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Venae cavae
Venae cavae
Venae cavae
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Venae cavae
The human heart and other structures, with superior and inferior vena cava labeled on left
Identifiers
MeSHD014684
FMA321896
Anatomical terminology

In anatomy, the venae cavae (/ˈviːni ˈkeɪvi/;[1] sg. vena cava /ˈviːnə ˈkeɪvə/; from Latin 'hollow veins')[2] are two large veins (great vessels) that return deoxygenated blood from the body into the heart. In humans they are the superior vena cava and the inferior vena cava, and both empty into the right atrium.[3] They are located slightly off-center, toward the right side of the body.

The right atrium receives deoxygenated blood through coronary sinus and two large veins called venae cavae. The inferior vena cava (or caudal vena cava in some animals) travels up alongside the abdominal aorta with blood from the lower part of the body. It is the largest vein in the human body.[4]

The superior vena cava (or cranial vena cava in animals) is above the heart, and forms from a convergence of the left and right brachiocephalic veins, which contain blood from the head and the arms.

(made in (1883))
Anatomy of the horse, with other arteries: spermatic artery (21), which is posterior (posterior) to vena cava, venae portae, as well as the External iliac artery, and the mesenteric vessels, Internal iliac and renal arteries labelled. The posterior venae cavae (vena cava) is labelled 22.

References

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Venae cavae

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from Grokipedia
The venae cavae (singular: vena cava) are the two largest veins in the human body, consisting of the superior vena cava (SVC) and the inferior vena cava (IVC), which collectively return deoxygenated blood from the systemic circulation to the right atrium of the heart for subsequent pulmonary oxygenation. These principal veins play a critical role in maintaining venous return, with the SVC draining the upper body—including the head, neck, upper extremities, and thorax—while the IVC collects blood from the lower body, encompassing the abdomen, pelvis, and lower extremities. Structurally, both venae cavae feature thin walls composed of three layers—the intima (endothelial lining), (elastic and smooth muscle fibers), and (connective tissue)—contributing to the venous system's high , which accommodates nearly three-fourths of the body's at low , with nourishment supplied by . Blood flow through these veins is primarily passive, augmented by contractions, respiratory dynamics, and one-way valves in peripheral tributaries, though the venae cavae themselves largely lack valves to prevent . Anatomical variants, such as a duplicated or left-sided IVC (prevalence 0.2–3%) or persistent left SVC (prevalence 0.3–0.5%), may arise from embryological development and can influence clinical interventions like placement.

Anatomy

Superior vena cava

The superior vena cava (SVC) is formed by the union of the right and left brachiocephalic veins posterior to the lower border of the first right . It descends vertically for approximately 7 cm along the right side of the , passing posterior to the second and third intercostal spaces before piercing the fibrous to drain into the superior aspect of the right atrium at the level of the third . This short, wide vessel is valveless and thin-walled, measuring about 2 cm in diameter in adults. The primary tributaries of the SVC are the right and left brachiocephalic veins, which themselves receive blood from the internal jugular, subclavian, vertebral, and , among others. Additional tributaries include the , which joins the posterior aspect of the SVC at the level of the right main via an arch over the right lung root, as well as smaller veins draining the and . In terms of anatomical relations, the SVC lies anterior to the parietal pleura of the right and the root of the right , with the right positioned laterally and the right posteromedially. It is situated posterior to the and superior to the right . The SVC carries deoxygenated from the head, , upper limbs, and thoracic structures above the diaphragm to the right atrium.

Inferior vena cava

The inferior vena cava (IVC) is the largest vein in the body and serves as the principal conduit for venous return from the lower extremities, , , and retroperitoneal structures to the right atrium of the heart. It forms at the level of the fifth lumbar vertebra (L5) by the confluence of the right and left common iliac veins, anterior to the fifth lumbar vertebral body and inferior to the bifurcation of the , then ascends paralleling the right side of the in the retroperitoneum. The IVC lies posterior to the and is crossed anteriorly by structures such as the third part of the and the liver in its upper course. The course of the IVC can be divided into abdominal and thoracic segments. The abdominal segment, the longest portion measuring approximately 18 cm, extends from its origin at L5 upward along the right anterolateral aspect of the vertebral column to the diaphragm, remaining within the ; its upper (hepatic) portion traverses the groove on the posterior surface of the liver, where the IVC lies partially embedded in a deep groove covered by hepatic tissue. It then transitions to the short thoracic segment, about 2 cm in length, which pierces the central tendon of the diaphragm at the level of the eighth thoracic vertebra (T8) through the caval opening before opening into the inferior aspect of the right atrium. Major tributaries join the IVC along its course, contributing deoxygenated blood from various regions. At its origin, it receives the common iliac veins at L5, followed by 4 to 5 pairs of lumbar veins draining the posterior abdominal wall between L1 and L5. The right enters at approximately L2, while the s join at the L1-L2 level, with the right renal vein being shorter and more direct. At L1, the right suprarenal vein drains the , and near the diaphragm at T8, the inferior phrenic veins and (typically three main ones) enter just before the IVC reaches the heart. The left gonadal and suprarenal veins typically drain indirectly via the left renal vein rather than the IVC itself. The IVC is a thin-walled, valveless vessel throughout most of its length, relying on respiratory movements and pumps for forward flow, though rudimentary valves may occasionally be present in the proximal portions of the common iliac veins. In the , its diameter measures up to 3 cm, reflecting its capacity to handle substantial venous volume, and it gradually narrows superiorly.

Function

Venous return

The venae cavae serve as the principal conduits for systemic venous return, collecting deoxygenated blood from the body's capillaries and transporting it to the right atrium of the heart for subsequent pulmonary circulation. The superior vena cava (SVC) drains the upper body, receiving blood primarily from the head, neck, arms, and thoracic structures via the right and left brachiocephalic veins, which form by the union of the internal jugular and subclavian veins. In contrast, the inferior vena cava (IVC) collects venous blood from the lower body and abdomen, integrating inputs from the common iliac veins (which merge at the L5 vertebral level) as well as visceral tributaries such as the renal, hepatic, and gonadal veins. Both venae cavae empty separately into the right atrium, with the SVC entering superiorly and the IVC inferiorly, ensuring efficient delivery without intermixing of regional flows. In resting adults, the IVC handles approximately 60-70% of total as venous return, while the SVC accounts for the remaining 30-40%, reflecting the larger venous drainage area below the diaphragm. This distribution maintains steady-state equilibrium where venous return equals over time, supporting overall circulatory balance. The proportion can vary with posture or activity; for instance, upright positioning may transiently increase IVC contribution due to gravitational effects on lower body venous pooling. As part of the low-pressure venous system, the venae cavae facilitate cardiac preload by accommodating compliant venous reservoirs that optimize end-diastolic volume in the right ventricle. Their distensibility allows blood volume storage and gradual release, enhancing ventricular filling without excessive pressure buildup. Respiratory movements further modulate flow: during inspiration, negative intrathoracic pressure promotes SVC inflow while causing partial IVC collapse (typically 20-50% diameter reduction at the hepatic level), augmenting overall venous return to the thorax. Blood flow through the venae cavae remains unidirectional toward the heart, driven by right atrial contraction, venous wall compliance, and extrinsic factors like the muscle pump in limbs, despite the absence of valves along their lengths (noting only a vestigial Eustachian valve remnant at the IVC-atrial junction).

Hemodynamic characteristics

The hemodynamic characteristics of the venae cavae are defined by low-pressure, high-volume blood flow that facilitates efficient venous return to the right atrium. (CVP), which reflects the pressure in the (SVC) and () near the right atrium, typically ranges from 0 to 8 mmHg in healthy individuals and serves as a key indicator of right heart filling and volume status. This pressure is routinely measured using central venous catheters inserted into the SVC or for clinical monitoring of and cardiac preload. At rest, blood flow rates in the venae cavae approximate one-third of cardiac output through the SVC (approximately 1.5-2 L/min) and two-thirds through the IVC (approximately 3-4 L/min), reflecting the distribution of venous drainage from the upper and lower body, respectively. These rates increase substantially during physiological demands such as exercise, where venous return can rise up to fivefold to match elevated cardiac output, driven by enhanced skeletal muscle contraction and sympathetic activation. The venae cavae exhibit high compliance and capacitance, with the SVC demonstrating distensibility of about 20 mL/mmHg and the IVC showing even greater values (around 22 mL/mmHg in adults), enabling them to function as expandable reservoirs that buffer fluctuations in venous return and maintain steady preload to the heart. Several factors modulate vena caval . Gravity exerts orthostatic effects, particularly on the IVC, reducing its flow in upright postures due to pooling in lower extremity veins, which can decrease IVC flow by up to 50% compared to conditions. Respiration influences flow through diaphragmatic descent during inspiration, which compresses abdominal veins and boosts IVC inflow by 20-30% per cycle, while also aiding SVC return via intrathoracic pressure changes. Flow in both venae cavae is synchronized with the , exhibiting phasic patterns with systolic and diastolic peaks that align with atrial relaxation and ventricular contraction to optimize right heart filling. The venae cavae lack functional valves along their lengths, relying instead on external compression from surrounding structures (such as respiratory muscles and intra-abdominal pressure) and the momentum of upstream venous flow to propel blood unidirectionally toward the heart. This valveless design contributes to minimal turbulence, as blood velocities remain low—typically 10-20 cm/s on average—ensuring predominantly laminar flow with Reynolds numbers well below the threshold for chaotic patterns.

Embryological development

Development of the superior vena cava

The (SVC) originates primarily from the right anterior cardinal vein and the right common cardinal vein during early embryonic development. These structures form part of the symmetrical venous system that drains the head, neck, and upper limbs into the of the primitive heart. The common cardinal veins, formed by the union of anterior and posterior cardinal veins, initially provide symmetric drainage on both sides, but the left-sided components largely regress to favor right-sided dominance. Embryonic formation of the SVC begins around the fourth week of , when the cardinal vein system emerges. By weeks 4 to 5, the right anterior cardinal vein contributes to the proximal SVC, while the right common cardinal vein forms its distal portion. The s develop subsequently, with the right arising directly from the right anterior cardinal vein and the left forming via an between the left and right anterior cardinal veins around week 7; these fuse to create the mature SVC by the eighth week. Key developmental processes include the between the anterior cardinal veins—which give rise to the future internal jugular veins—and connections to the vitelline veins via the common cardinals, alongside the regression of the left common cardinal vein to establish unilateral right-sided drainage. The SVC also derives mainly from the right horn of the and incorporates contributions from the subclavian veins, which develop from venous plexuses in the limb buds and connect to the anterior cardinals. Anomalies in SVC development arise from incomplete regression or persistence of embryonic structures. A persistent left SVC, resulting from the failure of the left anterior cardinal vein to regress, occurs in 0.3-0.5% of the population and typically drains into the in 80-92% of cases, often coexisting with a right SVC to form a double SVC configuration. Double SVC, or bilateral SVC, is similarly prevalent at 0.3-0.5% and is attributed to inadequate development of the anastomosing branch between anterior cardinals, such as due to thymic vein influences. These variants highlight the plasticity of cardinal vein remodeling during weeks 7-8.

Development of the inferior vena cava

The development of the inferior vena cava (IVC) is a complex process involving the integration of multiple primitive venous systems during early embryogenesis, primarily between the 4th and 8th weeks of gestation. It arises from the cardinal and vitelline venous systems, where the posterior cardinal veins, which initially drain the caudal embryo, largely regress and contribute only to the formation of the common iliac veins. The subcardinal veins emerge around weeks 6-7 and develop anastomoses with the posterior cardinals via the subcardino-posterior cardinal anastomosis, while the supracardinal veins appear by week 8 and form connections through the sub-supracardinal and suprasupracardinal anastomoses, predominantly on the right side due to asymmetric regression of the left-sided structures. This rightward shift ensures the IVC's typical position, with full structural assembly completed by weeks 8-10. The IVC is segmented based on its embryonic origins: the iliac portion derives from the posterior cardinal veins; the renal segment forms from the sub-supracardinal ; the prerenal segment arises from the right subcardinal vein; and the posthepatic (suprahepatic) segment develops from the right vitelline vein. The hepatic segment is uniquely shaped by the incorporation of the liver, where the vitelline veins traverse the developing hepatic sinusoids, creating the retrohepatic IVC through with the subcardinal veins. At its termination in the right atrium, the Eustachian valve represents a remnant of the embryonic valve of the , which directs blood flow from the IVC toward the foramen ovale during . Anomalies in IVC development often result from incomplete regressions or persistent bilateral structures, leading to variants such as interrupted IVC with azygos or hemiazygos continuation, where the infrarenal IVC is absent and lumbar veins drain into the azygos system (prevalence 3-5%); left-sided IVC due to failure of the right supracardinal vein to develop (0.2-0.5%); and double IVC from bilateral supracardinal persistence (1-3%). These congenital variations are typically asymptomatic but can impact surgical planning or endovascular procedures.

Clinical significance

Disorders of the superior vena cava

Superior vena cava syndrome (SVCS) is the most common disorder affecting the superior vena cava, resulting from partial or complete obstruction of blood flow through the vessel, leading to a constellation of symptoms due to impaired venous drainage from the head, neck, upper extremities, and thorax. The primary causes include malignancy, accounting for approximately 70% of cases, with lung cancer being the most frequent etiology (60-85% of malignant SVCS), followed by non-Hodgkin lymphoma and other thoracic tumors that compress or invade the vessel. Non-malignant causes, such as thrombosis related to indwelling central venous catheters or pacemakers, contribute to about 25% of cases, exacerbated by the superior vena cava's anatomical vulnerability—its short length, thin walls, and lack of valves make it susceptible to extrinsic compression and intrinsic occlusion. An estimated 15,000 cases of SVCS occur annually in the United States, with incidence rising due to increased use of long-term central venous devices. Symptoms of SVCS typically develop gradually but can progress to life-threatening complications; common manifestations include facial and edema, dyspnea, , distended and chest wall veins, upper extremity swelling, and , with severe cases involving headache, visual disturbances, or from elevated venous pressure. Collateral circulation via azygos and internal mammary veins may develop over time, mitigating symptoms in chronic cases, but acute obstruction often presents emergently. Other disorders of the include isolated , which arises from central venous catheterization, hypercoagulable states, or , leading to clot formation without full development. Rare conditions encompass rupture, primarily from blunt thoracic trauma such as accidents, which can cause or and carries high mortality if undiagnosed. may be congenital, resulting from anomalous development, or iatrogenic, often following or surgical interventions near the vessel. Diagnosis of superior vena cava disorders relies on clinical evaluation, including elevated jugular venous pressure and visible collateral veins, supplemented by imaging such as contrast-enhanced CT venography to identify obstruction site and etiology, or MRI for detailed vascular assessment in patients with contraindications to iodinated contrast. Management is tailored to the underlying cause; for malignant SVCS, initial supportive measures like head elevation and oxygen are followed by radiation therapy or chemotherapy to reduce tumor burden, with endovascular stenting providing rapid symptom relief in 70-90% of cases. Thrombotic SVCS or isolated thrombosis is treated with systemic anticoagulation (e.g., heparin followed by warfarin or direct oral anticoagulants) and, if acute, thrombolysis or thrombectomy within 2-5 days of onset; catheter removal is recommended when feasible. For stenosis or obstruction, balloon angioplasty or stenting offers durable patency, while traumatic rupture requires urgent surgical repair, potentially aided by endovascular balloon occlusion for hemostasis. Prognosis varies significantly, with non-malignant causes yielding better outcomes (survival >90%), whereas malignant SVCS portends poorer survival tied to the primary tumor's aggressiveness.

Disorders of the inferior vena cava

Inferior vena cava (IVC) involves the formation of a blood clot within the IVC, a condition linked to high morbidity due to its potential for (PE) and . It often results from proximal extension of lower extremity deep vein (DVT), occurring in 4% to 15% of DVT cases, while other etiologies include malignancy-related hypercoagulability and pregnancy-associated stasis. Symptoms typically manifest as bilateral lower extremity , leg pain or heaviness, and nonspecific abdominal or flank discomfort, with approximately 12% of cases progressing to PE. In the United States, IVC affects an estimated 13,000 patients annually, underscoring its clinical burden within the broader spectrum of venous thromboembolism. Compression syndromes of the IVC or its tributaries contribute significantly to venous pathology, often precipitating or chronic symptoms. May-Thurner syndrome arises from extrinsic compression of the left common iliac by the overlying right , a variant present in up to 24% of the population but symptomatic in a minority, leading to left lower extremity pain, swelling, and recurrent iliofemoral DVT. Similarly, results from entrapment of the left between the and , commonly causing intermittent (in 79% of cases), flank pain (38%), and orthostatic due to elevated venous pressure gradients exceeding 3 mm Hg relative to the IVC. These syndromes heighten the risk of pelvic congestion and formation, particularly in younger adults with low or rapid . Congenital anomalies of the IVC further predispose individuals to thrombotic events by altering venous flow dynamics. Interrupted IVC, frequently associated with heterotaxy syndrome (including polysplenia or situs inversus), features azygos or hemiazygous continuation of infrahepatic venous return, occurring in about 1% of the population and elevating DVT risk through venous stasis in the lower extremities. Duplication of the IVC, with a prevalence of 0.2% to 3%, stems from failed regression of embryonic supracardinal veins and is linked to recurrent venous thromboembolism, particularly in young patients without other risk factors, due to turbulent flow and potential compression at confluence sites. These anomalies, while rare, account for a disproportionate share of idiopathic thrombosis cases in otherwise healthy individuals. Management of IVC disorders emphasizes preventing embolic complications while addressing underlying causes. IVC filters, deployed infrarenally via jugular or femoral access, serve as mechanical barriers to PE in patients with contraindications to anticoagulation; retrievable types allow removal once risk subsides, though permanent filters are used in recurrent cases. Complications occur in 10% to 20% of placements, including filter migration (2-4%), (1-5%), and caval (up to 11%), necessitating vigilant follow-up. Adjunctive therapies include catheter-directed to dissolve acute thrombi and venous stenting to relieve compression in syndromes like May-Thurner, with studies showing reduced rates when combined with anticoagulation. Overall, early intervention improves outcomes, though long-term anticoagulation remains cornerstone for most patients.

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