Inferences about Respiratory Muscle Use after Cardiac Surgery from Compartmental Volume and Pressure Measurements

Background: After upper abdominal surgery, patients have been observed to have alterations in respiratory movements of the rib cage and abdomen and respiratory shifts in pleural and abdominal pressure that suggest dysfunction of the diaphragm. The validity of making such deductions about diaphragm function from these observations is open to discussion.

Methods: In eight adult patients, American Society of Anesthesiologists physical status 2, scheduled for elective cardiac surgery, we measured respiratory rate, tidal volume, rib cage and abdominal cross-section changes, and esophageal (Pes) and gastric (Pga) pressures preoperatively, 1 day postoperatively, and 5 days postoperatively. These data were analyzed in detail by following the variables through each respiratory cycle.

Results: Mean Delta Pga/Delta Pes decreased from 0.73 preoperatively to -0.56 1 day postoperatively and recovered to 0.47 5 days postoperatively. Plots of Pes against Pga and rib cage against abdominal expansion (Konno-Mead diagrams) were constructed. Six patients showed a postoperative pattern of breathing similar to that seen in patients who have undergone abdominal surgery: a decrease in the ratio of delta Pga/delta Pes and a shift toward rib cage expansion, with an increase in breathing rate and a decrease in tidal volume. This change was accomplished in most cases by the use of abdominal muscles in expiration with an increase in inspiratory intercostal muscle action without an increase in diaphragm activation, that is, a shift in the normal balance of respiratory muscle use in favor of muscles other than the diaphragm. A different ventilatory pattern was observed in the other two patients, consisting of minimal rib cage excursion and a large abdominal excursion. In these cases tidal volume was generated largely by contraction and relaxation of abdominal muscles with probable reduction in diaphragm activity. In addition, five patients exhibited positive changes in Pes at the end of inspiration that corresponded to closure of the upper airway, relaxation of inspiratory muscles, and subsequent opening of the airway with sudden exhalation, producing a grunt.     

Recovery of costal and crural diaphragmatic contractility from partial paralysis

Since the two muscles (costal and crural) that constitute the diaphragm are separate and histologically different, their individual recovery pattern from neuromuscular blockade also may be different. Therefore, we studied the recovery of force and shortening in the in vivo diaphragm from atracurium-induced neuromuscular blockade in seven pentobarbital anesthetized dogs to assess segmental differences. Transdiaphragmatic pressure (Pdi), shortening of costal and crural segments, integrated electromyogram (EMG), and tidal volume (VT) were measured during spontaneous breathing. After atracurium had reduced VT to 30% of control, breathing parameters were followed until recovered to 90% of control values. In addition, force-frequency curves generated by supramaximal tetanic stimuli of the phrenic nerve were measured. Recovery times for tidal Pdi, tidal EMG, tidal shortening, low-frequency shortening, and twitch Pdi were twice as fast as for VT (40 +/- 4 min), reflecting a slower rate of recovery of accessory inspiratory muscles. High-frequency recovery was typically slower than that of VT. During tidal breathing and tetanic stimulation, costal and crural shortening recovered simultaneously. On the other hand, comparison between costal and crural by analysis of pressure-shortening relationships showed a segmental difference (crural shortened 30% more than costal at the same Pdi), which implied reduced afterload on the crural segment. However, since shortening and pressure were linearly related during paralysis and recovery, measurements of Pdi alone can accurately reflect changes in contractile mass when heterogeneity and afterload are controlled.     

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.     

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.     

Modifications of Diaphragmatic Activity Induced by Midline Laparotomy and Changes in Abdominal Wall Compliance

Introduction and ObjectiveDiaphragmatic activity varies with the initial length of the muscle. Our objective was to evaluate the influence of surgery and changes in abdominal wall compliance on diaphragmatic activity.MethodsBoth phrenic nerves in 7 mongrel dogs were stimulated electrically with single supramaximal pulses (twitch). The gastric (Pga) and transdiaphragmatic (Pdi) pressures generated and muscle shortening (sonomicrometry) were used to evaluate diaphragmatic activity, which was determined at baseline, after midline laparotomy, with an elastic abdominal bandage, and with a rigid circular cast. Abdominal pressure was then gradually increased in order to induce progressive lengthening of the diaphragm.ResultsAfter laparotomy, the pressures were somewhat lower (by 12%) than at baseline. The elastic bandage produced a slight increase in the pressure generated by the diaphragm (mean [SE] values: Pga, from 4.2 [0.3] cm H₂O to 6.3 [0.9] cm H₂O, P<.01; Pdi, from 12.1 [2.0] cm H₂O to 15.4 [1.8] cm H₂O, P<.05]), and these values increased even further with the rigid cast (Pga, to 12.6 [1.5] cm H₂O; Pdi, to 20.2 [2.3] cm H₂O; P<.01 for both comparisons); this occurred despite smaller degrees of muscle shortening: by 57% [5%] of the initial length at functional residual capacity at baseline, by 49% [5%] with the bandage (P<.05), and by 39% [6%] with the cast (P<.01). With progressive lengthening of the muscle, its contractile efficacy increased up to a certain point (105% of the length at functional residual capacity), after which it began to decline.ConclusionsAbdominal wall compliance plays an important role in the diaphragmatic response to stimulation. This appears to be due mainly to changes in its length at rest.     

Eventration of the diaphragm

OBJECTIVE: Eventration of the diaphragm (ED) is defined as the abnormal elevation of the diaphragm. Although asymptomatic ED may be amenable to conservative treatment, symptomatic ED in children, either congenital or acquired, may require surgical treatment. This study evaluated the results of diaphragmatic plication in children with unilateral ED. METHODS: Fifteen patients who had undergone diaphragmatic plication for ED between 1997 and 2003 were evaluated retrospectively. The diagnosis of ED was established by routine chest radiographs and fluoroscopy. Patients who failed to respond to nonoperative treatment were referred for surgery. Nine patients underwent diaphragmatic fluoroscopy 1-5 years following plication to assess function. RESULTS: Indications for diaphragmatic plication were respiratory symptoms such as tachypnoea, dyspnoea, recurrent pneumonia and failure to thrive. In 14 patients, the position of the diaphragm was normal after plication, but the diaphragm was elevated without symptoms in one patient during postoperative follow-up. The motion of the diaphragm was investigated in nine patients. Fluoroscopic studies showed that the operated hemidiaphragm was immobile and there was no paradoxical motion. No return of symptoms was found during follow-up. CONCLUSION: ED is the abnormal elevation of the diaphragm as a result of paralysis or aplasia of the muscular fibres. The abnormally elevated diaphragm may compress the ipsilateral lung, and with respiratory effort the mediastinum may shift towards the normal side. Therefore, diaphragmatic plication is performed to restore normal pulmonary parenchymal volume by replacing the diaphragm in its normal location. After plication, there was immediate remission of symptoms in most patients and decreasing symptoms were observed for a year in others. During follow-up, the location of the diaphragm was normal and no paradoxical movement was observed. Relapse of symptoms was not noted in patients with immobile diaphragms.     

Flumazenil recovers diaphragm muscle dysfunction caused by midazolam in dogs

We studied the effects of flumazenil on diaphragm muscle dysfunction caused by midazolam in dogs. Animals were divided into three groups of eight each. In each group, anesthetic doses (0.1 mg/kg initial dose plus 0.5 mg. kg(-1). h(-1) maintenance dose) of midazolam were administered for 60 min. Immediately after the end of midazolam administration, Group 1 received no study drug; Group 2 was infused small-dose (0.004 mg. kg(-1). h(-1)) flumazenil; Group 3 was infused with large-dose (0.02 mg. kg(-1). h(-1)) flumazenil. We assessed diaphragm muscle function (contractility and electrical activity) by transdiaphragmatic pressure (Pdi) and integrated electrical activity of the diaphragm (Edi). After midazolam was administered in each group, Pdi at low-frequency (20-Hz) and high-frequency (100-Hz) stimulation decreased from baseline values (P < 0.05), and values of Edi at 100-Hz stimulation were less than those obtained during baseline (P < 0.05). In Group 1, Pdi and Edi to each stimulus did not change from midazolam-induced values. In Groups 2 and 3, with an infusion of flumazenil, Pdi at both stimuli and Edi at 100-Hz stimulation increased from midazolam-induced values (P < 0.05). The increase in Pdi and Edi was more in Group 3 than in Group 2 (P < 0.05). We conclude that flumazenil recovers the diaphragm muscle dysfunction (reduced contractility and inhibited electrical activity) caused by anesthetic doses of midazolam in dogs. IMPLICATIONS: In dogs, flumazenil recovers diaphragm muscle dysfunction (reduced contractility and inhibited electrical activity) caused by midazolam in a dose-related manner.     

The effect of inhaled colforsin daropate on contractility of fatigued diaphragm in dogs

We studied the effect of inhaled colforsin daropate, a water-soluble forskolin derivative, on the contractility of fatigued diaphragm in dogs. Animals were divided into 3 groups of 8. In each group, diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20-Hz stimulation applied for 30 min. Immediately after the end of the fatigue-producing period, Group 1 received inhaled vehicle, Group 2 received inhaled colforsin daropate 0.1 mg/mL, and Group 3 received inhaled colforsin daropate 0.2 mg/mL. We assessed diaphragmatic contractility by transdiaphragmatic pressure (Pdi). After fatigue was produced, in each group, Pdi at low-frequency (20-Hz) stimulation decreased from baseline values (P < 0.05), and there was no change in Pdi at high-frequency (100-Hz) stimulation. In Groups 2 and 3, during colforsin daropate inhalation, Pdi at both stimuli increased from fatigued values (P < 0.05). The increase in Pdi was significantly larger in Group 3 than in Group 2. The integrated electrical activity of the diaphragm did not change in any group. We conclude that inhaled colforsin daropate causes an increase in contractility of fatigued canine diaphragm in a dose-related fashion. IMPLICATIONS: Diaphragmatic fatigue may contribute to the development of respiratory failure. Inhaled colforsin daropate improves, in a dose-dependent manner, the contractility of fatigued diaphragm in dogs.     

Effects of diltiazem on contractility and electromyographic activity of non-fatigued diaphragm in dogs

BACKGROUND: No data are available for diltiazem on muscle function (contractility and electomyographic activity) of non-fatigued diaphragm. METHODS: Eighteen pentobarbital-anesthetized dogs were divided into 3 groups of 6 each: Group I received no drug; Group II received small-dose of diltiazem (0.1 mg.kg-1.h-1); Group III received large-dose of diltiazem (0.5 mg.kg-1.h-1). Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi), the difference between esophageal and gastric pressures. Diaphragmatic electromyographic activity (Edi) was measured by means of electrodes placed at the anterior portion of the crural and costal parts of the diaphragm. After measuring baseline values of Pdi and Edi at 20 Hz and 100 Hz stimulation, the study drug was administered for 30 min. RESULTS: With infusion of diltiazem, Pdi and Edi to each stimulus did not change in Groups II and III. In Group I, these variables also showed no change. CONCLUSIONS: Diltiazem, at doses below 0.5 mg.kg-1.h-1, does not affect contractility and electromyographic activity of non-fatigued canine diaphragm.     

Changes in ventilatory mechanics and diaphragmatic function after lung volume reduction surgery in patients with COPD

BACKGROUND: Lung volume reduction (LVR) has recently been used to treat severe emphysema. About 25% of the volume of each lung is removed with this method. Little is known about the mechanism of functional improvement so a study was undertaken to investigate the changes in ventilatory mechanics and diaphragmatic function in eight patients after LVR. METHODS: Measurements of work of breathing (WOB), intrinsic positive end expiratory pressure (PEEPi), dynamic compliance (Cdyn), and arterial carbon dioxide tension (PaCO2) were performed on the day before surgery and daily for seven days after surgery, as well as one, three, and six months after surgery. All measurements were performed on spontaneously breathing patients, simultaneously assessing oesophageal pressure via an oesophageal balloon catheter and air flow via a tightly adjusted mask. Diaphragmatic function was evaluated by measuring oesophageal and transdiaphragmatic pressure (Pdi) preoperatively and at one, three, and six months postoperatively. RESULTS: Mean forced expiratory volume in one second (FEV1) was 23 (3.6)% predicted, and all patients were oxygen dependent before the-operation. One day after LVR the mean decrease in WOB was 0.93 (95% confidence interval (CI) 0.46 to 1.40) joule/l, the mean decrease in PEEPi was 0.61 (95% CI 0.35 to 0.87) kPa, and the mean increase in Cdyn was 182.5 (95% CI 80.0 to 284.2) ml/kPa. Similar changes were found seven days and six months after surgery. PaCO2 was higher on the day after the operation but was significantly reduced six months later. Pdi was increased three and six months after surgery. CONCLUSIONS: Ventilatory mechanics improved immediately after LVR, probably by decompression of lung tissue and relief of thoracic distension. An improvement in diaphragmatic function three and six months postoperatively also contributes to improved respiratory function after LVR.


     

RETRACTED ARTICLE: Different effects of olprinone on contractility in nonfatigued and fatigued diaphragm in dogs

PURPOSE: To evaluate the effects of low-dose olprinone, a phosphodiesterase III inhibitor, on contractility and its mechanism in nonfatigued and fatigued diaphragm in dogs. METHODS: Thirty six pentobarbitone-anesthetized dogs were studied. In Group Ia (n=6), animals without fatigue, received no study drug. In Group Ib (n=6), dogs were given a bolus injection (10 ug x kg(-1)) followed by continuous infusion (0.1 microg x kg(-1) x min(-1)) of olprinone. In Groups IIa, IIb, and IIc (n=8 each), diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20-Hz applied for 30 min. After producing fatigue, Group IIa received no study drug; Group IIb was infused with olprinone (10 ug x kg(-1) loading dose plus 0.1 microg-kg(-1) min(-1) maintenance dose); Group IIc was infused with nicardipine (5 microg x kg(-1) x min(-1)) during olprinone administration. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi). RESULTS: No difference in Pdi was observed between Groups Ia and Ib. After fatigue, in Groups IIa, IIb, and IIc, Pdi at low-frequency (20-Hz) stimulation decreased from prefatigued (baseline) values (P < 0.05), whereas there was no change in Pdi at high-frequency stimulation (100-Hz). In Group IIb, during olprinone administration, Pdi at both stimuli increased from fatigued values (P < 0.05). In Group IIc, the augmentation of Pdi to each stimulus in fatigued diaphragm by olprinone was abolished with an infusion of nicardipine. CONCLUSION: Low-dose olprinone does not affect contractility in nonfatigued diaphragm, but increases contractility in fatigued diaphragm via its effect on transmembrane calcium movement in dogs.     

Robotic thoracoscopic plication for symptomatic diaphragm paralysis

Diaphragmatic paralysis is an uncommon condition characterized by significant elevation of a hemidiaphragm, and can cause dyspnea. The goal of diaphragm plication is to improve dyspnea by correcting the dysfunctional movement of a diaphragm during inspiration. Minimally invasive thoracoscopic diaphragm plication has been widely used and has been reported to lead to significant improvements in dyspnea and postoperative pulmonary function. Advantages of thoracoscopic plication compared to open thoracotomy are less postoperative pain and shorter hospitalization, yet technical difficulties due to limited workspace afforded by the ribcage and the elevated hemidiaphragm have been a major drawback in using the thoracoscopic approach for this disorder. We describe our experience with robotic thoracoscopic plication for the treatment of diaphragmatic paralysis. This is, to our knowledge, the first report of this kind.     

The dose-range effects of propofol on the contractility of fatigued diaphragm in dogs.

Diaphragmatic fatigue may contribute to the development of respiratory failure. We studied the dose-range effects of propofol on the contractility of fatigued diaphragm in dogs. Animals were divided into three groups of eight each. In each group, diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20-Hz stimulation for 30 min. Immediately after the end of a fatigue-producing period, Group 1 received no study drug; Group 2 was infused with small-dose propofol (0.1 mg/kg initial dose plus 1.5 mg x kg(-1) x h(-1) maintenance dose); Group 3 was infused with large-dose propofol (0.1 mg/kg initial dose plus 6.0 mg x kg(-1) x h(-1) maintenance dose). We assessed diaphragmatic contractility by transdiaphragmatic pressure (Pdi). After the fatigue-producing period, in each group, Pdi at low-frequency (20-Hz) stimulation decreased from baseline values (P < 0.05), whereas there was no change in Pdi at high-frequency (100-Hz) stimulation. In Groups 2 and 3, with an infusion of propofol, Pdi at 20-Hz stimulation decreased from fatigued values (P < 0.05). Compared with Group 1, Pdi at 20-Hz stimulation decreased from fatigued values (P < 0.05) during propofol administration in Groups 2 and 3. The decrease in Pdi was more in Group 3 than in Group 2 (P < 0.05). We conclude that propofol decreases the contractility of fatigued canine diaphragm in a dose-related fashion. IMPLICATIONS: Propofol is a widely used IV anesthetic for the induction and maintenance of general anesthesia and sedation. It decreases, in a dose-related fashion, the contractility of fatigued diaphragm in dogs.     

Twitch pressures in the assessment of diaphragm weakness.

To assess the value of phrenic nerve stimulation in the investigation of diaphragm function, transdiaphragmatic pressures were measured in 20 healthy subjects and in 15 patients with diaphragm weakness, during unilateral and bilateral transcutaneous phrenic nerve stimulation at 1 Hz at functional residual capacity (twitch Pdi). Diaphragm function was initially assessed by measuring transdiaphragmatic pressure during a voluntary manoeuvre, the maximal sniff (sniff Pdi); normal readings were confirmed in the control subjects (102-157 (normal greater than 98) cm H2O in the 10 men, 79-102 (normal greater than 70) cm H2O in the 10 women) and reduced values were found in the 15 patients with diaphragm weakness (7.5-90 cm H2O in the 13 men, 23 and 53 cm H2O in the two women). Twitch Pdi during bilateral phrenic nerve stimulation ranged from 8.8 to 33 cm H2O in the control subjects and from 3.1 to 27 cm H2O in the 10 patients in whom a measurement could be obtained. Bilateral twitch Pdi correlated with sniff Pdi both in the control subjects and in the patients with diaphragm weakness (r = 0.75). Only four patients had a bilateral twitch Pdi below the lowest value seen in the control group, including the three with the lowest sniff Pdi (3.1-8.5 cm H2O). These results indicate that transdiaphragmatic pressure recorded during bilateral phrenic nerve stimulation discriminated between control subjects and patients with known weakness of the diaphragm only when this was severe.     

Effect of aminophylline on the human diaphragm.

The effect of intravenous aminophylline on the contractile function of the diaphragm was studied in four normal subjects. The contractility of the diaphragm was assessed by the measurement of transdiaphragmatic pressure (Pdi) after right phrenic nerve stimulation at 1 Hz. Pdi was measured before and during aminophylline infusion (6 mg/kg over 30 minutes), during which therapeutic concentrations of theophylline were attained (mean 13.8 mg/l, range 8.5-20.2). The Pdi achieved was not affected by aminophylline. This result suggests that theophylline at therapeutic concentrations has little effect on the contractility of the normal human diaphragm.     

Diaphragm plication in adult patients with diaphragm paralysis leads to long-term improvement of pulmonary function and level of dyspnea.

OBJECTIVE: There is still controversy about the feasibility and long-term outcome of surgical treatment of acquired diaphragm paralysis. We analyzed the long-term effects on pulmonary function and level of dyspnea after unilateral or bilateral diaphragm plication. METHODS: Between December 1996 and January 2006, 22 consecutive patients underwent diaphragm plication. Before surgery, spirometry in both seated and supine positions and a Baseline Dyspnea Index were assessed. The uncut diaphragm was plicated as tight as possible through a limited lateral thoracotomy. Patients with a follow-up exceeding 1 year (n=17) were invited for repeat spirometry and assessment of changes in dyspnea level using the Transition Dyspnea Index (TDI). RESULTS: Mean follow-up was 4.9 years (range 1.2-8.7). All spirometry variables showed significant improvement. Mean vital capacity (VC) in seated position improved from 70% (of predicted value) to 79% (p<00.03), and in supine position from 54% to 73% (p=0.03). Forced expiratory volume in 1s (FEV1) in supine position improved from 45% to 63% (p=0.02). Before surgery the mean decline in VC changing from seated to supine position was 32%. At follow-up this had improved to 9% (p=0.004). For FEV1 these values were 35% and 17%, respectively (p<0.02). TDI showed remarkable improvement of dyspnea (mean+5.69 points on a scale of -9 to +9). CONCLUSION: Diaphragm plication for single- or double-sided diaphragm paralysis provides excellent long-term results. Most patients were severely disabled before surgery but could return to a more or less normal way of life afterwards.     

Plication of the diaphragm for symptomatic phrenic nerve paralysis

Paralysis of the diaphragm in infants may produce severe respiratory difficulty because of the paradoxic motion of the affected diaphragm and shift of a mobile mediastinum to the contralateral side. Six infants with diaphragmatic paralysis and severe respiratory distress underwent plication of the diaphragm by a simple technique. Five of the six infants had significant improvement in respiratory effort and were ultimately weaned from ventilatory support. One patient with bilateral paralysis had only minimal improvement. Diaphragmatic function returned in two patients after plication. Plication of the diaphragm is a safe and useful procedure to improve ventilation in infants with a paralyzed diaphragm. Since this technique does not prevent return of diaphragmatic function, it should be employed prior to the development of sequelae of prolonged assisted ventilation and sooner if the phrenic nerve is permanently injured.     

Improvement of diaphragmatic function by a thoracic extradural block after upper abdominal surgery

The effects on diaphragmatic function of a thoracic epidural block were assessed in 13 patients after upper abdominal surgery (UAS). Lung volumes and tidal changes in chest wall circumferences and gastric (delta Pgas) and esophageal (delta Pes) pressures were measured pre- and postoperatively. Volume displacement of the abdomen divided by tidal volume (delta VAB/VT) and delta Pgas/delta Pes were taken as indices of the diaphragmatic contribution to tidal breathing. These respiratory variables were obtained in the postoperative period, before and after epidural injection of 0.5% plain bupivacaine to achieve a block up to the T4 segment. UAS was constantly associated with a decrease in VT, delta VAB/VT, delta Pgas/delta Pes, and forced vital capacity (FVC). Epidural block was associated with an increase in VT, delta VAB/VT, and FVC. delta Pgas and delta Pgas/delta Pes returned to their preoperative values. It is concluded that: 1) diaphragmatic dysfunction observed after UAS is partially reversed by thoracic epidural block; and 2) that inhibitory reflexes of phrenic activity arising from the abdominal compartment (abdominal wall and/or viscera) could be involved in this diaphragmatic dysfunction.     

Ventilatory muscle recruitment and work of breathing in patients with respiratory failure after thoracic surgery.

OBJECTIVES: Increased work of breathing (WOB) and respiratory muscle weakness have been identified as major causes of respiratory failure after thoracic surgery. This study was undertaken firstly to characterize the mechanical impairment in patients with respiratory failure after cardio-thoracic surgery, and secondly, to determine how diaphragmatic paralysis affects deterioration in the ventilatory mechanics. METHODS: We evaluated the respiratory mechanics of 24 patients following cardiac and thoracic surgery. Ten patients without respiratory problems were examined as control subjects. There were nine patients with phrenic nerve injury and five patients without phrenic nerve injury who required mechanical ventilation for more than 7 days. Phrenic nerve injury was assessed with a phrenic nerve stimulation test. We measured the respiratory variables, the esophageal, gastric and transdiaphragmatic pressure swing (deltaPes, deltaPga and deltaPdi, respectively), and the work of breathing during quiet tidal breathing. RESULTS: Both the groups requiring mechanical ventilation exhibited abnormally negative deltaPga/deltaPes values, compared with the control subjects. A significant increase in WOB with the normal generation of deltaPdi was seen in the patients without phrenic nerve injury. In contrast, the poor generation of deltaPdi with a slight increase in work of breathing was noted in patients with phrenic nerve injury. CONCLUSIONS: These results demonstrated two different types of respiratory failure in thoracic surgery patients, focusing on the impact of phrenic nerve paralysis. Diaphragmatic dysfunction should not be overlooked in postoperative care, and the amelioration of this compromise in respiratory mechanics is an important aspect of good patient management.     

Experimental study on diaphragm fatigue during diaphragm pacing

An experimental study was performed to determine the main site of fatigue associated with diaphragm pacing. Using 24 mature mongrel dogs, weighing 7.5 to 12.7 kg, direct phrenic nerve pacing was conducted from the right cervical area at three different respiration rates, 37 (Group 1, n = 6), 25 (Group 2, n = 6) and 12 (Group 3, n = 6) times per minute, under fixed stimulation conditions (pulse duration, 200 microseconds; frequency, 25 Hz; pulse train repetition time, 1.2 sec). Diaphragm fatigue was defined as the reduction in transdiaphragmatic pressure (Pdi) to less than or equal to 60% of the initial value. In each animal, tidal volume (Vt), induced muscle action potential (Edi), conduction time (CT) and electrical current (E) between two electrodes were examined at various periods until fatigue. In addition, after fatigue, aminophylline (10 mg/kg) was injected and each parameter was observed for an additional 45 min. In 10 animals, the polarity of stimulation was changed from anodal to cathodal current after fatigue and changes in Pdi and Edi were examined. The time to fatigue was 70 +/- 20 min for Group 1, 149 +/- 48 min for Group 2, and 371 +/- 97 min for Group 3, showing a significant stimulation rate dependency (P less than 0.05). Vt and Edi showed a significant decrease (P less than 0.05) at fatigue in all of the groups. However, no significant differences of CT and E were seen between pre- and postfatigue values. Pdi and Edi did not change even when polarity was changed after fatigue. Following administration of aminophylline, Pdi showed a significant (P less than 0.05) increase over time in all groups: 19.8 +/- 13.5% at 5 min, 23.0 +/- 13.5% at 15 min, and 16.2 +/- 14.9% at 30 min for Group 1; 23.6 +/- 11.6% at 5 min, 27.3 +/- 15.5% at 15 min, and 19.0 +/- 16.1% at 30 min for Group 2; and 29.9 +/- 21.1% at 5 min, 29.5 +/- 18.6% at 15 min, 22.3 +/- 13.8% at 30 min, and 15.5 +/- 13.4% at 45 min for Group 3. In contrast, administration of aminophylline caused no significant changes in Edi. Based upon the finding that aminophylline was significantly effective at the time of diaphragm fatigue, it is concluded that fatigue of the muscle itself constitutes one of the contributing factors for the fatigue phenomenon associated with diaphragm pacing.