Increase In End-expiratory Volume Research Articles

Effects of positive expiratory pressure on chest wall volumes in subjects with stroke compared to healthy controls: a case–control study

BackgroundAlterations in respiratory system kinematics in stroke lead to restrictive pattern associated with decreased lung volumes. Chest physical therapy, such as positive expiratory pressure, may be useful in the treatment of these patients;however, the optimum intensity to promote volume and motion changes of the chest wall remains unclear. ObjectiveTo assess the effect of different intensities of positive expiratory pressure on chest wall kinematics in subjects with stroke compared to healthy controls. Methods16 subjects with chronic stroke and 16 healthy controls matched for age, gender, and body mass index were recruited. Chest wall volumes were assessed using optoelectronic plethysmography during quiet breathing, 5 minutes,and recovery. Three different intensities of positive expiratory pressure (10, 15, and 20cmH2O) were administered in a random order with a 30 minutes rest interval between intensities. ResultsDuring positive expiratory pressure, tidal chest wall expansion increased in both groups compared to quiet breathing; however, this increase was not significant in the subjects with stroke (0.41 vs. 1.32L, 0.56 vs. 1.54L, 0.52 vs. 1.8L, at 10, 15, 20cmH2O positive expiratory pressure, for stroke and control groups; p<0.001). End-expiratory chest wall volume decreased in controls, mainly due to the abdomen, and increased in the stroke group, mainly due the pulmonary rib cage. ConclusionPositive expiratory pressure administration facilitates acute lung expansion of the chest wall and its compartments in restricted subjects with stroke. Positive expiratory pressure intensities above 10cmH2O should be used with caution as the increase in end-expiratory volume led to hyperinflation in subjects with stroke.

Determination of 'recruited volume' following a PEEP step is not a measure of lung recruitability.

It has been proposed that the analysis of positive end-expiratory pressure (PEEP)-induced volume changes can quantify alveolar recruitment. The potential of a lung to be recruited is expected to be high in acute respiratory distress syndrome (ARDS), where collapsed lung tissue is very common. The volume change that is beyond the delta volume because of the patient's compliance has been termed 'recruited volume' (RecV). However, data of patients with low and high RecV showed less severe lung disease in high 'recruiters', indicating that RecV may not equal the 'potentially recruitable lung tissue' seen in computed tomography scans. We hypothesized that RecV is higher in lung-healthy (LH) patients with little collapsed lung compared with ARDS patients. RecV and inspiratory capacity (IC) were determined in 12 LH and in 25 ARDS patients during incremental PEEP (steps of 2 cmH2 O). RecV was determined as the time-dependent increase in end-expiratory volume following the first expiration to the new PEEP level (ΔTDV). Gas distribution in LH patients was analyzed by electric impedance tomography. Cumulative RecV(ΔTDV) and IC were higher (P < 0.01) in LH compared with ARDS patients, 1739 ml vs. 832 ml and 4432 ml vs. 2020 ml, respectively. In both groups, RecV correlated excellently with IC (R(2) = 0.86). In LH, RecV emanated mainly from nondependent lung regions at PEEP below 15 cmH2O. Maximum plateau pressure was reached with fewer PEEP steps in ARDS compared with LH patients (11 vs. 14, P < 0.01). Our findings suggest that RecV predominately measures a slow fraction of inflation of already aerated lung tissue and not recruitment of collapsed alveoli.

Quantification of Improvements in Static and Dynamic Ventilatory Measures Following Lung Volume Reduction Surgery for Severe COPD

Rationale: This study quantitatively measured the effects of lung volume reduction surgery (LVRS) on spirometry, static and dynamic lung and chest wall volume subdivision mechanics, and cardiopulmonary exercise measures. Methods: Patients with severe COPD (mean FEV1 = 23 ± 6% predicted) undergoing LVRS evaluation were recruited. Spirometry, plethysmography and exercise capacity were obtained within 6 months pre-LVRS and again within 12 months post- LVRS. Ventilatory mechanics were quantified using stationary optoelectronic plethysmography (OEP) during spontaneous tidal breathing and during maximum voluntary ventilation (MVV). Statistical significance was set at P< 0.05. Results:Ten consecutive patients met criteria for LVRS (5 females, 5 males, age: 62±6yrs). Post -LVRS (mean follow up 7 months ± 2 months), the group showed significant improvements in dyspnea scores (pre 4±1 versus post 2 ± 2), peak exercise workload (pre 37± 21 watts versus post 50 ± 27watts ), heart rate (pre 109±19 beats per minutes [bpm] versus post 118±19 bpm), duty cycle (pre 30.8 ± 3.8% versus post 38.0 ± 5.7%), and spirometric measurements (forced expiratory volume in 1 second [FEV1] pre 23 ± 6% versus post 32 ± 13%, total lung capacity / residual lung volume pre 50 ± 8 versus 50 ± 11) . Six to 12 month changes in OEP measurements were observed in an increased percent contribution of the abdomen compartment during tidal breathing (41.2±6.2% versus 44.3±8.9%, P=0.03) and in percent contribution of the pulmonary ribcage compartment during MVV (34.5±10.3 versus 44.9±11.1%, P=0.02). Significant improvements in dynamic hyperinflation during MVV occurred, demonstrated by decreases rather than increases in end expiratory volume (EEV) in the pulmonary ribcage (pre 207.0 ± 288.2 ml versus post -85.0 ± 255.9 ml) and abdominal ribcage compartments (pre 229.1 ± 182.4 ml versus post -17.0 ± 136.2 ml) during the maneuver. Conclusions: Post-LVRS, patients with severe COPD demonstrate significant favorable changes in ventilatory mechanics, during tidal and maximal voluntary breathing. Future work is necessary to determine if these findings are clinically relevant, and extend to other environments such as exercise.

Raising end-expiratory volume relieves air hunger in mechanically ventilated healthy adults

Air hunger is an unpleasant urge to breathe and a distressing respiratory symptom of cardiopulmonary patients. An increase in tidal volume relieves air hunger, possibly by increasing pulmonary stretch receptor cycle amplitude. The purpose of this study was to determine whether increasing end-expiratory volume (EEV) also relieves air hunger. Six healthy volunteers (3 women, 31 +/- 4 yr old) were mechanically ventilated via a mouthpiece (12 breaths/min, constant end-tidal Pco(2)) at high minute ventilation (Ve; 12 +/- 2 l/min, control) and low Ve (6 +/- 1 l/min, air hunger). EEV was raised to approximately 150, 400, 725, and 1,000 ml by increasing positive end-expiratory pressure (PEEP) to 2, 4, 6, and 8 cmH(2)O, respectively, for 1 min during high and low Ve. The protocol was repeated with the subjects in the seated and supine positions to test for the effect of shifting baseline EEV. Air hunger intensity was rated at the end of each breath on a visual analog scale. The increase in EEV was the same in the seated and supine positions; however, air hunger was reduced to a greater extent in the seated position (13, 30, 31, and 44% seated vs. 3, 9, 23, and 27% supine at 2, 4, 6, and 8 cmH(2)O PEEP, respectively, P < 0.05). Removing PEEP produced a slight increase in air hunger that was greater than pre-PEEP levels (P < 0.05). Air hunger is relieved by increases in EEV and tidal volume (presumably via an increase in mean pulmonary stretch receptor activity and cycle amplitude, respectively).

Effects of PEEP on oxygenation and respiratory mechanics during one-lung ventilation

One-lung ventilation-related hypoxaemia (OLV-RH) can occur in patients with healthy lungs. In this case, PEEP frequently improves oxygenation. The aim of this study was to determine, in a healthy lung model of OLV, whether the increase in PEEP improved oxygenation and whether the mechanisms involved include both inspiratory lung recruitment and an end-expiratory lung volume increase. Since inhaled nitric oxide (iNO) may have a synergistic effect on oxygenation in the case of PEEP-induced recruitment, their association was also tested. Twenty pigs were studied during open-chest, left OLV. Arterial blood gases and haemodynamic variables were measured at different levels of PEEP (0, 5, 10 and 15 cm H(2)O) applied in random order with or without iNO 4 p.p.m. Pressure-volume curves were measured at each level of PEEP. PEEP(5) and PEEP(10) improved Pa(O(2))/FI(O(2)) ratio (P<0.005) and shunt (P<0.005) regardless of the presence of iNO. PEEP(15) improved oxygenation and shunt only when it was associated with iNO (P<0.001). Whereas PEEP(5), PEEP(10) and PEEP(15) were associated with a significant increase in end-expiratory volume (P<0.001), only PEEP(5) and PEEP(10) were associated with continuous lung volume recruitment (P<0.01). Moreover, PEEP(15) induced a significant decrease in linear compliance (P<0.001). In a healthy porcine lung model of OLV-RH, moderate PEEP can improve oxygenation. This effect implies both expiratory and inspiratory pulmonary recruitment. Co-administration of 4 p.p.m. iNO was ineffective.

Fluctuations in End-Expiratory Lung Volume during Cheyne-Stokes Respiration

We hypothesized that patients with Cheyne-Stokes respiration exhibit periodic increases in end-expiratory lung volume, mediated by changes in breath components, postinspiratory inspiratory muscle activity, or both. Calibrated inductive plethysmography revealed that 12 of 12 patients with Cheyne-Stokes respiration experienced increases in end-expiratory volume during hyperpnea: maximum 412 +/- 112 (SE) ml (range 75-1,543 ml). Compared with quiet breathing, the breath with largest increase in end-expiratory volume had larger tidal volume (867 +/- 107 vs. 567 +/- 38 ml, p < 0.01) and shorter expiratory time (1.25 +/- 0.11 vs. 1.66 +/- 0.15 seconds, p < 0.05). During decrescendo, the breath with largest decrease in end-expiratory volume had smaller tidal volume (p < 0.01) and longer expiratory time (p < 0.01). Cross-correlation of time series revealed that end-expiratory volume was related to both breath components (p < 0.0001). Bipolar needle electrodes revealed that scalene muscle activity at end-expiration was 50.7 +/- 14.0% higher at highest increase in lung volume than during preceding apnea (p < 0.05). Time series for scalene activity and end-expiratory volume were cross-correlated (p < 0.008). Increase in tonic scalene activity at end-expiration, however, was equivalent during crescendo and decrescendo phases: 50.6 +/- 22.1 versus 42.0 +/- 12.9% (p = 0.48). In conclusion, patients with Cheyne-Stokes respiration exhibit fluctuations in end-expiratory lung volume, primarily because of alterations in tidal volume and expiratory time rather than postinspiratory inspiratory muscle activity.

Chest wall hyperinflation during acute bronchoconstriction in asthma.

The mechanics of the chest wall was studied in seven asthmatic patients before and during histamine-induced bronchoconstriction (B). The volume of the chest wall (VCW) was calculated by three-dimensional tracking of 89 chest wall markers. Pleural (Ppl) and gastric (Pga) pressures were simultaneously recorded. VCW was modeled as the sum of the volumes of the pulmonary-apposed rib cage (VRC,p), diaphragm-apposed rib cage (VRC,a), and abdomen (VAB). During B, hyperinflation was due to the increase in end-expiratory volume of the rib cage (0.63 +/- 0.09 L, p < 0.01), whereas change in VAB was inconsistent (0.09 +/- 0.07 L, NS) because of phasic recruitment of abdominal muscles during expiration. Changes in end-expiratory VRC,p and VRC,a were along the rib cage relaxation configuration, indicating that both compartments shared proportionally the hyperinflation. VRC,p-Ppl plot during B was displaced leftward of the relaxation curve, suggesting persistent activity of rib cage inspiratory muscles throughout expiration. Changes in end-expiratory VCW during B did not relate to changes in FEV(1) or time and volume components of the breathing cycle. We concluded that during B in asthmatic patients: (1) rib cage accounts largely for the volume of hyperinflation, whereas abdominal muscle recruitment during expiration limits the increase in VAB; (2) hyperinflation is influenced by sustained postinspiratory activity of the inspiratory muscles; (3) this pattern of respiratory muscle recruitment seems to minimize volume distortion of the rib cage at end-expiration and to preserve diaphragm length despite hyperinflation.

Effects of chest wall counterpressures on lung mechanics under high levels of CPAP in humans.

We assessed the respective effects of thoracic (TCP) and abdominal/lower limb (ACP) counterpressures on end-expiratory volume (EEV) and respiratory muscle activity in humans breathing at 40 cmH2O of continuous positive airway pressure (CPAP). Expiratory activity was evaluated on the basis of the inspiratory drop in gastric pressure (DeltaPga) from its maximal end-expiratory level, whereas inspiratory activity was evaluated on the basis of the transdiaphragmatic pressure-time product (PTPdi). CPAP induced hyperventilation (+320%) and only a 28% increase in EEV because of a high level of expiratory activity (DeltaPga = 24 +/- 5 cmH2O), contrasting with a reduction in PTPdi from 17 +/- 2 to 9 +/- 7 cmH2O . s-1 . cycle-1 during 0 and 40 cmH2O of CPAP, respectively. When ACP, TCP, or both were added, hyperventilation decreased and PTPdi increased (19 +/- 5, 21 +/- 5, and 35 +/- 7 cmH2O . s-1 . cycle-1, respectively), whereas DeltaPga decreased (19 +/- 6, 9 +/- 4, and 2 +/- 2 cmH2O, respectively). We concluded that during high-level CPAP, TCP and ACP limit lung hyperinflation and expiratory muscle activity and restore diaphragmatic activity.

Effects of Doxapram on Hypercapnic Response during Weaning from Mechanical Ventilation in COPD Patients

Failure of weaning from mechanical ventilation in COPD patients is often related to diaphragmatic fatigue. Whether there is a central respiratory drive fatigue and a reserve of excitability is still debated. The purpose of this study was to analyze the following in 13 COPD patients weaned from mechanical ventilation: (1) ventilatory (VE/PETCO2) and neuromuscular (P0.1/PETCO2) response to hypercapnia; (2) the maximum reserve capacity measured through changes in the VE/PETCO2 and P0.1/PETCO2 slopes after doxapram (DXP) infusion, which, given during the test, allows measurement of the maximum response capacity to overstimulation; and (3) analyze the influence of these changes on the outcome of weaning. The results show a variable P0.1/PETCO2 response and a low VE/PETCO2. DXP infusion does not change the slopes of these relations but increases the end-expiratory volume (delta FRCd); (p less than 0.02). Since there was no change in the VE/PETCO2, P0.1/PETCO2, and delta FRC values with or without DXP, there was no excitability reserve in patients who were successfully weaned. When weaning failed, DXP did not change VE/PETCO2 and P0.1/PETCO2 slope, but delta FRCd was greater the delta FRC (p less than 0.001). The excitability reserve in these patients leads to an increase in end-expiratory volume, probably worsening the diaphragm dysfunction.

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.

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.

Effects of an increase in end-expiratory volume on the pattern of thoracoabdominal movement

Changes in end-expiratory lung volume can alter the mechanical function of the muscles of inspiration and may affect the pattern of thoracoabdominal movements. The present study examined the effect of increasing end-expiratory lung volume on the motion of the rib cage and abdomen during inspiration. In six seated subjects, end-expiratory volume was increased by expiratory threshold loading. The end-expiratory thoracoabdominal configuration shifted to the left of the relaxation curve presumably as a result of the activation of the abdominal expiratory muscles. There was outward displacement of both the rib cage and the abdomen with inspiration at the elevated volume but the relative volumetric contribution of abdominal displacement to the inspired volume was significantly less than during breathing from FRC. When at an enlarged lung volume subjects were constrained to initiate inspiration from a point on the thoracoabdominal relaxation configuration, there was inward movement of the abdomen and a decrease in abdominal dimensions during inspiration. Inward abdominal movement occurred despite large increases in diaphragm electrical activity and was associated with an inspiratory fall in gastric pressure. These results suggest that at large lung volumes, the function of the diaphragm as an agonist is lost and its function as a fixator may be impaired unless there is an activation of the abdominal muscles and the diaphragm is appropriately lengthened.

Effects of hyperinflation of the thorax on the mechanics of breathing.

ARTICLESEffects of hyperinflation of the thorax on the mechanics of breathingA. E. Grassino, G. E. Lewinsohn, and J. M. TylerA. E. Grassino, G. E. Lewinsohn, and J. M. TylerPublished Online:01 Sep 1973https://doi.org/10.1152/jappl.1973.35.3.336MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByHyperinflation and expiratory muscle recruitment during NREM sleep in humansRespiration Physiology, Vol. 82, No. 1Effect of Helium Concentration on Experimental Upper Airway Obstruction28 June 2016 | Annals of Otology, Rhinology & Laryngology, Vol. 99, No. 7Load compensation during positive pressure breathing in anesthetized manRespiration Physiology, Vol. 65, No. 3Effects of an increase in end-expiratory volume on the pattern of thoracoabdominal movementRespiration Physiology, Vol. 53, No. 3Respiratory mechanics of Pekin ducks under four conditions: Pressure breathing, anesthesia, paralysis or breathing CO2-enriched gasRespiration Physiology, Vol. 47, No. 2Muscle activity during chest wall restriction and positive pressure breathing in manRespiration Physiology, Vol. 35, No. 3The effect of hyperoxia, hypoxia and hypercapnia on FRC and occlusion pressure in human subjectsRespiration Physiology, Vol. 33, No. 2Airway occlusion pressures in awake and anesthetized goatsRespiration Physiology, Vol. 27, No. 1Effect of inspiratory resistance on occlusion pressure in hypoxia and hypercapniaRespiration Physiology, Vol. 24, No. 3Occlusion pressure as a measure of respiratory center output cm conscious manRespiration Physiology, Vol. 23, No. 2 More from this issue > Volume 35Issue 3September 1973Pages 336-342 Copyright & PermissionsCopyright © 1973 the American Physiological Societyhttps://doi.org/10.1152/jappl.1973.35.3.336PubMed4269954History Published online 1 September 1973 Published in print 1 September 1973 Metrics

Relative contribution of rib cage and abdomen to ventilation during exercise.

Relative contribution of rib cage and abdomen to ventilation during exercise.

Measurement of the separate volume changes of rib cage and abdomen during breathing.

Measurement of the separate volume changes of rib cage and abdomen during breathing.

Characteristics of an inspiration-augmenting reflex in anesthetized cats.

Overinflation or release from deflation of the lungs in anesthetized cats induced a vagally mediated, inspiration-augmenting reflex, characterized by a sudden phrenic motor discharge and an increase in rate and depth of inspiration. It resulted in an increase in end-expiratory volume and lung compliance. In a series of sinusoidal inflations, the reflex could exhibit summation to occur on any single inflation, but having occurred, was temporarily refractory to further inflations. The spontaneous deep breath was shown to be the same reflex, being vagally mediated, and similarly related to changes in mechanical properties of the lungs. The effective stimulus was shown to be a function of velocity and duration of inflation, while the refractoriness shown by the reflex was related to the accompanying increase in end-expiratory volume. The inspiration-augmenting reflex, by increasing functional residual capacity and compliance, was presumed to open alveolar units. It may interact with the Hering-Breuer inspiration-limiting reflex in controlling the respiratory cycle. Submitted on January 8, 1962