ABSTRACT
Introduction: Remaining respiratory symptoms is common after covid-19. The pathophysiology behind this is unclear, with spirometry often within the normal range. We hypothesised that impairment in the small airways can be an explanation. Aim(s): To investigate if the function of the small airways is impaired after covid-19. Method(s): 28 (18 females) post covid-19 subjects aged 27-63 yrs performed spirometry, DLCO, nitrogen (N ) multiple breath washout (MBW) and impulse oscillometry (IOS). Three out of 28 were hospitalized due to covid-19. Median (IQR) days between first symptom and participation was 216 (108;372). Results were compared to findings in 10 (7 females) non-covid-19 subjects, aged 29-63 yrs, and reported in z-score (z) related to GLI reference equations for spirometry and DLCO, while two healthy cohorts (n=400 and n=158) provided local reference values for N MBW and IOS, respectively. Result(s): IOS derived frequency dependence of resistance (FDR) and MBW derived Sacin were the only outcomes significantly different in post covid-19 subjects, median (IQR), 0.01 kPa/L/s (0.00;0.02) vs 0.04 kPa/L/s (0.01;0.06), p=0.028 for FDR and 0.070 (0.046;0.076) vs 0.009 (0.075;0.121), p=0.017 for Sacin. FDR was >1.96 z in 2/28 whileS >1.96 z was found in 14/28. In post covid-19 subjects with S >1.96 z, dyspnea were more common than in those with normal Sacin, (8/14 vs 2/14, p=0.049). FEV1 and DLCO were > -1.96 z in all but one subject. Conclusion(s): Ventilation heterogeneity at the entrance to the acinar airways were common in this small sample of post covid-19 subjects, as assessed by Sacin, and may explain the experience of dyspnea in these subjects, despite normal spirometry and DLCO. A larger study is ongoing.
ABSTRACT
Background: SARS-CoV-2 displays high affinity for ACE2 receptors, expressed on type 2 alveolar cells. These cells produce pulmonary surfactant - a crucial thin layer of surface-active lipid rich fluid - fundamental for proper gas exchange. Aims and objectives: To investigate changes in surfactant lipid composition and the relationship to prolonged symptoms of post covid-19 among patients treated in intensive care unit for covid-19 infection. Method(s): Patients (n=43, 17 female, aged 44-80 years) treated in an intensive care unit with covid-19 infection in average six months prior to enrollment were recruited. Particles in exhaled air were collected with PExA-instrument (PExA AB) and we also conducted body plethysmograph and diffusion capacity of the lungs for carbon monoxide. Twenty-two healthy, non-infected, age- and gender-matched controls were also enrolled. Lipids were analysed using liquid chromatography with a triple quadrupole mass spectrometer. Statistical analyses were performed with Qlucore. Result(s): Preliminary results suggest a significant change in the composition of surfactant lipids. Analysis show significant reductions of all measured phosphatidyl-glycerols (PG, n=14) an increase of all measured phosphatidyl- inositols (PI, n=4), e.g. PG 18:1-18:1 22 % lower (p<0.001, q=0.04) and PI:16:0:18:1 67% higher (p<0.001, q=0.0003) among the post-covid patients compared to controls. Conclusion(s): Our findings suggest that surfactant composition is altered also in the recovery phase after covid-19 infection which could be a key component in the post-covid syndrome with lingering effects on the respiratory system.
ABSTRACT
Background: SARS-CoV-2 displays high affinity for ACE2 receptors as a vector of pathogenesis. ACE2 receptors are highly expressed on surfactant producing type 2 alveolar cells. These cells produce pulmonary surfactant - a crucial thin layer of surface-active fluid mainly composed of lipids, lining the alveolar epithelial surface. The main function, to reduce the surface tension, is fundamental for proper gas exchange. Aims and Objectives: To investigate changes in surfactant lipid composition and the relationship to longstanding symptoms of post Covid-19 among patients treated in intensive care for Covid-19 infection. Methods: We recruited 43 patients (17 women, aged 44-80 years) who had previously been treated in ICU in a major Swedish hospital, in average 6 months before inclusion. The participants answered a questionnaire regarding symptoms, we collected particles in exhaled air with PExA-instrument (PExA AB) and conducted pulmonary function tests, body plethysmography, and diffusion capacity of the lungs for carbon monoxide. Twenty-two healthy, non-infected, ageand gender-matched controls were enrolled. Lipids were analysed using liquid chromatography with a triple quadrupole mass spectrometer. Statistical analyses were performed with Qlucore. Results: Early results suggest a significant change in the composition of surfactant lipids among post-Covid -19 patients treated in intensive care compared to controls. Early analysis show significant reductions of all measured phosphatidyl-glycerols (PG, n = 14) an increase of all measured phosphatidyl-inositols (PI, n = 4), for example were PG 18:1-18:1 22% lower (p < 0.001, q = 0.04) and PI:16:0:18:1 67% higher (p < 0.001, q = 0.0003) in subjects post-Covid compared to controls. Conclusions: Our findings suggest that surfactant composition is altered also in the recovery after Covid-19 infection, which could be a key component in the post-Covid syndrome and the lingering effects on the respiratory system.
ABSTRACT
Exhaled droplets are composed of water, salts and organic material and the physical designation is particles. These particles vary in size from 0.01 microm to very large, e g produced during coughing. The respiratory tract lining fluid (RTLF) is the main source of the particles. Large and small exhaled particles are produced in central airways, vocal cords and mouth whereas small particles (< about 5 microm) are produced also in small airways, generated during inspiration by the airway closure/opening mechanism. These particles are composed mainly of surfactant. Exhaled small particles may carry virus and cause airborne transmission and infection, which may be an important transmission route indoors. Ventilation, concentration of people, activities and face mask occurrence influence the risk of infection. Outdoor transmission is in addition influenced by outdoor pollution and wind speed.