardiographic Assessment
Qualitative Assessment
 Visual assessment of RV enlargement in PLAX view.
 Normally, right ventricular size is approximately two-thirds
that of the left ventricle as seen in apical 4 chamber view.
Enlargement is suspected if RV is equal to or larger than
LV.

35. Quantitative Assessment
 From the apical four-chamber view, through careful
alignment of the imaging plane, a long axis of the right
ventricle is recorded at end-diastole
 Short-axis dimensions are measured at the base and mid
chamber level

37. The chamber area can be measured by
planimetry

41. Measuring Right Ventricular Volume
 Area-length method (2D)
 3D Echocardiographic Methods

42. Measuring Right Ventricular Function
 TAPSE : Tricuspid valve annular motion during systole
(M-Mode)
 FAC : Fractional area change (2D)
 Tissue Doppler Imaging (Tricuspid Annulus)
 TEI Index
 Regional right ventricular wall motion abnormalities
 RV ejection fraction by volume measurement

43. TAPSE

45. RV Function
Tricuspid Annular Plane Systolic Excursion
Surrogate for global
RV systolic function
• 5 mm  20% EF
• 10 mm  30% EF
• 15 mm  40% EF
• 20 mm  50% EF
– Correlates with RV
EF
Lateral Annulus
Tricuspid annular motion during systole is
normally between 1.5 and 2.0 cm.

46. (End-diastolic area) – (end-systolic area)
x 100
(end-systolic area)
FAC : Fractional area change
(2D)

47. Fractional Area Change
2D FAC <32% indicates RV systolic dysfunction
• Correlates with MRI RV EF (r = 0.69 - 0.88)
• Related to outcome in a number of conditions

48. TISSUE DOPPLER IMAGING
 An apical four chamber view is used
 The pulsed Doppler sample volume is placed in either the
tricuspid annulus or the middle of the basal segment of
the RV free wall
 The S’ velocity is read as the highest systolic velocity
without over-gaining the Doppler envelope
 Normal S’ velocity is > 9 - 10 cm/s

50. Advantages
 A simple, reproducible
technique with good
discriminatory ability to
detect normal versus
abnormal RV function
 Pulsed Doppler is available
on all modern systems
 Maybe obtained and
analyzed off-line
Disadvantages
 Less reproducible for
nonbasal segments
 Is angle dependent
 Limited normative data in
all ranges and in both
sexes
 It assumes that the
function of a single
segment represents the
function of the entire right
ventricle
TISSUE DOPPLER IMAGING

51. TEI Index = Right Ventricular MPI
(Myocardial Performance Index)
TEI Index =
𝐼𝑉𝐶𝑇 + 𝐼𝑉𝑅𝑇
𝐸𝑇
TEI Index =
𝑇𝐶𝑂 − 𝐸𝑇
𝐸𝑇
IVCT = Isovolumetric contraction time
IVRT = Isovolumetric relaxation time
ET = Ejection Time
TCO = Tricuspid closing to opening time
Index of Global RV function
(Systolic & Diastolic)

52. TEI Index = Right Ventricular MPI
(Myocardial Performance Index)
 Can be measured either with Pulsed wave doppler or
Tissue Doppler
 In PW doppler two different views are needed. First in
apical 4 chamber view PW doppler recording across
tricuspid valve is obtained.
 Later in PSAX RVOT view , PW doppler recording across
pulmonary valve is obtained.

55. End of A wave to beginning of E wave

56.  TCO time is obtained with this view.
 To obtain ET (ejection time) PSAX RVOT view is used.
 Here PW doppler recording across pulmonary valve is
recorded
 Ejection time is interval between beginning of ejection
tracing to end of tracing.

59. TEI Index =
𝑇𝐶𝑂 − 𝐸𝑇
𝐸𝑇

60. TEI Index using Tissue doppler
 Only single Apical 4 chamber view is needed
 In Tissue doppler mode , PW sample volume is positioned
at tricuspid annulus with cursor parallel to RV free wall
 In this tracing IVCT, ET and IVRT are measured.

63. End of A’ to
beginning of
S’

64. Beginning of S’ to end of S’

65. End of S’ to beginning of E’

66. TEI Index =
𝐼𝑉𝐶𝑇 + 𝐼𝑉𝑅𝑇
𝐸𝑇

67. MPI Correction for Heart Rate
(if HR > 100 or < 75 )

68. Pulsed Doppler Method Pulsed Tissue Doppler Method
>0.4 >0.55RV Dysfunction

69. Advantages
 This approach is
feasible in a large
majority of subjects
 The MPI is reproducible
 It avoids geometric
assumptions and
limitations of the complex
RV geometry
 The pulsed TDI method allows
for measurement of MPI as
well as S´,E´ and A´all from a
single image
 The MPI is unreliable
when RV ET and TR
time are measured with
differing R-R intervals,
as in atrial fibrillation
 It is load dependent
and unreliable when RA
pressures are elevated
Dis-advantages

70. RV DIASTOLIC FUNCTION
 From the apical 4-chamber view, the Doppler beam
should be aligned parallel to RV inflow
 Sample volume is placed at the tips of the tricuspid valve
leaflets
 Measure at held end-expiration and/or take the average
of ≥5 consecutive beats
 Measurements are essentialy the same as those used for
the left side

71. Variable Lower reference
value
Upper reference
value
E (cm/s) 35 73
A (cm/s) 21 58
E/A ratio 0.8 <2.
Decelerationtime (ms) 120 220
IVRT (ms) 23 73
E’(cm/s) 8 20
A’(cm/s) 7 20
E’/A’ratio 0.5 1.9
E/E’ 2 6
RV DIASTOLIC FUNCTION

72. RECOMMENDATIONS
 Measurement of RV diastolic function should be
considered in patients with suspected RV impairment as a
marker of early or subtle RV dysfunction, or in patients with
known RV impairment as a marker for poor prognosis
 Transtricupsid E/A ratio, E/E’ ratio, and RA size have been
most validated are the preferred measures
Grading of RV Diastolic Dysfunction should be done as follows:
E/A ratio < 0.8 suggests impaired relaxation
E/A ratio 0.8 to 2.0 with an E/E’ ratio > 6 or
diastolic prominence in the hepatic veins suggest
pseudo normal filling
E/A ratio > 2 with deceleration time < 120 ms suggests restrictive filling

73. RA PRESSURE DETERMINATION
 Measurement of the IVC should be obtained at end-
expiration and just proximal to the junction of the hepatic
veins that lie approximately 0.5 to 3.0 cm proximal to the
ostium of the right atrium
 To accurately assess IVC collapse, the change in diameter
of the IVC with a sniff and also with quiet respiration
should be measured, ensuring that the change in diameter
does not reflect a translation of the IVC into another plane

75. ESTIMATION OF RA PRESSURE FROM IVC DIAMETER
IVC SIZE BSA
NORMAL 17 mm < 1.55 m2
20 mm 1.55 to 1.71 m2
21 mm > 1.71 m2
IVC COLLAPSE RAP
Size Normal IVC >50% 05 mm hg
Normal IVC <50% 10 mm hg
Dilated IVC >50% 15 mm hg
Dilated IVC <50% 20 mm hg

76. RV PATHOLOGY
 RV volume overload
 RV pressure overload
 RV infarction
 ARVD
 Pulmonary Embolism
 Cardiac Tamponade

77. Right Ventricular Overload
 RV free wall hypertrophy along with IVS hypertrophy
compared to LV posterior wall (from medially angulated
PLAX view)
 Flattening of the interventricular septum in PSAX
 A characteristic feature of right ventricular pressure
overload is the persistence of this septal flattening
throughout the cardiac cycle, that is, in both systole and
diastole. This is in contrast to right ventricular volume
overload, which leads to septal flattening predominantly
during diastole.

79. HEMODYNAMIC ASSESSMENT
Systolic pulmonary artery or RV pressure
• Estimated with TR jet velocity using simplified Bernoulli’s
equation ( provided there is no RVOT obstruction )
RVSP = 4(VTR)2 + RA pressure
• Normal peak RVSP is 35 to 36 mmHg assuming RA
pressure of 3 to 5 mmHg
Measure TR jet velocity from various views to get the highest
velocity

81. HEMODYNAMIC ASSESSMENT
Pulmonary artery diastolic pressure ( PADP )
Estimated from velocity of end diastolic pulmonary
regurgitant jet
PADP = 4(VPR)2+ RA pressure
Mean Pulmonary Pressure
MAP =1/3 (PASP ) + 2/3 (PADP)

82.  If the transducer is not parallel to the flow of TR jet
, peak velocity of the jet will be reduced and
underestimation of PASP will occur.
 Incorrectly estimating mean RA pressure from the
IVC can lead to under or overestimation of
pulmonary pressure

83.  Pulmonary flow has a symmetric contour with a peak
velocity occurring in mid systole. As pulmonary pressure
increases, peak velocity occurs earlier in systole and late
systolic notching is often present.
 The acceleration time (time from onset to peak flow
velocity) can be measured and provides a rough estimate
of the degree of increase in pulmonary artery pressure.
The shorter the acceleration time, the higher the
pulmonary artery pressure.
 Elevated pulmonary regurgitation velocity (> 2 m/sec) is
consistent with increased pulmonary artery diastolic
pressure

86. Right Ventricular Dysplasia
Echocardiography has been used extensively for the diagnosis
of this abnormality, although it is less sensitive & non-specific.
Cardiac MRI is preferred now.
ECHO Findings:
 Right ventricular enlargement
 Focal right ventricular wall motion abnormalities
 Localized aneurysms of the free wall
 The affected right ventricular myocardium may exhibit a
characteristic echogenic appearance, reflecting the
presence of fat and/or scar tissue within the free wall.

87. Right Ventricular Dysplasia