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

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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 languageEnglish
Pages (from-to)178-182
Number of pages5
JournalInternational Journal of Cardiology
Volume259
DOIs
Publication statusPublished - May 15 2018

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Hyperventilation
Pulmonary Hypertension
Ventilation
Exercise
Hypercapnia
Blood Gas Analysis
Tidal Volume
Exercise Test
Carbon Dioxide
Reference Values
Perfusion

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

@article{8315673e1616464ebb8337332c630faa,
title = "Physiological insights of exercise hyperventilation in arterial and chronic thromboembolic pulmonary hypertension",
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.",
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",
author = "Stefania Farina and Noemi Bruno and Cecilia Agalbato and Mauro Contini and Roberto Cassandro and Davide Elia and Sergio Harari and Piergiuseppe Agostoni",
note = "Copyright {\circledC} 2017 Elsevier Ireland Ltd. All rights reserved.",
year = "2018",
month = "5",
day = "15",
doi = "10.1016/j.ijcard.2017.11.023",
language = "English",
volume = "259",
pages = "178--182",
journal = "International Journal of Cardiology",
issn = "0167-5273",
publisher = "Elsevier Ireland Ltd",

}

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 -