Are you talking about an acute increase in pulmonary vascular resistance or chronic thromboembolic pulmonary hypertension (WHO group 4 Pulmonary Hypertension).
In the former, it's both obstruction and reactive pulmonary vasoconstriction (hypoxia, platelet/inflammatory mediators). That leads to an increase in PVR, which requires higher pressures to move the same CO over the pulmonary vascular bed.