Ventricular septal defect

Last updated: September 12, 2024

Ventricular septal defect

MD2_HDF_II

MD2_HDF_II

Antituberculosis medications
Cardiac work
Pressure-volume loops
Blood pressure, blood flow, and resistance
Pressures in the cardiovascular system
Laminar flow and Reynolds number
Measuring cardiac output (Fick principle)
Anatomy clinical correlates: Heart
Tricuspid valve disease
Pulmonary valve disease
Mitral valve disease
Aortic valve disease
Cardiomyopathies: Pathology review
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Cardiac conduction system
Cardiac conduction velocity
ECG basics
ECG normal sinus rhythm
ECG rate and rhythm
ECG cardiac infarction and ischemia
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart failure: Pathology review
Cor pulmonale
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Development of the cardiovascular system
Heart failure: Clinical
Adrenergic antagonists: Beta blockers
Loop diuretics
ACE inhibitors, ARBs and direct renin inhibitors
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Heart failure
Fetal circulation
Persistent truncus arteriosus
Transposition of the great vessels
Tetralogy of Fallot
Patent ductus arteriosus
Ventricular septal defect
Coarctation of the aorta
Atrial septal defect
Cardiac muscle histology
Hypertension: Pathology review
Hypertension
Thiazide and thiazide-like diuretics
Calcium channel blockers
Angina pectoris
Myocardial infarction
Peripheral artery disease
Atherosclerosis and arteriosclerosis: Pathology review
Aortic dissections and aneurysms: Pathology review
Vasculitis: Pathology review
Kawasaki disease
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Antiplatelet medications
Thrombolytics
Reading a chest X-ray
The role of the kidney in acid-base balance
Acid-base map and compensatory mechanisms
Acid-base disturbances: Pathology review
Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis
Plasma anion gap
Obstructive lung diseases: Pathology review
Chronic obstructive pulmonary disease (COPD): Clinical
Asthma: Clinical
Alpha 1-antitrypsin deficiency
Bronchiectasis
Chronic bronchitis
Cystic fibrosis
Emphysema
Restrictive lung diseases
Idiopathic pulmonary fibrosis
Sarcoidosis
Deep vein thrombosis and pulmonary embolism: Pathology review
Pulmonary hypertension
Pulmonary edema
Tuberculosis: Pathology review
Pneumonia: Clinical
Chlamydia pneumoniae
Klebsiella pneumoniae
Mycoplasma pneumoniae
Streptococcus pneumoniae
Upper respiratory tract infection
Bacterial epiglottitis
Respiratory syncytial virus
Influenza virus
Mesothelioma
Bronchodilators: Leukotriene antagonists and methylxanthines
Bronchodilators: Beta 2-agonists and muscarinic antagonists

Transcript

Watch video only

Content Reviewers

If you look at the heart, you’ve got the right and left atrium up top, and the right and left ventricles down low. Each of these pairs is separated by a wall, called a septum. A ventricular septal defect is when this lower wall—the ventricular septum—has a gap in it after development. 

The septum is formed during development as this muscular ridge of tissue grows upward from the apex, or the tip, and then fuses with a thinner membranous region coming down from the endocardial cushions. Voila—two separate chambers. If these don’t fuse though, then a gap is left between the two chambers; in other words, a ventricular septal defect, or VSD. The majority of cases are caused by a defect in the membranous portion of the septum.

Among babies, VSDs are actually the most common congenital defect overall, but 30 to 50% of VSDs can spontaneously close during childhood, which makes ventricular defects less common with adults. VSDs are associated with fetal alcohol syndrome and Down syndrome, and are often associated with other cardiac deformities as well. 

Alright so now let’s check out what happens with blood flow, now that there’s this opening between the two ventricles. I’m going to actually switch to this super duper simplified heart instead, just because it’s easier to show what’s going on with blood flow. Alright, so deoxygenated blood comes from the body to the right atrium, and then flows down into the right ventricle, where now it can either be pumped out to the lungs, as normal, or pop over to the left ventricle. Since the pressure on the left side of the heart is actually higher than on the right, and blood likes to flow from high pressure to low pressure, it actually prefers to just keep going on to the lungs. When oxygenated blood comes back from the lungs to the left atrium, and then the left ventricle, now again, it’s got two choices: it can either be pumped out to the body, or flow over to the right ventricle through the gap. Since now it’s in the left ventricle which has higher pressure, some of the blood flows over to the lower-pressure right ventricle, so a left-to-right shunt has been set up, where oxygenated blood takes an extra trip to the lungs.

Key Takeaways

Ventricular septal defect (VSD) is a type of congenital heart defect that affects the septum, the wall that separates the two ventricles of the heart. In VSD, there is an abnormal opening in the septum that allows blood to flow between the two ventricles. This results in increased blood flow to the lungs, causing pulmonary hypertension and, in severe cases, heart failure. VSD is typically diagnosed during infancy or childhood, and imaging tests such as echocardiography or cardiac catheterization may be used to confirm the diagnosis. Treatment options for VSD depend on the size and location of the defect, and can include medications, surgery, or catheter-based procedures to close the hole and restore normal blood flow in the heart.