Right ventricle (RV) anatomy and functions

RIGHT VENTRICLE
ANATOMY,PHYSIOLOGY,
ASSESSMENT
&
CLINICAL SIGNIFICANCE
21/06/2013

RIGHT VENTRICLE ANATOMY,PHYSIOLOGY, ASSESSMENT & CLINICAL SIGNIFICANCE
• In 1616, Sir William Harvey was the first to
describe the importance of right ventricular
(RV) function in his seminal treatise, De Motu
Cordis:
“Thus the right ventricle may be said to be
made for the sake of transmitting blood
through the lungs, not for nourishing them.”

DEVELOPMENT OF RV

ANATOMY
• Crescent shaped chamber
• As suggested by “Goor and Lillehi”,
• Inlet
• Trabecular
• Outflow/Conus/
Infundibulum

• Within the right ventricle, a nearly circular ring of
muscle known as the crista supraventricularis
(supraventricular crest) forms an unobstructed
opening into the outlet region. It consists of –
• Parietal band
• Outlet septum
• Septal band, and
• Moderator band

PHYSIOLOGY OF RV
• The primary function of the RV is to receive
systemic venous return and to pump it into the
pulmonary arteries
• PRE LOAD
• AFTERLOAD
• CONTRACTILE FUNCTION
• Also by heart rhythm, synchrony of ventricular
contraction and ventricular interdependence

STRUCTURE OF RV
• Morphologically,ultrastructurally, and biochemically,
the RV differs dramatically from the LV.
• Normal RV seldom exceeds 2–3 mm wall thickness at
end diastole, compared with 8–11 mm for the LV.
• 1/6th
LV mass
• Biochemically,RV has a higher proportion of the alpha-
myosin heavy chain isoform that results in more rapid
but less energy efficient contraction.

PRELOAD
• 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.

PRELOAD/FILLING OF RV
•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

AFTER LOAD
• Normally afterload minimal - 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), and the endothelin pathway
(vasoconstriction).

U-shaped relationship between lung volume
and PVR.

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

RV CONTRACTION
• RV consists of
– 1.The superficial oblique myocardial fibers , in continuity
with the LV fibers
– 2.Deeper layer of longitudinally arranged
• LV has additional middle transverse fibres
• 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.

Higher ratio of RV volume change to RV free wall surface area change and
allows the RV to eject a large volume of blood with little alteration in RV
wall stretch.
Poorly adapted to generating high pressure.

RV PRESSURE VOLUME LOOP
• External mechanical work is substantially lower in the right ventricle
• Trapezoidal shape
• 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
• External mechanical work is substantially lower in the right ventricle
• Trapezoidal shape
• 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
LV RV

• Maximal RV elastance
better reflects RV
contractility than does
the end-systolic
elastance.
• The normal maximal RV
elastance is 1.3 +/-0.84
mm Hg/mL(study by
Dell’Italia and Walsh)
[LV -5.48 +/-1.23]

RV PRESSURE TRACING
• Right-sided pressures are –
• Significantly lower than comparable left-sided
• Show an early peaking and a rapidly 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.

HANGOUT INTERVAL
• Measure of impedence 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 impedence
• Accounts for the normal split S2
• In cases of PAH narrows down.

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, or chronic RV failure

VENTRICULAR INTERDEPENDENCE
• The size, shape, and compliance of 1 ventricle may
affect the size, shape, and pressure-volume
relationship of the other ventricle through direct
mechanical interactions.
• Systolic – Mainly through the interventricular septum
& continuity of muscle fibres
• Diastolic – Mainly through the pericardium

SUMMARY
• Thin walled,more complaint,higher ED volumes(RV -49-101 ;
LV-44-89 ml/m2 )
• Equal cardiac output at less energy expenditure
• Ejects equal amount of blood at lower RVEF (40% - 45%)than
LV( 50%–55%)
• Tolerates volume overload better
• More efficient work output
• Preload and afterload sensitive
• Hang out interval
• Ventricular interdependence

EVALUATION OF RIGHT VENTRICLE
• Chest X ray
• 2d ECHO
• Cardiac MRI
• Nuclear Studies
• Right heart catheterisation
• Other studies

CHEST X RAY
• The lateral view is best suited for the detection of RV enlargement, which
can be noted when the cardiac silhouette occupies more than 40% of the
lower retrosternal space.
• Has reasonable sensitivity but poor specificity

2D ECHO
• Inexpensive,portable,non invasive
• Limitations –retrosternal location, anatomy,
and contractile mechanism of the RV,
markedly load dependent indices of RV
function.
– Guidelines for the Echocardiographic Assessment of the Right
Heart in Adults: A Report from the American Society of
Echocardiography
J Am Soc Echocardiogr 2010

The basal diameter is the maximal short-axis dimension in the basal
one third of the RV . The upper reference limit for the RV basal dimension is 4.2 cm
The midcavity diameter is measured in the middle third of the right ventricle at the level of
the RV papillary muscles. Normal <3.2cm
The longitudinal dimension is drawn from the plane of the tricuspid annulus to the RV apex
Normal<8.6cm

RV FRACTIONAL AREA CHANGE
• The percentage RV FAC, defined as end-diastolic area
end-systolic area)/end-diastolic area x100
• Shown to correlate with RV EF by magnetic
resonance imaging (MRI)
• RV FAC was found to be an independent predictor of
heart failure, sudden death, stroke, and/or mortality
in studies of patients after PTE & MI
• Lower reference value for normal RV fractional area
change- 35%.

RV EF
• Calculating RV volume can be divided into area-
length methods, disk summation methods, and other
methods
• It is inferior in comparison with 3D
echocardiographic methods of RV volume estimation
• Normal reference range by 2D-38 – 50%
• By 3D echocardiography lower reference limit of
44%

INTERVENTRICULAR SEPTAL
POSITION
• In the PSAX, the left ventricle assumes a progressively more
D-shaped cavity as the ventricular septum flattens and
progressively loses its convexity with respect to the center of
the RV cavity
• In Isolated RV volume overload have the most marked shift of
the ventricular septum away from the center of the right
ventricle at end-diastole
• With relatively isolated RV pressure overload have leftward
septal shift away from the center of the right ventricle at both
end-systole and end-diastole, with the most marked
deformation at endsystole

The ratio between the LV anteroposterior dimension and the the septolateral
dimension.
This ‘‘eccentricity index’’ is abnormal and suggests RV overload when this ratio
is >1.0

TAPSE
• TAPSE or TAM(Tricuspid Annular motion) is a method
to measure the distance of systolic excursion of the RV
annular segment along its longitudinal plane, from a
standard apical 4-chamber window.
• TAPSE is usually acquired by placing an M-mode cursor
through the tricuspid annulus and measuring the
amount of longitudinal motion of the annulus at peak
systole
• Normal lower reference value for impaired RV systolic
function of 16 mm.
• More specific,less sensitive

TAPSE
5mm =20% RVEF
10mm =30%
15mm =40%
20mm =50%

HEMODYNAMIC ASSESSMENT OF THE
RV
• RVSP
• RVSP can be reliably
determined from peak TR jet
velocity
• By the simplified Bernoulli
equation and combining this
value with an estimate of the
RA pressure: RVSP = 4(V)2 +
RA pressure
• In the absence of a gradient of
across the pulmonic valve or
RVOT, SPAP is equal to RVSP

RA PRESSURE

PVR
• Pressure gradient = flow x resistance.
• PVR = peak TR velocity (in meters per second) /RVOT
velocity-time integral (in centimeters) x10 +0.16
• This relationship is not reliable in patients with very
high PVR, with measured PVR > 8 Wood units
• Peak TR velocity/RVOT TVI = normally 0.15

RV dP/dT
• Time required for the TR jet to increase in velocity from 1 to 2
m/s
• The dP/dt is therefore calculated as 12 mm Hg divided by this
time (in seconds), yielding a value in mm of Hg per second.
• RV dP/dt < 400 mm Hg/s is likely abnormal

RIMP
• The MPI, also known as the RIMP or Tei index, is a global
estimate of both systolic and diastolic function of the
right ventricle
• The MPI is defined as the ratio of isovolumic time divided
by ET, or [(IVRT + IVCT)/ET]
• Normal right-sided MPI = 0.28+/-0.04
• Yoshifuku and colleaguesdescribed pseudonormalized values in
acute and severe RV myocardial infarction, which can probably be
explained by a decrease in isovolumic contraction time associated
with an acute increase in RV diastolic pressure

PULSED TISSUE DOPPLER
Peak systolic velocity < 11.5 cm/s identifies the presence
of RV dysfunction with
a sensitivity and specificity of 90% and 85%, respectively

STRAIN IMAGING

COLOUR TISSUE DOPPLER

SPECKLE TRACKING-STRAIN IMAGING

IVA
Isovolumic Myocardial acceleration(IVA) is defined as the peak isovolumic myocardial
velocity divided by time to peak velocity at the lateral tricuspid annulus
The lower reference limit by pulsed-wave Doppler tissue imaging is 2.2 m/s2(1.4 to 3.0)

Measurement of RV Diastolic Function
• From the apical 4-chamber view, the Doppler beam
should be aligned parallel to the RV inflow.
Grading of RV diastolic dysfunction
• Tricuspid E/A ratio < 0.8 suggests impaired relaxation,
• Tricuspid E/A ratio of 0.8 to 2.1 with an E/e’ ratio > 6
or diastolic flow predominance in the hepatic veins
suggests pseudonormal filling
• Tricuspid E/A ratio > 2.1 with a deceleration
Time < 120 ms and late diastolic antegrade flow in the
pulmonary artery suggests restrictive filling

RV DYSFUNCTION (RVEF)-
MILD -35-44
MOD -26-34
SEVERE -<25

REGIONAL FUNCTION
• RCA –
Inferior &
lateral
• PDA –
Inferior

Mc Connell’s Sign
• Severe hypokinesia of the RV mid free wall, with
normal contraction of the apical segment.
• Sensitivity of 77% and specificity of 94% for acute
pulmonary embolism.
• Recently, casazza and colleaguesalso recognized this
pattern in patients with acute RV myocardial
infarction.

“Reverse McConnell’s Sign”: A
Unique Right Ventricular Feature of
Takotsubo Cardiomyopathy
• Motion of the basilar and middle segments of the RV
free wall is often .However, the motion of the apical
segment of the RV free wall is usually hypokinetic

ARVD
• Regional wall-motion abnormalities occur in
79% of probands
• Most common sites of these abnormalities-
–Apex (72%)
–Anterior wall (70%)

TEE

NUCLEAR IMAGING
• First-pass radionuclide ventriculography
• Detects transit of a 99mTc labeled tracer
through the RV.
• Normal values have been reported as 52%+/-
6%(lower limit of normal of 40%).
• Considered the nuclear method of choice for
RV assessment because of reasonably good
correlations with CMR.

• Gated equilibrium blood pool imaging
• Requires longer acquisition periods, but is technically less
demanding.
• Nuclear techniques restricted by limited spatial resolution,
relatively prolonged imaging times, and need for
radioisotopes

CARDIAC MRI

• PET SCAN –
• FDG accumulation in RV free wall correlates -
– Negatively with RV EF
– Positvely with PVR and mean PAP in patients with PAH.
• MAGNETIC RESONANCE SPECTROSCOPY-
• Quantifies intracellular TG content-correlates to RV systolic and
diastolic function in diabetics.

Right Heart Pressures Tracings

Normal RV waveform artifact
• Note the notch on the
top of RV pressure
waveform
– This represents “ringing”
of a fluid-filled catheter
– Ringing can also be
noted on the diastolic
portion of the waveform

In advanced RV
failure is a reduction
in the PAP coincident
with a decrease in
cardiac index

RV DYSFUNCTION
• RV dysfunction refers to abnormalities of filling or
contraction without reference to signs or symptoms of HF
• RV failure is a complex clinical syndrome that can result from
any structural or functional cardiovascular disorder that
impairs the ability of the RV to fill or to eject blood
• The most common cause of RV dysfunction is chronic left-
sided HF.
• PAH is the second important cause of RV dysfunction
The survival rate associated with severe RV
failure may be as low as 25%–30%

The cardinal clinical
manifestations of RV failure are
•(1) fluid retention, which may
lead to peripheral edema, ascites,
and anasarca
•(2) decreased systolic reserve or
low cardiac output, exercise
intolerance and fatigue
•(3) atrial or ventricular
arrhythmias

VOLUME OVERLOAD
• RV can handle large volumes
easily.
• The highly compliant RV &
low-resistance pulmonary
vasculature is able to
accommodate the increased
flow without an increase in
pressure.
• However,chronic right
ventricular volume overload
eventually leads to high-
output RV failure
PRESSURE OVERLOAD
• In the early stages, RVH is
mostly an adaptive response
(compensated state).
• As the disease progresses, the
RV dilates and RV failure
eventually occurs (maladaptive
right ventricular remodeling).
• The compensatory phase
during the progressive
increasing afterload is shorter
in the RV compared with the
LV.
• The same is true with acute
increases in the afterload
• Probably due to due inability to
switch back to the fetal gene
program

• RV adaptation to disease is complex and depends on
many factors.
1. The type and severity of myocardial injury or stress,
2. The time course of the disease (acute or chronic),
3. The time of onset of the disease process (newborn,
pediatric, or adult years)
4. Neurohormonal activation,
5. Altered gene expression,
6. Pattern of ventricular remodelling
The role of RV dysfunction in various clinical settings..

IMPORTANT CONDITIONS INVOLVING
RV DYSFUCTION
• Left Heart Failure with RV involvement
• Cor pulmonale
• Ischemia – RVMI
• Congenital conditions
• Arrhythmic conditions

RV DYSFUNCTION IN LEFT HEART
FAILURE
• Mechanisms-
1. Pulmonary venous hypertension
2. Intrinsic myocardial involvement
3. Ventricular interdependence
4. Neurohormonal interactions
5. Myocardial ischemia
• RV dysfunction appears to be more common in
nonischemic cardiomyopathy than in ischemic
cardiomyopathy and more closely parallels LV
dysfunction

INCIDENCE
• RV failure is estimated to account for 3% of all
acute heart failure admissions and confers worse
mortality rates than acutely decompensated left
heart failure
Nieminen MS,et al,EuroHeart Failure Survey II (EHFS II),Heart J 2006; 27:2725–
2736
• Reeves and Groves reported that 44% of patients
with coronary artery disease at the time of
coronary arteriography and right heart
catheterization have pulmonary hypertension.
Approach to the patient with pulmonary hypertension. In: Weir EK, Reeves JT, eds. Pulmonary
Hypertension. Mt Kisco, New York: Futura Publishing Company Inc; 1984:1– 44

PROGNOSIS

RVEF & PAP -normal
Low RVEF
High PAP
Low RVEF & High PAP

OTHER INDICES
• RVEF represents a strong and independent
predictor of mortality in left HF
• Additive effect has been found with presence
of PAH
• Other indexes of RV function like RV
myocardial performance index and systolic
and diastolic tricuspid annular velocities also
are important.

Volume 15, Issue 4,Pg- 408-414

• Only a few studies have addressed the prognostic importance
of RV diastolic function.
• In patients with left HF, Yu and colleagues showed that RV
diastolic dysfunction defined by abnormal filling profiles is
associated with an increased risk of nonfatal hospital
admissions for HF or unstable angina.
• Exercise capacity, a strong predictor of mortality in HF,
appears to be more closely related to RV function than LV
function.
• Baker and colleagues and Di Salvo and colleagues observed a
significant correlation between RVEF and exercise capacity in
HF

COR PULMONALE
• Definition of cor pulmonale is RV enlargement or hypertrophy
secondary to pulmonary disease in the absence of LV
failure/congenital heart disease.
• May present with RV hypertrophy,asymptomatic RV dysfunction, or RV
failure
• Chronic obstructive pulmonary disease (COPD) is the most common
cause of cor pulmonale in North America (20 to 30% develop cor
pulmonale)
• Diseases complicated by cor pulmonale have worse survival than the
same disease without cor pulmonale. As an example, four-year survival
is roughly 75 percent among patients with COPD of varying severity ,
but <50 percent among patients whose COPD is complicated by cor
pulmonale
– Cor pulmonale: an overview.Budev MM, Arroliga AC, Wiedemann HP, Matthay RA,Semin
Respir Crit Care Med. 2003;24(3):233.

• In a study for outcomes by Campo et al In-hospital
mortality of PAH patients with cor pulmonale was 14 %, but
this increased to 45 to 50 % among patients who required
inotropic medications or were admitted to the intensive
care unit.
• Mortality following discharge was 13, 26, and 35 % at 3, 6,
and 12 months, respectively.
– Outcomes of hospitalisation for right heart failure in pulmonary
arterial hypertension,Eur Respir J. 2011;38(2):359
• In a recent study, Burgess and colleagues showed that RV
end-diastolic diameter index and the velocity of late
diastolic filling were independent predictors of survival

IDIOPATHIC PAH
• Increased afterload is the primary cause of right
ventricular adaptation and, ultimately, RV failure.
• Severity of symptoms and survival are strongly
associated with right ventricular function, and right
heart failure is the main cause of death in patients with
PAH.
• Survival rates at 1 year, 68% ; at 3 years, 48% ;and at 5
years, 34%. Measures of right ventricular pump
function, such as right atrial pressure, cardiac index
and PAP as important prognostic measures
– D’Alonzo GE, Barst RJ, Ayres SM, et al. Survival in patients with primary pulmonary
hypertension. Results from a national prospective registry. Ann Intern Med 1991; 115:
343–349

EMF
• Disease of tropical countries
• Isolated RV involvement -10%;BV involvement -50%
• Fibrous lesions affect the inflow of the right
ventricle,may also involve the atrioventricular valves,
thereby producing regurgitant lesions.
• Presents as Right heart failure
• Obliteration of apex and normotensive TR occur.
• Biospy-rarely diagnostic
• TV repair/replacement & endocardiectomy may be
needed.

The fibrotic retraction of the right ventricular apex
produces the typical apical dimple.

PTE
• PE is the most common cause of acute cor
pulmonale in the adult.
• The mortality of PE is closely related to the degree of
RV failure and hemodynamic instability.
• Thus, patients may be divided into 3 groups:
Expected mortality
Hemodynamically stable <4 %
RV dysfunction +,no shock 5 – 15 %
Cardiogenic shock 20 – 50 %

RV dysfunction means the presence of at least 1 of the
following:
— RV dilation (apical 4-chamber RV diameter divided by
LV diameter >0.9) or RV systolic dysfunction on
echocardiography
— RV dilation (4-chamber RV diameter divided by LV diameter
>0.9) on CT
— Elevation of BNP (>90 pg/mL)
— Elevation of N-terminal pro-BNP (>500 pg/mL);
--- Electrocardiographic changes (new complete or incomplete
right bundle-branch block, anteroseptal ST elevation
or depression, or anteroseptal T-wave inversion)
RV dysfunction means the presence of at least 1 of the
following:
— RV dilation (apical 4-chamber RV diameter divided by
LV diameter >0.9) or RV systolic dysfunction on
echocardiography
— RV dilation (4-chamber RV diameter divided by LV diameter
>0.9) on CT
— Elevation of BNP (>90 pg/mL)
— Elevation of N-terminal pro-BNP (>500 pg/mL);
--- Electrocardiographic changes (new complete or incomplete
right bundle-branch block, anteroseptal ST elevation
or depression, or anteroseptal T-wave inversion)

• RV dysfunction may also predict recurrent PE or
DVT
– Association of persistent right ventricular dysfunction at hospital discharge after
acute pulmonary embolism with recurrent thromboembolic events.Grifoni S et al,
Arch Intern Med. 2006
• Although the presence of RV dysfunction and co-
morbidities are associated with an increased risk
of death in the long-term, quantifiable tools that
accurately predict outcome are lacking
• Evidence of RV dysfunction is an indication for
TLT in sub massive PTE(class IIb)

RV MI
• 30 - 50 % cases of IWMI,upto 13-15 % cases of AWMI
• RCA is usually the culprit,typically a proximal
occlusion
• 25 % -Cardiogenic shock with raised JVP(prominent
x) is a common presentation

DIAGNOSIS
• The clinical syndrome of RVMI was first recognized by Saunders in
1930 when he described the triad of
1. Hypotension,
2. Elevated jugular veins, and
3. Clear lung fields
• Hemodynamic consequences of RVMI depend on the extent of RV
free wall dysfunction, presence of concomitant right atrial ischemia
& extent of simultaneous left ventricular impairment.
• Clinically evident hemodynamic manifestations are seen in less than
50 percent of affected patients

• Pattern of
equalized
diastolic
pressures
and RV “dip
and
plateau”press
ure tracing

MANAGEMENT
•The initial therapy for hypotension in patients with right
ventricular infarction should almost always be volume
expansion. The reported efficacy of this approach is variable, a
probable reflection of differences in initial volume status
•Opioids, nitrates,vasodilators,CCB and beta blockers should be
used with caution
•Ventricular pacing may fail to increase cardiac output and
atrioventricular sequential pacing may be required

OUTCOMES
• Many patients spontaneously improve within 3 to 10
days regardless of the patency status of the infarct-
related artery.
• Furthermore, global RV performance typically
recovers, with normalization within 3 to 12 months.
• Although RV function may recover despite persistentAlthough RV function may recover despite persistent
RCA occlusion, acute RV ischemia contributes to earlyRCA occlusion, acute RV ischemia contributes to early
morbidity and mortalitymorbidity and mortality.

EARLY PROGNOSIS
• Prior to the use of primary percutaneous coronary
intervention, meta-analyses found that right
ventricular involvement in patients with an acute
inferior MI was associated with a worse in-hospital
outcome due primarily to persistent hypotension and
arrhythmias
• Among patients who are diagnosed with RVMI and
cardiogenic shock, in-hospital and 30-day mortality
have been reported to be 53 and 23 percent,
respectively.

LONG TERM PROGNOSIS
• In those who survive RVMI, the long-term prognosis is primarily
determined by the extent of left ventricular involvement.
• Nearly complete recovery of RV function has been shown to occur in 62 to
82 percent of patients within the first few months
– Frequency and significance of right ventricular dysfunction during inferior wall left ventricular myocardial infarction treated with
thrombolytic therapy (results from the thrombolysis in myocardial infarction [TIMI]II trial). The TIMI Research Group,Am J
Cardiol. 1993;71(13):1148
– Prognostic significance of persistent right ventricular dysfunction as assessed by radionuclide angiocardiography in patients with
inferior wall acute myocardial infarction,Am J Cardiol. 2000;85(8):939
• Chronic right heart failure attributable only to right ventricular infarction
is rare,even in those without successful reperfusion
• Over the long term, a persistent reduction in right ventricular function
appears to be associated with a worse long-term prognosis
• During a mean follow-up of 17 months, patients with an RVEF <40 percent
had a significantly higher mortality compared to those with an RVEF >40
percent (adjusted hazard ratio 2.9).

RV IN CHD

SHUNT PHYSIOLOGY
• ASD causes volume overload of RV,while VSD & PDA cause
pressure overload of RV.
• In those patients with non-restrictive defects, right ventricular
wall thickness does not regress.
• With aging and growth, right ventricular wall thickness
increases at a rate equal to that of the left ventricle and the
thickness of the right and left ventricular free walls remains
equal resembling fetal heart.
• Normal right ventricular function is thus the rule rather than
the exception
• Even with development of eisenmengerisation, RV
dysfunction is rare

EISENMENGER’S SYNDROME
• Eisenmenger’s has good long-term prognosis
among other causes of PAH
• Long-term survival of 80% at 10 years, 77% at
15 years, and 42% at 25 years
-Kidd L, Driscoll DJ, Gersony WM, et al. Second natural history study of congenital
heart defects. Results of treatment of patients with ventricular septal defects.
Circulation. 1993;87(2 Suppl):I38–51.
-Saha A, Balakrishnan KG, Jaiswal PK, et al. Prognosis for patients with Eisenmenger
syndrome of various aetiology. Int J Cardiol. 1994;45(3):199–207

“Comparison of the hemodynamics and survival of adults with severe
primary pulmonary hypertension or Eisenmenger syndrome”
Journal of Heart & Lung Transplant, Volume 15, 1996, Hopkins et al,

WHY??

It is all about timing!
• The better prognosis of Eisenmenger patients is
believed to be to the fact that the subpulmonary
ventricle has been exposed to high pressures and
has been primed since birth; it is betterbetter adaptedadapted
because of the long-standing volume and pressure
overload

POST OP TOF
• With Surgical repair-RV remodels with regression of wall
thickness.
• Significant post-op PR (regurgitant fractions of >50%) Leads to
volume overload of the right ventricle and chamber dilatation
• It can lead to exertional dyspnea, right ventricular failure &
increased incidence of atrial and ventricular arrhythmias and
SCD
• Severe RV dilatation, especially when progressive, may be an
early sign of a failing RV and should prompt consideration of
pulmonary valve replacement.
• QRS width may reflect the degree of right ventricular dilation and, when
extreme (>180 milliseconds) or rapidly progressive, may be a risk factor
for sustained ventricular tachycardia and sudden death

“RESTRICTIVE RV PHYSIOLOGY”
• Defined by the presence of forward and laminar late
diastolic pulmonary flow throughout respiration due to stiff
RV with RA systole required to maintain forward flow.
• EarlyEarly after TOF repair, restrictive RV physiology is
associated with a low cardiac output and longer intensive
care stay.
• LateLate after TOF repair, however, restrictive RV physiology
counteracts the effects of chronic pulmonary regurgitation.
• It is associated with a smaller RV, shorter QRS duration,
and increased exercise tolerance.

RVOT OBSTRUCTION
• Isolated PS is found in 80%-90% of all patients with RVOT
obstruction.
• A hypertrophied RV can maintain its function for years,
even when RV pressures are near systemic.May cause RV
failure on long term.
• After pulmonary valve commissurotomy,open valvotomy or
a transannular patch placement invariably result in various
degrees of PR & RV volume overload.
• Eventually RV dysfunction ensues and patients develop
symptoms, such as dyspnea, fatigue and substantial
arrhythmia.

SUICIDAL RV
• A dynamic right ventricular outflow obstruction has
been referred to as “suicide” RV.
• It has been reported in both children and adults
following either surgical or catheter relief of valvular
obstruction, particularly in patients who have an initial
supra-systemic right ventricular pressure.
• In some cases, the obstruction may become severe
enough to produce low cardiac output.
• This is frequently related to infundibular hypertrophy
and may gradually resolve spontaneously.
• Immediate treatment-hydration & beta blocker
therapy

EBSTEIN’S ANOMALY
• Rare CHD
• Results from failure or
incomplete delamination of
the inner layers of the inlet
zone of the ventricles.
• 1)Apical displacement of
septal & posterior leaflets
• 2)Dilation of the “atrialized”
portion of the right ventricle,
with various degrees of
hypertrophy and thinning of
the wall
• (3)Redundancy, fenestrations,
and tethering of the anterior
leaflet

• RV failure in Ebstein’s anomaly results primarily from
volume overload of the RV and from a hypoplastic RV
chamber incapable of adequately handling the systemic
venous return
• Size of functional ventricle(as measured by GOSE score)is a
marker of early mortality.
• As noted in the 2008 ACC/AHA adult congenital heart
disease guidelines, indications for surgical repair of
Ebstein’s anomaly beyond infancy include:
1. Symptoms or deteriorating exercise capacity
2. Cyanosis (oxygen saturation less than 90 percent)
3. Paradoxical embolism
4. Progressive cardiomegaly on chest x-ray
5. Progressive right ventricular (RV) dilation or reduction of RV
systolic function

Uhl’s Anomaly
• Parchment heart
• Aplasia/hypoplasia of most if not all of the
myocardium of trabecular portion of RV,with normally
functioning tricuspid valve.
• RV acts as a passive conduit that channels blood from
RA to pulmonary trunk.
• Survival into adulthood possible
• The clinical picture of Uhl’s anomaly is dominated by
congestive HF,which may result in death in infancy

ARVD
• Genetic disorder involving desmosomal protein
• Unusual myopathy that involves predominantly the RV and results
in fibrofatty replacement of the myocardium.
• The most frequently involved areas of the RV are the posterior
base, apex, and the infundibulum. These areas are collectively
called the triangle of dysplasia.
• Sudden cardiac death frequently is the first manifestation of the
disease.
• Risk factors for sudden death include RV dilatation, precordial
repolarization abnormalities, LV involvement, documented or
suspected ventricular tachycardia or fibrillation, and 1 affected
family member.

• Classified into four clinico-
pathologic stages
1. Concealed phase or silent
phase
2. Overt arrhythmic phase
3. Global right ventricular
dysfunctional phase -
isolated right heart
failure(6%).
4. Bi-ventricular pump failure
with LV involvement
EPSILON WAVES AND T WAVE
INVERSION

Pattern of RV involvment
• RV dilatation can be observed in 80% of patients
• RV free wall motion abnormalities(akinesia/dyskinesia)
can be found in 33% patients
• RV saccular aneursyms
• Upto 66.7% show systolic dysfunction
• Right ventricular outflow tract (RVOT) dilation
(diameter 30 mm) has been reported to have the
highest sensitivity and specificity (89% and 86%,
respectively) of echocardiographic parameters

MR imaging is the imaging modality of
choice in evaluating

DEVICE THERAPY-PPI
• RV apical pacing
• RVOT pacing
• Dual site RV pacing

RV APICAL PACING
• Asynchronous electrical activation –ventricular dyssynchrony
• Redistribution of mechanical load within the ventricular wall
and may lead to reduction of the blood flow and myocardial
wall thickness over the site of early activation,esp
inferoposterior and apical areas –ADVERSE REMODELLING
• This leads to RWMA and impaired LV function on long term in
9-26 % cases
- Ozcan C, Jahangir A,et al; N Engl J Med 2001;344:1043e51
- MOST TRIAL :Adverse effect of ventricular pacing on heart failure and atrial
fibrillation among patients with normal baseline QRS duration in a clinical
trial of pacemaker therapy for sinus node dysfunction.Sweeney Mo et
al,Circulation 2003

In the Dual Chamber and VVI Implantable Defibrillator (DAVID)
trial,RV pacing was associated with heart failure disease progression,
including an increased incidence of worsening heart failure

ALTERNATIVES
• Managed ventricular pacing — Devices with this
capability allow native conduction to occur, even
in the setting of substantial PR prolongation or
second degree atrioventricular (AV) block.
• Prolonged programmed AV intervals
• Eliminating rate responsive AV delay
• DDI or DDIR pacing
• RVOT pacing,septal pacing, and direct His bundle
pacing

RVOT PACING

DUAL SITE RV PACING
• Recently, the beneficial effects of dual site RV pacing
(RVOT + RV apex) in a small group of patients, in
whom CS lead implantation failed because of the
technical difficulties during CRT, has been reported.
– Pachon JC, Pachon EI, Albornoz RN, et al. Pacing Clin Electrophysiol
2001;24:1369e76.
– O Sai Satish ,Europace et al (2005) 7, 380e384,The European Society of
Cardiology.

CRT
• Patients with marked RV dysfunction (RVEF <
30%/TAPSE <1.5mm) have a particularly low
response rate to CRT.
• It is possible that significant RV dysfunction marks
extensive and irreversible adverse remodelling,
preventing reverse remodelling and functional
recovery after CRT implantation.
• Right ventricular function is also an important
predictor of major adverse events & mortality
following CRT
– Ghio S,et al: Long-term left ventricular reverse remodelling with cardiac
resynchronization therapy: results from the CARE-HF trial. Eur J,Heart Fail 2009, 11:480-
488.
– Burri H,et al: Right ventricular systolic function and cardiac resynchronization therapy.
Europace 2010, 12:389-394.

Heart 2013;99:722–728. doi:10.1136/heartjnl-2012-303076

OTHERS
• In patients with ARDSARDS,Significant RV dysfunction occurs in 15% of
patients(usually is related to microvasculature dysfunction and/or the
effects of mechanical ventilation).It is an independent predictor of
mortality.
• In Sepsis, RV dysfunction is related to myocardial depression or PAH.
Persistence of RV dysfunction in sepsis appears to be associated with an
increased risk of mortality.
• In severe MSsevere MS RV dysfunction may be the cause of mortality in 60% to 70%
of untreated patients
• In unoperated chronic MRchronic MR patients, subnormal RVEF at rest is associated
with decreased exercise tolerance, complex arrhythmias, and mortality.

• Preoperative RV systolic dysfunction has been shown to predict late
survival after coronary artery bypass surgery and mitral valve surgery.
• Severe RV failure after Cardiac surgeryCardiac surgery occurs in 0.1% of patients and is
associated with high mortality rates.
• Examples
• Coronary artery bypass surgery
• Valve replacement
• LV assist device placement-20-30%
• Heart transplantation-2-3%,20% in some reports
• Factors involved in the pathophysiology of RV failure in cardiac surgery
include RV ischemia, PAH, reperfusion lung injury, pulmonary emboli,
sepsis.
• After insertion of LV assist deviceLV assist device the underlying reasons-- higher cardiac
output after LVAD implantation, decrease in the septal contribution to
ventricular interdependence or septal suck down effect).

• Many factors contribute to the development of acute RV
failure after heart transplantation-after heart transplantation-
1)Preexisting or acquired pah(preoperative PVR >6 wood units &
transpulmonary gradient >15 mm hg)
2) Marginal organ preservation and long ischemic time,
3) Mechanical obstruction at the level of the pulmonary artery
anastomosis
4) Significant donor-recipient mismatch with a much smaller donor heart
(more than 20% mismatch in size)
5) Acute allograft rejection.
• RV failure in this setting is associated with increased
perioperative mortality
• PregnancyPregnancy in patients with severe RV failure is associated
with high maternal and fetal mortality rate. The periods of
greater risk are the second trimester and the period of active
labour and delivery.

MANAGEMENT

PAH SPECIFIC THERAPIES
• Management of patients with acute and chronic RV failure
is more empiric than the management of patients with left
heart failure
• CCB- RV function return to normal in patients with PAH
who are vasoreactive.
• ERA- Not found to cause significant fall in PAP or reversal of
RV remodeling
• PDE5I –Additional inotropic, dose-related increases in
cardiac output
• PGI2 -Increase in contractility and cardiac output. Maintain
relatively normal RV function in the face of severe
pulmonary vascular disease

IPBP
• Earlier standard intraaortic balloon pump was
been inserted into a synthetic vascular graft &
anastomosed in an end-to-side fashion to the
pulmonary artery.
• Per cutaneous insertion of 8 ml balloon into
pulmonary artery has been shown to be possible in
an experiment in dogs.
• Have been found to be useful in cases of acute
PTE,PAH,Post CABG with RV failure.

RV ASSIST DEVICES
• When biventricular failure is refractory, mechanical circulatory
support may be considered as part of a bridge-to-transplant
strategy.
• Other indications for RVAD implantation are as follows:
– RV MI
– Acute myocarditis
– Postcardiotomy cardiogenic shock (including valve surgery, coronary
artery bypass, heart transplantation, LVAD insertion, and pulmonary
thromboendarterectomy)
– Acute rejection after orthotopic heart transplantation
– Refractory arrhythmias
– Bridge to decision following cardiac arrest
• Cardiac transplantation is the definitive treatment of patients with
advanced RV failure.

• 3 broad categories –
• Surgically implanted centrifugal pump
devices-Centrimag
• Percutaneous systems (also mostly centrifugal
pump devices) – Tandem heart
• Extracorporeal membrane oxygenation
(ECMO) system

CENTRIMAG

HEART TRANSPLANTATION
• Indicated for selected patients with advanced
refractory RV failure,with arrhythmogenic RV
dysplasia and refractory tachyarrhythmias .
• Advanced RV failure secondary to PAH (PVR >
6 WU)-heart-lung or isolated lung
transplantation been useful.
• Complex CHD with PH should be considered
candidates for heart-lung transplantation.

Thank you

Right ventricle (RV) anatomy and functions

More Related Content

What's hot

Similar to Right ventricle (RV) anatomy and functions

More from Malleswara rao Dangeti

Recently uploaded

Right ventricle (RV) anatomy and functions

Editor's Notes