Abstract
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/O2Sat 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.
| Original language | English |
|---|---|
| Pages (from-to) | 178-182 |
| Number of pages | 5 |
| Journal | International Journal of Cardiology |
| Volume | 259 |
| DOIs | |
| Publication status | Published - May 15 2018 |
Fingerprint
Keywords
- Adult
- Aged
- Chronic Disease
- Exercise/physiology
- Exercise Test/methods
- Exercise Tolerance/physiology
- Female
- Humans
- Hypertension, Pulmonary/diagnosis
- Hyperventilation/diagnosis
- Male
- Middle Aged
- Pulmonary Embolism/diagnosis
Cite this
Physiological insights of exercise hyperventilation in arterial and chronic thromboembolic pulmonary hypertension. / Farina, Stefania; Bruno, Noemi; Agalbato, Cecilia; Contini, Mauro; Cassandro, Roberto; Elia, Davide; Harari, Sergio; Agostoni, Piergiuseppe.
In: International Journal of Cardiology, Vol. 259, 15.05.2018, p. 178-182.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Physiological insights of exercise hyperventilation in arterial and chronic thromboembolic pulmonary hypertension
AU - Farina, Stefania
AU - Bruno, Noemi
AU - Agalbato, Cecilia
AU - Contini, Mauro
AU - Cassandro, Roberto
AU - Elia, Davide
AU - Harari, Sergio
AU - Agostoni, Piergiuseppe
N1 - Copyright © 2017 Elsevier Ireland Ltd. All rights reserved.
PY - 2018/5/15
Y1 - 2018/5/15
N2 - 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/O2Sat 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.
AB - 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/O2Sat 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.
KW - Adult
KW - Aged
KW - Chronic Disease
KW - Exercise/physiology
KW - Exercise Test/methods
KW - Exercise Tolerance/physiology
KW - Female
KW - Humans
KW - Hypertension, Pulmonary/diagnosis
KW - Hyperventilation/diagnosis
KW - Male
KW - Middle Aged
KW - Pulmonary Embolism/diagnosis
U2 - 10.1016/j.ijcard.2017.11.023
DO - 10.1016/j.ijcard.2017.11.023
M3 - Article
C2 - 29579597
VL - 259
SP - 178
EP - 182
JO - International Journal of Cardiology
JF - International Journal of Cardiology
SN - 0167-5273
ER -