Ventricles of the heart
The definition of heart ventricles can be summed up as the large, lower chambers of the fibromuscular organ that work to keep blood moving through the body. Although all parts of the heart work together to carry out its daily function, the ventricles have an enormous role in maintaining adequate cardiac output to keep blood flowing. The heart works continuously from the 4th gestational week until the end of life. Throughout this time, the muscular ventricles have the tremendous responsibility of pumping blood out of the heart and into the systemic and pulmonary circuits.
|Interventricular septum||Separates the left and right ventricles
Upper, thin membranous part
Lower, thick muscular part
Carries the atrioventricular bundles of His
|Ventricular function||Right - pumps blood to pulmonary circulation
Left - pumps blood to systemic circulation
|Embryology||Left ventricle arises from the primitive ventricle
Right ventricle arises from the bulbus cordis
|Ventricular pathology||Congenital ventricular disorders - ventricular septal defects, double outlet right ventricle, hypoplastic ventricles
Acquired - hypertrophy, pseudoaneurysm, arrhythmia, bundle-branch block
This article aims to discuss the development, anatomy, and function of the ventricles of the heart with an accompanying heart diagram to aid in understanding. Additional discussion regarding disorders of the ventricle (both congenital and acquired) will also be included.
- Review of cardiac anatomy
- Right ventricle
- Left ventricle
- Interventricular septum
- Ventricular function
- Ventricular pathology
Review of cardiac anatomy
The heart is a mediastinal structure that has the most important role in the circulatory system. In the anatomical position, the heart is obliquely positioned, with its anatomical base (formed by the left atrium) pointing posterolaterally to the right and the apex of heart directed anteroinferiorly to the left. The right cardiac chambers account for most of the anterior or sternocostal surface of the heart. However, the walls of both ventricles constitute the inferior or diaphragmatic surface.
An overview of the heart and its surfaces is given in the following resource:
The outer surface of the heart is marked by depressions known as grooves. They act as landmarks for the interatrial and interventricular septa inside the heart. The left and right pulmonary surfaces are made up by the left ventricle and right atrium, respectively. Of note, the left pulmonary surface rests in the cardiac notch of the left lung. The heart is made up of four muscular chambers that work synergistically to propel blood throughout the body. The heart is divided into two sides by the interatrial and interventricular septa. Each half of the heart has two chambers: an atrium, and a lower chamber called the ventricle. The function of the atria is to collect and pump blood into the ventricles. The function of the ventricles is to pump blood into systemic and pulmonary circulations. Details regarding the direction of the flow of blood can be found in the cardiac cycle article.
The atria are separated from the ventricles by the atrioventricular septa. This is a fibroelastic structure that not only prevents inappropriate blood flow from the atrium to the ventricle, but it also prevents unwanted electrical conduction from the atrial myocardium to the ventricles. In the absence of this structure, there would be backflow of blood and electrical activity across the myocardium.
However, blood is able to flow from each atrium into the ipsilateral ventricle via the respective atrioventricular valves, the tricuspid valve on the right and mitral valve on the left. Blood also leaves each ventricle via their respective ventricular outflow tracts that are guarded by the semilunar valves. On the left-hand side, this outflow tract is the aorta, which is guarded by the aortic valve. From here, blood flows into systemic circulation. On the right-hand side, the outflow tract is the pulmonary artery, which is guarded by the pulmonary valve. From here, blood flows into pulmonary circulation.
The following resources provide you with clarifications and details about the heart valves:
Location and external features
The right ventricle is the smaller of the two lower chambers of the heart–it is only one-third of the thickness of its counterpart. In spite of the size disparity, the right ventricle still pumps the same volume of blood as the left ventricle. However, it does less work since the resistance in the pulmonary circulation is much lower than that in the systemic circulation.
The majority of the sternocostal surface of the heart is occupied by the anterosuperior part of the right ventricle. This part of the ventricle is convex and lies between the 3rd and 6th costal cartilages. The anterior margin of the left lung, as well as the left pleura, are superolaterally (toward the left) related to the anterior surface of the right ventricle. The inferior surface of the right ventricle accounts for a small part of the diaphragmatic surface of the heart. It sits over the central tendon of the diaphragm and a small muscular portion of the left hemidiaphragm. The interventricular septum functions as the posterior and left wall of the right ventricle. The right ventricle is anterior to the left ventricle and anteroinferior to the right atrium.
It begins at the orifice of the tricuspid valve (right atrioventricular valve) and continues inferolaterally towards the apex of the heart. The natural contour of the chamber then turns superiorly toward the conus arteriosus (also called the infundibulum) and terminates at the orifice of the pulmonary valve (right semilunar valve). It is a bit difficult to assign an approximate geometrical shape to the right ventricle. When the structure is viewed laterally, it appears triangular. But when it is viewed in transverse section, it has a crescentic appearance due to the inward bulging of the free wall (the part not attached to the apex or the interventricular septum).
Another important structure is the tendon of infundibulum (or conus ligament). This is a band of collagenous tissue that extends from the posterior part of the conus arteriosus to the aortic root.
Structurally, the right ventricle can be subdivided into an inlet, an apical part, and an outlet. The inlet of the right ventricle, the tricuspid valve, provides a scaffold for the tricuspid annulus and other valvular structures. It is lined by trabeculae carneae and continues into a central area that becomes increasingly trabeculated. The apical part of the right ventricle is marked by numerous raised, interlacing ridges called trabeculae carneae. The muscular outflow tract is smooth and supports components of the pulmonary valve. The outlet, conus arteriosus, and pulmonary valve is relatively smooth in contrast and leads away from the trabeculated area. Of note, the inlet and outlet are separated from each other by the supraventricular crest, which is also called the crista supraventricularis. The crest is a thick, muscular band with septal and mural limbs that extend to the anterolateral wall of the right ventricle from a high point on the interventricular septal wall. It acts as a scaffold for the anterosuperior tricuspid leaflet. Additionally, it directs the flow of blood as it enters the ventricular cavity, and prevents it from going directly to the outflow tract. Both the inlet and outlet of the right ventricle are located in the roof of the chamber.
The other important internal features of the right ventricle are the papillary muscles, of which there are three:
- Anterior - is the largest of the three muscles. It originates from the anterior wall of the right ventricle. It is indirectly connected to the anterior and posterior tricuspid leaflets by way of the chordae tendineae.
- Posterior - originates from the inferior wall of the right ventricle, is smaller than the anterior papillary muscle, and is indirectly attached to the posterior and septal tricuspid leaflets.
- Septal - has attachments to the interventricular septum and indirect attachments to the anterior and septal tricuspid leaflets.
These muscular, finger-like projections are attached to the inner ventricular walls at one end and to the collagen-rich chordae tendineae at the other. The chordae tendineae are attached to the free edges of the tricuspid valve. Contraction of the papillary muscles precedes ventricular contraction. It results in the apposition of the tricuspid leaflets, thus occluding the valve orifice and preventing backflow of blood during ventricular contraction. Therefore the papillary muscles indirectly regulate the status of the tricuspid valve as it opens and closes throughout the cardiac cycle. Another important elevation within the right ventricle is the septal band, which gives added support to the papillary muscles of the tricuspid valve and the septomarginal (moderator) band.
The septomarginal (moderator) band is a thick, muscular structure that arises from the caudal part of the interventricular septum. It travels across the floor of the right ventricle toward the anterior papillary muscle. It acts as a conduit for part of the right atrioventricular bundle tract, which is a part of the electrical circuit of the heart. This muscle provides a shorter route for electrical impulses to reach the anterior papillary muscle so that it contracts with the rest of the ventricle.
For more information about the right ventricle, take a look below:
Location and external features
The left ventricle is responsible for maintaining pulsatile blood flow against the relatively high-pressure systemic circulation. It is a muscular chamber of the heart that receives oxygenated blood from the left atrium. The walls of the left ventricle are three times as thick as the right ventricle. It is roughly conical in shape and more elongated than its right counterpart. The base of the left ventricle begins at the left atrioventricular valve (a.k.a. the mitral valve, bicuspid valve) and continues toward the apex of the heart. The ventricular lumen then curves around toward the aortic valve, where blood is ejected into the aorta and systemic circulation. The external walls of the relatively large ventricle account for much of the left pulmonary, sternocostal, and diaphragmatic surfaces of the heart.
Other important landmarks located over the ventricles are the cardiac grooves. The interventricular groove extends over the sternocostal and diaphragmatic surfaces, where it marks the separation between the two ventricles. This groove also provides an external landmark to delineate between the territories of each ventricle.
The internal surface of the left ventricle is generally unremarkable. The lumen is oval and trabeculated toward the apex like in the right ventricle. However, the trabecular network is finer and appears mesh-like. The valves on the left side of the heart are more closely associated with each other than those on the right side. In fact, the mitral, aortic, and tricuspid valves are in continuity with each other via the fibroelastic cardiac skeleton (where they are attached by the left and right fibrous trigones. In fact, there is a fibrous subaortic curtain that descends from the left and right posterior arches of the aortic valve to separate the mitral valve from the aortic valve.
The left ventricle also has papillary muscles (anterior and posterior) that are attached to chordae tendineae as observed in the right ventricle. However, the papillary muscles of the left ventricle are much larger than those seen on the right. The free edge of each mitral leaflet will receive multiple chordae tendineae from both papillary muscles. This is most likely related to the fact that these papillary muscles must resist greater pressure in order to keep the mitral valve closed during ventricular systole.
If you want to cement your knowledge about the left ventricle and related structures, study the following resources:
An important structure that separates the two ventricles is the interventricular septum. Anatomically it is divided into two parts: a thick, muscular part and a relatively thin membranous part. The muscular part of the interventricular septum separates most of the left and right ventricles from each other. However, the membranous part of the interventricular septum – which is positioned posteriorly and superiorly within the left ventricle – separates the right chambers from the subaortic area. There is an additional division system used to segregate parts of the septum. With echocardiography, the interventricular septum can be divided into five parts. These are listed in no particular order:
- Basal anteroseptal
- Basal inferoseptal
- Apical septal
In addition to separating the ventricles, the interventricular septum also functions as a conduit for part of the conducting system of the heart. The atrioventricular bundle of His, which arises from the atrioventricular node, arborizes within the septum to reach its target points.
The interventricular septum is quite dynamic during each cardiac cycle. It contracts with the ventricles during systole such that it shortens longitudinally (from the base to the apex) and becomes thicker. This is because cardiomyocytes become shorter longitudinally, thinner circumferentially, and wider radially during muscle contraction. Additionally, the septum allows for complex motions of the heart during each contraction. It acts as a support structure against which the free wall of the right ventricle contracts against during systole.
The principal role of the ventricles is to pump blood out of the heart and into either systemic or pulmonary circulation. During diastole (relaxation) the ventricle is in the phase of passive filling where blood passes through the atria and into the ventricles. The atrioventricular valves are particularly important here because if they are not functioning (like in valvular stenosis), ventricular filling is impaired. When the atria depolarize and contract toward the end of diastole, they force any residual blood from the atria into their respective ventricles. As the ventricles fill, they dilate until they become depolarized and contract. Blood not only flows toward the semilunar valves but also toward the atrioventricular valves as well. The force of blood will cause competent atrioventricular valves to close (preventing reflux of blood into the atria) but will cause the semilunar valves to open.
Overwhelmed by the anatomical details of the ventricles and heart? Simplify your learning, cement your knowledge, and test yourself with our diagrams, quizzes & worksheets of the heart!
While the electrical activity throughout the heart is important for each cardiac cycle to occur in a timely manner, the pressure gradient across the valves and within the chambers are equally as important. The pressure dynamics within the ventricles are important to force the semilunar valves open, and to keep the atrioventricular valves closed. In the early phase of systole (contraction), intraventricular pressure (that is, the pressure within the ventricle) rapidly rises in order to overcome the pressure on the other side of the respective valves. However, until the intraventricular pressure is sufficient to open the semilunar valves, no blood will leave the ventricle. This state is known as isovolumetric contraction because even though there is ventricular contraction, there is no loss of blood from the ventricles. The ventricles enter the ejection phase when intraventricular pressure exceeds the pressure within the outflow tract: approximately 8 mmHg on the right side, and 85 mmHg on the left. The valves will open and blood will be ejected from the respective ventricle into systemic or pulmonary circulation.
The heart is one of the first organs to begin development. A heartbeat can be detected on ultrasound as early as the 6th gestational week. Early development and activity are necessary so that blood can be adequately circulated throughout the developing embryo.
Towards the end of the 3rd gestational week, the primitive heart tube begins pumping blood throughout the primitive embryo. It is a mesodermal derivative that appears like a tubular structure but subsequently undergoes significant morphological changes. The process starts with the appearance of the cardiogenic area (region of the growing heart near the head end (cephalic pole)) of the developing embryo. Subsequently, two strands of cardiogenic cords (mesenchymal derivatives with cardiac potential) arise within the cardiogenic area. As the embryo continues to grow, the cardiogenic tubes migrate centrally and fuse, giving rise to the endocardial tubes (18th - 22nd day of development).
The endocardial tubes are characterized by a truncus arteriosus (gives rise to the pulmonary trunk and aorta) in the cephalic aspect. This is followed by the bulbus cordis, primitive ventricle, primitive atrium (future atria), and the sinus venosus (future coronary sinus and oblique vein). By the end of the 4th gestational week, the heart has begun its intricate process of cardiac origami–where the heart undergoes significant changes and folding. The folding of the endocardial tubes results in the bulbus cordis assuming a ventral relationship with respect to the ventricle. Eventually, both the bulbus cordis (which will form the right ventricle) and primitive ventricle (forms the left ventricle) will be inferiorly related to the atria. Also important to note that the truncus arteriosus gives rise to the aorta and pulmonary artery–the outflow tracts of the left and right ventricles, respectively.
The bulbus cordis and primitive ventricle are in communication with each other and form a common ventricle. There is a median ridge on the floor of the common ventricle near the apical aspect of the chamber. This is known as the muscular interventricular septum which is subsequently populated by myocytes (muscle cells) originating from precursor ventricles. Myoblasts (precursors to myocytes) within the developing septum contribute to the growth of the interventricular septum as well. Endocardial cushions (which are located superior to the cushions) are also quite important in the formation of the interventricular septum. They are aggregates of modified cardiac tissue that contribute to the formation of the cardiac valves. This septal proliferation continues with a crescent-shaped defect intervening between the endocardial cushion and the interventricular septum. This ventricular septal defect persists up until the 7th gestational week when the bulbar ridge and the endocardial cushions meet. The point of fusion of the two membranes gives rise to the membranous part of the interventricular septum.
The trabecular patterns of the luminal surface of the ventricles develop after heart folding has begun. Initially, the lumen is covered with a two-layered epithelial lining that subsequently develops into sheets of myocardial elevations. The elevations extend into the lumen of the ventricle and concentrate near the inlets and apical areas, but recede near the outlet. The trabeculae carneae continue to acquire more cellular layers as they continue to mature.
The ultimate function of the heart is to get blood ejected from the ventricles into either systemic or pulmonary circuits. Unfortunately, both congenital and acquired disorders can directly affect the ventricles, resulting in suboptimal activity. While some of the pathologies are amenable to surgical intervention, other disorders are irreversible and are associated with life-long morbidity and mortality. Below is a list of congenital and acquired disorders that affect the ventricles. Not all of the disorders listed below will be addressed in this article.
|Congenital ventricular disorders||Ventricular septal defect
Double outlet right ventricle
Hypoplastic right ventricle
|Acquired ventricular disorders||Ventricular hypertrophy (left and right)
Ventricular arrhythmias - Ventricular tachycardia, Ventricular flutter, Ventricular fibrillation, Torsade de Pointe
Bundle branch block
Congenital ventricular disorders
Congenital ventricular disorders – much like other forms of congenital cardiac anomalies – occur early in development. They can arise either in isolation (hypoplastic ventricles) or as a part of a syndrome (tetralogy of Fallot). Furthermore, the cause may be a random genetic mutation or one precipitated by exposure to a teratogen (a drug that can cause a mutation).
Ventricular septal defect
A ventricular septal defect is an abnormal communication between the two ventricles via a perforation in the interventricular septum. It can be observed as a stand-alone defect or in association with syndromic disorders such as tetralogy of Fallot, transposition of the great arteries, or other concomitant atrioventricular septal defects. The major concern with ventricular septal defects is the fact that there is mixing of oxygenated and deoxygenated blood. This concern is minimal as long as blood flow is predominantly from the left side to the right (left to right shunt). However, chronic exposure of the right ventricle to the high pressures of the left ventricle results in subsequent right ventricular hypertrophy and eventually reversal of the shunt (right to left). This leads to predominantly deoxygenated blood entering systemic circulation. The patient may develop symptoms of hypoxia and their sequelae.
Ventricular septal defects rarely occur following an acquired etiology. One example of this acquired disorder is following a myocardial infarction (heart attack). Irrespective of the location, the walls of the heart are susceptible to rupture following an infarction. This phenomenon is based on the fact that as the myocardium heals, dead muscle cells are replaced with fibrous tissue which is unable to adequately accommodate the fluctuations in pressure. Therefore the affected walls are at risk of rupture.
Acquired ventricular disorders
There is a limited list of pathologies that can affect the ventricles of the heart. However, when they do occur, they can have a lasting effect on the heart due to the poor healing capability of cardiomyocytes (heart muscle cells).
Like all muscle cells, cardiomyocytes increase in size following an increasing workload. In the case of the heart, the increased workload comes in the form of increased resistance to blood flow. In the systemic circulatory pathway, this is commonly due to vascular narrowing as a result of atherosclerosis, where blood vessels become less compliant due to the excess plaque build-up in the arterial walls. Therefore higher pressures are needed to overcome the systemic resistance in order to maintain adequate blood flow. The left ventricle increases in size in response to the increased systemic resistance (left ventricular hypertrophy). Another cause of left ventricular hypertrophy includes aortic valvulopathy. Unfortunately, as the left ventricle continues to increase in size, it becomes less efficient. Eventually left ventricular output becomes suboptimal and the patient begins to experience symptoms of left ventricular failure (left heart failure).
Similarly, the right ventricle can undergo hypertrophic changes following an increase in its workload. Pulmonary hypertension, pulmonary valve stenosis, tricuspid valve regurgitation, and left heart failure can all increase the demand on the right ventricle, resulting in ventricular hypertrophy.