How RVH eventually screws all the other chambers?

[Ven0m]

If there is RV hypertrophy, with a decreased ejection fraction and filling capacity, then will this lead to RA hypertrophy because RA still has the same amount of blood it wants to pump, but has to pump against a smaller (and thus higher internal pressure) RV chamber? And the RV hypertrophy will also cause pulmonary hypotension because its not pumping enough blood to the lungs? And systemic hypertension because not enough blood can come back through the IVC and SVC into the failing right heart? And then will the systemic hypertension lead to LV hypertrophy? And the LV hypertrophy will lead to LA hypertrophy?

I know there's a lot of regulating mechanisms that the body does to try to control this from spiraling out of control, but if we didnt have any regulating mechanisms, is this how it would go (based on physics and shiz)?

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[Ven0m]

Bump

 

[Instatewaiter]

If there is RV hypertrophy, with a decreased ejection fraction and filling capacity, then will this lead to RA hypertrophy because RA still has the same amount of blood it wants to pump, but has to pump against a smaller (and thus higher internal pressure) RV chamber? And the RV hypertrophy will also cause pulmonary hypotension because its not pumping enough blood to the lungs? And systemic hypertension because not enough blood can come back through the IVC and SVC into the failing right heart? And then will the systemic hypertension lead to LV hypertrophy? And the LV hypertrophy will lead to LA hypertrophy?

I know there's a lot of regulating mechanisms that the body does to try to control this from spiraling out of control, but if we didnt have any regulating mechanisms, is this how it would go (based on physics and shiz)?

Let us assume you have someone with RVH and reduced RV systolic function.

1) The RA does not really hypertrophy much mainly because the pressures arent ever THAT high. The highest I have ever seen is about 30mmHg. Compare this to high RV systolic pressures which can be in the 130s. What happens in this circumstance is that the venous pressure (and RA pressure) rises to overcome the diastolic pressure of the RV. This means you get venous congestion often with hepatic and renal insults due to high venous pressures.

2) Let us now assume the RV cardiac output is low enough. This will cause systemic hypotension. Your RV output is low enough that it underfills the LV. This means the LV preload is reduced and you get systemic hypotension. This then means the venous return to the RA and RV drops as well.

Hypertrophy of the ventricle also takes a long, long time.

 

[Ven0m]

Let us assume you have someone with RVH and reduced RV systolic function.

1) The RA does not really hypertrophy much mainly because the pressures arent ever THAT high. The highest I have ever seen is about 30mmHg. Compare this to high RV systolic pressures which can be in the 130s. What happens in this circumstance is that the venous pressure (and RA pressure) rises to overcome the diastolic pressure of the RV. This means you get venous congestion often with hepatic and renal insults due to high venous pressures.

2) Let us now assume the RV cardiac output is low enough. This will cause systemic hypotension. Your RV output is low enough that it underfills the LV. This means the LV preload is reduced and you get systemic hypotension. This then means the venous return to the RA and RV drops as well.

Hypertrophy of the ventricle also takes a long, long time.

Thank you so much. I understand now.