Contents

Right VentricleEdit

The right ventricle is one of the four chambers of the heart, responsible for guiding venous blood from the right atrium into the lungs for oxygenation. It forms the anterior portion of the heart’s lower surface and works under far lower pressure than the left ventricle, reflecting its role in pulmonary circulation rather than systemic circulation. Blood reaches the right ventricle from the right atrium through the tricuspid valve and is ejected into the pulmonary trunk via the pulmonary valve.

The right ventricle is structurally distinct from its left-sided counterpart. It tends to have a thinner wall and a more crescent-shaped silhouette in cross-section, with a highly trabeculated interior that contrasts with the more compact, thick-walled left ventricle. The chamber contains an inflow region that receives blood from the right atrium and an outflow tract that leads to the pulmonary valve and then to the pulmonary circulation. Its interior includes features such as the moderator band (septomarginal trabecula) and multiple papillary muscles that anchor the tricuspid valve apparatus. The inflow and outflow portions are separated by the infundibulum, sometimes referred to as the conus arteriosus, which is relatively smooth-walled compared with the trabeculated inflow. The right ventricle’s conduction and coronary blood supply are tailored to its lower pressure environment, with the right bundle branch and the right coronary artery providing essential support.

Anatomy

  • Location and shape: The right ventricle lies mostly to the anterior aspect of the heart, wrapping around the left ventricle. Its shape is more crescentic in the standard anatomical view, reflecting its integration with the right atrium and the outflow tract to the lungs. Left ventricle is the counterpart in the heart’s other main pumping chamber.
  • Inflow tract: The tricuspid valve governs flow from the right atrium into the RV. The interior shows prominent trabeculations, or ridges, known as trabeculae carneae.
  • Outflow tract: The infundibulum leads to the pulmonary valve and the pulmonary artery, forming the smooth-walled RVOT (right ventricular outflow tract) that transitions blood toward the lungs.
  • Internal features: The moderator band (septomarginal trabecula) runs from the interventricular septum to the anterior papillary muscle, and multiple papillary muscles anchor the tricuspid valve. The interior contains numerous trabeculations that differ from the LV’s more compact geometry.
  • Wall thickness and perfusion: The right ventricular free wall is thinner than the left ventricle and has different perfusion demands, with a coronary circulation largely supplied by branches of the right coronary artery in most individuals. Coronary arteries and Right coronary artery are relevant pages for understanding this supply.
  • Relation to other structures: The RV shares contact with the interventricular septum and the right atrium, and it interacts with the sternum and anterior chest wall in imaging and clinical assessment. The septum plays a role in ventricular interdependence, a topic of interest in cardiology.

Physiology and function

  • Flow through the heart: Blood returns to the heart via the superior and inferior vena cavae into the right atrium, then passes through the tricuspid valve to the right ventricle, which contracts to propel blood into the pulmonary trunk via the pulmonary valve for gas exchange in the lungs. The process is driven by pressure differences across the tricuspid and pulmonary valves during the cardiac cycle.
  • Pressure environment: The RV operates at substantially lower afterload than the left ventricle. Its systolic pressures are typically much lower than LV pressures, reflecting the low-resistance pulmonary circulation. This low-pressure system is sensitive to changes in pulmonary vascular resistance.
  • Function measurements: Right ventricular function can be assessed with imaging and hemodynamic indices such as the right ventricular ejection fraction (RVEF), fractional area change, and tricuspid annular plane systolic excursion (TAPSE). Modern practice often uses cardiac MRI or echocardiography to quantify RV function. Echocardiography and Cardiac MRI are common modalities for these assessments.
  • Interdependence and physiology: The RV’s performance is influenced by the pulmonary circulation’s resistance (afterload) and by the ventricle’s interaction with the left heart. Ventricular interdependence means changes in LV size or pressure can affect RV filling and function, and vice versa.
  • Developmental and evolutionary context: The right ventricle develops from distinct embryologic origins compared with the LV, and its structure reflects its function in handling venous return and pulmonary circulation. See Embryology of the heart for broader developmental context.

Development and comparative anatomy

  • Embryology: The right ventricle arises from segments of the primitive heart tube that form the right-sided inflow and outflow tracts, with the infundibulum contributing to the outflow portion toward the pulmonary artery. The left ventricle forms from its own distinct outflow tract and myocardial wall, facilitating high-pressure systemic circulation.
  • Comparative anatomy: Across mammals, the RV’s basic plan—thin-walled, trabeculated inflow region and smoother outflow tract toward the pulmonary circulation—reflects the demands of pumping blood into short, low-resistance pulmonary vessels, a contrast to the high-resistance systemic circuit managed by the LV.

Clinical significance

  • Right ventricular failure and cor pulmonale: The RV is particularly vulnerable to conditions that raise pulmonary vascular resistance, such as chronic lung disease or thromboembolic disease. Prolonged high afterload can lead to right-sided heart failure, a condition sometimes described as cor pulmonale when primarily driven by lung pathology. Cor pulmonale and Pulmonary hypertension are key topics in this area.
  • Pulmonary hypertension: Elevated pressures in the pulmonary arteries increase RV afterload and can lead to remodeling, dilation, and impaired contractility. Management focuses on reducing afterload or improving oxygenation and lung function, depending on the underlying cause. Pulmonary hypertension is a central concept in this discussion.
  • Congenital and acquired conditions: The right ventricle is involved in congenital heart diseases such as Tetralogy of Fallot and tricuspid valve anomalies, and it may be affected by acquired conditions like myocarditis or arrhythmogenic right ventricular cardiomyopathy (ARVC). Understanding RV structure helps explain the clinical manifestations and surgical approaches in these diseases. Tetralogy of Fallot and Arrhythmogenic right ventricular cardiomyopathy provide context for these conditions.
  • Diagnostic imaging and assessment: Noninvasive imaging strategies, including Echocardiography and Cardiac MRI, are essential for evaluating RV size, shape, wall thickness, and function. Specific measures such as TAPSE, FAC, and RVEF guide prognosis and therapy. Clinicians also monitor signs of venous congestion and hepatic involvement in advanced RV disease.
  • Therapeutic considerations: Treating RV disorders often requires addressing the underlying cause (lung disease, pulmonary vascular disease, or congenital anatomy) and supporting RV function with diuretics or afterload-reducing therapies when appropriate. In advanced, refractory cases, devices that support or bypass the RV may be considered in specialized centers. The choice of therapy is tailored to the patient’s overall condition and comorbidities.

See also