Maximal Inspiratory Efforts Research Articles

Respiratory effects of the scalene and sternomastoid muscles in humans.

Previous studies have shown that in normal humans the change in airway opening pressure (DeltaPao) produced by all the parasternal and external intercostal muscles during a maximal contraction is approximately -18 cmH(2)O. This value is substantially less negative than DeltaPao values recorded during maximal static inspiratory efforts in subjects with complete diaphragmatic paralysis. In the present study, therefore, the respiratory effects of the two prominent inspiratory muscles of the neck, the sternomastoids and the scalenes, were evaluated by application of the Maxwell reciprocity theorem. Seven healthy subjects were placed in a computed tomographic scanner to determine the fractional changes in muscle length during inflation from functional residual capacity to total lung capacity and the masses of the muscles. Inflation induced greater shortening of the scalenes than the sternomastoids in every subject. The inspiratory mechanical advantage of the scalenes thus averaged (mean +/- SE) 3.4 +/- 0.4%/l, whereas that of the sternomastoids was 2.0 +/- 0.3%/l (P < 0.001). However, sternomastoid muscle mass was much larger than scalene muscle mass. As a result, DeltaPao generated by a maximal contraction of either muscle would be 3-4 cmH(2)O, which is about the same as DeltaPao generated by the parasternal intercostals in all interspaces.

The role of mean inspiratory effort on daytime sleepiness.

This study has investigated the role of average maximum inspiratory effort in excessive daytime sleepiness in patients with obstructive sleep apnoea syndrome (OSAS) and upper airway resistance syndrome (UARS). Fifteen patients diagnosed with UARS and 32 patients with OSAS, with >5.5 h total sleep time (TST) during 8 h of nocturnal polygraphic recordings, were included in the study. Demographical data, polysomnographical data and data about daytime sleepiness, including Epworth sleepiness scale (ESS) and multiple sleep latency test (MSLT), were evaluated. In order to compute the average maximum inspiratory effort from oesophageal pressure (Poes) measurements, maximum Poes was obtained from 20 representative obstructive respiratory events (obstructive apnoeas, hypopnoeas or flow limitations) for each sleep stage in both supine and side positions. From Poes measurements during sleep, the increase in Poes (deltaPoes) during respiratory events was also calculated. The average maximum Poes, deltaPoes, respiratory disturbance index (RDI) and arousal index were significantly correlated with ESS in OSAS patients. In patients with UARS, the only significant correlation was obtained between average maximum Poes and ESS. The MSLT score did not show any significant correlation with arousal index, number of stage variations, RDI, average Poes, deltaPoes, minimum oxygen saturation (Sa,O2) and percentage of TST with an Sa,O2 <90% in both UARS and OSAS patients. The results of multiple regression analysis showed that average maximum Poes correlates best with the variance in ESS for OSAS patients. In conclusion, the data from this study indicate the possible important role of average inspiratory effort in determining subjective sleepiness in both obstructive sleep apnoea syndrome and upper airway resistance syndrome patients.

Lung deposition of salbutamol in healthy human subjects from the MAGhaler dry powder inhaler

The MAGhaler (Mundipharma GmbH) is a multidose dry powder inhaler (DPI) containing a novel formulation of drug and lactose compacted by an isostatic pressing technique (GGU GmbH). On actuation, a precise dose is metered from a compacted ring-shaped drug tablet. In this study, the lung deposition of salbutamol from this device has been assessed. Ten healthy non-smoking subjects completed a two-way cross-over study, assessing the pulmonary deposition of salbutamol (200 μg) from the MAGhaler at high (60 l/min) and low (30 l/min) peak inhaled flow rates (PIFRs), representing maximal and sub-maximal inspiratory efforts. The formulation was radiolabelled with 99mTc, and lung and oropharyngeal depositions were quantified by gamma scintigraphy. The mean ( SD)% of the delivered dose deposited in the lungs was 26.4 (4.3)% at 60 l/min and 21.1 (5.1)% at 30 l/min ( P<0.05), corresponding to mean lung depositions of 52.8 and 42.2 μg salbutamol, respectively. The distribution of drug within different lung regions did not vary significantly with inhaled flow rate. The data provided proof of concept for the novel inhaler device and the innovative drug formulation. In comparison with previous deposition data obtained with other DPIs, the lung deposition was relatively high, relatively reproducible (coefficient of variation 16% at 60 l/min) and relatively insensitive to the change in peak inhaled flow rate.

Deposition and pharmacokinetics of budesonide from the Miat Monodose inhaler, a simple dry powder device

Dry powder inhalers (DPIs) are used to deliver asthma drugs to patients, but lung deposition may depend upon the degree of inspiratory effort. The pulmonary deposition of the glucocorticosteroid budesonide (SMB-Galephar) has been assessed in 12 asthmatic patients when delivered by the Monodose inhaler (Miat, Milan, Italy); the Pulmicort Turbuhaler DPI (AstraZeneca, Lund, Sweden) was used as a comparator product. Patients inhaled from each device with maximal or sub-maximal inspiratory effort: Monodose inhaler 90 vs 45 l/min; Turbuhaler DPI 60 vs 30 l/min. The formulations were radiolabelled with 99mTc, and deposition of budesonide was quantified by gamma scintigraphy. Mean (SD) whole lung deposition for the Monodose inhaler (% capsule dose), was independent of inspiratory effort (maximal: 21.4 (4.3)%; sub-maximal: 21.4 (7.5)%), while lung deposition for the Turbuhaler DPI (% metered dose) fell significantly with decreasing inspiratory effort (maximal: 25.1 (6.1)%; sub-maximal: 18.5 (6.5)%; P<0.05). The plasma concentrations of budesonide showed the same trends as the whole lung deposition data. The Monodose inhaler showed inspiratory effort-independent drug delivery characteristics, and could prove be a valuable low-cost alternative to more complex devices such as the Turbuhaler DPI. The Monodose inhaler may be especially useful in groups of patients unable to inhale maximally through DPIs, including young children and adult patients with severe respiratory impairment.

Assessing Inspiratory Muscle Strength in Patients With Neurologic and Neuromuscular Diseases: Comparative Evaluation of Two Noninvasive Techniques

Static mouth pressure during maximal inspiratory efforts is commonly used to evaluate inspiratory muscle strength. However, maximal inspiratory pressure (MIP) presents some potential limitations likely to be overcome by the measure of mouth pressure during a maximal sniff maneuver in patients with respiratory muscle weakness. The aim of the present study was to assess whether mouth pressure during sniff maneuver (Pmosn) is a better index of inspiratory muscle strength than MIP in patients with neurologic and neuromuscular diseases (NNMD) with and without inspiratory muscle weakness. Both MIP and Pmosn were measured in 30 patients affected by various types of NNMD and in 41 control subjects. Pmosn was measured with a 5-cm latex balloon-catheter system, the balloon being held in the oral cavity with the lips closed. In control subjects, MIP was either similar (in female subjects) or higher (in male subjects) than Pmosn, the variation coefficients for the two tests being similar both in male subjects (19.3% vs 19.1% for MIP and Pmosn, respectively) and in female subjects (27.5% vs 26.2%, respectively). There was no difference in the Pmosn/MIP ratios observed in the different diseases (one-way analysis of variance, F = 0.29, p = 0.91). In control subjects, a significant inverse relationship between Pmosn/MIP ratio and MIP (r = - 0.66, p < 0.00001) was found, ie, the lower the MIP, the higher the Pmosn/MIP ratio, suggesting an increasing difficulty in performing MIP as MIP values decreased. The majority of patients were between the prediction limits of the regression calculated for control subjects. At variance, patients with Duchenne dystrophy and low MIP were under the prediction limits of the regression calculated for control subjects, indicating a lower-than-expected PMOSN. In patients with NNMD, irrespective of the etiology, we found the following: (1) Pmosn does not overcome the limitations of MIP measurement; (2) the two maneuvers are not interchangeable, but rather complement one another in the assessment of inspiratory muscle strength; (3) Pmosn may underestimate muscle strength as assessed by MIP in patients with NNMD with inspiratory muscle weakness; and (4) in patients with low MIP, the lower-than-expected Pmosn/MIP ratio confirms inspiratory muscle weakness.

Inferences on force transmission from muscle fiber architecture of the canine diaphragm.

Functional properties of the diaphragm are mediated by muscle structure. Modeling of force transmission necessitates a precise knowledge of muscle fiber architecture. Because the diaphragm experiences loads both along and transverse to the long axes of its muscle fibers in vivo, the mechanism of force transmission may be more complex than in other skeletal muscles that are loaded uniaxially along the muscle fibers. Using a combination of fiber microdissections and histological and morphological methods, we determined regional muscle fiber architecture and measured the shape of the cell membrane of single fibers isolated from diaphragm muscles from 11 mongrel dogs. We found that muscle fibers were either spanning fibers (SPF), running uninterrupted between central tendon (CT) and chest wall (CW), or were non-spanning fibers (NSF) that ended within the muscle fascicle. NSF accounted for the majority of fibers in the midcostal, dorsal costal, and lateral crural regions but were only 25-41% of fibers in the sternal region. In the midcostal and dorsal costal regions, only approximately 1% of the NSF terminated within the fascicle at both ends; the lateral crural region contained no such fibers. We measured fiber length, tapered length, fiber diameters along fiber length, and the taper angle for 271 fibers. The lateral crural region had the longest mean length of SPF, which is equivalent to the mean muscle length, followed by the costal and sternal regions. For the midcostal and crural regions, the percentage of tapered length of NSF was 45.9 +/- 5.3 and 40.6 +/- 7.5, respectively. The taper angle was approximately 0.15 degrees for both, and, therefore, the shear component of force was approximately 380 times greater than the tensile component. When the diaphragm is submaximally activated, as during normal breathing and maximal inspiratory efforts, muscle forces could be transmitted to the cell membrane and to the extracellular intramuscular connective tissue by shear linkage, presumably via structural transmembrane proteins.

Supine fall in lung volumes in the assessment of diaphragmatic weakness in neuromuscular disorders

Fromageot C, Lofaso F, Annane D, Falaize L, Lejaille M, Clair B, Gajdos P, Raphaël JC. Supine fall in lung volumes in the assessment of diaphragmatic weakness in neuromuscular disorders. Arch Phys Med Rehabil 2001;82:123-8. Objective: To determine whether diaphragmatic function can be determined by noninvasive respiratory indices in neuromuscular disease. Design: Vital capacity (VC) and mouth pressure generated during a maximal static inspiratory effort (Pi max) were measured with patients in both sitting and supine positions. Setting: Rehabilitation hospital. Patients: Twenty-four patients with generalized neuromuscular disease. Main Outcome Measures: Changes in indices from sitting to supine position were compared with invasive diaphragmatic function indices consisting of transdiaphragmatic pressures during maximal sniff (Pdi sniff) and the ratio of gastric pressure (Pga) increases over transdiaphragmatic pressure (ΔPga/ΔPdi) during quiet breathing. Results: The fall in VC in the supine position was greater in the 15 patients who had spontaneous paradoxical diaphragmatic motion (ΔPga/ΔPdi < 0) than in the 9 patients who did not. Specificity and sensitivity of a greater than 25% supine fall in VC for the diagnosis of diaphragmatic weakness (ΔPga/ΔPdi < 0 and/or Pdi sniff < 30cmH2O) were 90% and 79%, respectively. Stepwise multiple regression analysis of Pdi sniff showed that both the supine fall in VC and Pi max were associated with diaphragmatic weakness (R2 =.66; p <.0001). These factors contributed 52% and 14% of the Pdi sniff variance, respectively. Conclusions: Simple VC measurement in the sitting and supine positions may be helpful in detecting severe or predominant diaphragmatic weakness. © 2001 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation

Effect of digoxin on global respiratory muscle strength after cholecystectomy: a double blind study

BACKGROUNDUpper abdominal surgery has been shown to impair the function of the respiratory muscles. In addition, controversial results have been reported concerning the effect of digoxin on the diaphragm. The...

The effect of fixed load incremental inspiratory muscle training in the elite athlete: a pilot study

This study sought to investigate whether a regime of high density inspiratory muscle training (IMT) would increase respiratory muscle strength (RMS) and respiratory muscle endurance (RME) in maximally trained subjects. Twelve endurance athletes (nine men) with a mean age of 25 years (±5·6 S.D.) were selected for a three times weekly training programme, performed over 8 weeks. Using a computerized system, subjects were required to perform three sustained maximal inspiratory efforts (SMIP) from residual volume to total lung capacity, and to subsequently attain repeated sub maximal pressure profiles at progressively reduced time intervals. With the use of biofeedback, subjects were required to match or exceed a pressure curve which was derived by reducing the best SMIP to 80% of peak at each training session. Maximal inspiratory pressure (MIP) values were recorded as measures of RMS. SMIP values were calculated in arbitrary pressure/time units (PTUs). RME was expressed as summated PTUs at programme completion. These results demonstrate a significant increase in RMS (P<0·001) and RME (P<0·0001) with a reported decrease in exertional dyspnoea. We conclude that this method of incremental IMT, which is set at a level consistent with high density training regimes, increases RMS and RME in highly trained subjects. These results also suggest that the application of this regime may result in greater pressure generation at higher lung volumes thereby affecting the length/tension relationship of the inspiratory muscles and hence ameliorate dyspnoea during periods of sustained aerobic performance.

Experimental reinnervation of a strap muscle with a few roots of the phrenic nerve in rabbits.

In order to compare application of the roots of the phrenic nerve to the ansa hypoglossi for laryngeal muscle neurotization, 1 or more roots from the phrenic nerve were implanted into the right sternothyroid (RST) muscle of rabbits (n = 36). Controls were intact animals (in which RST innervation is provided by the ansa; n = 6) and denervated ones (n = 6). At 66 +/- 2 days (mean +/- SE) after neurotization, during quiet breathing, inspiratory electromyographic activity and isometric contraction force were observed in all reinnervated RST muscles (n = 24). During maximal inspiratory effort, electromyographic activity and force increased. In animals reinnervated by the C4 root alone, forces (46.22 +/- 7.8 g) were significantly higher than in intact animals (10.83 +/- 5.0 g). Retrograde labeling proved the phrenic origin of the neurotization. Electromyography of the diaphragm was recorded. We conclude that in rabbits, neurotization of a strap muscle by 1 or 2 roots of the phrenic nerve allows inspiratory contraction, even during quiet breathing. Such inspiratory activity is not observed in sternothyroid muscles of intact animals innervated by the ansa hypoglossi.

Clinical Effects of Theophylline on Inspiratory Muscle Drive in Tetraplegia

Theophylline has been shown to restore diaphragmatic function in animals following cervical spinal cord hemisection, which induces hemidiaphragm paralysis. Although theophylline had been used clinically in the treatment of various pulmonary diseases, its effects on respiratory muscle function in cervical spinal cord injured tetraplegics has not been studied. In the present case study, we evaluated a patient injured in 1979 with a chronic asymmetric C5-7 tetraplegia (left C5-6, right C6-7) before and after receiving theophylline chronically by mouth for three weeks and again before and after receiving acute intravenous (IV) aminophylline after the effects of the chronic drug administration wore off. Neural activation to inspiratory muscles was assessed by right and left parasternal intercostal and diaphragm EMGs during quiet breathing and max imal inspiratory efforts. Global respiratory drive was assessed by P100, and inspiratory muscle force was assessed by maximal inspiratory pressures and vital capacity. Both long-term orally administered and acute IV theophylline increased neural activation to the diaphragm, especially on the more affected left side. Theophylline treatment was also associated with an increase in global central respiratory drive and inspiratory muscle force, without changing expiratory airflows. Left diaphragm EMG activity was markedly increased following the administration of theophylline. Of interest, upper parasternal intercostal EMG activity was also recruited on the left in spite of being below the level of cervical injury. We speculate that the administration of theophylline in selected patients with an asymmetric cervical spinal cord injury may activate la tent bulbospinal respiratory pathways and improve inspiratory muscle function, re ducing the likelihood of associated respiratory failure.

Effect of Lung Volume Reduction Surgery on Bony Thorax Configuration in Severe COPD

Hyperinflation in patients with severe COPD is associated with an increased anteroposterior (AP) rib cage diameter. We sought to determine whether bilateral lung volume reduction surgery (LVRS) affects bony thorax configuration. Prospective of clinical data collection before and after LVRS. Tertiary-care university medical center. We measured multiple AP and transverse thoracic diameters, by using plain chest roentgenograms (CXRs) in 25 patients (11 men, 14 women), and thoracic CT scans in 14 patients (7 men, 7 women), preoperatively and 3 months postoperatively. A subgroup of 7 patients (reference data) also had CXR thoracic diameter measurements made, using films obtained previously within a year of their presurgical evaluation. Another subgroup of 10 patients had CT scan measurements also made 12 months postoperatively. CXR dimensions were taken at the level of the manubrium sterni (M) and thoracic T7 and T11 levels. CT dimensions were taken at T4, T6, T8, and T10 levels. At each level, left (L), midsagittal (C), and right (R) AP and maximal transverse diameters were measured. The sum of the three AP diameters (Total) was used for calculations. Patients also underwent tests such as spirometry, lung volumes, diffusing capacity of the lung for carbon monoxide, 6-min walk distance (6MWD), and transdiaphragmatic pressures during maximum static inspiratory efforts (Pdimax sniff) measured before and 3 months after LVRS. Patients were (mean +/- SD) 58+/-8 years old, with severe COPD and hyperinflation (FEV1, 0.68+/-0.23 L; FVC, 2.56+/-7.3 L; and total lung capacity [TLC], 143+/-22% predicted). After LVRS, AP diameters were reduced at thoracic level T7 (from 24.2+/-2.0 cm to 23.3+/-2.2 cm, p = 0.0002), and transverse diameters were reduced at T7 (from 26.8+/-1.9 cm to 26.4+/-1.7 cm, p = 0.001) and T11 (from 29.9+/-2.2 cm to 29.5+/-2.2 cm, p = 0.03), as measured using the CXR. In contrast, thoracic diameters were similar in subjects with CXRs before LVRS and within 1 year before evaluation. CT-measured AP diameters were significantly reduced 3 months after LVRS at T6, (from 48.8+/-6.0 cm to 46.7+/-5.4 cm, p = 0.02), T8 (from 54.2+/-7.0 cm to 52.3+/-6.5 cm, p = 0.004), and T10 (from 53.8+/-7.5 cm to 51.2+/-8.0 cm, p = 0.001), but not at T4. These AP diameter reductions directly correlated with the postoperative reductions in TLC and residual volume, and also with the increases in Pdimax sniff and 6MWD after LVRS. The reduction in AP diameters at thoracic levels T8 and T10 seen 3 months after LVRS remained stable at 12-month follow-up, whereas those measured at T6 lost statistical significance. CT-measured transverse diameters were unchanged at all levels after LVRS. We conclude that LVRS decreases mid-to-lower AP rib cage diameter as assessed by CXR and thoracic CT. Although transverse diameters were reduced on CXR, the magnitude was small and was not confirmed with CT. After LVRS, AP diameter reductions are most likely the result of reduction in lung volume, and they are associated with improvements in diaphragm strength and exercise endurance.

Maximum Static Respiratory Pressures in Healthy Elderly Men and Women: Issues of Reproducibility and Interpretation

Background: Respiratory muscle strength is assessed using the static pressure generated at the mouth during a maximal inspiratory or expiratory effort [PI_max and PE_max, respectively (MSRPs)]. Interpretation of MSRPs relies upon comparison with ‘normal’ values, but MSRPs show very weak associations with predictors such as physical characteristics. The influence of habitual physical activity upon MSRPs remains undefined. Objectives: We examined measurement reproducibility, as well as the influence of physical characteristics and habitual physical activity upon MSRPs in healthy elderly people. Methods: MSRPs were assessed in 41 healthy subjects using a portable mouth pressure meter on two occasions, 1 week apart. Physical activity was assessed in 10 subjects by diary record. Pearson product-moment correlation coefficients were used to assess the association of MSRPs with other measured variables. Results: There was good measurement reproducibility of MSRPs, with coefficients of reproducibility of 10.2 and 12.8% for PI_max and PE_max, respectively. MSRPs showed statistically significant negative correlations with age, but correlations with physical characteristics were poor. In contrast, MSRPs were highly correlated with physical activity. Conclusions: We conclude that MSRPs can be measured reproducibly and that they decline with advancing age. Physical characteristics are not good predictors of MSRPs; this may be due to a strong confounding influence of physical activity making interpretation of measurements problematic. We suggest that the poor predictive power of physical characteristics indicate that reference to ‘normal’ values be made with caution and that it may be more appropriate to consider functional interpretations of MSRPs based upon factors such as lung and chest wall elastance.

Inspiratory muscle adaptations following pressure or flow training in humans.

Skeletal muscle adapts differently to training with high forces or with high velocities. The effects of these disparate training protocols on the inspiratory muscles were investigated in ten healthy volunteers. Five subjects trained using high force (pressure) loads (pressure trainers) and five trained using high velocity (flow) loads (flow trainers). Pressure training entailed performing 30 maximal static inspiratory efforts against a closed airway. Flow training entailed performing 30 sets of three maximal dynamic inspiratory efforts against a minimal resistance. Training was supervised and carried out 5 days a week for 6 weeks. Inspiratory flow rates and oesophageal pressure-time curves were measured before and after training. Peak inspiratory pressures during maximal static and dynamic efforts and peak flows during the maximal dynamic efforts were calculated. The time-to-peak pressure and rate of rise in peak pressure during maximal static and dynamic manoeuvres were also calculated before and following training. Maximal static pressure increased in the pressure training group and maximal dynamic pressure increased in the flow training group. Both groups increased the rate of pressure production (dP/dt) during their respective maximal efforts. The post-training decrease in time-to-peak pressure was proportionately greater in the flow trainers than in the pressure trainers. The differences in time-to-peak pressure between the two groups were consistent with the different effects of force and velocity training on the time-to-peak tension of skeletal muscle.

Effect of lung volume reduction surgery on diaphragm length in severe chronic obstructive pulmonary disease.

Lung volume reduction surgery (LVRS) has been suggested as improving respiratory mechanics in patients with severe chronic obstructive pulmonary disease (COPD). We hypothesized that LVRS might lengthen the diaphragm, increase its area of apposition with the chest wall, and thereby improve its mechanical function. To determine the effect of bilateral LVRS on diaphragm length, we measured diaphragm length at TLC, using plain chest roentgenograms (CXRs), in 25 patients (11 males and 14 females) before LVRS and 3 to 6 mo after LVRS. A subgroup of seven patients (reference data) also had diaphragm length measurements made with CXRs, using films made within a year before their presurgical evaluation. Right hemidiaphragm silhouette length (PADL) and the length of the most vertically oriented portion of the right hemidiaphragm muscle (VDML) were measured. Diaphragm dome height was determined from the: (1) distance between the dome and transverse diameter at the manubrium; and (2) highest point of the dome referenced horizontally to the vertebral column. Patients also underwent spirometry, measurements of lung volumes and diffusion capacity, an incremental symptom-limited maximum exercise test, and measurements of 6 min walk distance (6MWD) and transdiaphragmatic pressures during maximum static inspiratory efforts (Pdimax sniff) and bilateral supramaximal electrophrenic twitch stimulation (Pditwitch) both before and 3 mo after LVRS. Patients were 58 +/- 8 yr of age, with severe COPD and hyperinflation (FEV1 = 0.68 +/- 0.23 L, FVC = 2.56 +/- 7.3 L, and TLC = 143 +/- 22% predicted). Following LVRS, PADL increased by 4% (from 13.9 +/- 1.9 cm to 14.5 +/- 1.7 cm; p = 0.02), VDML increased by 44% (from 2.08 +/- 1.5 cm to 3.00 +/- 1.6 cm, p = 0.01), and diaphragm dome height increased by more than 10%. In contrast, diaphragm lengths were similar in subjects with CXRs made before LVRS and within 1 yr before evaluation. The increase in diaphragm length correlated directly with postoperative reductions in TLC and RV, and also with increases in transdiaphragmatic pressure with maximal sniff (Pdimax sniff), maximal oxygen consumption (V O2max), maximal minute ventilation (V Emax), and maximum voluntary ventilation following LVRS. We conclude that LVRS leads to a significant increase in diaphragm length, especially in the area of apposition of the diaphragm with the rib cage. Diaphragm lengthening after LVRS is most likely the result of a reduction in lung volume. Increases in diaphragm length after LVRS correlate with postoperative improvements in diaphragm strength, exercise capacity, and maximum voluntary ventilation.

Effects of different expiratory maneuvers on inspiratory muscle force output.

We assessed the effects of two different expiratory maneuvers (fast [F] or slow [S]) on the ability of normal subjects (n = 12, age 35 +/- 6 yr) to generate maximal inspiratory pressures and maximal inspiratory flows near residual volume (RV). With the F maneuver, the subject exhaled rapidly to RV and immediately performed a maximal inspiratory effort, whereas with the S maneuver the subject exhaled slowly to RV, paused for 4 to 6 s at RV, and then inspired forcefully. Maximal static inspiratory pressure against an occluded airway (PImax), and maximal dynamic inspiratory pressure (PIdyn) and maximal inspiratory flow (V Imax) with no added resistance, as well as the electromyographic activity of the parasternal muscles, were measured during each maneuver. Both maneuvers were initiated from TLC and were performed randomly. In comparison with the S maneuver, the F maneuver yielded values of higher (mean +/- SE) PImax (148 +/- 5 cm H2O versus 135 +/- 7 cm H2O, p < 0.05), PIdyn (33 +/- 2 cm H2O versus 28 +/- 2 cm H2O, p < 0.05), and V Imax (12.3 +/- 0.4 L/s versus 11.4 +/- 0.6 L/s, p < 0.05). In addition, the rate of rise of PImax, the rate of rise of PIdyn, and the integrated peak electromyographic activity of the parasternal muscles were significantly greater with the F than with the S maneuver, suggesting greater inspiratory muscle (IM) activation. The enhanced IM activation may be related to a specific inspiratory-expiratory muscle interaction similar to the agonist-antagonist interactions described for a pair of skeletal muscles.

Neurogenesis of patterns of automatic ventilatory activity

Normal respiration, termed eupnea, is characterized by periodic filling and emptying of the lungs. Eupnea can occur ‘automatically’ without conscious effort. Such automatic ventilation is controlled by the brainstem respiratory centers of pons and medulla. Following removal of the pons, eupnea is replaced by gasping, marked by brief but maximal inspiratory efforts. The mechanisms by which the respiratory rhythms are generated have been examined intensively. Evidence is discussed that ventilatory activity can be generated in multiple regions of pons and medulla. Eupnea and gasping represent fundamentally different ventilatory patterns. Only for gasping has a critical region for neurogenesis been identified, in the rostral medulla. Gasping may be generated by the discharge of ‘pacemaker’ neurons. In eupnea, this pacemaker activity is suppressed and incorporated into the pontile and medullary neuronal circuit responsible for the neurogenesis of eupnea. Evidence for ventilatory neurogenesis which has been obtained from a number of in vitro preparations is discussed. A much-used preparation is that of a ‘superfused’ brainstem of the neonatal rat. However, activities of this preparation differ greatly from those of eupnea, as recorded in vitro or in arterially perfused in vitro preparations. Activities of this ‘superfused’ preparation are identical with gasping and, hence, results must be reinterpreted accordingly. The possibility is presented that mechanisms responsible for generating respiratory rhythms may differ from those responsible for shaping respiratory-modulated discharge patterns of cranial and spinal nerves. The importance of pontile mechanisms in the neurogenesis and control of eupnea is reemphasized.

Effect of lung volume reduction surgery on diaphragm strength.

Since lung volume reduction surgery (LVRS) reduces end-expiratory lung volume, we hypothesized that it may improve diaphragm strength. We evaluated 37 patients for pulmonary rehabilitation and LVRS. Before and 8 wk after pulmonary rehabilitation, 24 patients had spirometry, lung volumes, diffusion capacity, incremental symptom limited maximum exercise test, 6-min walk test, maximal static inspiratory and expiratory mouth pressures, and transdiaphragmatic pressures during maximum static inspiratory efforts and bilateral supramaximal electrophrenic twitch stimulation measured. Twenty patients (including 7 patients who crossed over after completing pulmonary rehabilitation) had baseline measurements postrehabilitation, and 3 mo post-LVRS. Patients were 58 +/- 8 yr of age, with severe COPD and hyperinflation (FEV1, 0.69 +/- 0.21 L; RV, 4.7 +/- 1.4 L). Nineteen patients had bilateral LVRS performed via median sternotomy and stapling, and 1 patient had unilateral LVRS via thorascopy with stapling. After rehabilitation, spirometry and DL(CO)/VA were not different, and lung volumes showed a slight worsening in hyperinflation. Gas exchange, 6-min walk distance, maximum oxygen uptake (VO2max), and breathing pattern during maximum exercise did not change after rehabilitation, but total exercise time was significantly longer. Inspiratory muscle strength (PImax, Pdi(max combined), Pdi(max sniff), Pdi(max), Pdi(twitch)), was unchanged after rehabilitation. In contrast, after LVRS, FVC increased 21%, FEV1 increased 34%, TLC decreased 13%, FRC decreased 23%, and FRC(trapped gas) and RV decreased by 57 and 28%, respectively. PCO2 was lower (44 +/- 6 versus 48 +/- 6 mm Hg, p < 0.003) and 6-min walk distance increased (343 +/- 79 versus 250 +/- 89 m, p < 0.001), as did total exercise time during maximum exercise (9.2 +/- 1.9 versus 6.9 +/- 2.7 min, p < 0.01). Minute ventilation (29 +/- 8 versus 21 +/- 6 L/min, p < 0.001) and tidal volume (1.0 +/- 0.33 versus 0.84 +/- 0.25 L, p < 0.001) during maximum exercise increased whereas respiratory rate was lower (28 +/- 6 versus 32 +/- 7 breaths/min, p < 0.02). Measurements of respiratory muscle strength (PImax, 74 +/- 28 versus 50 +/- 18 cm H2O, p < 0.002; Pdi(max combined), 80 +/- 25 versus 56 +/- 29 cm H2O, p < 0.01; Pdi(max sniff), 71 +/- 7 versus 46 +/- 27 cm H2O, p < 0.01; Pdi(twitch), 15 +/- 5 versus 7 +/- 5 cm H2O, p < 0.01) were all greater post-LVRS. Inspiratory muscle workload as measured by Pdi TTI was lower following LVRS (0.07 +/- 0.02 versus 0.09 +/- 0.03, p < 0.03). On multiple regression analysis, increases in PImax correlated significantly with decreases in RV and FRC(trapped gas) after LVRS (r = 0.67, p < 0.03). We conclude that LVRS significantly improves diaphragm strength that is associated with a reduction in lung volumes and an improvement in exercise performance. Future studies are needed to determine the relationship and stability of these changes over time.

Equipment review: Measurement of occlusion pressures in critically ill patients

The evaluation of airway pressure tracings during complete airway occlusion provides interesting functional data for weaning patients from mechanical ventilation. The occlusion manoeuvre may be achieved either by maintaining occlusion for a prolonged period during maximal inspiratory effort (PiMax) or for a shorter time period (200–300 ms). The inspiratory depression of airways pressure, achieved after 100 ms of occlusion, is generally defined as the occlusion pressure or P0.1 and represents a valid indirect measurement of the activity of the respiratory centres. P0.1 is a reliable measurement of the intensity of the stimuli from the neurological centres to the peripheral respiratory muscles [1,2]. Whitelaw et al elegantly demonstrated the reliability of this measurement [1] in human healthy volunteers spontaneously breathing at rest and during hypercapnic challenge. P0.1 can represent a more precise respiratory drive measurement than other measurements such as tidal volume, respiratory rate, minute ventilation or mean inspiratory flow (VT/Ti) since it is relatively independent of modification by respiration machines. The aim of this article is to analyse the technical aspects relating to the acquisition of occlusion pressures, taking into account the possible bias represented by specific physiopathologic situations and to define some future uses of P0.1 during weaning procedures. A complete review of the literature dedicated to P0.1 measurement in different clinical settings has been recently published [3].

Inspiratory muscle endurance in patients with chronic heart failure.

To assess the significance of changes in respiratory muscle endurance in relation to respiratory and limb muscle strength in patients with mild to moderate chronic heart failure using a threshold loading technique. 20 patients with chronic heart failure (17 male) aged 63.8 (SD 7.4) years and 10 healthy men aged 63.1 (5.6) years. Heart failure severity was New York Heart Association (NYHA) grade II (n = 11) and NYHA grade III/IV (n = 9). Respiratory muscle strength was measured from mouth pressures during maximum inspiratory effort (MIP) at functional residual capacity (FRC) and limb muscle strength was measured using a hand grip dynamometer. Inspiratory muscle endurance was measured using a threshold loading technique. The total endurance duration, the maximum threshold pressure achieved (P-Max), and the inspiratory load (% ratio of P-Max/MIP) were recorded in all subjects. Inspiratory muscles were weaker in patients with heart failure than in the controls [MIP 53.6 (16.5) v 70.9 (20.2) cm H2O, P < 0.05]. Hand grip strength was similar in both subject groups [31.6 (SD) v 36.1 (15.9) dynes]. Total endurance duration was significantly reduced in the patient group [494 (223) v 996 (267) s, P < 0.01], as was the maximal threshold pressure achieved [P-Max 18.5 (6.4) v 30.7 (6.6) cm H2O, P < 0.01]. When expressed as a percentage of MIP, P-Max was also lower in the patients [35.2 (11.8) v 44.8 (11.4)%, P < 0.05]. There was no significant correlation between any measure of endurance and limb muscle strength. Respiratory muscle endurance is reduced in patients with chronic heart failure. These changes probably reflect a generalised skeletal myopathy and provide further evidence of respiratory muscle dysfunction in patients with this disease. Respiratory muscle endurance needs now to be related to symptoms and the effects of treatment and respiratory muscle training should also be explored.