Ventricular Septal Defect
Ventricular Septal Defect
Ventricular Septal Defect
Echocardiographic image of a moderate ventricular septal defect in the mid-muscular part of the septum. The trace in the lower left shows the flow during one complete cardiac cycleand the red mark the time in the cardiac cycle that the image was captured. Colours are used to represent the velocity of the blood. Flow is from the left ventricle (right on image) to theright ventricle (left on image). The size and position is typical for a VSD in the newborn period.
ICD-10
Q21.0
ICD-9
745.4
DiseasesDB
13808
eMedicine
med/3517
MeSH
C14.240.400.560.540
A ventricular septal defect (VSD) is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart. The ventricular septum consists of an inferior muscular and superior membranous portion and is extensively innervated with conducting cardiomyocytes. The membranous portion, which is close to the atrioventricular node, is most commonly affected in adults and older children in the United States.[1][2] It is also the type that will most commonly require surgical intervention, comprising over 80% of cases.[3] Membranous ventricular septal defects are more common than muscular ventricular septal defects, and are the most common congenital cardiac anomaly. [4] Contents
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6 Epidemiology and Etiology 7 See also 8 Additional images 9 References 10 External links
[edit]Diagnosis
A VSD can be detected by cardiac auscultation. Classically, a VSD causes a pathognomonic holoor pansystolic murmur. Auscultation is generally considered sufficient for detecting a significant VSD. The murmur depends on the abnormal flow of blood from the left ventricle, through the VSD, to the right ventricle. If there is not much difference in pressure between the left and right ventricles, then the flow of blood through the VSD will not be very great and the VSD may be silent. This situation occurs a) in the fetus (when the right and left ventricular pressures are essentially equal), b) for a short time after birth (before the right ventricular pressure has decreased), and c) as a late complication of unrepaired VSD. Confirmation ofcardiac auscultation can be obtained by non-invasive cardiac ultrasound(echocardiography). To more accurately measure ventricular pressures, cardiac catheterization, can be performed.
[edit]Pathophysiology
During ventricular contraction, or systole, some of the blood from the left ventricle leaks into the right ventricle, passes through the lungs and reenters the left ventricle via the pulmonary veins and left atrium. This has two net effects. First, the circuitous refluxing of blood causes volume overload on the left ventricle. Second, because the left ventricle normally has a much higher systolic pressure (~120 mm Hg) than the right ventricle (~20 mm Hg), the leakage of blood into the right ventricle therefore elevates right ventricular pressure and volume, causingpulmonary hypertension with its associated symptoms. In serious cases, the pulmonary arterial pressure can reach levels that equal the systemic pressure. This reverses the left to right shunt, so that blood then flows from the right ventricle into the left ventricle, resulting in cyanosis, as blood is by-passing the lungs for oxygenation.[5] This effect is more noticeable in patients with larger defects, who may present with breathlessness, poor feeding and failure to thrive in infancy. Patients with smaller defects may be asymptomatic. Four different septal defects exist, with perimembranous most common, outlet, atrioventricular, and muscular less commonly.[6]
[edit]Signs
and symptoms
Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.
[edit]Symptoms
VSD is an acyanotic congenital heart defect, aka a Left-to-right shunt, so there are no signs of cyanosis.
[edit]Signs
Pansystolic (Holosystolic) murmur (depending upon the size of the defect) +/- palpable thrill (palpable turbulence of blood flow). Heart sounds are normal. Larger VSDs may cause a parasternal heave, a displaced apex beat (the palpable heartbeat moves laterally over time, as the heart enlarges). An infant with a large VSD will fail to thrive and become sweaty and tachypnoeic (breathe faster) with feeds.[7]
CAUSES: The cause of VSD ( ventricular septal defect) includes the incomplete looping of the heart during days 24-28 of development. Faults with NKX2.5 gene can cause this.
[edit]Treatment
A nitinol device for closing muscular VSDs, 4 mm diameter in the centre. It is shown mounted on the catheter into which it will be withdrawn during insertion.
Most cases do not need treatment and heal at the first years of life. Treatment is either conservative or surgical. Smaller congenital VSDs often close on their own, as the heart grows, and in such cases may be treated conservatively. Some cases may necessitate surgical intervention, i.e. with the following indications: 1. Failure of congestive cardiac failure to respond to medications 2. VSD with pulmonic stenosis 3. Large VSD with pulmonary hypertension 4. VSD with aortic regurgitation For the surgical procedure, a heart-lung machine is required and a median sternotomy is performed. Percutaneous endovascular procedures are less invasive and can be done on a beating heart, but are only suitable for certain patients. Repair of most VSDs is complicated by the fact that the conducting system of the heart is in the immediate vicinity.
Ventricular septum defect in infants is initially treated medically with cardiac glycosides (e.g., digoxin 1020mcg/kg per day), loop diuretics(e.g., furosemide 13 mg/kg per day) and ACE inhibitors (e.g., captopril 0.5 2 mg/kg per day).
[edit]Surgical
a) Surgical closure of a Perimembranous VSD is performed on cardiopulmonary bypass with ischemic arrest. Patients are usually cooled to 28 degrees. Percutaneous Device closure of these defects is rarely performed in the United States because of the reported incidence of both early and late onset complete heart block after device closure, presumably secondary to device trauma to the AV node. b) Surgical exposure is achieved through the right atrium. The tricuspid valve septal leaflet is retracted or incised to expose the defect margins. c) Several patch materials are available, including native pericardium, bovine pericardium, PTFE (Gore-Tex or Impra), or Dacron. d) Suture techniques include horizontal pledgeted mattress sutures, and running polypropylene suture. e) Critical attention is necessary to avoid injury to the conduction system located on the left ventricular side of the interventricular septum near the papillary muscle of the conus. f) Care is taken to avoid injury to the aortic valve with sutures. g) Once the repair is complete, the heart is extensively deaired by venting blood through the aortic cardioplegia site, and by infusing Carbon Dioxide into the operative field to displace air. h) Intraoperative transesophageal echocardiography is used to confirm secure closure of the VSD, normal function of the aortic and tricuspid valves, good ventricular function, and the elimination of all air from the left side of the heart. i) The sternum, fascia and skin are closed, with potential placement of a local anesthetic infusion catheter under the fascia, to enhance postoperative pain control. j) A video of Perimembranous VSD repair, including the operative technique, and the daily postoperative recovery, can be seen here: VSD Repair, Perimembranous Ventricular Septal Defect
[edit]Epidemiology
and Etiology
VSDs are the most common congenital cardiac anomalies. They are found in 30-60% of all newborns with a congenital heart defect, or about 2-6 per 1000 births. During heart formation, when the heart begins life as a hollow tube, it begins to partition, forming septa. If this does not occur properly it can lead to an opening being left within the ventricular septum. It is debatable whether all those defects are true heart defects, or if some of them are normal phenomena, since most of the trabecular VSDs close spontaneously.[8] Prospective studies
give a prevalence of 2-5 per 100 births of trabecular VSDs that closes shortly after birth in 80-90% of the cases.
[9][10]
Congenital VSDs are frequently associated with other congenital conditions, such as Down syndrome.[11] A VSD can also form a few days after a myocardial infarction[12] (heart attack) due to mechanical tearing of the septal wall, before scar tissueforms, when macrophages start remodeling the dead heart tissue.
Abnormality: A defect allowing blood flow between the left and right ventricle. The defect on the right side is usually beneath the septal leaflet of the tricuspid valve. The defect on the left side is usually beneath the aortic valve. The hemodynamic consequences of VSD consist of:
a. eccentric hypertrophy of the left ventricle, and right ventricle. The right ventricle is more distensible
than the left ventricle thus reduced left ventricular distensibility becomes the main problem leading to congestive heart failure. It appears that flow across the defect usually streams directly into the pulmonary artery without significant mixing and distention of the right ventricle b. a marked % of LV cardiac output is detoured from its true target pulmonary artery hyperplasia resulting in severe pulmonary artery hypertension. This will result in a reversal of blood shunt flow from right to left. This causes systemic hypoxemia. We have never documented such a scenario. top Congenital Heart Disease: General
c. if the volume of shunt flow is very high, the pulmonary vasculature may respond with profound
2.
History: An incidental finding at the time of puppy vaccination if small defect large defect - stunted growth, fail to thrive A murmur may be detected as an incidental finding in the adult A systolic heart murmur with a PMI over the right sternal border Thrill may be present over right hemithorax If shunt flow reverses - signs of right to left shunt flow will be noted and signs of right heart failure Large defects may show congestive heart failure
2.
Physical examination:
top
a. Auscultation of a right sternal border systolic heart murmur. b. Radiographic evidence of pulmonary overcirculation.
The re-circulation circuit is: right ventricle, right ventricular outflow tract, pulmonary arteries, pulmonary veins, left atrium and left ventricle. Diagnostic Findings:
c. Echocardiography:
Comment (Right to left VSD): It is reported that chronic large volume of flow across the VSD into the pulmonary arteries can result in pulmonary artery hypertension and elevated right ventricular pressure. This can eventually result in right to left flow across the VSD. It is my belief that a right to left shunt does not occur due to this etiology of excessive blood flow as described in man. When a right to left shunt does occur it is a result of a hypoplastic pulmonary vasculature or congenital pulmonary artery hypertension. When right to left flow occurs across the VSD: 1. Historical signs develop: reduced exercise tolerance syncope fatigue
2.
3.
jugular venous distention cyanosis weakness possibly heart murmur right ventricular enlargement right atrial enlargement pleural effusion ascites right ventricular enlargement right atrial enlargement reduced arterial oxygen content right ventricular enlargement right atrial enlargement right to left contrast flow across VSD
4.
5.
Congenital Heart Disease: General Mild VSD c. d. causes no hemodynamic embarrassment and thus warrants no therapy may require surgical repair of the defect a number of procedures are available Severe VSD
Arterial vasodilators will reduce the degree of left to right shunting. Pulmonary artery banding procedures can spare pulmonary vascular damage a result of excessive fluid flowing through the pulmonary circulation. Congenital Heart Disease: General
top 1. 2.
Comments:
chronic excessive fluid flow through the pulmonary circulation may result in pulmonary hypertension and right to left shunt flow. this is likely a rare occurrence. if it does occur, polycythemia (increase in RBC mass of the blood) may develop and can be treated with hydroxyurea, which suppresses bone marrow production of RBCs.
http://www.vetgo.com/cardio/concepts/concsect.php?conceptkey=149#149
Programs & Treatments How are ventricular septal defects (VSDs) treated?
If your child has a ventricular septal defect, your pediatric cardiologist will want to carefully monitor him or her to make sure the condition is not causing damage to the heart. You will likely have frequent appointments and repeated tests at our Heart Institute to track the condition.
Medication
If your child has symptoms like shortness of breath or trouble nursing, he or she will be given medications to help treat these symptoms and help the heart beat more efficiently. Some VSDs will close on their own, without a surgical procedure. However, if your child has symptoms despite the medications, or if the hole is large enough that it is unlikely to close on its own, then surgery should be performed to close the hole. Some VSDs should be closed regardless of their size because of their position within the heart wall.
Heart Surgery
Ventricular septal defects are usually repaired with open-heart surgery by a pediatric cardiac surgeon. In some situations, minimally invasive surgical approaches may be used. This type of surgery is relatively low risk and most children are home within 3-5 days after surgery. Learn why Childrens Colorado is the best place for your childs heart surgery.
What are the signs and symptoms of ventricular septal defects (VSDs)?
A childs symptoms depend on the size of the hole and where it is located along the septum. Many children seem to have no symptoms. They grow and gain weight normally. Doctors may be able to tell that a child has VSD while listening to his or her heart during a physical exam. Some VSDs may be identified on a fetal ultrasound exam before a baby is born. Children with larger, more severe VSD generally have noticeable symptoms as babies. They may have difficulty feeding, which can slow their growth. Children with ventricular septal defects can experience shortness of breath, look pale, fail to gain weight or sweat while eating. Some children have frequent respiratory infections.
Diagnosis & Tests How do doctors diagnose ventricular septal defects (VSDs)?
Most ventricular septal defects are first identified by a childs pediatrician during a routine checkup. Blood passing irregularly from the left ventricle to the right causes a swooshing sound, also called a murmur, that a doctor can hear while listening to the heart with a stethoscope. If your doctor suspects your child may have VSD, he or she will request more tests to identify the size and location of the septal hole. Common tests for VSD include:
Helpful resources
If youd like to learn more about VSD, visit:
The U.S. National Library of Medicine The American Heart Association Childrens Hospital Colorado Health Library
http://www.childrenscolorado.org/conditions/heart/conditions/ventricular-septaldefect.aspx#4
Ventricular septal defect is one of the most common congenital heart defects. The baby may have no symptoms, and the hole can eventually close as the wall continues to grow after birth. If the hole is large, too much blood will be pumped to the lungs, leading to heart failure. The cause of VSD is not yet known. This defect often occurs along with other congenital heart defects. In adults, ventricular septal defects are a rare but serious complication of heart attacks. These holes are related to heart attacks and do not result from a birth defect. Symptoms Patients with ventricular septal defects may not have symptoms. However, if the hole is large, the baby often has symptoms related to heart failure. The most common symptoms include: Shortness of breath Fast breathing Hard breathing Paleness Failure to gain weight Fast heart rate Sweating while feeding Frequent respiratory infections
Exams and Tests Listening with a stethoscope usually reveals a heart murmur (the sound of the blood crossing the hole). The loudness of the murmur is related to the size of the defect and amount of blood crossing the defect. Tests may include: Chest x-ray -- looks to see if there is a large heart with fluid in the lungs ECG -- shows signs of an enlarged left ventricle Echocardiogram -- used to make a definite diagnosis Cardiac catheterization (rarely needed, unless there are concerns of high blood pressure in the lungs) MRI of the heart -- used to find out how much blood is getting to the lungs
Treatment
If the defect is small, no treatment is usually needed. However, the baby should be closely monitored by a health care provider to make sure that the hole eventually closes properly and signs of heart failure do not occur. Babies with a large VSD who have symptoms related to heart failure may need medicine to control the symptoms and surgery to close the hole. Medications may include digitalis (digoxin) and diuretics. If symptoms continue despite medication, surgery to close the defect with a Gore-tex patch is needed. Some VSDs can be closed with a special device during a cardiac catheterization, although this is infrequently done. Surgery for a VSD with no symptoms is controversial. This should be carefully discussed with your health care provider. Outlook (Prognosis) Many small defects will close on their own. For those defects that do not spontaneously close, the outcome is good with surgical repair. Complications may result if a large defect is not treated. Possible Complications
Heart failure Infective endocarditis (bacterial infection of the heart) Aortic insufficiency (leaking of the valve that separates the left ventricle from the aorta) Damage to the electrical conduction system of the heart during surgery (causing arrhythmias) Delayed growth and development (failure to thrive in infancy) Pulmonary hypertension (high blood pressure in the lungs) leading to failure of the right side of the heart
When to Contact a Medical Professional Most often, this condition is diagnosed during routine examination of an infant. Call your infant's health care provider if the baby seems to be having difficulty breathing, or if the baby seems to have an unusual number of respiratory infections. Prevention Except for the case of heart-attack-associated VSD, this condition is always present at birth. Drinking alcohol and using the antiseizure medicines depakote and dilantin during pregnancy have been associated with increased incidence of VSDs. Other than avoiding these things during pregnancy, there is no known way to prevent a VSD. Alternative Names
VSD; Interventricular septal defect References Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. St. Louis, Mo: WB Saunders; 2007. Update Date: 12/21/2009 Updated by: Kurt R. Schumacher, MD, Pediatric Cardiology, University of Michigan Congenital Heart Center, Ann Arbor, MI. Review provided by VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc. Browse the Encyclopedia
http://www.nlm.nih.gov/medlineplus/ency/article/001099.htm
Hard breathing Paleness Failure to gain weight Fast heart rate Sweating while feeding Frequent respiratory infections
Exams and Tests Listening with a stethoscope usually reveals a heart murmur (the sound of the blood crossing the hole). The loudness of the murmur is related to the size of the defect and amount of blood crossing the defect. Tests may include: Chest x-ray -- looks to see if there is a large heart with fluid in the lungs ECG -- shows signs of an enlarged left ventricle Echocardiogram -- used to make a definite diagnosis Cardiac catheterization (rarely needed, unless there are concerns of high blood pressure in the lungs) MRI of the heart -- used to find out how much blood is getting to the lungs
Treatment If the defect is small, no treatment is usually needed. However, the baby should be closely monitored by a health care provider to make sure that the hole eventually closes properly and signs of heart failure do not occur. Babies with a large VSD who have symptoms related to heart failure may need medicine to control the symptoms and surgery to close the hole. Medications may include digitalis (digoxin) and diuretics. If symptoms continue despite medication, surgery to close the defect with a Gore-tex patch is needed. Some VSDs can be closed with a special device during a cardiac catheterization, although this is infrequently done. Surgery for a VSD with no symptoms is controversial. This should be carefully discussed with your health care provider. Outlook (Prognosis) Many small defects will close on their own. For those defects that do not spontaneously close, the outcome is good with surgical repair. Complications may result if a large defect is not treated.
Possible Complications
Heart failure Infective endocarditis (bacterial infection of the heart) Aortic insufficiency (leaking of the valve that separates the left ventricle from the aorta) Damage to the electrical conduction system of the heart during surgery (causing arrhythmias) Delayed growth and development (failure to thrive in infancy) Pulmonary hypertension (high blood pressure in the lungs) leading to failure of the right side of the heart
When to Contact a Medical Professional Most often, this condition is diagnosed during routine examination of an infant. Call your infant's health care provider if the baby seems to be having difficulty breathing, or if the baby seems to have an unusual number of respiratory infections. Prevention Except for the case of heart-attack-associated VSD, this condition is always present at birth. Drinking alcohol and using the antiseizure medicines depakote and dilantin during pregnancy have been associated with increased incidence of VSDs. Other than avoiding these things during pregnancy, there is no known way to prevent a VSD
NCP for Ventricular Septal Defect Ventricular Septal Defect Definition A ventricular septal defect (VSD) is a heart malformation present at birth. Any condition that is present at birth can also be termed a "congenital" condition. A VSD, therefore, is a type of congenital heart disease (CHD). The heart with a VSD has a hole in the wall (the septum) between its two lower chambers (the ventricles). http://www.medicinenet.com Signs and Symptoms Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth. Symptoms VSD is an acyanotic congenital heart defect, aka a Left-to-right shunt, so there are no signs of cyanosis. Signs Pansystolic (Holosystolic) murmur (depending upon the size of the defect) +/- palpable thrill (palpable turbulence of blood flow). Heart sounds are normal. Larger VSDs may cause a parasternal heave, a displaced apex beat (the palpable heartbeat moves laterally over time, as the heart enlarges). An infant with a large VSD will fail to thrive and become sweaty and tachypnoiec (breathe faster) with feeds [Textbook of Paediatric Emergency Medicine. p116-117 eds Cameron P. et al Elsevier 2006]. CAUSES: The cause of VSD ( ventricular septal defect) includes the incomplete looping of the heart during
days 24-28 of development. Faults with NKX2.5 gene can cause this. en.wikipedia.org Pathophysiology During ventricular contraction, or systole, some of the blood from the left ventricle leaks into the right ventricle, passes through the lungs and reenters the left ventricle via the pulmonary veins and left atrium. This has two net effects. First, the circuitous refluxing of blood causes volume overload on the left ventricle. Second, because the left ventricle normally has a much higher systolic pressure (~120 mm Hg) than the right ventricle (~20 mm Hg), the leakage of blood into the right ventricle therefore elevates right ventricular pressure and volume, causing pulmonary hypertension with its associated symptoms. This effect is more noticeable in patients with larger defects, who may present with breathlessness, poor feeding and failure to thrive in infancy. Patients with smaller defects may be asymptomatic. Four different septal defects exist, with perimembranous most common, outlet, atrioventricular, and muscular less commonly. en.wikipedia.org Nursing Diagnosis Decrease in cardiac output associated with heart malformations Objective: improve the heart Rainfall Outcome criteria: signs of improvement in cardiac output Nursing Intervention : Observation of the quality and strength of heart rate, peripheral pulse, skin color and warmth. Set the degree of cyanosis (mucous membranes, clubbing) Monitor signs of CHF (anxiety, tachycardia, tachipnea, cramped, tired while drinking milk, periorbital edema, and hepatomegaly Oliguria. Collaboration for the administration of drugs (diuretics, to reduce afterload) as indicated.
pressure is higher than the right (pulmonary), the shunt is left to right and increased blood is circulated through the lungs. Eventually, the increased flow rates through the pulmonary circulation lead to obliteration of the lung tissue and pulmonary hypertension. When the pulmonary circulatory pressure is equal to or greater than the systemic, the shunt reverses and becomes right to left. This is called "Eisenmenger's syndrome." When this occurs, less blood flows through the pulmonary circulation and the patient may become cyanosed (skin and mucous membranes turn blue) as a result of poor blood oxygenation. Ventricular septal defects are rarely "acquired," as in myocardial infarction involving the ventricular septum.
http://www.virtualmedicalcentre.com/diseases.asp?did=46&title=ventricular-septaldefect-vsd