ability to explain exercise intolerance [18]. Specifically, it has been recognised that constraints to VT expansion [19], as determined by a critical IRV, are paramount to exertional dyspnoea in obstructive and restrictive lung diseases [20] this is considered further in chapters about COPD [21] and ILD [22] later in this Monograph. In this context, the strengths and limitations of performing IC manoeuvres to uncover these constraints are now better recognised compared with 10 years ago. A great deal of work has helped better standardise this approach as well as the strategies used to interpret the derived variables (as reviewed in [23]). Exercise IC manoeuvres also allow tidal flow–volume loops to be correctly placed relative the maximum pre-exercise loop, thereby allowing better recognition of expiratory flow limitation [24]. Owing to these advances, most of the commercially available CPET systems now offer IC recording with tidal-to-maximal flow–volume loop displays. Another pathophysiological feature that is important to the genesis of dyspnoea is excess exercise ventilation (“ventilatory inefficiency”) as reflected by increased V′E as a function of metabolic demand (i.e. V′CO 2 ) (a chapter by WARD [25] in this Monograph discusses the determinants of physiological responses to muscular exercise in healthy subjects). The potential for high indices of ventilatory inefficiency (V′E–V′CO 2 or the minimum ventilatory equivalent (V′E/V′CO 2 min)) to trigger uncomfortable respiratory sensations in cardio-respiratory disease has long been recognised [26, 27]. More recently, several studies have demonstrated that a high ventilatory inefficiency is an early sign of impaired gas exchange efficiency (increased “wasted” ventilation) and/or excessive afferent stimuli to ventilation (as recently reviewed in [28]) as it is related to a high respiratory neural drive and dyspnoea in symptomatic smokers [29, 30] and patients with mild COPD [31, 32], heart failure [8], heart failure–COPD [33, 34], ILD [35] and pulmonary hypertension (PH) [36, 37]. Thus, the use of different indices of the V′E–V′CO 2 relationship has proved useful in the interpretation of CPET responses in patients with unexplained or disproportionate exertional dyspnoea [38]. Investigating potential pulmonary vascular disease In the past decade, pulmonary vascular disease, particularly PH, has been more frequently recognised as a cause of exertional dyspnoea [36, 37]. Several studies found that a cluster of 400 450 500 Clinical Exercise Testing ERS Monographs 350 300 250 150 200 100 50 0 Year Figure 1. Number of publications on CPET indexed in the Web of Science (https://apps.webofknowledge. com) since 1978. Note that 70% were published in the past 10 years. The content of the current ERS Monograph (published in 2018) is based on literature published up to the end of 2017. xii https://doi.org/10.1183/2312508X.10015318 Publications n 1978 1979 1980 1981 1982 1983 1984 1985 1986 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 2015 2016 2017
Previous Page Next Page