Can Non-invasive Ventilation Modulate Cerebral, Respiratory, and Peripheral Muscle Oxygenation During High-Intensity Exercise in Patients With COPD-HF?

Abstract

Aim: To evaluate the effect of non-invasive positive pressure ventilation (NIPPV) on (1) metabolic, ventilatory, and hemodynamic responses; and (2) cerebral (Cox), respiratory, and peripheral oxygenation when compared with SHAM ventilation during the high-intensity exercise in patients with coexisting chronic obstructive pulmonary disease (COPD) and heart failure (HF).

Methods and results: On separate days, patients performed incremental cardiopulmonary exercise testing and two constant-work rate tests receiving NIPPV or controlled ventilation (SHAM) (the bilevel mode-Astral 150) in random order until the limit of tolerance (Tlim). During exercise, oxyhemoglobin (OxyHb+Mb) and deoxyhemoglobin (DeoxyHb+Mb) were assessed using near-infrared spectroscopy (Oxymon, Artinis Medical Systems, Einsteinweg, The Netherlands). NIPPV associated with high-intensity exercise caused a significant increase in exercise tolerance, peak oxygen consumption ( $\stackrel{·}{V}{\text{O}}_2$ in mlO₂·kg^-1·min^-1), minute ventilation peak ( ${\stackrel{·}{V}}_{\text{E}}$ in ml/min), peak peripheral oxygen saturation (SpO₂, %), and lactate/tlim (mmol/s) when compared with SHAM ventilation. In cerebral, respiratory, and peripheral muscles, NIPPV resulted in a lower drop in OxyHb+Mb (p < 0.05) and an improved deoxygenation response DeoxyHb+Mb (p < 0.05) from the half of the test (60% of Tlim) when compared with SHAM ventilation.

Conclusion: Non-invasive positive pressure ventilation during constant work-rate exercise led to providing the respiratory muscle unloading with greater oxygen supply to the peripheral muscles, reducing muscle fatigue, and sustaining longer exercise time in patients with COPD-HF.

Keywords: COPD; blood flow muscle; cardiovascular physiology; heart failure; oxygen consumption.

Figure 1

Protocol of our ventilation study adapted with the gas analysis measured breath-by-breath in which the trachea was connected with the pneumotach.

Figure 2

Flow diagram representing the sample recruitment and loss.

Figure 3

Comparison between HR and cardiac output during ventilation and NIPPV. Heart rate (HR); non-invasive positive pressure ventilation (NIPPV); (A) HR peak. (B) cardiac output. Student's t-test.

Figure 4

Comparative analysis of the effects of NIPPV (closed symbols) and SHAM ventilation (open symbols) on Cox, respiratory, and peripheral muscle oxygenation. During high-intensity exercise (N = 14). (A) (OxyHb+Mb) cerebral p interaction: 0.87; (B) (OxyHb+Mb) peripheral muscle (vastus lateralis muscle) p interaction: 0.10; (C) (OxyHb+Mb) respiratory muscle (intercostal muscle) p interaction: 0.79; (D) (DeoxyHb+Mb) cerebral p interaction: 0.03; (E) (DeoxyHb+Mb) peripheral muscle (right vastus lateralis muscle) p interaction: 0.79; (F) (DeoxyHb+Mb) respiratory muscle (intercostal muscle) p interaction < 0.01. *p < 0.05 100% NIPPV vs. 20–40% NIPPV; ^α100% SHAM vs. 60–80% NIPPV; ^#100% NIPPV vs. 100% SHAM. Two-way variance analysis with Bonferroni post-hoc.

Figure 5

A comparative analysis in Cox, peripheral, and respiratory muscle during rest and limit of tolerance (Tlim) (SHAM 98 s and NIPPV 129 s). *p < 0.05, ANOVA two-way. (A) (OxyHb+Mb) cerebral; (B) (OxyHb+Mb) peripheral muscle (vastus lateralis muscle); (C) (OxyHb+Mb) respiratory muscle (intercostal muscle); (D) (DeoxyHb+Mb) cerebral p interaction: 0.03; (E) (DeoxyHb+Mb) respiratory muscle (intercostal muscle); (F) (DeoxyHb+Mb) peripheral muscle (right vastus lateralis muscle).