Ninaber, M.K.; Hamersma,
W.B.G.J.; Schouffoer, A.A.; van ’t Wout, E.F.A.; Stolk, J.. QJM:

An International Journal of Medicine, January 2015, Vol. 108 Issue: Number
1 p33-33, 1p;

Abstract:

Background: Exercise intolerance (EI) in
systemic sclerosis (SSc) is difficult to manage by the clinician. The
peripheral chemoreflex drive compensates for metabolic acidosis during
exercise and may be related to EI. Aim: To assess the global peripheral
chemoreflex drive (GPCD) in patients with SSc at rest and during
exercise.

Methods: Consecutively tested SSc patients (n = 49) were
evaluated by pulmonary function tests, carbon dioxide (CO2)
rebreathing studies and non-invasive cardiopulmonary exercise testing
(CPET). Results of their CO2 rebreathing tests were compared
with those of controls (n = 32). Respiratory compensation for
metabolic acidosis during CPET was defined by the occurrence of a sharp
increase in minute ventilation (VdotE) and the ventilatory equivalent
for CO2 (V’E and V’CO2) at the end of the
isocapnic buffer phase. Euoxic (eVHR) and hyperoxic (hVHR) ventilatory
responses to hypercapnia were measured and its difference (eVHR − hVHR)
was considered to reflect the GPCD. Results: In 45 patients with SSc,
CPET results showed respiratory compensation at the occurrence of
metabolic acidosis. eVHR − hVHR in patients with diffuse cutaneous SSc
(dcSSc) differed significantly from that in patients with limited
cutaneous SSc (lcSSc) and from that in controls (0.47 ± 0.38 (dcSSc)
vs. 0.90 ± 0.77 (lcSSc) and 0.90 ± 0.49 (controls) l/min/mmHg; P =
0.04 and P = 0.03, respectively).

Conclusions: Respiratory
compensation for metabolic acidosis occurred in all patients. However,
the GPCD was diminished in dcSSc patients, suggesting an altered
control of breathing. Its assessment may help the clinician to better
understand reported EI and exertional dyspnea in dcSSc patients.;