Cardiovascular diseases, especially left-ventricular diastolic dysfunction, are among the most frequent reasons for morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD).
Dynamic hyperinflation is one of the expected pathophysiological mechanisms in the multifactorial genesis of this left-ventricular diastolic dysfunction in patients with COPD.
The novel concept of Expiratory Stenosis Breathing (ESB) is based on the method of Metronome-Paced Tachypnea (MPT) of Cooper et al. Therefore the investigators use a metronome to indicate a specific breathing frequency (BF) and the relation of inspiration : expiration (I : E) in order to let subjects hyperinflate.
Subjects get split into two groups each hyperinflating three times for 90sec by one of the two methods before doing a cross-over and switch groups to do the same in the other group. At the end of the 90sec there is a measurement of the Inspiratory Capacity (IC) and an echocardiography in order to objectify dynamic hyperinflation respectively the change in diastolic function.
During ESB participants hyperinflate with a BF - 30/min and a I : E - 1 : 3. In addition they have to breathe through an expiratory-effective stenosis (3, 2 and 1,5mm) on the mouthpiece of the pneumotachograph to simulate the collapsing airways in COPD-patients. In contrast, during MPT subjects hyperinflate with a BF - 40/min, I : E - 1 : 1; BF - 40/min, I : E - 1 : 2; BF - 30/min, I : E - 1 : 2.
During the whole trial investigators measure Intrinsic Positive Endexpiratory Pressure (PEEPi) in order to objectify the dynamic hyperinflation more significantly.
The primary goal of this study is to assess if actively induced dynamic hyperinflation can affect diastolic function of the left ventricle.
Furthermore a correlation between the extent of dynamic hyperinflation and diastolic dysfunction should be quantified.
In addition measurement of PEEPi should validate the method of Metronome-paced Tachypnea (MPT) because the investigators hypothesize that this method does not simulate the pathophysiological circumstances in patients with COPD sufficiently.
