Ventricular septal defect history and symptoms: Difference between revisions

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{{Ventricular septal defect}}
{{Ventricular septal defect}}
{{CMG}}, Leida Perez, M.D.; '''Associate Editor-In-Chief:''' [[User:KeriShafer|Keri Shafer, M.D.]] [mailto:kshafer@bidmc.harvard.edu],Atif Mohammad, M.D., [[Priyamvada Singh]], [[MBBS]]


==History and Symptoms ==


{{CMG}}and Leida Perez, M.D.
Depends on the size of the defect and the [[pulmonary vascular resistance]] (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.<ref> Braunwald Zipes Libby.  Heart disease: A textbook of cardiovascular medicine, 6th Edition chapter 43:W.B. Saunders ;.pp 1533</ref>
 
'''Associate Editor-In-Chief:''' [[User:KeriShafer|Keri Shafer, M.D.]] [mailto:kshafer@bidmc.harvard.edu],Atif Mohammad, M.D., [[Priyamvada Singh]], [[MBBS]]
 
__NOTOC__
 
 
 
==Clinical Features <ref> Braunwald Zipes Libby.  Heart disease: A textbook of cardiovascular medicine, 6th Edition chapter 43:W.B. Saunders ;.pp 1533</ref> ==
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===
===Clinical Features of Small VSDs===
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Common in infancy, rarely seen in adults.
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.
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===
===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.
From age 1 to 12 months severe symptoms are due to [[LV failure]] secondary to a large [[left-to-right shunt]].
 
* [[Tachypnea]]
a) tachypnea
* Excess sweating
 
* Fatigue with feeding
b) excess sweating
 
c) fatigue with feeding


All these become progressively worse. They respond well to medical therapy and the development of LVH also allows the LV to handle larger flows.
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:
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
* May be due to spontaneous closure of the defect
* There may be a progressive increase in the Pulmonary vascular resistance (PVR, the most frequent cause).
* 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.


b) there may be a progressive increase in the Pulmonary vascular resistance (PVR, the most frequent cause).
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.


c) occasionally there is protective hypertrophy of the outflow tract of the RV. This increases resistance through the pulmonary  
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".
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.
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:
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".
* [[Chest pain]] resembling [[angina]]
 
* Exertional [[syncope]]
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:
* [[Hemoptysis]]
 
* [[Cerebral thrombosis]] related to the high [[hematocrit]] value
a) chest pain resembling angina
* [[Cerebral abscesses]] related to paradoxic [[emboli]]
 
* Death in the third decade, usually is sudden, particularly high mortality rate in pregnant women.
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==
==References==
{{reflist|2}}
{{reflist|2}}
 
[[Category:Cardiology]]
[[Category: Cardiology]]
[[Category:Congenital heart disease]]
[[Category:Pediatrics]]
[[Category:Disease]]
[[Category:Needs overview]]


{{WH}}
{{WH}}


{{WS}}
{{WS}}

Latest revision as of 17:17, 8 January 2013

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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

History and Symptoms

Depends on the size of the defect and the pulmonary vascular resistance (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.[1]

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.

  • Tachypnea
  • Excess sweating
  • 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:

  • May be due to spontaneous closure of the defect
  • There may be a progressive increase in the Pulmonary vascular resistance (PVR, the most frequent cause).
  • 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:

References

  1. Braunwald Zipes Libby. Heart disease: A textbook of cardiovascular medicine, 6th Edition chapter 43:W.B. Saunders ;.pp 1533

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