To the Editor: Recently, the Surviving Sepsis Campaign COVID-19 guidelines and ATS suggest that a ventilatory strategy complying with the ARDSnet protocol should be applied to manage COVID-19 pneumonia [1-3]. However, "COVID-19 lung" pathophysiology seems to be divergent from the "ARDS lung"; hence, heart-lung interactions may be more pronounced than initially considered [2, 3]. We studied 17 patients (March 20-April 14, 2020) treated in two Greek University Intensive Care Units. Patients had COVID-19 pneumonia fulfilling the Berlin criteria of acute respiratory distress syndrome (ARDS) and were on the 2nd or 3rd day of invasive mechanical ventilation. Positive endexpiratory pressure (PEEP) was set according to predefined criteria [1-3]. Mean tidal volume (± standard deviation) was 6.8 ± 0.9 ml/kg ideal body weight (469 ± 64 ml), respiratory rate was 29.5 ± 3.7 breaths/min, and the fraction of inspired oxygen was 82 ± 12%. After measuring respiratory mechanics, arterial blood gases, and hemodynamics, we decreased PEEP by 25-30% (other mechanical ventilation variables remained stable). We re-evaluated measurements (1 h later) focusing on the effects of PEEP reduction on respiratory mechanics, hemodynamics, and fluid balance in a 12-h window before and after the PEEP change. Mean PEEP reduction by 29% significantly increased respiratory system compliance and reduced hypercapnia, while oxygenation (PaO 2 /FiO 2) did not worsen (Table 1). PEEP reduction was not accompanied by lung derecruitment, as oxygenation was not deteriorated. Rather PEEP reduction decreased lung overdistension as interpreted by the increase in respiratory system compliance and decrease in dead space ventilation (reduced PaCO 2). Concerning hemodynamics, PEEP reduction was followed by a substantial decrease in noradrenaline dose,
In chronic lung diseases physical activity limitation is multifactorial involving respiratory, hemodynamic, and peripheral muscle abnormalities. The mechanisms of limitation discussed in this paper relate to (i) the imbalance between ventilatory capacity and demand, (ii) the imbalance between energy demand and supply to working respiratory and peripheral muscles, and (iii) the factors that induce peripheral muscle dysfunction. In practice, intolerable exertional symptoms (i.e., dyspnea) and/or leg discomfort are the main symptoms that limit physical performance in patients with chronic lung diseases. Furthermore, the reduced capacity for physical work and the adoption of a sedentary lifestyle, in an attempt to avoid breathlessness upon physical exertion, cause profound muscle deconditioning which in turn leads to disability and loss of functional independence. Accordingly, physical inactivity is an important component of worsening the patients' quality of life and contributes importantly to poor prognosis. Identifying the factors which prevent a patient with lung disease to easily carry out activities of daily living provides a unique as well as important perspective for the choice of the appropriate therapeutic strategy.
Although there is a strong correlation between oral/oro-nasal breathing and apnoea/ hypopnoea index in patients with obstructive sleep apnoea and normal nasal resistance at wakefulness, it remains unknown whether the pharmacological prevention of potential nasal obstruction during sleep could decrease oral/oro-nasal breathing and increase nasal breathing and subsequently decrease the apnoea/ hypopnoea index. This study evaluated the effect of a combination of a nasal decongestant with corticosteroid on breathing route pattern and apnoea/hypopnoea index.21 patients with obstructive sleep apnoea (mean apnoea/hypopnoea index 31.1 events per hour) and normal nasal resistance at wakefulness were enrolled in a randomised crossover trial of 1 weeks' treatment with nasal tramazoline and dexamethasone compared with 1 weeks' treatment with nasal placebo. At the start and end of each treatment period, patients underwent nasal resistance measurement and overnight polysomnography with attendant measurement of breathing route pattern.Nasal tramazoline with dexamethasone was associated with decrease in oral/oro-nasal breathing epochs and concomitant increase in nasal breathing epochs, and mean decrease of apnoea/hypopnoea index by 21%. The change in nasal breathing epochs was inversely related to the change in apnoea/hypopnoea index (R s 50.78; p,0.001).In conclusion, nasal tramazoline with dexamethasone in OSA patients with normal nasal resistance at wakefulness can restore the preponderance of nasal breathing epochs and modestly improve apnoea/ hypopnoea index. @ERSpublications Nasal tramazoline with dexamethasone in OSA patients can restore nasal breathing epochs and improve AHI modestly
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