Inspiratory Maneuvers Research Articles

Pneumothorax Caused by Aggressive Use of an Incentive Spirometer in a Patient With Emphysema

A 68-year-old man presented to the emergency department with a small pneumothorax following aggressive use of an incentive spirometer. The patient had a baseline chest radiograph consistent with emphysema. He was initially treated with oxygen in the emergency department, with resolution of his symptoms. The pneumothorax resolved spontaneously over a period of 3 days. The development of the pneumothorax was likely due to the patient's repeated forceful inspiratory maneuvers in the setting of emphysema and lung hyperinflation. Inspiratory resistive breathing can cause large negative swings in intrathoracic pressure, which may result in mechanical stress of lung tissue. This is the first report of a secondary pneumothorax associated with use of an incentive spirometer. Patients with bullous emphysema should be counseled to avoid frequent high intensity maneuvers with an incentive spirometer if the potential benefits of the procedure are marginal.

Peripheral vascular response to inspiratory breath hold in paediatric homozygous sickle cell disease

New Findings• What is the central question of this study?Autonomic nervous dysfunction is implicated in complications of sickle cell anaemia (SCA). In healthy adults, a deep inspiratory breath hold (IBH) elicits rapid transient SNS- mediated vasoconstriction detectable using Laser Doppler Flux (LDF) assessment of the finger-tip cutaneous micovasculature.• What is the main finding and its importance?We demonstrate significantly increased resting peripheral blood flow and sympathetic activity in African children with SCA compared to sibling controls and increased sympathetic stimulation in response to vasoprovocation with DIG.This study is the first to observe an inverse association between resting peripheral blood flow and haemoglobin oxygen saturation (SpO2). These phenomena may be an adaptive response to the hypoxic exposure in SCA.There is increasing evidence that autonomic dysfunction in adults with homozygous sickle cell (haemoglobin SS) disease is associated with enhanced autonomic nervous system-mediated control of microvascular perfusion. However, it is unclear whether such differences are detectable in children with SS disease. We studied 65 children with SS disease [38 boys; median age 7.2 (interquartile range 5.1–10.6) years] and 20 control children without symptoms of SS disease [8 boys; 8.7 (5.5–10.8) years] and recorded mean arterial blood pressure (ABP) and daytime haemoglobin oxygen saturation (). Cutaneous blood flux at rest (RBF) and during the sympathetically activated vasoconstrictor response to inspiratory breath hold (IBH) were measured in the finger pulp of the non-dominant hand using laser Doppler fluximetry. Local factors mediating flow motion were assessed by power spectral density analysis of the oscillatory components of the laser Doppler signal. The RBF measured across the two study groups was negatively associated with age (r=−0.25, P < 0.0001), ABP (r=−0.27, P= 0.02) and daytime (r=−0.30, P= 0.005). Children with SS disease had a higher RBF (P= 0.005) and enhanced vasoconstrictor response to IBH (P= 0.002) compared with control children. In children with SS disease, higher RBF was associated with an increase in the sympathetic interval (r=−0.28, P= 0.022). The SS disease status, daytime and age explained 22% of the variance in vasoconstrictor response to IBH (P < 0.0001). Our findings suggest that blood flow and blood flow responses in the skin of young African children with SS disease differ from those of healthy control children, with increased resting peripheral blood flow and increased sympathetic stimulation from a young age in SS disease. They further suggest that the laser Doppler flowmetry technique with inspiratory breath hold manoeuvre appears to be robust for use in young children with SS disease, to explore interactions between , ABP and autonomic function with clinical complications, e.g. skin ulceration.

Atividade mioelétrica dos músculos respiratórios em crianças asmáticas durante manobra inspiratória máxima

OBJETIVOS: avaliar a atividade dos músculos escalenos e esternocleidomastóideo (ETMD) no período basal e durante manobra de pressão inspiratória máxima (PImax) em crianças asmáticas. MÉTODOS: foram estudadas 15 crianças, divididas em grupo asma (n=8) e grupo controle (n=7). Foi realizada a análise da função pulmonar e da PImax através da espirometria e da manovacuometria, respectivamente. A atividade mioelétrica dos músculos escaleno e ETMD foram realizadas pela eletromiografia de superfície durante período basal e manobra de PImax. RESULTADOS: a eletromiografia de superfície (EMGs) basal do músculo escaleno é maior no grupo asma quando comparado ao grupo controle. Diferentemente, a EMGs basal do músculo ETMD não apresentou diferença significativa nos grupos estudados. O percentual da EMGs dos músculos escaleno e ETMD durante manobra de PImax foi maior no grupo asma quando comparado ao grupo controle. CONCLUSÕES: EMGs do escaleno durante o período basal está aumentada em crianças asmáticas. A atividade eletromiográfica do músculo ETMD no período basal é similar em ambos os grupos estudados. A EMGs dos músculos ETMD e escaleno na geração de pressão intratorácica, durante a manobra de PImax, está aumentada em crianças asmáticas.

Respiratory Muscle Fatigue following Exercise in Patients with Interstitial Lung Disease

Background: It is not known whether respiratory muscle fatigue occurs as a consequence of exercise in patients with interstitial lung disease (ILD) and, if so, to what extent it is related to changes in dynamic lung volumes. Objectives: To assess the development of respiratory muscle fatigue in patients with ILD and relate it to the respiratory pattern during exercise. Methods: Sixteen ILD patients (11 women) performed incremental, symptom-limited cycle ergometry with inspiratory capacity manoeuvres used to measure changes in end-expiratory lung volume (EELV). Twitch transdia-phragmatic pressure (TwPdi) and twitch gastric pressure (TwT₁₀Pga), in response to magnetic stimulation, were used to assess the development of fatigue. Results: TwPdi did not differ significantly before and after exercise (21.8 ± 8 vs. 20.2 ± 8 cm H₂O; p = 0.10), while TwT₁₀Pga fell from 28.6 ± 18 to 25.2 ± 14 cm H₂O (p = 0.02). EELV fell from 2.18 ± 0.65 to 1.91 ± 0.59 liters following exercise (p = 0.04). The fall in TwT10Pga correlated with peak oxygen uptake at peak of exercise (r = -0.52, p = 0.041), increase in heart rate (r = 0.53, p = 0.032) and with the decrease of EELV during exercise (r = 0.57, p = 0.021). Abdominal muscle fatiguers (n = 9, 56%), defined as having a ≥10% fall in TwT10Pga, had a fall in EELV of 22 ± 22% compared to 0.7 ± 8% in non-fatiguers (p = 0.016). Conclusion: Abdominal muscle fatigue develops during exercise in some ILD patients in association with increased expiratory muscle activity manifested by reduced EELV.

Bedside Assessment of Total Systemic Vascular Compliance, Stressed Volume, and Cardiac Function Curves in Intensive Care Unit Patients

Mean systemic filling pressure (Pmsf) can be measured at the bedside with minimally invasive monitoring in ventilator-dependent patients using inspiratory hold maneuvers (Pmsf(hold)) as the zero flow intercept of cardiac output (CO) to central venous pressure (CVP) relation. We compared Pmsf(hold) with arm vascular equilibrium pressure during vascular occlusion (Pmsf(arm)) and their ability to assess systemic vascular compliance (Csys) and stressed volume by intravascular fluid administration. In mechanically ventilated postoperative cardiac surgery patients, inspiratory holds at varying airway pressures and arm stop-flow maneuvers were performed during normovolemia and after each of 10 sequential 50-mL bolus colloid infusions. We measured CVP, Pmsf(arm), stroke volume, and CO during fluid administration steps to construct CVP to CO (cardiac function) curves and Δvolume/ΔPmsf (compliance) curves. Pmsf(hold) was measured before and after fluid administration. Stressed volume was determined by extrapolating the Pmsf-volume curve to zero pressure intercept. Fifteen patients were included. Pmsf(hold) and Pmsf(arm) were closely correlated. Csys was linear (64.3 ± 32.7 mL · mm Hg(-1), 0.97 ± 0.49 mL · mm Hg(-1) · kg(-1) predicted body weight). Stressed volume was estimated to be 1265 ± 541 mL (28.5% ± 15% predicted total blood volume). Cardiac function curves of patients with an increase of >12% to 500 mL volume extension (volume responsive) were steep, whereas the cardiac function curves of the remaining patients were flat. Csys, stressed volume, and cardiac function curves can be determined at the bedside and can be used to characterize patients' hemodynamic status.

Tracheobronchoplasty for the treatment of tracheobronchomalacia

Patients with tracheobronchomalacia (TBM) typically present with dyspnea, recurrent infections, intractable cough, or retained secretions. Airway stabilization may be accomplished with silicone stenting, which provides patients with symptom relief in a minimally invasive manner. However, this technique is not without complications, which mostly occur by 3 weeks. Surgical stabilization is the definitive treatment of TBM. We review the evaluation of TBM and options for treatment.

The influence of rowing-related postures upon respiratory muscle pressure and flow generating capacity

During the rowing stroke, the respiratory muscles are responsible for postural control, trunk stabilisation, generation/transmission of propulsive forces and ventilation (Bierstacker et al. in Int J Sports Med 7:73-79, 1986; Mahler et al. in Med Sci Sports Exerc 23:186-193, 1991). The challenge of these potentially competing requirements is exacerbated in certain parts of the rowing stroke due to flexed (stroke 'catch') and extended postures (stroke 'finish'). The purpose of this study was to assess the influence of the postural role of the trunk muscles upon pressure and flow generating capacity, by measuring maximal respiratory pressures, flows, and volumes in various seated postures relevant to rowing. Eleven male and five female participants took part in the study. Participants performed two separate testing sessions using two different testing protocols. Participants performed either maximal inspiratory or expiratory mouth pressure manoeuvres (Protocol 1), or maximal flow volume loops (MFVLs) (Protocol 2), whilst maintaining a variety of specified supported or unsupported static rowing-related postures. Starting lung volume was controlled by initiating the test breath in the upright position. Respiratory mouth pressures tended to be lower with recumbency, with a significant decrease in P (Emax) in unsupported recumbent postures (3-9% compared to upright seated; P=0.036). There was a significant decrease in function during dynamic manoeuvres, including PIF (5-9%), FVC (4-7%) and FEV(1) (4-6%), in unsupported recumbent postures (p<0.0125; Bonferroni corrected). Thus, respiratory pressure and flow generating capacity tended to decrease with recumbency; since lung volumes were standardised, this may have been, at least in part, influenced by the postural co-contraction of the trunk muscles.

Simulation of apneas at the end of argon inhalation, using seven parallel regions of the lung

Jeng et al. (Ann. Biomed. Eng, 28:453, 2000) could not simulate apneas after argon (Ar) inhalation because the convection‐diffusion equation, solved by diluting the inhaled Ar with FRC, obtained too much Ar in the alveoli. Using the model of 7 parallel regions to simulate a normal breath of O2, and CO2, new concepts were introduced in mixing the inhaled gas with the expiratory reserve volume (ERV), by the mechanism of convection‐diffusion during inspiration. During the time of expiration, gases diffused from RV to ERV for CO2 and from ERV to RV for O2 (Caucha et al. Am. J. Respir. Crit. Care Med. 183: A5180, 2011). These concepts are now applied to forced inspiratory (2s) and expiratory (3s) maneuvers by inhaling 1.9 L of 21% O2, 79% Ar from FRC and exhaling to RV. The breath was held at the end of inspiration for 5s, 10s and 20s. The simulated expired curves are shown in the Figure. The last 8, 9 and 10 generations of Weibel's anatomical model were used at the base, middle and apical regions, respectively, at 5s a 10s of apnea. For 20s it was necessary to use the last 10th and 11th generations for the base and apical regions. In conclusion, the model described is capable of simulating the experiments of Cruz (Respir. Physiol. 86:1, 1991).

Determination of Vascular Waterfall Phenomenon by Bedside Measurement of Mean Systemic Filling Pressure and Critical Closing Pressure in the Intensive Care Unit

Mean systemic filling pressure (Pmsf) can be determined at the bedside by measuring central venous pressure (Pcv) and cardiac output (CO) during inspiratory hold maneuvers. Critical closing pressure (Pcc) can be determined using the same method measuring arterial pressure (Pa) and CO. If Pcc > Pmsf, there is then a vascular waterfall. In this study, we assessed the existence of a waterfall and its implications for the calculation of vascular resistances by determining Pmsf and Pcc at the bedside. In 10 mechanically ventilated postcardiac surgery patients, inspiratory hold maneuvers were performed, transiently increasing Pcv and decreasing Pa and CO to 4 different steady-state levels. For each patient, values of Pcv and CO were plotted in a venous return curve to determine Pmsf. Similarly, Pcc was determined with a ventricular output curve plotted for Pa and CO. Measurements were performed in each patient before and after volume expansion with 0.5 L colloid, and vascular resistances were calculated. For every patient, the relationship between the 4 measurements of Pcv and CO and of Pa and CO was linear. Baseline Pmsf was 18.7 ± 4.0 mm Hg (mean ± SD) and differed significantly from Pcc 45.5 ± 11.1 mm Hg (P < 0.0001). The difference of Pcc and Pmsf was 26.8 ± 10.7 mm Hg, indicating the presence of a systemic vascular waterfall. Volume expansion increased Pmsf (26.3 ± 3.2 mm Hg), Pcc (51.5 ± 9.0 mm Hg), and CO (5.5 ± 1.8 to 6.8 ± 1.8 L · min(-1)). Arterial (upstream of Pcc) and venous (downstream of Pmsf) vascular resistance were 8.27 ± 4.45 and 2.75 ± 1.23 mm Hg · min · L(-1); the sum of both (11.01 mm Hg · min · L(-1)) was significantly different from total systemic vascular resistance (16.56 ± 8.57 mm Hg · min · L(-1); P = 0.005). Arterial resistance was related to total resistance. Vascular pressure gradients in cardiac surgery patients suggest the presence of a vascular waterfall phenomenon, which is not affected by CO. Thus, measures of total systemic vascular resistance may become irrelevant in assessing systemic vasomotor tone.

Procedural Aspects and Physiologic Mechanisms of the Deep Inspiratory Maneuver

Sir, we have read the paper by S. Preau et al. “Hemodynamic changes during a deep inspiration maneuver predict fluid responsiveness in spontaneously breathing patients” with great interest. Based on the fundamental ideas of dynamic hemodynamic monitoring, inducing cardiac preload variations and monitoring corresponding pulse pressure variations [1], the paper presents a novel technique of varying cardiac preload in spontaneously breathing (SB) patients that does not necessitate specialised equipment apart from routine clinical monitoring. The paper is indeed relevant because it is, to our knowledge, the first to present the feasibility of a deep breathing method (deep inspiratory maneuver, DIM) for inducing preload changes. For the purpose of better understanding the presented technique, we wish to pose the following questions for the authors. Concerning compliance and applicability in terms of intention-to-treat: it is not clear which proportion of SB patients with acute circulatory failure was able to comply with the DIM. Can compliance be expected to be as high as 87% (26 of 30) for this generally defined patient group? Concerning the calculations: DIM-induced changes are defined by the authors as. DIM-induced changes = (maximal value during DIM − minimal value during quiet SB prior to DIM)/((maximal value during DIM − minimal value during quiet SB prior to DIM)/2). How large was the time window when estimating the minimal value during quiet SB prior to DIM? Did the time window vary or was it fixed? The maximal value during DIM was found in either phase 2 or phase 4 of the DIM. In which phase was the maximal value typically found? Were the maximal values during the two phases generally of the same magnitude? Instructing the patients to perform the DIM: this is important should the technique be validated by other study groups and in turn gain widespread use. Did the authors in any way evaluate if the slow continuous inspiration strain was associated with a more or less constant inspiratory flow or was most air generally inspired in the first phase of inspiration, perhaps amplifying maximal value during DIM phase 2? How were instructions given on inspiratory flow rate? Did you make any instructions to the patients (directly or indirectly) what tidal volume should be during DIM? Did they inspire to, for example, maximal or convenient lung volume? Concerning the physiological mechanisms: did you experience any patients with significant heart rate variability (HRV)? The respiratory part of HRV (with its subsequent varying passive filling time of the ventricles) could be another mechanism inducing preload variations and as such it could confound results obtained with the DIM technique. On the other hand, HRV is known to be significantly reduced during sepsis [2]. We also have a few comments and suggestions to the proposed physiological mechanisms. The decrease in left ventricular stroke volume during DIM phase 1 is suggested to be induced by increasing ventricular afterload. However, we think that another and perhaps more important mechanism is the reduced intrathoracic pressure reducing left ventricular preload during the initial phase of inspiration—until the increasing right ventricular stroke volume with the delay of pulmonary transit time again increases left ventricular preload substantially. In line with this suggestion, but as a “reversed mechanism,” we also believe that the increasing intrathoracic pressure during passive expiration (DIM phase 4) contributes somewhat to the increasing left ventricular (preload and) stroke volume in DIM phase 4 in addition to the suggested overall increase in intrathoracic blood volume. As a last comment, we would like to suggest that the DIM phases 2 and 4 could potentially disclose right ventricular failure: a large maximal value during DIM phase 2 relies on biventricular preload responsiveness whereas a large value in DIM phase 4 relies mostly, if not fully, on left ventricular preload responsiveness. Even though the authors did not encounter any cases of preload unresponsiveness associated with high ΔPPdim (specificity was 100%) low phase 2 values associated with high phase 4 values could theoretically disclose right ventricular failure—even when taking interventricular dependence into account.

Hemodynamic Changes during a Deep Inspiration Maneuver Predict Fluid Responsiveness in Spontaneously Breathing Patients

Objective. We hypothesized that the hemodynamic response to a deep inspiration maneuver (DIM) indicates fluid responsiveness in spontaneously breathing (SB) patients. Design. Prospective study. Setting. ICU of a general hospital. Patients. Consecutive nonintubated patients without mechanical ventilation, considered for volume expansion (VE). Intervention. We assessed hemodynamic status at baseline and after VE. Measurements and Main Results. We measured radial pulse pressure (PP) using an arterial catheter and peak velocity of femoral artery flow (VF) using continuous Doppler. Changes in PP and VF induced by a DIM (ΔPPdim and ΔVFdim) were calculated in 23 patients. ΔPPdim and ΔVFdim ≥12% predicted responders to VE with sensitivity of 90% and specificity of 100%. Conclusions. In a restricted population of SB patients with severe sepsis or acute pancreatitis, ΔPPdim and ΔVFdim are accurate indices for predicting fluid responsiveness. These results should be confirmed in a larger population before validating their use in current practice.

Evoked corticospinal output to the human scalene muscles is altered by lung volume

Increases in lung volume inhibit the inspiratory output from the medulla, but the effect of lung inflation on the voluntary control of breathing in humans is not known. We tested corticospinal excitability using transcranial magnetic stimulation (TMS) to evoke a response in the scalene muscles. TMS was delivered at rest at three different lung volumes between functional residual capacity (FRC) and total lung capacity (TLC) during incremental inspiratory and incremental expiratory manoeuvres. Motor evoked potentials (MEPs) in scalenes were ∼50% larger at a high lung volume (FRC+∼90% inspiratory capacity [IC]) compared to lower lung volumes (FRC and FRC+∼40% IC) in both inspiratory and expiratory manoeuvres (p<0.001). The change in MEP size was not due to differences in pre-stimulus EMG amplitude (p=0.29). The results suggest a differential effect of lung inflation on the automatic and voluntary control of breathing in humans.

S117 Respiratory muscle fatigue following exercise in patients with interstitial lung disease

BackgroundPatients with interstitial lung disease (ILD) experience progressive breathlessness and exercise limitation. Although respiratory muscle fatigue has been investigated in healthy subjects and patients with COPD, it is unknown whether...

S115 The effect of posture on the 2nd intercostal space surface parasternal electromyogram (EMGpara): validating a novel clinical tool to measure neural respiratory drive

IntroductionAlthough neural respiratory drive (NRD), as measured by diaphragm EMG, has been shown to reflect the balance between the respiratory muscle load and capacity providing a marker of disease severity,...

Determinants of Expiratory Flow Limitation in Healthy Women during Exercise

Expiratory flow limitation (EFL) can occur in healthy young women during exercise. We questioned whether the occurrence and severity of EFL were related to aerobic fitness or anatomical factors. Twenty-two healthy young (<40 yr) women performed a progressive cycle test to exhaustion. The subjects' maximum expiratory flow-volume curve was compiled from several effort-graded vital capacity maneuvers before and after exercise. The maximum expiratory flow-volume curve, along with inspiratory capacity maneuvers, was used to determine lung volumes and expiratory flows and to quantify EFL. To determine relative airway size, we used a ratio sensitive to both airway size and lung volume, called the dysanapsis ratio. The subjects were partitioned into two groups based upon the appearance of >5% EFL. Ten subjects showed EFL during exercise. Forced vital capacities (4.4 ± 0.4 vs 3.7 ± 0.4 L, P < 0.001) and forced expiratory flows for any given lung volume were significantly larger in the non-expiratory flow-limited (NEFL) group. The NEFL group's dysanapsis ratio was significantly larger than that of the EFL group (0.27 ± 0.06 vs 0.21 ± 0.04, respectively, P < 0.05), indicating larger airways in the NEFL group. There was no difference between the NEFL and EFL groups with respect to maximal aerobic capacity (50.8 ± 10.0 vs 46.7 ± 5.9 mL·kg(-1)·min(-1), respectively, P = 0.264). At peak exercise, the NEFL group had a significantly higher end-expiratory lung volume than the EFL group (40.1% ± 4.8% vs 33.7% ± 5.7% FVC, respectively, P < 0.05). We conclude that EFL in women can largely be explained by anatomical factors that influence the capacity to generate flow and volume during exercise rather than fitness per se.

Neural respiratory drive as a physiological biomarker to monitor change during acute exacerbations of COPD

BackgroundAcute exacerbations of chronic obstructive pulmonary disease have a significant negative impact on both patients and healthcare systems. Currently, there are no physiological biomarkers that effectively monitor clinical change or...

Effects Of Carrying A Weighted Backpack On Lung Mechanics In Healthy Men

The use of a weighted backpack is common in occupational and recreational settings. However, it is not known if weighted backpacks alter breathing mechanics or increase the work of breathing (WOB). PURPOSE: To determine the effect of a weighted backpack on breathing mechanics during treadmill walking. METHODS: Subjects (n=7, age=28±6 yrs, ht =180±6 cm) completed five randomized exercise bouts on a treadmill: no backpack (NP), an un-weighted backpack (NW) or a backpack weighing 15, 25 or 35 kg. The backpack trials consisted of two 2.5 min stages, while the NP trial had five 2.5 min stages; to ensure there was an overlap in ventilations. An esophageal balloon catheter was used to estimate pleural pressure and calculate the work of breathing. A maximal expiratory flow volume curve was generated for each condition before and after exercise, while inspiratory capacity manoeuvres were performed during each stage to determine end-expiratory lung volume (EELV). RESULTS: Forced vital capacity (FVC) for the 25 and 35 kg pack trials was decreased compared to all other conditions (P<0.01); however, there was no difference between the NP and NW condition and the 15 kg and NW condition (P>0.05). There was no difference in expiratory flows at: peak, 75% FVC, 50% FVC and 25% FVC between all conditions (P>0.05). Two subjects displayed expiratory flow limitation (7-8% of tidal breath) during the final workload of the 35 kg trial. At the same treadmill grade and speed the 25 and 35 kg conditions had significantly different: minute ventilation, breathing frequency, EELV and WOB; when compared to the 15kg, NW and NP condition (P<0.05). There was no difference in the WOB when comparing different backpack weights at similar minute ventilations (P>0.05). At a similar minute ventilation, independent of trial speed and grade, values were different for the 35 kg backpack and NP condition for breathing frequency (27±4 vs. 22±4 bpm; P<0.01), EELV(25±3 vs. 32± 3 % FVC; P<0.01) and tidal volume (2.0±0.3 vs. 2.5±0.5 l; P<0.01), but were similar for WOB (481±200 vs. 407±116 J·min-1; P>0.05). CONCLUSION: Wearing a weighted backpack alters lung mechanics and the breathing strategy employed during mild to moderate exercise in a normoxic environment; without changing the specific WOB. Funding: The Natural Science and Engineering Research Council of Canada

Regional chest wall volume changes during various breathing maneuvers in normal men.

The purpose of this study is to investigate the regional chest wall volume changes during various breathing maneuvers in normal men with an optical reflectance system (OR), which tracks reflective markers in three dimensions. Chest wall volume was measured by the OR system [VL(CW)], and lung volume was measured by hot wire spirometry [VL(SP)] in 15 healthy men during quiet breathing (QB), during breathing at a rate of 50 tidal breaths/min paced using a metronome (MT: metronome-paced tachypnea), and during a maximal forced inspiratory and expiratory maneuver (MFIE maneuver). There were few discrepancies between VL(CW) and VL(SP) for QB and MT. In the MFIE maneuver, however VL(CW) was often underestimated compared with VL(SP), particularly during forced maximal expiration, because of pulmonary rib cage volume changes. Furthermore, the regional chest wall volume changes were affected by breathing maneuver alternation. In the pulmonary and abdominal rib cage, inspiratory reserve volume was larger than expiratory reserve volume, respectively, and in the abdomen, expiratory reserve volume was larger than inspiratory reserve volume. Alternation of breathing maneuvers affects regional chest wall volume changes.

P26 Home serial spirometry as an adjunct in the diagnosis of vocal cord dysfunction

IntroductionThe diagnosis of vocal cord dysfunction (VCD) is often difficult. Visualisation of the vocal cords using laryngoscopy is the current gold standard method of diagnosis, but may not be diagnostic...

P124 Neuroventilatory uncoupling during cycle and treadmill exercise in COPD

BackgroundIt is widely accepted that neuroventilatory uncoupling drives breathlessness in COPD. COPD patients are more likely to stop exercising because of breathlessness during treadmill exercise than whilst cycling.AimTo test the...