Pulmonary hypertension is defined as mPAP ≥ 25 mmHg (1 mmHg = 0.133 kPa) measured by the RHC at sea level and resting (Table
1). Including precapillary, postcapillary and mixed pulmonary hypertension (pulmonary artery and pulmonary vein pressure can be increased) [
1]. Precapillary pulmonary hypertension includes PAH pulmonary hypertension caused by respiratory diseases and/or hypoxia; pulmonary hypertension caused by chronic pulmonary artery obstruction and pulmonary hypertension caused by unknown causes. The hemodynamics of precapillary pulmonary hypertension were defined as mPAP ≥ 25 mmHg, PAWP ≤ 15 mmHg and PVR > 3 wood units measured by RHC. Postcapillary pulmonary hypertension refers to pulmonary hypertension caused by left heart disease and pulmonary hypertension caused by unknown factors. The hemodynamics of postcapillary pulmonary hypertension is defined as the RHC measuring mPAP ≥ 25 mmHg, PAWP > 15 mmHg, in which simple postcapillary pulmonary hypertension PVR ≤ 3 wood units, mixed postcapillary pulmonary hypertension PVR > 3 wood units. Simonneau and Montani et al. [
16] proposed a new definition of pulmonary hypertension hemodynamics. It is recommended to change mPAP ≥ 25 mmHg to ≥ 20 mmHg, and other indicators remain unchanged. Among them, mPAP is defined as a mild increase in 21–24 mmHg. PVR > 3 wood units, although relatively conservative, can more accurately diagnose precapillary and postcapillary pulmonary hypertension, and can distinguish increased pulmonary artery pressure caused by pulmonary vascular disease or increased PAWP. Thenappan et al. [
17] found that compared with patients with PAH, patients with pulmonary hypertension caused by left heart disease had lower mPAP and PVR, higher CO, and enlarged left atrium. Studies on pulmonary hypertension caused by respiratory diseases showed that when the pulmonary artery pressure increased significantly, the PVR also increased significantly [
18,
19]. Even if the pulmonary artery pressure increased only slightly, the increase in PVR would be greater than 3 wood units. Similar to the results of a prospective study on chronic thromboembolic pulmonary hypertension [
20]. The increase in PVR is mainly due to alveolar hypoxia or thrombotic obstruction leading to vasoconstriction or pulmonary vascular remodeling. However, some studies have shown that PVR has no significant difference in responsiveness to hypoxia or hyperoxia in a short period of time [
21,
22], and the significant increase in PVR may be related to a decrease in CO or other diseases. In short, PVR is an important indicator for diagnosing PAH, and we need to accurately interpret the data measured by the RHC.
Table 1
PVR on hemodynamic classification of PH
PH | ≥ 25 | | |
Precapillary PH (including PAH) | ≥ 25 | ≤ 15 | > 3 |
Postcapillary PH | ≥ 25 | > 15 | |
Simple | ≥ 25 | > 15 | ≤ 3 |
Mixed | ≥ 25 | > 15 | > 3 |