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

doi:10.1016/j.ijcard.2017.11.023

Cited by 42 publications

(59 citation statements)

References 36 publications

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“…Patients with PAH were found to have higher ventilatory response to hypoxia at rest compared to HA, which is consistent with previous work demonstrating higher carotid chemoreflex sensitivity in PAH (Farina et al . ). Patients with PAH also presented diminished HRR30s, HRR60s and HRR120s, as well as longer T30 during recovery from exercise, which collectively supports an alteration in early post‐exercise vagal reactivation (Pomeranz et al .…”

Section: Discussionmentioning

confidence: 97%

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Carotid chemoreflex activity restrains post‐exercise cardiac autonomic control in healthy humans and in patients with pulmonary arterial hypertension

Paula‐Ribeiro

Ribeiro

Aranda

et al. 2019

The Journal of Physiology

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Key pointsr Dysfunction of post-exercise cardiac autonomic control is associated with increased mortality risk in healthy adults and in patients with cardiorespiratory diseases.r The afferent mechanisms that regulate the post-exercise cardiac autonomic control remain unclear.r We found that afferent signals from carotid chemoreceptors restrain the post-exercise cardiac autonomic control in healthy adults and patients with pulmonary arterial hypertension (PAH).r Patients with PAH had higher carotid chemoreflex sensitivity, and the magnitude of carotid chemoreceptor restraint of autonomic control was greater in patients with PAH as compared to healthy adults.r The results demonstrate that the carotid chemoreceptors contribute to the regulation of post-exercise cardiac autonomic control, and suggest that the carotid chemoreceptors may be a potential target to treat post-exercise cardiac autonomic dysfunction in patients with PAH.Abstract Dysfunction of post-exercise cardiac autonomic control predicts mortality, but its underlying mechanisms remain unclear. We tested whether carotid chemoreflex activity restrains post-exercise cardiac autonomic control in healthy adults (HA), and whether such restraint is greater in patients with pulmonary arterial hypertension (PAH) who may have both altered carotid chemoreflex and altered post-exercise cardiac autonomic control. Twenty non-hypoxaemic patients with PAH and 13 age-and sex-matched HA pedalled until 90% of peak work rate observed in a symptom-limited ramp-incremental exercise test. Recovery consisted of unloaded pedalling for 5 min followed by seated rest for 6 min. During recovery, subjects randomly inhaled either 100% O 2 (hyperoxia) to inhibit the carotid chemoreceptor activity, or 21% O 2 (normoxia) as control. Post-exercise cardiac autonomic control was examined via heart rate (HR) recovery (HRR; HR change after 30, 60, 120 and 300 s of recovery, using linear and non-linear regressions of HR decay) and HR variability (HRV; time and spectral domain analyses). As expected, the PAH group had higher carotid chemosensitivity and worse post-exercise HRR and HRV than HA. Hyperoxia increased HRR at 30, 60 and 120 s and absolute spectral power HRV in both groups.Additionally, hyperoxia resulted in an accelerated linear HR decay and increased time domain HRV during active recovery only in the PAH group. In conclusion, the carotid chemoreceptors restrained recovery of cardiac autonomic control from exercise in HA and in patients with PAH, with the restraint greater for some autonomic indexes in patients with PAH.

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Section: Discussionmentioning

confidence: 97%

“…; Farina et al . ), likely enhance the contribution of the carotid chemoreflex to cardiac autonomic control.…”

Section: Introductionmentioning

confidence: 99%

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Carotid chemoreflex activity restrains post‐exercise cardiac autonomic control in healthy humans and in patients with pulmonary arterial hypertension

Paula‐Ribeiro

Ribeiro

Aranda

et al. 2019

The Journal of Physiology

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“…33 Recent studies have shown that autonomic nervous system disturbances may play an important role in ventilatory inefficiency, and that there may be an additional component of increased chemoreceptor sensitivity leading to hyperventilation in PAH. 34 Farina et al 35 demonstrated that ventilatory responses to brief periods of inspiratory hypoxia and steady-state hyperoxic hypercapnia in subjects with PAH were about twofold greater than in matched controls. 29,35 According to this study, hyperventilation in PAH is explained by a combination of increased dead space ventilation and an enhanced sensitivity of chemoreceptors.…”

Section: The Pulmonary Ventilation/perfusion Relationshipmentioning

confidence: 99%

“…34 Farina et al 35 demonstrated that ventilatory responses to brief periods of inspiratory hypoxia and steady-state hyperoxic hypercapnia in subjects with PAH were about twofold greater than in matched controls. 29,35 According to this study, hyperventilation in PAH is explained by a combination of increased dead space ventilation and an enhanced sensitivity of chemoreceptors.…”

Section: The Pulmonary Ventilation/perfusion Relationshipmentioning

confidence: 99%

Exercise Pathophysiology in Pulmonary Arterial Hypertension—The Physiologic Explanation for Why Pulmonary Arterial Hypertension Does What It Does

Dumitrescu

Oudiz

2019

Advances in Pulmonary Hypertension

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Pulmonary arterial hypertension (PAH) is a chronic disease that is associated with a significant and progressive limitation of exercise tolerance. The pathophysiological mechanisms of exercise intolerance during exercise are complex, multifactorial, and in fact not limited to the pulmonary circulation and the right ventricle. Disturbance of autonomic nervous function leads to an enhanced chemosensitivity, as well as respiratory and peripheral muscle weakness, and systemic endothelial dysfunction, which together play important roles in PAH pathophysiology and symptomatology. This article is focused on the different pathophysiological mechanisms of exercise intolerance in PAH, their interactions, and their relevance for clinical practice.

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Role of cardiopulmonary exercise test in the prediction of hemodynamic impairment in patients with pulmonary arterial hypertension

et al. 2022

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Periodic repetition of right heart catheterization (RHC) in pulmonary arterial hypertension (PAH) can be challenging. We evaluated the correlation between RHC and cardiopulmonary exercise test (CPET) aiming at CPET use as a potential noninvasive tool for hemodynamic burden evaluation. One hundred and forty‐four retrospective PAH patients who had performed CPET and RHC within 2 months were enrolled. The following analyses were performed: (a) CPET parameters in hemodynamic variables tertiles; (b) position of hemodynamic parameters in the peak end‐tidal carbon dioxide pressure (PETCO2) versus ventilation/carbon dioxide output (VE/VCO2) slope scatterplot, which is a specific hallmark of exercise respiratory abnormalities in PAH; (c) association between CPET and a hemodynamic burden score developed including mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR), cardiac index, and right atrial pressure. VE/VCO2 slope and peak PETCO2 significantly varied in mPAP and PVR tertiles, while peak oxygen uptake (peak VO2) and O2 pulse varied in the tertiles of all hemodynamic parameters. PETCO2 versus VE/VCO2 slope showed a strong hyperbolic relationship (R2 = 0.7627). Patients with peak PETCO2 > median (26 mmHg) and VE/VCO2 slope < median (44) presented lower mPAP and PVR (p < 0.005) than patients with peak PETCO2 < median and VE/VCO2 slope > median. Multivariate analysis individuated peak VO2 (p = 0.0158) and peak PETCO2 (p = 0.0089) as hemodynamic score independent predictors; the formula 11.584 − 0.0925 × peak VO2 − 0.0811 × peak PETCO2 best predicts the hemodynamic score value from CPET data. A significant correlation was found between estimated and calculated scores (p < 0.0001), with a precise match for patients with mild‐to‐moderate hemodynamic burden (76% of cases). The results of the present study suggest that CPET could allow to estimate the hemodynamic burden in PAH patients.

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

Cited by 42 publications

References 36 publications

Carotid chemoreflex activity restrains post‐exercise cardiac autonomic control in healthy humans and in patients with pulmonary arterial hypertension

Carotid chemoreflex activity restrains post‐exercise cardiac autonomic control in healthy humans and in patients with pulmonary arterial hypertension

Exercise Pathophysiology in Pulmonary Arterial Hypertension—The Physiologic Explanation for Why Pulmonary Arterial Hypertension Does What It Does

Role of cardiopulmonary exercise test in the prediction of hemodynamic impairment in patients with pulmonary arterial hypertension

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