Effect of acute arteriolar vasodilation on capacitance and resistance in pulmonary arterial hypertension

Abstract

Background: Pulmonary vascular capacitance (PVC) is reduced in pulmonary arterial hypertension (PAH). In normal lung, PVC is largely a function of vascular compliance. In PAH, increased pulmonary vascular resistance (PVR) arises from the arterioles. PVR and PVC share pressure and volume variables. The dependency between the two qualities of the vascular bed is unclear in a state of intense vasoconstriction.

Methods: We compared PVC and PVR before and during nitric oxide (NO) inhalation during right-sided heart catheterization in eight NO-responsive patients with PAH. NO only directly affects tone in parenchymal vessels.

Results: During NO inhalation, pulmonary arterial systolic pressure decreased, 80 ± 20 SD to 48 ± 20 mm Hg, and stroke volume increased, 62 ± 19 mL to 86 ± 24 mL (P < .01). PVR dropped from 10 ± 4.4 Wood units to 4.7 ± 2.2 Wood units (P < .012), and PVC increased from 1.4 ± 1.1 mL/mm Hg to 3.2 ± 1.8 mL/mm Hg (P < .018). The magnitude of PVR drop was 57% ± 6% and the decrease in 1/PVC was 54% ± 14% (P = not significant).

Conclusions: In vasoresponsive PAH, PVC is a function of the pressure response of the vasoconstricted arterioles to stroke volume. Immediately upon vasodilation, the capacitance increases markedly. The compliance vessels are, thus, the same as the resistance vessels. The immediate reduction in pulmonary arterial pressure during NO inhalation suggests that large vessel remodeling is not a major contributor to systolic pressure in these patients.

Figure 1 –

Plot of PVC vs PVR for 157 patients with pulmonary hypertension. Data were calculated from values taken at the time of a single cardiac catheterization. The inverse relationship is similar to those reported from other centers and registries. PVC = stroke volume (SV)/(pulmonary arterial systolic pressure [Pa sys] − pulmonary arterial diastolic [Pa dias]). PVR = (mean pulmonary arterial pressure [Pa mean] − wedge pressure [P wedge])/cardiac output in milliliters per second. SV in milliliters. ○ = baseline data for the eight NO vasoresponsive patients; NO = nitric oxide; PVC = pulmonary vascular capacitance; PVR = pulmonary vascular resistance.

Figure 2 –

Plot of hemodynamic data before and during NO inhalation in eight vasoresponsive patients. PA systolic, diastolic, and pulse pressure all decreased while SV increased. The data indicate that proximal arterial stiffness was not a major feature of the high PA systolic pressure but that capacitance increased markedly as resistance decreased. PA = pulmonary arterial. See Figure 1 legend for expansion of other abbreviation.

Figure 3 –

Product of PVC × PVR (product of resistance × capacitance [RC] time) for eight patients with pulmonary hypertension with extreme vasodilator responses to inhaled NO. As in Table 3, in addition to large changes in PA pressure and PVR, the NO responders also had a decrease in heart rate and increase in SV. Paired differences analyzed using Wilcoxon signed-rank test. RC time decreased. See Figure 1 legend for expansion of abbreviations.