Impaired central hemodynamics in chronic obstructive pulmonary disease during submaximal exercise

Research output: Contribution to journalArticle

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Abstract

It is unknown whether central hemodynamics are impaired during exercise in chronic obstructive pulmonary disease (COPD) patients. We hypothesized that, at a similar absolute V· O2 during exercise, COPD patients would have a lower stroke volume and cardiac output compared with healthy controls. Furthermore, we hypothesized that greater static hyperinflation [ratio of inspiratory capacity to total lung capacity (IC/TLC)] and expiratory intrathoracic pressure would be significantly related to the lower cardiac output and stroke volume responses in COPD patients. Clinically stable COPD (n = 13; FEV1/FVC: 52 ± 13%) and controls (n = 10) performed constant workload submaximal exercise at an absolute V· O2 of ~1.3 L/min. During exercise, inspiratory capacity maneuvers were performed to determine operating lung volumes and cardiac output (via open-circuit acetylene rebreathe technique) and esophageal pressure were measured. At similar absolute V· O2 during exercise (P = 0.81), COPD had lower cardiac output than controls (COPD: 11.0 ± 1.6 vs. control: 12.2 ± 1.2 L/min, P = 0.03) due to a lower stroke volume (COPD: 107 ± 13 vs. control: 119 ± 19 mL, P = 0.04). The heart rate response during exercise was not different between groups (P = 0.66). FEV1 (%predicted) and IC/TLC were positively related to stroke volume (r = 0.68, P = 0.01 and r = 0.77, P < 0.01). Last, esophageal pressure-time integral during inspiration was positively related to cardiac output (r = 0.56, P = 0.047). These data demonstrate that COPD patients have attenuated cardiac output and stroke volume responses during exercise compared with control. Furthermore, these data suggest that the COPD patients with the most severe hyperinflation and more negative inspiratory intrathoracic pressures have the most impaired central hemodynamic responses. NEW & NOTEWORTHY Chronic obstructive pulmonary disease leads to cardiac structural changes and pulmonary derangements that impact the integrative response to exercise. However, it is unknown whether these pathophysiological alterations influence the cardiac response during exercise. Herein, we demonstrate that COPD patients exhibit impaired central hemodynamics during exercise that are worsened with greater hyperinflation.

Original languageEnglish (US)
Pages (from-to)691-697
Number of pages7
JournalJournal of applied physiology
Volume127
Issue number3
DOIs
StatePublished - Jan 1 2019

Fingerprint

Chronic Obstructive Pulmonary Disease
Hemodynamics
Exercise
Cardiac Output
Stroke Volume
Inspiratory Capacity
Total Lung Capacity
Pressure
Cardiac Volume
Acetylene
Lung
Workload
Heart Rate

Keywords

  • Cardiac output
  • Hyperinflation
  • Intrathoracic pressure
  • Stroke volume
  • Ventilatory constraints

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Impaired central hemodynamics in chronic obstructive pulmonary disease during submaximal exercise. / Smith, Joshua R.; Johnson, Bruce D.; Olson, Thomas P.

In: Journal of applied physiology, Vol. 127, No. 3, 01.01.2019, p. 691-697.

Research output: Contribution to journalArticle

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abstract = "It is unknown whether central hemodynamics are impaired during exercise in chronic obstructive pulmonary disease (COPD) patients. We hypothesized that, at a similar absolute V· O2 during exercise, COPD patients would have a lower stroke volume and cardiac output compared with healthy controls. Furthermore, we hypothesized that greater static hyperinflation [ratio of inspiratory capacity to total lung capacity (IC/TLC)] and expiratory intrathoracic pressure would be significantly related to the lower cardiac output and stroke volume responses in COPD patients. Clinically stable COPD (n = 13; FEV1/FVC: 52 ± 13{\%}) and controls (n = 10) performed constant workload submaximal exercise at an absolute V· O2 of ~1.3 L/min. During exercise, inspiratory capacity maneuvers were performed to determine operating lung volumes and cardiac output (via open-circuit acetylene rebreathe technique) and esophageal pressure were measured. At similar absolute V· O2 during exercise (P = 0.81), COPD had lower cardiac output than controls (COPD: 11.0 ± 1.6 vs. control: 12.2 ± 1.2 L/min, P = 0.03) due to a lower stroke volume (COPD: 107 ± 13 vs. control: 119 ± 19 mL, P = 0.04). The heart rate response during exercise was not different between groups (P = 0.66). FEV1 ({\%}predicted) and IC/TLC were positively related to stroke volume (r = 0.68, P = 0.01 and r = 0.77, P < 0.01). Last, esophageal pressure-time integral during inspiration was positively related to cardiac output (r = 0.56, P = 0.047). These data demonstrate that COPD patients have attenuated cardiac output and stroke volume responses during exercise compared with control. Furthermore, these data suggest that the COPD patients with the most severe hyperinflation and more negative inspiratory intrathoracic pressures have the most impaired central hemodynamic responses. NEW & NOTEWORTHY Chronic obstructive pulmonary disease leads to cardiac structural changes and pulmonary derangements that impact the integrative response to exercise. However, it is unknown whether these pathophysiological alterations influence the cardiac response during exercise. Herein, we demonstrate that COPD patients exhibit impaired central hemodynamics during exercise that are worsened with greater hyperinflation.",
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