Physiological insights of exercise hyperventilation in arterial and chronic thromboembolic pulmonary hypertension.

BACKGROUND: Pulmonary hypertension (PH) patients show, during exercise, an excessive increase in ventilation (VE ) compared to carbon dioxide output (VCO2 ), determining a high VE /VCO2 slope. There are several possible causes, including an elevated dead space ventilation (VD ), VE /perfusion (Q) mismatch and/or an enhanced peripheral or central chemoreceptor activity. We evaluated the causes of exercise hyperventilation in PH patients.

METHODS: Eighteen group I and IV PH patients underwent cardiopulmonary exercise test with blood gas analysis at every minute. VE , alveolar ventilation (VA ) and VD vs. VCO2 relationship were calculated. Resting chemoreceptor sensitivity was analyzed through hypoxia/hypercapnia tests.

RESULTS: PeakVO2 and VE /VCO2 slopes were 1.06±0.24l/min and 39.1±9.0, respectively. Throughout the exercise, 30% of VE was due to VD . VE /VCO2 slope significantly correlated with VD /VCO2 slope (r=0.82, p<0.001) but not with VA /VCO2 slope (r=0.3, p=ns). Peak exercise end-tidal CO2 (PetCO2 ) correlated with VD /VCO2 slope (r=-0.79, p<0.001) and VE /VCO2 slope (r=-0.91, p<0.001). Dead space(DS)/Tidal volume and P(arterial-et)CO2 were elevated without arterial hypoxemia suggesting a high VE /Q mismatch. Chemoreceptor peripheral response to hypoxia and central CO2 response were both enhanced being peripheral responses to hypoxia and hypercapnia 0.416±0.402 (normal ref values=0.285±0.221) l/min/O2 Sat and 0.076±0.047 (0.066±0.430) l/min/mmHg, respectively; central hypercapnic chemosensitivity was 4.475±3.99 (2.352±0.936) l/min/mmHg.

CONCLUSIONS: Increased DS, VE /Q mismatch and chemorecptor response are among the main mechanisms involved in exercise hyperventilation in PH. ClinicalTrial.govNCT02892981.