PT - JOURNAL ARTICLE AU - Roberta Pulcheri Ramos AU - Jaquelina Sonoe Ota Arakaki AU - Eloara Vieira Machado Ferreira AU - Adriano Acedo AU - Melline Almeida AU - Luiz Eduardo Nery AU - J. Alberto Neder TI - Portioning out the contribution of dead space ventilation and low CO<sub>2</sub> set point to ventilatory inefficiency during exercise in chronic thromboembolic pulmonary hypertension DP - 2012 Sep 01 TA - European Respiratory Journal PG - P4437 VI - 40 IP - Suppl 56 4099 - http://erj.ersjournals.com/content/40/Suppl_56/P4437.short 4100 - http://erj.ersjournals.com/content/40/Suppl_56/P4437.full SO - Eur Respir J2012 Sep 01; 40 AB - Rationale: The individual relevance of enlarged dead space ventilation as a fraction of tidal volume (VD/VT) and low CO2 set-point in promoting exercise ventilatory inefficiency in chronic thromboembolic pulmonary hypertension (CTEPH) remains controversial. Objective: To determine the contributing role of VD/VT and PaCO2 on the excessive ventilatory response to exercise in patients with CTEPH. Material and methods: 20 patients (47 ± 14 yrs, mean pulmonary artery pressure= 52 ± 10 mmHg) underwent an incremental exercise test and a steady-state test with arterial blood gases measurements. Results: Compared to normal standards, patients showed lower resting PaCO2 and peak V'O2 but greater ΔV'E/ΔV'CO2 slope (68 ± 16). Peak V'O2 and ΔV'E/ΔV'CO2 were inversely correlated (r= -0.70; p&lt;0.05). V'E/V'CO2 ratio during the constant work rate test was also abnormally high (62 ± 15). VD/VT increased from 0.31±0.08 at rest to 0.39±0.11 during exercise; on the other hand, end-tidal partial pressure (PET) for CO2 decreased despite a stable PaCO2 (p&gt;0.05). Consequently, P(a-ET)CO2 became wider (4 ± 3 mmHg to 8 ± 5 mmHg), a finding related to greater V'E/V'CO2 (r= 0.81; p&lt;0.05). On a multiple regression analysis VD/VT (partial r = 0.89) and PaCO2 (partial r = -0.37) explained up to 90% of V'E/V'CO2 variability (125.9 VD/VT - 2.3 PaCO2 + 77.1; p&lt;0.001). Conclusion: Increased VD/VT is the main pathophysiological mechanism leading to an excessive ventilatory response to exercise in patients with CTEPH. Low CO2 set-point responds for a relatively minor portion of this abnormal feature.