Diaphragmatic Strength Research Articles

37 Respiratory failure and ventilation

Forced vital capacity (FVC) and maximal inspiratory pressure correlate with nocturnal hypoventilation in adults with neuromuscular disease, but children may not be able to perform these volitional tests.To identify volitional and non-volitional parameters reflecting lung and respiratory muscle function which differ in children treated or not with nocturnal noninvasive positive pressure ventilation (NPPV).Parameters reflecting lung function and respiratory muscle performance were measured in 27 children not treated with NPPV (Unventilated group) and 8 children treated with NPPV (Ventilated group).Concerning noninvasive tests, the Ventilated group had a rapid shallow breathing and a lower ventilatory response to carbon dioxide compared to the Unventilated group. FVC (performed by 69% of the patients) and sniff nasal inspiratory pressure were lower in the Ventilated group. Concerning invasive tests, the non-volitional measurement of diaphragmatic strength by magnetic stimulation of the phrenic nerves showed lower results in the Ventilated group as compared to the Unventilated group. Volitional tests evaluating inspiratory and expiratory muscle strength and endurance by means of the sniff and cough manoeuvres and the tension time indexes, revealed lower values in the Ventilated group as compared to the Unventilated group.Several lung function and respiratory muscle function tests are lower in children treated with NPPV as compared to children not treated with NPPV. A prospective hierarchical evaluation of these tests, according to their feasibility and invasiveness, may be helpful to identify children with neuromuscular disease at risk for nocturnal hypoventilation.

Spontaneous recovery of diaphragmatic strength in unilateral diaphragmatic paralysis

The aim of the present study was to evaluate diaphragmatic strength in patients with unilateral diaphragmatic paralysis and to determine whether patients with recent diaphragm paralysis develop lower inspiratory pressure than patients with longstanding diaphragmatic paralysis. Twenty patients (16 men and 4 women, 62+/-12 years) and six control subjects were included (4 men and 2 women, 53+/-15 years) in the study. Esophageal pressure during sharp sniff (Pes,sniff), bilateral cervical phrenic nerve magnetic stimulation (Pes,cms) and unilateral phrenic nerve stimulation (Pes,ums) (in nine patients) were measured. Sixteen patients presented right diaphragmatic paralysis and four, left diaphragmatic paralysis. Pes,sniff was higher in control subjects than in patients with diaphragmatic paralysis (respectively 110+/-22 cmH2O and 82+/-24 cmH2O, P<0.05). There was no difference in Pes,cms between patients with diaphragmatic paralysis and control subjects (14+/-7 cmH2O vs. 16+/-4 cmH2O; ns). Pes,ums after stimulation of the affected phrenic nerve was less than 4 cmH2O, was 8+/-2 cmH2O after stimulation of the intact phrenic nerve and was correlated to Pes,cms (R=0.87, P<0.01). There was a positive correlation between Pes,cms, Pes,ums of the intact hemidiaphragm, Pes,sniff and the time from the onset of symptoms and the diaphragmatic explorations (respectively R=0.86, P<0.0001; R=0.72, P<0.05; R=0.48, P<0.05). In conclusion, diaphragmatic strength after unilateral diaphragmatic paralysis seems to improve with time.

Effect of Lung Volume Reduction Surgery on Diaphragmatic Neuromechanical Coupling At 2 Years

We previously reported that patients with emphysema show an increase in diaphragmatic neuromechanical coupling at 3 months after lung volume reduction surgery. Diaphragmatic neuromechanical coupling was quantified as the quotient of tidal volume (normalized to total lung capacity) to tidal change in transdiaphragmatic pressure (normalized to maximal transdiaphragmatic pressure). As such, neuromechanical coupling estimates the fraction of diaphragmatic capacity used to generate tidal breathing. The present investigation was conducted to determine whether benefit is maintained at 2 years. Fifteen patients with severe COPD, 8 of whom completed the 2-year study. Lung volumes, exercise capacity (6-min walking distance), diaphragmatic function (maximal transdiaphragmatic pressure and twitch transdiaphragmatic pressure elicited by phrenic nerve stimulation), and diaphragmatic neuromechanical coupling were recorded before surgery, and at 3 months and 2 years after surgery. Two years after surgery, lung volumes deteriorated to preoperative values, but patients showed persistent improvements in 6-min walking distance (p < 0.05). Three months after surgery, maximal transdiaphragmatic pressure (p < 0.05), twitch transdiaphragmatic pressure (p < 0.01), and diaphragmatic neuromechanical coupling (p < 0.01) had increased over preoperative values. The improvements in neuromechanical coupling resulted from improvements in diaphragmatic strength and, to a lesser extent, from a decrease in transdiaphragmatic pressure required to maintain tidal breathing. The change in respiratory muscle function at 2 years varied among patients: diaphragmatic contractility was > 10% of preoperative value in half of the patients who concluded our study, and neuromechanical coupling was > 10% of preoperative value in three fourths of the patients who concluded our study. Patients who maintained their gains in neuromechanical coupling also maintained their gains in 6-min walking distance. Patients undergoing lung volume reduction surgery can maintain early gains in neuromechanical coupling and exercise capacity 2 years later.

MULTIDISCIPLINARY PAIN ABSTRACTS: 1 . Anesthesia (1)

Stellate ganglion block is a procedure frequently used for the management of patients with chronic sympathetically mediated pain affecting the arm, neck or head. In this study, the authors looked at the effect of the stellate ganglion block on ipsilateral phrenic nerve function, and hence diaphragmatic strength, in 11 adult patients with chronic sympathetically mediated pain. Pre‐block and post‐block forced vital capacity (FVC) measurements were recorded using a pneumotachograph and a Magstim nerve stimulator was used to generate pre‐block and post‐block twitch mouth pressures (P[TWM]). This device can be used to stimulate the phrenic nerves and hence the diaphragm. The resulting change in airway pressure was measured at the mouth and has previously been shown to reflect diaphragm strength. There was no statistically significant difference in FVC or P(TWM) before or after the stellate ganglion block. In conclusion, a stellate ganglion block has no adverse effect on ipsilateral phrenic nerve function or diaphragm strength in healthy adult patients.

Increased diaphragmatic strength and tolerance to fatigue after bilateral lung transplantation: an electromyographic study

We evaluated the diaphragmatic function of seven patients with severe chronic respiratory failure before and after a bilateral lung transplantation (BLT), with follow-up at one year of pulmonary function tests, maximal inspiratory mouth pressure (MIP) and surface diaphragmatic electromyogram (Edi). The patients were asked to sustain target inspiratory pressures at −15, −30, and −50 cmH 2O. We measured the endurance time (Tlim) to sustain inspiratory efforts and the power spectrum density function of Edi at each inspiratory maneuver. The Edi power spectra was analysed in terms of median frequency (MF), total power (TP) and energies in high-and low-frequency bands (EL and EH). Before BLT, a defect of the diaphragmatic function was evident: MIP was 62±7% of the predicted value and the Tlim measured at each inspiratory effort was very short (13±1 s, 10±1 s and 8±1 s at pressures of −15, −30, and −50 cmH 2O, respectively). One month after BLT, the Tlim began to increase at all target inspiratory pressures and at 6 months MIP recovered to normal values. One month after BLT, there was a significant decrease in TP measured at the beginning of each inspiratory efforts and also an increase in the concomitant MF value. BLT markedly accentuated the maximal variations of TP, MF and low-frequency Edi energy. Some hypotheses are raised to explain this dramatic improvement in diaphragmatic function after BLT.

Effect of Ammonia on in vitro Diaphragmatic Contractility, Fatigue and Recovery

Background: Following strenuous exercise, in vivo diaphragmatic strength has been reported to decrease. This decrease has been suggested to result from an increase in metabolic by-products of intense exercise. Objective: We tested the hypothesis that physiological NH₃ concentrations adversely affect diaphragmatic contractility, fatigability, and recovery. Methods: Rat diaphragm strips were exposed to one of six experimental conditions (n = 6 per condition): Krebs-Ringer control solution, or the control solution with NH₃ added (in mM): 0.11, 2.5, 5.0, 10.0, or 14.0. Initial diaphragmatic contractility was assessed with the force-frequency response in the control solution. Following the first force-frequency response, the solution was replaced with one of the six solutions and a second force-frequency response was measured. Strips were then subjected to a short fatigue protocol and contractility was reassessed with a third force-frequency response. A longer fatigue protocol was then administered, followed by a 20-min recovery assessment period. Results: Ammonia significantly (p < 0.05) reduced diaphragmatic contractility, but only at concentrations of 5 mM or greater. Additionally, ammonia did not alter the rate of fatigue. Conclusions: This study suggests that physiological NH₃ concentrations do not adversely affect in vitro diaphragmatic contractility, fatigue, or recovery. These data are not consistent with diaphragmatic fatigue associated with exercise induced by arterial concentrations of NH₃ seen in humans, although further testing in situ or in vivo is needed.

Prevalence of diaphragmatic muscle weakness and dyspnoea in Graves' disease and their reversibility with carbimazole therapy.

Dyspnoea is a common complaint among patients with thyrotoxicosis. However, its causative mechanisms have not been identified. We assessed the role of thoracic diaphragmatic muscle weakness in dyspnoea among patients with active Graves' disease. Twenty-seven patients (19 female, 8 male) with active Graves' disease were assessed for the clinical severity of dyspnoea, functional (pressure generating capacity) and anatomical aspects (thickness and excursion) of the diaphragm at presentation. The severity of dyspnoea was assessed using a visual analogue scale (VAS) and the 6 min walk test. Lung function tests, diaphragmatic strength (sniff oesophageal pressure, SniffP(oeso)), maximum inspiratory and expiratory pressures, diaphragmatic thickness and movements on real time ultrasonography were evaluated during normal and deep respiration. Twenty of the 27 patients were reassessed after achieving euthyroidism with carbimazole therapy at a mean interval of 5+/-2 months. Reevaluation after carbimazole therapy revealed a significant reduction in dyspnoea on the VAS (59+/-26 to 23+/-13%). Patients covered a similar distance during the 6 min walk before and after euthyroidism. Significant improvement was observed in the vital capacity (2.57+/-0.62 to 2.94+/-0.60 l), forced expiratory volume in the first second (2.21+/-0.49 to 2.45+/-0.47 l), total lung capacity (3.57+/-1.19 to 4.1+/-1.12 l), diaphragmatic movement during deep respiration (5.5+/-1.0 to 6.6+/-1.1 cm) and SniffP(oeso) (68.7+/-23 to 93.1+/-25.2 cmH(2)O). There was no significant change in the distance walked in 6 min, tidal volume, lung diffusion capacity and diaphragmatic thickness. There was no significant correlation between the net change in dyspnoea score and net change in lung function tests, diaphragmatic movement and SniffP(oeso). Significant functional weakness of diaphragm muscle is present in patients with active Graves' disease. This weakness is more marked during a maximal respiratory manoeuvre, indicating a diminished diaphragmatic reserve which could be the cause of dyspnoea observed on exertion among patients with thyrotoxicosis.

Spirometry in the Supine Position Improves the Detection of Diaphragmatic Weakness in Patients With Amyotrophic Lateral Sclerosis

To determine which respiratory function tests best predicted diaphragmatic strength in patients with amyotrophic lateral sclerosis. Patients referred for pulmonary evaluation were included (n = 25) if they underwent measurement of transdiaphragmatic pressure (Pdi) and one or more of the following on the same day: upright FVC, supine FVC, upright FEV(1), supine FEV(1), maximal inspiratory pressure (MIP), maximal expiratory pressure (MEP), and PaCO(2). Abdominal paradox and use of accessory muscles were also assessed. Bivariate analyses were performed using simple linear regression. Sensitivity and specificity of the potential predictors to detect an abnormal Pdi (< 70 cm H(2)O) were calculated. Pulmonary function laboratory of an academic medical center. Upright FVC, FEV(1), and MEP were all significantly correlated with Pdi, while MIP and PaCO(2) were not. Supine FVC was the most highly correlated predictor of Pdi (R(2) = 0.76). A cutoff of supine FVC that was < 75% predicted was 100% sensitive and specific for predicting an abnormally low Pdi. Accessory muscle use and abdominal paradox were both significantly associated with Pdi, and the presence of accessory muscle use had a sensitivity of 84% and a specificity of 100% for detecting a low Pdi. Our findings suggest that supine FVC is an excellent and simple test of diaphragmatic weakness.

Unsuspected pseudophysiologic emphysema in chronic persistent asthma.

The current literature emphasizes the role of airway remodeling in chronic persistent asthma and its putative effect on causing fixed expiratory airflow limitation. We studied 18 adults with chronic persistent asthma; 12 men, six women, age 59 +/- 15 yr (mean +/- SD) with fixed expiratory airflow obstruction. We measured lung elastic recoil and examined the mechanism of expiratory airflow limitation. Diaphragmatic strength was also measured in six asthmatics, using both sniff and partially occluded airway technique. All 18 asthmatics had markedly abnormal maximal expiratory flow-volume curves at both high and low lung volumes. Hyperinflation was present at residual volume (RV), FRC, and TLC in all subjects. Diffusing capacity was normal or elevated and lung computed tomography (CT) was normal in all 18 asthmatic subjects. There was a significant loss of lung elastic recoil in three of four asthmatics age 30 to 49, all five age 51 to 60 yr, and seven of nine age 61 to 82 yr. Maximal expiratory airflow limitation in only four elderly asthmatics and only at low lung volumes was due completely to loss of lung elastic recoil. In the others, we estimate the reduction in lung elastic recoil was responsible for 35% reduction in maximal expiratory airflow at 80% of TLC, and 55% at 70% of TLC. Despite hyperinflation, transdiaphragmatic pressures and strength were normal. The mechanisms responsible for loss of lung elastic recoil remain elusive. The high incidence of loss of lung elastic recoil in chronic persistent asthma was unexpected, and its contribution to abnormal lung function needs to be emphasized.

Neural Drive to the Diaphragm After Lung Volume Reduction Surgery

The aim of this study was to investigate prospectively the changes in neural drive to the diaphragm in the first year after lung volume reduction surgery (LVRS) in patients with COPD. In 14 patients with severe emphysema (mean +/- SD; age, 53.7 +/- 8.3 years; FEV(1), 0.64 +/- 0. 18 L; residual volume [RV], 5.33 +/- 1.25 L; PaO(2), 62.3 +/- 9.0 mm Hg; PaCO(2), 39.0 +/- 6.0 mm Hg), we assessed lung function, arterial blood gases, maximal exercise capacity (Wmax), and oxygen uptake (f1.gif" BORDER="0">O(2)max); intrinsic positive end-expiratory pressure (PEEPi); diaphragmatic strength (transdiaphragmatic pressure, Pdisniff) and endurance capacity (tlim); central diaphragmatic drive assessed by root mean square analysis of the esophageal electromyogram (rmsdia); and isotime dyspnea during loaded breathing tests (BS). Despite a significant increase (expressed as a percentage of baseline) in FEV(1) (40.6%) and a decrease in RV (30.0%) and PEEPi (75.7%) 1 month after LVRS, the improvements in Wmax (31.2%) and f1.gif" BORDER="0">O(2)max (13.7%); Pdisniff (25.4%) and tlim (64.9%); rmsdia (34.6%); and BS (21.7%) did not reach statistical significance (p < 0.05) until 6 months after LVRS. Arterial blood gases did not change significantly. Significant correlations were found between decrease in rmsdia and changes in PEEPi (r = 0.69), Wmax (r = -0.56), Pdisniff (r = -0.65), tlim (r = -0.59), and BS (r = 0.71) 6 months after LVRS. Our results show that LVRS is able to increase the efficacy of the respiratory pump and by this way reduce ventilatory drive and respiratory effort sensation.

Alteration in diaphragmatic function induced by acute necrotizing pancreatitis in a rodent model.

Some of the common complications of acute necrotizing pancreatitis also involve pulmonary complications. These manifestations are often associated with a cephalad diaphragmatic shift. We hypothized that diaphragmatic function might be directly compromised by the acute abdominal process. This hypothesis was tested on an acute necrotizing pancreatitis (ANP) rat model. We assessed the diaphragm and peripheral (Extensor Digitorum Longus and Soleus) muscle properties in vitro using strips in control (C) and ANP animals. Contractile parameters included single twitch and a force-frequency curve (10 to 100 Hz), and an endurance capacity index (T50%) was calculated after a repetitive stimulation (30 Hz). Breathing pattern was not different between control and ANP animals, and muscular histologic examination was normal. However, ANP was associated with a marked decrease in diaphragmatic strength for all frequencies of stimulation when compared with C. Endurance capacity was also reduced in ANP animals as assessed by a lower T50% (ANP: 31 +/- 10.5 s; C: 49 +/- 10.3 s; p < 0.05). By contrast, no significant change in peripheral muscle function was observed in both groups. We conclude that ANP causes impairment in diaphragmatic strength and endurance capacity, whereas peripheral muscles are spared. These findings suggest that alterations in the respiratory pump may be involved in the genesis of acute respiratory failure in ANP.

A non-invasive system to evaluate diaphragmatic strength in ventilated patients

In this paper we describe a system that allows an indicator of diaphragmatic strength to be determined non-invasively in mechanically ventilated patients. The system is comprised of an occlusion device that can be incorporated into the ventilator tubing and an occlusion control unit to operate the occlusion. The system electronically coordinates the timing of airway occlusion at the mouthpiece, application of a magnetic phrenic nerve stimulus and rapid removal of the occlusion once the measurement has been made. The system therefore permits measurement of the change in airway pressure produced by a stimulated diaphragm contraction, without disconnection from the ventilator. Other important respiratory measurements such as twitch mouth pressure, simulated cough and P0.1 can also be performed on non-ventilated patients in a repeatable and systematic manner. Keywords: twitch mouth pressure, respiratory muscle strength, magnetic stimulation, ventilator weaning, simulated coughs, P0.1

Transvenous versus perinervous stimulation of the phrenic nerve to assess the diaphragmatic strength in rabbits

Diaphragmatic strength can be measured by transdiaphragmatic pressure during phrenic nerve stimulation. In order to avoid phrenic nerve dissection, a transjugular approach of the phrenic nerve can be performed. The objective of this study was to verify the identity of perinervous and transvenous techniques of phrenic nerve stimulation to assess diaphragmatic force. In intact ( n=9) or right phrenicotomized ( n=12) rabbits, we compared esophageal pressure (Peso) induced by supramaximal perinervous stimulation of the phrenic nerve with that obtained by transvenous stimulation of the phrenic nerve. Electromyography (EMG) of the thoracic muscles was studied in four animals. We found no difference between Peso induced by perinervous (PNS) and transvenous (TVS) unilateral or bilateral phrenic nerve stimulation. During unilateral stimulation, no EMG activity was recorded in the non stimulated diaphragm, or in the middle part of the esophagus, or in ipsi- and contralateral accessory inspiratory muscles. We conclude that in rabbits, unilateral or bilateral TVS of the phrenic nerve is functionally equivalent to PNS, whatever the side of stimulation; Peso is not altered by esophageal contraction in TVS. Transvenous stimulation can replace perinervous stimulation in experimental studies, when cervical access is difficult.

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.

Assessment and management of dyspnoea.

The terms 'dyspnoea' or 'breathlessness' refer to an individual's subjective awareness of discomfort related to the act of breathing. Elevations in CO2 above normal levels have been shown to cause breathlessness although it is unlikely to be the sole cause of breathlessness in a clinical setting. Several studies suggest that supplemental O2 during exercise will diminish the sensation of breathlessness although not all work has confirmed this finding. Much about the role of gas exchange in dyspnogenesis remains controversial. Phrenic blockade can abolish dyspnoea in response to breath-holding, while work in quadriplegics suggests that the intercostal muscles are not involved. A separate and direct pathway from the respiratory centre to the sensory cortex has also be implicated. Threshold discrimination has established that patients with chronic airflow limitation (CAL) have a blunted response to the addition of resistive loads to breathing, while category scaling methods (e.g. the Borg scale) have added descriptive terms to these physiological measures. Questionnaires often appear limited by their subjectivity and lack of correlation with physiological changes, but remain a useful tool in the clinical setting. In regard to therapy of dyspnoea high fat diets have a theoretical advantage in the CAL group but are generally not well tolerated. Resistive training devices and exercise training in CAL have been widely researched but in general, measures of lung remain unaltered and many of the studies would suggest that they have little, if any, inpact on functional status. Beta-agonists have been widely shown to be useful in CAL patients, despite the fact that bronchodilatation is not always demonstrable. Anticholinergics have be shown to be effective bronchodilators, but whether there is an improvement in dyspnoea above that expected from improvement in lung function is unclear. Animal studies and work in normal individuals would suggest that methylxanthines have a theoretical role in CAL possibly by increasing diaphragmatic muscle strength and decaying fatigue, but toxicity and lack of clear benefit in this group suggest that they should not be used as monotherapy. There is little evidence to support the use of opioids in chronic CAL although their role in the acute dyspnoea of end-stage CAL remains defined. The use of benzodiazepines has also been disappointing. Bullectomy remains widely accepted in clinical practice. New techniques such as 'reduction surgery' for diffuse emphysema are showing promise, although still in need of further testing and validation.

Effects of nitric oxide on diaphragmatic muscle endurance and strength in pigs.

The aim of the study was to evaluate the effects of nitric oxide (NO) on diaphragmatic fatigue in fifteen anaesthetized, mechanically ventilated pigs, divided into three groups. The animals were pre-treated with indomethacin (3 mg kg-1, i.v.) to block the cyclo-oxygenase pathway. To group 1 pigs (n = 6) NG-nitro-L-arginine methyl ester (L-NAME, 5 mg kg-1 i.v.) was administered as a bolus to block endogenous NO production, while group 2 pigs (n = 6) were infused with sodium nitroprusside (SNP, 0.023 mg kg-1, i.v.), a donor of NO. Group 3 pigs (n = 3) were used as the controls. We evaluated diaphragmatic strength by measuring the transdiaphragmatic pressure (P di) generated during bilateral phrenic nerve stimulation at 10, 20, 30 and 50 Hz, 15 V, while the diaphragmatic endurance was assessed by a 30s stimulation at 10 Hz, 15 V. Diaphragmatic index was assessed as the ratio of peak force between single twitches performed before and after the 30 s stimulation west. We also evaluated mean systemic (MAP) and pulmonary (MPAP) arterial pressures, pulmonary wedge pressure (PW), systemic (SVR) and pulmonary vascular resistance (PVR) and cardiac output (CO). L-NAME increased MAP, MPAP, PW, SVR and PVR, but decreased CO. SNP caused a decrease in MAP, MPAP, PW and SVR, while PVR and CO did not change. The main finding of this study was that diaphragmatic strength was not significantly weakened after L-NAME administration, except at 10 Hz, while it did not change after SNP infusion. However, both L-NAME and SNP caused significant decreases in diaphragmatic endurance capacity. The fatigue appearing after L-NAME is probably correlated with a decline in diaphragmatic blood flow, as evidenced by the increase in SVR and the decrease in CO, and consequently in oxygen supply. In contrast, the decrease in endurance capacity after SNP infusion can be attributed to a direct action of NO on skeletal muscle.

Effects of steroid on diaphragmatic functions in rabbits.

The effects of steroid on diaphragmatic contractility and endurance were examined in 24 New Zealand rabbits. Diaphragmatic contractility was determined by measuring gastric pressure (Pga) with the lower thorax and the abdomen of the animal being fixed with a rigid cast. Endurance procedure was done by continuous 15 Hz stimulation of the bilateral phrenic nerves, and diaphragmatic endurance was expressed as the time from the initiation of the endurance procedure to the moment when transdiaphragmatic pressure 15 Hz (Pdi-15 Hz) decreased to 25% of Pdimax-15 Hz. Our data suggested that intravenous administration of dexamethasone 2.5 mg daily for 7 days did not affect the diaphragmatic contractility significantly, but could cause a significant decrease in diaphragmatic endurance. When delivered intravenously at the dose of 2.0 mg daily for 14 days, dexamethasone induced a significant decrease both in diaphragmatic contractility and endurance. The recovery of the diaphragmatic strength from fatigue, however, was not influenced by dexamethasone in either circumstance. The influence of dexamethasone on diaphragmatic contractility and endurance may have important clinical implications.

Respiratory muscle activity and oxygenation during sleep in patients with muscle weakness

Patients with respiratory muscle weakness show nocturnal hypoventilation, with oxygen desaturation particularly during rapid eye movement (REM) sleep, but evidence in individuals with isolated bilateral diaphragmatic paresis (BDP) is conflicting. The effect of sleep on relative activity of the different respiratory muscles of such patients and, consequently, the precise mechanisms causing desaturation have not been clarified. We have studied eight patients, four with generalized muscle weakness and four with isolated BDP during nocturnal sleep with measurements including oxygen saturation and surface electromyographic (EMG) activity of various respiratory muscle groups. Nocturnal oxygenation correlated inversely with postural fall in vital capacity, an index of diaphragmatic strength. During REM sleep, hypopnoea and desaturation occurred particularly during periods of rapid eye movements (phasic REM sleep). In most subjects, such events were "central" in type and associated with marked suppression of intercostal muscle activity, but two subjects had recurrent desaturation due to "obstructive" hypopnoea and/or apnoea. Expiratory activity of the external oblique muscle was present whilst awake and during non-rapid eye movement (NREM) sleep in seven of the eight subjects in the semirecumbent posture. This probably represents an "accessory inspiratory" effect, which aids passive caudal diaphragmatic motion as the abdominal muscles relax at the onset of inspiration. Expiratory abdominal muscle activity was suppressed in phasic REM sleep, suggesting that loss of this "accessory inspiratory" effect may contribute to "central" hypopnoea. We conclude that, in patients with muscle weakness, nocturnal oxygenation correlates with diaphragmatic strength.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of cortisone and testosterone on diaphragmatic function and biochemistry in the rabbit.

The effects of cortisone and testosterone on in vivo diaphragmatic function and biochemistry were assessed in rabbits to determine whether androgens can prevent the effects of corticosteroids on diaphragmatic function and biochemistry and what mechanisms of muscle function may be altered. Cortisone altered respiratory muscle endurance and diaphragmatic glycogen and lactate levels but had little effect on diaphragmatic strength. Testosterone had no significant impact on diaphragmatic strength, endurance, or biochemistry. However, concomitant administration of testosterone with cortisone blunted the effect of cortisone on respiratory muscle endurance, even though it failed to block the effects of cortisone on diaphragmatic glycogen and lactate levels. Alterations in respiratory muscle endurance were not due to low- or high-frequency contractile fatigue of the diaphragm or diaphragmatic glycogen depletion or lactate accumulation in any of the treatment conditions. On the other hand, alterations in central drive played a dominant role, as evidenced by alterations in inspiratory duty cycle and a falloff in the intensity of central drive during loading. Although the exact mechanisms underlying the alterations in central drive remain unknown, concomitant administration of androgens with corticosteroids blunted the impact of corticosteroids on respiratory muscle function.

Pathophysiological response of bovine diaphragm function to gastric distension.

Because of the anatomic association of an exceptionally bulky stomach with a striking compartmentation of the chest wall, leading to the most cranial insertion of the diaphragm among mammals, gastric overdistension in the bovine species offers a unique pathophysiological condition for the diaphragm. The purpose of the present study was to determine whether increased intragastric pressure (Pga) (1, 2, 3, 4, and 5 kPa) leads to perturbations of respiratory and diaphragm function in calves. Changes in diaphragmatic strength and inspiratory action followed a biphasic pattern: 1) transdiaphragmatic pressure (Pdi) in response to constant bilateral maximal phrenic nerve stimulation at 30 Hz increased with moderate gastric distension and then fell abruptly as Pga continued to rise and 2) the magnitude of the ratio of the fall in pleural pressure to total Pdi was maintained up to a Pga amounting to 2 kPa but declined at higher pressures. We conclude that gastric distension in the bovine species provokes physiologically significant alterations of the diaphragm excitation-to-pressure generation coupling as well as of its capacity to convert Pdi into useful inspiratory pleural pressure. We suggest that these perturbations resulted from the combination of 1) altered tension-generating capacity due to compromised perfusion, 2) altered diaphragm geometry capable of altering tension-to-pressure generation coupling, and 3) modified coupling of the diaphragm with the chest wall that reduced its ability to drive inspiration.