In the second case, if there is no explanation for the high wedge pressure (i.e. no LV dysfunction or prosthetic dysfunction), can the high wedge pressure be explained by the severe TR alone? Because of RV dilation and compression of the LA-LV.
Good thought, but I don't believe so. Severe TR and RV dilatation indeed causes ventricular interdependence and equalization of RV-LV diastolic pressures, and secondary rise of LVEDP even if LV is normal per se. LVEDP will match RVEDP, and LA pressure will ~ match LVEDP and RVEDP, but without large V wave (like in constrictive pericarditis). Isolated RV failure or constriction causes left underfilling, hence it is hard to generate a big V wave.
Thanks for such an elaborated demonstration
The last hemodynamic, PA and RV, can be seen in patent ductus arteriosus?
In the second case, if there is no explanation for the high wedge pressure (i.e. no LV dysfunction or prosthetic dysfunction), can the high wedge pressure be explained by the severe TR alone? Because of RV dilation and compression of the LA-LV.
Good thought, but I don't believe so. Severe TR and RV dilatation indeed causes ventricular interdependence and equalization of RV-LV diastolic pressures, and secondary rise of LVEDP even if LV is normal per se. LVEDP will match RVEDP, and LA pressure will ~ match LVEDP and RVEDP, but without large V wave (like in constrictive pericarditis). Isolated RV failure or constriction causes left underfilling, hence it is hard to generate a big V wave.