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In the heart, a ventricle is one of two large chambers that collect and expel blood received from an atrium towards the peripheral beds within the body and lungs. The atrium (an adjacent/upper heart chamber that is smaller than a ventricle) primes the pump. Interventricular means between the ventricles (for example the interventricular septum), while intraventricular means within one ventricle (for example an intraventricular block).
In a four-chambered heart, such as that in humans, there are two ventricles that operate in a double circulatory system: the right ventricle pumps blood into the pulmonary circulation to the lungs, and the left ventricle pumps blood into the systemic circulation through the aorta.
Ventricles have thicker walls than atria and generate higher blood pressures. The physiologic load on the ventricles requiring pumping of blood throughout the body and lungs is much greater than the pressure generated by the atria to fill the ventricles. Further, the left ventricle has thicker walls than the right because it needs to pump blood to most of the body while the right ventricle fills only the lungs.
On the inner walls of the ventricles are irregular muscular columns called trabeculae carneae which cover all of the inner ventricular surfaces except that of the conus arteriosus, in the right ventricle. There are three types of these muscles. The third type, the papillary muscles give origin at their apices to the chordae tendinae which attach to the cusps of the tricuspid valve.
The right ventricle is equal in size to that of the left ventricle, and contains roughly 85 millilitres (3 imp fl oz; 3 US fl oz) in the adult. Its upper front surface is circled and convex, and forms much of the sternocostal surface of the heart. Its under surface is flattened, forming part of the diaphragmatic surface of the heart that rests upon the diaphragm.
Its posterior wall is formed by the ventricular septum, which bulges into the right ventricle, so that a transverse section of the cavity presents a semilunar outline. Its upper and left angle forms a conical pouch, the conus arteriosus, from which the pulmonary artery arises. A tendinous band, called the tendon of the conus arteriosus, extends upward from the right atrioventricular fibrous ring and connects the posterior surface of the conus arteriosus to the aorta.
The left ventricle is shorter and more conical in shape than the right, and on transverse section its concavity presents an oval or nearly circular outline. It forms a small part of the sternocostal surface and a considerable part of the diaphragmatic surface of the heart; it also forms the apex of the heart. The left ventricle is thicker and more muscular than the right ventricle because it pumps blood at a higher pressure.
The right ventricle is triangular in shape and extends from the tricuspid valve in the right atrium to near the apex of the heart. Its wall is thickest at its base and thins towards the atrium.
By early maturity, the walls of the left ventricle have thickened from three to six times greater than that of the right ventricle. This reflects the typical five times greater pressure workload this chamber performs while accepting blood returning from the pulmonary veins at ~80mmHg pressure (equivalent to around 11 kPa) and pushing it forward to the typical ~120mmHg pressure (around 16.3 kPa) in the aorta during each heartbeat. (The pressures stated are resting values and stated as relative to surrounding atmospheric which is the typical "0" reference pressure used in medicine.)
The left ventricle receives oxygenated blood from the left atrium via the mitral valve and pumps it through the aorta via the aortic valve, into the systemic circulation. The left ventricular muscle must relax and contract quickly, and be able to increase or lower its pumping capacity under the control of the nervous system. In the diastolic phase, it has to relax very quickly after each contraction so as to quickly fill with the oxygenated blood flowing from the pulmonary veins. Likewise in the systolic phase, the left ventricle must contract rapidly and forcibly to pump this blood into the aorta, overcoming the much higher aortic pressure. The extra pressure exerted is also needed to stretch the aorta and other arteries to accommodate the increase in blood volume.
The typical healthy adult heart pumping volume is ~5 liters/min, resting. Maximum capacity pumping volume extends from ~25 liters/min for non-athletes to as high as ~45 liters/min for Olympic level athletes.
In cardiology, the performance of the ventricles are measured with several volumetric parameters, including end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV)and ejection fraction (Ef).
|Measure||Typical value||Normal range|
|end-diastolic volume (EDV)||120 mL[non-primary source needed]||65–240 mL[non-primary source needed]|
|end-systolic volume (ESV)||50 mL[non-primary source needed]||16–143 mL[non-primary source needed]|
|stroke volume (SV)||70 mL||55–100 mL|
|ejection fraction (Ef)||58%||55–70%|
|heart rate (HR)||75 bpm||60–100 bpm|
|cardiac output (CO)oo||5.25 L/minute||4.0–8.0 L/min|
The heart and its performance are also commonly measured in terms of dimensions, which in this case means one-dimensional distances, usually measured in millimeters. This is not as informative as volumes, but may be much easier to estimate with e.g. M-Mode echocardiography or with sonomicrometry (mostly used for animal model research). Optimally, it is specified with which plane the distance is measured in, e.g. the dimension of the longitudinal plane.
|End-diastolic dimension||EDD||The diameter across a ventricle at the end of diastole, if not else specified then usually referring to the transverse (left-to-right) internal (luminal) distance, excluding thickness of walls, although it can also be measured as the external distance.|
|LVEDD or sometimes LVDD||The end-diastolic dimension of the left ventricle.||48 mm,|
Range 36 – 56 mm
|RVEDD or sometimes RVDD||The end-diastolic dimension of the right ventricle.||Range 10 – 26 mm|
|End-systolic dimension||ESD||ESD is similar to the end-diastolic dimension, but is measured at the end of systole (after the ventricles have pumped out blood) rather than at the end of diastole.|
|LVESD or sometimes LVSD||The end-systolic dimension of the left ventricle.||Range 20 – 40 mm|
|RVESD or sometimes RVSD||The end-systolic dimension of the right ventricle.||Range 10 – 26 mm|
|Interventricular septal end diastolic dimension||IVSd||The thickness of the interventricular septum.||8.3 mm,|
Range 7 – 11 mm
|Left ventricular end diastolic posterior wall dimension||LVPWd||The thickness of the posterior left ventricular wall.||8.3 mm,|
Range 7 – 11 mm
|Left atrial dimension||LA||Range 24 – 40 mm|
Fractional shortening (FS) is the fraction of any diastolic dimension that is lost in systole. When referring to endocardial luminal distances, it is EDD minus ESD divided by EDD (times 100 when measured in percentage). Normal values may differ somewhat dependent on which anatomical plane is used to measure the distances. Normal range is 25-45%, Mild is 20-25%, Moderate is 15-20%, and Severe is <15%. Cardiology Diagnostic Tests Midwall fractional shortening may also be used to measure diastolic/systolic changes for inter-ventricular septal dimensions and posterior wall dimensions. However, both endocardial and midwall fractional shortening are dependent on myocardial wall thickness, and thereby dependent on long-axis function. By comparison, a measure of short-axis function termed epicardial volume change (EVC) is independent of myocardial wall thickness and represents isolated short-axis function.
Cardiac dysrhythmia or arrhythmia is an irregular heartbeat that can occur in the ventricles or atria. Normally the heartbeat is initiated in the SA node of the atrium but initiation can also occur in the Purkinje fibres of the ventricles giving rise to premature ventricular contractions, also called ventricular extra beats. When these beats become grouped the condition is known as ventricular tachycardia.
Another form of arrhythmia is that of the ventricular escape beat. This can happen as a compensatory mechanism when there is a problem in the conduction system from the SA node.