A sigh of relief or a sigh of expected relief: Sigh rate in response to dyspnea relief

Dyspnoea is a debilitating symptom that affects quality of life, exercise tolerance and mortality in various disease conditions/states. In patients with chronic obstructive pulmonary disease (COPD), it has been shown to be a better predictor of mortality than forced expiratory volume in 1 s. In patients with heart disease it is a better predictor of mortality than angina. Dyspnoea is also associated with decreased functional status and worse psychological health in older individuals living at home. It also contributes to the low adherence to exercise training programmes in sedentary adults and in COPD patients. The mechanisms of dyspnoea are still unclear. Recent studies have emphasised the multidimensional nature of dyspnoea in the sensory-perceptual (intensity and quality), affective distress and impact domains. The perception of dyspnoea involves a complex chain of events that depend on varying cortical integration of several afferent/efferent signals and coloured by affective processing. This review, which stems from the European Respiratory Society research symposium held in Paris, France in November 2012, aims to provide state-of-the-art advances on the multidimensional and multidisciplinary aspects of dyspnoea, by addressing three different themes: 1) the neurophysiology of dyspnoea, 2) exercise and dyspnoea, and 3) the clinical impact and management of dyspnoea.

Posttraumatic stress disorder (PTSD) and panic disorder (PD) are two anxiety disorders with prominent psychophysiological symptoms. The PTSD criterion of persistent hyperarousal suggests autonomic dysregulation, and the disorder has been associated with elevated heart rate. In contrast, PD has been associated with respiratory abnormalities such as low end-tidal Pco(2). An integrated analysis of automatic and respiratory function in a direct comparison of these anxiety disorders is currently lacking. Electrodermal, cardiovascular, and respiratory psychophysiology was examined in 23 PTSD patients, 26 PD patients, and 32 healthy individuals at baseline and during threat of shock. At baseline, the PTSD patients, in contrast to the other two groups, were characterized by attenuated parasympathetic and elevated sympathetic control, as evidenced by low respiratory sinus arrhythmia (a measure of cardiac vagal control) and high electrodermal activity. They also displayed elevated heart rate and cardiovascular sympathetic activation in comparison with healthy controls. PD patients exhibited lower Pco(2) (hypocapnia) and higher cardiovascular sympathetic activation compared with healthy controls. PTSD patients, but not PD patients, sighed more frequently than controls. During the threat of shock phase, the PTSD group demonstrated blunted electrodermal responses. Persistent hyperarousal symptoms in PTSD seem to be due to high sympathetic activity coupled with low parasympathetic cardiac control. Respiratory abnormalities were also present in PTSD. Several psychophysiological measures exhibited group-comparison effect sizes in the order of 1.0, supporting their potential for enhancing differential diagnosis and possibly suggesting utility as endophenotypes in genetic studies of anxiety disorders.