Approach to evaluation of the right ventricle in adults - UpToDate 05/08/20 16.

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Approach to evaluation of the right ventricle in adults

Authors: Peter G Danias, MD, PhD, FACC, FESC, James D Chang, MD
Section Editor: Heidi M Connolly, MD, FACC, FASE
Deputy Editors: Susan B Yeon, MD, JD, FACC, Brian C Downey, MD, FACC

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jul 2020. | This topic last updated: Sep 04, 2019.

INTRODUCTION

Evaluation of the right ventricle (RV) is a key component of the clinical assessment of many cardiovascular and pulmonary disorders. There are many ways
to evaluate the RV, most of which can be accomplished noninvasively and without radiation exposure.

This topic will discuss the approach to evaluation of RV structure and function. The evaluation of left ventricular (LV) structure and function is discussed
separately. (See "Tests to evaluate left ventricular systolic function" and "Echocardiographic evaluation of left ventricular diastolic function" and
"Echocardiographic recognition of cardiomyopathies".)

ANATOMY

Morphologic features of the RV that permit differentiation between the anatomic RV and LV in cases of complex congenital anomalies include:

● Separate inflow and outflow tracts arranged in series such that the tricuspid atrioventricular (AV) valve (inlet) is not in direct fibrous continuity with the
pulmonic semilunar valve (outlet). Unlike the other three cardiac valves, the pulmonic valve is not in continuity with any part of the fibrous cardiac
skeleton, but rather, it arises directly from infundibular myocardium.

● Highly trabeculated endocardial surfaces with multiple discrete muscular ridges, the most prominent of which is the moderator band.

● Apical displacement of the septal leaflet of the tricuspid valve relative to the corresponding (anterior) leaflet of the mitral valve.

In contrast to the LV cavity which is readily modeled as a symmetrical prolate hemispheroid, the RV cavity is divided into three asymmetrical segments
which include the trabeculated inflow tract, the trabeculated apex, and the smooth outflow tract (figure 1). Several discrete muscular ridges or bands are
present in the RV, for which inconsistent and often confusing nomenclature has been used [1].

● The crista supraventricularis (also called the ventriculo-infundibular fold) separates the RV inflow tract from the RV outflow tract and is continuous with
the parietal band.

● The moderator band (through which the right bundle branch passes) is continuous with the septomarginal band. Abnormal development or
hypertrophy of these muscular bands can lead to the syndrome of double-chambered RV, characterized by muscular obstruction between the RV inlet
and RV outlet [2].

● The RV outflow tract is also referred to as the infundibulum, the supracristal segment, and the conus (arteriosus).

The anatomically distinct walls of the RV are the inferior (also known as diaphragmatic) wall, anterior wall, and infundibulum (conus arteriosus). An apex
and lateral wall of the RV are often identified separately, but are actually parts of the anterior wall. The juncture of anterior and inferior walls forms an acute
angle (the acute margin of the heart), in contrast to the rounded contour of the obtuse margin of the heart, which is formed by the lateral wall of the LV.

Septal, anterior, and posterior leaflets comprise the tricuspid valve and are supported via chordae tendinae by anterior and posterior papillary muscles;
some of the chordae attach directly to the interventricular septum, right ventricular free wall, or moderator band, unlike the mitral valve apparatus which is
entirely supported by papillary muscles. The septal portion of the tricuspid annulus is supported by the right fibrous trigone, while the mural portion of the
annulus abuts the RV free wall, lacking support from the fibrous cardiac skeleton and therefore prone to elongation under chronic pressure or volume
overload, leading to annular dilation and valvular regurgitation (figure 2).

PATHOPHYSIOLOGY

Acquired dysfunction of the RV is most often secondary to pressure and/or volume overload. RV dysfunction may also be caused by conditions directly
affecting the right ventricular myocardium (eg, cardiomyopathy or ischemic heart disease).

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Under normal conditions, the requirement for stroke work (the product of stroke volume and mean pulmonary artery systolic pressure) by the RV is one-
seventh to one-sixth that of the LV [3], since mean pulmonary arterial systolic pressure is approximately one-sixth to one-seventh mean systemic arterial
systolic pressure while stroke volume is identical. Accordingly, RV mass is normally one-sixth to one-seventh that of the LV [4]. Hence, when an RV not
chronically preconditioned to generate increased stroke work is required to eject its entire stroke volume against a pathologically elevated afterload (as in
acute pulmonary embolism or acute left heart failure [HF]), one or more of the following can occur: dilation, hypokinesis, leftward displacement of the
interventricular septum, and tricuspid regurgitation; which results in elevated filling pressure into and reduced antegrade ejection out of both sides of the
heart.

In states of RV volume overload there is predominantly diastolic flattening of the interventricular septum, accounting for the D-shaped short axis
configuration of the LV during diastole. In states of RV pressure overload, flattening of the septum is constant throughout the cardiac cycle, accounting for
the D-shape of the LV throughout the entire cardiac cycle.

Volume overload causes RV dilation (eccentric hypertrophy). As is the case for mitral regurgitation, tricuspid regurgitation tends to beget more tricuspid
regurgitation due to the effects of chronic volume overload, including chamber and annular dilatation, leaflet tethering, and loss of coaptation, which worsen
the tricuspid regurgitation and create a positive feedback loop or vicious cycle. Dilation of the RV can also occur in a variety of other diseases that affect
the myocardium of the RV, including RV infarct, RV dysplasia (including arrhythmogenic right ventricular dysplasia, Naxos disease, and Uhl's anomaly),
and as a result of cardiotoxic chemotherapy, myocarditis, and myositis. Thickening of the RV free wall (concentric hypertrophy) is a consequence of
pressure overload. (See "Etiology, clinical features, and evaluation of tricuspid regurgitation" and "Echocardiographic assessment of the right heart".)

LV function can be adversely affected by RV pressure and/or volume overload by direct ventricular interaction [5] between the conjoined pumping
chambers (the reverse Bernheim effect, so-named because it is the reciprocal of what Bernheim originally hypothesized [6] as a mechanism of right HF,
secondary to hypertrophic cardiomyopathy). This effect is mediated by the constraining effects of the pericardium, the shared interventricular septum, and
the superficial layer of cardiac myofibers which encircle both ventricles parallel to the AV groove. Mitigation of the reverse Bernheim effect by pressure- or
volume-unloading of the RV can therefore result in marked improvement of LV filling and ejection.

CONDITIONS ASSOCIATED WITH RV DYSFUNCTION

RV dysfunction may develop secondary to hemodynamic (pressure and/or volume) overload or from a primary disease of the myocardium.

Causes of secondary RV dysfunction — RV dysfunction may be caused by pressure and/or volume overload.

● The most common cause of pressure overload is pulmonary hypertension; other causes include RV outflow obstruction such as pulmonic stenosis
(subvalvular or valvular), pulmonic atresia, and pulmonary artery stenosis (which may be caused by conditions such as Williams syndrome, rubella
exposure during pregnancy, mediastinal radiation therapy, surgical banding, or sequelae of surgical shunts). (See "Clinical features and diagnosis of
pulmonary hypertension of unclear etiology in adults" and "Clinical manifestations and diagnosis of pulmonic stenosis in adults".)

● Causes of RV volume overload include left-to-right shunts at or above the atrial level (eg, atrial septal defect, unroofed coronary sinus, anomalous
pulmonary vein connection to the right atrium and/or the vena cava), tricuspid regurgitation, and pulmonic regurgitation. (See "Etiology, clinical
features, and evaluation of tricuspid regurgitation" and "Pulmonic regurgitation" and "Clinical manifestations and diagnosis of atrial septal defects in
adults".)

Pulmonary hypertension — Acute or chronic pulmonary hypertension (PH) adversely impacts RV function. Causes of PH are classified as follows
(table 1) (see "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults"):

● Group 1: Pulmonary arterial hypertension. This group includes pulmonary arterial hypertension arising from a variety of causes, including from
congenital heart disease (PH-CHD). In this group, vascular resistance occurs at the level of the precapillary arterioles. (See "The epidemiology and
pathogenesis of pulmonary arterial hypertension (Group 1)" and "Clinical manifestations and diagnosis of pulmonary hypertension in adults with
congenital heart disease".)

● Group 2: PH due to left heart disease (including HF due to LV systolic, diastolic, or valvular dysfunction, and other causes of post-capillary PH such as
pulmonary vein stenosis or thrombosis and fibrosing mediastinitis) is the most common type of PH. (See "Pulmonary hypertension due to left heart
disease (group 2 pulmonary hypertension) in adults".)

● Group 3: PH due to lung disease and/or hypoxia. (See "Pulmonary hypertension due to lung disease and/or hypoxemia (group 3 pulmonary
hypertension): Epidemiology, pathogenesis, and diagnostic evaluation in adults" and "Pulmonary hypertension due to lung disease and/or hypoxemia
(group 3 pulmonary hypertension): Treatment and prognosis".)

● Group 4: PH due to pulmonary artery obstruction (including chronic thromboembolic PH). (See "Clinical manifestations and diagnosis of chronic
thromboembolic pulmonary hypertension" and "Chronic thromboembolic pulmonary hypertension: Medical treatment".)

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● Group 5: PH with unclear and/or multifactorial mechanisms (includes hematologic disorders and complex congenital heart disease). (See "Clinical
features and diagnosis of pulmonary hypertension of unclear etiology in adults".)

Chronic PH induces concentric RV hypertrophy, similar to the occurrence of LV hypertrophy in patients with systemic hypertension. The shape of the RV,
however is not well suited to sustain high pressure loads and is more prone to failure than the LV, even at significantly lower pressure loads.

Heart failure — Left-sided HF is the most common cause of PH (known as PH due to left heart disease or PH-LHD). In patients with HF, RV size and
RV ejection fraction (RVEF) have been shown to be independent prognostic factors of outcome, including among patients with reduced or preserved LV
ejection fraction (LVEF). (See "Pulmonary hypertension due to left heart disease (group 2 pulmonary hypertension) in adults".)

Left ventricular assist device-supported hearts — Patients with HF requiring mechanical circulatory support continue to be at risk of right heart
dysfunction due to PH-LHD. The acute effects of LV assist device (LVAD) support are the transfer of the burden of stroke work generation from the LV to
the LVAD, reduction of RV afterload, and an increase in RV preload. Thorough and accurate assessment of RV function is paramount prior to and after
implantation of an LVAD, since overall circulatory function will be limited by whatever capacity to generate useful stroke work remains in the (usually
dysfunctional) RV. RV failure (defined variously as a requirement for mechanical or pharmacologic support to augment RV output) occurs in 13 to 40
percent of continuous flow LVAD recipients [7].

Echocardiographic assessment of RV dysfunction in LVAD patients involves assessment of RV parameters and identification of abnormalities including RV
dilation, RV hypokinesis, leftward displacement of the interventricular septum, and tricuspid regurgitation. These findings may be identified when the RV
cannot "keep up" with the native LV or an LVAD-supported LV. RV and LV parameters are assessed during echocardiographic "ramp" studies performed to
optimize LVAD pump speed to maintain balance between antegrade left- and right-sided output. (See "Echocardiographic assessment of the right heart"
and "Practical management of long-term mechanical circulatory support devices", section on 'Device interrogation' and "Practical management of long-term
mechanical circulatory support devices", section on 'Thrombosis'.)

Acute pulmonary embolism — The hallmarks of acute RV pressure overload caused by acute pulmonary embolism are chamber dilation, free wall
hypokinesis, leftward displacement of the interventricular septum, and the development or worsening of tricuspid regurgitation. However,
echocardiographic manifestations of these phenomena have limited specificity and sensitivity for the diagnosis of acute pulmonary embolism. The role of
additional echocardiographic parameters for diagnosis and prognosis is discussed separately. (See "Clinical presentation, evaluation, and diagnosis of the
nonpregnant adult with suspected acute pulmonary embolism", section on 'Echocardiography' and "Treatment, prognosis, and follow-up of acute
pulmonary embolism in adults", section on 'Prognostic factors'.)

Chronic respiratory disorders — In patients with chronic respiratory disorders who develop PH (group 3), there is pressure overload of the RV.
Within this group, chronic obstructive pulmonary disease is the most common underlying etiology; other causes include interstitial lung disease and sleep
disordered breathing. (See "Pulmonary hypertension due to lung disease and/or hypoxemia (group 3 pulmonary hypertension): Epidemiology,
pathogenesis, and diagnostic evaluation in adults" and "Obstructive sleep apnea and cardiovascular disease in adults", section on 'Pulmonary
hypertension'.)

For some patients in this group (eg, those with chronic obstructive pulmonary disease), the changes in the geometry of the thoracic cavity may pose
additional difficulties for the assessment of RV size and function. Hyperinflation of the lungs in patients with asthma or chronic obstructive pulmonary
disease makes cardiac auscultation more difficult, as sounds are attenuated by the interfering lung, electrocardiographic (ECG) voltage decreases,
echocardiographic windows may be suboptimal, and breath-holding capacity is reduced, although adequate cardiovascular magnetic resonance (CMR)
imaging can generally be performed.

Congenital heart disease — For patients with a variety of congenital cardiac conditions (with or without surgical correction), the size and function of the
RV are important prognostic markers and determine the timing of intervention. Congenital conditions associated with risk of progressive RV dilation and
dysfunction include pulmonic regurgitation, pulmonic stenosis with prior intervention, repaired tetralogy of Fallot, PH-CHD, and lesions associated with
severe tricuspid and severe pulmonary valve regurgitation. Patients with these conditions require periodic monitoring of RV size and function. Some
examples are discussed here:

Atrial septal defect/ anomalous pulmonary venous return — In patients with atrial septal defect and/or anomalous pulmonary venous return, the
right heart is presented with increased blood volume comprised of the systemic circulatory volume plus the additional shunt volume. Larger shunts result in
greater RV dilatation and greater risk of arrhythmias, right HF, and adverse outcomes. (See "Indications for closure and medical management of atrial
septal defects in adults" and "Clinical manifestations and diagnosis of atrial septal defects in adults".)

Tetralogy of Fallot — In patients with uncorrected tetralogy of Fallot, RV outflow tract obstruction and ventricular septal defect with overriding aortic
root (resulting in the RV ejecting to the systemic circulation) both increase RV afterload, leading to RV pressure overload and free wall hypertrophy.
Patients who undergo surgical repair almost invariably develop pulmonic regurgitation which over time causes progressive RV dilation and, if left untreated,
RV failure, ventricular arrhythmias, and increased mortality. (See "Pathophysiology, clinical features, and diagnosis of tetralogy of Fallot" and "Management
and outcome of tetralogy of Fallot", section on 'Chronic postoperative complications'.)

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PH-CHD — Approximately 3 to 10 percent of adults with CHD develop pulmonary arterial hypertension (PAH), termed pulmonary hypertension-
congenital heart disease (PH-CHD). PAH may develop in patients with CHD with left-to-right intracardiac or extracardiac shunts (atrial, ventricular, and
great artery defects), especially when they are large and hemodynamically nonrestrictive, due to increased pulmonary blood volume and/or pressure
overload. Elevated flow through the pulmonary vasculature activates cellular mechanisms leading to PAH. Evaluation of PH-CHD is discussed separately.
(See "Clinical manifestations and diagnosis of pulmonary hypertension in adults with congenital heart disease".)

Causes of primary or secondary RV dysfunction — Conditions that are associated with primary and/or secondary RV dysfunction include ischemic
heart disease, cardiomyopathies involving the RV (including congenital cardiac disorders such as Ebstein anomaly), and heart transplantation.

Ischemic heart disease — Ischemic heart disease may directly involve the RV or may cause RV dysfunction secondary to PH-LHD. Patients with
ischemic heart disease commonly have RV as well as LV dysfunction [8]. (See 'Heart failure' above and "Pulmonary hypertension due to left heart disease
(group 2 pulmonary hypertension) in adults".)

In the clinical syndrome of RV myocardial infarction (MI), RV ischemia or infarction causes RV dysfunction, which is commonly but not always
accompanied by at least focal LV dysfunction. The extent and severity of RV and LV dysfunction in this setting varies depending upon the amount of
ischemia caused by the culprit lesion, as well as other conditions such as prior MI. Thus, clinical hemodynamic manifestations include no apparent
hemodynamic compromise or hemodynamically significant LV and/or RV dysfunction.

In the minority of patients with isolated RV infarction, the clinical and echocardiographic picture may be similar to that with acute pulmonary embolism (with
the dyad of dilated hypokinetic RV and small hyperdynamic LV). When this occurs, the most salient differentiating feature is the pulmonary artery pressure,
which will usually be normal or reduced in isolated RV infarction, and elevated in pulmonary embolism. RV dysfunction and fibrosis following infarction are
also well-visualized by CMR. (See "Right ventricular myocardial infarction".)

Cardiomyopathies — Although cardiomyopathies that predominantly affect the RV are less common than those affecting primarily the LV, they are an
important cause of morbidity and mortality. The most important of these is arrhythmogenic RV cardiomyopathy (ARVC), the diagnosis of which is based on
a combination of findings on imaging (echocardiography/CMR), tissue characterization (endomyocardial biopsy), ECG (depolarization and repolarization
abnormalities), ambulatory cardiac rhythm monitoring, and family history (including genetic analysis) [9]. ARVC should be carefully distinguished from
"athlete's heart", since features of physiological adaptation (such as dilation) of the right heart in response to exercise training may often overlap features of
ARVC [10]. (See "Arrhythmogenic right ventricular cardiomyopathy: Diagnostic evaluation and diagnosis".)

RV dysfunction is commonly seen with dilated cardiomyopathy (from various causes) and other types of cardiomyopathy, including LV noncompaction.
(See "Familial dilated cardiomyopathy: Prevalence, diagnosis and treatment" and "Isolated left ventricular noncompaction in adults: Clinical manifestations
and diagnosis", section on 'RV involvement'.)

Transplanted hearts — Cardiac transplant recipients may have right heart dysfunction secondary to PH-LHD and/or primary RV dysfunction related to
primary graft dysfunction (with causes including ischemia and reperfusion imaging), rejection, cardiac allograft vasculopathy, and other causes.

Assessment of RV morphology and function in heart transplant recipients is similar to that in other patients. However, echocardiography plays a limited role
in the detection of two major cardiac complications of orthotopic heart transplantation: acute cellular rejection and cardiac allograft vasculopathy [11]. The
mainstays for assessment of these complications are endomyocardial biopsy and invasive coronary angiography, respectively. (See "Heart transplantation
in adults: Diagnosis of acute allograft rejection" and "Heart transplantation: Clinical manifestations, diagnosis, and prognosis of cardiac allograft
vasculopathy" and "Heart transplantation in adults: Graft dysfunction".)

Because the target of endomyocardial biopsy is the right side of the interventricular septum, from which chordae tendinae arise to support the tricuspid
valve, chordal damage and tricuspid regurgitation are common and frequently identified by echocardiography.

APPROACH TO EVALUATION OF THE RV

When to evaluate RV function — Cardiac imaging to assess RV function should be undertaken in patients with clinical conditions associated with RV
dysfunction, including patients with congenital heart disease affecting the right heart, known or suspected pulmonary hypertension (PH), ischemic heart
disease, or cardiomyopathy. Patients should have an initial evaluation at the onset of symptoms or signs of disease. The frequency of subsequent
evaluation varies depending upon the underlying pathology and the response to initial therapies.

Initial evaluation — We begin the evaluation of patients with suspected or known RV dysfunction as follows:

● History and physical examination – In addition to the general cardinal symptoms of HF, including dyspnea, fatigue, and fluid retention, symptoms of
abdominal visceral congestion are common in patients with RV dysfunction. These include bloating, pain, and tenderness (especially in the right upper
quadrant), loss of appetite, and malabsorption syndromes leading to diarrhea (less frequently to constipation) and malnutrition (in its extreme form,
cardiac cachexia). Malabsorption due to intestinal edema may lead not only to diarrhea, but more importantly, can also lead to the development of
diuretic (and other drug) refractoriness as a result of failure of the drug to enter the bloodstream when taken orally.

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Physical examination findings in patients with RV dysfunction and/or right-sided HF may include jugular venous distention (with or without large V
waves indicating the presence of significant tricuspid regurgitation), peripheral or dependent edema, ascites, hepatosplenomegaly, and the presence
of one or more cardiac exam findings. The cardiac exam may reveal a right-sided third heart sound (which indicates the presence of elevated RV filling
pressure and is distinguished from a third heart sound emanating from the LV by its respirophasic variation and its optimal locus of auscultation at or
near the left lower sternal border), a murmur of tricuspid regurgitation, an RV heave or lift, and a loud pulmonic component of the second heart sound
(indicating the presence of pulmonary hypertension).

● 12-lead ECG – ECG findings are often nonspecific but may include signs of right HF such as RV hypertrophy, right bundle branch block and/or right
axis deviation. Atrial fibrillation is a common but highly non-specific finding.

● Chest radiograph – A chest radiograph is commonly obtained to assess causes of dyspnea. (See "Approach to the patient with dyspnea", section on
'Initial testing in chronic dyspnea'.)

● Baseline laboratory testing – Recommended initial blood tests for patients with symptoms and signs of HF include:

• Cardiac troponin T or I in patients with acute decompensated HF, suspected acute coronary syndrome, or myocarditis. (See "Troponin testing:
Clinical use" and "Diagnosis of acute myocardial infarction" and "Initial evaluation and management of suspected acute coronary syndrome
(myocardial infarction, unstable angina) in the emergency department".)

• A complete blood count, which may suggest concurrent or alternate conditions. Anemia or infection can exacerbate pre-existing HF. (See
"Evaluation and management of anemia and iron deficiency in adults with heart failure".)

• Serum electrolytes, blood urea nitrogen, and creatinine may indicate associated conditions. Hyponatremia generally indicates severe HF, though
other causes should be considered [12]. Renal impairment may be caused by, and/or contribute to, HF exacerbation. Baseline evaluation of
electrolytes and creatine is also necessary when initiating therapy with diuretics and/or angiotensin converting enzyme inhibitors.

• Liver injury may be caused by hepatic congestion as well as low cardiac output. The most common liver biochemical abnormality in patients with
HF is elevated serum bilirubin. Elevated serum aminotransferase levels and an abnormal prothrombin time are also common. Hypoalbuminemia is
common in patients with HF but is likely caused by malnutrition and protein-losing gastroenteropathy due to intestinal lymphatic pressure. (See
"Congestive hepatopathy".)

• Fasting blood glucose to detect underlying diabetes mellitus. (See "Heart failure in patients with diabetes mellitus: Epidemiology, pathophysiology
and management".)

● Echocardiography – Transthoracic echocardiography (TTE) should be performed as the initial test for evaluation of RV structure and function.
Transesophageal echocardiography (TEE) may provide additional or complementary information about RV structure and function in select patients. It
may also provide information about the cause of RV dysfunction. (See 'How to evaluate RV disease' below and 'Echocardiography' below and
"Echocardiographic assessment of the right heart" and "Echocardiographic evaluation of the tricuspid valve" and "Echocardiographic evaluation of the
pulmonic valve and pulmonary artery".)

Additional evaluation — Following echocardiography, additional evaluation is indicated for selected patients.

● For patients with non-diagnostic echocardiographic imaging (eg, RV size or function is uncertain) or complex congenital heart disease (eg, monitoring
of patients with repaired tetralogy of Fallot) or with a suspected diagnosis that requires further imaging (eg, arrhythmogenic RV cardiomyopathy or
sarcoidosis), cardiovascular magnetic resonance (CMR) is the preferred approach. CMR can help identify anomalous venous connection to the
superior or inferior vena cava when this is not adequately imaged by TEE.

● If CMR is unavailable or contraindicated (eg, patient with severe claustrophobia), cardiac computed tomography (CT) and scintigraphic approaches
are alternative methods for evaluating the RV:

• Cardiac CT is an option if CMR cannot be performed. CT may provide additional useful information about the RV, as described below. (See 'How
to evaluate RV disease' below and 'Cardiac computed tomography' below.)

• Scintigraphic approaches (first pass and gated radionuclide ventriculography, gated single photon emission CT, and positron emission
tomography) are rarely used when the primary clinical question is RV function. However, useful information on RV size and function may arise in
patients who undergo such scintigraphic testing for other indications (eg, stress testing to evaluate ischemic heart disease). (See 'How to evaluate
RV disease' below and 'SPECT/RVG' below.)

● Cardiac catheterization is indicated in select patients with suspected right heart disease or evidence of PH. (See "Clinical features and diagnosis of
pulmonary hypertension of unclear etiology in adults", section on 'Right heart catheterization' and "Pulmonary hypertension due to left heart disease
(group 2 pulmonary hypertension) in adults", section on 'When to perform right heart catheterization' and 'Cardiac catheterization' below.)

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In addition, invasive measurements are indicated in patients for whom noninvasive techniques do not suffice to document the diagnosis (eg, in patients
with constriction versus restriction in whom surgical therapy is contemplated). (See "Differentiating constrictive pericarditis and restrictive
cardiomyopathy", section on 'Cardiac catheterization'.)

HOW TO EVALUATE RV DISEASE

The complete assessment of the RV size and function includes evaluation of the following parameters:

RV size — Conditions resulting in RV volume overload (eg, left-to-right shunts or tricuspid and pulmonary valve regurgitation) as well as certain RV
cardiomyopathies result in an increased RV size. A physical exam may demonstrate the displaced RV impulse and ECG may suggest RV dilation. Although
two-dimensional (2D) echocardiography is most frequently used, it provides a semi-quantitative measure of the RV dimension (table 2 and movie 1 and
image 1). Volumetric assessment of the RV with three-dimensional (3D) TTE has shown promise in studies using cardiac magnetic resonance (CMR)-
derived volumes as the gold standard [13-15], but its use in the day-to-day quantitation of the RV is fraught with technical limitations of acquisition and
quantification [16]. CMR and CT using the disk-summation approach (Simpson's rule) provide a more accurate quantitative assessment. Radionuclide
ventriculography (RVG) has been used extensively in the past and may provide semi-quantitative assessment of the RV size. Similarly, though not
commonly used for this indication, single photon emission CT (SPECT) and positron emission tomography (PET) may also be able to provide a gross semi-
quantitative assessment of RV dilation. Invasive catheterization with right ventriculography may be used to visualize RV size, but in modern practice is
primarily used for patients with congenital heart disease that undergo invasive hemodynamic assessment, usually with another indication for the procedure.

RV wall thickness — Conditions resulting in RV pressure overload (eg, pulmonic stenosis, pulmonary hypertension [PH]) can result in RV wall
hypertrophy. A physical exam and an ECG may provide clues that RV hypertrophy may be present (RV heave, right axis deviation and voltage criteria for
RV hypertrophy) but are more qualitative characteristics. Imaging methods (primarily CMR and CT, but also echocardiography and SPECT/PET) can
readily visualize wall thickness. CMR (and CT) may also provide information regarding the structure of the RV wall (eg, scarring, fatty infiltration, etc) which
may be helpful in certain conditions (eg, evaluation for arrhythmogenic RV cardiomyopathy, sarcoidosis, etc). Invasive cardiac catheterization with right
ventriculography may demonstrate thickened RV trabeculations and thus provide indirect evidence of RV hypertrophy, but is rarely used for this indication.

RV contractile function — Physical signs (including third and fourth heart sounds emanating from the RV, edema, and RV heave) are neither sensitive
nor specific for assessing RV function [17]. Echocardiography remains the most commonly used test to estimate RVEF. Quantitation of RV free wall
deformation by speckle-tracking (strain) echocardiography may be superior to the more commonly obtained echocardiographic measures of RV contractile
function, including tricuspid annular plane systolic excursion (TAPSE), because unlike TAPSE, strain measurements are not subject to errors introduced by
the plane of M-mode imaging and cardiac translation [18]. CMR is currently considered the most accurate and reproducible method to quantitate RV
function. The accuracy of measurement of the RVEF is generally similar to that of the LVEF [19], although the free wall trabeculations may interfere with
accurate endocardial tracing and the difficulty in defining the plane of the tricuspid and pulmonic valves may increase variability and compromise accuracy
and reproducibility of the measurement. RVG has been used extensively in the past for this indication, and is still considered highly accurate and
reproducible, but its clinical use has substantially decreased for this indication as the other imaging methods have evolved. With cardiac CT, when radiation
is delivered throughout the entire cardiac cycle the RVEF can be measured, but is generally avoided as it results in high radiation dosimetry. SPECT/PET
with ECG-gating can also provide a semi-quantitative assessment of RV function and may be clinically useful in patients who undergo stress imaging for
other indications.

Right heart pressures — Invasive right heart/pulmonary artery catheterization is the standard reference for assessment of intracardiac pressures. The
relations among pulmonary artery and left atrial (pulmonary capillary wedge pressure), right atrial pressure, and LV pressure can be useful in defining
pathology in a variety of diseases with impaired hemodynamics. A complete discussion of the invasive hemodynamic assessment of the RV is presented
separately. (See "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults".)

Assessment of the height of the jugular venous pulsation and the amplitude of the pulmonic component of the second heart sound are employed to
estimate right atrial and pulmonary artery pressure, respectively, but surprisingly limited data are available to evaluate their diagnostic accuracy, and the
data that do exist demonstrate low sensitivity and specificity of these (and other) physical findings for the detection of pathologically elevated right-sided
pressures, which in part explains reliance on echocardiography and catheterization to assess right heart pressures [17]. Right atrial pressure equals the
diastolic RV pressure and can be used in combination with data from imaging (echocardiography) to assess the systolic pressure of the RV (and pulmonary
artery if there is no pulmonary stenosis).

Echocardiography can measure pressure gradients across valves and only indirectly or by estimation assess absolute values of intracardiac pressures.
Similarly, CMR (and less so CT) can provide indirect evidence of RV pressure overload.

Right heart valves — Echocardiography is the standard reference for visualization of all cardiac valves. Tricuspid and pulmonic valve regurgitation can be
visually assessed by Doppler and 2D/3D color flow imaging. Another option, including quantitative assessment of the severity of regurgitation, can be
obtained by CMR with a technique called phase-contrast, alone (for pulmonic regurgitation) or in combination with volumetric data (for tricuspid
regurgitation) [20]. Pulmonic stenosis is primarily evaluated by echocardiography and invasive catheterization if interventional therapy is elected, while

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CMR also can be useful towards this assessment.

MODALITIES

The RV is less symmetric than the LV and is significantly more complex in its internal geometry. Its cavity can be roughly modeled as a stack of crescents
with diminishing dimensions from base to apex. However there is significant interindividual variability, which is one of several reasons why its volume
cannot be calculated by entering linear dimensions into simple mathematical equations the way that LV volume can be. Two-dimensional (2D)
echocardiography remains the mainstay of noninvasive evaluation of the RV, but newer imaging modalities are assuming an increasing role (table 2). (See
"Echocardiographic assessment of the right heart" and "Echocardiographic evaluation of the tricuspid valve" and "Echocardiographic evaluation of the
pulmonic valve and pulmonary artery".)

Echocardiography — Echocardiography is the key initial imaging modality for evaluation of RV structure and function. Assessment of the right heart is
important component of all complete echocardiographic studies. Measurement of chamber dimensions, evaluation of RV systolic function, and estimation
of hemodynamic parameters should be routinely performed. (See "Echocardiographic assessment of the right heart".)

When feasible, the following core measurements (table 3) should be included in each study (with additional measurements performed and reported as
clinically indicated):

● RV basal diameter from the RV-focused apical four-chamber view (normal ≤4.1 cm), or, if feasible, RV volume from a three-dimensional (3D)
acquisition. (See "Echocardiographic assessment of the right heart", section on 'Right ventricular size'.)

● RA volume from the apical four-chamber view using the single-plane Simpson's method. (See "Echocardiographic assessment of the right heart",
section on 'Right atrial size'.)

● Right atrial (RA) pressure from the inferior vena cava size and collapse. (See "Echocardiographic assessment of the right heart", section on 'RA
pressure'.)

● Pulmonary arterial systolic pressure from the tricuspid regurgitation velocity and estimated RA pressure. (See "Echocardiographic assessment of the
right heart", section on 'Pulmonary artery pressure'.)

● RV systolic function using at least one quantitative parameter: tricuspid annular plane systolic excursion (TAPSE; normal ≥1.7 cm), tricuspid annular
velocity (S'; normal ≥9.5 cm/second), fractional area change (normal ≥35 percent), myocardial performance index (normal ≤0.43 by pulsed Doppler or
≤0.55 by tissue Doppler). In addition, 3D-derived RVEF is recommended when suitable technology and expertise is available. (See
"Echocardiographic assessment of the right heart", section on 'Right ventricular function'.)

Limitations of echocardiographic imaging may include:

● The RV is located immediately behind the sternum (anterior wall) and above the diaphragm (inferior/diaphragmatic wall). The sternum limits the
acoustic windows through which right heart structures can be imaged by TTE. This limitation does not apply to TEE, in which imaging of the RV does
not require acoustic penetration of the chest wall, but transesophageal imaging of the RV has its own limitation in that the imaging transducer is far
away from the target. However, imaging from the transgastric views often yields high quality images of the RV as well as of the tricuspid valve due to
the proximity of these structures to the diaphragm abutting the gastric fundus [21].

● Acoustic shadowing and scattering from implanted electronic device leads can degrade the tricuspid regurgitation color-flow Doppler signal during
echocardiography.

Cardiovascular magnetic resonance — Cardiovascular magnetic resonance (CMR) is the most accurate and reproducible imaging method to
quantitatively assess RV (and LV) size and function. It also enables quantitation of shunts and valvular regurgitant flow, assessment of myocardial disease,
identification of anomalous pulmonary venous connection (including attachment to superior or inferior vena cava), and evaluation of the pulmonary artery
and aorta [22]. CMR is recommended when echocardiographic imaging is non-diagnostic or insufficient for diagnosis and evaluation. Gadolinium-based
contrast is not required for imaging ventricular chamber size and function and great vessels but is used for evaluation of myocardial contrast effects
(including delayed enhancement for detection of infarction, scar, or inflammation), disease, and MR angiography (movie 2). (See "Clinical utility of
cardiovascular magnetic resonance imaging" and "Cardiac imaging with computed tomography and magnetic resonance in the adult".)

Limitations of CMR imaging may include difficulty with defining the valve plane for tricuspid and pulmonic valves. Without slice tracking techniques, a fixed
plane is imaged. This plane contains different levels of the RV wall at each phase of the cardiac cycle as the RV moves through the plane. This can be
mostly overcome when imaging the RV in the longitudinal (two-chamber) and four-chamber orientations, while it remains a significant issue for short-axis
imaging, unless a slice tracking technique is used. When RV volumes and ejection fraction are quantified using short axis images, the through-plane
motion must be accounted for.

Cardiac computed tomography — Cardiac CT refers to CT imaging of the heart with multidetector (eg, 64 and higher) CT systems using ECG techniques

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to synchronize the image acquisition with the cardiac cycle. Global RV systolic function can be qualitatively and quantitatively evaluated. Visual
assessment of RV global wall motion can be graded qualitatively by viewing cine volume loops encompassing the entire cardiac cycle. Cardiac CT image
acquisition is rapid relative to other techniques. Fast automated tools for analysis of segmental and global function have been shown to have high
reproducibility and excellent correlation with echocardiography. The temporal resolution with cardiac CT is still inferior to other techniques, including TTE
and CMR, which leads to CT overestimation of end systolic volumes, and, as a consequence, underestimation of RVEF. Cardiac CT exposes the patient to
radiation associated with the acquisition of the scan, although lower radiation dose protocols have been proposed that limit radiation exposure to less than
5 mSv. Additionally, cardiac CT exposes the patient to intravenous administration of iodinated contrast.

Limitations of CT imaging may include:

● Radiation exposure
● Low temporal resolution
● Low contrast-to-noise ratio between wall and cavity

SPECT/RVG — Radionuclide ventriculography (RVG) is performed using a radioactive tracer to label the patient's red blood cell pool and a gamma-ray
camera to capture images of the blood circulating through the heart. RVG provides a detailed and accurate assessment of RVEF and LVEF, with the most
common indication being the quantification of ventricular volumes and LVEF when this diagnostic information is unreliable or unavailable by other imaging
modalities. RVG can also be used to quantify shunt fractions for patients with congenital heart disease and intracardiac shunts. As with CT, there is
associated radiation exposure estimated to be approximately 6 to 7 mSv.

Single photon emission CT-myocardial perfusion imaging (SPECT-MPI) is commonly used for assessment of ischemic heart disease, and generally
includes evaluation of LV volumes and LVEF. Precise information on the RV size and RVEF is not typically available using SPECT.

Limitations of SPECT/RVG imaging may include:

● Low spatial resolution. Mural trabeculations result in partial volume effects.

● For radionuclide angiography, there is limited definition of RV borders and overlap with adjacent cardiac chambers.
● Low temporal resolution.
● Radiation exposure.

Cardiac catheterization — Cardiac catheterization is the reference standard for assessment of right heart hemodynamics but is indicated in only select
patients with suspected right heart disease or pulmonary hypertension. (See 'Additional evaluation' above.)

Cardiac catheterization may be used to assess intracardiac, pulmonary artery, pulmonary capillary wedge and aortic pressure, and may also be used to
estimate cardiac output and shunt fraction. These procedures are discussed separately. (See "Pulmonary artery catheterization: Indications,
contraindications, and complications in adults" and "Pulmonary artery catheters: Insertion technique in adults" and "Pulmonary artery catheterization:
Interpretation of hemodynamic values and waveforms in adults" and "Clinical manifestations and diagnosis of ventricular septal defect in adults" and
"Clinical manifestations and diagnosis of ventricular septal defect in adults", section on 'Cardiac catheterization' and "Cardiac catheterization techniques:
Normal hemodynamics" and "Clinical manifestations and diagnosis of atrial septal defects in adults", section on 'Approach to diagnosis and evaluation' and
"Clinical manifestations and diagnosis of atrial septal defects in adults".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society
guideline links: Multimodality cardiovascular imaging appropriate use criteria" and "Society guideline links: Pulmonary hypertension in adults".)

SUMMARY AND RECOMMENDATIONS

● Evaluation of the right ventricle (RV) is a key component of the clinical assessment of many cardiovascular and pulmonary disorders. Cardiac imaging
to assess RV function should be undertaken in patients with clinical conditions associated with RV dysfunction, including patients with congenital heart
disease (CHD) affecting the right heart, known or suspected pulmonary hypertension (PH), ischemic heart disease, or cardiomyopathy. (See 'When to
evaluate RV function' above.)

● Acquired dysfunction of the RV is most often secondary to pressure and/or volume overload. RV dysfunction may also be caused by conditions directly
affecting the RV myocardium (eg, cardiomyopathy or ischemic heart disease). (See 'Pathophysiology' above and 'Conditions associated with RV
dysfunction' above.)

● The most common cause of pressure overload is PH; other causes include RV outflow obstruction such as pulmonic stenosis (subvalvular or valvular),
pulmonic atresia, and pulmonary artery stenosis (which may be caused by conditions such as Williams syndrome, rubella exposure during pregnancy,

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mediastinal radiation therapy, or surgical banding). (See "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults" and
"Clinical manifestations and diagnosis of pulmonic stenosis in adults".)

● Causes of RV volume overload include left-to-right shunts at the atrial level or above (eg, atrial septal defect, unroofed coronary sinus, anomalous
pulmonary vein connection to the right atrium and/or the vena cava), tricuspid regurgitation, and pulmonic regurgitation. (See "Etiology, clinical
features, and evaluation of tricuspid regurgitation" and "Pulmonic regurgitation" and "Clinical manifestations and diagnosis of atrial septal defects in
adults".)

● The initial evaluation of a patient with impaired RV function includes history and physical examination, electrocardiogram, baseline laboratory testing,
and echocardiography.

● Echocardiography is the key initial imaging modality for evaluation of RV structure and function. (See 'Initial evaluation' above and 'Echocardiography'
above.)

● For patients with non-diagnostic echocardiographic imaging (eg, RV size or function is uncertain) or complex CHD (eg, monitoring of patients with
repaired tetralogy of Fallot) or with a suspected diagnosis that requires further imaging (eg, arrhythmogenic RV cardiomyopathy or sarcoidosis),
cardiovascular magnetic resonance (CMR) is the preferred approach, as the most accurate and reproducible imaging method to assess RV size and
function. If CMR is unavailable or contraindicated (eg, patient with severe claustrophobia, or devices which are CMR incompatible), cardiac computed
tomography and scintigraphic approaches are alternative methods for evaluating the RV. (See 'Additional evaluation' above.)

● Cardiac catheterization is the reference standard for hemodynamic assessment but is indicated only in patients with suspected right heart disease or
PH. (See 'Cardiac catheterization' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. Anderson RH, Becker AE, Van Mierop LH. What should we call the 'crista'? Br Heart J 1977; 39:856.

2. Loukas M, Housman B, Blaak C, et al. Double-chambered right ventricle: a review. Cardiovasc Pathol 2013; 22:417.

3. Haddad F, Hunt SA, Rosenthal DN, Murphy DJ. Right ventricular function in cardiovascular disease, part I: Anatomy, physiology, aging, and functional
assessment of the right ventricle. Circulation 2008; 117:1436.

4. Kohli P, Schiller NB. The physiologic basis of RV echocardiography. In: ASE's Comprehensive Echocardiography, 2nd ed, Lang RM, Goldstein SA, Kr
onzon I, et al (Eds), Elselvier Saunders, Philadelphia 2016. p.142.

5. Friedberg MK. Imaging Right-Left Ventricular Interactions. JACC Cardiovasc Imaging 2018; 11:755.

6. Bernheim PI. De l’asystolie veineuse dans l'hypertrophie du coeur gauche par stenose concomitante du ventricule droit. Rev Med 1910; 30:785.

7. Hayek S, Sims DB, Markham DW, et al. Assessment of right ventricular function in left ventricular assist device candidates. Circ Cardiovasc Imaging
2014; 7:379.

8. Sabe MA, Sabe SA, Kusunose K, et al. Predictors and Prognostic Significance of Right Ventricular Ejection Fraction in Patients With Ischemic
Cardiomyopathy. Circulation 2016; 134:656.

9. Marcus FI, McKenna WJ, Sherrill D, et al. Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task
force criteria. Circulation 2010; 121:1533.

10. D'Ascenzi F, Solari M, Corrado D, et al. Diagnostic Differentiation Between Arrhythmogenic Cardiomyopathy and Athlete's Heart by Using Imaging.
JACC Cardiovasc Imaging 2018; 11:1327.

11. Olymbios M, Kwiecinski J, Berman DS, Kobashigawa JA. Imaging in Heart Transplant Patients. JACC Cardiovasc Imaging 2018; 11:1514.

12. WRITING COMMITTEE MEMBERS, Yancy CW, Jessup M, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the
American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation 2013; 128:e240.

13. Park JB, Lee SP, Lee JH, et al. Quantification of Right Ventricular Volume and Function Using Single-Beat Three-Dimensional Echocardiography: A
Validation Study with Cardiac Magnetic Resonance. J Am Soc Echocardiogr 2016; 29:392.

14. Leibundgut G, Rohner A, Grize L, et al. Dynamic assessment of right ventricular volumes and function by real-time three-dimensional

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echocardiography: a comparison study with magnetic resonance imaging in 100 adult patients. J Am Soc Echocardiogr 2010; 23:116.

15. Gopal AS, Chukwu EO, Iwuchukwu CJ, et al. Normal values of right ventricular size and function by real-time 3-dimensional echocardiography:
comparison with cardiac magnetic resonance imaging. J Am Soc Echocardiogr 2007; 20:445.

16. Laser KT, Horst JP, Barth P, et al. Knowledge-based reconstruction of right ventricular volumes using real-time three-dimensional echocardiographic
as well as cardiac magnetic resonance images: comparison with a cardiac magnetic resonance standard. J Am Soc Echocardiogr 2014; 27:1087.

17. Braganza M, Shaw J, Solverson K, et al. A Prospective Evaluation of the Diagnostic Accuracy of the Physical Examination for Pulmonary
Hypertension. Chest 2019; 155:982.

18. Carluccio E, Biagioli P, Alunni G, et al. Prognostic Value of Right Ventricular Dysfunction in Heart Failure With Reduced Ejection Fraction: Superiority
of Longitudinal Strain Over Tricuspid Annular Plane Systolic Excursion. Circ Cardiovasc Imaging 2018; 11:e006894.

19. Mooij CF, de Wit CJ, Graham DA, et al. Reproducibility of MRI measurements of right ventricular size and function in patients with normal and dilated
ventricles. J Magn Reson Imaging 2008; 28:67.

20. Addetia K, Harb SC, Hahn RT, et al. Cardiac Implantable Electronic Device Lead-Induced Tricuspid Regurgitation. JACC Cardiovasc Imaging 2019;
12:622.

21. Hahn RT. State-of-the-Art Review of Echocardiographic Imaging in the Evaluation and Treatment of Functional Tricuspid Regurgitation. Circ
Cardiovasc Imaging 2016; 9.

22. Galea N, Carbone I, Cannata D, et al. Right ventricular cardiovascular magnetic resonance imaging: normal anatomy and spectrum of pathological
findings. Insights Imaging 2013; 4:213.

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GRAPHICS

Right ventricular anatomy

Netter

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Cross sectional heart anatomy

Cross sectional anatomy of the heart from a superior perspective (atria removed).

Netter

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Clinical classification of pulmonary hypertension (6 th World Symposium on Pulmonary Hypertension)

1 PAH

1.1 Idiopathic PAH

1.2 Heritable PAH

1.3 Drug- and toxin-induced PAH

1.4 PAH associated with:

1.4.1 Connective tissue disease

1.4.2 HIV infection

1.4.3 Portal hypertension

1.4.4 Congenital heart disease

1.4.5 Schistosomiasis

1.5 PAH long-term responders to calcium channel blockers

1.6 PAH with overt features of venous/capillaries (PVOD/PCH) involvement

1.7 Persistent PH of the newborn syndrome

2 PH due to left heart disease

2.1 PH due to heart failure with preserved LVEF

2.2 PH due to heart failure with reduced LVEF

2.3 Valvular heart disease

2.4 Congenital/acquired cardiovascular conditions leading to post-capillary PH

3 PH due to lung disease and/or hypoxia

3.1 Obstructive lung disease

3.2 Restrictive lung disease

3.3 Other lung disease with mixed restrictive/obstructive pattern

3.4 Hypoxia without lung disease

3.5 Developmental lung disorders

4 PH due to pulmonary artery obstructions (refer to the UpToDate table on PH due to PA obstruction)

4.1 Chronic thromboembolic PH

4.2 Other pulmonary artery obstructions

5 PH with unclear and/or multifactorial mechanisms (refer to the UpToDate table on PH due to unclear or multifactorial mechanisms)

5.1 Hematologic disorders

5.2 Systemic and metabolic disorders

5.3 Others

5.4 Complex congenital heart disease

PAH: pulmonary arterial hypertension; PVOD: pulmonary veno-occlusive disease; PCH: pulmonary capillary hemangiomatosis; PH: pulmonary hypertension; LVEF: left ventricular ejection
fraction.

Reproduced with permission of the © ERS 2019: European Respiratory Journal 53 (1) 1801913; DOI: 10.1183/13993003.01913-2018. Published 24 January 2019.

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Comparison of techniques for assessing the right heart

Exam ECG Echo CMR CT Cath RVG SPECT/PET

Cavity size + + +++ ++++ ++++ +++ ++ ++

Wall thickness + ++ +++ ++++ ++++ – - ++

Ejection fraction – – +++ ++++ ++++ +++ ++++ ++

TR ++ – ++++ ++++ - ++ + –

PS ++ – +++ +++ ++ ++++ - -

PR + – ++++ ++++ - +++ - –

RV pressure ++ – +++ ++ + ++++ - +

+++− = Not applicable.

++++ = Poor.
++++ = Fair.
++++ = Good.
++++ = Gold standard.

ECG: electrocardiogram; ECHO: echocardiography; CATH: cardiac catheterization; CMR: cardiovascular magnetic resonance; RVG: radionuclide ventriculogram; SPECT: single photon emission
computed tomography; PET: positron emission tomography; CT: computed tomography; TR: tricuspid regurgitation; PS: pulmonary stenosis; PR: pulmonic regurgitation; RV: right ventricle.

Courtesy of James Chang, MD.

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Diastolic interventricular septal flattening in right ventricular volume overload

Parasternal short-axis transthoracic echocardiographic views of the left ventricle (LV) and right ventricle (RV) in a patient with RV volume overload and anasarca.
(A) View at end-diastole. The RV is markedly dilated. The LV should normally be circular in this view, with the interventricular septum concave toward the LV. However the interventricular
volume overloading of the RV within a constraining pericardium. This septal flattening is maximal when the RV is maximally distended, at end-diastole.
(B) View at end-systole. Note that the interventricular septum which was flattened at end-diastole (A), recovers its normal curvature and concavity toward the LV at end-systole.

LVEDD: left ventricular end-diastolic dimension; LVESD: left ventricular end-systolic dimension.

Courtesy of James Chang, MD.

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Echocardiographic parameters for right heart

Variable Unit Normal

Chamber dimensions

RV basal diameter cm ≤4.1

RV wall thickness in subcostal view cm ≤0.5

RVOT diameter in PLAX view cm ≤3.0 1

RA end-systolic volume index mL/m 2 ≤39 in men / ≤33 in women 1

RA end-systolic area cm 2 ≤18.5

Systolic function

TAPSE cm ≥1.7 1

Pulsed Doppler peak annular velocity (S') cm/s ≥9.5 1

Pulsed Doppler MPI – ≤0.43 1

Tissue Doppler MPI – ≤0.54

FAC percent ≥35

3D-derived RVEF (percent) percent ≥45 1

Diastolic function

E/A ratio – 0.8 to 2.1

E/E' ratio – ≤6

IVC diameter in subcostal view cm ≤2.1 1

IVC collapse during inspiratory sniff percent ≥50 1

Hepatic vein velocity ratio in subcostal view – Systolic > Diastolic

FAC: fractional area change; MPI: myocardial performance index; PLAX: parasternal long-axis; PSAX: parasternal short-axis; RA: right atrium; RV: right ventricle; RVD: right ventricular
diameter; RVOT: right ventricular outflow tract; TAPSE: tricuspid annular plane systolic excursion.

Reference:
1. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography
and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr 2015; 28:1.
Original figure modified for this publication. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society
of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J
Am Soc Echocardiogr 2010; 23:685. Table used with the permission of Elsevier Inc. All rights reserved.

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Contributor Disclosures
Peter G Danias, MD, PhD, FACC, FESC Nothing to disclose James D Chang, MD Nothing to disclose Heidi M Connolly, MD, FACC, FASE Nothing to disclose Susan B
Yeon, MD, JD, FACC Nothing to disclose Brian C Downey, MD, FACC Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and
through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards
of evidence.

Conflict of interest policy

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