The primary determinant of pulmonary artery systolic pressure is . . . ?
- Pulmonary arterial tone
- Pulmonary venous pressure
- RV contractility
- Pulmonary blood flow
Answer : All of the above
But what is the relative contribution of each ?
I am 100 % sure , no one can answer this question correctly !
It is true , in some pathological situations one can be fairly certain about cause of elevated pulmonary arterial pressure .
When we confront a patient with left heart disease it is the transmission of mean venous pressure .
Whatever be our understanding ( Pre/Post capillary pulmonary hyper tension and the related stuff ! ), the one parameter that makes mystery contribution to PA pressure is RV contractility !
In physiology RV generates about 30mmhg systolic pressure that becomes the pulmonary systolic pressure .The diastolic pressure will be around 15 and mean around 20 . During exercise contractility of both RV and LV increase .There has been documented PASP up to 50 mmhg in normal healthy adults during exertion .
Here one can assume RV contractility is causing a entity called transient Isolated systolic pulmonary arterial hypertension.(ISPAH)
Consider a entirely different situation
A patient with COPD with raised PASP . The right ventricle pressure has to equilibrate with PASP during systole .For this to happen it has to generate the 60mmhg . If the RV fails to augment it’s contractility for some reason , will the ineffective RV contraction will lower the PASP ? This is the perplexing question !
While the popular understanding is , RV dysfunction will under- estimate the severity of pulmonary hypertension . . . still . . . we are not sure whether RV dysfunction will reduce the PASP per-se ( and subsequently PA diastolic pressure as well )
We often see a good example . A patient who develops tricuspid valve disease and RV dysfunction get symptomatic relief from lung congestion .
The relationship between RV function and pulmonary artery pressure is a real enigma. Though hyper functioning RV is expected to elevate PASP and hypo functioning RV would pull it down , the relationship is not that simple. If only we decode this mysteries we can try specific RV negative inotropic agents as a modality to treat pulmonary hypertension .
Total artificial hearts are going to come in a big way in the coming decades .It will specifically address this issue , as RV and LV contractility need to be individually tuned to avoid pulmonary congestion.
While RV function is critical for human survival , Fontan principle simply says entire RV is dispensable . How ?