COVID-19: persistence of symptoms and lung alterations after 3-6 months from hospital discharge.

PURPOSE: Few data are currently available on persistent symptoms and late organ damage in patients who have suffered from COVID-19. This prospective study aimed to evaluate the results of a follow-up program for patients discharged from a nonintensive COVID-19 ward. METHODS: 3-6 months after hospital discharge, 59 of 105 COVID-19 patients (31 males, aged 68.2 ± 12.8 years) were recruited in the study. Forty-six patients were excluded because of nontraceability, refusal, or inability to provide informed consent. The follow-up consisted of anamnesis (including a structured questionnaire), physical examination, blood tests, ECG, lower limb compression venous ultrasound (US), thoracic US, and spirometry with diffusion lung capacity for carbon monoxide (DLCO). RESULTS: 22% of patients reported no residual symptoms, 28.8% 1 or 2 symptoms and 49.2% 3 or more symptoms. The most frequently symptoms were fatigue, exertional dyspnea, insomnia, and anxiety. Among the inflammatory and coagulation parameters, only the median value of fibrinogen was slightly above normal. A deep vein thrombosis was detected in 1 patient (1.7%). Thoracic US detected mild pulmonary changes in 15 patients (25.4%), 10 of which reported exertional dyspnea. DLCO was mildly or moderately reduced in 19 patients (37.2%), 13 of which complained of exertional dyspnea. CONCLUSION: These results highlight that a substantial percentage of COVID-19 patients (77.8%) continue to complain of symptoms 3-6 months after hospital discharge. Exertional dyspnea was significantly associated with the persistence of lung US abnormalities and diffusing capacity alterations. Extended follow-up is required to assess the long-term evolution of postacute sequelae of COVID-19.

Thoraco-abdominal motion/displacement does not affect dyspnea following exercise training in COPD patients.

PURPOSE: The interrelations among chest wall kinematics (displacement and configuration), ventilatory profile and dyspnea relief following cycle exercise training (EXT) have not been systematically evaluated in hyperinflated chronic obstructive pulmonary disease (COPD) patients. We hypothesize that a decrease in ventilation affects dyspnea relief, regardless of the changes in chest wall kinematics. METHODS: Fourteen patients were studied before and after 24-session exercise training program. We evaluated the volumes of chest wall and its compartments (rib cage, and abdomen) using optoelectronic plethysmography. RESULTS: At iso-time EXT (i) reduced ventilation, respiratory frequency and dyspnea (by Borg scale), mildly improved rib cage configuration, but left operational volumes unchanged; (ii) Borg was much smaller for any comparable inspiratory reserve volume (IRVcw), and a decrease in IRVcw was tolerated much better for any given Borg. CONCLUSIONS: Regardless of the changes in chest wall kinematics, a decrease in ventilation attenuates dyspnea following EXT.

Obstructive sleep apnea (OSA) does not affect ventilatory and perceptual responses to exercise in morbidly obese subjects.

We have tested the hypothesis that high mass loading effects and obstructive sleep apnea (OSA) constrain the ventilatory response to exercise in morbidly obese subjects as compared to their counterparts without OSA. Fifteen obese patients with (8) and without OSA and 12 lean healthy subjects performed incremental cycle exercise. The functional evaluation included ventilation, oxygen uptake, carbon dioxide production, end-expiratory-lung-volumes (EELV), inspiratory capacity, heart rate, dyspnea and leg effort (by a modified Borg scale). Changes in ventilation and dyspnea per unit changes in work rate and metabolic variables were similar in the three groups. Breathing pattern and heart rate increased from rest to peak exercise similarly in the three groups. Leg effort was the prevailing symptom for stopping exercise in most subjects. In conclusion, OSA does not limit exercise capacity in morbidly obese subjects. Ventilation contributes to exertional dyspnea similarly as in lean subjects and in obese patients regardless of OSA.

Do obstructive and restrictive lung diseases share common underlying mechanisms of breathlessness?

This review tries to answer two main questions: (i) What are the neurophysiological underpinnings of the most commonly selected cluster descriptors which define the qualitative dimension of dyspnea in patients? (ii) How do mechanical constraints affect dyspnea? (iii) Do obstructive and restrictive lung diseases share some common underlying mechanisms? Qualitative dimensions of dyspnea, which allude to increased respiratory work/effort breathing, reflect a harmonious coupling between increased respiratory motor output and lung volume displacement in healthy subjects. Descriptors that allude to unsatisfied inspiration are the dominant qualitative descriptors in patients with a variety of respiratory diseases. It is possible that sensory feedback from a multitude of mechanoreceptors throughout the respiratory system (in the muscle, chest wall, airways and lung parenchyma) collectively convey information to the consciousness that volume/flow or chest wall displacement is inadequate for the prevailing respiratory drive. The data would lend support to the idea that: (i) an altered afferent proprioceptive peripheral feedback signals that ventilatory response is inadequate to the prevailing motor drive, reflecting neuromechanical uncoupling (NMU), (ii) mechanical constraints on volume expansion (dynamic restriction) play a pivotal role in dyspnea causation in patients with a variety of either obstructive or restrictive respiratory disorders, and (iii) all of the physiological adaptations that optimize neuromechanical coupling in obstructive and restrictive disorders are seriously disrupted so that an NMU underpins cluster descriptors of dyspnea which are similar in obstructed and in restricted patients.