Echocardiographic image of a moderate ventricular septal defect in the mid-muscular part of the septum. The size and location is typical for a VSD in a new-born child.  The trace in the lower left shows the flow during one complete cardiac cycle and 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 the right ventricle (left on image).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 withrawn during insertion.
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Ventricular septal defect

A ventricular septal defect (or VSD) is a defect in the ventricular septum (the wall dividing the left and right ventricles of the heart). more...

VACTERL association
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The ventricular septum consists of a muscular (inferior) and membranous portion (superior). The membranous portion (which is close to the atrioventricular node) is most commonly affected.

Congential VSDs are collectively the most common congenital heart defect.


VSDs can be detected by cardiac auscultation, as they typically cause systolic murmurs. Confirmation of findings from cardiac auscultation can be obtained with a cardiac ultrasound (echocardiography) (less invasive) and cardiac catheterization (more invasive).

Auscultation is generally considered sufficient for ruling-out a significant VSD, if done by a pediatric cardiologist. This holds true as long as the pressures on the right side of the heart is low.


Large VSDs result in a significant left-to-right shunt and increase load on the right ventricle. If untreated, they result in hypertrophy of the right ventricle, which ultimately leads to right heart failure and death.


Treatment is either surgical (open or percutaneous endovascular) or conservative. Smaller congenital VSDs often close on their own (as the heart grows) and are thus treated conservatively. Open surgical procedures require a heart-lung machine and are done with a median sternotomy. 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.


VSDs are the most common congenital cardiac anomaly. It is found in 30% of all newborns with a congenital heart defect, or about 2-3 per 1000 births.

Congential VSDs are frequently associated with other congential conditions, such as Down syndrome.

A VSD can form a few days after a myocardial infarction (heart attack) due to mechanical tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead (heart) tissue.


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Continuous murmur caused by a ventricular septal defect post-myocardial infarction : visual display with a handheld computer
From CHEST, 8/1/05 by Jeff Olson

Ventricular septal defects do not typically result in a continuous murmur. The only previously reported case involved a congenital ventricular septal defect. We report a ease of an acquired ventricular septal defect following a large anterior myocardial infarction resulting in a continuous murmur. The continous nature was confirmed both with 2D echocardiography and a specially equipped stethoscope in conjuntion with a handheld computer to provide a visual display of the murmur. A proposed mechanism for the continuous murmur was discussed.

Key words: cardiology physical diagnosis; coronary artery disease; echocardiography; myocardial infarction; shock

Abbreviations: LAD = left anterior descending; VSD = ventricular septal defect


A 64-year-old man without a previously known history of coronary artery disease or cardiomyopathy was transferred from an outside facility after presenting with 36 h of continuous chest pain. His initial creatinine kinase level was 2,982 U/L with a troponin-I level of > 50 ng/mL. On hospital admission, the patient had ongoing chest pain with ST elevation in the anterior precordial leads. The patient was sent for cardiac catheterization; however, prior to this procedure, he developed third-degree heart block. The patient was resuscitated and a transvenous pacemaker was inserted. The diagnostic catheterization showed a proximal left anterior descending (LAD) artery occlusion. Percutaneous transluminal coronary angioplasty was attempted on the occluded LAD. Unfortunately, while attempting to cross the lesion there was a wire perforation of the LAD artery, and the procedure was aborted.

An intraaortic balloon pump was placed. Left ventricular pressures were 105/28 prior to insertion of this device. An echocardiogram was performed that showed a large hypokinetic segment involving the anterior, anteroseptal, and apical portions of the left ventricle with an estimated ejection fraction of 15%. There was no evidence for a pericardial effusion or tamponade. A repeat echoeardiogram was performed the following day, and the findings were unchanged. The patient remained hemodynamically stable and was started on therapy with aspirin, clopidogrel, atorvastatin, metoprolol tartrate, and ramipril. Treatment with the intraaortic balloon pump was discontinued after 3 days.

On the fifth hospital day, a harsh continuous III/VI murmur along the lower left sternal border was noted during physical examination. The murmur intensified during systole but continued throughout diastole. A waveform and spectral display of the murmur are shown in Figure 1. The murmur was recorded using a standard stethoscope equipped with an electronic recording device (Prosteth; Point of Care., Toronto, CA) and was displayed on a standard handheld computer (IPAC; Hewlett-Packard; Palo Alto, CA) possessing software designed for this purpose (Sounds Easy; Point of Care). A repeat echocardiogram then showed a small muscular ventricular septal defect (VSD) near the apex but was otherwise unchanged (Fig 2). The color Doppler image displayed left-to-right shunting both during systole and diastole. To our knowledge, this is the first continuous murmur associated with an acquired VSD. In fact, there has been only one instance of a continuous VSD murmur reported in a patient with a congenital VSD. (1,2) We postulate that the murmur was continuous as a result of elevated left ventricular diastolic pressure secondary to the acute anterior myocardial infarction. A marked pressure disparity between the left and right ventricles during diastole could explain the continued left-to-right shunting during this latter period. Continued shunting during diastole was likely facilitated by the small diameter of the defect, which prevented the rapid equilibration of pressures between the two chambers.


The specially equipped stethoscope in conjunction with a handheld computer used in this study was valuable in the assessment and teaching of cardiac sounds. In this instance, the visual displays provided confirmation of the continuous nature of this murmur; moreover, this apparatus allowed for repeated playback at both full speed and half-speed, providing a means for additional auditory review.


(1) Assey ME, Stalheim RM, Usher BW. Ventricular septal defect with aneurysm of the membranous septum presenting as a systolic and early diastolic murmur. Chest 1979; 75:504-506

(2) Tavel ME. Clinical phonocardiography and external pulse recording. 4th ed. Chicago, IL: Year Book Medical Publishers, 1985; 181 and 326

Manuscript received January 30, 2005; revision accepted March 23, 2005.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml).

Correspondence to: Jeff Olson, St Vincent's Hospital, Cardiology, 8333 Naab Rd, Indianapolis, IN 46260; e-mail: jakjiolson@

* From the Department of Cardiology (Dr. Olson), St Vincent's Hospital, Indianapolis, IN; and the Cardiology Department (Dr. Tavel), The Care Group, Indianapolis, IN.

COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group

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