Delta Pdi Research Articles

Reduction of Psychosis Proneness in a Daycare Hospital Program for Patients with Severe Alcohol Use Disorder

Objectives Anxiety and depressive symptoms, as well as cognitive dysfunctions, improve with abstinence in individuals with alcohol use disorders (AUD), but less is known about psychotic features. The objective of this study was to evaluate the psychosis proneness in a sample of individuals with severe AUD and potential changes after alcohol withdrawal. Method An observational study was conducted, assessing prospectively Peter’s Delusional Inventory scale (PDI); anxiety and depression symptoms by MADRS and cognitive functioning by the MoCA at entry in daycare hospital (D0) and after 30 days (D30). Individuals with schizophrenia, chronic delusional disorder and bipolar disorder were excluded. Wilcoxon tests were used to evaluate the evolution between D0 and D30, and linear regressions were conducted to test the association between delta PDI and the variables that could be potential confounders. Results Forty individuals (72% males) with a mean age of 50 ± 9 years old and AUD evolved for 15 ± 11 years were included. After one month, PDI score decreased significantly (p = .001), and several biological and clinical parameters improved significantly with abstinence or consumption reduction: GGT (p = .003), MoCA (p < .001), MADRS (p = .047). Conclusion We observed a decrease in delusional thinking along abstinence and/or consumption reduction. To our knowledge, this is the first research to study psychosis proneness evolution in patients with severe AUD. Replications are required in independent samples with larger sample size.

In normal subjects bracing impairs the function of the inspiratory muscles.

Normal subjects can increase their capacity to sustain hyperpnoea by bracing their arms on fixed objects, a procedure which is also known to reduce dyspnoea in patients with chronic obstructive pulmonary disease (COPD). In the present study, it was tested whether bracing per se could improve the function of the diaphragm. The effect of bracing on diaphragm function was studied in six normal subjects by recording changes in oesophageal (delta Poes) and transdiaphragmatic (delta Pdi) pressure during inspiratory capacity (IC) manoeuvres in the seated and upright postures, and in the seated posture, also during bilateral phrenic nerve stimulation (BPNS) at functional residual capacity (FRC). The pattern of ribcage motion and deformation associated with bracing and with diaphragm contraction was also evaluated using inductance plethysmography and magnetometers. Bracing increased FRC by >300 mL and reduced IC by approximately 200 mL, in both postures. Delta Pdi during BPNS decreased on average by 15% indicating an impaired diaphragmatic function. The ribcage was deformed with bracing and was more distortable during BPNS. In conclusion, in normal subjects, bracing impairs the function of the inspiratory muscles and reduces ribcage stability. These negative effects cannot explain the improved capacity to sustain hyperpnoea when the arms are braced.

Differential inspiratory muscle pressure contributions to breathing during dynamic hyperinflation.

During dynamic hyperinflation, the ventilatory pump is facing increased demand because it must overcome the intrinsic positive end-expiratory pressure (PEEPi) and decreased capacity since it must operate at a dynamically increased end-expiratory lung volume (EELV). The aim of this study was to evaluate the relative pressure contribution by the diaphragm and inspiratory rib cage muscles (RCMs) during dynamic hyperinflation. In six healthy subjects, dynamic hyperinflation was induced by limiting expiratory flow. The global inspiratory muscle pressure (delta Pmus,i) and transdiaphragmatic pressure (delta Pdi) were partitioned into the portion used to overcome PEEPi and the portion used to inflate the respiratory system. The delta Pdi/delta Pmus,i ratio was used to estimate the pressure contribution of RCMs relative to that of the diaphragm. Our results suggest that (1) with increasing severity of dynamic hyperinflation, there is a significant increase in the inspiratory pressure contribution of RCMs relative to that of the diaphragm for inflating the respiratory system; (2) during dynamic hyperinflation, especially at high EELV, the major pressure contribution of the diaphragm is to overcome the PEEPi-imposed inspiratory threshold load, whereas the inspiratory pressure needed for the subsequent task of inflating the respiratory system is largely contributed by RCMs. This arrangement is consistent with the change in mechanical advantages of RCMs and the diaphragm during the development of dynamic hyperinflation.

Effects of Diaphragmatic Plication on Respiratory Mechanics in Dogs With Unilateral and Bilateral Phrenic Nerve Paralyses

To examine the effects of diaphragmatic plication on respiratory mechanics during spontaneous breathing, we grouped 28 dogs into left phrenicotomy and plication (group L, n = 11), bilateral phrenicotomy and plication (group B, n = 9), and sham operations (group C, n = 8). In groups L and B, phrenicotomy caused significant (p < 0.05) decreases in tidal volume (VT), transdiaphragmatic pressure (delta Pdi), the ratio of gastric to esophageal pressure (delta Pga/delta Pes) and dynamic lung compliance (Cdyn), and significant (p < 0.05) increases in esophageal pressure (delta Pes), and the work of breathing (WOB) per liter of ventilation. In group L, plication resulted in significant (p < 0.05) increases in VT, delta Pdi, delta Pga/delta Pes, and Cdyn, and a significant reduction of WOB compared with phrenicotomy condition, indicating an improvement in the respiratory mechanics. However, in group B, no significant changes were observed after plication except for increased VT. In eight left-phrenicotomized open-chest dogs, transdiaphragmatic pressure (Pdi) and fractional shortening (FS) of right hemidiaphragm by right phrenic nerve stimulation increased significantly (p < 0.05) after plication, compared with the phrenicotomy condition, suggesting more effective kinetics of the right hemidiaphragm after plication of the left hemidiaphragm. Our results showed that diaphragmatic plication for unilateral paralysis is more effective than for bilateral paralysis, indicating that an improvement in kinetics of the intact hemidiaphragm plays an important role in functional recovery.

Thoracic epidural anesthesia increases diaphragmatic shortening after thoracotomy in the awake lamb.

Prolonged inhibition of diaphragmatic function occurs after thoracic and upper abdominal surgery. It was hypothesized that thoracic epidural anesthesia on the day after a thoracotomy could block inhibitory neural pathways and increase the shortening of costal and crural diaphragmatic segments. Pairs of sonomicrometer crystals were implanted into the costal and crural regions of the diaphragm through a right lateral thoracotomy in 14 30-kg, 4-5-month-old lambs. One day after surgery, a thoracic epidural catheter was placed at the T8-T9 level. Regional diaphragmatic shortening normalized to end-expiratory length (%LFRC), was measured by sonomicrometry in these awake lambs. Changes in gastric (delta Pgas), esophageal (delta Pes), and transdiaphragmatic (delta Pdi) pressures were measured with transnasal balloon catheters. End-tidal carbon dioxide (FETCO2), costal and crural electromyogram (Edi), and tidal volume (VT) were measured. Inductance plethysmography was used in four lambs to assess relative contributions of the rib cage and abdomen to VT. Control values were obtained during quiet breathing and while rebreathing at up to 10% FETCO2. To block thoracic dermatomes, 1% or 2% lidocaine was injected through the epidural catheter. Measurements were repeated after each lidocaine injection. There was no change of resting length with 1% lidocaine; costal resting length increased by 22% with 2% lidocaine. After 2% lidocaine, costal %LFRC increased from control both during quiet breathing (8.7 +/- 0.7 to 18.1 +/- 1, mean +/- SEM%) and at FETCO2 10% (22.1 +/- 2 to 33.7 +/- 3%). VT during quiet breathing was unchanged after 1% lidocaine but increased from 235 +/- 16 to 283 +/- 28 ml after 2% lidocaine. At 10% FETCO2, delta Pdi was unchanged after 1% lidocaine and decreased from 36.5 +/- 4.3 to 26.3 +/- 4.9 cmH2O after 2% lidocaine. Regional delta Edi was unchanged with both 1% and 2% lidocaine at rest and during carbon dioxide rebreathing. Plethysmography in three lambs showed a reduction in rib cage contribution to tidal volume with 2% lidocaine during quiet breathing. Improved postoperative tidal volume and diaphragmatic shortening after thoracic epidural blockade may be due to changes of chest wall conformation and resting length and a shift of the workload of breathing from the rib cage to the diaphragm caused by intercostal muscle paralysis.

Effects of thoracic extradural block on diaphragmatic electrical activity and contractility after upper abdominal surgery.

Upper abdominal surgery (UAS) induces diaphragmatic dysfunction. Thoracic extradural block (TEB) using 0.5% bupivacaine improves some pressure and motion indices of diaphragmatic function. However, no direct information on diaphragmatic activity is available after UAS. The aim of this study was to assess diaphragmatic electrical activity (Edi) after UAS before and after TEB. A postoperative electromyogram was obtained, using intramuscular electrodes inserted by the surgeon in the costal and crural parts of the diaphragm, in 14 patients undergoing abdominal aortic surgery. Tidal changes in abdominal (VAB) and rib-cage (VRC) volumes, and gastric (delta Pgas), esophageal (delta Pes), and transdiaphragmatic (delta Pdi) pressures were used to measure tidal volume (VT) and respiratory rate and to provide indirect indices of diaphragmatic activity from the two ratios VAB/VT and delta Pgas/delta Pdi. These respiratory variables were obtained preoperatively. Postoperatively, measurements including Edi were obtained before and after a segmental epidural block, reaching a T4 level was achieved with 0.5% plain bupivacaine. Upper abdominal surgery induced an increase in respiratory rate (+28 +/- 15%; P < .01), associated with a decrease in VAB/VT (from 0.75 +/- 0.11 to 0.07 +/- 0.08; P < .01), delta Pgas/delta Pdi (from 0.3 +/- 0.08 to 0.01 +/- 0.19; P < .05), and VT (-30 +/- 14%; P < .01). After surgery, all patients exhibited electrical diaphragmatic activity that increased with TEB by 48 +/- 28% (P < .01) and 60 +/- 22% (P < .001) for the cural and costal segments, respectively. The ratio delta Pdi/Edi, used to evaluate diaphragmatic contractility, was not modified by TEB. Tidal volume, respiratory rate, and delta Pgas/delta Pdi returned to preoperative levels, whereas VAB/VT increased but remained different from preoperative values. This study demonstrates that TEB produces an increase in diaphragmatic activity, identical for the two segments of the muscle. Interruption of afferents that produce an inhibitory effect on diaphragmatic activity appears the most attractive hypothesis to explain the consequences of TEB after UAS.

Effects of aminophylline on regional diaphragmatic shortening after thoracotomy in the awake lamb.

Aminophylline has been reported to augment diaphragmatic contraction, although this remains a controversial finding. We studied the effect of aminophylline on regional diaphragmatic shortening, changes in transdiaphragmatic pressure (delta Pdi), and integrated regional electromyographic (EMG) activity of the diaphragm (Edi) after a right thoracotomy in nine lambs using sonomicrometry, esophageal and gastric balloons, and EMG. Sonomicrometer crystals and EMG leads were implanted into the costal and crural regions of the diaphragm through a right thoracotomy, and a tracheostomy was performed. The animals were studied while awake within 4 days after surgery. Fractional costal and crural diaphragmatic shortening was measured using the sonomicrometer; delta Pdi was calculated from esophageal and gastric pressures. Respiratory variables were measured through the tracheostomy. Data were collected during quiet breathing and during CO2 rebreathing. After control measurements, aminophylline (10 mg/kg) was administered intravenously, producing a serum concentration of 17.7 +/- 1.5 micrograms/ml. Aminophylline did not augment shortening, increase delta Pdi, or overcome postoperative diaphragmatic inhibition acutely in the awake sheep after a right lateral thoracotomy. A small decrease of end-tidal CO2, from 5.2% to 4.9%, was measured at rest during aminophylline infusion, but Edi was unchanged. Although during CO2 rebreathing diaphragmatic shortening increased, the addition of aminophylline did not further augment shortening. Our data in awake lambs suggest that aminophylline does not improve diaphragmatic contraction in the acute postoperative period.

Respiratory Response to Arm Elevation in Patients with Chronic Airflow Obstruction

We have shown that patients with chronic airflow obstruction (CAO) complain of disabling dyspnea when performing seemingly trivial tasks with unsupported arms. Surprisingly little is known about the metabolic and ventilatory responses to unsupported upper extremity activity even though some of the muscles of the upper torso and shoulder girdle are used to perform simple and complex everyday tasks as well as partake in ventilation. To determine the effect of simple arm elevation in 20 patients with CAO we studied their lung function, VO2, VCO2, and VE, with arms down at the side (AD), during 2 min with arms extended forward up to shoulder level (AE), and during recovery. To determine the pattern of ventilatory muscle recruitment we also measured endoesophageal (Ppl), gastric (Pg), and transdiaphragmatic (Pdl) pressures. In five of the patients the electromyographic signal (EMG) of the sternocleidomastoid (Sm) muscle was recorded and analyzed in its time domain (amplitude) and power spectrum density (median frequency). Within 30 s of arm elevation VO2, VCO2, and VE rose and remained elevated for 1 min after the arms were lowered. The increase in VE resulted from increases in respiratory rate and minimal rise in tidal volume (VT). With AE, FEV1 decreased by 5% (p less than 0.02) but FRC increased by 2% (p less than 0.05). Peak inspiratory pressure (Pimax) dropped from 54 +/- 4 to 48 +/- 4 cm H2O (p less than 0.005); Pdimax remained unchanged. Immediately after raising the arms Pgi, inspiratory swing in Pdi (delta Pdi), end-expiratory Ppl, and end-expiratory Pg increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of lung inflation on diaphragmatic shortening

The effect of lung inflation on chest wall mechanics was studied in 11 vagotomized pentobarbital sodium-anesthetized dogs. Diaphragmatic shortening (percent change from initial length at functional residual capacity, %LFRC) and transdiaphragmatic pressure swings (delta Pdi) were compared with control values over a range of positive-pressure breathing that produced a maximum increase in lung volume to 40% of inspiratory capacity. There was no change in the electromyogram of the diaphragm or parasternal intercostals during positive-pressure breathing. delta Pdi and tidal volume (VT) fell to 52 +/- 3.3 and 42.5 +/- 5% (SE) of control. This was associated with a reduction in the initial resting length of 13 +/- 1.9 and 21 +/- 2.2%LFRC (SE) in the costal and crural diaphragms, respectively. Tidal diaphragmatic shortening, however, decreased to 66 +/- 7 and 57 +/- 7 and the mean velocity decreased to 78 +/- 10 and 63 +/- 8% (SE) of control for the costal and crural diaphragms, respectively. We conclude that the reduction in diaphragmatic shortening is the main determinant of the reduced delta Pdi and VT during lung inflation and relate this to what is currently known about diaphragmatic contractile properties.

Pleural pressure between diaphragm and rib cage during inspiratory muscle activity.

We measured the changes in pleural surface pressure (delta Ppl) in the area of apposition of the rib cage to the diaphragm (Aap) in anesthetized dogs during spontaneous breathing, inspiratory efforts after airway occlusion at functional residual capacity, and phrenic stimulation. Intact dogs were in supine or lateral posture; partially eviscerated dogs were in lateral posture. delta Ppl,ap often differed significantly from changes in abdominal pressure (delta Pab); sometimes they differed in sign (except during phrenic stimulation). Changes in transdiaphragmatic pressure in Aap (delta Pdi,ap) could be positive or negative and were less in eviscerated than in intact dogs. delta Pdi,ap could differ in sign among respiratory maneuvers and over different parts of Aap. Hence average delta Pdi,ap should be closer to zero than delta Pdi,ap at a given site. Since delta Ppl,ap = delta Prc,ap, where Prc,ap represents rib cage pressure in Aap, delta Pdi,ap = delta Pab - delta Prc,ap. Hence, considering that delta Pab and delta Prc depend on different factors, delta Pdi,ap may differ from zero. This pressure difference seems related to the interaction between two semisolid structures (contracted diaphragm and rib cage in Aap) constrained to the same shape and position.

Transdiaphragmatic pressure and rib motion in area of apposition during paralysis.

Changes in pleural surface pressure in area of apposition of diaphragm to rib cage (delta Ppl,ap), changes in abdominal pressure (delta Pab), and redial displacement of the 11th rib have been recorded in anesthetized, paralyzed dogs during lung inflation or deflation. Above functional residual capacity (FRC) changes in transdiaphragmatic pressure in area of apposition (delta Pdi,ap) were essentially nil in intact (INT) dogs either in lateral or supine posture, and in partially eviscerated (EVS) dogs in lateral posture, either in the 10th or 11th intercostal space. Below FRC delta Pdi,ap could be positive (INT lateral and EVS), nil (EVS), or negative (INT supine and EVS); it could be different in the 10th and 11th intercostal spaces. Hence, with stretched (like with contracted) diaphragm, delta Ppl,ap measured at one site often differs from delta Pab and is not representative of average pressure acting on area of apposition. With volume increase above FRC, the 11th rib moved slightly in and then out in EVS and linearly out in INT. With volume decrease below FRC it moved out progressively in EVS, and it moved in and eventually reversed in INT. In paralyzed dogs in lateral posture the factor having the greatest influence on displacement of the abdominal rib cage is Pab. Mechanical linkage with pulmonary rib cage becomes relevant at large volume, whereas insertional traction of diaphragm becomes relevant at low volume.

Diaphragmatic contractility after upper abdominal surgery

Postoperative dysfunction of the diaphragm has been reported after upper abdominal surgery. This study was designed to determine whether an impairment in diaphragmatic contractility was involved in the genesis of the diaphragmatic dysfunction observed after upper abdominal surgery. Five patients undergoing upper abdominal surgery were studied. The following measurements were performed before and 4 h after surgery: vital capacity (VC), functional residual capacity (FRC), and forced expiratory volume in 1 s. Diaphragmatic function was also assessed using the ratio of changes in gastric pressure (delta Pga) over changes in transdiaphragmatic pressure (delta Pdi). Finally contractility of the diaphragm was determined by measuring the change in delta Pdi generated during bilateral electrical stimulation of the phrenic nerves (Pdi stim). Diaphragmatic dysfunction occurred in all the patients after upper abdominal surgery as assessed by a marked decrease in delta Pga/delta Pdi from 0.480 +/- 0.040 to -0.097 +/- 0.152 (P less than 0.01) 4 h after surgery compared with preoperative values. VC also markedly decreased after upper abdominal surgery from 3,900 +/- 630 to 2,060 +/- 520 ml (P less than 0.01) 4 h after surgery. In contrast, no change in FRC and Pdi stim was observed 4 h after surgery. In contrast, no change in FRC and Pdi stim was observed 4 h after upper abdominal surgery compared with the preoperative values. We conclude that contractility of the diaphragm is not altered after upper abdominal surgery, and diaphragmatic dysfunction is secondary to other mechanisms such as possible reflexes arising from the periphery (chest wall and/or peritoneum), which could inhibit the phrenic nerve output.

Diaphragmatic Strength during Weaning from Mechanical Ventilation

Respiratory muscle weakness is considered to be a factor in the inability to wean from mechanical ventilation. To assess this possibility, the present study examined the mechanical behavior of the diaphragm by measuring the change in transdiaphragmatic pressure (delta Pdi) during weaning. Nine "T-piece" weanings were carried out in seven patients with prior weaning failure and were terminated with the development of hypercapnia, hypoxemia, or severe tachypnea. Serial measurements of delta Pdi during these weans revealed that (1) in no case was there a decrease in delta Pdi at termination of weaning, and (2) in the subgroup of patients whose weaning failed because of hypercapnia, the increase in arterial carbon dioxide tension (mean increase of 12 mm Hg) was associated with a significant increase in delta Pdi, from the beginning (21.1 +/- 12.1 cm H2O) to the end (24.8 +/- 13.4 cm H2O) of the trial (p less than 0.05). We conclude that failure to wean in these patients, in particular the development of carbon dioxide retention, was not due to failure of the diaphragm as a pressure generator.

Pulmonary Involvement in Mixed Connective Tissue Disease

To determine the frequency of pulmonary function abnormalities in mixed connective tissue disease (MCTD), we studied 16 consecutive patients. Spirometry, total lung capacity (TLC), diffusing capacity (Dco), static lung compliance (Cst), and tests of respiratory muscle function (peak inspiratory pressure [PIP] and the maximum change in transdiaphragmatic pressure [delta PDI] during a diaphragmatic Müeller maneuver) were obtained. Airway resistance (RAW) and frequency dependence of compliance were also measured. Static lung compliance was less than 0.2 L/cm H2O in four of nine patients. The PIP was less than 75 cm H2O in only one patient and delta PDI was greater than 45 cm H2O in all ten patients evaluated. Frequency dependence of compliance was abnormal in seven of ten patients, whereas RAW was increased in only three of eight patients. The TLC and DCO were less than 80 percent of the predicted values in ten of 16 and 14 of 16 patients respectively. There was no correlation between the level of extractable nuclear antigen and pulmonary function abnormalities. The study did not identify significant abnormalities in respiratory muscle function.

Effects of aminophylline on diaphragmatic dysfunction after upper abdominal surgery.

The effects of upper abdominal surgery on diaphragmatic function were studied in eight supine patients before and after administration of aminophylline. Changes in pleural (delta Ppl) and gastric pressure (delta Pga) swings were measured with balloon catheter systems. Transdiaphragmatic pressure change (delta Pdi) was calculated as the difference delta Pga-delta Ppl. The ratio delta Pga/delta Pdi, used as an index of the diaphragmatic contribution to the quiet breathing process, decreased significantly as early as 1 h after operation without any further change throughout the 6-h period studied. Administration of aminophylline (6 mg/kg), six hours postoperatively, produced a significant increase in this diaphragmatic index. These data indicate that the early reduced diaphragmatic activity, after upper abdominal surgery, partially may be reversed by administration of aminophylline. The mechanism of its action may involve central nervous stimulation and/or a direct inotropic effect on diaphragmatic muscle. Further studies are needed to evaluate if the correction of altered diaphragmatic motion by aminophylline improves postoperative lung function.

Electrical and mechanical activity of the diaphragm accompanying body position in severe chronic obstructive pulmonary disease.

Using a special gastroesophageal catheter, electromyographic measurements of the diaphragm (Edi) and transdiaphragmatic pressure (Pdi) were taken in the supine, standing, erect sitting, and leaning forward (sitting) positions in 8 normal subjects and 6 patients with severe chronic obstructive pulmonary disease (COPD) with marked hyperinflation and low fat diaphragms. Four patients had pronounced postural relief of their dyspnea from assuming the supine and/or leaning forward positions. All 8 normal subjects and 4 of the 6 patients with COPD showed substantial (2- to 5-fold) increases in delta Edi, the phasic inspiratory amplitude of Edi, on assuming the standing and erect sitting postures. In the normal subjects, delta Pdi, the phasic inspiratory increment in Pdi, was maintained in all 4 postures, whereas in all patients with COPD, it decreased significantly in the erect sitting and standing postures. In 2 of the 6 patients with COPD, the delta Edi did not increase in the erect postures. This suggested that in these patients a reflex, which normally compensates for reduced diaphragmatic efficiency because of shortened muscle fibers in the erect postures, was not operating. Although it is not clear what mechanism(s) might account for suppression of this compensatory reflex, such reflex suppression might be advantageous from the viewpoint of diaphragmatic muscle energetics. The diaphragm would be thus spared energetically wasteful attempts to accomplish a fatiguing mechanical task.

Relationship of Rib Cage and Abdomen Motion to Diaphragm Function During Quiet Breathing

Although rib cage (RC) and abdomen (Ab) motion is believed to reflect intercostal and diaphragm contributions to breathing, systematic investigations have failed to confirm this. We measured inspiratory changes in RC and Ab anterior-posterior diameter (delta RC and delta Ab) both corrected for volume equivalence (isovolume) and not corrected (isodistance, observed), and correlated these with simultaneous changes in gastric (delta Pab) and esophageal (delta Ppl) pressure: delta Pab - delta Ppl = delta Pdi, the change in transdiaphragmatic pressure. The delta Pab/delta Pdi was used as an index of the relative contribution of diaphragm motion to the breathing process. Relative abdomen motion was expressed as delta Ab/(delta Ab + delta RC). Isodistance and isovolume delta Ab/(delta Ab + delta RC) correlated, R = 0.69; observed abdomen motion overestimated abdomen-diaphragm contribution to tidal volume. Isodistance delta Ab/(delta Ab + delta RC) was less for women than men; isovolume delta Ab/(delta Ab + delta RC) was similar for the two sexes. Among individuals, isodistance delta Ab/(delta Ab + delta RC) correlated with delta Pab/delta Pdi (R = 0.73, P less than 0.001). Within a given individual, the mean R for seven subjects for delta Pab/delta Pdi vs delta Ab/(delta Ab + delta RC) was 0.90. We conclude that observed rib cage and abdomen motion reflects intercostal and diaphragm contributions to breathing; the correlation is better within a given subject than among individuals.