Background The aim of the present work was to study the influence of body position on resting and exercise pulmonary hemodynamics in patients assessed for pulmonary hypertension (PH). Methods and Results Data from 483 patients with suspected PH undergoing right heart catheterization for clinical indications (62% women, age 61±15 years, 246 precapillary PH, 48 postcapillary PH, 106 exercise PH, 83 no PH) were analyzed; 213 patients (main cohort, years 2016–2018) were examined at rest in upright (45°) and supine position, such as under upright exercise. Upright exercise hemodynamics were compared with 270 patients (historical cohort) undergoing supine exercise with the same protocol. Upright versus supine resting data revealed a lower mean pulmonary artery pressure 31±14 versus 32±13 mm Hg, pulmonary artery wedge pressure 11±4 versus 12±5 mm Hg, and cardiac index 2.9±0.7 versus 3.1±0.8 L/min per m 2 , and higher pulmonary vascular resistance 4.1±3.1 versus 3.9±2.8 Wood P <0.001. Exercise data upright versus supine revealed higher work rates (53±26 versus 33±22 watt), and adjusting for differences in work rate and baseline values, higher end‐exercise mean pulmonary artery pressure (52±19 versus 45±16 mm Hg, P =0.001), similar pulmonary artery wedge pressure and cardiac index, higher pulmonary vascular resistance (5.4±3.7 versus 4.5±3.4 Wood units, P =0.002), and higher mean pulmonary artery pressure/cardiac output (7.9±4.7 versus 7.1±4.1 Wood units, P =0.001). Conclusions Body position significantly affects resting and exercise pulmonary hemodynamics with a higher pulmonary vascular resistance of about 10% in upright versus supine position at rest and end‐exercise, and should be considered and reported when assessing PH.

BackgroundPure oxygen breathing (hyperoxia) may improve hemodynamics in patients with pulmonary hypertension (PH) and allows to calculate right-to-left shunt fraction (Qs/Qt), whereas breathing normobaric hypoxia may accelerate hypoxic pulmonary vasoconstriction (HPV). This study investigates how hyperoxia and hypoxia affect mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance (PVR) in patients with PH and whether Qs/Qt influences the changes of mPAP and PVR.Study Design and MethodsAdults with pulmonary arterial or chronic thromboembolic PH (PAH/CTEPH) underwent repetitive hemodynamic and blood gas measurements during right heart catheterization (RHC) under normoxia [fractions of inspiratory oxygen (FiO2) 0.21], hypoxia (FiO2 0.15), and hyperoxia (FiO2 1.0) for at least 10 min.ResultsWe included 149 patients (79/70 PAH/CTEPH, 59% women, mean ± SD 60 ± 17 years). Multivariable regressions (mean change, CI) showed that hypoxia did not affect mPAP and cardiac index, but increased PVR [0.4 (0.1–0.7) WU, p = 0.021] due to decreased pulmonary artery wedge pressure [−0.54 (−0.92 to −0.162), p = 0.005]. Hyperoxia significantly decreased mPAP [−4.4 (−5.5 to −3.3) mmHg, p &lt; 0.001] and PVR [−0.4 (−0.7 to −0.1) WU, p = 0.006] compared with normoxia. The Qs/Qt (14 ± 6%) was &gt;10 in 75% of subjects but changes of mPAP and PVR under hyperoxia and hypoxia were independent of Qs/Qt.ConclusionAcute exposure to hypoxia did not relevantly alter pulmonary hemodynamics indicating a blunted HPV-response in PH. In contrast, hyperoxia remarkably reduced mPAP and PVR, indicating a preserved vasodilator response to oxygen and possibly supporting the oxygen therapy in patients with PH. A high proportion of patients with PH showed increased Qs/Qt, which, however, was not associated with changes in pulmonary hemodynamics in response to changes in FiO2.

Background: High-altitude pulmonary edema is associated with elevated systolic pulmonary artery pressure (sPAP) and increased extravascular lung water (EVLW). We investigated sPAP and EVLW during repeated exposures to high altitude (HA). Methods: Healthy lowlanders underwent two identical 7-day HA-cycles, where subjects slept at 2900 m and spent 4-8 h daily at 5050 m, separated by a weeklong break at low altitude (LA). Echocardiography and EVLW by B-lines were measured at 520 m (baseline, LA 1 ), on day one, two and six at 5050 m (HA 1-3 ) and after descent (LA 2 ). Results: We included 21 subjects (median 25 years, body mass index 22 kg/m 2 , SpO 2 98%). SPAP rose from 21 mmHg at LA 1 to 38 mmHg at HA 1 , decreased to 30 mmHg at HA 3 (both p < 0.05 vs LA 1 ) and normalized at 20 mmHg at LA 2 (p = ns vs LA 1 ). B-lines increased from 0 at LA 1 to 6 at HA 2 and 7 at HA 3 (both p < 0.05 vs LA 1 ) and receded to 1 at LA 2 (p = ns vs LA 1 ). Overall, in cycle two, sPAP did not differ (mean difference (95% confidence interval) −0.2(−2.3 to 1.9) mmHg, p = 0.864) but B-lines were more prevalent (+2.3 (1.4-3.1), p < 0.001) compared to cycle 1. Right ventricular systolic function decreased significantly but minimally at 5050 m. Conclusions: Exposure to 5050 m induced a rapid increase in sPAP. B-lines rose during prolonged exposures to 5050 m, despite gradual decrease in sPAP, indicating excessive hydrostatic pressure might not be solely responsible for EVLW-development. Repeated HA-exposure had no acclimatization effect on EVLW. This may affect workers needing repetitive ascents to altitude and could indicate greater B-line development upon repeated exposure.

Background: Exact and simultaneous measurements of mean pulmonary artery pressure (mPAP) and cardiac output (CO) are crucial to calculate pulmonary vascular resistance (PVR), which is essential to define pulmonary hypertension (PH). Simultaneous measurements of mPAP and CO are not feasible using the direct Fick (DF) method, due to the necessity to sample blood from the catheter-tip. We evaluated a modified DF method, which allows simultaneous measurement of mPAP and CO without needing repetitive blood samples.Methods: Twenty-four patients with pulmonary arterial or chronic thromboembolic PH had repetitive measurements of CO at rest and end-exercise during three phases of a crossover trial. CO was assessed by the original DF method using oxygen uptake, measured by a metabolic unit, and arterial and mixed venous oxygen saturations from co-oximetry of respective blood gases served as reference. These CO measurements were then compared with a modified DF method using pulse oximetry at the catheter- and fingertip.Results: The bias among CO measurements by the two DF methods at rest was −0.26 L/min with limits of agreement of ±1.66 L/min. The percentage error was 28.6%. At the end-exercise, the bias between methods was 0.29 L/min with limits of agreement of ±1.54 L/min and percentage error of 16.1%.Conclusion: Direct Fick using a catheter- and fingertip pulse oximetry (DFp) is a practicable and reliable method for assessing CO in patients with PH. This method has the advantage of allowing simultaneous measurement of PAP and CO, and frequent repetitive measurements are needed during exercise.Clinical Trial Registration:https://clinicaltrials.gov/ct2/show/NCT02755259, identifier: NCT02755259.