{"id":1953,"date":"2025-02-16T00:00:00","date_gmt":"2025-02-15T22:00:00","guid":{"rendered":"https:\/\/gynaikologos-komotini.gr\/?p=1953"},"modified":"2026-08-16T13:04:35","modified_gmt":"2026-08-16T10:04:35","slug":"ventricular-septal-defect-2","status":"publish","type":"post","link":"https:\/\/gynaikologos-komotini.gr\/en\/ventricular-septal-defect-2\/","title":{"rendered":"Ventricular Septal Defect"},"content":{"rendered":"\t\t
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Communications between the two circulatory systems (pulmonary and systemic) are located in the septa separating the atria (atrial septal defects) or the ventricles (ventricular septal defects), or involve communication between the great vessels (aortopulmonary communication). The result is blood shunting from the high-pressure system (systemic circulation) to the low-pressure system (pulmonary circulation). The shunt is left-to-right, while in very large defects it may become bidirectional.<\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t

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Anatomy<\/h3>

The interventricular septum is formed by the union of several septal components:<\/p>

Muscular septum<\/strong>, divided into:<\/p>

  1. Inlet septum (near the atrioventricular valves)<\/li>
  2. Trabeculated septum (extending to the apex)<\/li>
  3. Outlet septum (separating the right ventricular outflow tract\/infundibulum from the left ventricle)<\/li><\/ol>

    Membranous septum<\/strong>
    (located below the aortic valve and in the upper part of the muscular septum)<\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t

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    Types of ventricular septal defects<\/figcaption>\n\t\t\t\t\t\t\t\t\t\t<\/figure>\n\t\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t
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    Ventricular Septal Defect (VSD)<\/th>

    Location<\/p><\/th><\/tr><\/thead><\/table>

    Muscular type \u2013 trabeculated septum (muscular VSD)<\/td>Most common form of VSD, often small in size with a high likelihood of spontaneous closure<\/td><\/tr><\/tbody><\/table><\/div>
    Membranous\/perimembranous VSD<\/td>Common type extending into the membranous septum and adjacent septa. Possible spontaneous closure through aneurysm formation from neighboring tricuspid valve tissue attachments. Often large defects<\/td><\/tr><\/tbody><\/table><\/div>
    Muscular type \u2013 inlet septum (inlet VSD)<\/td>Defects located directly beneath the atrioventricular valves, without a tendency for spontaneous closure. Included among endocardial cushion defects<\/td><\/tr><\/tbody><\/table><\/div>
    Muscular type \u2013 outlet septum (malalignment VSD)<\/td>Large defects between the outlet septum and the remaining muscular septum due to failed alignment and connection. Severe congenital heart diseases such as Tetralogy of Fallot are characterized by this type of VSD<\/td><\/tr><\/tbody><\/table>

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    Hemodynamics and Clinical Manifestations<\/h2>

    Hemodynamics<\/h3>

    The presence of an intra- or extracardiac communication allows part of the blood flow to deviate from its normal course and pass through the defect into the opposite circulation. The direction and magnitude of the shunt depend on both the size of the defect and the pressure difference between the two circulations at the level of the communication.<\/p>

    Since systemic circulation has higher pressures than pulmonary circulation, blood flow through the defect is directed from the systemic to the pulmonary circulation (left-to-right shunt). If the defect is small to moderate, maintaining the pressure difference between the circulations, the amount of blood flow through the defect depends mainly on the size of the communication.<\/p>

    The left-to-right shunt reduces systemic cardiac output and increases pulmonary blood flow. Oxygenated blood from the left chambers (or aorta) escapes into the right chambers (or pulmonary artery), recirculating through the lungs without contributing to systemic oxygenation, thereby increasing pulmonary perfusion.<\/p>

    Small defects are termed restrictive because they significantly limit shunting between circulations. Large defects are nonrestrictive and minimally impede blood flow through the communication. In this case, the pressure difference between the two circulations decreases or pressures equalize, leading to pulmonary hypertension.<\/p>\t\t\t\t\t\t\t\t<\/div>\n\t\t\t\t\t<\/div>\n\t\t\t\t<\/div>\n\t\t

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    Clinical Manifestations<\/h3>

    The common clinical manifestations depend on the extent of the left-to-right shunt. When the shunt is limited, patients are asymptomatic. However, extensive left-to-right shunting leads to reduced systemic output and pulmonary recirculation, resulting in signs and symptoms of heart failure:<\/p>