Maximal Transdiaphragmatic Pressure Research Articles

Diaphragm dimensions of the healthy term infant

Human neonatal diaphragm development has not been extensively studied. Previous work in children and adults suggests that diaphragm thickness (t(di)) is in scale with body size such that maximal transdiaphragmatic pressure (P(dimax)) remains relatively constant. Such assessments have not been made in healthy term infants. This study was designed to evaluate the relationships among t(di), body dimensions and P(dimax) in healthy term infants. It was hypothesized that in healthy term infants 1) t(di) is positively correlated with body size and 2) calculated P(dimax) is independent of body weight and length. Fifteen clinically stable term infants (8 males and 7 females) were recruited [birthweight (BW), 3.3 +/- 0.7 kg, (mean +/- SD); head circumference (HC), 33.7 +/- 2 cm; body length (BL) 50 +/- 3 cm; gestational age (GA) 39 +/- 1 wk; and postnatal age 1.7 +/- 0.8 day]. Ultrasound was used to visualize the diaphragm at the level of the zone of apposition and measure t(di). Standard techniques were used to measure the anthropometric dimensions of the rib cage. P(dimax) was calculated using the piston-in-cylinder model of diaphragm function. Significant correlations were found among t(di) and BW (R = 0.58), BL (R = 0.58) and HC (R = 0.65) but not between GA (R = 0.20). Larger infants tended to have thicker diaphragms and larger cross-sectional areas of the lower rib cage (A(ZAP)). For the group, calculated P(dimax) was independent of either body weight or length and was greater than that calculated for adults. It is concluded that diaphragm mass in healthy term infants is proportional to body size, whereas calcuated P(dimax) is independent of body size. Since calculated P(dimax) is greater than that predicted for adults, there may be perinatal diaphragm strengthening. This may assist the infant in generating sufficient pressure to overcome the enormous elastic and resistive loads imposed during perinatal pulmonary transition.

Altered diaphragm contractile properties with controlled mechanical ventilation

This study shows that, over time, diaphragm inactivity with controlled mechanical ventilation (CMV) decreases diaphragm force and produces myofibril damage contributing to the reduced force. We measured in vivo and in vitro diaphragm contractile and morphological properties in 30 sedated rabbits grouped (n = 6) as follows: 1 or 3 days of CMV, 1 or 3 days of 0 cmH(2)O continuous positive airway pressure, and control. The CMV rate was set sufficient to suppress diaphragm electrical activity. Compared with the control group, phrenic-stimulated maximum transdiaphragmatic pressure did not decrease with continuous positive airway pressure but decreased to 63% after 1 day of CMV and to 49% after 3 days of CMV. The in vitro tetanic force decreased to 86% after 1 day of CMV and to 44% after 3 days of CMV. After 3 days of CMV, significant myofibril damage occurred in the diaphragm but not in the soleus. The decrease in tetanic force correlated with the volume density of abnormal myofibrils. We conclude that CMV had a detrimental effect on diaphragm contractile properties.

Respiratory Muscle Evaluation of the Patient with Neuromuscular Disease

This review presents clinically relevant issues regarding the assessment of respiratory muscles in individuals with neuromuscular disorders, and discusses the advantages and disadvantages of methods generally available to the clinician. Vital capacity (VC) and total lung capacity (TLC) are routinely measured in pulmonary function laboratories and are typically reduced in the context of severe respiratory muscle weakness, but the sensitivity and specificity of these measures are limited. Better measures of respiratory muscle weakness are maximal static inspiratory and expiratory pressures (PI max and PE max). PI max is reduced even with mild or moderate degrees of inspiratory muscle weakness, but low values also may be related to submaximal effort. To circumvent this problem, pressures can be measured using simpler maneuvers such as a maximal sniff. Specific tests of diaphragm function such as measurements of maximal transdiaphragmatic pressure are invasive and not routinely available to the clinician. Recently, noninvasive methods that specifically assess diaphragm function, such as diaphragm ultrasound of the zone of apposition and magnetic or electrophrenic nerve stimulation, have shown promise as new techniques for clinical use.

Effect of maturity on maximal transdiaphragmatic pressure in infants during crying.

The aim of this study was to determine the effect of maturation on diaphragmatic function. In addition, we investigated whether noninvasive assessment yielded similar results to invasive measurement. Twenty-eight infants, median gestational age (GA) 35.5 wk (range, 25 to 42 wk) and postconceptional age (PCA), 37.6 wk (range, 32 to 44 wk), were examined. Diaphragmatic function was assessed by measuring the maximal transdiaphragmatic pressure during crying (cPdi) using balloon catheters in the midesophagus (Pes) and the stomach (Pgas). In 14 of the infants, a noninvasive measurement of inspiratory muscle strength, maximal inspiratory pressure (PImax), was also made. cPdi and PImax were recorded during a crying effort with the airway occluded at end-expiration. The median cPdi and Pes during crying (cPes), but not Pgas during crying (cPgas), were significantly lower in those studied at a PCA of less than term compared with those studied at an older age (p < 0.05). cPdi and cPes, but not cPgas, correlated significantly with PCA (r = 0.44, p < 0.02; r = 0.43, p < 0.03; respectively) and gestational age (r = 0.46, p < 0.02 and r = 0.56, p < 0.01; respectively). In the 14 infants, the median PImax was lower, but it correlated significantly with cPdi (r = 0.79, p < 0.01). We conclude maturation does affect diaphragm function, and PImax may provide a noninvasive index of diaphragm strength.

The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD.

How do the respiratory centres of patients with chronic obstructive pulmonary disease (COPD) and hypercapnia respond to acute increases in inspiratory load? A depressed respiratory motor output has long been postulated, but studies on this issue have yielded inconsistent results, partly due to limitations of investigative techniques. Many of these limitations can be overcome by the twitch interpolation technique, which is capable of accurately quantifying the degree of diaphragmatic activation, termed the voluntary drive to breathe. The hypothesis that patients with COPD and hypercapnia compensate for an acute increase in mechanical load on the inspiratory muscles with a lower voluntary drive to breathe than is the case with normocapnic patients was tested. Measurements were obtained in 15 patients with COPD, six of whom displayed hypercapnia and nine normocapnia. The maximum degree of diaphragmatic activation, expressed as a voluntary activation index (mean +/- SEM), was higher in hypercapnic than in normocapnic patients (98.7 +/- 0.7 versus 94.5 +/- 0.9% (p = 0.006)), as was the mean value (94.5 +/- 0.7 versus 88.5 +/- 1.9% (p = 0.01)). Within-patient values of the index were also less variable in the hypercapnic patients (coefficients of variation, 3.4 +/- 0.3 versus 6.1 +/- 0.9%, p = 0.01). Multiple regression analysis revealed the ratio of dynamic elastance to maximum transdiaphragmatic pressure, an index of inspiratory muscle loading, and pH as the only variables that correlated with maximum voluntary activation index (r2 = 0.69, p = 0.02 for each variable). Contrary to the hypothesis, it was concluded that voluntary activation of the diaphragm was greater and less variable in hypercapnic patients than normocapnic patients with severe chronic obstructive pulmonary disease during an acute increase in inspiratory mechanical load. Whether greater diaphragmatic recruitment during episodes of a severe exacerbation of chronic obstructive pulmonary disease provides a survival advantage for hypercapnic patients with chronic obstructive pulmonary disease remains to be determined.

The Shrinking Lungs Syndrome in Systemic Lupus Erythematosus

The Shrinking Lungs Syndrome in Systemic Lupus Erythematosus

Variability of electrophrenic diaphragm twitch stimulation over time in normal subjects

Transcutaneous electrophrenic twitch stimulation is a potentially powerful way to assess diaphragm contractile function in response to interventions which may alter respiratory muscle strength and endurance. At present, the variability of the transdiaphragmatic twitch pressure (Pdi T) over a several hour period is not well described. The present study examines the reproducibility of Pdi T amplitude and the twitch occlusion technique of assessing maximum transdiaphragmatic pressure (Pdi max) in seven normal adults stimulated intermittently every hour for a total 4-h period. In one subject, data were obtained on two occasions separated by a 2-month interval. Among all subjects, the Pdi T amplitude expressed as a percentage of the Pdi max was highly reproducible over 4 h (coefficient of variation 5.3). Peak Pdi T was inversely related to graded voluntary Pdi ( r=−0.0996) and the relationship was virtually identical over 4 h ( r=−0.999, P=0.96). These data show that Pdi T at functional residual capacity and the twitch occlusion relationship are highly reproducible.

Bilateral Apical vs Nonapical Stapling Resection During Lung Volume Reduction Surgery

To determine whether biapical stapling resection alone or resection of diseased, nonapical areas of emphysematous lung provides comparable physiologic outcomes or alters morbidity and mortality after lung volume reduction surgery (LVRS). Consecutive case-series analysis. Urban university hospital. Forty-seven patients ([mean +/- SD] aged 58+/-8 years; 18 men) with severe emphysema (FEV1, 0.7+/-0.2 L; total lung capacity [TLC], 139+/-23% predicted). Thirty-two patients underwent biapical LVRS, 27 by median sternotomy (MS) and 5 by video-assisted thoracoscopic surgery (VATS), and 15 underwent nonapical resection, 9 by MS and 6 by VATS. Patients were assessed for postoperative complications (respiratory tract infections, air leak duration, and death), length of stay, and physiologic parameters, which included a 6-min walk distance, spirometry, lung volume, gas exchange, diaphragm strength, and quality-of-life measures. Patients were studied at baseline and at 3 months postoperatively. At the preoperative baseline, both groups had similar ages (57 vs 60 years; p = 0.2), 6-min walk distance (294 vs 263 m; p = 0.3), FEV1 (28% vs 29% predicted; p = 0.6), degree of hyperinflation (TLC, 138% vs 141% predicted; p = 0.8), gas exchange (PaO2/fraction of inspired oxygen, 344 vs 313, p = 0.1; PaCO2 46 vs 48 mm Hg, p = 0.4), and diaphragm strength (maximal transdiaphragmatic pressure sniff, 54 vs 46 cm H2O, p = 0.4). Resected tissue weight was similar in both groups (94 vs 93 g, p = 0.9). There were no differences in the mean percentage of change from baseline for these physiologic parameters or for quality-of-life measures between the two groups. The 6-min walk distances increased by 20% and 33%, FEV1 increased by 37% and 38%, the degrees of hyperinflation (residual volume/TLC) decreased by 16% and 15%, and the quality-of-life scores improved by 51% and 41%, respectively, in the groups that underwent biapical and nonapical resections at 3 months post-LVRS. The length of stay in the hospital for LVRS (18 vs 23 days; p = 0.4) and the duration of air leak (10 vs 15 days; p = 0.4) were also similar. Complications between the two groups (biapical vs nonapical) were similar (respiratory tract infection, 47% vs 60%, p = 0.2; reintubation, 34% vs 33%, p = 0.2; reoperation, 9% vs 20%, p = 0.4; and death, 9% vs 7%, p = 0.2). LVRS, by biapical or nonapical resection, produces similar improvements in lung function, exercise, diaphragm strength, and quality of life, with comparable morbidity and mortality.

Testing the competency of the hemostasis valve in introducer catheters.

Testing the competency of the hemostasis valve in introducer catheters.

Structure and function relationships of the respiratory muscles.

Potential relationships between the structure of the diaphragm and external intercostals and several indices of respiratory muscle function, lung function and nutrition in 27 patients (61+/-10 yrs of age) subjected to thoracotomy as a result of a lung neoplasm have been investigated. Prior to surgery the nutritional status of the patients was assessed and lung function (spirometry, lung volumes, transfer factor of the lungs for carbon monoxide, arterial blood gases) and respiratory muscle function (maximal inspiratory pressure (MIP) and diaphragmatic function were measured). Biopsies of the diaphragm (and external intercostals) were obtained during surgery. On average, patients showed mild airflow limitation (forced expiratory volume in one second (FEV1), 70+/-14% of predicted value, FEV1/forced vital capacity (FVC), 70+/-9%) with some air trapping (residual volume (RV), 139+/-50% pred) and normal gas exchange (arterial oxygen tension (Pa,O2), 11.3+/-1.33 kPa (85+/-10 mmHg)) and arterial carbon dioxide tension (Pa,CO2) 5.4+/-0.5 kPa (40.6+/-4 mmHg). MIP was 77+/-25% pred; maximal transdiaphragmatic pressure was 90+/-27 cmH2O. Most morphometric measurements of the diaphragm and external intercostals were within the range of values reported previously in other skeletal muscles. The size of the fibres of these two respiratory muscles was positively related (p<0.05) to MIP (% pred). There were no significant relationships between the structure of both muscles and nutritional status or any index of lung function. In conclusion, in the population studied, the fibre size of the diaphragm and external intercostals appears to relate to their ability to generate force.

Effect of lung volume reduction surgery on neuromechanical coupling of the diaphragm.

The mechanisms for symptomatic improvement following lung volume reduction surgery for emphysema are poorly understood. We hypothesized that enhanced neuromechanical coupling of the diaphragm is an important factor in this improvement. We studied seven patients with diffuse emphysema before and 3 mo after surgery. Patients showed improvements in 6-min walking distance (p = 0.002) and dyspnea (p = 0.04). The pressure output of the respiratory muscles, quantified as pressure-time product per minute (PTP/min), decreased after surgery (p = 0.03), as did PaCO2 (p = 0.02). Maximal transdiaphragmatic pressures (Pdi(max)) increased from 80.3 +/- 9.5 (SE) to 110.8 +/- 9.3 cm H2O after surgery (p = 0.03), and the twitch transdiaphragmatic pressure response to phrenic nerve stimulation (Pdi(tw)) increased from 17.2 +/- 2.4 to 25.9 +/- 3.0 cm H2O (p = 0.02); these increases were greater than could be accounted for by a decrease in lung volume. The contribution of the diaphragm to tidal breathing, assessed by relative changes in gastric and transdiaphragmatic pressures, increased after surgery (p = 0.008). Net diaphragmatic neuromechanical coupling, quantified as the quotient of tidal volume (normalized to total lung capacity) to tidal change in Pdi (normalized to Pdi(max)), improved after surgery (p = 0.03) and was related to the increase in 6-min walking distance (r = 0.86, p = 0.03) and decrease in dyspnea (r = 0.76, p = 0.08). In conclusion, lung volume reduction surgery effects an improvement in diaphragmatic function, greater than can be accounted for by a decrease in operating lung volume, and enhances diaphragmatic neuromechanical coupling.

Recovery of PdiTwitch following the induction of diaphragm fatigue in normal subjects.

Low frequency diaphragm fatigue (LFF) may play a major role in the pathogenesis of ventilatory failure; however, recovery from LFF is not well studied. We measured transdiaphragmatic twitch pressure (PdiT) at FRC (using a reduction of PdiT as an index of LFF) and maximum transdiaphragmatic pressure (Pdimax) before and after the induction of diaphragm fatigue in seven normal subjects, age 31 +/- 3 yr (mean +/- SD). Fatigue was induced by breathing through an inspiratory resistive load. PdiT produced by bilateral transcutaneous supramaximal electrophrenic stimulation was measured at baseline, 15, 30 min, 1, 2, 3, 4 h, and then 1 to 3 times between hour 20-25 post-fatigue. Pdimax estimated by twitch occlusion was measured at baseline, 30 min, 2-3, and 20-25 h post-fatigue. Pre-fatigue values (mean +/- SE) were: PdiT 23.6 +/- 2.5 cm H2O. The mean +/- SD time to fatigue was 25.3 +/- 12.3 min. Post-fatigue PdiT was reduced to 50%, and by 3 h was 72% of the initial value; 100% by 25 h. Pdimax was reduced to 75% post-fatigue, but recovered to 87% by 3 h, and 100% by 25 h. We concluded that recovery of PdiT and Pdimax in normal subjects starts to occur within the first few hours following diaphragm fatigue, and is complete by 25 h.

Kinematics and mechanics of midcostal diaphragm of dog.

Radiopaque markers were attached to the peritoneal surface of three neighboring muscle bundles in the midcostal diaphragm of four dogs, and the locations of the markers were tracked by biplanar video fluoroscopy during quiet spontaneous breathing and during inspiratory efforts against an occluded airway at three lung volumes from functional residual capacity to total lung capacity in both the prone and supine postures. Length and curvature of the muscle bundles were determined from the data on marker location. Muscle lengths for the inspiratory states, as a fraction of length at functional residual capacity, ranged from 0.89 +/- 0.04 at end inspiration during spontaneous breathing down to 0.68 +/- 0.07 during inspiratory efforts at total lung capacity. The muscle bundles were found to have the shape of circular arcs, with the three bundles forming a section of a right circular cylinder. With increasing lung volume and diaphragm displacement, the circular arcs rotate around the line of insertion on the chest wall, the arcs shorten, but the radius of curvature remains nearly constant. Maximal transdiaphragmatic pressure was calculated from muscle curvature and maximal tension-length data from the literature. The calculated maximal transdiaphragmatic pressure-length curve agrees well with the data of Road et al. (J. Appl. Physiol. 60: 63-67, 1986).

Respiratory mechanics in patients with tense cirrhotic ascites.

Lung volumes are decreased by tense ascites and increase after large volume paracentesis (LVP). The overall effect of ascites and LVP on the respiratory function is poorly understood. We studied eight cirrhotic patients with tense ascites before and after LVP. Inspiratory muscle force (maximal transdiaphragmatic pressure (Pdi,max), and the lowest pleural pressure (Pp1,min)) was assessed while the patients were seated. Rib cage and abdominal volume displacements, as well as pleural and gastric pressures were measured during quiet breathing while the patients were supine. Pdi,max and Ppl,min were normal and did not change after LVP (from 84.2+/-19.7 to 85.2+/-17.0 cmH2O and from 68.3+/-19.7 to 74+/-15.9 cmH2O, respectively). The abdominal contribution to the generation of tidal volume was greater than that of the rib cage (79 vs 21%), a pattern which did not change after LVP (73 and 27%). Before LVP, tidal swings both of pleural pressure (Ppl,sw) and transdiaphragmatic pressure (Pdi,sw) were large (15.3+/-4.3 and 18.5+/-3.9 cmH2O, respectively) and the load on inspiratory muscles was increased as a consequence of elevated dynamic elastance of the lung (El,dyn) (11.4+/-2.6 cmH2O x L(-1)) and ("intrinsic") positive end-expiratory pressure (PEEPi) (4.3+/-3.5 cmH2O). LVP reduced the load on the inspiratory muscles, as shown by the significant decrease in Ppl,sw (10.6+/-2.0 cmH2O), Pdi,sw (12.8+/-3.0 cmH2O), El,dyn (10.0+/-2.0 cmH2O x L(-1)) and PEEPi (1.1+/-1.3 cmH2O). The amount of fluid removed was closely related to changes in Ppl,sw and PEEPi. We conclude that the strength of the inspiratory muscles is normal or reduced in seated cirrhotic patients. In the supine position, tense ascites results in an increase in lung elastic load and development of positive end-expiratory pressure, with a consequent overload and increased activation of inspiratory muscles. Large volume paracentesis decreases overloading and activation, but does not change the strength of the inspiratory muscles.

Effects of prolonged controlled mechanical ventilation on diaphragmatic function in healthy adult baboons.

To study diaphragmatic strength and endurance after a prolonged period of mechanical ventilation. Prospective animal study. Animal research laboratory. Seven uninjured adult baboons (Papio cynocephalus) were anesthetized with ketamine, sedated, paralyzed, and mechanically ventilated. Animals were monitored with pulmonary arterial and peripheral arterial catheters. Mechanical ventilation was provided for 11 days with an FIO2 of 0.21 and tidal volume of 15 mL/kg. Pulmonary function tests, including lung volumes, arterial blood gases, and chest radiographs were also monitored. Nursing care procedures included frequent turning, chest physiotherapy, and endotracheal suction. Antacids and prophylactic antibiotics (intravenous penicillin, topical polymyxin B, and gentamicin sulfate) were administered. In three animals, fishhook electrodes were surgically placed around both phrenic nerves on both day 0 and after 11 days of mechanical ventilation for diaphragmatic stimulation. On day 0, the electrodes were removed after phrenic nerve stimulation studies were performed. After 11 days of mechanical ventilation, animals were electively killed and full autopsy performed. Hemodynamic and pulmonary function parameters were measured at baseline and every day during the 11 days of mechanical ventilation. Diaphragmatic strength and endurance were measured on days 0 and 11. Diaphragmatic endurance was determined by an inspiratory resistive loading protocol. There were no significant changes in hemodynamics, lung volumes, or gas exchange during the period of mechanical ventilation. On day 7, the chest radiographs showed patchy lobar atelectasis in six animals, which cleared by day 11 in all but two of the animals. Lung pathology showed mild, focal pneumonitis. By day 11, maximum transdiaphragmatic pressure had decreased by 25% from day 0 and diaphragmatic endurance had decreased by 36%. Eleven days of mechanical ventilation and neuromuscular blockade in healthy baboons resulted in nonsignificant changes in hemodynamics, oxygenation, and/or lung function. However, significant impairment in diaphragmatic endurance and strength were seen. Based on these results, it is likely that prolonged mechanical ventilation by itself impairs diaphragmatic function independent of underlying lung disease.

Maximal inspiratory pressures and dimensions of the diaphragm.

We postulated that the variation of maximal voluntary inspiratory pressures (PI,max and Pdi,max) among individuals largely reflects the variation of the structural attributes of the inspiratory muscles, in particular the muscular cross-sectional area of the diaphragm (CSAdi) and its axially projected area (A(thor)). To test this postulate, we measured PI,max in 36 healthy subjects, including 3 children and 15 weight-lifters, and Pdi,max in 11 subjects. Structural measurements by ultrasonography and anthropometric calipers were available as reported in the companion manuscript. We found a high degree of correlation of Pdi,max with diaphragm thickness (tdi), CSAdi, and CSAdi/A(thor) (r2 = 0.89, 0.89, and 0.77, respectively). PI,max was also correlated with diaphragm structural measurements, although less well. The weight-lifters had greater pressures, thicker diaphragms, and greater diaphragm maximal stress (sigma(max)) than adults of similar stature who had not trained with weights. We conclude (1) that both Pdi,max and PI,max reflect in part structural attributes of the respiratory muscles; (2) that the variation of maximal transdiaphragmatic pressures is largely attributable to the normal variation of diaphragm structure; (3) weight lifting increases diaphragm structure and pressures.

The effect of lung transplantation on the neural drive to the diaphragm in patients with severe COPD.

Little is known about the effects of lung transplantation (LT) on the neural drive to the diaphragm and on the endurance of respiratory muscles in patients with severe chronic obstructive pulmonary disease (COPD). The aim of this study was to evaluate these effects of single-lung (SLT) and double-lung transplantation (DLT). The neural drive to the diaphragm was assessed during fatiguing inspiratory threshold loading manoeuvres in six SLT recipients, six DLT recipients and seven patients with severe COPD, by using diaphragmatic surface electromyograms. During threshold loading, the patients had to generate 80% of their maximal transdiaphragmatic pressure with each breath. The endurance of inspiratory muscles was defined as the time from the beginning of a resistive breathing trial until exhaustion (t lim). In DLT recipients and even in SLT recipients (on both sides), neural activation of the diaphragm was significantly lower than in COPD patients (p < 0.05). However, no statistically significant difference in t lim was seen between LT recipients and COPD patients. The data suggest that single-lung and double-lung transplantations cause a significant decrease of the neural drive to the diaphragm, while the endurance of inspiratory muscles is well-preserved in patients with advanced chronic obstructive pulmonary disease. This may contribute to reduced sensation of inspiratory effort during ventilatory stress, thus improving the quality of life.

Respiratory muscle and cardiopulmonary function during exercise in very severe COPD.

Chronic obstructive pulmonary disease (COPD) is thought to limit exercise capacity through a decreased ventilatory reserve, with cardiovascular factors playing a minimal role. We assessed respiratory muscle (RM) and cardiopulmonary function during exercise in very severe COPD (FEV1 0.79 +/- 0.17 L). We determined minute ventilation (VE), oxygen consumption (VO2), carbon dioxide production (VCO2), heart rate (HR), respiratory rate (RR), and O2 pulse with a metabolic cart. RM function was assessed from esophageal and gastric pressures. Dyspnea was assessed with a visual analog scale (VAS). Exercise capacity (peak VO2 = 36 +/- 31%), ventilatory reserve (VE/maximum voluntary ventilation [MW] = 89 +/- 31%), HR = 76 +/- 15%, and O2 pulse (O2Pmax = 45 +/- 15%) were abnormal. Peak VO2 correlated with O2Pmax(r = 0.82), the change in end-inspiratory pleural pressure (deltaPpli) (r = -0.74), maximal transdiaphragmatic pressure (Pdimax) (r = 0.68), and VEmax (r = 0.58). There were similar correlations with exercise endurance time. Multiple regression analysis revealed O2Pmax to be the best predictor of peak VO2. Thereafter, only VEmax and deltaPpli remained significant (r2 = 0.87). O2Pmax correlated with inspiratory muscle function (Pplimax, r = -0.58; Pdimax, r = 0.53; deltaPpli, r = -0.47; and PImax, r = -0.47). By multiple regression analysis, the predictors of O2Pmax were Pplimax and deltaPpli (r2 = 0.47). In very severe COPD, the impressive swings in intrathoracic pressure resulting from deranged ventilatory mechanics are the most likely cause of exercise limitation and reduced O2 pulse. The contributions of factors such as deconditioning, hypoxemia, and concurrent heart disease remain unknown.

Assessment of the voluntary activation of the diaphragm using cervical and cortical magnetic stimulation.

The twitch occlusion technique is a promising tool for use in accessing central drive to the diaphragm and determining maximal transdiaphragmatic pressure (Pdi) from submaximal efforts. It clinical use is limited by difficulties inherent to bilateral electrical stimulation (BES) of the phrenic nerves. This study was designed to revisit the technique using cervical magnetic stimulation (CMS). In addition, the effects of a voluntary contraction on diaphragm response to magnetic stimulation of the cortex (CxMS) were studied. Seven volunteers aged 23-33 yrs were studied. Pdi was determined at relaxed functional residual capacity (FRC) in response to BES (Pdi,P-ES) and CMS (Pdi,p-CMS), and the effects of an increasing voluntary contraction (Pdi, vol) were assessed, The same procedure was applied to CxMS. Pdi,p-CMS at relaxed FRC was 27.5 +/- 2.2 cmH2O (mean+/-SEM), about 20% higher than Pdi,p-ES, and reported previously. Pd,p-CMS linearly decreased with Pdi, vol, and six out of seven subjects were capable of producing voluntary contractions sufficient to extinguish the twitch. More complex patterns were observed with CxMS. Cervical magnetic stimulation provides diaphragmatic twitch occlusion data very similar to bilateral electrical phrenic stimulation. Magnetic stimulation, be it cervical or cortical, could probably be helpful for the assessment of central and peripheral mechanisms of diaphragmatic dysfunction in the clinical setting.

Effects of Body Position, Hyperinflation, and Blood Gas Tensions on Maximal Respiratory Pressures in Patients with Chronic Obstructive Pulmonary Disease

BACKGROUND--Inspiratory muscle strength in patients with chronic obstructive pulmonary disease (COPD) can be affected by mechanical factors which influence the length of the diaphragm, and by non-mechanical factors. The aim of the present study was to evaluate firstly the effects of body position on respiratory pressures and, secondly, to determine the relative contribution of age, body mass index (BMI), lung volumes, and arterial blood gas tensions to respiratory muscle strength. METHODS--Thirty male patients with stable COPD (mean FEV1 40.4% predicted) participated in the study. Maximal inspiratory and expiratory mouth pressures (PImax, PEmax) and maximal inspiratory transdiaphragmatic pressures (PDI) in the sitting and supine position, lung function, and arterial blood gas tensions were measured. RESULTS--Mean (SD) PImax in the sitting position was higher than in the supine position (7.1(2.3)kPa v 6.4(2.2)kPa respectively). In contrast, PDI in the sitting position was lower than in the supine position (10.0(3.5)kPa v 10.8(3.7)kPa respectively). PEmax was higher in the sitting position (9.3(3.0)kPa) than in the supine position (8.7(2.8)kPa). Significant correlations were found between inspiratory muscle strength on the one hand, and lung function parameters, BMI, and arterial blood gas tensions on the other. CONCLUSIONS--Inspiratory muscle strength in patients with COPD is influenced by mechanical factors (body position, lung volumes) and non-mechanical factors (BMI, FEV1, and blood gases). PImax and PEmax are lower in the supine position while, in contrast to healthy subjects, PDI is higher in the supine position than in the sitting position.