Ventricular septal defect history and symptoms
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]and Leida Perez, M.D.
Associate Editor-In-Chief: Keri Shafer, M.D. [2],Atif Mohammad, M.D., Priyamvada Singh, MBBS
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3] and Leida Perez, M.D.
Associate Editor-in-Chief: Keri Shafer, M.D. [4], Priyamvada Singh, MBBS
Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [5] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
Clinical Features
Depends on the size of the defect and the pulmonary vascular resistence (PVR). Defects in the muscular septum and subtricuspid defects frequently close or get smaller with time. Subaortic defects do not close spontaneously because the superior border is the aortic valve.
Clinical Features of Small VSDs
Generally, the course is benign throughout infancy and childhood.
Clinical Features of Medium-Sized VSDs
Common in infancy, rarely seen in adults.
More common in adulthood is a medium-sized left to right shunt of other causes, either a large VSD with protective infundibular stenosis, or a large VSD partially occluded by a septal leaflet of the tricuspid valve.
Clinical Features of Large VSDs
From age 1 to 12 months severe symptoms are due to LV failure secondary to a large left-to-right shunt.
a) tachypnea
b) excess sweating
c) fatigue with feeding
d) all these become progressively worse
e) respond well to medical therapy and the development of LVH also allows the LV to handle larger flows.
From 6 to 24 months, there are decreased symptoms due to a decrease in left-to-right shunting. Causes of the decreased shunt include:
a) may be due to spontaneous closure of the defect
b) there may be a progressive increase in the Pulmonary vascular resistance (PVR, the most frequent cause).
c) occasionally there is protective hypertrophy of the outflow tract of the RV. This increases resistance through the pulmonary circuit and decreases the shunt to that of a moderate-sized defect. Usually this obstruction becomes severe and the patient develops a tetralogy of Fallot type of syndrome.
These patients must be studied during the first year of life. It is within the first year that these patients develop pulmonary vascular obstructive disease, and unless surgical repair is undertaken they become inoperable.
Because of the rise in the Puylmonary vascular resistance, the majority of these patients become fairly asymptomatic at age 12 to 24 months, but in adolescence, the pulmonary vascular resistance becomes so high that right-to-left shunting develops and the patients develop cyanosis and the "Eisenmenger's complex".
The definition of Eisenmenger's syndrome is officially any defect which allows free communication between the pulmonary and systemic circuits with a predominant right-to-left shunt secondary to a large rise in the PVR. Features include:
a) chest pain resembling angina
b) exertional syncope
c) hemoptysis
d) cerebral thrombosis related to the high hematocrit value
e) cerebral abscesses related to paradoxic emboli
f) death in the third decade, usually is sudden, particularly high mortality rate in pregnant women.
References