End-inspiratory Lung Volume Research Articles

Sensation of inspiratory difficulty during inspiratory threshold and hyperinflationary loadings. Effect of inspiratory muscle strength.

Dynamic hyperinflation loads the inspiratory muscles by increasing end-expiratory lung volume (EELV) and imposing intrinsic positive end-expiratory pressure (PEEPi), the latter behaving as an inspiratory threshold load (ITL). The aim of the current study was to examine how induced-inspiratory muscle fatigue affects the independent effects of the imposed ITL and increasing operating lung volume on the perceived inspiratory difficulty. Dynamic hyperinflation in healthy subjects was induced by positive end-expiratory pressure (PEEP). Increasing operating lung volume alone (without PEEPi) and increasing ITL alone (without change in EELV) were induced by continuous positive airway pressure (CPAP) and external ITL, respectively. Inspiratory difficulty was quantified by the modified Borg scale and analyzed by step forward multiple regression, using the imposed ITL, EELV, and end-inspiratory lung volume (EILV) as independent variables. When fresh, the first entered variable was the imposed ITL (r(2), 0.38). Adding EILV into the model increased r(2) to 0.67. After fatigue, the first entered variable became EILV (r(2), 0.50) and the second selected variable was the imposed ITL, which increased r(2) to 0.66. EELV was insignificant under both conditions. The coefficient of EILV increased significantly from 0.039 +/- 0.005 to 0.092 +/- 0.012 (% inspiratory capacity(-)(1)) after fatigue run (p < 0.001), whereas that of the imposed ITL did not change. It is concluded that in the experimental conditions studied, inspiratory muscle fatigue increased the importance of lung volume over that of inspiratory threshold load in determining the perceived inspiratory difficulty.

Emerging Concepts in the Evaluation of Ventilatory Limitation During Exercise: The Exercise Tidal Flow-Volume Loop

Traditionally, ventilatory limitation (constraint) during exercise has been determined by measuring the ventilatory reserve or how close the minute ventilation (VE) achieved during exercise (i.e., ventilatory demand) approaches the maximal voluntary ventilation (MVV) or some estimate of the MVV (i.e., ventilatory capacity). More recently, it has become clear that rarely is the MVV breathing pattern adopted during exercise and that the VE/MVV relationship tells little about the specific reason(s) for ventilatory constraint. Although it is not a new concept, by measuring the tidal exercise flow-volume (FV) loops (extFVLs) obtained during exercise and plotting them according to a measured end-expiratory lung volume (EELV) within the maximal FV envelope (MFVL), more specific information is provided on the sources (and degree) of ventilatory constraint. This includes the extent of expiratory flow limitation, inspiratory flow reserve, alterations in the regulation of EELV (dynamic hyperinflation), end-inspiratory lung volume relative to total lung capacity (or tidal volume/inspiratory capacity), and a proposed estimate of ventilatory capacity based on the shape of the MFVL and the breathing pattern adopted during exercise. By assessing these types of changes, the degree of ventilatory constraint can be quantified and a more thorough interpretation of the cardiopulmonary exercise response is possible. This review will focus on the potential role of plotting the extFVL within the MFVL for determination of ventilatory constraint during exercise in the clinical setting. Important physiologic concepts, measurements, and limitations obtained from this type of analysis will be defined and discussed.

Progressive mechanical ventilatory constraints with aging.

To investigate the progressive nature of mechanical ventilatory constraints with aging, we studied 20 young (age 39 +/- 3 yr), 14 senior (70 +/- 2 yr), and 11 elderly (88 +/- 2 yr) men and women during exercise. All subjects had normal pulmonary function and performed graded cycle ergometry to exhaustion. Minute ventilation (V E), lung volume, and expiratory airflow limitation (EAFL) were measured during each 1-min increment in work rate. Data were analyzed by two-way analysis of variance (ANOVA; age x gender) at rest, ventilatory threshold (VTh), and peak exercise. If an interaction was present, each gender was analyzed with a one-way ANOVA. Aging resulted in an increased V E for a given submaximal work rate, although V E during peak exercise was lowest in the elderly group (p < 0.01). End-expiratory lung volume (EELV, % of TLC) in men increased progressively with age and all groups were different at VTh (p < 0.01) and peak exercise (p < 0.01). In women, EELV (% of TLC) also increased with aging, the senior and elderly subjects had a greater EELV at VTh (p < 0.01) and peak exercise (p < 0.01) than the young group. Additionally, the normal decrease in EELV during the early stages of exercise was not observed in elderly subjects. End-inspiratory lung volume (EILV) also progressively increased with aging; senior and elderly subjects had a higher EILV at rest (p < 0.05), VTh (p < 0.01), and peak exercise (p < 0.01) than young subjects. EAFL (% of VT) increased with aging; elderly subjects experienced greater EAFL at rest (p < 0.05), VTh (p < 0.01), and peak exercise (p < 0.01) than both young and senior subjects. We conclude that mechanical ventilatory constraints are progressive with aging, elderly subjects demonstrating marked mechanical ventilatory constraints during exercise. The impact of these constraints on exercise tolerance cannot be determined from this investigation and remains unclear.

Closing Pressure Rather Than Opening Pressure Determines Optimal Positive End-Expiratory Pressure and Avoids Overdistention

Ventilator-induced lung injury can result from either low lung volume ventilation with its associated cyclic alveolar collapse1 or from lung overdistention2,3 and volutrauma. Positive end-expiratory pressure (PEEP) is the main determinant of end-expiratory lung volume (EELV).4 If PEEP is set too low, alveolar and bronchiolar collapse can occur. Tidal volume in conjunction with PEEP determines end-inspiratory lung volume (EILV), which is a key determinant in volutrauma.5 When PEEP is determined by the inflation limb inflection point, or the “opening pressure” (OP), of the pressure-volume (P-V) curve, it can be used to recruit collapsed alveoli, improving oxygenation as well as compliance.

Perceived inspiratory difficulty during inspiratory threshold and hyperinflationary loadings.

Dynamic hyperinflation loads the inspiratory muscles by increasing end-expiratory lung volume (EELV) and imposing intrinsic positive end-expiratory pressure (PEEPi), the latter behaving as an inspiratory threshold load (ITL). The major purpose of this study was to describe the independent effects of the imposed ITL and changes in operating lung volume on the perception of inspiratory difficulty. In eight healthy subjects, independent increases in EELV and ITL were induced by continuous positive airway pressure (CPAP) and external ITL applications, respectively; increase in both EELV and PEEPi (thus the imposed ITL) was induced by application of positive end-expiratory pressure (PEEP). The perceived inspiratory difficulty increased significantly when either EELV or ITL was increased, and was always greater during combined increase in EELV and the imposed ITL (during PEEP) than when either factor was increased independently, suggesting that the imposed ITL and EELV each contribute independently to inspiratory difficulty. Inspiratory difficulty of each subject under all conditions was then fitted into a step-forward multiple regression model. The imposed ITL was a significant contributor to inspiratory difficulty in all subjects and was the first parameter to be selected in six of the eight subjects. When the results of all the subjects were pooled, the imposed ITL alone explained 40% of variations in inspiratory difficulty. Adding the change in end-inspiratory lung volume (DeltaEILV) to the model explained an additional 24% of variations in inspiratory difficulty. The coefficients (slopes) of the imposed ITL and DeltaEILV were 0.21 +/- 0.02 cm H2O-1 and 0.051 +/- 0.006 %IC-1, respectively. It is concluded that under our experimental conditions, the imposed ITL is a better predictor for explaining the variability of the perceived inspiratory difficulty than the operating lung volume.

Airway hyperresponsiveness in asthma. Not just a problem of smooth muscle relaxation with inspiration.

Airway hyperresponsiveness in asthma has been attributed to impaired ability of deep inspiration (DI) to stretch airway smooth muscle. We have retested this hypothesis by comparing the responses to methacholine of 10 asthmatic and 10 control subjects. After each dose subjects breathed tidally without deep inspiration for 4 min, followed by a forced partial expiration from which flow was measured at a constant volume, 35% baseline VC (Vp 35). This index is independent of both DI and increases in end-inspiratory lung volume (EILV). EILV increased significantly more in the asthmatic group than in the control group (15.0 versus 2.5% of baseline VC, p = 0. 019), a factor that if not taken into account would tend to mask the difference in the two responses. Comparisons were made after a cumulative dose of 50 microg methacholine, which was the highest dose common to all subjects. The asthmatic response was significantly greater than that seen in the control group, with reductions to 25.9 and 72.1% of baseline Vp 35, respectively (p = 0. 0007). We conclude that the sensitivity of asthmatic airways to methacholine is greater than that of normal airways even when DI is prohibited. Therefore, the hyperresponsiveness of asthmatic airways is not attributable simply to an inability of DI to stretch airway smooth muscle.

Respiratory Muscle Overloading and Dyspnoea During Bronchoconstriction in Asthma: Protective Effects of Fenoterol

Whether, and to what extent, β2-agonists protect against respiratory muscle overloading and breathlessness during bronchoconstriction remains to be defined in patients with asthma. In a double blind placebo-controlled study, 100 μg of fenoterol were administered to six stable asthmatics before a bronchial provocation test, performed by inhaling doubling concentrations of histamine from a Devilbiss 646 nebulizer. We recorded breathing pattern (tidal volume VT, inspiratory time TI, total time of the respiratory cycle TTOT), inspiratory capacity (IC), dynamic pleural pressure swing (Pplsw), total lung resistance (RL) and FEV1. VTwas expressed both in actual values and as % of IC. Changes in VT(%IC) during histamine inhalation reflected changes in dynamic end-inspiratory lung volume (EILV). Pplswwas expressed as % of maximal (the most negative in sign) pleural pressure, obtained under control conditions during a sniff manoeuvre (Pplsn). Pplsw(%Pplsn) is an index of inspiratory muscle effort. The test ended when the concentration of histamine which caused a decrease in FEV1of ≥40% post-saline was reached. Dyspnoea rating was scored by a modified Borg scale. At the ultimate degree of bronchoconstriction (UDB) with histamine: (i) decrease in FEV1was similar after placebo and fenoterol, while increase in RLwas lower after fenoterol (P<0.005); (ii) VT(%IC) increased less after fenoterol (P<0.027); (iii) increases in Pplsw(%Pplsn) was lower after fenoterol (P<0.001); (iv) ΔBorg (from saline) was lower (P<0.01) after fenoterol; (v) differences in ΔBorg, from placebo to fenoterol, related to concurrent changes in VT(%IC) (r2=0.67). In conclusion, at UDB 100 μg of fenoterol produced a beneficial effect on the degree of inspiratory muscle loading and breathlessness, an effect greater than it would be expected from measuring FEV1alone.

AIRFLOW LIMITATION AND REGULATION OF END EXPIRATORY LUNG VOLUME DURING EXERCISE 522

Increases in end expiratory lung volume (EELV) during exercise have been noted in patients, fit elderly subjects and some highly fit young athletes. Elevation seems to occur with the onset of expiratory air flow limitation(AFL). To test the hypothesis that AFL influences the regulation of EELV during exercise, eleven subjects with normal lung function performed steady state (SS) exercise on an ergometer, with and without AFL. AFL was achieved by increasing the density of inspired air in a hyperbaric chamber, at a depth of 3 atmospheres (3 ATA). SS exercise also was performed with the same apparatus at atmospheric pressure (SL). Six subjects achieved AFL, and 5 did not achieve AFL during the 3 ATA phase, none of the subjects had AFL during SL exercise. EELV was significantly higher during exercise at 3 ATA compared with SL exercise in the subjects with AFL at 3 ATA (SL=46+6%; 3 ATA-AFL=53+9%; (% of TLC) BTPS; p=0.012). However, in subjects with no AFL during exercise at 3 ATA, EELV was not different from that seen at SL (SL=43+6%; 3 ATA = 44+4%; p=0.74). End inspiratory lung volume also was significantly elevated during exercise at 3 ATA compared with SL, but only in those subjects with AFL at 3 ATA (SL=81+6%; 3 ATA-AFL=86+5%; p=0.01; in subjects without AFL, SL=82+4%; 3 ATA=83+4%; p=0.65). Tidal volume and ventilation were not different for either group. These data suggest that the occurrence of AFL influences the regulation of EELV during SS exercise.

Ventilation with constant versus decelerating inspiratory flow in experimentally induced acute respiratory failure.

Recognition of the potential for ventilator-associated lung injury has renewed the debate on the importance of the inspiratory flow pattern. The aim of this study was to determine whether a ventilatory pattern with decelerating inspiratory flow, with the major part of the tidal volume delivered early, would increase functional residual capacity at unchanged (or even reduced) inspiratory airway pressures and improve gas exchange at different positive end-expiratory pressure levels. Surfactant depletion was induced by repeated bronchoalveolar lavage in 13 anesthetized piglets. Decelerating and constant inspiratory flow ventilation was applied at positive end-expiratory pressure levels of 22, 17, 13, 9, and 4 cm H(2)O. Tidal volume, inspiration-to-expiration ratio, and ventilatory frequency were kept constant. Airway pressures, gas exchange, functional residual capacity (using a wash-in/washout method with sulfurhexafluoride), central hemodynamics, and extravascular lung water (using the thermo-dye-indicator dilution technique) were measured. Decelerating inspiratory flow yielded a lower arterial carbon dioxide tension compared to constant flow, that is, it improved alveolar ventilation. There were no differences between the flow patterns regarding end-inspiratory occlusion airway pressure, end-inspiratory lung volume, static compliance, or arterial oxygen tension. No differences were seen in hemodynamics and oxygen delivery. The decelerating inspiratory flow pattern increased carbon dioxide elimination, without any reduction of inspiratory airway pressure or apparent improvement in arterial oxygen tension. It remains to be established whether these differences are sufficiently pronounced to justify therapeutic consideration.

Aerosol derived airway morphometry in healthy subjects

Monodisperse aerosol particles can be used to non-invasively probe intrapulmonary airspace dimensions. In this study, the aerosol-derived airway morphometry technique was used to study airspace dimensions in 79 healthy subjects, in order to assess reference data for the future clinical application of aerosol-derived airway morphometry, and to investigate the effect of lung inflation, anthropometric, and lung function parameters on aerosol-derived airway morphometry. Intrapulmonary airspace dimensions were assessed by measuring the deposition of monodisperse, hydrophobic submicron aerosol particles during breathholding. Additionally, measurements of spirometric and body plethysmographic lung function were performed. Airspace dimensions were in good agreement with morphometric lung data. Airspace dimensions increased with increasing lung inflation. Interindividual variation of airspace dimensions was lowest in the lung periphery, at high levels of lung inflation, and when the volumetric lung depth was normalized to the end-inspiratory lung volume. Analysis of variance showed an increase of airspace dimensions with age. The results of this study indicate that aerosol-derived airway morphometry is dependent on the level of lung inflation and the age of the subject. These results suggest that in contrast to conventional lung function techniques, aerosol-derived airway morphometry might be a powerful tool for the detection of small changes in peripheral airway geometry.

Different ventilatory approaches to keep the lung open

To study the ability of different ventilatory approaches to keep the lung open. Different ventilatory patterns were applied in surfactant deficient lungs with PEEP set to achieve pre-lavage PaO2. Experimental laboratory of a University Department of Anaesthesiology and Intensive Care. 15 anaesthetised piglets. One volume-controlled mode (L-IPPV201:1.5) and two pressure-controlled modes at 20 breaths per minute (bpm) and I:E ratios of 2:1 and 1.5:1 (L-PRVC202:1 and L-PRVC201.5:1), and two pressure-controlled modes at 60 bpm and I:E of 1:1 and 1:1.5 (L-PRVC601:1 and L-PRVC601:1.5) were investigated. The pressure-controlled modes were applied using "Pressure-Regulated Volume-Controlled Ventilation" (PRVC). Gas exchange, airway pressures, hemodynamics, FRC and intrathoracic fluid volumes were measured. Gas exchange was the same for all modes. FRC was 30% higher with all post-lavage settings. By reducing inspiratory time MPAW decreased from 25 cmH2O by 3 cmH2O with L-PRVC201.5:1 and L-PRVC601:1.5. End-inspiratory airway pressure was 29 cmH2O with L-PRVC201.5:1 and 40 cmH2O with L-IPPV201:1.5, while the other modes displayed intermediate values. End-inspiratory lung volume was 65 ml/kg with L-IPPV201:1.5, but it was reduced to 50 and 49 ml/kg with L-PRVC601:1 and L-PRVC601:1.5. Compliance was 16 and 18 ml/cmH2O with L-PRVC202:1 and L-PRVC201.5:1, while it was lower with L-IPPV201:1.5, L-PRVC601:1 and L-PRVC601:1.5. Oxygen delivery was maintained at pre-lavage level with L-PRVC201.5:1 (657 ml/min.m2), the other modes displayed reduced oxygen delivery compared with pre-lavage. Neither the rapid frequency modes nor the low frequency volume-controlled mode kept the surfactant deficient lungs open. Pressure-controlled inverse ratio ventilation (20 bpm) kept the lungs open at reduced end-inspiratory airway pressures and hence reduced risk of barotrauma. Reducing I:E ratio in this latter modality from 2:1 to 1.5:1 further improved oxygen delivery.

Pulmonary dead space and airway dimensions in dogs at different levels of lung inflation.

The quasi-stationary front that separates inspired gas from mixed alveolar gas is largely determined by the balance between diffusive and convective forces of gas transport. To investigate parameters influencing this balance, a study was performed on eight anesthetized ventilated beagle dogs. Measurements were made of the volume of pulmonary dead space corresponding to four end-inspiratory lung volumes. Aerosol recovery techniques were used to determine airway sizes at lung depths corresponding to those respective dead space volumes as well as at fixed volumetric depths between 70 and 250 ml. Mean dead space volumes as measured by a single inhalation of He (and SF6) were 112 +/- 15 (SD) ml (127 +/- 15 ml), 120 +/- 18 ml (137 +/- 20 ml), 127 +/- 18 ml (145 +/- 20 ml), and 133 +/- 19 ml (155 +/- 21 ml) at end-inspiratory lung volumes of 64, 71, 79, and 86%, respectively, of total lung capacity. At fixed lung depths the airway diameters increased with higher levels of lung inflation. However, airway diameters "at the end of the dead space" did not change significantly. They were approximately 0.5 mm for SF6 dead space and approximately 0.75 mm for He dead space. These findings support the theoretical prediction that the position of the diffusion front during breathing is strongly dependent on airway geometry and much less dependent on parameters of the breathing maneuver.

Exertional breathlessness in patients with chronic airflow limitation. The role of lung hyperinflation.

There is considerable intersubject variability in the perceived intensity of breathlessness for a given level of activity among patients with chronic airflow limitation (CAL). To examine possible factors contributing to this variability we compared breathing pattern parameters, dynamic operational lung volumes, and Borg dyspnea ratings in 23 patients with severe CAL and in 10 healthy age-matched normal subjects during cycle ergometry to symptom-limitation. Patients with CAL had significantly (p < 0.01) higher levels of ventilation (% maximal voluntary ventilation) for a given work rate (slope of VE(%MVV)/WR(% pred max) = 1.51 +/- 0.18 versus 0.63 +/- 0.10; mean +/- SEM) and greater dynamic lung hyperinflation (DH) (change [delta] in end-expiratory lung volume [EELVdyn] = +0.31 +/- 0.11 L versus -0.16 +/- 0.22 L). Compared with normal subjects at a standardized VE (30 L/min), the CAL group was more breathless Borg = 4 +/- 1 versus 2 +/- 1, p < 0.01) and hyperinflated (EELVdyn = 75 +/- 3 versus 46 +/- 6% TLC, p < 0.001; end-inspiratory lung volume [EILVdyn] = 85 +/- 3 versus 67 +/- 5% TLC, p < 0.01). Within the CAL group, change in Borg ratings correlated with delta VE(%MVV) (r = 0.77, p < 0.001) and with slope of VE(%MVV)/WR(% pred max) (r = 0.48, p < 0.01). Regression analysis selected delta EILVdyn (or delta inspiratory reserve volume [delta IRVdyn]) from various dynamic ventilatory parameters as the strongest predictor of delta Borg (r = 0.63, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Selecting ventilator settings according to variables derived from the quasi-static pressure/volume relationship in patients with acute lung injury.

Knowledge of the pressure/volume (P/V) relationship of the lung may allow selection of tidal volume and positive end-expiratory pressure (PEEP) to optimize gas exchange without adversely affecting lung function or hemodynamics. Ten patients with acute lung injury were stabilized on controlled mechanical ventilation, based on conventional practice, using criteria from arterial blood gas data. The P/V relationship was determined under quasi-static conditions (end-expiratory and end-inspiratory, no flow periods > 0.8 s) during mechanical ventilation with an automated procedure that changed PEEP in a stepwise fashion. Differences in expiratory tidal volumes before and after a change in PEEP equaled the change in functional residual capacity (delta FRC). PEEP was set above the lowest point of the steepest section of the P/V curve (inflection pressure) to prevent end-expiratory lung collapse. Inspiratory tidal volumes (VTI) were adjusted to avoid an end-inspiratory lung volume reaching the flat part of the P/V curve. Averaged delta FRC versus PEEP curves were shifted to the left and the slope increased 1, 6, and 12 h after changing ventilator settings compared to baseline (P < 0.01). Averaged baseline delta FRC versus PEEP curves showed a marked inflection pressure that decreased after adjusting ventilator settings (P < 0.01). PEEP was increased from 7.4 +/- 1.8 cm H2O (baseline) to 11.9 +/- 1.6 cm H2O (1 h) (P < 0.001) according to measured baseline inflection pressures. Simultaneously, VTI had to be reduced from 759 +/- 161 mL (baseline) to 664 +/- 101 mL (1 h) (P < 0.01) to avoid end-inspiratory overinflation. To maintain minute volume constant ventilator frequency was increased from 14 +/- 1.2 (baseline) to 16 +/- 1.2 breaths/min (1 h) (P < 0.01). Maximum quasi-static compliance of 38 +/- 7 mL/cm H2O (baseline) increased to 46 +/- 9 mL/cm H2O (1 h) (P < 0.01). Maintaining FIO2 constant, PaO2 increased from a baseline of 90 +/- 16 mm Hg to 122 +/- 24 mm Hg (1 h) (P < 0.001), to 130 +/- 20 mm Hg (6 h) (P < 0.01), and to 138 +/- 19 mm Hg (12 h) (P < 0.01). Intrapulmonary shunt decreased from 0.28 +/- 0.08 (baseline) to 0.14 +/- 0.05 (12 h) (P < 0.001). Hemodynamic variables did not change. Our data suggest that using variables derived from a quasi-static P/V loop during mechanical ventilation under muscle paralysis is clinically superior compared to blood gas criteria for titration of ventilator settings.

Effects of ventilation inhomogeneity on DLcoSB-3EQ in normal subjects.

In patients with airflow obstruction, we found that ventilation inhomogeneity during vital capacity single-breath maneuvers was associated with decreases in the three-equation single-breath CO diffusing capacity of the lung (DLcoSB-3EQ) when breath-hold time (tBH) decreased. We postulated that this was due to a significant resistance to diffusive gas mixing within the gas phase of the lung. In this study, we hypothesized that this phenomenon might also occur in normal subjects if the breathing cycle were altered from traditional vital capacity maneuvers to those that increase ventilation inhomogeneity. In 10 normal subjects, we examined the tBH dependence of both DLcoSB-3EQ and the distribution of ventilation, measured by the mixing efficiency and the normalized phase III slope for helium. Preinspiratory lung volume (V0) was increased by keeping the maximum end-inspiratory lung volume (Vmax) constant or by increasing V0 and Vmax. When V0 increased while Vmax was kept constant, we found that the tBH-independent and the tBH-dependent components of ventilation inhomogeneity increased, but DLcoSB-3EQ was independent of V0 and tBH. Increasing V0 and Vmax did not change ventilation inhomogeneity at a tBH of 0 s, but the tBH-dependent component decreased. DLcoSB-3EQ, although independent of tBH, increased slightly with increases in Vmax. We conclude that in normal subjects increases in ventilation inhomogeneity with increases in V0 do not result in DLcoSB-3EQ becoming tBH dependent.

Mechanical constraints on exercise hyperpnea in endurance athletes.

We determined how close highly trained athletes [n = 8; maximal oxygen consumption (VO2max) = 73 +/- 1 ml.kg-1.min-1] came to their mechanical limits for generating expiratory airflow and inspiratory pleural pressure during maximal short-term exercise. Mechanical limits to expiratory flow were assessed at rest by measuring, over a range of lung volumes, the pleural pressures beyond which no further increases in flow rate are observed (Pmaxe). The capacity to generate inspiratory pressure (Pcapi) was also measured at rest over a range of lung volumes and flow rates. During progressive exercise, tidal pleural pressure-volume loops were measured and plotted relative to Pmaxe and Pcapi at the measured end-expiratory lung volume. During maximal exercise, expiratory flow limitation was reached over 27-76% of tidal volume, peak tidal inspiratory pressure reached an average of 89% of Pcapi, and end-inspiratory lung volume averaged 86% of total lung capacity. Mechanical limits to ventilation (VE) were generally reached coincident with the achievement of VO2max; the greater the ventilatory response, the greater was the degree of mechanical limitation. Mean arterial blood gases measured during maximal exercise showed a moderate hyperventilation (arterial PCO2 = 35.8 Torr, alveolar PO2 = 110 Torr), a widened alveolar-to-arterial gas pressure difference (32 Torr), and variable degrees of hypoxemia (arterial PO2 = 78 Torr, range 65-83 Torr). Increasing the stimulus to breathe during maximal exercise by inducing either hypercapnia (end-tidal PCO2 = 65 Torr) or hypoxemia (saturation = 75%) failed to increase VE, inspiratory pressure, or expiratory pressure. We conclude that during maximal exercise, highly trained individuals often reach the mechanical limits of the lung and respiratory muscle for producing alveolar ventilation. This level of ventilation is achieved at a considerable metabolic cost but with a mechanically optimal pattern of breathing and respiratory muscle recruitment and without sacrifice of a significant alveolar hyperventilation.

Flow Limitation and Regulation of Functional Residual Capacity during Exercise in a Physically Active Aging Population

In 29 older (69 +/- 1 yr), physically active subjects (VO2max = 44 +/- 2 ml.kg-1.min-1), we determined the effect of an age-related decline in elastic lung recoil (i.e., Vmax50 = 65% of 30-yr-old adults) on the ventilatory response to progressive exercise. More specifically, we assessed if expiratory airflow limits were achieved and how this may modulate the regulation of end-expiratory lung volume (EELV). We found that with only mild to moderate (50 to 75% VO2max) exercise, the mean EELV was reduced 0.38 +/- 0.07 L, and that expiratory flow limitation was present over 25 +/- 4% of the VT. In 11 subjects during this intensity of exercise, EELV was within their closing capacity. As exercise intensity progressed, VT plateaued at 58 +/- 2% of the vital capacity, and increased expiratory air flow rates were achieved by significantly increasing the EELV back to near resting levels, thereby moving a portion of the expiratory tidal flow-volume envelope away from the constraints of the effort independent portion of the maximal flow-volume curve. During heavy exercise, end-inspiratory lung volume (EILV) approached 90% of TLC. To achieve greater expiratory flow with maximal exercise, EELV remained similar to the previous intensity, and a significantly greater portion of the tidal expiratory flow-volume envelope (greater than 40% of the VT) became flow-limited. Despite this significant expiratory limitation, a rise in EELV, and an EILV approaching TLC, TI/Ttot remained constant throughout exercise, and the ventilatory response for the metabolic demand (VA/VCO2) was appropriate.(ABSTRACT TRUNCATED AT 250 WORDS)

Lung volumes during low-intensity steady-state cycling

The use of inspiratory capacity (IC) to estimate end-expiratory lung volume (EELV) during exercise has been questioned because of the assumption of constant total lung capacity (TLC). To investigate lung volumes during low-intensity steady-state cycling, we measured EELV by the open-circuit N2 washout method (MR-1, currently Sensormedics 2100) in eight healthy men while at rest and during unloaded and 60-W cycling. TLC was calculated by adding EELV and IC. Measurement variation of TLC was 142 ml at rest, 121 ml during unloaded cycling, and 158 ml during 60-W cycling. TLC did not differ significantly among the three conditions studied. EELV decreased during unloaded (P less than 0.002) and 60-W cycling (P less than 0.001) compared with rest. End-inspiratory lung volume increased only during 60-W cycling (P = 0.03). The decrease in EELV accounted for 100% of the increase in tidal volume during unloaded cycling. Although minute ventilation was similar in the subjects during unloaded cycling, we noted that breathing patterns varied among the subjects. The increase in respiratory frequency was negatively correlated to the change in tidal volume (R2 = 0.54, P = 0.038) and to the change in end-inspiratory lung volume (R2 = 0.68, P = 0.012). We conclude that TLC does not differ significantly during low-intensity steady-state cycling and that use of IC to estimate changes in EELV is appropriate.

Adverse Effects of Large Tidal Volume and Low PEEP in Canine Acid Aspiration

When normal lungs are ventilated with large tidal volumes (VT) and end-inspired pressures (Pei), surfactant is depleted and pulmonary edema develops. Both effects are diminished by positive end-expiratory pressure (PEEP). We reasoned that ventilatory with large VT-low PEEP would similarly increase edema following acute lung injury. To test this hypothesis, we ventilated dogs 1 h after hydrochloric acid (HCl) induced pulmonary edema with a large VT (30 ml/kg) and low PEEP (3 cm H2O) (large VT-low PEEP) and compared their results with dogs ventilated with a smaller VT (15 ml/kg) and 12 cm H2O PEEP (small VT-high PEEP). The small VT was the smallest that maintained eucapnia in our preparation; the large VT was chosen to match Pei and end-inspired lung volume. Pulmonary capillary wedge transmural pressure (Ppwtm) was kept at 8 mm Hg in both groups. Five hours after injury, the median lung wet weight to body weight ratio (WW/BW) was 25 g/kg higher in the large VT-low PEEP group than in the small VT-high PEEP group (p less than 0.05). Venous admixture (Qva/Qt) was similarly greater in the large VT-low PEEP group (49.8 versus 23.5%) (p less than 0.05). We conclude that small VT-high PEEP is a better mode of ventilating acute lung injury than large VT-low PEEP because edema accumulation is less and venous admixture is less. These advantages did not result from differences in Pei, end-inspiratory lung volume, or preload (Ppwtm).(ABSTRACT TRUNCATED AT 250 WORDS)

Some mechanical characteristics of the respiratory system of the fresh-water turtle Mauremys casplca

1. 1. Respiratory mechanics were evaluated for the total pulmonary system of the turtle Mauremys casplca. 2. 2. Compliance (3.56 ml/cm H 2O) and hysteresis (2.99cm) values are comparable to those of reptiles with similar pulmonary structure. 3. 3. Maximal lung volume, resting lung volume, end-inspiratory lung volume and body volume, were determined. 4. 4. The slope of the relationship of these parameters with body weight reaches values until twice that of other turtles.