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Ventricle
Computer generated animation of cut section of the human heart showing both ventricles.
Details
Identifiers
Latinventriculus cordis
MeSHD006352
TA98A12.1.00.012
FMA7100
Anatomical terminology

A ventricle is one of two large chambers located toward the bottom of the heart that collect and expel blood towards the peripheral beds within the body and lungs. The blood pumped by a ventricle is supplied by an atrium, an adjacent chamber in the upper heart that is smaller than a ventricle. 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.

Structure

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Heart section showing ventricles and ventricular septum

Ventricles have thicker walls than atria and generate higher blood pressures. The physiological 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.[1][citation needed][2]

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 and to the mitral valve.

The mass of the left ventricle, as estimated by magnetic resonance imaging, averages 143 g ± 38.4 g, with a range of 87–224 g.[3]

The right ventricle is equal in size to the left ventricle[citation needed] 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.[citation needed]

Shape

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The left ventricle is longer 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 the apex and thins towards its base at the atrium. When viewed via cross section however, the right ventricle seems to be crescent shaped.[4][5] The right ventricle is made of two components: the sinus and the conus. The Sinus is the inflow which flows away from the tricuspid valve.[6] Three bands made from muscle, separate the right ventricle: the parietal, the septal, and the moderator band.[6] The moderator band connects from the base of the anterior papillary muscle to the ventricular septum.[5][7]

Development

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By young adulthood, 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.)

Function

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During systole, the ventricles contract, pumping blood through the body. During diastole, the ventricles relax and fill with blood again.

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 right ventricle receives deoxygenated blood from the right atrium via the tricuspid valve and pumps it into the pulmonary artery via the pulmonary valve, into the pulmonary circulation.

Pumping volume

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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.

Volumes

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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).

Wiggers diagram of various events of a cardiac cycle, showing left ventricular volume as a red trace.
Ventricular volumes
Measure Right ventricle Left ventricle
End-diastolic volume 144 mL (± 23 mL)[8] 142 mL (± 21 mL)[9]
End-diastolic volume / body surface area (mL/m2) 78 mL/m2 (± 11 mL/m2)[8] 78 mL/m2 (± 8.8 mL/m2)[9]
End-systolic volume 50 mL (± 14 mL)[8] 47 mL (± 10 mL)[9]
End-systolic volume / body surface area (mL/m2) 27 mL/m2 (± 7 mL/m2)[8] 26 mL/m2 (± 5.1 mL/m2)[9]
Stroke volume 94 mL (± 15 mL)[8] 95 mL (± 14 mL)[9]
Stroke volume / body surface area (mL/m2) 51 mL/m2 (± 7 mL/m2)[8] 52 mL/m2 (± 6.2 mL/m2)[9]
Ejection fraction 66% (± 6%)[8] 67% (± 4.6%)[9]
Heart rate 60–100 bpm[10] 60–100 bpm[10]
Cardiac output 4.0–8.0 L/minute[11] 4.0–8.0 L/minute[11]

Pressures

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Partial Wiggers diagram.

Red = aortic pressure
Blue = left ventricular pressure
Yellow = left atrial pressure.
Site Normal
pressure range
(in mmHg)[12]
Central venous pressure 3–8
Right ventricular pressure systolic 15–30
diastolic 3–8
Pulmonary artery pressure systolic 15–30
diastolic 4–12
Pulmonary vein/

Pulmonary capillary wedge pressure

2–15
Left ventricular pressure systolic 100–140
diastolic 3–12

Ventricular pressure is a measure of blood pressure within the ventricles of the heart.[13]

Left

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During most of the cardiac cycle, ventricular pressure is less than the pressure in the aorta, but during systole, the ventricular pressure rapidly increases, and the two pressures become equal to each other (represented by the junction of the blue and red lines on the diagram on this page), the aortic valve opens, and blood is pumped to the body.

Elevated left ventricular end-diastolic pressure has been described as a risk factor in cardiac surgery.[14]

Noninvasive approximations have been described.[15]

An elevated pressure difference between the aortic pressure and the left ventricular pressure may be indicative of aortic stenosis.[16]

[edit]

Right ventricular pressure demonstrates a different pressure-volume loop than left ventricular pressure.[17]

Dimensions

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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[18] or with sonomicrometry, which is 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.[19]

Dimension Abbreviation Definition Normally
End-diastolic dimension EDD The diameter across a ventricle at the end of diastole, if not else specified then usually referring to the transverse[20] (left-to-right) internal (luminal) distance, excluding thickness of walls, although it can also be measured as the external distance.
Left ventricular end-diastolic dimension
 LVEDD or sometimes LVDD The end-diastolic dimension of the left ventricle. 48 mm,[21]
Range 36 – 56 mm[22]
Right ventricular end-diastolic dimension
 RVEDD or sometimes RVDD The end-diastolic dimension of the right ventricle. Range 10 – 26 mm[22]
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.
Left ventricular end-systolic dimension
 LVESD or sometimes LVSD The end-systolic dimension of the left ventricle. Range 20 – 40 mm[22]
Right ventricular end-systolic dimension
 RVESD or sometimes RVSD The end-systolic dimension of the right ventricle. Range 10 – 26 mm[22]
Interventricular septal end diastolic dimension IVSd The thickness of the interventricular septum. 8.3 mm,[21]
Range 7 – 11 mm[22]
Left ventricular end diastolic posterior wall dimension LVPWd The thickness of the posterior left ventricular wall. 8.3 mm,[21]
Range 7 – 11 mm[22]
Mean left ventricular myocardial thickness Mean LVMT Average thickness of the left ventricle, with numbers given as 95% prediction interval for the short axis images at the mid-cavity level[23] Women: 4 - 8 mm[23]
Men: 5 - 9 mm[23]
Mean right ventricular myocardial thickness Mean RVMT Average thickness of the right ventricle, with numbers given as 95% prediction interval.[24] 4 - 7 mm[24]
Left ventricular end systolic dimension As above but measured during systole. This measurement is not commonly used clinically. 16  mm[25]
Left atrial dimension LA Range 24 – 40 mm[22]

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).[26] 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%.[27] Cardiology Diagnostic Tests Midwall fractional shortening may also be used to measure diastolic/systolic changes for inter-ventricular septal dimensions[28] and posterior wall dimensions. However, both endocardial and midwall fractional shortening are dependent on myocardial wall thickness, and thereby dependent on long-axis function.[29] 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.[29]

Clinical significance

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An 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.[citation needed]

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.[citation needed]

The most severe form of arrhythmia is ventricular fibrillation which is the most common cause of cardiac arrest and subsequent sudden death.

See also

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Ventricle (heart)

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The ventricles of the heart are the two lower muscular chambers that function as the primary pumps for systemic and , propelling blood out of the heart to the lungs and the rest of the body, respectively. The right ventricle receives deoxygenated blood from the right atrium through the and pumps it via the into the to reach the lungs for oxygenation. In contrast, the left ventricle receives oxygenated blood from the left atrium through the and ejects it through the into the for distribution throughout the systemic circulation. Structurally, both ventricles are thick-walled chambers separated by the , with the left ventricle featuring significantly thicker myocardial walls—approximately three times thicker than those of the right ventricle—due to the higher pressure required to against systemic . This wall thickness difference reflects their specialized roles: the right ventricle operates under lower pressure to propel a shorter distance to the lungs, while the left ventricle generates greater force to sustain circulation to distant body tissues. The ventricles contract simultaneously during , coordinated by electrical impulses from the , ensuring efficient flow without backflow, which is prevented by semilunar valves at their outlets. Notably, the ventricles' robust design, including (muscular ridges) on their inner surfaces, enhances contraction efficiency and anchors that secure the atrioventricular valves. Disruptions in ventricular function, such as or dilation, can lead to conditions like , underscoring their critical role in maintaining cardiovascular .

Anatomy

Location and Relations

The heart's ventricles are located within the , the central compartment of the situated between the lungs and posterior to the . They form the inferior portion of the heart, positioned below the atria and oriented such that their apex, primarily contributed by the left ventricle, points downward and to the left, resting on the diaphragm. This positioning places the ventricles in a slightly oblique plane, with the right ventricle occupying a more anterior and rightward location relative to the left ventricle. The right ventricle is the most anterior cardiac chamber, lying immediately behind the and forming the acute right margin of the heart, while its diaphragmatic surface contacts the central tendon of the diaphragm inferiorly. In contrast, the left ventricle is situated more posteriorly and to the left, wrapping around the that divides it from the right ventricle. The left ventricle maintains close spatial relations with the descending posteriorly and the left atrium superiorly, whereas the right ventricle relates anteriorly to the chest wall and indirectly to the via its outflow tract. The , a thick , separates the two ventricles and curves such that the right ventricle assumes a crescentic shape enveloping the left ventricle from the front and right sides. This arrangement ensures the ventricles' efficient contribution to the heart's overall compact structure within the , with minimal overlap in their projections on frontal imaging.

Shape and Dimensions

The left ventricle possesses a conical shape characterized by thicker muscular walls adapted for high-pressure systemic circulation, whereas the right ventricle adopts a crescent-shaped morphology in cross-section with thinner walls suited to lower-pressure pulmonary flow. In healthy adults, left ventricular wall thickness at end-diastole averages 6–10 mm in men and 6–9 mm in women, as measured by echocardiography, with the internal end-diastolic diameter typically spanning 4.2–5.8 cm in men and 3.8–5.2 cm in women. The right ventricular wall thickness is thinner, normally 3–5 mm, and its internal volume is comparably large to that of the left ventricle in diastole but appears more irregular due to extensive trabeculation. Ventricular dimensions exhibit variations influenced by age, sex, and body size; for example, athletes often display increased left ventricular wall thickness up to 13–15 mm and larger cavity dimensions as a benign physiological to chronic exercise demands. These morphological features and sizes are quantified using established imaging standards from and cardiac MRI, such as those from the American Society of Echocardiography, which define normal ranges adjusted for demographic factors to aid in clinical assessment.

Internal Features

The is a robust, obliquely oriented muscular wall that divides the left and right ventricles, ensuring separation of oxygenated and deoxygenated flows. It primarily consists of a thick muscular component formed by three continuous layers of myocardium, with a smaller membranous portion located superiorly just beneath the . This membranous segment, derived from , is thin and fibrous, measuring a few millimeters (typically 3-6 mm) in length in adults, and serves as a critical junction for the conduction system. The septum's thickness varies, averaging 8-12 mm in the muscular part, contributing to the mechanical synchrony of ventricular contraction. Within both ventricles, the endocardial surface features , which are irregular, raised muscular ridges and columns projecting from the inner walls, lined by and arranged in a crisscross pattern to enhance myocardial strength without impeding blood flow. These structures are more prominent and coarser in the right ventricle, where they form prominent elevations up to several millimeters in height, particularly in the apical region, compared to the finer, less extensive trabeculations in the left ventricle that create a relatively smoother cavity overall. The integrate with the ventricular myocardium, providing structural support and facilitating efficient contraction by increasing surface area for force transmission. Papillary muscles arise as conical projections from the ventricular walls, typically three in the right ventricle (anterior, posterior, and septal) and two in the left (anterolateral and posteromedial), serving as anchors for the . These are thin, fibrous cords composed of and fibers that extend from the apices of the papillary muscles to the free edges and ventricular surfaces of the atrioventricular valve leaflets, preventing valve prolapse and regurgitation during by tensing as the muscles contract. In the right ventricle, the papillary muscles attach to the leaflets, while in the left, they support the , with classified as marginal, basal, and strut types based on their insertion points. This apparatus ensures unidirectional blood flow through the valves. The right ventricle exhibits a tripartite internal , comprising distinct , trabecular, and outlet zones that reflect its specialized geometry for low-pressure pumping. The zone, adjacent to the , includes the papillary muscles and , forming a smooth, valve-supporting region about 3-4 cm long. The central trabecular zone occupies the apex, characterized by coarse, interconnecting muscular ridges that wrap around the , enhancing contractility in this irregular, crescent-shaped cavity. The outlet zone, or infundibulum, transitions smoothly to the , featuring minimal trabeculation to allow unobstructed ejection. In contrast, the left ventricle maintains a more uniform, ovoid cavity with subtler trabeculations, optimized for high-pressure systemic output.

Embryonic Development

The embryonic development of the heart ventricles begins during the third week of , when cardiogenic mesoderm cells, derived from the splanchnic , migrate and differentiate into cardiac progenitor cells under the influence of signaling molecules such as (BMP). These progenitors form bilateral endocardial tubes that fuse in the midline by the end of week 3 (Carnegie stage 9-10), establishing the primitive linear heart tube, which initially consists of an inner endocardial layer surrounded by myocardium and cardiac jelly. By the fourth week (Carnegie stage 12), the heart tube undergoes rightward looping due to differential growth rates, forming the bulboventricular fold that positions the future ventricles caudally and establishes the basic left-right asymmetry essential for ventricular orientation. This looping process expands the ventricular regions, with the proximal contributing to the trabeculated portions of both ventricles and the primitive ventricle forming the trabeculated myocardium of the main ventricular chambers. Trabeculation, the formation of myocardial ridges, begins around day 28 and supports early contractile function while facilitating in the absence of a coronary vasculature. Ventricular septation commences in the fourth week (Carnegie stage 13-14), with the interventricular septum arising from the apposition and merger of the medial walls of the developing ventricles, driven by localized proliferation of myocardial cells. in the atrioventricular canal and outflow tract swell and fuse starting in week 5 (Carnegie stage 14), while cells migrate into the outflow cushions by week 6 (Carnegie stage 16), contributing to the membranous portion of the by closing the interventricular . By week 7 (Carnegie stage 19), the interventricular septum is largely complete, dividing the ventricles and directing blood flow appropriately, with the membranous septum forming the final closure through fusion of the cushions with the . Differential growth occurs concurrently, with the left ventricle undergoing greater myocardial thickening to prepare for systemic circulatory pressures, while the right ventricle incorporates more of the trabeculated and adapts for lower pulmonary pressures, a process influenced by hemodynamic forces and regional by week 8 (Carnegie stage 23). This results in the mature that is predominantly muscular with a small membranous component. Incomplete septation during these stages can lead to congenital anomalies such as ventricular septal defects (VSDs), where failure of cushion fusion or muscular septum growth creates a persistent communication between the ventricles, most commonly in the membranous or muscular regions. These defects arise from genetic factors, such as mutations in PITX2, or environmental teratogens disrupting migration, and represent the most frequent congenital heart malformation.

Physiology

Role in Blood Circulation

The ventricles of the heart function as the main pumping chambers, driving through the pulmonary and systemic circulatory pathways to sustain oxygenation and delivery across the body. The left ventricle receives oxygenated from the left atrium and propels it into the during contraction, thereby initiating systemic circulation that distributes to all peripheral tissues via arteries, capillaries, and veins. Conversely, the right ventricle receives deoxygenated from the right atrium and pumps it into the , facilitating where reaches the lungs for carbon dioxide removal and oxygen uptake. Within the cardiac cycle, the ventricles fill passively during as they relax and the atrioventricular valves open, allowing inflow from the atria; the atria augment this filling with a brief contraction in late . In , ventricular contraction closes the atrioventricular valves and opens the semilunar valves, enabling forceful ejection of into the outflow tracts while preventing . This cyclical filling and ejection mechanism underpins , with each ventricle ejecting roughly 70 mL of blood per beat in a typical , maintaining steady blood flow to support organ function and metabolic demands.

Contraction and Pumping Action

Ventricular contraction begins with excitation-contraction coupling, where action potentials originating from the propagate rapidly across the ventricular myocardium to individual cardiomyocytes. These action potentials depolarize the , activating voltage-gated L-type calcium channels that permit extracellular calcium influx. This influx triggers from the via ryanodine receptors, elevating cytosolic calcium levels and enabling actin-myosin cross-bridge formation for force generation. During , the ventricles first enter an phase after atrioventricular valve closure, during which myocardial fibers shorten without altering ventricular volume as pressure builds to exceed that in the and . Semilunar valves then open, initiating rapid ejection of blood into the great arteries. The Frank-Starling mechanism modulates this process by linking end-diastolic preload—increased by greater venous return—to enhanced stretch, which boosts sensitivity to calcium and thereby increases to match circulatory demands. Diastole involves active relaxation to facilitate ventricular refilling, an ATP-dependent process that rapidly lowers cytosolic calcium through into the via pumps and extrusion via the sodium-calcium exchanger. also detaches actin-myosin cross-bridges, allowing of the myocardium and restoring low diastolic stiffness for passive filling from the atria. The energy for these contraction and relaxation cycles derives primarily from ATP produced via in the mitochondria-dense myocardium, which accounts for over 95% of cardiac ATP under normal conditions, supporting the high metabolic demands of continuous pumping.

Hemodynamic Measurements

Hemodynamic measurements provide quantitative assessment of ventricular performance through key parameters such as volumes, , and pressures, which reflect the heart's ability to pump blood effectively. Stroke volume (SV) is defined as the difference between (EDV) and end-systolic volume (ESV), calculated by the formula SV = EDV - ESV, representing the amount of ejected from the ventricle per beat; a typical value in adults is approximately 70 mL. (EF), a critical indicator of systolic function, is computed as EF = (SV / EDV) × 100, with normal ranges typically falling between 50% and 70%. Ventricular pressures are measured during and to evaluate loading conditions and contractility. In the left ventricle, systolic pressure is approximately 120 mmHg, while diastolic pressure is around 10 mmHg; in the right ventricle, systolic pressure is about 25 mmHg, and diastolic pressure is roughly 5 mmHg. These parameters are obtained using invasive and non-invasive techniques. directly measures intracardiac pressures by inserting a into the ventricles, providing precise hemodynamic data. offers a non-invasive method to estimate ventricular volumes and derive SV and EF through imaging of chamber dimensions and Doppler flow assessment.

Left vs. Right Ventricle Differences

The left and right ventricles exhibit profound structural asymmetries adapted to their distinct roles in the . The left ventricular wall is substantially thicker, typically measuring 8-12 mm, compared to the right ventricular wall at 3-5 mm, resulting in the left ventricle having approximately three times the myocardial mass of the right to generate the high pressures required for systemic circulation. This disparity in wall thickness and mass enables the left ventricle to pump blood against the high-resistance systemic circuit, while the right ventricle's thinner, more compliant walls suit the low-pressure pulmonary circuit. Morphologically, the left ventricle adopts a conical or bullet-shaped form, which facilitates efficient ejection into the , whereas the right ventricle has a more crescent-shaped or bellows-like structure in cross-section, optimized for handling larger of blood with lower . These shapes reflect evolutionary adaptations: the left ventricle's robust evolved to support high-output systemic demands in mammals, while the right ventricle's compliant architecture, derived from earlier structures like the , excels as a pump for pulmonary flow. Functionally, both ventricles achieve equivalent cardiac outputs of approximately 5 L/min at rest in healthy adults, despite the left ventricle operating against much higher pressures; the right ventricle compensates through its larger cavity volume and lower impedance pulmonary vasculature, requiring only about one-fifth the expenditure of the left. This balance ensures steady-state circulation, with the right ventricle's greater offsetting its reduced contractility relative to the left. Under stress, the ventricles respond differently based on their loading conditions. The left ventricle tends toward in response to pressure overload, such as , thickening its walls further to maintain output against elevated . In contrast, the right ventricle is more prone to eccentric dilation under volume or stress from pulmonary conditions, expanding its cavity to accommodate increased preload while risking impaired function due to its lower baseline reserve. These adaptive patterns highlight the left ventricle's greater resilience to increases compared to the right's sensitivity to impedance changes in the pulmonary circuit.

Clinical Relevance

Pathophysiological Conditions

Pathophysiological conditions affecting the heart ventricles include a spectrum of acquired and congenital disorders that disrupt normal structure and function, often leading to impaired pumping efficiency, altered , and increased risk of complications. These conditions can arise from pressure or , ischemic injury, or developmental anomalies, contrasting with the ventricles' typical robust myocardial architecture designed for high-pressure ejection. Ventricular hypertrophy represents an adaptive response to chronic stress but can progress to maladaptive remodeling. of the left ventricle, characterized by increased wall thickness with preserved or reduced chamber size, commonly develops in response to pressure overload from , where the narrowed valve imposes elevated on the ventricle. This remodeling aims to normalize wall stress but may eventually impair diastolic filling and coronary . In contrast, eccentric hypertrophy involves chamber dilation with proportional wall thickening, often triggered by secondary to myocardial ischemia, as seen in ischemic , where infarct-related remodeling leads to progressive ventricular enlargement. Heart failure manifests through ventricular dysfunction, broadly categorized into systolic and diastolic subtypes. Systolic heart failure, or heart failure with reduced ejection fraction (HFrEF), results from impaired contractile function, typically reducing ejection fraction below 40%, which diminishes the ventricle's ability to eject blood effectively and is frequently caused by prior ischemic damage or cardiomyopathy. Diastolic heart failure, or heart failure with preserved ejection fraction (HFpEF), stems from impaired ventricular relaxation and increased stiffness, hindering diastolic filling despite normal systolic ejection, often linked to hypertrophy or fibrosis that elevates end-diastolic pressures. Arrhythmias such as (VT) frequently originate from structural abnormalities in the ventricular myocardium. Post-myocardial infarction, scarred tissue creates heterogeneous conduction zones within the infarct border, facilitating reentrant circuits that sustain VT, a life-threatening disturbance increasing sudden cardiac risk. Congenital ventricular defects, though originating in embryonic development, profoundly impact postnatal ventricular function. Ventricular septal defects (VSDs) involve openings in the , permitting left-to-right shunting of oxygenated blood into the , which overloads the right ventricle and can lead to if unrepaired. represents a severe developmental defect where the left ventricle and associated structures are underdeveloped, rendering the left ventricle incapable of supporting systemic circulation and necessitating immediate postnatal interventions.

Diagnostic Techniques

Diagnostic techniques for assessing the and function of the heart's ventricles are essential in clinical practice to identify abnormalities such as impaired contractility or structural changes. These methods range from non-invasive imaging and electrical assessments to invasive hemodynamic measurements, allowing clinicians to evaluate ventricular performance in relation to conditions like ischemia or . Echocardiography serves as a primary non-invasive tool for ventricular evaluation, utilizing waves to produce real-time images of cardiac structures. Two-dimensional (2D) echocardiography provides cross-sectional views to assess wall motion abnormalities and calculate (EF), a key measure of systolic function, while three-dimensional (3D) imaging enhances accuracy in volumetric assessments. complements these by measuring blood flow velocities across ventricular outlets and inlets, aiding in the detection of valvular gradients or regurgitant flows. Cardiac (MRI) is considered the gold standard for precise quantification of ventricular volumes and myocardial tissue characterization, particularly in identifying through techniques like late enhancement. This modality offers high-resolution, multi-planar imaging without , enabling detailed evaluation of both left and right ventricular function and detecting subtle pathological changes such as from prior ischemia. Electrocardiography (ECG) provides an accessible, non-invasive method to infer ventricular abnormalities through analysis of electrical activity. It detects via increased voltage or duration criteria, such as Sokolow-Lyon or Cornell indices, and identifies ischemia through ST-segment changes or T-wave inversions reflecting altered . While ECG has limitations in sensitivity for anatomic , it remains valuable for initial screening and risk stratification in ventricular pathologies. Cardiac catheterization offers the invasive gold standard for direct measurement of ventricular pressures and intracardiac gradients, particularly in assessing valve-related diseases affecting ventricular loading. Performed via femoral or radial access, it involves advancing catheters into the heart chambers to record pressures in the left and right ventricles, pulmonary artery, and wedge positions, providing critical hemodynamic data not fully captured by non-invasive methods.

Therapeutic Interventions

Therapeutic interventions for ventricular disorders primarily aim to alleviate symptoms, improve ventricular function, and prevent progression of conditions such as and ischemia. Pharmacotherapy forms the cornerstone of management for , with guideline-directed medical therapy (GDMT) including four foundational classes for heart failure with reduced (HFrEF): receptor-neprilysin inhibitors (ARNIs; preferred over [ACE] inhibitors or receptor blockers [ARBs]), evidence-based beta-blockers, antagonists (MRAs), and sodium-glucose cotransporter-2 inhibitors (SGLT2is). These agents reduce , inhibit neurohormonal activation, provide cardioprotection, and improve outcomes, leading to reverse remodeling, decreased hospitalization, and reduced mortality risks. SGLT2is are also recommended for heart failure with preserved (HFpEF). Beta-blockers additionally control heart rate in arrhythmias. These therapies are typically initiated in stable patients with systolic dysfunction and titrated to target doses for optimal benefit. Surgical options are reserved for advanced or structural ventricular issues. Ventricular assist devices (VADs), particularly left VADs, serve as bridge or destination therapy for end-stage , mechanically supporting ventricular pumping to enhance and quality of life while awaiting transplant or as permanent support. Surgical repair of ventricular septal defects involves open-heart procedures using patches to close congenital or acquired holes, preventing shunting and right ventricular overload, with high success rates in restoring normal . Interventional procedures target ischemic or valvular contributions to ventricular strain. Percutaneous coronary intervention (PCI), including angioplasty and stenting, restores blood flow in obstructive coronary arteries to limit ischemic damage to the ventricles, reducing infarct size and improving ejection fraction in acute settings. Valve replacement surgeries, such as aortic or mitral valve procedures, alleviate abnormal loading on the ventricles; for instance, aortic valve replacement in stenosis reduces left ventricular hypertrophy and pressure overload, promoting regression of myocardial changes over time. Lifestyle and supportive measures, including , play a vital role post-myocardial infarction to enhance ventricular recovery. Structured exercise programs improve left ventricular remodeling and function by boosting and reducing , while also addressing risk factors to prevent recurrent events. These interventions are integrated into multidisciplinary care for sustained ventricular health.

References

  1. https://www.cdc.gov/heart-defects/how-the-heart-works/index.html
  2. https://training.seer.cancer.gov/anatomy/cardiovascular/heart/structure.html
  3. https://pmc.ncbi.nlm.nih.gov/articles/PMC8975613/
  4. https://oertx.highered.texas.gov/courseware/lesson/2210/student/?section=2
  5. https://www.ncbi.nlm.nih.gov/books/NBK470256/
  6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1860731/
  7. https://pmc.ncbi.nlm.nih.gov/articles/PMC5100240/
  8. https://www.ahajournals.org/doi/10.1161/circulationaha.113.001375
  9. https://www.asecho.org/wp-content/uploads/2016/02/2015_ChamberQuantificationREV.pdf
  10. https://www.ncbi.nlm.nih.gov/books/NBK499876/
  11. https://www.ahajournals.org/doi/10.1161/circimaging.113.000690
  12. https://www.ahajournals.org/doi/10.1161/01.cir.101.3.336
  13. https://pmc.ncbi.nlm.nih.gov/articles/PMC8031199/
  14. https://anatomy.ttuhscep.edu/cardiovascular_system/heart_tables.html
  15. https://connects.catalyst.harvard.edu/Profiles/profile/1224000
  16. https://pmc.ncbi.nlm.nih.gov/articles/PMC9181036/
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