left sided hypertrophy from left to right VSD shunt?

[automaton]

how do you get left sided hypertrophy if the blood is flowing out to the right side? seems very counterintuitive to me. can anyone explain this?

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[omarsaleh66]

Im not sure but I think that u get left to right shunt and after a while the pulmonary artery cant handle the increased load from the right heart so the shunt reverses and u get left sided hypertrophy and a late onset of cyanosis. Did that help? No? ok my bad...

 

[north2southOMFS]

RVH actually overtakes the LV ability to push blood from left to right, so the shunt reverses and you get right to left shunting. (its a bad thing)

Called Eisenmengers syndrome.

 

[Idiopathic]

how do you get left sided hypertrophy if the blood is flowing out to the right side? seems very counterintuitive to me. can anyone explain this?

The LVH comes after the RVH, which is a direct result of the shunt. Most commonly, this happens in late childhood in a tetralogy of fallot patient, but can also happen in isolated VSD cases. So..

1. Shunted blood travels from L-->R
2. Increased preload on the R causes RVH
3. Increased force of ejection from the R, d/t hypertrophy, causes the shunt to reverse
4. Reversal of shunt causes increased preload on the LV and resultant LVH

Eisenmenger's is the correct term for this process.

 

[HiddenTruth]

The LVH comes after the RVH, which is a direct result of the shunt. Most commonly, this happens in late childhood in a tetralogy of fallot patient, but can also happen in isolated VSD cases. So..

1. Shunted blood travels from L-->R
2. Increased preload on the R causes RVH
3. Increased force of ejection from the R, d/t hypertrophy, causes the shunt to reverse
4. Reversal of shunt causes increased preload on the LV and resultant LVH

Eisenmenger's is the correct term for this process.

Actually this whole phenomena of Eisenmenger's suyndrome (when the shunt is reversed: R--> L) occurs in all late cyanosis congenital heart defects, i.e. VSD, ASD, PDA.

Additionally, just to add to what everyone else has said, the RVH occurs secondary to the increaed preload from the left side and is FURTHER exacerbated due to the subsequent PH that develops.

The reversing of the shunt is directly related to rt sided pressures and reistance eventually reaching that of systemic pressures and resistance over time because of the increased preload and PH that develops.

Also, I don't think the LVH occurs AFTER the reversal of the shunt. It may be a much stronger/exacerbated phenomena after the reversal; however, I think the stimulus for LVH and dilation is present throghout the course of the L-->R shunt, because of increased volume overload to the L. heart, secondary to RVH and an increased EF.

 

[lewtin]

agree with Hiddentruth

Actually this whole phenomena of Eisenmenger's suyndrome (when the shunt is reversed: R--> L) occurs in all late cyanosis congenital heart defects, i.e. VSD, ASD, PDA.

Additionally, just to add to what everyone else has said, the RVH occurs secondary to the increaed preload from the left side and is FURTHER exacerbated due to the subsequent PH that develops.

The reversing of the shunt is directly related to rt sided pressures and reistance eventually reaching that of systemic pressures and resistance over time because of the increased preload and PH that develops.

Also, I don't think the LVH occurs AFTER the reversal of the shunt. It may be a much stronger/exacerbated phenomena after the reversal; however, I think the stimulus for LVH and dilation is present throghout the course of the L-->R shunt, because of increased volume overload to the L. heart, secondary to RVH and an increased EF.

 

[razorback831]

agree with Hiddentruth

Tetralogy is cyanotic at birth in most cases...preceding the chance to have Eisenmenger's syndrome....correct?

 

[Ramoray]

The reversal of the shunt actually has minimal to due with LVH seen in L->r shunt. The reversal comes much later. the LVH is a direct result of the left ventr. working almost twice as hard. For one think of half or a good portion of each pump the blood is escaping to the RV instead of the system therefore system requirements are not being met and therefore the LV must pump 2 or 3 times harder and more frequent to compensate for the loss to the right ventricle since each pump is producing less to the system therefore it hypertrophies. Later when pulmonary resistance builds and pressure in the right side increases higher than the left the shunt reverses. At this point the RV has hypertrophied as well since it has been pumping more blood than its used to recieving due to the shunt as well as pumping against a continuing increased pul resis. Therefore you have RVH and LVH. The LVH at this point will continue due to the reversed shunt putting more blood into the LV and the LV having to work harder to pump it out. Therefore the LV kind of traded one problem for another-both of which made it work harder and hypertrophy

 

[HiddenTruth]

Tetralogy is cyanotic at birth in most cases...preceding the chance to have Eisenmenger's syndrome....correct?

Well, first off, the damage in tet and the extent of the disease all depends on the severity of the pulmonary steonosis. If it's severe, then it acts like a pure R-->L shunt through the VSD secondary to tremendously ncreased pressures in RV. So, in that scenario there is no such thing as Eisenmenger's syndrome. And, classically tet is described as R-->L shunt with early cyanosis at birth usually. But on the same note, you can have a milder form of tet with mild pulm stenosis, and that acts like an isolated VSD with a L-->R shunt initially, (hence the term, "pink tetralogy") and over time, with the severity of the pulm stenosis and PH and increased RVH, you get the reversal and classic Eisenmenger's, I imagine.

Keep in mind, I think Eisenmenger is a term given to a reversal of the shunt that is INITIALLY L-->R. If tet is cyanotic at birth, it is a R-->L shunt.

 

[HiddenTruth]

automaton: dude, u and everyone else who has read this thread, should know everything to know about the consequences and implications of some of the congenital heart disease--lol--sheesh, i don't think there is anything missing onthe topic of EISENMENGER'S syndrome

 

[bchengreat]

12 yrs late to the thread, but Hiddentruth is right! just confirmed this with a pediatric cardiologist =)

 

[Instatewaiter]

Pathophysiology of a VSD:
Blood flows from LV to RV. This leads to pulmonary overcirculation and Pulmonary hypertension. In addition it causes a larger volume of blood being dumped into the LA/LV which causes volume overload and therefore LA and LV dilation. RV dilation and RVH is a later finding.

Isolated VSDs (ie not associated with TOF) cause predominantly left sided findings even though they shunt blood to the R.