Right Ventricular Anatomy and Function

Acknowledgments

The authors wish to acknowledge Anjali Vaidya, MD, and James N. Kirkpatrick, MD, the authors of related chapters in previous editions of The Practice of Clinical Echocardiography.

The right ventricle (RV) is a complex but critical structure for normal cardiovascular function. Descriptions of the role of the RV in normal cardiovascular physiology have evolved throughout history. Some of the earliest documented studies of cardiac anatomic structures were performed by Leonardo da Vinci in his cadaveric dissections. His interest in the RV structure is catalogued in notebook sketches of an anatomic study of an ox heart, with careful detailing of RV papillary muscles, chordae tendineae, and the tricuspid valve.

The 20th century was a period of increased understanding of modern cardiovascular physiology. Initial human in vivo cardiac catheterization procedures in the 1920s first visualized dynamic RV function with invasive right ventriculography using iodinated contrast media. This laid the foundation for work in the 1940s and 1950s in which the technique of right heart catheterization was refined and extensively used for the in vivo study of cardiac and pulmonary physiology. Much of this work was done in canine studies, which showed that an extensively injured RV led to no significant acute increase in central venous filling pressure or decrease in RV systolic pressures. ^, This finding was later reinforced by the use of the Fontan procedure to provide a direct passive conduit of venous flow to the pulmonary arteries.

From these and other studies, it was concluded that normal RV contractility played a minor role in normal cardiovascular function. Although this concept has had extraordinary resilience, there has been increasing recognition that it is an incomplete simplification of a complex issue.

With improved availability of echocardiographic imaging and rapid percutaneous intervention techniques, isolated RV ischemia has become recognized as a unique and potentially catastrophic clinical entity. Although the adverse hemodynamics of acute RV myocardial infarction can potentially be reversed with acute coronary reperfusion, acute mortality rates remain high. This clinical point has become further relevant due to the high risk of death from left or right coronary obstruction as a complication of transcatheter aortic valve replacement (TAVR). ^,

If patients survive beyond the acute phase of cardiogenic shock, those with right heart failure may have improved survival rates compared with those with left-sided pump failure. However, persistent perturbations in normal RV function have important prognostic implications for a wide variety of cardiovascular conditions, and there is renewed interest in better understanding the nuances of RV function. Whereas early tools for the interrogation of RV physiology were invasive, current noninvasive imaging techniques can provide high-quality and reproducible assessments of the RV.

Echocardiography is the first-line modality for imaging the RV, and it has well-established guidelines for application ( Table 6.1 ). ^, The advantages of echocardiography lie in its wide availability, high temporal resolution, integrative Doppler physiologic assessments, lack of ionizing radiation, rapid improvements in image quality, and new technologies such as strain and three-dimensional (3D) imaging. They provide a comprehensive toolset for the integrative assessment of RV anatomy and physiology.

TABLE 6.1

Echocardiography Guidelines for RV Assessment.

Year	Title	Authors	Journal
2010	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	Rudski et al.	Journal of the American Society of Echocardiography
2015	Recommendations for cardiac chamber quantification by echocardiography in adults: An update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging	Lang et al.	Journal of the American Society of Echocardiography

This chapter provides an in-depth review of advanced echocardiographic topics regarding RV anatomy and function and focuses on the technical aspects of image acquisition and data prognostication. It also discusses the specific advantages, limitations, and correlations of echocardiography with complementary imaging technologies.

RV Anatomy and Physiology

RV External Anatomy

The RV is the most anterior cardiac chamber, lying immediately posterior to the sternum ( Fig. 6.1 ). The RV rests inferiorly on the diaphragm; posteriorly, it wraps the obliquely oriented left ventricle (LV). This oblique orientation aligns the RV apex anteriorly and inferiorly. The base of the RV is the tricuspid annular plane, which lies posteriorly and to the right as it communicates with the right atrium (RA). Superiorly, the RV outflow tract (RVOT) tapers at the muscular infundibulum as it gives rise to the pulmonic valve and pulmonary artery.

Fig. 6.1, RV external anatomic structure.

The RV structure is complex and does not readily conform to common geometric shapes. From the short-axis view, the RV has the appearance of an asymmetric crescent. When viewed in a horizontal or vertical long-axis projection, the RV has a more triangular appearance. The full 3D structure of the RV can be conceptualized as a flexible triangular pouch wrapped around the LV.

RV Internal Anatomy

The internal anatomy of the RV can be roughly divided into an inflow region, an outflow region, and a main body ( Fig. 6.2 ). These regions have distinct morphologic characteristics and can provide helpful localization of pathology, such as a ventricular septal defect (VSD). Membranous or perimembranous VSDs are located in the inflow region. Supracrystal or outflow tract VSDs are located in the outflow region. Muscular VSDs are located in the main body of the RV.

Fig. 6.2, RV internal anatomic structure.

The inflow region of the RV borders the tricuspid annulus and is demarcated superiorly by the crista supraventricularis, a muscular ridge that is contractile and extends from the tricuspid annulus along the interventricular septum (IVS) before forming the moderator band near the apex. The outflow region (i.e., infundibulum) of the RV is a smooth and cylindrical muscular structure. Overdevelopment of this musculature can lead to pulmonary stenosis as an isolated entity or as part of the tetralogy of Fallot. The main body of the RV is highly trabeculated and includes a network of tricuspid chordae and associated tricuspid papillary muscles. Hypertrophied anomalous muscle bundles in the main body of the RV can lead to a dual-chambered RV physiology.

Tricuspid Valve

The tricuspid valve and its supporting apparatus are inexorably tied to the internal structure of the RV ( Table 6.2 ). Although the tricuspid valve often comprises a varied number of leaflets and scallops, it is classically described as having septal, anterior, and posterior leaflets. Given the compliant nature of the RV cavity and the tricuspid annulus, right-sided volume loads readily lead to tricuspid annular dilation and secondary tricuspid regurgitation (TR) ( Fig. 6.3 ).

TABLE 6.2

Tricuspid Valve Anatomy.

Papillary Muscles	Tricuspid Valve Leaflets	Associated Structures in the RV
Anterior	Anterior, posterior	Moderator band, anterior wall
Posterior	Septal	Posterior free wall
Septal	Anterior, septal	Interventricular septum

Fig. 6.3, Tricuspid valve evaluation with TEE.

The base of the tricuspid valve leaflets inserts into the tricuspid annulus, which is anteriorly displaced compared with the mitral annulus. The anterior tricuspid annular displacement and identification of the moderator band and extensive RV trabeculation can help in distinguishing the morphologic RV from the LV in congenital heart disorders. Failure of delamination of the septal and posterior leaflets of the tricuspid valve can cause an apparent apical displacement of the tricuspid annulus (i.e., Ebstein anomaly).

Right Atrium and Inferior Vena Cava

The RA and RV are anatomic neighbors whose functions are closely intertwined. The RV receives blood from the RA by passive flow, active RV relaxation, and right atrial contraction. The RA is filled by the superior and inferior vena cavae and the coronary sinus. Isolated RA dilation can be a sign of TR or restrictive RV filling. Conversely, a large volume load from an atrial septal defect can cause RV and RA dilation. Because of the close physiologic relationship of these structures, an abnormality of either one warrants a comprehensive evaluation of all right-sided cardiac structures ( Fig. 6.4 ).

Fig. 6.4, Multimodality imaging of the sinus venosus atrial septal defect.

Pulmonic Valve and Pulmonary Artery

The pulmonic valve connects the RVOT with the pulmonary arteries. The pulmonic valve is a tricuspid structure with leaflets that are thinner than the aortic valve leaflets. The anterior and superior location of the pulmonic valve and the thin pulmonic leaflets render the valve challenging to image with almost all imaging modalities ( Fig. 6.5 ).

Fig. 6.5, Multimodality imaging of pulmonary regurgitation.

The pulmonary artery is a thin-walled, high-flow, low-pressure system that provides flow from the RV into the pulmonary vascular bed. The normally low-pressured nature of the pulmonary vascular system means that the RV is poorly suited for increases in pulmonary pressures resulting from pulmonary hypertension ( Table 6.3 ).

TABLE 6.3

Classification of Pulmonary Hypertension.

Type of Pulmonary Hypertension	Subtypes and Associations
Pulmonary arterial hypertension (PAH)	Idiopathic PAH Heritable PAH Drug and toxin induced Associated with connective tissue, HIV infection, portal hypertension, congenital heart disease, schistosomiasis Pulmonary veno-occlusive disease and/or pulmonary capillary hemangiomatosis Persistent pulmonary hypertension of the newborn LV systolic dysfunction LV diastolic dysfunction Valvular disease Congenital/acquired left heart inflow/outflow tract obstruction and congenital cardiomyopathies Chronic obstructive pulmonary disease Interstitial lung disease Other pulmonary diseases with mixed restrictive and obstructive pattern Sleep-disordered breathing Alveolar hypoventilation disorders Chronic exposure to high altitude Developmental lung diseases
Chronic thromboembolic pulmonary hypertension (CTEPH)	No subcategories
Pulmonary hypertension with unclear multifactorial mechanisms	Hematologic disorders: chronic hemolytic anemia, myeloproliferative disorders, splenectomy Systemic disorders: sarcoidosis, pulmonary histiocytosis, lymphangioleiomyomatosis Metabolic disorders: glycogen storage disease, Gaucher disease, thyroid disorders Others: tumoral obstruction, fibrosing mediastinitis, chronic renal failure, segmental pulmonary hypertension

HIV , Human immunodeficiency virus.

Adapted from Simonneau G, Robbins IM, Beghetti M, et al. Updated clinical classification of pulmonary hypertension. J Am Coll Cardiol . 2009;30;54(1 suppl):S43–S54.

RV Blood Supply

The RV blood supply predominantly arises from the right coronary artery (RCA), with accessory contribution along the IVS from the left coronary artery (LCA) system ( Fig. 6.6 ). The RCA ostium normally arises in an anterior direction from the right coronary cusp of the sinus of Valsalva. It has proximal, middle, and distal segments, which are delineated by the superior and inferior margins of the RV. The proximal portion of the RCA commonly provides an atrioventricular nodal branch and a conus branch that supplies blood to the RVOT or infundibulum.

The midportion of the RCA gives off multiple RV acute marginal branches that supply blood to the RV free wall. In most individuals, the RCA is dominant and gives rise to a right posterior descending artery (rPDA) branch and a right posterolateral branch. The rPDA typically supplies the basal and mid-inferoseptum, and the LCA supplies the remainder of the IVS, primarily through septal perforators from the left anterior descending coronary artery.

Acute RV ischemia can lead to cardiogenic shock that is associated with a high mortality rate. Historically, the RV was thought to tolerate ischemia better than the LV. This was attributed to the lower metabolic demands of the RV, greater thickness of the LV myocardium, and differences in coronary physiology, with RCA flow being less phasic and augmented in systole compared with LCA flow, which occurs primarily in diastole. ^, However, in TAVR patients, early coronary occlusion of the RCA or LCA leads to acute ischemia and a combined hospital mortality rate of 50%. This suggests that the adverse outcomes from acute RCA occlusion may be related more to the territory of myocardial involvement than to differences in coronary and myocardial physiology. This is further supported by data in patients with acute RV infarctions who underwent late gadolinium enhancement imaging by cardiac magnetic resonance imaging (CMR). In these patients, evidence of RV injury was noted in 57% of patients, which persisted at 13 months ( Fig. 6.7 ).

RV Physiology

In anatomically normal hearts, RV and LV systolic functions mirror each other. Differences in appearance of the RV size on traditional 2D imaging results from the anatomic location of the RV in the thoracic cavity and the inability of a planar 2D ultrasound beam to capture a 3D structure. Although the RV appears smaller than the LV in most 2D projections, the total RV volume is larger than the LV in normal individuals. This means that the RV ejection fraction must be lower than the LV ejection fraction for any given cardiac output. These relationships are defined by the following formulas:

Cardiac output = Stroke volume × Heart rate

Stroke volume = End diastolic volume − End systolic volume

Ejection fraction = Stroke volume ÷ End diastolic volume

RV and LV functions have direct interactions, called ventricular interdependence . Ventricular interdependence is multifactorial, but a primary contributor is the shared space in the pericardial cavity ( Fig. 6.8 ). During normal inspiration, decreased intrathoracic pressure augments flow into the RV. As the RV preload increases, RV cardiac output is augmented by normal Frank-Starling interactions. Although the pericardium is a tough fibrous structure, there is a normal physiologic capacity that can accommodate this additional flow. Loss of this normal pericardial capacity in pathologic states such as pericardial constriction or pericardial tamponade can lead to an inspiratory RV septal shift that impinges on normal LV filling. Other situations of significant RV pressure and/or volume overload due to factors such as pulmonary hypertension, pulmonary embolism, or RV infarction can also displace the IVS and similarly affect LV filling ( Fig. 6.9 ).

Fig. 6.8, Relationship of the RV and pericardium.

Fig. 6.9, Pulmonary hypertension and RV function.

Another contributor to ventricular interdependence is the shared ventricular muscle fibers. The LV has three distinct layers of muscle fibers, whereas the RV contains only a superficial and an endocardial layer. The superficial layer of the RV myocardial fibers is circumferential and is contiguous with the LV; the thicker RV endocardial layer of muscle fibers is longitudinally oriented and forms the RV side of the shared IVS. The difference in myocardial fiber orientation contributes to a unique RV contractile pattern that is more reliant on longitudinal shortening than on free wall motion.

In addition to normal ventricular interactions, the RV is highly sensitive to small changes in preload and afterload, likely related to its thin walls. This may lead to perturbations in RV diastolic function. Although RV diastolic function is less well described than that of the LV, it is driven by same parameters of active relaxation, passive filling, and ventricular chamber compliance.

Basic Principles of Image Acquisition

RV imaging should use an integrative approach that includes multiple echocardiographic and Doppler techniques to evaluate all right-sided cardiac structures ( Fig. 6.10 ). Transthoracic echocardiographic (TTE) imaging of the RV can be challenging because of its location in the anterior chest. In parasternal views, the sternum and ribs may limit the available echocardiographic windows, and the proximity of the RV to the transducer probe may degrade image quality due to near-field clutter artifact. From the parasternal imaging windows, a standard phased array ultrasound transducer has a triangular beam that is unable to provide full visualization of the entire RV in a single field of view and may require apical or subcostal windows for improved visualization.

Fig. 6.10, RV diagnostic approach with TTE.

RV Anatomic Evaluation

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