The previous definition of exercise pulmonary hypertension (PH) with a mean pulmonary artery pressure (mPAP) >30 mmHg was abandoned because healthy individuals can exceed this threshold at high cardiac output (CO). We hypothesised that incorporating assessment of the pressure-flow relationship using the mPAP/CO ratio, i.e. total pulmonary resistance (TPR), might enhance the accuracy of diagnosing an abnormal exercise haemodynamic response.Exercise haemodynamics were evaluated in 169 consecutive subjects with normal resting mPAP ⩽20 mmHg. Subjects were classified into controls without heart or lung disease (n=68) versus patients with pulmonary vascular disease (PVD) (n=49) and left heart disease (LHD) (n=52).TPR and mPAP at maximal exercise produced diagnostic accuracy with area under the receiver operating curve of 0.99 and 0.95, respectively, for discriminating controls versus patients with PVD and LHD. The old criterion of mPAP >30 mmHg had sensitivity of 0.98 but specificity of 0.77. Combining maximal mPAP >30 mmHg and TPR >3 mmHg·min·L −1 retained sensitivity at 0.93 but improved specificity to 1.0. The accuracy of the combined criteria was high across different age groups, sex, body mass index and diagnosis (PVD or LHD).Combining mPAP >30 mmHg and TPR >3 mmHg·min·L −1 is superior to mPAP >30 mmHg alone for defining a pathological haemodynamic response of the pulmonary circulation during exercise. @ERSpublications Mean PAP >30 mmHg and total pulmonary resistance >3 WU may be used as new criteria for exercise PH

Simultaneous determination of the kinetics of cardiac output, systemic O 2 delivery, and lung O2 uptake at exercise onset in men. Am J Physiol Regul Integr Comp Physiol 290: R1071-R1079, 2006. First published October 20, 2005 doi:10.1152/ajpregu.00366.2005.-We tested whether the kinetics of systemic O 2 delivery (Q aO2) at exercise start was faster than that of lung O 2 uptake (V O2), being dictated by that of cardiac output (Q ), and whether changes in Q would explain the postulated rapid phase of the V O2 increase. Simultaneous determinations of beat-by-beat (BBB) Q and Q aO 2, and breath-by-breath V O2 at the onset of constant load exercises at 50 and 100 W were obtained on six men (age 24.2 Ϯ 3.2 years, maximal aerobic power 333 Ϯ 61 W). V O2 was determined using Grønlund's algorithm. Q was computed from BBB stroke volume (Q st, from arterial pulse pressure profiles) and heart rate (f H, electrocardiograpy) and calibrated against a steadystate method. This, along with the time course of hemoglobin concentration and arterial O 2 saturation (infrared oximetry) allowed computation of BBB Q aO 2. The Q , Q aO2 and V O2 kinetics were analyzed with single and double exponential models. f H, Qst, Q , and V O2 increased upon exercise onset to reach a new steady state. The kinetics of Q aO 2 had the same time constants as that of Q . The latter was twofold faster than that of V O2. The V O2 kinetics were faster than previously reported for muscle phosphocreatine decrease. Within a two-phase model, because of the Fick equation, the amplitude of phase I Q changes fully explained the phase I of V O2 increase. We suggest that in unsteady states, lung V O2 is dissociated from muscle O 2 consumption. The two components of Q and Q aO2 kinetics may reflect vagal withdrawal and sympathetic activation. cardiovascular response AT THE ONSET OF SQUARE-WAVE light aerobic exercise, O 2 consumption increases to attain a steady level, proportional to the exerted mechanical power. Its increase rises at a finite rate in response to the step increase in power, so that an O 2 deficit is incurred in the first minutes of exercise. The O 2 deficit reflects the decrease in high-energy phosphate concentration that is necessary to accelerate aerobic metabolic pathways (5,19,35,37). Analogous to the charge of a single capacitance, the increase in O 2 consumption was described by monoexponential equations (5,15,19). The monoexponential decrease in phosphocreatine concentration upon square-wave exercise onset (6, 46) is perhaps the strongest evidence provided so far in favor of this single capacitance model for O 2 consumption. Assuming close correspondence between O 2 consumption by the working muscles and O 2 uptake at the lungs (V O 2 ), the V O 2 was investigated to gain information on O 2 consumption (15, 16).This correspondence, however, was questioned. In fact, the kinetics of O 2 consumption requires that it be sustained by adequate O 2 transfer from ambient air to mitochondria. Thus, concomitant with the increase in O 2 consumption, th...

Results: From 996 (53% female) PH patients, 549 had pulmonary arterial hypertension (PAH), 36 PH due to left heart disease, 127 due to lung disease, 249 to chronic thromboembolic PH (CTEPH) and 35 to miscellaneous PH. Age and BMI significantly increased over time, whereas hemodynamic severity decreased. Overall, event-free survival was 84, 72, 64 and 58% for the years 1-4 and similar for time periods since 2000, but better during the more recent periods for PAH and CTEPH. Of all PAH cases, 89% had target medical therapy and 43% combination therapy. Of CTEPH patients, 14 and 2% underwent pulmonary endarterectomy or transplantation, respectively; 87% were treated with PAH target therapy. Conclusion: Since 2000, the incident Swiss PH patients registered were older, hemodynamically better and mostly treated with PAH target therapies. Survival has been better for PAH and CTEPH diagnosed since 2008 compared with earlier diagnosis or other classifications. © 2015 S. Karger AG, Basel Key WordsRegistry · Pulmonary hypertension · Pulmonary arterial hypertension · Chronic thromboembolic pulmonary hypertension Abstract Background: Registries are important for real-life epidemiology on different pulmonary hypertension (PH) groups. Objective: To provide long-term data of the Swiss PH registry of 1998-2012. Methods: PH patients have been classified into 5 groups and registered upon written informed consent at 5 university and 8 associated hospitals since 1998. New York Heart Association (NYHA) class, 6-min walk distance, hemodynamics and therapy were registered at baseline. Patients were regularly followed, and therapy and events (death, transplantation, endarterectomy or loss to follow-up) registered. The data were stratified according to the time of diagnosis into prevalent before 2000 and incident during 2000-

Rationale and objectivesProne positioning as a complement to oxygen therapy to treat hypoxemia in coronavirus disease (COVID-19) pneumonia in spontaneously breathing patients has been widely adopted, despite a lack of evidence for its benefit.To test the hypothesis that a simple incentive to self-prone for a maximum of 12 h per day would decrease oxygen needs in patients admitted to the ward for COVID-19 pneumonia on low-flow oxygen therapy.MethodsTwenty-seven patients with confirmed COVID-19 pneumonia admitted to Geneva University Hospitals were included in the study. Ten patients were randomised to self-prone positioning and 17 to usual care.Measurements and Main ResultsOxygen needs assessed by oxygen flow on nasal cannula at inclusion were similar between groups. Twenty-four hours after starting the intervention, the median oxygen flow was 1.0 L·min−1 (interquartile range, 0.1–2.9) in the prone position group and 2.0 L·min−1 (interquartile range, 0.5–3.0) in the control group (p=0.507). Median oxygen saturation/fraction of inspired oxygen ratio was 390 (interquartile range, 300–432) in the prone position group and 336 (interquartile range, 294–422) in the control group (p=0.633). One patient from the intervention group who did not self-prone was transferred to the high-dependency unit. Self-prone positioning was easy to implement. The intervention was well tolerated and only mild side-effects were reported.ConclusionsSelf-prone positioning in patients with COVID-19 pneumonia requiring low-flow oxygen therapy resulted in a clinically meaningful reduction of oxygen flow, but without reaching statistical significance.