End-expiratory Volume Research Articles

Effect on breathing of raising end-expiratory lung volume in sleeping laryngectomized man

In animals, tonic vagal activity from lung receptors provides a means by which changes in end-expiratory lung volume can influence respiratory timing. We wished to examine whether increasing the end-expiratory lung volume within the tidal volume range had a similar effect in man. In order to minimize behavioral influences on breathing, the study was performed in subjects during deep non-rapid eye movement sleep. Five laryngectomized subjects were chosen for the study since their permanent tracheal stomata allow simple, airtight connection to respiratory apparatus and avoided problems with glottic closure. During EEG-documented sleep, end-expiratory volume was increased by up to 350 ml with the addition of expiratory threshold loads of 1 to 10 cm H 2O. End-expiratory volume increased linearly with expiratory pressure. Inspiratory and expiratory times (T I and T E) were not affected by increases in end-expiratory volume. Tidal volume (V T) was decreased such that end-inspiratory volume remained unchanged. The decrease in V T may result from a reduction in inspiratory muscle efficiency at a higher lung volume. The results of the study provide no evidence that tonic vagal afferent information from the lungs is important in controlling respiratory rhythm within the tidal volume range in man when behavioral control of breathing is minimized.

Chest wall motion and expiratory muscle use during phonation in normal humans

The pattern of rib cage (RC) and abdomen (AB) motion and the electromyograms of the triangularis sterni (TS) and abdominal external oblique (EO) muscles were studied during speech and reading in six normal uninformed subjects in the sitting posture. Most phrases were started from within the tidal breathing range and extended below RC and AB spontaneous end-expiratory volumes. On the average, 75% of the change in chest wall volume occurred below the resting end-expiratory level. The expired volume resulted from a large predominance of RC displacement, and this was accompanied by marked recruitment of the TS. The EO was also generally activated, but the pattern of activation was less consistent. We conclude that 1) speech occurs primarily below the spontaneous end-expiratory level; 2) most of the volume change is caused by active emptying of the RC produced, at least in part, by contraction of the TS; 3) concomitant activation of the abdominal muscles serves to optimize the inspiratory function of the diaphragm, which has to contract rapidly between phrases to refill the respiratory system.

Mechanical effects of PEEP in patients with adult respiratory distress syndrome

In 10 patients with adult respiratory distress syndrome, we studied the effects on respiratory system mechanics of two levels of positive end-expiratory pressure (PEEP), best PEEP (BP) and half of this value (HBP), using a respiratory inductive plethysmograph (RIP) combined with a super syringe. We found the following. 1) Inflation compliance of pressure-volume (PV) curves did not change significantly. 2) End-expiratory volume increased with HBP and further with BP (278 +/- 186 and 464 +/- 313 ml, respectively, P less than 0.01). This increase was positively correlated with inflation compliance for HBP and BP (r = 0.794, P less than 0.01 and r = 0.876, P less than 0.01, respectively). 3) No dynamic hyper-inflation was detected on mechanical ventilation at zero end-expiratory pressure (ZEEP), and the time constant of the respiratory system was in the normal range (0.79 +/- 0.21 s). 4) Hysteresis of PVrip curves, which were corrected for gas exchange, decreased significantly with PEEP (P less than 0.05). We conclude that PEEP does not change inflation PV curve but induces an increase in intrathoracic volume whose magnitude is related to compliance and PEEP level. The reduction of hysteresis with PEEP suggests less gas trapping and thus a functional improvement.

Pulmonary Effects due to Subchronic Exposure to Oil Fog

Male and in some cases female rats were exposed to an oil fog generated by flash vaporization and subsequent condensation of light-weight lubricating oil. Exposures were for 3.5 h/d, 4d/wk for 13 wk. Males were exposed at concentrations of 1.5, 0.5, 0.2 or 0.0 mg/l (1500, 500, 200, and 0 mg/m3) and a particle size of approximately 1 micron (mass median aerodynamic diameter). A number of biologic endpoints were assessed the day after the last exposure and, in some cases, after a 4 wk recovery period. Effects of 1.5 mg/l on male and female rats were compared. Diffuse accumulation of macrophages in the alveoli was observed in all oil fog exposed groups. The degree of severity was concentration dependent. Histopathologic changes were more prominent in males than in females and represented the most notable gender-related differences. Histologic effects observed one day and 4 wk post exposure were similar. Minimal histopathologic changes and minimal increase in lavage fluid protein were the only effects observed at the 0.2 mg/l exposure level. There was a significant increase in lavage fluid protein, percent lavagable polymorphonuclear leukocytes and lung wet and dry weight following exposure to both 0.5 and 1.5 mg/l. At the highest exposure concentration effects on lung weights were still evident 4 wk post exposure. Pulmonary function endpoints including total lung capacity, vital capacity, residual volume, diffusing capacity to CO, compliance, and end expiratory volume (EEV) were unaffected by oil fog exposure with the exception of EEV in males exposed at the 1.5 mg/l level. All of the changes observed following oil fog exposure were consistent with a mild inflammatory edema.

Transition from dynamically maintained to relaxed end-expiratory volume in human infants.

Newborn infants, in contrast to adults, dynamically maintain end-expiratory lung volume (EEV) above relaxation volume. The purpose of this study was to determine at what age children develop a breathing strategy that is relaxed, i.e., determined by the mechanical characteristics of the lung and chest wall. Forty studies were performed in 27 healthy infants and children aged 1 mo to 8 yr during natural sleep. Volume changes were recorded with the use of respiratory inductance plethysmography (RIP). The volume signal was differentiated to yield flow. Flow-volume representations were generated for a random sample of the recorded breaths to determine the predominant breathing strategy utilized, i.e., relaxed, interrupted, or indeterminate. The respiratory pattern was predominantly interrupted below 6 mo of age and predominantly relaxed over 1 yr of age. Mixed patterns were observed in children 6-12 mo of age. The number of breaths that could not be classified (indeterminate) decreased with age. Respiratory frequency measured from the sample of breaths decreased with age and was accompanied by an increase in expiratory time. We conclude that a relaxed EEV develops at the end of the first year of life and may be related to changes in the mechanical properties of the chest wall associated with growth as well as changes in respiratory timing.

Effects of continuous positive- and negative-pressure breathing on the pattern of breathing in man during exercise.

Breathing pattern and static lung volumes were studied in 10 subjects at rest and during incremental-load cycle ergometry under three different conditions, viz. with normal pressure in the airways (control) and during continuous positive- and negative-pressure breathing (CPPB, CNPB) of +15 and -15 cmH2O. End-expiratory, end-inspiratory and mid-expiratory volumes were increased by CPPB and decreased by CNPB; these effects were especially pronounced at rest and during mild exercise. Both at rest and during exercise mean inspiratory flow (VT/TI) was exaggerated by CPPB and attenuated by CNPB. At rest these changes were due mainly to concomitant changes in tidal volume (VT) which was increased by CPPB and decreased by CNPB, while inspiratory time duration (TI) was relatively unaffected by pressure breathing. The transition from rest to loadless pedalling induced an increase in VT but no change in TI in the control condition, whereas in the CPPB and CNPB conditions TI decreased and VT remained unaltered. This CPPB- and CNPB-induced change in the volume-time threshold relationship at the onset of pedalling is attributed to increased stretch receptor activity in the extrathoracic portion of the trachea as a result of the increments in transmural pressure. During the course of exercise there was an inverse relationship between the slope of the VT-TI curve and the mid-expiratory volume in that the slope was greater in the control than in the CPPB condition and greatest during CNPB, suggesting that in exercise hyperpnoea the VT-TI relationship is also determined by pulmonary and/or thoracic wall stretch receptors capable of sensing the absolute lung volume.

Determination of Auto-PEEP During Spontaneous and Controlled Ventilation by Monitoring Changes in End-Expiratory Thoracic Gas Volume

Auto-PEEP, or PEEPi, occurs when alveolar pressure fails to decrease to zero at the end of exhalation. While PEEPi can be measured in paralyzed or apneic patients by occlusion of the ventilator expiratory valve at end-exhalation (PEEPi-OC), this may not be possible in patients with spontaneous respiratory efforts. When adjusting the ventilator PEEP valve, FRC increases only after PEEPi has been exceeded. In both mechanically ventilated and spontaneously breathing patients, changes in FRC are mirrored by changes in end-expiratory TGV as measured with RIP set in the DC mode. We compared PEEPi as measured by RIP to PEEPi-OC in 20 patients receiving mechanical ventilator support. Noninvasive measurement of changes in end-expiratory TGV by RIP is a convenient alternative method to estimate PEEPi in both controlled, assisted, and spontaneously ventilating patients.

INFLUENCE OF END-EXPIRATORY LUNG VOLUME ON CARBON DIOXIDE ELIMINATION DURING HIGH FREQUENCY VENTILATION IN DOGS

We have examined the effect of varying end-expiratory lung volume on carbon dioxide elimination in 10 mongrel dogs undergoing conventional mechanical ventilation at 12 b.p.m. and forced diffusion ventilation (FDV) at 6 Hz and 50 Hz and continuous flow. End-expiratory volumes were altered by changing the pressure in a plethysmographic box in which the dogs underwent ventilation. The pressures studied were atmospheric, sub-atmospheric (box pressure -1.0 kPa) and increased atmospheric (box pressure + 0.5 kPa). The results indicated that more carbon dioxide was eliminated at low lung volumes and this was most pronounced with HFV at 50 Hz and continuous flow. It is postulated that changes in airway geometry and different lung volumes may alter the distance between the gas interface in the conductive airways and the respiratory zone and so alter the efficiency of ventilation during FDV.

Thyroarytenoid muscle activity during wakefulness and sleep in normal adults.

To determine the respiratory-related activity of the thyroarytenoid (TA) muscle in normal adults, intramuscular electromyographic recordings were performed in eight normal adult males during wakefulness and sleep. Phasic expiratory TA activity was present during normal tidal breathing in all subjects during wakefulness. Tonic activity was frequently present during inspiration. After an initial rapid rise in activity near the onset of expiration, phasic TA activity generally exhibited one of three different discharge patterns: a plateau, a progressive increase, or, less commonly, a progressive decrease in activity. In four of five subjects examined, peak TA activity during quiet breathing in wakefulness appeared to be directly related to time of expiration. At a particular lung volume above end-expiratory volume during wakefulness, measurements of expiratory resistance were directly related to the level of TA activity. TA activity disappeared during stable periods of non-rapid-eye-movement sleep and exhibited paroxysmal bursts of activity during rapid-eye-movement sleep. The results during wakefulness indicate that the TA contributes to an active adduction of the vocal cords in expiration and suggest the presence of an active laryngeal braking mechanism during exhalation.

Effects of Posture on Stimulated Ventilation in Quadriplegia

Quadriplegics are able to compensate for alterations of operational length of the diaphragm by reflexly increasing neural drive to the diaphragm. This increase in neural drive is adequate to maintain required tidal volume and minute ventilation during quiet breathing in these patients with limited inspiratory muscle function. It is not known, however, if this neural compensation is sufficient to preserve ventilation when the diaphragm is stressed by simultaneously changing its operational length and increasing ventilatory demands. This issue was explored in 7 quadriplegics whose vital capacity was reduced to 15 to 53% of predicted. The diaphragm was stressed by shortening its length from the supine to a 60 degree tilted position, and also by inducing hyperventilation by having the subjects rebreathe 7% CO2. Response to this stress was recorded by monitoring the ventilatory response to rebreathing CO2 (delta VE/delta PCO2), and also by measuring mouth pressure 0.1 s after occluding the airway at the start of inspiration during CO2 rebreathing (delta P0.1/delta PCO2). A change from the supine to the tilted position caused an increase in resting end-expiratory volume of 0.8 +/- 0.2 L (SD) and therefore shortened the diaphragm. Despite this shortening of diaphragm length and the stress of CO2 rebreathing, there was no significant change in delta VE/delta PCO2 and delta P0.1/delta PCO2 with changes in posture. The delta VE/delta PCO2 was 0.82 +/- 0.42 L/min/mm Hg supine versus 0.95 +/- 0.65 L/min/mm Hg when tilted. The delta P0.1/delta PCO2 was 0.18 +/- 0.08 cm H2O/mm Hg supine versus 0.20 +/- 0.10 cm H2O/mm Hg tilted.(ABSTRACT TRUNCATED AT 250 WORDS)

Inspiratory muscles during exercise: a problem of supply and demand.

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Assisted ventilation using cuirass respirators

The effects of cuirass-assisted ventilation have been studied in 25 subjects with chest wall disease. Cuirass respirators increase ventilation in proportion to the peak negative pressure within the cuirass shell and the respiratory rate. Positive pressure applied during expiration produces little additional ventilation. During cuirass-assisted ventilation end-expiratory volume increases, arterial carbon dioxide tension (PaCO2) falls and arterial oxygen tension (PaO2) rises. Cardiac output is unchanged. Paradoxical chest wall motion is corrected by cuirass-assisted ventilation and restriction of chest wall expansion by the cuirass shell is minimal. Jacket-type respirators can produce larger tidal volumes than the cuirass at the same peak negative pressure, but are associated with greater air leakage.

Breathing strategy of the adult horse (Equus caballus) at rest.

To investigate the mechanism underlying the polyphasic airflow pattern of the equine species, we recorded airflow, tidal volum, rib cage and abdominal motion, and the sequence of activation of the diaphragm, intercostal, and abdominal muscles during quiet breathing in nine adult horses standing at rest. In addition, esophageal, abdominal, and transdiaphragmatic pressures were simultaneously recorded using balloon-tipped catheters. Analysis of tidal flow-volume loops showed that, unlike humans, the horse at rest breathes around, rather than from, the relaxed volume of the respiratory system (Vrx). Analysis of the pattern of electromyographic activities and changes in generated pressures during the breathing cycle indicate that the first part of expiration is passive, as in humans, with deflation toward Vrx, but subsequent abdominal activity is responsible for a second phase of expiration: active deflation to below Vrx. From this end-expiratory volume, passive inflation occurs toward Vrx, followed by a second phase of inspiration: active inflation to above Vrx, brought about by inspiratory muscle contraction. Under these conditions the abdominal muscles appear to share the principal pumping duties with the diaphragm. Adoption of this breathing strategy by the horse may relate to its peculiar thoracoabdominal anatomic arrangement and to its very low passive chest wall compliance. We conclude that there is a passive and active phase to both inspiration and expiration due to the coordinated action of the respiratory pump muscles responsible for the resting adult horse's biphasic inspiratory and expiratory airflow pattern. This unique breathing pattern perhaps represents a strategy of minimizing the high elastic work of breathing in this species, at least at resting breathing frequencies.

Effects of high-frequency jet ventilation on arterial baroreflex regulation of heart rate.

Fifteen anesthetized mechanically ventilated patients recovering from multiple trauma were studied to compare the effects of high-frequency jet ventilation (HFJV) and continuous positive-pressure ventilation (CPPV) on arterial baroreflex regulation of heart rate. Systolic arterial pressure and right atrial pressure were measured using indwelling catheters. Electrocardiogram (ECG) and mean airway pressure were continuously monitored. Lung volumes were measured using two linear differential transformers mounted on thoracic and abdominal belts. Baroreflex testing was performed by sequential intravenous bolus injections of phenylephrine (200 micrograms) and nitroglycerin (200 micrograms) to raise or lower systolic arterial pressure by 20-30 Torr. Baroreflex regulation of heart rate was expressed as the slope of the regression line between R-R interval of the ECG and systolic arterial pressure. In each mode of ventilation the ventilatory settings were chosen to control mean airway pressure and arterial PCO2 (PaCO2). In HFJV a tidal volume of 159 +/- 61 ml was administered at a frequency of 320 +/- 104 breaths/min, whereas in CPPV a tidal volume of 702 +/- 201 ml was administered at a frequency of 13 +/- 2 breaths/min. Control values of systolic arterial pressure, R-R interval, mean pulmonary volume above apneic functional residual capacity, end-expiratory pulmonary volume, right atrial pressure, mean airway pressure, PaCO2, pH, PaO2, and temperature before injection of phenylephrine or nitroglycerin were comparable in HFJV and CPPV. Baroreflex regulation of heart rate after nitroglycerin injection was significantly higher in HFJV (4.1 +/- 2.8 ms/Torr) than in CPPV (1.96 +/- 1.23 ms/Torr).(ABSTRACT TRUNCATED AT 250 WORDS)

Analytic Reviews : Hemodynamic Management of the Adult Respiratory Distress Syndrome

Hemodynamic management is an essential aspect of the care of patients with adult respiratory distress syn drome (ARDS). On the basis of current knowledge, our proposed goals of management are to maximize pe ripheral oxygen delivery while attempting to minimize further lung damage or dysfunction. The major patho physiologic abnormalities of ARDS are an increased lung vascular permeability, right-to-left intrapulmonary shunting, and pulmonary vascular resistance. These abnormalities must be understood to select the proper therapy. Although all patients with ARDS share these abnormalities, they differ in their associated clinical conditions and underlying cardiovascular status. Be cause each ARDS patient may respond differently to therapy, hemodynamic management must be selected empirically with the goal of therapy as a guide. We have considered available therapeutic options including posi tive end-expiratory pressure, volume depletion, volume expansion, vasopressors, and vasodilators. In the future hemodynamic management of patients with ARDS will likely change as better methods of patient assessment and treatment are developed.

Evaluating the toxicity of urban patterns of oxidant gases. II. Effects in mice from chronic exposure to nitrogen dioxide.

The study reported herein evaluates the influence of a chronic exposure to an urban pattern of NO2 (continuous baseline exposure of 0.2 ppm, on which were superimposed two 1-h spikes of 0.8 ppm NO2, 5 d/wk) as compared to the baseline exposure to determine the contribution of the spikes to toxicity. Mice were exposed for up to 52 wk with interim examinations. Multivariate analysis of variance revealed a statistically significant treatment effect on infectivity (p = 0.05) and pulmonary function (p = 0.03) parameters. Infectivity mortality of mice in the spiked exposure regimen was significantly greater than that in either the NO2-background-exposed mice or in control mice. Four of the pulmonary function variables exhibited the greatest differences among the treatment groups: end expiratory volume, vital capacity, respiratory-system compliance, and multiple-breath nitrogen washout. Results from the pulmonary-function analyses indicate that the spiked exposures to 0.8 ppm NO2 may have induced a subtle lesion. The chronic study results indicate that the presence of spikes of NO2 is contributing significantly to effects on antibacterial lung defenses and pulmonary function of mice.

Pulmonary effects due to short-term exposure to oil fog.

Rats were exposed to an oil fog generated by flash vaporation and subsequent condensation of lightweight lubricating oil. Exposures were for 3.5 h/d, 4 d/wk, for 4 wk, at concentrations of 1.5, 0.5, or 0.0 mg/l and a particle size of approximately 1 micron. Samples of respiratory tissues were taken for histopathologic analyses, lavage fluid samples were collected, and pulmonary function measurements were made the day after the last exposure. An accumulation of macrophages within the alveolar lumen, an increase in lavage fluid protein content, and an increase in total cell content in lavage fluid due to an influx of polymorphonuclear leukocytes was noted in rats exposed at the 1.5-mg level. Also, for this exposure group there was an increase in lung wet and dry weight and an increase in end-expiratory volume, and pneumonitis was observed histopathologically in 4 of 10 male rats exposed. Pneumonitis was not observed among six female rats examined. Oil fog had no effect on total lung capacity, residual volume, vital capacity, lung compliance, or the distribution of ventilated air within the lung. Effects following exposure to 0.5 mg/l were limited to slight accumulation of macrophages in the alveolar lumen and an increase in the total cells in lavage fluid, which could not be attributed to an increase in any particular cell type.

Left ventricular external constraint: relationship between pericardial, pleural and esophageal pressures during positive end-expiratory pressure and volume loading in dogs.

Left ventricular (LV) diastolic filling is limited by the constraining effects exerted by the pericardium (PE) and the lung/chest wall. The aim of the present study was to assess the validity of various estimates of external cardiac constraint, compared to pericardial surface pressure (Ppe) measured lateral to the LV myocardium. In nine anesthetized dogs we measured Ppe, pleural surface pressure (Ppt) (lateral to the pericardium) and esophageal pressure (Pes) under conditions of volume loading and positive end-expiratory pressure (PEEP). We measured Ppe and Ppl with flat, liquid-containing silastic rubber balloons and Pes with an air-containing cylindrical balloon. After instrumentation, the chest was resealed and continuous suction (-5 mm Hg, 1 mm Hg = 0.133 kPa) was maintained. Volume loading with incremental intravenous infusions of saline was used to increase LV end-diastolic pressure to 20-25 mm Hg. PEEP of 0, 10 and 20 mm Hg were applied at baseline and after each increment of volume loading. At low volume, increases in PEEP caused simultaneous increases in LV end-diastolic pressure (P less than 0.01) and in Ppe (P less than 0.0001) but a reduction in transmural LV pressure (P less than 0.0005). Ppl and Pes both increased with PEEP (P less than 0.001 and P less than 0.01, respectively). However, Ppe always exceeded Ppl, while Pes remained at only approximately 1/3 Ppl throughout. Volume loading caused a significant increase in Ppe (P less than 0.0001) and a smaller, but significant increase in Ppl (P less than 0.05). Pes remained unchanged during volume loading. Thus external cardiac constraint increased markedly during volume loading and PEEP as evidenced by a marked elevation of Ppe. Both Ppl and Pes markedly underestimated this increase. Therefore, calculation of transmural LV pressure by subtracting pleural or esophageal pressure from intracavitary pressure can lead to overestimation of LV preload. The decrease in cardiac output during PEEP occurs secondary to decreased preload, i.e. decreased transmural pressure and end-diastolic dimension. Analysis of performance using cardiac function curves does not suggest a change in contractility with PEEP.

Expiratory volume clamping: a new method to assess respiratory mechanics in sedated infants.

During breathing under sedation via a two-way valve, airflow (V), volume (delta V), and airway pressure (P) were recorded in eight normal (N) infants, seven with reversible obstructive airway disease (ROAD), and seven with chronic lung disease (CLD). Intermittently, expiratory volume clamping (EVC) was applied, involving selective occlusion of the expiratory valve for three to five breaths. The latter produced cumulative increases in delta V that, due to progressive recruitment of the Hering-Breuer reflex, were accompanied by increasing expiratory plateaus in P (i.e., apneas). The resultant passive inflation delta V-P relationships were closely approximated by the expression: delta V = aP2 + bP + c, wherein a represented the pressure-related changes in chord compliance (Crs), b the Crs at P = 0, and c the difference between the dynamic end-expiratory and relaxation volumes of the respiratory system. Relative to N, the ROAD and CLD infants had significantly reduced weight-specific values of a/kg, their b/kg values were increased, whereas the c/kg measurements did not significantly vary. Moreover, for each subject we determined the net Crs/kg obtaining at P = 20 cmH2O (i.e., Crs20/kg), an estimate of the net deflation compliance; the passive respiratory time constant (tau rs) based on the slope of the expired delta V/V relationship; and the respiratory system conductance (Grs/kg). Relative to N, the mean Crs20/kg was significantly reduced only in the infants with CLD and, due to increases in tau rs, both patient groups depicted significantly diminished values of Grs/kg, suggesting the presence of airways obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)