Topic Importance Oscillometry is becoming increasingly recognized as an important method to measure pulmonary function. However, the methodology is unfamiliar and sometimes intimidating to clinicians due to the complex physiology and math commonly used to explain the technique. This review aims to demystify oscillometry by explaining it in more intuitive terms related to acoustic waves, using tuning forks as an analogy. In addition, we highlight recent literature describing various clinical applications of oscillometry. Review Findings Oscillometry can be explained by considering how tuning forks generate sound of different frequencies to impact the cochlea. In the case of oscillometry, acoustic waves of different frequencies are chosen to specifically target different depths of the respiratory system. The information derived is interpreted in the context of a simple structural model based on the equation of motion. Recent applications of oscillometry include obstructive and restrictive lung disease, pediatrics, population studies, occupational exposures, and monitoring of mechanical ventilation. Summary Oscillometry is a valuable tool that complements spirometry and other lung function testing and can allow us to better understand the physiological impacts of a wide variety of lung disease.

An exciting aspect of oscillometry is the ability to detect small airways disease (SAD), particularly through frequency dependence of resistance, commonly measured as R5-R20. While SAD influences oscillometry measurements, it is important to realize that oscillometry is not specific for SAD. In addition, oscillometry measurements do not take into account lung volume, which can influence the measurements and make interpretation less clear. Finally, while oscillometry is very sensitive at detecting abnormalities of lung function, it is not specific for distinct lung diseases. These limitations should be considered when using oscillometry in respiratory physiology and medicine, where oscillometry provides valuable complimentary information to other lung function tests in evaluation of lung health.

Background:Determination of reference values of respiratory impedance (Z) measured by oscillometry is of utmost importance for its clinical usefulness. The aim of our study was to develop reference values for within-breath and total oscillometry measurements in adults (18-90 years of age). Methods:Healthy asymptomatic never-smoking adults of the Austrian LEAD study cohort were included in the analysis. Healthy never-smoking adults without any respiratory disease, with normal weight (body mass index (BMI) ≤35 kg·m-2) and normal lung volumes (total lung capacity ≥ lower limit of normal) were included. Data were collected with the Resmon Pro FULL® device using a multiple frequency mode of 5-11-19 Hz. Sex-specific reference equations were developed for within-breath and total resistance, reactance and the impedance modulus, as well as for the frequency dependence of resistance (R 5-R 19), the resonant frequency and the area under the reactance curve using the lambda, mu, sigma method. Results:A total of 887 participants were included in the analysis. We developed sex-specific reference equations for 30 total and within-breath oscillometry parameters. Height, age and BMI were included in the modelling, and height showed the strongest association. Predicted values showed a narrower normality range compared with existing reference equations. Conclusion:Our study provides highly accurate, adult reference equations derived from a large sample size with a wide age span. Development of reference equations supports further research on positioning of oscillometry in respiratory diagnostics.

Background:The pattern of preserved ratio impaired spirometry (PRISm) has gained increased attention in the last few years. While PRISm has been linked to increased morbidity and mortality, the underlying physiological causes remain unclear and the stability of PRISm over time remains uncertain. Methods:We investigated 6571 individuals (≥25 years, 51.4% female) from the Austrian population-based, longitudinal LEAD (Lung, hEart, sociAl, boDy) study who underwent post-bronchodilator spirometry and body plethysmography twice within a 4-year interval. Individuals were classified into normal spirometry (forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC)≥0.7 and FEV1≥80% predicted Global Lung Function Initiative (GLI)); airflow limitation (AFL) (FEV1/FVC<0.7); and PRISm (FEV1/FVC≥0.7 and FEV1<80% predicted GLI). Body composition was assessed by bone density scanning. Results:PRISm was present in 2.6% of individuals (n=171) at baseline. Different subgroups of PRISm were identified: after 4 years, 45.6% had persistent PRISm, 37.4% PRISm-to-normal and 17.0% had PRISm-to-AFL. Persistent PRISm individuals were characterised by significantly lower total lung capacity (TLC), with two-thirds meeting TLC criteria for restriction. PRISm-to-AFL had a higher TLC and lower airway conductance as well as a higher FEV1 decline. Participants with new PRISm after 4 years (n=71) had the highest decline of vital capacity and TLC. Smoking status was not associated with PRISm progression or resolution as never- and ever-smokers with PRISm showed no difference in frequency of transitions after 4 years. Conclusion:PRISm is primarily defined by low lung volumes and is characterised by a dynamic course, with more than two-thirds demonstrating stable or improving lung function. Lung volume assessment in PRISm is mandatory for precise evaluation of pulmonary function. Similar transition patterns in smokers and never-smokers challenge the assumption of PRISm as an early smoking-related obstructive state and emphasise the importance of repeated lung function testing over time.

RATIONALE: People with obesity and asthma experience worse asthma control and have increased rates of hospitalizations compared to lean people with asthma. Standard inhaler therapy, such as inhaled corticosteroids, are not as effective in people with obesity compared to lean people. This is thought to be due to the low lung volumes caused by obesity, which can increase airway reactivity even in the absence of asthma. Lung volumes can be increased through use of continuous positive airway pressure (CPAP). We sought to determine the efficacy of nocturnal CPAP for reducing airway reactivity in obese people both with and without asthma. METHODS: This was a two-site double-blinded randomized control trial. Participants with BMI ≥ 30 kg/m2 with (n=20) and without (n=20) asthma were randomized to 7 nights of CPAP of 10 cmH2O or sham CPAP (4cmH2O). Baseline airway physiology and response to methacholine were measured by oscillometry before and after the CPAP intervention, and compared using Student's t-test. Airway reactivity was quantified by the PC100, defined as the dose of methacholine producing a 100% increase in the area under the reactance curve from 5 Hz to the resonant frequency (Ax). The changes in ln(PC100) resulting from the intervention were compared by ANOVA. RESULTS: Control participants in both the CPAP and sham groups had similar BMI's (34.3 vs 34.1, respectively), as did the participants with asthma (BMI's of 40.1 vs 37.3, respectively). Participants with asthma had higher magnitudes of resistance and reactance, lower FEV1, and higher residual volume (percent predicted) than controls. On average, participants used CPAP for less than 5 hours per night. In the participants receiving 10 cmH2O CPAP, there were no significant differences in baseline oscillometry parameters between those with asthma versus controls, except for improved resistance at 19 Hz in participants with asthma (-0.29±0.08 vs -0.07±0.31, p=0.07). ln(PC100) increased, although non-significantly, with CPAP in controls only (1.53 [SEM 0.98] vs 0.42 [SEM 0.27]; p=0.17, respectively). CONCLUSIONS: These data suggest that nocturnal CPAP is unlikely to have a significant impact on asthma outcomes in people with obesity, and that airway reactivity in people with obesity and asthma is not related to low lung volumes. A larger, longer trial with greater adherence to CPAP and possible higher CPAP pressure may provide more power to see any small changes.

BACKGROUND:While effects of COVID-19 on lung function are commonly described in those with severe illness, less is known about those with less severe illness, and most studies do not extend beyond 6 months following initial presentation. RESEARCH QUESTION:What are the effects of COVID-19 on lung function in a cohort of participants that included those with more severe and less severe disease over a 1 year period from time of enrollment? STUDY DESIGN:We enrolled 52 participants who included those with more severe (had been hospitalized) and less severe (not hospitalized) illness and measured spirometry, lung volumes, diffusing capacity, oscillometry, maximal muscle pressures, inspiratory drive, exercise capacity, and symptom and quality of life surveys at presentation, and repeated the measurements 6 and 12 months later. RESULTS:While participants who had been hospitalized had consistently lower lung function in all measures, all values were within normal reference ranges. The pattern of lung function change suggested a predominant restrictive physiologic defect with reduced exercise capacity. Over 1 year, there was no significant improvement in lung function. Similar findings were seen when participants were stratified by whether they had shortness of breath at presentation. INTERPRETATION:In our cohort of participants with both more severe and less severe disease, there were only minor differences in lung function associated with severe illness or whether participants had shortness of breath. COVID-19 resulted in subtle changes related to physiologic restriction, but overall lung function remained in the normal range with little change over time, suggesting that other factors besides lung function contribute to shortness of breath in participants following COVID-19.