Pulmonary circulation is a low pressure , low impedance but a high capacitance system . The job of pulmonary circulation is not only to ferry the blood from right ventricle to left atrium , it should also ensure smooth gas exchange as it traverses the circuit . (How vital it’s job is . . . but we tend to be obsessed with heart !)
The paradox is , for the flow of blood to occur you need a pressure head . (Note : the pressure head is 120mmhg in systemic circulation.) The pulmonary pressure head is only about 5-10mmhg it has to push the entire blood .(Pulmonary pressure head = Mean pulmonary artery pressure -mean LA pressure )
In healthy persons
- Pulmonary artery pressure (PAP) is not supposed to increase beyond few mmhg.
- The diastolic pulmonary artery pressure can not afford to increase even those few mm.
If it does , it can cause serious hemodynamic and oxygenation issues. Both these statements are based on strong scientific beliefs But now we realise the margin of these elevation has been revised a little higher in normal persons .
- In health , athletes can reach a systolic PAP up to 40mmhg .
- Diastolic PAP still largely remain a mystery . You can’t measure it when the patient is running you know !
Here is a recent article from chest (2011) which documents pulmonary artery systolic pressure in trained athletes .
Relationship between exertional dyspnea and PA pressure.
The mechanism of exertional dyspnea in any individual is largely attributable to exercise induced pulmonary vascular stretch .(J receptors etc ) . Many still believe human functional capacity is limited primarily by the lung function and the cross sectional areas of pulmonary microvascular bed .( Is this the reason two patients with 25% EF has vastly different functional capacity ?)
* Note : Exercise induced pulmonary artery pressure elevation are well-recognized in pathological states.
- Mitral valve disease
- In established COPD
- In patients with LV dysfunction