Ventricular septal defect history and symptoms: Difference between revisions
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c) Occasionally there is protective hypertrophy of the outflow tract of the RV. This increases resistance through the pulmonary | 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 | circuit and decreases the shunt to that of a moderate-sized defect. Usually this obstruction becomes severe and the patient develops | ||
a [[ | a [[Tetralogy of Fallot]] type of syndrome'''. | ||
These patients must be followed from 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. | These patients must be followed from 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. | ||
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The [[Eisenmenger's syndrome]] can be defined as 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 Pulmonary vascular resistance. Features include: | The [[Eisenmenger's syndrome]] can be defined as 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 Pulmonary vascular resistance. Features include: | ||
a) | a) [[Chest pain]] resembling [[angina]] | ||
b) | b) Exertional [[syncope]] | ||
c) | c) [[Hemoptysis]] | ||
d) | d) [[Cerebral thrombosis]] related to the high [[hematocrit]] value | ||
e) | e) [[Cerebral abscesses]] related to paradoxic [[emboli]] | ||
f) | f) Death in the third decade, usually is sudden, particularly high mortality rate in pregnant women. | ||
==References== | ==References== | ||
Revision as of 17:35, 25 August 2012
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Ventricular septal defect Microchapters | |
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Differentiating Ventricular Septal Defect from other Diseases | |
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Diagnosis | |
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ACC/AHA Guidelines for Surgical and Catheter Intervention Follow-Up | |
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Case Studies | |
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Ventricular septal defect history and symptoms On the Web | |
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American Roentgen Ray Society Images of Ventricular septal defect history and symptoms | |
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Risk calculators and risk factors for Ventricular septal defect history and symptoms | |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Leida Perez, M.D.; Associate Editor-In-Chief: Keri Shafer, M.D. [2],Atif Mohammad, M.D., Priyamvada Singh, MBBS
Overview
History and Symptoms
[1] 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
With progression of time these features may worsen. They 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 followed from 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 Pulmonary 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 Eisenmenger's syndrome can be defined as 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 Pulmonary vascular resistance. 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
- ↑ Braunwald Zipes Libby. Heart disease: A textbook of cardiovascular medicine, 6th Edition chapter 43:W.B. Saunders ;.pp 1533