Expiratory Contraction Research Articles

Gastric Pressure Monitoring Unveils Abnormal Patient-Ventilator Interaction Related to Active Expiration: A Retrospective Observational Study.

Patient-ventilator dyssynchrony is frequently observed during assisted mechanical ventilation. However, the effects of expiratory muscle contraction on patient-ventilator interaction are underexplored. The authors hypothesized that active expiration would affect patient-ventilator interaction and they tested their hypothesis in a mixed cohort of invasively ventilated patients with spontaneous breathing activity. This is a retrospective observational study involving patients on assisted mechanical ventilation who had their esophageal pressure (Peso) and gastric pressure monitored for clinical purposes. Active expiration was defined as gastric pressure rise (ΔPgas) greater than or equal to 1.0 cm H2O during expiratory flow without a corresponding change in diaphragmatic pressure. Waveforms of Peso, gastric pressure, diaphragmatic pressure, flow, and airway pressure (Paw) were analyzed to identify and characterize abnormal patient-ventilator interaction. 76 patients were identified with Peso and gastric pressure recordings, of whom 58 demonstrated active expiration with a median ΔPgas of 3.4 cm H2O (interquartile range = 2.4 to 5.3) observed in this subgroup. Among these 58 patients, 23 presented the following events associated with expiratory muscle activity: (1) distortions in Paw and flow that resembled ineffective efforts, (2) distortions similar to autotriggering, (3) multiple triggering, (4) prolonged ventilatory cycles with biphasic inspiratory flow, with a median percentage (interquartile range) increase in mechanical inflation time and tidal volume of 54% (44 to 70%) and 25% (8 to 35%), respectively and (5) breathing exclusively by expiratory muscle relaxation. Gastric pressure monitoring was required to identify the association of active expiration with these events. Respiratory drive, assessed by the rate of inspiratory Peso decrease, was significantly higher in patients with active expiration (median [interquartile range] dPeso/dt: 12.7 [9.0 to 18.5] vs 9.2 [6.8 to 14.2] cmH2O/sec; P < 0.05). Active expiration can impair patient-ventilator interaction in critically ill patients. Without documenting gastric pressure, abnormal patient-ventilator interaction associated with expiratory muscle contraction may be mistakenly attributed to a mismatch between the patient's inspiratory effort and mechanical inflation. This misinterpretation could potentially influence decisions regarding clinical management.

Impact Of Repeated, Hyperoxic Exercise Dives On Pulmonary Force Production Before And After Endurance Runs

Few studies have described maximal inspiratory/expiratory pressures (MIP/MEP) following hyperoxic dives. PURPOSE: Quantify changes in pulmonary force production pre- and post- run-to-fatigue before, after, and 72 hr post single and consecutive 6-hr hyperoxic exercise dives. METHODS: 14 military trained divers (age 30.6 ± 2.2 yrs) performed a single 6-hr dive (SD) and five consecutive 6-hr dives with 18-hr surface intervals (DW) breathing 100% oxygen at 1.35 ATA while alternating between 30-minute rest and exercise periods. An 85% V̇O2max endurance run was performed three days before SD and DW (PRE), within 2 hrs (2-POST) and 72 hrs (72-POST) after SD or dive 5 of DW. Three trials of MIP/MEP were recorded before and after each run. Data were analyzed using a 2 (Run: pre/post run) x 3 (Diving: PRE, 2-POST, 72-POST) repeated measures analysis of variance (ANOVA) with significance set at p < 0.05. Data presented as mean ± SEM. RESULTS: There was a significant main effect of the run on MIP for both SD (pre-run: -116.5 ± 0.8 cm H2O vs. post-run: -111.5 ± 0.5 cm H2O, p = 0.016) and DW (pre-run: -118.2 ± 1.3 cm H2O vs. post-run: -111.1 ± 0.5 cm H2O, p = 0.034). There was no main effect of diving or run x diving interaction on MIP for SD or DW. There was a significant main effect of the run on MEP (pre-run: 150.2 ± 4.4 cm H2O vs post-run: 144.6 ± 3.9 cm H2O, p = 0.032), and a significant main effect of diving (Pre-dive: 154.7 ± 5.8 cm H2O vs 2-POST: 140.4 ± 6.4 cm H2O vs 72-POST 147.1 ± 5.8 cm H2O p = 0.002). DW post-test analysis showed that 2-POST pre-run (143.2 ± 9.4 cm H2O, p < 0.001), 2-POST post-run (137.6 ± 9.1 cm H2O, p < 0.001), 72-POST pre-run (149.0 ± 8.4 cm H2O, p = 0.015), and 72-POST post-run (145.2 ± 8.3 cm H2O, p < 0.001) were significantly lower than PRE pre-run MEP (158.4 ± 8.4 cm H2O). There was no significant difference compared to PRE post-run (151.1 ± 8.3 cm H2O). There were no significant main effects or interactions for MEP during SD. There were no significant correlations between percent change in run time and percent change in MIP or MEP. CONCLUSION: Reductions in expiratory, but not inspiratory, force following repeated, long-duration hyperoxic immersions suggests repetitive 100% O2 exposure differentially affects expiratory force production, potentially due to hyperoxia-induced impairment of expiratory muscle contraction. Funded by ONR and NAVSEA DSBD

Airway pressure morphology and respiratory muscle activity during end-inspiratory occlusions in pressure support ventilation

BackgroundThe driving pressure of the respiratory system is a valuable indicator of global lung stress during passive mechanical ventilation. Monitoring lung stress in assisted ventilation is indispensable, but achieving passive conditions in spontaneously breathing patients to measure driving pressure is challenging. The accuracy of the morphology of airway pressure (Paw) during end-inspiratory occlusion to assure passive conditions during pressure support ventilation has not been examined.MethodsRetrospective analysis of end-inspiratory occlusions obtained from critically ill patients during pressure support ventilation. Flow, airway, esophageal, gastric, and transdiaphragmatic pressures were analyzed. The rise of gastric pressure during occlusion with a constant/decreasing transdiaphragmatic pressure was used to identify and quantify the expiratory muscle activity. The Paw during occlusion was classified in three patterns, based on the differences at three pre-defined points after occlusion (0.3, 1, and 2 s): a “passive-like” decrease followed by plateau, a pattern with “clear plateau,” and an “irregular rise” pattern, which included all cases of late or continuous increase, with or without plateau.ResultsData from 40 patients and 227 occlusions were analyzed. Expiratory muscle activity during occlusion was identified in 79% of occlusions, and at all levels of assist. After classifying occlusions according to Paw pattern, expiratory muscle activity was identified in 52%, 67%, and 100% of cases of Paw of passive-like, clear plateau, or irregular rise pattern, respectively. The driving pressure was evaluated in the 133 occlusions having a passive-like or clear plateau pattern in Paw. An increase in gastric pressure was present in 46%, 62%, and 64% of cases at 0.3, 1, and 2 s, respectively, and it was greater than 2 cmH2O, in 10%, 20%, and 15% of cases at 0.3, 1, and 2 s, respectively.ConclusionsThe pattern of Paw during an end-inspiratory occlusion in pressure support cannot assure the absence of expiratory muscle activity and accurate measurement of driving pressure. Yet, because driving pressure can only be overestimated due to expiratory muscle contraction, in everyday practice, a low driving pressure indicates an absence of global lung over-stretch. A measurement of high driving pressure should prompt further diagnostic workup, such as a measurement of esophageal pressure.

Feedforward discharges couple the singing central pattern generator and ventilation central pattern generator in the cricket abdominal central nervous system

We investigated the central nervous coordination between singing motor activity and abdominal ventilatory pumping in crickets. Fictive singing, with sensory feedback removed, was elicited by eserine-microinjection into the brain, and the motor activity underlying singing and abdominal ventilation was recorded with extracellular electrodes. During singing, expiratory abdominal muscle activity is tightly phase coupled to the chirping pattern. Occasional temporary desynchronization of the two motor patterns indicate discrete central pattern generator (CPG) networks that can operate independently. Intracellular recordings revealed a sub-threshold depolarization in phase with the ventilatory cycle in a singing-CPG interneuron, and in a ventilation-CPG interneuron an excitatory input in phase with each syllable of the chirps. Inhibitory synaptic inputs coupled to the syllables of the singing motor pattern were present in another ventilatory interneuron, which is not part of the ventilation-CPG. Our recordings suggest that the two centrally generated motor patterns are coordinated by reciprocal feedforward discharges from the singing-CPG to the ventilation-CPG and vice versa. Consequently, expiratory contraction of the abdomen usually occurs in phase with the chirps and ventilation accelerates during singing due to entrainment by the faster chirp cycle.

Respiratory muscle activation and action during voluntary cough in healthy humans

Cough is a defensive airway reflex consisting of a modified respiratory act which involves the sequential activation of several laryngeal and respiratory muscles. The contraction of the latter results in thoraco-abdominal volume variations in order to provide enough amount of air available, the operating volume (OV), to be expelled. Because both posture and OV could influence muscular activation and thoraco-abdominal displacements during voluntary cough, we aimed to verify if and how they play a role during inspiratory (ICP) and expiratory (ECP) cough phases, in terms of flow, volumes and surface electromyography activity (sEMG). In 10 healthy subjects, we measured sEMG of 7 muscles (scalene, sternocleidomastoid, parasternal, intercostal, diaphragm (assessed at the 8th intercostal space), external abdominal oblique and rectus abdominis) in supine and seated position during cough maneuvers performed at 4 different OV measured by opto-electronic plethismography: total lung capacity (TLC), functional residual capacity and two intermediate volumes. The amplitude of sEMG signals tended to be maximal at TLC (p < 0.005) during ICP in the neck and parasternal muscles and during ECP in abdominal muscles. Postures slightly affected only sEMG of the thoracic muscles. sEMG data were similar (p > 0.05) in the other OV, but cough peak flow increased with OV. Thoraco-abdominal volume variations during cough were unaffected by posture and OV as well, being predominantly thoracic (supine: 60 and 64%; seated: 68 and 69%, respectively during ICP and ECP).Our results suggest that voluntary cough OV or posture do not have an important effect on voluntary cough that seems more likely to be resulting from a motor mechanism that activates a synergetic antagonistic contraction of inspiratory and expiratory muscles leading to a specific thoraco-abdominal pattern, in which the rib cage is the predominant.

Specific anesthesia-induced lung volume changes from induction to emergence: a pilot study.

Studies aimed at maintaining intraoperative lung volume to reduce post-operative pulmonary complications have been inconclusive because they mixed up the effect of general anesthesia and the surgical procedure. Our aims were to study: (1) lung volume during the entire course of anesthesia without the confounding effects of surgical procedures; (2) the combination of three interventions to maintain lung volume; and (3) the emergence phase with focus on the restored activation of the respiratory muscles. Eighteen ASA I-II patients undergoing ENT surgery under general anesthesia without muscle relaxants were randomized to an intervention group, receiving lung recruitment maneuver (LRM) after induction, 7cmH2 O positive end-expiratory pressure (PEEP) during anesthesia and continuous positive airway pressure (CPAP) during emergence with 0.4 inspired oxygen fraction (FiO2 ) or a control group, ventilated without LRM, with 0cmH2 O PEEP, and 1.0 FiO2 during emergence without CPAP application. End-expiratory lung volume (EELV) was continuously estimated by opto-electronic plethysmography. Inspiratory and expiratory ribcage muscles electromyography was measured in a subset of seven patients. End-expiratory lung volume decreased after induction in both groups. It remained low in the control group and further decreased at emergence, because of active expiratory muscle contraction. In the intervention group, EELV increased after LRM and remained high after extubation. A combined intervention consisting of LRM, PEEP and CPAP during emergence may effectively maintain EELV during anesthesia and even after extubation. An unexpected finding was that the activation of the expiratory muscles may contribute to EELV reduction during the emergence phase.

Review of Epidural Spinal Cord Stimulation for Augmenting Cough after Spinal Cord Injury.

Spinal cord injury (SCI) remains a debilitating condition for which there is no cure. In addition to loss of somatic sensorimotor functions, SCI is also commonly associated with impairment of autonomic function. Importantly, cough dysfunction due to paralysis of expiratory muscles in combination with respiratory insufficiency can render affected individuals vulnerable to respiratory morbidity. Failure to clear sputum can aggravate both risk for and severity of respiratory infections, accounting for frequent hospitalizations and even mortality. Recently, epidural stimulation of the lower thoracic spinal cord has been investigated as novel means for restoring cough by evoking expiratory muscle contraction to generate large positive airway pressures and expulsive air flow. This review article discusses available preclinical and clinical evidence, current challenges and clinical potential of lower thoracic spinal cord stimulation (SCS) for restoring cough in individuals with SCI.

The Diaphragm Acts as a Brake during Expiration to Prevent Lung Collapse.

The diaphragm is the major inspiratory muscle and is assumed to relax during expiration. However, electrical postinspiratory activity has been observed. Whether there is an expiratory diaphragmatic contraction that preserves lung patency has yet to be explored. We hypothesized the occurrence of an expiratory diaphragmatic contraction directed at stabilizing peripheral airways and preventing or reducing cyclic expiratory lung collapse. Mild acute respiratory distress syndrome was induced in 10 anesthetized, spontaneously breathing pigs. Lung volume was decreased by lowering end-expiratory airway pressure in a stepwise manner. We recorded the diaphragmatic electric activity during expiration, dynamic computed tomographic scans, and respiratory mechanics. In five pigs, the same protocol was repeated during mechanical ventilation after muscle paralysis. Diaphragmatic electric activity during expiration increased by decreasing end-expiratory lung volume during spontaneous breathing. This enhanced the diaphragm muscle force, to a greater extent with lower lung volume, indicating a diaphragmatic electromechanical coupling during spontaneous expiration. In turn, the resulting diaphragmatic contraction delayed and reduced the expiratory collapse and increased lung aeration compared with mechanical ventilation with muscle paralysis and absence of diaphragmatic activity. The diaphragm is an important regulator of expiration. Its expiratory activity seems to preserve lung volume and to protect against lung collapse. The loss of diaphragmatic expiratory contraction during mechanical ventilation and muscle paralysis may be a contributing factor to unsuccessful respiratory support.

Spirometry improvement after muscular exercise in elite swimmers.

An increased sympathetic activity during muscular effort is a well established physiological response, whose intensity is known to increase with the muscular load. Spirometry was described to improve as an effect of swimming training in healthy and asthmatic subjects, suggesting a decrease in airway resistance The aim was to investigate the possible effect of muscular exercise (swimming) on spirometry, in particular searching for possible differences because of different swimming times. The measurements were performed on 9 highly trained male competitive swimmers (age: 41±12.79 years, height: 1.69±0.06 meters, weight: 66.14±14.28 kg, BMI: 22.8±3.61 kg/m2) during an official competition. The data were collected at the border of the swimming-pool before (control, C) and few minutes after the swimming sessions (exercise, E), which consisted either of 800 meter (7 subjects) or 1500 meter (5 subjects) free style. A general trend indicating a postexercise increase in spirometry was observed. We found post-exercise significant increments in FEV1 and in MEF75 for both the 800 and 1500 meter swimming sessions, and in FEF25-75 and in MEF25 for the shorter distance. We conclude that, as it may be expected, muscular exercise induces an improvement of spirometry both because of a smooth muscle relaxation-induced modulation of airway diameter and resistance to airflow, and because of an enhanced expiratory muscle contraction strength. Both of these mechanisms are related to an increased sympathetic activity which is well known to accompany muscular exercise.

Simulation of late inspiratory rise in airway pressure during pressure support ventilation.

Late inspiratory rise in airway pressure (LIRAP, Paw/ΔT) caused by inspiratory muscle relaxation or expiratory muscle contraction is frequently seen during pressure support ventilation (PSV), although the modulating factors are unknown. We investigated the effects of respiratory mechanics (normal, obstructive, restrictive, or mixed), inspiratory effort (-2, -8, or -15 cm H2O), flow cycle criteria (5-40% peak inspiratory flow), and duration of inspiratory muscle relaxation (0.18-0.3 s) on LIRAP during PSV using a lung simulator and 4 types of ventilators. LIRAP occurred with all lung models when inspiratory effort was medium to high and duration of inspiratory muscle relaxation was short. The normal lung model was associated with the fastest LIRAP, whereas the obstructive lung model was associated with the slowest. Unless lung mechanics were normal or mixed, LIRAP was unlikely to occur when inspiratory effort was low. Different ventilators were also associated with differences in LIRAP speed. Except for within the restrictive lung model, changes in flow cycle level did not abolish LIRAP if inspiratory effort was medium to high. Increased duration of inspiratory relaxation also led to the elimination of LIRAP. Simulation of expiratory muscle contraction revealed that LIRAP occurred only when expiratory muscle contraction occurred sometime after the beginning of inspiration. Our simulation study reveals that both respiratory resistance and compliance may affect LIRAP. Except for under restrictive lung conditions, LIRAP is unlikely to be abolished by simply lowering flow cycle criteria when inspiratory effort is strong and relaxation time is rapid. LIRAP may be caused by expiratory muscle contraction when it occurs during inspiration.

0434. Simulation of late inspiratory rise in airway pressure during pressure support ventilation

Late inspiratory rise in airway pressure (LIRAP, ΔPaw/Δt, Fig. ​Fig.1)1) caused by inspiratory muscle relaxation or expiratory muscle contraction is frequently seen during pressure support ventilation [1, 2], although the factors that modulate LIRAP are unknown. Figure 1 Objectives The aim of current study was to determine the factors related to LIRAP during PSV using a simulation lung model. Influence of inspiratory muscle relaxation was assessed under various combinations of lung models and ventilator settings. Influence of expiratory muscle contraction was assessed through its intervention at various time points during the inspiratory phase.

Reading Pulmonary Vascular Pressure Tracings. How to Handle the Problems of Zero Leveling and Respiratory Swings

The accuracy of pulmonary vascular pressure measurements is of great diagnostic and prognostic relevance. However, there is variability of zero leveling procedures, and the current recommendation of end-expiratory reading may not always be adequate. A review of physiological and anatomical data, supported by recent imaging, leads to the practical recommendation of zero leveling at the cross-section of three transthoracic planes, which are, respectively midchest frontal, transverse through the fourth intercostal space, and midsagittal. As for the inevitable respiratory pressure swings, end-expiratory reading at functional residual capacity allows for minimal influence of elastic lung recoil on pulmonary pressure reading. However, hyperventilation is associated with changes in end-expiratory lung volume and increased intrathoracic pressure, eventually exacerbated by expiratory muscle contraction and dynamic hyperinflation, all increasing pulmonary vascular pressures. This problem is amplified in patients with obstructed airways. With the exception of dynamic hyperinflation states, it is reasonable to assume that negative inspiratory and positive expiratory intrathoracic pressures cancel each other out, so averaging pulmonary vascular pressures over several respiratory cycles is most often preferable. This recommendation may be generalized for the purpose of consistency and makes sense, as pulmonary blood flow measurements are not corrected for phasic inspiratory and expiratory changes in clinical practice.

A human model of the pathophysiology of chronic obstructive pulmonary disease

This short review summarizes a series of studies on the effects of expiratory flow limitation (EFL) at approximately 1 L/s during incremental exercise to maximal workload (Wmax) in normal subjects on exercise performance, respiratory muscle dynamics and control, and CO(2) elimination. Each subject served as his or her own control by performing the same protocol without EFL. Additionally, an index of cardiac output was measured before and after imposing EFL while the subjects exercised at Wmax, Wmax was reduced to 65% of control by severe dyspnoea. EFL forced a decrease in the shortening velocity of expiratory muscles, resulting in increased expiratory pressures which accounted for 66% of the variance in Borg scale ratings of dyspnoea. In spite of an increase in the shortening velocity of inspiratory muscles, inspiratory pressures and power increased, because EFL exercise induced hypercapnia, which increased the chemical drive to breathe. This was in part due to an increased alveolar dead space presumably resulting from a reduction in pulmonary capillary blood volume secondary to the high expiratory pressures. A vicious circle was established in which expiratory muscle pressures induced hypercapnia, which resulted in an even stronger expiratory muscle contraction. The imposition of EFL reduced cardiac output by 10% and decreased arterial O(2) saturation, reducing energy supplies to working locomotor and respiratory muscles. This model reproduces the most important clinical features of COPD, and these arise from ventilatory pump dysfunction rather than from the lung. It also leads to hypotheses that can be tested in patients with COPD.

Respiratory muscles

Maintenance of oxygen/carbon dioxide homeostasis requires continuous movement of air into and out of the alveolus. In healthy humans, inspiration occurs when the inspiratory muscles contract to generate a sub-atmospheric pressure in the thorax; in contrast, expiration is passive at rest, though it can be assisted by expiratory muscle contraction in the absence of flow limitation. The respiratory muscles are histologically and physiologically identical to peripheral skeletal muscle. The fibre-type mix of the diaphragm, the most important inspiratory muscle, is similar to that of the quadriceps − 50% type I and 50% type II. Diaphragm contraction results in downwards movement of the diaphragmatic dome (Figure 1). This generates a negative pressure change in the thorax (resulting in inspiratory airflow) and a positive pressure change in the abdomen. Unopposed diaphragm action (as in high tetraplegia) therefore results in inwards movement of the ribcage. In healthy humans, this is opposed by co-contraction of the upper thoracic inspiratory muscles (scalenes and sternomastoid) and by expansion of the lower ribcage, achieved by transmission of the abdominal pressure through the zone of apposition.

Effects of expiratory muscle work on muscle sympathetic nerve activity.

We hypothesized that contractions of the expiratory muscles carried out to the point of task failure would cause an increase in muscle sympathetic nerve activity (MSNA). We measured MSNA directly in six healthy men during resisted expiration (60% maximal expiratory pressure) leading to task failure with long [breathing frequency (f(b)) = 15 breaths/min; expiratory time (TE)/total respiratory cycle duration (TT) = 0.7] and short (f(b) = 30 breaths/min; TE/TT = 0.4) TE. Both of these types of expiratory muscle contractions elicited time-dependent increases in MSNA burst frequency that averaged +139 and +239%, respectively, above baseline at end exercise. The increased MSNA coincided with increases in mean arterial pressure (MAP) for both the long-TE (+28 +/- 6 mmHg) and short-TE (+22 +/- 14 mmHg) trials. Neither MSNA nor MAP changed when the breathing patterns and increased tidal volume of the task failure trials were mimicked without resistance or task failure. Furthermore, very high levels of expiratory motor output (95% maximal expiratory pressure; f(b) = 12 breaths/min; TE/TT = 0.35) and high rates of expiratory flow and expiratory muscle shortening without task failure (no resistance; f(b) = 45 breaths/min; TE/TT = 0.4; tidal volume = 1.9 x eupnea) had no effect on MSNA or MAP. Within-breath analysis of the short-expiration trials showed augmented MSNA at the onset of and throughout expiration that was consistent with an influence of high levels of central expiratory motor output. Thus high-intensity contractions of expiratory muscles to the point of task failure caused a time-dependent sympathoexcitation; these effects on MSNA were similar in their time dependency to those caused by high-intensity rhythmic contractions of the diaphragm and forearm muscles taken to the point of task failure. The evidence suggests that these effects are mediated primarily via a muscle metaboreflex with a minor, variable contribution from augmented central expiratory motor output.

Contribution of Expiratory Muscle Pressure to Dynamic Intrinsic Positive End-Expiratory Pressure

In spontaneously breathing (SB) patients expiratory muscle contraction leads to an overestimation of dynamic intrinsic PEEP (PEEP(i),dyn). To quantify this overestimation, PEEP(i),dyn measured with the esophageal balloon technique was corrected for the increase in Pga over the course of expiration (Pga,exp rise), for the whole decay of Pga during inspiration (Pga,total decay) or for the part of Pga decay restricted between the onset of inspiratory effort and the point of zero flow (Pga,zf decay). Corrections were compared with the reference PEEP(i),dyn (PEEP(i),dyn ref ), calculated by using the Campbell diagram. In 15 ventilator-dependent, SB, and actively expiring patients, we found that the difference PEEP(i),dyn - Pga, total decay (mean +/- SD, 5.7 +/- 1.9 cm H(2)O) was quite similar to PEEP(i),dyn ref (5.3 +/- 1.9 cm H(2)O). Their mean difference was 0. 37 cm H(2)O with limits of agreement -0.09 to 0.83 cm H(2)O, indicating strong agreement between these methods. PEEP(i),dyn - Pga, exp rise (6.0 +/- 2.1 cm H(2)O) was also similar to PEEP(i),dyn ref. Their mean difference was 0.72 cm H(2)O with limits of agreement -1. 69 to 3.13 cm H(2)O, indicating good agreement. In contrast, mean difference of PEEP(i),dyn - Pga,zf decay and PEEP(i),dyn ref was 3. 14 cm H(2)O with limits of agreement -0.46 to 6.74 cm H(2)O, indicating lack of agreement. The error in measurement due to the subtraction of Pga,zf decay from PEEP(i),dyn (i.e., [PEEP(i),dyn - Pga,zf decay] - PEEP(i),dyn ref ) was proportional to the intensity of expiratory muscle contraction, as expressed by the Pga,exp rise (r = 0.903, p < 0.001). We conclude that in actively expiring patients an adequate correction of PEEP(i),dyn for the overestimation caused by expiratory muscle contraction can be made by subtracting either Pga,total decay or Pga,exp rise from PEEP(i), dyn, the former achieving the best performance.

Expiratory muscle pressure and breathing mechanics in chronic obstructive pulmonary disease.

Expiratory muscle recruitment is common in stable chronic obstructive pulmonary disease (COPD) patients. Due to airway obstruction, there is little reason to believe that active expiration in COPD would be mechanically effective in lowering operating lung volume. The physiological significance of expiratory muscle recruitment in COPD, therefore, remains unknown. The purpose of this study was to assess, in COPD patients breathing at rest, the effect of expiratory muscle contraction on force generating ability of the diaphragm. The force generating ability of the diaphragm was evaluated from its pressure swing (Pdi) for a given diaphragm electrical activity (Edi), where Edi was normalized as % of its maximal value (Pdi/Edi/Edi,max). Phasic expiratory muscle contraction was measured as the total expiratory rise in gastric pressure (Pga,exp.rise). Nineteen seated patients with moderate to severe COPD, participated in the study and 10 exhibited phasic rise in Pga during expiration with a mean Pga,exp.rise of 1.91+/-0.89 cmH2O. The patients were thus divided into passive expiration (PE) and active expiration (AE) groups. There was no significant difference in various lung function and breathing pattern parameters between the two groups. Pdi/Edi/Edi,max was 0.63+/-0.07 and 0.54+/-0.07 cmH2O/% in PE and AE groups, respectively, and was not significantly different between each other. Compared with PE group, AE group not only recruited expiratory muscles, but also preferentially recruited inspiratory rib cage muscles and derecruited the diaphragm. The results do not support a significant improvement of the force-generating ability of the diaphragm by phasic contraction of expiratory muscles at rest in chronic obstructive pulmonary disease patients.

Correcting static intrinsic positive end-expiratory pressure for expiratory muscle contraction. Validation of a new method.

We have recently shown (Eur. Respir. J. 1997;10:522-529) that in spontaneously breathing and actively expiring patients, static intrinsic positive end-expiratory pressure (PEEPi,st) can be corrected for expiratory muscle contraction by subtracting the average expiratory rise in gastric pressure (Pga,exp rise), calculated from three breaths just prior to an airway occlusion, from the end-expiratory airway pressure (Paw) of the first occluded inspiratory effort (PEEPi,st avg). However, since in some patients there is substantial variability in the intensity of expiratory muscle activity and hence in Pga,exp rise, this method may be inaccurate because the Pga,exp rise of breaths preceding airway occlusion may differ from that of the first postocclusion breath. In the present study, we introduced a new method consisting of synchronous subtraction of Pga,exp rise from Paw, both occurring during airway occlusion (PEEPi,st sub). PEEPi,st sub and PEEPi,st avg were each compared with the reference PEEPi,st (PEEPi,st ref), which was obtained during muscular paralysis and simulation of the spontaneous breathing pattern by the ventilator. We found that, in 25 critically ill patients, PEEPi,st sub (mean +/- SD, 5.3 +/- 2.6 cm H(2)O) was nearly identical to PEEPi,st ref (5.4 +/- 2.4 cm H(2)O). Their mean difference was -0.06 cm H(2)O with limits of agreement -0.96 to 0.84 cm H(2)O, indicating a strong agreement between these methods. In contrast, mean difference of PEEPi,st avg and PEEPi,st ref was 0.73 cm H(2)O with limits of agreement -3.97 to 5.43 cm H(2)O, indicating lack of agreement. Coefficient of variation of Pga,exp rise was 14.3 +/- 7.2% (range, 5.2 to 28.3%). There was a good correlation between the coefficient of variation of Pga,exp rise and the difference between PEEPi,st avg and PEEPi,st ref (r = 0.909; p < 0.001). We conclude that PEEPi,st can be accurately measured in spontaneously breathing patients by synchronous subtraction of Pga,exp rise from Paw during airway occlusion.

Physiological basis and pharmacology of motion sickness: an update

Motion sickness can occur when sensory inputs regarding body position in space are contradictory or are different from those predicted from experience. Signals from the vestibular system are essential for triggering motion sickness. The evolutionary significance of this malady is unclear, although it may simply represent the aberrant activation of vestibuloautonomic pathways that typically subserve homeostasis. The neural pathways that produce nausea and vomiting during motion sickness are presumed to be similar to those that generate illness after ingestion of toxins. The neural substrate of nausea is unknown but may include neurons in the hypothalamus and inferior frontal gyrus of the cerebral cortex. The principal motor act of vomiting is accomplished through the simultaneous contractions of inspiratory and expiratory respiratory muscles and is mediated by neurons in the lateral medullary reticular formation and perhaps by cells near the medullary midline. Cocontraction of the diaphragm and abdominal muscles increases pressure on the stomach, which causes gastric contents to be ejected through the mouth. Effective drugs for combating motion sickness include antihistamines, antimuscarinics, 5-HT 1A (serotonergic) receptor agonists and neurokinin type 1 receptor antagonists. However, considerable information concerning the physiological basis and pharmacology of motion sickness is unknown; future research using animal models will be required to understand this condition.

"Intrinsic" PEEP (PEEPi): role of expiratory muscles

In normal subjects breathing at rest, lung volume at end-expiration corresponds with the elastic equilibrium volume, or relaxation volume (Vr), of the respiratory system. If expiratory duration is not long enough, then inspiration may begin before the system has returned to Vr, such that end-expiratory lung volume is higher than Vr. This condition is named dynamic pulmonary hyperinflation and intrinsic positive end-expiratory pressure (PEEPi), also called auto PEEP, corresponds to the elastic recoil of the lung at end-expiration [1, 2]. In the spontaneously breathing subject, this dynamic hyperinflation occurs mainly when the rate of lung emptying is decreased owing to high respiratory resistance or flow limitation. The highest degrees of dynamic hyperinflation are, thus, encountered in patients with airway diseases, particularly chronic obstructive pulmonary disease (COPD) patients. In the ventilated patient, external determinants may also induce dynamic pulmonary hyperinflation, or increase the magnitude of dynamic hyperinflation that was already present before the onset of mechanical ventilation. These additional external determinants include a preceding inflation volume that is too large, a time available for expiration that is reduced or a decreased rate of lung emptying owing to high resistance associated with the tube, the ventilator tubing or devices [3]. Dynamic pulmonary hyperinflation has important pathophysiological and therapeutic implications mainly in critical care medicine [3]. In particular, it implies that as the inspiratory muscles start to contract they must first offset the elastic recoil pressure of the system before inspiratory flow can begin and lung volume can increase. PEEPi associated with dynamic pulmonary hyperinflation thus corresponds to an inspiratory threshold load and is associated with an increased inspiratory work of breathing. This has led several investigators to give external PEEP or continuous positive airway pressure (CPAP) in the belief that this would unload the inspiratory muscles and, therefore, reduce the inspiratory work of breathing [4–6]. It must be stressed, however, that PEEPi and dynamic pulmonary hyperinflation are not always linked. In fact, alveolar pressure can also remain positive throughout expiration when the expiratory muscles contract [1, 5]. With respect to this, recent studies have shown that in many patients with stable but severe COPD [7] as well as in many mechanically ventilated patients [8, 9], expiration is a mechanically active process. These observations, thus, provide strong evidence that the active nature of expiration is an important determinant of PEEPi in such patients and, therefore, that the importance of dynamic pulmonary hyperinflation has been overestimated. Since a positive end-expiratory alveolar pressure resulting from an expiratory muscle contraction does not represent an inspiratory threshold load, the level of external PEEP that is needed in such patients must be significantly less than conventionally thought. The contribution of expiratory muscle contraction to the increase in end-expiratory alveolar pressure has to be taken into account when applying external PEEP or CPAP to offset PEEPi or these procedures might, in fact, result in enhanced pulmonary dynamic hyperinflation with further deleterious consequences [4, 10]. In this issue of the European Respiratory Journal, ZAKYNTHINOS and co-workers [11] report on a method for detecting expiratory muscle use and quantifying its contribution to PEEPi. The two points at issue in this and other studies [7–9] are: