Effect of intravenous midazolam on breathing pattern and chest wall mechanics in human

Breathing pattern, thoracoabdominal motion, and separate end-expiratory positions of the rib cage and abdomen were measured noninvasively in eight healthy subjects before and after intravenous administration of either placebo or midazolam, a short-acting benzodiazepine. Compared with placebo, midazolam produced a significant (P less than 0.01) decrease in mean inspiratory flow of 29% from preinjection values, resulting in a 39% reduction in tidal volume (VT). This ventilatory depression was partly compensated by a 35% decrease in expiratory time producing an increase in respiratory rate (+39%). The fall in VT was almost entirely (91%) mediated by a reduction of the abdominal contribution to tidal breathing while sparing rib cage motion. This fact contrasts with the effects of inhalational anesthetics or morphine, which preferentially depress rib cage expansion, indicating that thoracoabdominal motion may selectively be depressed by different pharmacological agents. In addition, continuous recording of end-expiratory levels showed a significant transient fall in the rib cage's end-tidal position 2 min after midazolam administration associated with the occurrence of central apneas.     

Effect of changes in lung volume on respiratory system compliance in newborn infants

Total respiratory system compliance (Crs) at volumes above the tidal volume (VT) was studied by use of the expiratory volume clamping (EVC) technique in 10 healthy sleeping unsedated newborn infants. Flow was measured with a pneumotachograph attached to a face mask and integrated to yield volume. Volume changes were confirmed by respiratory inductance plethysmography. Crs measured by EVC was compared with Crs during tidal breathing determined by the passive flow-volume (PFV) technique. Volume increases of approximately 75% VT were achieved with three to eight inspiratory efforts during expiratory occlusions. Crs above VT was consistently greater than during tidal breathing (P less than 0.0005). This increase in Crs likely reflects recruitment of lung units that are closed or atelectatic in the VT range. Within the VT range, Crs measured by PFV was compared with that obtained by the multiple-occlusion method (MO). PFV yielded greater values of Crs than MO (P less than 0.01). This may be due to braking of expiratory airflow after the release of an occlusion or nonlinearity of Crs. Thus both volume recruitment and airflow retardation may affect the measurement of Crs in unsedated newborn infants.     

Effects of changes in CO2 partial pressure on the sensation of respiratory drive

The purpose of this study was to determine whether a change in respiratory sensation accompanies an increase in CO2 partial pressure (PCO2) in the absence of any changes in the level and pattern of thoracic displacement and respiratory muscle force. Eleven normal subjects were artificially hyperventilated with a positive-pressure mechanical respirator. In separate trials the tidal volume (VT) was set at 10 and 18 ml/kg and the frequency of ventilation (f) was adjusted to maintain the base-line end-tidal PCO2 at approximately 30 Torr. Thereafter, at a constant controlled VT and f, the PCO2 was progressively increased by raising the inspired CO2 concentration. There were no changes in respiratory motor activity as determined from the peak inspiratory airway pressure (Paw) until the PCO2 reached 40.8 +/- 1.0 and 40.1 +/- 1.0 (SE) Torr in the large and small VT trials, respectively. Initially there was no conscious awareness of the change in respiratory activity. Subjects first signaled that ventilatory needs were not being satisfied only after a further increase in PCO2 to 44.7 +/- 1.3 and 42.3 +/- 1.0 (SE) Torr in the large and small VT trials and after the Paw had fallen to 55-60% of the base-line value. The results suggest that changes in respiratory sensation produced by increasing chemical drive are a consequence of increases in respiratory efferent activity, but a direct effect of changes in PCO2 on respiratory sensation cannot be excluded.     

Inductance plethysmography measurement of CPAP-induced changes in end-expiratory lung volume

The respiratory inductance plethysmograph (RIP) has recently gained popularity in both the research and clinical arenas for measuring tidal volume (VT) and changes in functional residual capacity (delta FRC). It is important however, to define the likelihood that individual RIP measurements of VT and delta FRC would be acceptably accurate (+/- 10%) for clinical and investigational purposes in spontaneously breathing individuals on continuous positive airway pressure (CPAP). Additionally, RIP accuracy has not been compared in these regards after calibration by two commonly employed techniques, the least squares (LSQ) and the quantitative diagnostic calibration (QDC) methods. We compared RIP with pneumotachographic (PTH) measurements of delta FRC and VT during spontaneous mouth breathing on 0-10 cmH2O CPAP. Comparisons were made after RIP calibration with both the LSQ (6 subjects) and QDC (7 subjects) methods. Measurements of delta FRC by RIPLSQ and RIPQDC were highly correlated with PTH measurements (r = 0.94 +/- 0.04 and r = 0.98 +/- 0.01 (SE), respectively). However, only an average of 30% of RIPQDC determinations per subject and 31.4% of RIPLSQ determinations per subject were accurate to +/- 10% of PTH values. An average of 55.2% (QDC) and 68.8% (LSQ) of VT determinations per subject were accurate to +/- 10% of PTH values. We conclude that in normal subjects, over a large number of determinations, RIP values for delta FRC and VT at elevated end-expiratory lung volume correlate well with PTH values. However, regardless of whether QDC or LSQ calibration is used, only about one-third of individual RIP determinations of delta FRC and one-half of two-thirds of VT measurements will be sufficiently accurate for clinical and investigational use.     

Enkephalin-induced changes in ventilation and ventilatory pattern in adult dogs

We studied the changes in ventilation induced by intracisternal administration of enkephalins in four unanesthetized adult dogs. Instantaneous minute ventilation (VT/TT) decreased markedly after D-Ala-Met-enkephalinamide (DAME). Mean VT/TT decreased maximally by 20-50 min after DAME and lasted an additional 15-60 min; by 2 h, VT/TT had returned to base line. Four doses (5, 25, 60, and 125 micrograms/kg) of DAME were used, and the ventilatory response depended on the dose. Mean inspiratory time decreased but mean expiratory time and mean TT showed a marked prolongation. Periodic breathing (2-3 breaths separated by long apneic pauses) occurred in every study and the frequency of sighs increased considerably. All these ventilatory changes were reversed by low doses of naloxone or naltrexone; in addition, VT/TT increased well above base line after the administration of these antagonists. However, naloxone did not increase VT/TT when injected without prior administration of DAME. We conclude that 1) the decrease in VT/TT is due to a decrease in respiratory duty cycle; 2) periodic breathing and increased frequency of sighs constitute part of the changes in the ventilatory pattern induced by DAME; 3) a ventilatory withdrawal reaction may occur after a receptor-agonist interaction of short duration; and 4) although enkephalins can modulate ventilation and the breathing pattern in a major way, these data provide no evidence suggesting that this modulation is tonic.     

Ventilatory response to fatiguing and nonfatiguing resistive loads in awake sheep

To study the changes in ventilation induced by inspiratory flow-resistive (IFR) loads, we applied moderate and severe IFR loads in chronically instrumented and awake sheep. We measured inspired minute ventilation (VI), ventilatory pattern [inspiratory time (TI), expiratory time (TE), respiratory cycle time (TT), tidal volume (VT), mean inspiratory flow (VT/TI), and respiratory duty cycle (TI/TT)], transdiaphragmatic pressure (Pdi), functional residual capacity (FRC), blood gas tensions, and recorded diaphragmatic electromyogram. With both moderate and severe loads, Pdi, TI, and TI/TT increased, TE, TT, VT, VT/TI, and VI decreased, and hypercapnia ensued. FRC did not change significantly with moderate loads but decreased by 30-40% with severe loads. With severe loads, arterial PCO2 (PaCO2) stabilized at approximately 60 Torr within 10-15 min and rose further to levels exceeding 80 Torr when Pdi dropped. This was associated with a lengthening in TE and a decrease in breathing frequency, VI, and TI/TT. We conclude that 1) timing and volume responses to IFR loads are not sufficient to prevent alveolar hypoventilation, 2) with severe loads the considerable increase in Pdi, TI/TT, and PaCO2 may reduce respiratory muscle endurance, and 3) the changes in ventilation associated with neuromuscular fatigue occur after the drop in Pdi. We believe that these ventilatory changes are dictated by the mechanical capability of the respiratory muscles or induced by a decrease in central neural output to these muscles or both.     

Ventilation heterogeneity in excised lobes: effect of tidal volume.

Although several factors are known to influence nonuniformity of ventilation, including lung mechanical properties (regional structure and compliance), external factors (chest wall, pleural pressure, heart), and ventilatory parameters (tidal and preinspiratory volume, flow rate), their relative contributions are poorly understood. We studied five excised, unperfused, canine right-middle lobes under varied levels of tidal volume (VT), thus eliminating many factors affecting heterogeneity. Multiple-breath washouts of N(2) were analyzed for anatomic dead space volume (VD(anat)), nonuniformity of N(2) washout, and nonuniformity between joined acinar regions vs. that occurring between larger joined regions. Approximately 80% of ventilation heterogeneity was found among joined acinar regions at resting levels of VT, but increasing VT reduced intra-acinar heterogeneity to about 25% of that found at resting levels. Increasing VT had essentially no effect on VD(anat) and heterogeneity among larger joined regions. The results indicate that the magnitude of VT is a major influence on the dominant intra-acinar component of ventilation heterogeneity and that VT effects on VD(anat) are likely due to perfusion and/or influences normally external to the lobar structure.     

Carbon dioxide effects on the ventilatory response to sustained hypoxia

We examined the interrelation between CO2 and the ventilatory response to moderate (80% arterial saturation) sustained hypoxia in normal young adults. On a background of continuous CO2-stimulated hyperventilation, hypoxia was introduced and sustained for 25 min. Initially, with the introduction of hypoxia onto hypercapnia, there was a brisk additional increase in inspiratory minute ventilation (VI) to 284% of resting VI, but the response was not sustained and hypoxic VI declined by 36% to a level intermediate between the initial increase and the preexisting hypercapnic hyperventilation. Through the continuous hypercapnia, the changes in hypoxic ventilation resulted from significant alterations in tidal volume (VT) and mean inspiratory flow (VT/TI) without changes in respiratory timing. In another experiment, sustained hypoxia was introduced on the usual background of room air, either with isocapnia or without maintenance of end-tidal CO2 (ETCO2) (poikilocapnic hypoxia). Regardless of the degree of maintenance of ETCO2, during 25 min of sustained hypoxia, VI showed an initial brisk increase and then declined by 35-40% of resting VI to a level intermediate between the initial response and resting room air VI. For both isocapnia and poikilocapnic conditions, the attenuation of VI was an expression of a diminished VT. Thus the decline in ventilation with sustained hypoxia occurred regardless of the background ETCO2, suggesting that the mechanism underlying the hypoxic decline is independent of CO2.     

Beta-blockade reduces tidal volume during heavy exercise in trained and untrained men

The effects of beta-blockade on tidal volume (VT), breath cycle timing, and respiratory drive were evaluated in 14 endurance-trained [maximum O2 uptake (VO2max) approximately 65 ml X kg-1 X min-1] and 14 untrained (VO2max approximately 50 ml X kg-1 X min-1) male subjects at 45, 60, and 75% of unblocked VO2max and at VO2max. Propranolol (PROP, 80 mg twice daily), atenolol (ATEN, 100 mg once a day) and placebo (PLAC) were administered in a randomized double-blind design. In both subject groups both drugs attenuated the increases in VT associated with increasing work rate. CO2 production (VCO2) was not changed by either drug during submaximal exercise but was reduced in both subject groups by both drugs during maximal exercise. The relationship between minute ventilation (VE) and VCO2 was unaltered by either drug in both subject groups due to increases in breathing frequency. In trained subjects VT was reduced during maximal exercise from 2.58 l/breath on PLAC to 2.21 l/breath on PROP and to 2.44 l/breath on ATEN. In untrained subjects VT at maximal exercise was reduced from 2.30 l/breath on PLAC to 1.99 on PROP and 2.12 on ATEN. These observations indicate that 1) since VE vs. VCO2 was not altered by beta-adrenergic blockade, the changes in VT and f did not result from a general blunting of the ventilatory response to exercise during beta-adrenergic blockade; and 2) blockade of beta 1- and beta 2-receptors with PROP caused larger reductions in VT compared with blockade of beta 1-receptors only (ATEN), suggesting that beta 2-mediated bronchodilation plays a role in the VT response to heavy exercise.     

Postural effects on measurements of tidal volume from body surface displacements

Tidal volume measurements based on the sum of volume displacements of the rib cage (RC) and abdomen (Ab) are limited in accuracy when changes in posture occur. To elucidate the underlying sources of error, five subjects performed spinal flexion-extension isovolume maneuvers and then performed Konno-Mead isovolume maneuvers at different lung volumes while erect, with the spine fully flexed, and at intermediate degrees of spinal flexion. RC and Ab dimensions were measured with respiratory inductance plethysmograph belts, and spinal flexion was assessed by a pair of magnetometers measuring the xiphi-Ab distance (Xi). RC and Ab volume-motion coefficients (alpha and beta, respectively) were calculated from the slope (-beta/alpha) of the Konno-Mead isovolume lines. We found that 1) spinal flexion with constant lung volume mainly increases the RC dimension, thereby displacing the Konno-Mead isovolume lines, and 2) spinal flexion decreases the -beta/alpha by decreasing beta. The error related to displacement averaged 28.4 +/- 15% of vital capacity, whereas the error related to changes in beta averaged 14 +/- 6% (SD). The systematic relationship of these errors with the degree of spinal flexion provides a mechanism whereby the addition of Xi to RC and Ab displacements significantly (P less than 0.001) improves volume estimates.     

Airway obstruction during periodic breathing in premature infants

To characterize changes in pulmonary resistance, timing, and respiratory drive during periodic breathing, we studied 10 healthy preterm infants (body wt 1,340 +/- 240 g, postconceptional age 35 +/- 2 wk). Periodic breathing in these infants was defined by characteristic cycles of ventilation with intervening respiratory pauses greater than or equal to 2 s. Nasal airflow was recorded with a pneumotachometer, and esophageal or pharyngeal pressure was recorded with a fluid-filled catheter. Pulmonary resistance at half-maximal tidal volume, inspiratory time (TI), expiratory time (TE), and mean inspiratory flow (VT/TI) were derived from computer analysis of five cycles of periodic breathing per infant. In 80% of infants periodic breathing was accompanied by completely obstructed breaths at the onset of ventilatory cycles; the site of airway obstruction occurred within the pharynx. The first one-third of the ventilatory phase of each cycle was accompanied by the highest airway resistance of the entire cycle (168 +/- 98 cmH2O.l-1.s). In all infants TI was greatest at the onset of the ventilatory cycle, VT/TI was maximal at the midpoint of the cycle, and TE was longest in the latter two-thirds of each cycle. A characteristic increase and subsequent decrease of 4.5 +/- 1.9 ml in end-expiratory volume also occurred within each cycle. These results demonstrate that partial or complete airway obstruction occurs during periodic breathing. Both apnea and periodic breathing share the element of upper airway instability common to premature infants.     

Driving and timing components of the breathing pattern during hypoxia in anaesthetized cats

The effects of acute hypoxic hypoxia elicited by N2 inhalation on the driving and timing components of the breathing pattern were studied in 18 adult anaesthetized cats. Two phases could be distinguished in the ventilatory response to acute hypoxia. During the first phase, mean inspiratory flow (VT/TI) increased exponentially up to 240% of the initial value. During the second phase, VT/TI gradually decreased, reaching the control values in the last preapnoeic breaths during the first exposure and remained higher than normal with earlier respiratory arrest in three repeated N2 inhalations. No significant changes could be observed in the timing component of breathing pattern (TI/TT) in the course of the first hypoxic exposure, and the changes in TI/TT did not exceed 7% in repeated attacks. This suggests that the shortening of both inspiratory and expiratory durations increased the breathing frequency up to 130% of its resting value. Moreover, tachypnoea was preserved until respiratory arrest. Accordingly, it is concluded that the decrease in ventilation with the appearance of apnoea during the second phase of N2 inhalation in anaesthetized cats is not due to a failure of respiratory timing, but to a depression of the driving mechanisms which are responsible for this phenomenon.     

Mild obesity does not limit change in end-expiratory lung volume during cycling in young women.

To investigate the effects of obesity on the regulation of end-expiratory lung volume (EELV) during exercise we studied nine obese (41 +/- 6% body fat and 35 +/- 7 yr, mean +/- SD) and eight lean (18 +/- 3% body fat and 34 +/- 4 yr) women. We hypothesized that the simple mass loading of obesity would constrain the decrease in EELV in the supine position and during exercise. All subjects underwent respiratory mechanics measurements in the supine and seated positions, and during graded cycle ergometry to exhaustion. Data were analyzed between groups by independent t-test in the supine and seated postures, and during exercise at ventilatory threshold and peak. Total lung capacity (TLC) was reduced in the obese women (P < 0.05). EELV was significantly lower in the obese subjects in the supine (37 +/- 6 vs. 45 +/- 5% TLC) and seated (45 +/- 6 vs. 53 +/- 5% TLC) positions and at ventilatory threshold (41 +/- 4 vs. 49 +/- 5% TLC) (P < 0.01). In conclusion, despite reduced resting lung volumes and alterations in respiratory mechanics during exercise, mild obesity in women does not appear to constrain EELV during cycling nor does it limit exercise capacity. Also, these data suggest that other nonmechanical factors also regulate the level of EELV during exercise.     

Effect of the mechanical ventilatory cycle on thermodilution right ventricular volumes and cardiac output.

The purpose of this study was to evaluate right ventricular (RV) loading and cardiac output changes, by using the thermodilution technique, during the mechanical ventilatory cycle. Fifteen critically ill patients on mechanical ventilation, with 5 cmH(2)O of positive end-expiratory pressure, mean respiratory frequency of 18 breaths/min, and mean tidal volume of 708 ml, were studied with help of a rapid-response thermistor RV ejection fraction pulmonary artery catheter, allowing 5-ml room-temperature 5% isotonic dextrose thermodilution measurements of cardiac index (CI), stroke volume (SV) index, RV ejection fraction (RVEF), RV end-diastolic volume (RVEDV), and RV end-systolic volume (RVESV) indexes at 10% intervals of the mechanical ventilatory cycle. The ventilatory modulation of CI and RV volumes varied from patient to patient, and the interindividual variability was greater for the latter variables. Within patients also, RV volumes were modulated more by the ventilatory cycle than CI and SV index. Around a mean value of 3.95 +/- 1.18 l. min(-1). m(-2) (= 100%), CI varied from 87.3 +/- 5.2 (minimum) to 114.3 +/- 5.1% (maximum), and RVESV index varied between 61.5 +/- 17.8 and 149.3 +/- 34.1% of mean 55.1 +/- 17.9 ml/m(2) during the ventilatory cycle. The variations in the cycle exceeded the measurement error even though the latter was greater for RVEF and volumes than for CI and SV index. For mean values, there was an inspiratory decrease in RVEF and increase in RVESV, whereas a rise in RVEDV largely prevented a fall in SV index. We conclude that cyclic RV afterloading necessitates multiple thermodilution measurements equally spaced in the ventilatory cycle for reliable assessment of RV performance during mechanical ventilation of patients.     

Cross-validation of ventilatory threshold prediction equations on aerobically trained men and women

The purpose of this investigation was to determine the validity of the non-exercise-based equations of Davis et al. (13), Jones et al. (20), and Neder et al. (30) for estimating the ventilatory threshold (VT) in samples of aerobically trained men and women. One hundred and forty-four aerobically trained men (mean +/- SD age, 41.0 +/- 11.6 years; N = 83) and women (37.1 +/- 9.0 years, N = 61) performed a maximal incremental test to determine VO2max and observed VT on a cycle ergometer. The observed VT was determined by gas exchange measurements using the V-slope method (VCO2/VO2) in conjunction with analyses of the ventilatory equivalents (i.e., minute ventilation VE/VO2 and VE/VCO2) and end-tidal gas tensions (i.e., P(ET)O2 and P(ET)CO2) for oxygen and carbon dioxide. The predicted VT values from 14 equations were compared to the observed VT values by examining the constant error (CE), standard error of estimate (SEE), Pearson correlation coefficient (r), and total error (TE). The results of this investigation indicated that all 14 equations resulted in significant (p < 0.008) CE values ranging from 1.13 to 1.72 L x min(-1) for the men and from 0.58 to 1.12 L x min(-1) for the women. Furthermore, the SEE, r, and TE values ranged from 0.37 to 0.54, from 0.36 to 0.53, and from 0.68 to 1.81 L x min(-1), respectively. The lowest TE values for the men and women represented 45 and 36% of the mean of the observed VT values, respectively. The results of this study indicated that the errors associated with all 14 equations were too large to be of practical value for estimating VT in aerobically trained men and women.     

Influence of anthropometric characteristics on changes in maximal exercise ventilation and breathing pattern during growth in boys.

The aim of this study was to investigate the effect of growth on ventilation and breathing pattern during maximal exercise oxygen consumption (VO2max) and their relationships with anthropometric characteristics. Seventy six untrained schoolboys, aged 10.5-15.5 years, participated in this study. Anthropometric measurements made included body mass, height, armspan, lean body mass, and body surface area. During an incremental exercise test, maximal ventilation (VEmax), tidal volume (VTmax), breathing frequency (fmax), inspiratory and expiratory times (tImax and tEmax), total duration of respiratory cycle (tTOTmax), mean inspiratory flow (VT/tImax), and inspiration fraction (tI/tTOTmax) were measured at VO2max. A power function was calculated between anthropometric characteristics and ventilatory variables to determine the allometric constants. The results showed firstly, that VEmax, VTmax, tImax, tEmax, tTOTmax, and VT/tImax increased with age and anthropometric characteristics (P less than 0.001), fmax decreased (P less than 0.001), and tI/tTOTmax remained constant during growth; secondly that lean body mass explained the greatest percentage of variance of VEmax (62.1%), VTmax (76.8%), and VT/tImax (70.6%), while anthropometric characteristics explained a slight percentage of variance of fmax and timing; and thirdly that VEmax, VTmax, and VT/tImax normalized by lean body mass did not change significantly with age. We concluded that at VO2max there were marked changes in ventilation and breathing pattern with growth. The changes in VEmax, VTmax, and VT/tImax were strongly related to the changes in lean body mass.     

Biomechanics and regulation of external respiration under conditions of five-day dry immersion

The functional state of external respiration and the features of its regulation in healthy persons were studied under conditions of microgravity simulated using dry immersion. The lung volume, the ratio of thoracic and abdominal components during quiet breathing and performing various respiratory maneuvers, as well as the parameters that characterize the regulation of breathing (the duration of breath holding and the ability to voluntarily control respiratory movements), were recorded during the baseline period, on days 2 and 4 of dry immersion, and after the end of the dry immersion. It has been shown that the breathing pattern did not significantly change under conditions of dry immersion compared to the baseline period; however, the inspiratory reserve volume increased (p < 0.05), while the expiratory reserve volume decreased (p < 0.01). Dry immersion did not alter pulmonary ventilation, yet most of the subjects trended toward an increase in the contribution of the abdominal component of breathing movements during quiet breathing and demonstrated a statistically significant increase in this parameter during the lung vital capacity maneuver. The durations of the inspiratory and expiratory maximal breath holding under conditions of immersion did not differ from the background values. During the immersion, the accuracy of voluntary control of breathing increased. We believe that immersion, similar to microgravity, leads to changes in the reserve lung volume, which are partly because of changes in the body position; changes in relative contributions of the thoracic and abdominal components in the breathing movements; and changes in voluntary breath regulation.     

Ventilatory response to sustained hypoxia in normal adults

We examined the ventilatory response to moderate (arterial O2 saturation 80%), sustained, isocapnic hypoxia in 20 young adults. During 25 min of hypoxia, inspiratory minute ventilation (VI) showed an initial brisk increase but then declined to a level intermediate between the initial increase and resting room air VI. The intermediate level of VI was a plateau that did not change significantly when hypoxia was extended up to 1 h. The relation between the amount of initial increase and subsequent decrease in ventilation during constant hypoxia was not random; the magnitude of the eventual decline correlated confidently with the degree of initial hyperventilation. Evaluation of breathing pattern revealed that during constant hypoxia there was little alteration in respiratory timing and that the changes in VI were related to significant alterations in tidal volume and mean inspiratory flow (VT/TI). None of the changes was reproduced during a sham control protocol, in which room air was substituted for the period of low fractional concentration of inspired O2. We conclude that ventilatory response to hypoxia in adults is not sustained; it exhibits some biphasic features similar to the neonatal hypoxic response.     

Quadriceps and Respiratory Muscle Fatigue Following High-Intensity Cycling in COPD Patients

Exercise intolerance in COPD seems to combine abnormal ventilatory mechanics, impaired O₂ transport and skeletal muscle dysfunction. However their relatie contribution and their influence on symptoms reported by patients remain to be clarified. In order to clarify the complex interaction between ventilatory and neuromuscular exercise limiting factors and symptoms, we evaluated respiratory muscles and quadriceps contractile fatigue, dynamic hyperinflation and symptoms induced by exhaustive high-intensity cycling in COPD patients. Fifteen gold II-III COPD patients (age = 67±6 yr; BMI = 26.6±4.2 kg.m^-2) performed constant-load cycling test at 80% of their peak workload until exhaustion (9.3±2.4 min). Before exercise and at exhaustion, potentiated twitch quadriceps strength (Q_tw), transdiaphragmatic (P_di,tw) and gastric (P_ga,tw) pressures were evoked by femoral nerve, cervical and thoracic magnetic stimulation, respectively. Changes in operational lung volumes during exercise were assessed via repetitive inspiratory capacity (IC) measurements. Dyspnoea and leg discomfort were measured on visual analog scale. At exhaustion, Q_tw (-33±15%, >15% reduction observed in all patients but two) and P_di,tw (-20±15%, >15% reduction in 6 patients) were significantly reduced (P<0.05) but not P_ga,tw (-6±10%, >15% reduction in 3 patients). Percentage reduction in Q_tw correlated with the percentage reduction in P_di,tw (r=0.66; P<0.05). Percentage reductions in P_di,tw and P_ga,tw negatively correlated with the reduction in IC at exhaustion (r=-0.56 and r=-0.62, respectively; P<0.05). Neither dyspnea nor leg discomfort correlated with the amount of muscle fatigue. In conclusion, high-intensity exercise induces quadriceps, diaphragm and less frequently abdominal contractile fatigue in this group of COPD patients. In addition, the rise in end-expiratory lung volume and diaphragm flattening associated with dynamic hyperinflation in COPD might limit the development of abdominal and diaphragm muscle fatigue. This study underlines that both respiratory and quadriceps fatigue should be considered to understand the complex interplay of factors leading to exercise intolerance in COPD patients.     

Development of a flexible cardiorespiratory monitor based on induction plethysmography]

Induction plethysmography (IP) utilizes changes in the inductance of sinusoidal wires embedded in elastic bands placed around the chest and abdomen to detect volume changes in the two compartments. These changes can be attributed to respiration or heart beat. To date, most applications have been tailored to an investigation of respiration. More sensitive systems have been employed for the detection of cardiac activity. The wires within the bands, which function as the coil in a resonant circuit, are excited by an oscillator. Among other factors, the inductance of the coil depends on the cross-sectional area of the coie, and changes with respiration in coils placed around the chest and abdomen. Using LabView software, the biosignals obtained undergo an analog-to-digital conversion prior to processing. The system was calibrated using the isovolume method. In 10 adults, IP was tested against a pneumotachograph (PNT) in different body positions (standing, sitting, supine, prone). Correlation between tidal volumes measured with IP and PNT was of r > or = 0.96 on average, recalibration being done after each change in position. The absolute mean error ranged between 3.7 and 8.5%, depending on body position. The smallest error (3.7%) and greatest agreement between the two methods was found in the supine position (93.3% of the IP measurements within +/- 10% of the PNT measurements). An IP application that could be used to collect data over the long term and which is in good agreement with PNT was developed by employing a "virtual instrument" (VI, LabView) for flexible data acquisition and data processing. Agreement was best when the volunteer adopted a supine position. A smaller correlation was found in standing or seated subjects. This might be due to the fact that in the latter two positions, the respiratory system may have more than 2 degrees of freedom, and thus cannot be adequately monitored by only two bands around the thorax and abdomen. Signals produced by cardiac activity were detectable on the surface of the body.