Decrease In End-expiratory Lung Volume Research Articles

Heart-lung interactions during mechanical ventilation: the basics.

The hemodynamic effects of mechanical ventilation can be grouped into three clinically relevant concepts. First, since spontaneous ventilation is exercise. In patients increased work of breathing, initiation of mechanical ventilatory support may improve O2 delivery because the work of breathing is reduced. Second, changes in lung volume alter autonomic tone, pulmonary vascular resistance, and at high lung volumes compress the heart in the cardiac fossa similarly to cardiac tamponade. As lung volume increases so does the pressure difference between airway and pleural pressure. When this pressure difference exceeds pulmonary artery pressure, pulmonary vessels collapse as they pass form the pulmonary arteries into the alveolar space increasing pulmonary vascular resistance. Hyperinflation increases pulmonary vascular resistance impeding right ventricular ejection. Anything that over distends lung units will increase their vascular resistance, and if occurring globally throughout the lung, increase pulmonary vascular resistance. Decreases in end-expiratory lung volume cause alveolar collapse increases pulmonary vasomotor tone by the process of hypoxic pulmonary vasoconstriction. Recruitment maneuvers that restore alveolar oxygenation without over distention will reduce pulmonary artery pressure. Third, positive-pressure ventilation increases intrathoracic pressure. Since diaphragmatic descent increases intra-abdominal pressure, the decrease in the pressure gradient for venous return is less than would otherwise occur if the only change were an increase in right atrial pressure. However, in hypovolemic states, it can induce profound decreases in venous return. Increases in intrathoracic pressure decreases left ventricular afterload and will augment left ventricular ejection. In patients with hypervolemic heart failure, this afterload reducing effect can result in improved left ventricular ejection, increased cardiac output and reduced myocardial O2 demand. This brief review will focus primarily on mechanical ventilation and intrathoracic pressure as they affect right and left ventricular function and cardiac output.

Defining a Ventilation Strategy for Flexible Bronchoscopy on Mechanically Ventilated Patients in the Medical Intensive Care Unit

Flexible bronchoscopy (FB) in intubated patients on mechanical ventilation increases airway resistance. During FB, two ventilatory strategies are possible: maintaining tidal volume (VT) while maintaining baseline CO2 or allowing reduction of VT. The former strategy carries risk of hyperinflation due to expiratory flow limitation with FB. The aim of the authors was too study end expiratory lung volume (EELV) during FB of intubated subjects while limiting VT. We studied 16 subjects who were intubated on mechanical ventilation and required FB. Changes in EELV were measured by respiratory inductance plethysmography. Ventilator mechanics, EELV, and arterial blood gases, were measured. FB insertions decreased EELV in 64% of cases (-325±371 mL) and increased it in 32% of cases (65±59 mL). Suctioning decreased EELV in 76% of cases (-120±104 mL) and increased it in 16% of cases (29±33 mL). Respiratory mechanics were unchanged. Pre-FB and post-FB, PaO2 decreased by 61±96 mm Hg and PaCO2 increased by 15±7 mm Hg. There was no clinically significant increase in EELV in any subject during FB. Decreases in EELV coincided with FB-suctioning maneuvers. Peak pressure limiting ventilation protected the subject against hyperinflation with a consequent, well-tolerated reduction in VT, and hypercapnea. Suctioning should be limited, especially in patients vulnerable to derecruitment effect.

Longitudinal inspiratory capacity changes in chronic obstructive pulmonary disease

BackgroundThe changes in inspiratory capacity (IC) over time in chronic obstructive pulmonary disease (COPD) patients are unknown. The Understanding Potential Long-term Impacts on Function with Tiotropium (UPLIFT®) trial included IC measurements.MethodsIC analysis from UPLIFT® (N = 5992) was performed at 1 and 6 months, and every 6 months through 4 years. Annualized rate of decline in pre- and post-bronchodilator IC and mean differences at each time point were analyzed by mixed-effects models. The relationships between baseline IC and exacerbation rate and mortality were explored using Cox regression analysis.ResultsBaseline characteristics: age, 65 years; 75% men; post-bronchodilator forced expiratory volume in 1 second, 1.32 L (48% predicted); pre- and post-bronchodilator IC, 2.03 and 2.33 L. Mean IC rate of decline (mL/year) was 34 ± 2 (1.7% of baseline) and 50 ± 3 (2.1% of baseline) pre- and post-bronchodilator, respectively, without significant between-group differences. Morning pre-bronchodilator (trough) IC improved with tiotropium versus placebo: 124 mL (1 month), 103 mL (1 year), 107 mL (2 years), 98 mL (3 years), and 97 mL (4 years) (all p < 0.001). Post-bronchodilator improvements were similar between treatment groups. Lower baseline IC values were associated with reduced time to first exacerbation. For the lowest quartile (n = 1413) the values in months were 14.3 (11.7–17.0) for tiotropium and 10.3 (8.8–11.7) for controls (p < 0.01).ConclusionIC declines from approximately 34 to 50 mL/year in patients with stage II to IV COPD. Tiotropium treatment does not change the IC decline rate but provides 24-hour improvements in IC sustained over the long term. Trough IC differences suggest that tiotropium provides sustained decrease in end-expiratory lung volume.

Changes in lung volume and diaphragm muscle activity at sleep onset in obese obstructive sleep apnea patients vs. healthy-weight controls

Obese obstructive sleep apnea (OSA) patients potentially defend end-expiratory lung volume (EELV) during wakefulness via increased expiratory diaphragmatic activity (eEMG(dia)). A reduction in eEMG(dia) and EELV at sleep onset could, therefore, increase upper airway collapsibility via reduced tracheal traction. The aim of this study was to establish if eEMG(dia) is greater in obese OSA patients vs. healthy-weight controls during wakefulness, and to compare eEMG(dia) and EELV changes at sleep onset between groups as a function of stable breathing, hypopnea vs. apnea events developing within the first few breaths after sleep onset. Eight obese men with OSA and eight healthy-weight men without OSA were studied in the supine position while instrumented with an intraesophageal catheter to measure eEMG(dia) and magnetometer coils to assess changes in EELV. While eEMG(dia) expressed as %maximal activity was not significantly different between groups during wakefulness, OSA patients experienced a greater fall in eEMG(dia) following sleep onset (group × breath, P < 0.001) and a greater decrease when respiratory events accompanied sleep onsets (category × breath, P < 0.001). The decrease in EELV by the third postsleep onset breath was small (OSA, 61.4 ± 8.0 ml, P < 0.001; controls, 34.0 ± 4.2 ml, P < 0.001), with the decrease significantly greater in OSA patients over time (group × breath, P = 0.007). There was a greater decrease with more severe events (category × breath, P < 0.001), with EELV decreasing by 89.6 ± 14.2 ml (P < 0.001) at the onset of apneas in the OSA group. These data support that diaphragm tone and EELV frequently decrease following sleep onset, with greater falls at transitions accompanied by respiratory events. In addition to decrements in upper airway dilator muscle activity, decreasing lung volume potentially contributes to an increased propensity for upper airway collapse in OSA patients at sleep onset.

Evaluation of acute bronchodilator reversibility in patients with symptoms of GOLD stage I COPD

Background:Patients with symptoms of GOLD stage I chronic obstructive pulmonary disease (COPD) can have significant abnormalities of ventilatory mechanics with greater exertional symptoms and exercise limitation than age-matched healthy subjects....

Fat Distribution and End-Expiratory Lung Volume in Lean and Obese Men and Women

Although obesity significantly reduces end-expiratory lung volume (EELV), the relationship between EELV and detailed measures of fat distribution has not been studied in obese men and women. To investigate, EELV and chest wall fat distribution (ie, rib cage, anterior subcutaneous abdominal fat, posterior subcutaneous fat, and visceral fat) were measured in lean men and women (ie, < 25% body fat) and obese men and women (ie, > 30% body fat). All subjects underwent pulmonary function testing, hydrostatic weighing, and MRI scans. Data were analyzed for the men and women separately by independent t test, and the relationships between variables were determined by regression analysis. All body composition measurements were significantly different among the lean and obese men and women (p < 0.001). However, with only a few exceptions, fat distribution was similar among the lean and obese men and women (p > 0.05). The mean EELV was significantly lower in the obese men (39 +/- 6% vs 46 +/- 4% total lung capacity [TLC], respectively; p < 0.0005) and women (40 +/- 4% vs 53 +/- 4% TLC, respectively; p < 0.0001) compared with lean control subjects. Many estimates of body fat were significantly correlated with EELV for both men and women. In both men and women, the decrease in EELV with obesity appears to be related to the cumulative effect of increased chest wall fat rather than to any specific regional chest wall fat distribution. Also, with only a few exceptions, relative fat distribution is markedly similar between lean and obese subjects.

Tiotropium and Simplified Detection of Dynamic Hyperinflation

Study objective:To detect dynamic hyperinflation (DH) by evaluating reduction in inspiratory capacity (IC) during metronome-paced hyperventilation (MPH) in patients with moderate-to-severe COPD, studied before and after treatment with tiotropium.Methods:IC and FEV1were measured before and immediately after MPH at two times resting the respiratory rate for 20 s in 60 COPD patients (28 men; mean age, 66 ± 10 years [± SD]) before and after 30 days of treatment with tiotropium bromide, 18 μg. Patients were encouraged to maintain a constant tidal volume during MPH.Results:At baseline, mean FEV1was 1.5 ± 0.1 L (± SE) [57 ± 1.6% of predicted], mean FVC was 2.6 ± 0.1L (77 ± 1.8% of predicted), and mean FEV1/FVC was 56 ± 1%. After 180 μg of aerosolized albuterol sulfate, mean FEV1was 1.7 ± 0.1 L (63 ± 1.5% of predicted) [p < 0.001] and mean FEV1/FVC was 58 ± 1%. Compared to baseline, after 30 days and 1.5 h after tiotropium there was an increase in IC of 0.18 ± 0.04L (p < 0.0001); FEV1of 0.13 ± 0.03 L (5.6 ± 0.8% of predicted; p = 0.0002); FVC of 0.22 ± 0.05 L (6.5 ± 1.3% of predicted; p < 0.001); and decrease in end-expiratory lung volume (EELV)/total lung capacity (TLC) of − 3.1 ± 0.6% (p = 0.0001); a decrease in end-inspiratory lung volume (EILV)/TLC of − 2.9 ± 1.3% (p = 0.03); and no change in TLC (− 0.06 ± 0.05 L). Results following MPH-induced DH at baseline and after 30 days of tiotropium were similar, with decreases in IC (− 0.35 ± 0.03 L; p < 0.001); FEV1(− 0.05 ± 0.04 L; p = 0.2); and FVC (− 0.22 ± 0.03 L; p < 0.0001); no change in TLC; and increases in EELV/TLC (11.8 ± 1.0% of predicted; p < 0.0001) and EILV/TLC (4.0 ± 1.3% of predicted, p < 0.003).Conclusion:In patients with moderate-to-severe COPD, tiotropium did not reduce MPH-induced DH and reduction in IC, compared to baseline. However, because tiotropium induced bronchodilation and increased baseline IC, lower operational lung volumes may blunt the effect of MPH-induced DH. The noninvasive simplicity of MPH-induced DH provides a clinically useful screening surrogate to monitor changes in IC following treatment with tiotropium.

Measuring end-expiratory lung volume and pulmonary mechanics to detect early lung function impairment in rabbits

We investigated whether end-expiratory lung volume (EELV) or lung mechanical parameters are more sensitive for the detection of a compromised gas exchange during bronchoconstriction and after surfactant depletion. EELV was determined via SF(6) multiple breath wash-outs in mechanically ventilated rabbits while a positive end-expiratory pressure (PEEP) of 1, 3 or 7 cm H(2)O was maintained. Airway resistance (R(aw)) and parenchymal elastance (H) were estimated from the pulmonary input impedance measured at each PEEP level by means of forced oscillations. Measurements were repeated during i.v. methacholine (MCh) infusions and following lung injury induced by saline lavage. MCh induced marked elevations in R(aw), with no significant change in EELV or H at any PEEP. After lavage, the severity of hypoxia was reflected systematically in significant decreases in EELV at all PEEP levels (-42+/-13%, -26+/-4%, and -18+/-5% at 1, 3 and 7 cm H(2)O, respectively), whereas compromised gas exchange was not associated with consistent changes in the mechanical parameters at a PEEP of 7 cm H(2)O (20+/-9% and 14+/-9% in R(aw) and H, respectively; p=0.2). We conclude that R(aw) is the only sensitive indicator for the detection of a compromised lung function during MCh infusions, whereas the estimation of EELV is necessary to follow the progression of a lung injury when a high PEEP level is applied.

Pathophysiology of exercise dyspnea in healthy subjects and in patients with chronic obstructive pulmonary disease (COPD)

In patients with a number of cardio-respiratory disorders, breathlessness is the most common symptom limiting exercise capacity. Increased respiratory effort is frequently the chosen descriptor cluster both in normal subjects and in patients with chronic obstructive pulmonary disease (COPD) during exercise. The body of evidence indicates that dyspnea may be due to a central perception of an overall increase in central respiratory motor output directed preferentially to the rib cage muscles. On the other hand, the disparity between respiratory motor output and mechanical response of the system is also thought to play an important role in the increased perception of exercise in patients. The expiratory muscles also contribute to exercise dyspnea: a decrease in Borg scores is related to a decrease in end-expiratory lung volume and to a decrease in end-expiratory gastric pressure at isowork after lung volume reduction surgery. Changes in respiratory mechanics and intrathoracic pressure surrounding the heart can reduce cardiac output by affecting the return of blood to the heart from the periphery, or by interfering with the ability of the heart to eject blood into the peripheral circulation. Change in arterial blood gas content may affect breathlessness via direct or indirect effects. Old and more recent data have demonstrated that hypercapnia makes an independent contribution to breathlessness. In hypercapnic COPD patients an increase in PaCO2 seems to be the most important stimulus overriding all other inputs for dyspnea. Hypoxia may act indirectly by increasing ventilation (VE), and directly, independent of change in VE. Finally, chemical (metabolic) ventilatory stimuli do not have a specific effect on breathlessness other than via their stimulation of VE. We conclude that exercise provides a stimulus contributing to dyspnea, which can be applied to many diseases.

High-Frequency Chest Compression: A Summary of the Literature

The purpose of the present literature summary is to describe high-frequency chest compression (HFCC), summarize its history and outline study results on its effect on mucolysis, mucus transport, pulmonary function and quality of life. HFCC is a mechanical method of self-administered chest physiotherapy, which induces rapid air movement in and out of the lungs. This mean oscillated volume is an effective method of mucolysis and mucus clearance. HFCC can increase independence. Some studies have shown that HFCC leads to more mucus clearance and better lung function compared with conventional chest physiotherapy. However, HFCC also decreases end-expiratory lung volume, which can lead to increased airway resistance and a decreased oscillated volume. Adding positive end-expiratory pressure to HFCC has been shown to prevent this decrease in end-expiratory lung volume and to increase the oscillated volume. It is possible that the HFCC-induced decrease in end-expiratory lung volume may result in more mucus clearance in airways that remain open by reducing airway size. Adjunctive methods, such as positive end-expiratory pressure, may not always be needed to make HFCC more effective.

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.

Reverse-thrust ventilation in hypercapnic patients with acute respiratory distress syndrome. Acute physiological effects.

Techniques of tracheal gas insufflation (TGI) have been shown to enhance CO(2) clearance efficiency in mechanically ventilated patients with acute respiratory distress syndrome (ARDS). Clinical studies have explored the effects of such techniques only at moderate intratracheal gas flow rates, with TGI superimposed to mechanical ventilation in a continuous fashion, or synchronized to the expiratory phase of the duty cycle. We examined the effects of intratracheal pulmonary ventilation (ITPV), delivering the entire tidal volume (VT) in the proximity of the tracheal carina, with all the gas flow supplied continuously through a reverse-thrust catheter (RTC). A potential limitation in the application of TGI is dynamic hyperinflation. Therefore, in a subgroup of patients, we also evaluated the effects of ITPV on end-expiratory lung volume (EELV) by respiratory inductive plethysmography (RIP). Eleven patients with ARDS under volume-cycled mechanical ventilation were subsequently switched to ITPV at the same baseline respiratory rate, I:E ratio, and VT. At the same minute volume, Pa(CO(2)) decreased from 70 +/- 12.3 to 59 +/- 9.5 mm Hg, with a percent reduction of 15 +/- 4% (range from 10 to 20%). The CO(2) decrease was greater in patients with higher baseline Pa(CO(2)) levels (DeltaPa(CO(2)) = 0.29 x Pa(CO(2)) - 9.48, r = 0.95). During transition from mechanical ventilation to ITPV, tracheal positive end-expiratory pressure (PEEP(tr)) decreased with a correspondent decrease in EELV. Both were restored by increasing the PEEP at the ventilator by 3.6 +/- 2.0 cm H(2)O. These data suggest that in patients with ARDS ITPV effectively reduces dead space ventilation and the employment of the RTC may limit or avoid dynamic hyperinflation.

End-expiratory lung volume during arm and leg exercise in normal subjects and patients with cystic fibrosis.

There are no reports concerning the regulation of end-expiratory lung volume (EELV) and flow-volume relationships during upper limb exercise in health and disease. We studied EELV during such exercise in 22 adults with cystic fibrosis (CF) and nine age-matched healthy control subjects. Subjects with CF were grouped according to the severity of their lung disease, as follows: mild = FEV1 > 80% predicted; moderate = FEV1 40 to 80% predicted, and severe = FEV1 < 40% predicted. EELV was calculated from measurements of inspiratory capacity (IC) made at each workload during an incremental arm and leg ergometer test to peak work capacity. In the control group, the decrease in EELV was significantly smaller for arm than for leg exercise at peak work (-0.13 L versus -0.53 L, p < 0.001) and for arm than for leg exercise at an equivalent submaximal ventilation (-0.13 L versus -0.46 L, p < 0.01). In the groups with moderate and severe CF, arm exercise resulted in an increase in EELV from resting levels (dynamic hyperinflation) that was not significantly different from the increase observed for leg exercise. For CF subjects there was a significant inverse relationship between FEV1 and changes in EELV from rest to peak arm exercise (r = -0.46, p < 0.05). In normal subjects, there was a difference in the EELV response for arm versus leg exercise. In CF subjects with airflow limitation, dynamic hyperinflation occurred with both forms of exercise.

Effects of Positive End-Expiratory Pressure on Oscillated Flow Rate During High-Frequency Chest Compression

To investigate the effects of positive end-expiratory pressure (PEEP) on end-expiratory lung volume (EELV) and mean oscillated flow rate (VOSC) during high-frequency chest compression (HFCC) in normal subjects and patients with severe COPD. Comparative study. Pulmonary function and lung mechanics laboratory, University of Alberta Hospitals. Six normal subjects (five male; one female) and six patients with clinically stable COPD (five male; one female) with hypercapnia. A pneumatic vest system was operated at 10 Hz with a mean chest wall pressure of 16 cm H2O to provide the HFCC. A closed-circuit spirometer system permitted measurement of HFCC- and PEEP-induced changes in EELV that were expressed as per cent baseline functional residual capacity (FRC). An isothermic chamber connected near the mouthpiece permitted measurement of VOSC. For the normal subjects, HFCC caused a significant decrease in EELV to 82.0% of FRC (p < or = 0.01) and the addition of 4.8+/-0.5 cm H2O of PEEP during HFCC increased EELV to 97.5% FRC. In the COPD patients, HFCC decreased EELV to 92.3% of FRC (p < or = 0.01), and the addition of 3.7+/-1.0 cm H2O of PEEP increased EELV to 98.4% FRC. For the normal subjects, increasing EELV to near FRC caused VOSC during expiration to increase 14.6% (p < or = 0.01), but there was no significant effect on VOSC during inspiration (5.1% increase). In the COPD patients, PEEP increased VOSC during both inspiration (30.5%) and expiration (57.0%) (both, p < or = 0.01). Addition of a modest amount of PEEP during HFCC prevents the decrease in EELV and increases VOSC during both phases of spontaneous breathing in COPD patients. This higher VOSC during HFCC+PEEP may improve the effectiveness of HFCC in clearing mucus from the lungs of patients with airway disease.

Mechanisms for episodes of hypoxemia in preterm infants undergoing mechanical ventilation

Objective: To ascertain possible mechanisms implicated in the development of transient episodes of hypoxemia (oxygen saturation <85%) frequently observed in preterm infants undergoing mechanical ventilation, even after the acute phase of respiratory failure has passed. Study design: Tidal flow, airway and esophageal pressure, and oxygen saturation were continuously recorded in 10 infants (mean ± SD, birth weight 733 ± 149 gm, gestational age 25.5 ± 2.2 weeks, age 26.3 ± 11.9 days) who had repeated episodes of hypoxemia without any evident cause. Measurements of minute ventilation (v̇ E), inspiratory compliance (C i), and inspiratory resistance (R i) were compared before and during episodes of hypoxemia. Results: All episodes of hypoxemia were preceded by an active exhalation that produced a mean decrease in end-expiratory lung volume of 6.4 ± 2.8 ml/kg. The reduction in lung volume was immediately followed by a sudden decrease in tidal flow and volume, despite continuation of mechanical ventilation at the same rate and peak pressure. The resulting hypoventilation was associated with a drop in C i to approximately one half and an increase in R i to more than double the baseline values. Approximately 30 seconds after the beginning of hypoventilation, the arterial oxygen saturation reached a hypoxemic level (oxygen saturation <85%). Conclusion: Most hypoxemic episodes were triggered by an expiratory effort that produced a large decrease in lung volume. This reduction in lung volume probably leads to closure of small airways and the development of intrapulmonary shunts, which would explain the rapid development of hypoxemia. (J P EDIATR 1995;127:767-73)

Effects of High Frequency Chest Compression on Respiratory System Mechanics in Normal Subjects and Cystic Fibrosis Patients

OBJECTIVE: To investigate the short term effects of high frequency chest compression (HFCC) on several indices of respiratory system mechanics in normal subjects and patients with cystic fibrosis (CF).DESIGN: Comparative physiological approach. Subjects were blinded to 10 randomized HFCC settings (5, 10, 15, 20 and 25 Hz) with each applied at the lowest and at the highest background vest pressure.SETTING: Pulmonary function and lung mechanics laboratory, University of Alberta.PARTICIPANTS: Ten normal male volunteers (24.2±3.8 years) and 11 clinically stable CF patients (23.4±6.7 years). Normal subjects were nonsmokers who had normal lung function. The CF patients had a wide range of airway obstruction.INTERVENTIONS: HFCC was supplied by oscillating a pneumatic vest that covered the entire torso. Balloon tipped catheters were used to measure esophageal (Pes) and external chest wall (Pew) pressures. Changes in end-expiratory lung volume (EELV) during HFCC were measured from a spirogram and were compared with baseline functional residual capacity (FRC). The HFCC induced air movement al the mouth, oscillated tidal volume (Vosc), was measured by reverse plethysmography.RESULTS: Both normals and CF patients had similar changes in Pes and EELV. At the highest background vest pressure and at the higher oscillation frequencies, EELV decreased approximately 30% from the no-HFCC baseline FRC. Vosc decreased with increasing oscillation frequency but normals had higher Vosc than CF patients at each frequency. Conversion of Vose to flow (V˙osc) revealed that the highest Vosc occurred between 10 and 15 Hz for both normals and CF patients. Also, Vosc was dependent on the overall airway function. Low forced expired volume in 1 s resulted in low Vosc, especially when Vosc was measured during spontaneous expiration.CONCLUSIONS: CF patients with moderate or severe airway obstruction may gain maximal benefit from HFCC therapy when low vest pressure is used at an oscillation frequency of 10 to 15 Hz. The low vest pressure minimizes the decrease in EELV and 10 to 15 Hz maximizes Vosc.

Ventilatory responses to inspiratory threshold loading and role of muscle fatigue in task failure.

To examine respiratory muscle recruitment pattern during inspiratory loading and role of fatigue in limiting endurance, we studied seven normal subjects on 17 +/- 6 days during breathing against progressive inspiratory threshold load. Threshold pressure (Pth) was progressively increased 14 +/- 5 cmH2O every 2 min until voluntary cessation (task failure). Subjects could adopt any breathing pattern. Tidal volume (VT), chest wall motion, end-tidal PCO2, and arterial O2 saturation were measured. At moderate loads [50-75% of maximum Pth (Pthmax)], inspiratory time (TI) decreased and VT/TI and expiratory time increased, increasing time for recovery of muscles between inspirations. At high loads (> 75% Pthmax), VT/TI decreased, which, with progressive decrease in end-expiratory lung volume (EELV) throughout, increased potential for inspiratory force development. Progressive hypoxia and hypercapnia occurred at higher work loads. Immediately after task failure all subjects could recover at high loads and still reachieve initial Pthmax on reimposition of progressive loading. Respiratory pressures were measured in subgroup of three subjects: transdiaphragmatic pressure response to 0.1-ms bilateral supramaximal phrenic nerve stimulation at end expiration initially increased with increasing load/decreasing EELV, consistent with increasing mechanical advantage of diaphragm, but decreased at highest loads, suggesting diaphragm fatigue. Full recovery had not occurred at 30 min after task failure. We demonstrated that progressive threshold loading is associated with systematic changes in breathing pattern that act to optimize muscle strength and increase endurance. Task failure occurred when these compensatory mechanisms were maximal. Inspiratory muscles appeared relatively resistant to fatigue, which was late but persistent.

Effect of global inspiratory muscle fatigue on ventilatory and respiratory muscle responses to CO2.

We evaluated the effect of global inspiratory muscle fatigue on ventilation and respiratory muscle control during CO2 rebreathing in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. CO2 response curves were measured before and after fatigue. During CO2 rebreathing, global fatigue caused a decreased tidal volume (VT) and an increased breathing frequency but did not change minute ventilation, duty cycle, or mean inspiratory flow. Both esophageal and transdiaphragmatic pressure swings were significantly reduced after global fatigue, suggesting decreased contribution of both rib cage muscles and diaphragm to breathing. End-expiratory transpulmonary pressure for a given CO2 was lower after fatigue, indicating an additional decrease in end-expiratory lung volume due to expiratory muscle recruitment, which leads to a greater initial portion of inspiration being passive. This, combined with the reduction in VT, decreased the fraction of VT attributable to inspiratory muscle contribution; therefore the inspiratory muscle elastic work and power per breath were significantly reduced. We conclude that respiratory control mechanisms are plastic and that the respiratory centers alter their output in a manner appropriate to the contractile state of the respiratory muscles to conserve the ventilatory response to CO2.

Activity of Lower Intercostal and Abdominal Muscle after Upper Abdominal Surgery

The decrease in end-expiratory lung volume after upper abdominal surgery has been attributed, in part, to reflex spasm of the abdominal muscles. To examine the influence of abdominal surgery on abdominal muscle tone, electromyographic (EMG) activity of abdominal and lower intercostal muscle was compared before operation with that at 3 hr and at 24 hr after operation in 18 healthy patients undergoing elective gastric or biliary surgery. After operation, EMG activity increased markedly and showed a phasic pattern of activity associated with respiration in most patients. This was characterized by a progressive increase in EMG activity during expiration with an abrupt decrease at the onset of inspiration. We conclude that increased expiratory activity in abdominal and lower intercostal muscle may be responsible for the decrease in lung volumes that occurs after upper abdominal surgery.

Changes in lung volume and breathing pattern during exercise and CO2 inhalation in humans.

Lung volume changes during CO2 inhalation and exercise were compared in seven human subjects. Expiratory reserve volume (ERV) normalized by vital capacity (VC) was used as an index of end-expiratory lung volume (EELV). Work loads tried were 30, 60, and 90 W and inspired CO2 concentrations were 3.5 and 5.0%. Exercise at 30 W led to a significant decrease in EELV, by 7% VC (P less than 0.005), with no further change at higher levels of exercise (P greater than 0.1). Both 3.5 and 5.0% CO2 inhalation resulted in an increase in EELV that was not statistically significant (3% VC, P greater than 0.1). A possible linkage of this different EELV behavior to breathing pattern was tested. The tidal volume-inspiratory duration curve shifted to a higher volume region during exercise compared with CO2 inhalation. Consequently, the volume-time threshold characteristic was better described by an end-inspiratory lung volume-inspiratory duration plot, resulting in a common relationship under these two different stimuli. These results suggest that the depth and rate of breathing in humans can be affected by not only phasic but also tonic components. A decrease in functional residual capacity or EELV was peculiar to exercise and should be associated with increased mechanical efficiency compared with CO2 inhalation. Theoretical predictions based on work of breathing optimization via a decreased EELV seemed to be capable of explaining isocapnic exercise hyperpnea in conjunction with proportional control of arterial CO2 tension.