In addition, adult Pulmonary hypertension clients experience an imbalance among the molecular messengers contributing to pulmonary vascular remodeling, systemic hypoxia, and pulmonary thrombosis, which leads to increased MPAP and the development of Pulmonary hypertension.
The levels of the molecular messengers prostacyclin and NO, which produce vasodilatation throughout the pulmonary circulation and prevent platelet aggregation, are reduced, while concurrently there is an overabundance of the vasoconstricting properties of the molecular messenger ET-1. As a result of the imbalance in the molecular messengers, pulmonary vascular resistance (PVR) and MPAP are increased and negatively affect cardiac output.