ABSTRACT
PURPOSE/HYPOTHESIS: Altered breathing patterns have been reported after SARS-CoV-2 infection, but it is unclear if they result from changes in chest wall kinematics, inspiratory muscle weakness, or both. Lung volumes can be estimated through chest wall motion via optoelectronic plethysmography (OEP). We hypothesized that poor inspiratory muscle performance would relate to impaired quiet breathing pattern as assessed by OEP in adults post COVID-19 infection. NUMBER OF SUBJECTS: 20. MATERIALS AND METHODS: A convenience sample of 20 subjects recovered from RT-PCR-confirmed COVID-19 (mean ± SD age = 52.45 ± 11.93 years and BMI = 30.89 ± 6.48 kg/m2) with no overt pulmonary disease underwent measures of maximal inspiratory pressure (MIP) using a digital manometer followed by OEP analysis to evaluate chest wall motion and its compartments during quiet breathing. All OEP data were collected with subjects in a seated position and with arms supported laterally. Eighty-nine reflective markers were distributed on the anterior surface, side and back of the participants' trunks, who were instructed to breathe normally for three minutes while the system was operated. The displacement of markers during the requested spontaneous quiet breathing was picked up by six synchronized cameras that recorded their coordinates, from which lung volumes were later estimated using algorithms. Statistical analyses included normality tests, descriptive statistics, Pearson's correlation and independent samples t-tests. RESULTS: The mean ± SD MIP and tidal volume (VT) of the sample were 82.15 ± 34.32 cmH2O and 369 ± 216.31 ml, respectively. 65% of the participants were below their predicted values for VT, and 70% had lower than predicted MIP values. MIP was significantly and positively associated with VT (r = 0.40, P=0.04), while a negative relationship was found between MIP and the percentage contribution of abdominal rib cage motion to VT (r=- 0.45, P=0.02). No further correlation was observed between MIP and other OEP variables. Additionally, subjects classified as having normal inspiratory muscle function (i.e. MIP > 80 cmH2O) had significantly greater VT when compared to those presenting with inspiratory muscle weakness (450.64 ± 262.57 versus 269.22 ± 67.67 ml, respectively;P = 0.04). CONCLUSIONS: The variability of post COVID-19 ventilatory impairment requires a complex screening process. In our sample, most subjects presented with lower than predicted VT and MIP. Moreover, a significant association existed between inspiratory muscle dysfunction and reduced tidal volume. Changes in abdominal rib cage motion were also observed and likely occurred to compensate for a less efficient diaphragm even during normal, regular breathing. CLINICAL RELEVANCE: Subjects recovering from COVID-19 may present with diaphragm myopathy and impairment, highlighting the need to screen for inspiratory muscle weakness which may help identify altered breathing patterns and guide management such as inspiratory muscle training to mitigate persistent symptoms related to abnormal ventilation.