Respiratory muscle function in interstitial lung disease

Walterspacher, Stephan; Schlager, Daniel; Walker, David; Müller–Quernheim, Joachim; Windisch, Wolfram; Kabitz, Hans‐Joachim

doi:10.1183/09031936.00109512

Cited by 43 publications

(43 citation statements)

References 39 publications

(64 reference statements)

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“…Thus, in these SSc patients, the respiratory compliance and airflow resistance did not affect occlusion pressures or the responsiveness to hypercapnia and is therefore considered to be normal. Furthermore, our data of mouth occlusion pressures during resting minute ventilation and during CO 2 rebreathing in patients with normal V’E/P0.1 are consistent with those of others [3,7,10,21]. However, in the present study no significant difference was seen in ∆V’E/∆PetCO 2 between the groups as classified by V’E/P0.1 (Table 2).…”

Section: Discussionsupporting

confidence: 93%

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Increased respiratory drive relates to severity of dyspnea in systemic sclerosis

et al. 2014

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BackgroundDyspnea may be a presenting symptom in progressive systemic sclerosis (SSc). Respiratory drive (mouth occlusion pressure, MOP, at rest and during CO2 rebreathing, 7% CO2, 93% O2) is a major determinant of dyspnea and may relate to the magnitude of dyspnea.MethodsIn a prospective design, MOP at 0.1 sec (P0.1) was measured in 73 SSc patients while breathing room air and during CO2 rebreathing. An abnormal V’E/P0.1 is defined as < 8 L/min/cm H2O. Dyspnea scores were assessed by a shortness of breath questionnaire (UCSD dyspnea scale).ResultsMean P0.1 in patients with normal V’E/P0.1 (n = 45) was 1.1 ± 0.04 and 1.6 ± 0.08 cm H2O in patients with abnormal V’E/P0.1 (n = 28), p <0.001. ∆P0.1/∆PetCO2 differed significantly between these groups (0.45 versus 0.75 cm H2O/mmHg, P < 0.001), but no significant difference was present in ∆V’E/∆PetCO2. V’E/P0.1 showed the highest significant correlation with the UCSD dyspnea score (r = -0.76, p <0.001). UCSD cut-off value for abnormal V’E/P0.1 was 8.5 (sensitivity 93%, specificity 96%, area under the curve 0.98).ConclusionsIn SSc patients an abnormal V’E/P0.1 better relates to the severity of dyspnea than traditional lung function parameters and can easily be assessed at first outpatient consultation.

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Section: Discussionsupporting

confidence: 93%

“…Although our reported values of the respiratory drive, as measured by P0.1, were approximately similar, differences from those previously reported by Walterspacher et al are present [21]. Potential reasons may include the differences in degree of restrictive lung function as measured by FVC% predicted.…”

Section: Discussionsupporting

confidence: 46%

Increased respiratory drive relates to severity of dyspnea in systemic sclerosis

et al. 2014

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“…So kann die Grunderkrankung des Patienten bereits eine atemmuskuläre Dysfunktion bedingen wie für pneumologische (z. B. COPD oder interstitielle Lungenerkrankungen [21,22]), kardio-zirkulatorische (z. B. pulmonale Hypertonie [23,24]), aber auch metabolische Krankheitsbilder (z.…”

Section: Kausalkette Der Vidd Beim Menschenunclassified

Ventilator induzierter Zwerchfellschaden: ein Update

2013

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There is rising evidence that ventilator-induced diaphragmatic dysfunction (VIDD) is not just an artifactual finding from animal studies, but actually occurs in humans undergoing invasive mechanical ventilation. Initial research findings in humans have demonstrated that periods of controlled invasive mechanical ventilation lasting just 18 - 69 hours can lead to a marked reduction in diaphragmatic myofibers. More recently, it has been shown that even short periods (e. g. two-hours) of controlled invasive mechanical ventilation are sufficient to initiate VIDD. The evidence available at present suggests that VIDD is most likely based on increased proteolysis of the respiratory muscles. Moreover, VIDD seems not to be part of a general muscle wasting process, as suggested by the fact that e. g. the human latissimus dorsi and the pectoralis major muscles seem not to be subjected to early muscle fiber atrophy when directly compared to the human diaphragm. Novel in vivo data have also revealed that VIDD in humans is associated with a reduction in diaphragmatic force generation after only one day of controlled invasive mechanical ventilation. This impairment was observed to progress further over the one-week investigation period. The introduction of a simple bedside ultrasound measurement of diaphragmatic function is of great importance to the clinician, as it may serve as a surrogate measure for VIDD, with high predictive value. Regarding potential therapeutic interventions against VIDD, the primary aim should be to encourage sufficient diaphragmatic use in susceptible patients so as to avoid VIDD; this approach remains in fundamental contrast to that of reducing respiratory muscle load by (invasive) mechanical ventilation.

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“…Patients with chronic heart failure [74], asthma [81,82] and pulmonary arterial hypertension [76] also suffer from significant exertional dyspnoea. The majority of these patients complain of exertional dyspnoea similar to that of COPD patients, which results from the inability of tidal volume to expand appropriately as ventilation increases because it is constrained: 1) from below by the effects of dynamic lung hyperinflation in COPD [83], and in selected patients with asthma [81,82], chronic heart failure [74], ILD [75,80,84,85] and pulmonary arterial hypertension [76], or by the already critically reduced resting inspiratory capacity in COPD [86]; or 2) from above (reflecting the reduced total lung capacity and inspiratory reserve volume, as may occur in some patients with chronic heart failure, ILD and pulmonary arterial hypertension).…”

Section: Exercise and Dyspnoeamentioning

confidence: 99%