Mechanical loading and control of breathing in patients with severe chronic obstructive pulmonary disease.

BACKGROUND--High neural drive to the respiratory muscles and rapid and shallow breathing are frequently observed in patients with chronic obstructive pulmonary disease (COPD), and both mechanical and chemical factors are thought to play a part. However, the interrelation between these factors and the modifications in the control of breathing are not clearly defined. The effects of an acute decrease in mechanical load by the administration of a high dose of a beta 2 agonist were studied. METHODS--Nine spontaneously breathing patients with severe COPD took part in the study. Criteria for entry were FEV1 of < 40% of predicted and an improvement in FEV1 of < 200 ml after inhalation of 400 micrograms fenoterol. The following parameters were measured: lung volumes, tidal volume (VT), respiratory frequency (Rf), maximal pleural pressure during a sniff manoeuvre (PPLmax), pleural pressure swings (PPLsw), lung resistance (RL), RL/PPLmax ratio, and surface electromyographic activity (EMG) of diaphragm (EDI) and parasternal (EPS) muscles. Arterial oxygen saturation (SaO2), end tidal carbon dioxide pressure (PETCO2), and the electrocardiogram were also monitored. Each variable was measured under control conditions and 20 and 40 minutes after the inhalation of 800 micrograms fenoterol. In five patients the effects of placebo were also studied. RESULTS--Fenoterol resulted in an increase in FEV1 and decrease in FRC. SaO2 did not change, while PETCO2 fell and heart rate increased. The VT increased, and Rf decreased, PPLsw fell and PPLmax increased, thus the PPLsw/PPLmax ratio fell. Both RL and RL/PPLmax also fell, and a substantial decrease in EDI and EPS was observed. Changes in PPLsw were related to changes in FEV1 and RL. Changes in VT and Rf, and EDI/TI and EPS/TI were also related to changes in PPLsw and RL/PPLmax ratio, but not to changes in FEV1. No variation was observed with placebo. CONCLUSIONS--In patients with severe COPD a decrease in inspiratory muscle loading relative to the maximal available strength, as expressed by the RL/PPLmax and PPLsw/PPLmax ratios, appears to be the major determinant of changes in breathing pattern and inspiratory muscle activity (decrease in EMG).     

Control of breathing in patients with limb girdle dystrophy: a controlled study.

BACKGROUND--In patients with limb girdle dystrophy the relative contribution of peripheral factors (respiratory muscle weakness, and lung and/or airway involvement) and central factors (blunted and/or inadequate chemoresponsiveness) in respiratory insufficiency has not yet been established. To resolve this, lung volumes, arterial blood gas tensions, respiratory muscle strength, breathing pattern and neural respiratory drive were investigated in a group of 15 patients with limb girdle dystrophy. An age-matched normal group was studied as a control. METHODS--Respiratory muscle strength was assessed as an arithmetic mean of maximal inspiratory (MIP) and expiratory (MEP) pressures. Breathing pattern was evaluated in terms of volume (ventilation VE, tidal volume VT) and time (respiratory frequency Rf, inspiratory time TI, expiratory time TE) components of the respiratory cycle. Neural respiratory drive was assessed as the mean inspiratory flow (VT/TI), mouth occlusion pressure (P0.1) and electromyographic activity (EMG) of the diaphragm (EMGd) and the intercostal parasternal (EMGp) muscles. In 10 of the 15 patients the responses to carbon dioxide (PCO2) stimulation were also evaluated. RESULTS--Most patients exhibited a moderate decrease in vital capacity (VC) (range 37-87% of predicted), MIP (range 23-84% of predicted), and/or MEP (range 13-41% of predicted). The arterial carbon dioxide tension (PaCO2) was increased in three patients breathing room air, while PaO2 was normal in all. Compared with the control group Rf was higher, and VT, TI and TE were lower in the patients. EMGd and EMGp were higher whilst VT/TI and P0.1 were normal in the patients. Respiratory muscle strength was inversely related to EMGd and EMGp. PaCO2 was found to relate primarily to VC and duration of illness, but not to respiratory muscle strength. During hypercapnic rebreathing delta VE/delta PCO2, delta VT/delta PCO2, and delta P0.1/delta PCO2 were lower than normal, whilst delta EMGd/delta PCO2 and delta EMGp/delta PCO2 were normal in most patients. A direct relation between respiratory muscle strength and delta VT/delta PCO2 was found. CONCLUSIONS--The respiratory muscles, especially expiratory ones, are weak in patients with limb girdle dystrophy. Reductions in respiratory muscle strength are associated with increased neural drive and decreased ventilatory output (delta VT/delta PCO2). The decrease in VC, together with the duration of disease, influence PaCO2. VC is a more useful test than respiratory muscle strength for following the course of limb girdle dystrophy.     

An analysis of the ventilatory response to carbon dioxide during halothane, isoflurane, or enflurane anesthesia in humans

To analyze the effects of halothane, isoflurane, or enflurane on the ventilatory response to CO2, minute volume (VE), respiratory rate (f), occlusion pressure, mean inspiratory flow rate (VT/TI), and effective elastance (Pmax/VT) were measured in 26 patients during quiet breathing and when the respiratory system was stressed by CO2. Comparison was made at equipotent anesthetic concentration (1 MAC) and all measurements were made in the absence of surgical stimulation. Respiratory rate and Pmax/VT were unchanged in all groups after end-tidal CO2 was elevated. By contrast, VE, VT/TI, and occlusion pressure increased in all the groups when the respiratory system was stressed by CO2. Among the parameters tested delta VE/delta PaCO2 and delta VT/TI/delta PaCO2 were significantly (P less than 0.05) greater during halothane anesthesia than during isoflurane or enflurane anesthesia. We conclude that, at equipotent anesthetic concentrations, isoflurane and enflurane depress CO2 chemosensitivity more than halothane does, and that such effect is primarily related to the greater depressant effects of isoflurane and enflurane on the respiratory driving mechanisms.     

Relation of lung function, maximal inspiratory pressure, dyspnoea, and quality of life with exercise capacity in patients with chronic obstructive pulmonary disease.

BACKGROUND--Several studies have shown that both objective and subjective measurements are related to exercise capacity in patients with chronic obstructive pulmonary disease (COPD). In this study the relative contribution of lung function, maximal inspiratory pressure, dyspnoea, and quality of life to the performance in a walking distance test and a bicycle ergometer test was investigated. METHODS--Static lung volumes, forced expiratory volume in one second (FEV1), inspiratory slow vital capacity (IVC), transfer factor for carbon monoxide (TLCO) divided by the alveolar volume (TLCO/VA), static compliance (Cst), and maximal inspiratory peak pressure (PImaxPOES) were measured in 40 patients with COPD with severe airways obstruction (mean FEV1 44% predicted, mean FEV1/IVC 37% predicted). Quality of life was assessed by the Chronic Respiratory Questionnaire (CRQ) and dyspnoea by the Borg category scale. Exercise capacity was measured by both a six minute walking distance (test) and a maximal work load of the bicycle ergometer test (Wmax). RESULTS--Spirometric values and maximal inspiratory pressure were modestly correlated with both the six minute walking test and Wmax, r values ranging from 0.50 to 0.58. The TLCO was strongly correlated with the six minute walking test (r = 0.62) and with Wmax (r = 0.78). Quality of life showed no correlation with exercise capacity, while there was a correlation between dyspnoea and the six minute walking test (r = -0.41). Backward linear regression analysis selected TLCO and PImaxPOES as the most significant determinants for exercise performance. They explained 54% and 69% of the variance in the six minute walking test and Wmax, respectively. CONCLUSIONS--The results show that exercise capacity in patients with COPD with severe airways obstruction is more strongly related to inspiratory muscle strength and lung function than to dyspnoea and quality of life. The significant correlation between dyspnoea and the six minute walking test suggests that subjective variables are more strongly related to walking tests than to bicycle ergometer tests.     

Physiopathology of acute respiratory failure in COPD and asthma

Asthma and chronic obstructive pulmonary diseases (COPD) lead to functional obstruction of airways, identified by increased inspiratory and expiratory resistances. Increased expiratory resistances cause, in turn, a reduction in expiratory flow. The analysis of flow-volume loops shows that, as the disease progresses, the flow generated during expiration of a tidal volume becomes very close to the flow generated during forced maximal expiration. In such condition, where there is little or no reserve of expiratory flow, higher tidal volumes need to be reached in order to increase the expiratory flow, and hyperinflation inevitably occurs. Hyperinflation, a key feature in COPD pathophysiology, is generated by two mechanisms: reduction of elastic recoil of the lung (static hyperinflation) and interruption of expiration at lung volumes still higher than FRC, due to reduction of expiratory flow (dynamic hyperinflation). When dynamic hyperinflation occurs, a residual positive pressure remains in the alveoli, which is defined as intrinsic positive end-expiratory pressure (PEEPi). Hyperinflation carries several consequences: 1) Respiratory mechanics: at lung volumes close to total lung capacity, lung compliance is physiologically reduced, and elastic work required to generate the same inspiratory volume is therefore increased; 2) Respiratory muscles: contractile properties of diaphragm deteriorate when the dome is pushed downward by an increased lung volume, inspiration is mainly performed by inspiratory muscles, and expiration becomes active; 3) Circulation: pulmonary vascular resistances increase due to compression exerted by hyperinflation on alveolar vessels and to hypoxic vasoconstriction; right ventricle afterload increases and right sided hypertrophy and dilation ensue; left ventricular afterload may increase due to increased negative intrapleural pressure which translates into an increased transmural pressure which needs to be overcome by ventricular contraction. Ventilatory support of COPD patients should decrease work of breathing and improve gas exchange without increasing hyperinflation. This target can be achieved during assisted ventilation by applying a positive pressure both during inspiration and expiration; the level of PEEP should equal PEEPi. During mechanical ventilation in sedated paralyzed patients hyperinflation should be limited by decreasing minute volume and by increasing expiratory time, eventually choosing controlled hypercapnia.     

Comparative effects of plasma exchange and pyridostigmine on respiratory muscle strength and breathing pattern in patients with myasthenia gravis.

BACKGROUND--Pyridostigmine, an acetylcholinesterase antagonist, is useful in improving respiratory function in patients with myasthenia gravis. More recently, plasma exchange has been employed in myasthenia gravis because it acts presumably by removal of circulating antibodies against acetylcholine receptors. Surprisingly, comparative data on the effects of pyridostigmine and plasma exchange on lung volumes, respiratory muscle strength, and ventilatory control system in patients with myasthenia gravis are lacking. METHODS--Nine consecutive patients with grade IIb myasthenia gravis were studied under control conditions and after a therapeutic dose of pyridostigmine. In a second study the patients were re-evaluated a few days after a cycle of plasma exchange, before taking pyridostigmine. In each subject pulmonary volumes, inspiratory (MIP) and expiratory (MEP) muscle force, and respiratory muscle strength, calculated as average MIP and MEP as percentages of their predicted values, were measured. The ventilatory control system was evaluated in terms of volume (tidal volume, VT) and time (inspiratory time, TI, and total time, TTOT) components of the respiratory cycle. Mean inspiratory flow (VT/TI)--that is, the "driving"--and TI/TTOT--that is, the "timing"--components of ventilation were also measured. RESULTS--In each patient treatment relieved weakness and tiredness, and dyspnoea grade was reduced with plasma exchange. Following treatment, vital capacity (VC) increased on average by 9.7% with pyridostigmine and by 14% with plasma exchange, and MIP increased by 18% and 26%, respectively. In addition, with plasma exchange but not with pyridostigmine forced expiratory volume in one second (FEV1) increased by 16% and MEP increased by 24.5%, while functional residual capacity (FRC) decreased a little (6.8%). The change in respiratory muscle strength was related to change in VC (r2 = 0.48). With plasma exchange, VT increased by 18.6% and VT/TI increased by 13.5%, while neither TI nor TI/TTOT changed. CONCLUSIONS--Plasma exchange can be used in patients with myasthenia gravis when symptoms are not adequately controlled by anticholinesterase agents. Plasma exchange increases respiratory muscle force and tidal volume due to changes in "driving" but not "timing" of the respiratory cycle.     

Nocturnal saturation and respiratory muscle function in patients with chronic obstructive pulmonary disease.

BACKGROUND--Nocturnal desaturations, mainly caused by hypoventilation, occur frequently in patients with chronic obstructive pulmonary disease (COPD). Daytime arterial oxygen and carbon dioxide tensions (PaO2 and PaCO2) appear to predict which patients will desaturate at night. It is unknown if respiratory muscle strength, which may be decreased in these patients, plays an additional part. METHODS--Polysomnography, maximal respiratory pressures, lung function, and arterial blood gas tensions were measured in 34 patients with COPD (mean (SD) forced expiratory volume in one second (FEV1) 41.7 (19.9)% pred). RESULTS--Significant correlations were found between the mean nocturnal arterial oxygen saturation and maximal inspiratory mouth pressure (r = 0.65), maximal inspiratory transdiaphragmatic pressure (r = 0.53), FEV1 (r = 0.61), transfer coefficient (KCO) (r = 0.38), arterial oxygen saturation (SaO2) (r = 0.75), and PaCO2 (r = -0.44). Multiple regression analysis showed that 75% of the variance in nocturnal SaO2 (70%) and FEV1 (5%). CONCLUSION--Inspiratory muscle strength and nocturnal saturation data are correlated, but daytime SaO2 and FEV1 remain the most important predictors of nocturnal saturation.     

Respiratory mechanics in airways obstruction associated with inspiratory dyspnoea.

Inspiratory muscle strength and the flow and elastic pressure opposing inspiration were measured in seven patients with severe airways obstruction who found inspiration difficult at rest. A comparison was made of measurements obtained from seven normal subjects and five patients with airways obstruction not experiencing inspiratory dyspnoea at rest. Measurements were also obtained when inspiratory dyspnoea was induced in the normal subjects by adding an inspiratory resistance or by voluntarily increasing lung volume. Compared with the controls the inspiratory muscle strength of the patients was reduced but was not significantly less than that of the patients without inspiratory dyspnoea. The pressure required to produce inspiratory flow was significantly greater when inspiratory dyspnoea was present (P = 0-01). However, there was considerable overlap in the pressures of those with and without inspiratory dyspnoea. A better relationship was obtained when muscle strength was considered. The ratio of inspiratory muscle strength to the pressure required to produce flow was 0-24 +/- 0-07 (mean +/- SD) in patient with inspiratory dyspnoea, 0-10 +/- 0-03 in patients without inspiratory dyspnoea, and 0-033 +/- 0-019 in normal subjects. There was no overlap between the two patient groups. The ratios of the normal subjects were increased when inspiratory dyspnoea was induced and, with the exception of two cases, were all above those obtained when inspiratory dyspnoea was absent. Inspiratory dyspnoea was experienced with lower ratios in the normals than in the patients with airways obstruction.     

Ventilation during steady-state exercise in patients with chronic obstructive pulmonary disease. A preliminary study

In this preliminary study 20 patients with chronic obstructive pulmonary disease (COPD) walked on the treadmill until symptoms limited further exercise. When minute volume exceeded 60% of the predicted maximum breathing capacity the arterial carbon dioxide partial pressure was frequently low, thus indicating hyperventilation; the arterial oxygen partial pressure also declined on exercise. In only 2 patients was there alveolar hypoventilation. Although other factors may be operative, the hyperventilation in some patients with COPD may be induced by an exertional decline in alveolar oxygen partial pressure. In 4 patients the exercise tidal volume exceeded the resting inspiratory capacity, indicating a decline in functional residual capacity and increased work of breathing. It is concluded that there is a need further to assess patients with COPD in respect of the association between exertional dyspnoea, alveolar ventilation and lung mechanics.     

Effect of CPAP on intrinsic PEEP,inspiratory effort,and lung volume in severe stable COPD

BACKGROUND: Intrinsic positive end expiratory pressure (PEEPi) constitutes an inspiratory threshold load on the respiratory muscles, increasing work of breathing. The role of continuous positive airway pressure (CPAP) in alleviating PEEPi in patients with severe stable chronic obstructive pulmonary disease is uncertain. This study examined the effect of CPAP on the inspiratory threshold load, muscle effort, and lung volume in this patient group. METHODS: Nine patients were studied at baseline and with CPAP increasing in increments of 1 cm H(2)O to a maximum of 10 cm H(2)O. Breathing pattern and minute ventilation (I), dynamic PEEPi, expiratory muscle activity, diaphragmatic (PTPdi/min) and oesophageal (PTPoes/min) pressure-time product per minute, integrated diaphragmatic (EMGdi) and intercostal EMG (EMGic) and end expiratory lung volume (EELV) were measured. RESULTS: Expiratory muscle activity was present at baseline in one subject. In the remaining eight, PEEPi was reduced from a mean (SE) of 2.9 (0.6) cm H(2)O to 0.9 (0.1) cm H(2)O (p<0.05). In two subjects expiratory muscle activity contributed to PEEPi at higher pressures. There were no changes in respiratory pattern but I increased from 9.2 (0.6) l/min to 10.7 (1.1) l/min (p<0.05). EMGdi remained stable while EMGic increased significantly. PTPoes/min decreased, although this did not reach statistical significance. PTPdi/min decreased significantly from 242.1 (32.1) cm H(2)O.s/min to 112.9 (21.7) cm H(2)O.s/min). EELV increased by 1.1 (0.3) l (p<0.01). CONCLUSION: High levels of CPAP reduce PEEPi and indices of muscle effort in patients with severe stable COPD, but only at the expense of substantial increases in lung volume.     

Physiological effects of flow and pressure triggering during non- invasive mechanical ventilation in patients with chronic obstructive pulmonary disease

BACKGROUND: The effect of the type of trigger system on inspiratory effort has been studied in intubated patients, but no data are available in non-invasive mechanical ventilation where the "trigger variable" may be even more important since assisted modes of ventilation are often employed from the beginning of mechanical ventilation. METHODS: The effect of flow triggering (1 and 5 1/min) and pressure triggering (-1 cm H2O) on inspiratory effort during pressure support ventilation (PSV) and assisted controlled mode (A/C) delivered non-invasively with a full face mask were compared in patients with chronic obstructive pulmonary disease (COPD) recovering from an acute exacerbation. The patients were studied during randomised 15 minute runs at zero positive end expiratory pressure (ZEEP). The oesophageal pressure time product (PTPoes), dynamic intrinsic PEEP (PEEPi,dyn), fall in maximal airway pressure (delta Paw) during inspiration, and ventilatory variables were measured. RESULTS: Minute ventilation, respiratory pattern, dynamic lung compliance and resistances, and changes in end expiratory lung volume (delta EELV) were the same with the two triggering systems. The total PTPoes and its pre-triggering phase (PTP due to PEEPi and PTP due to valve opening) were significantly higher during both PSV and A/C with pressure triggering than with flow triggering at both levels of sensitivity. delta Paw was larger during pressure triggering, and PEEPi,dyn was significantly reduced during flow triggering in the A/C mode only. CONCLUSIONS: In patients with COPD flow triggering reduces the inspiratory effort during both PSV and A/C modes compared with pressure triggering. These findings are likely to be due to a reduction in PEEPi,dyn and in the time of valve opening with a flow trigger.


     

Exertional dyspnoea in patients with airway obstruction, with and without CO2 retention

BACKGROUND: Dyspnoea is a common and disabling symptom in patients with cardiopulmonary disease. Unfortunately the mechanisms that produce dyspnoea are still poorly understood. The relationship between dyspnoea and the load on the ventilatory muscles, chemical drive, and ventilatory indices was therefore assessed in patients with obstructive pulmonary disease during an incremental exercise test. METHODS: Fifty patients with a wide range of obstructive pulmonary disease (mean forced expiratory volume in one second (FEV1) 66.1 (28.8)% predicted) performed an incremental cycle ergometer test. A subdivision was made between subjects with CO2 retention (delta PaCO2 > or = 0, n = 22) and subjects without CO2 retention (delta PaCO2 < 0, n = 28) during exercise. During the test dyspnoea (Borg score), oesophageal pressures (mechanical load on the ventilatory muscles (time tension index (TTI), blood gas tensions, and minute ventilation were measured. Correlations for changes in mechanical and chemical factors with changes in dyspnoea score were calculated to assess relevant factors. An analysis of covariance was used to examine whether there was a relationship between dyspnoea score and each of these factors and whether this relationship was different between the subgroups with and without CO2 retention. Multiple regression analysis was used to assess the independent effect of each parameter on dyspnoea sensation. Furthermore, the amplitude of pleural pressure swing ((Pi + Pe)act) generated at maximal work load (Ptot, an indication of the load on all respiratory muscles) was calculated. Analysis of covariance was used to assess whether there was a relationship between tidal volume (VT) and Ptot and whether this relationship was different between the groups (slopes are an expression of the length-tension inappropriateness, LTI). RESULTS: In the total group and the group without CO2 retention a significant correlation between dyspnoea and the increase in the inspiratory time tension index (TTIi) was present. In the group with CO2 retention a significant correlation was seen between dyspnoea and delta PaCO2. The factors delta PaO2, delta VE%MVV and delta (VT/Ti) showed a correlation with a p value of < or = 0.10 both in the total group and in those without CO2 retention. In an analysis of covariance the relationship between dyspnoea score and delta PaCO2 appeared to be significantly different between the two subgroups, being more pronounced in the group with CO2 retention. No other relationships with change in dyspnoea score were found. There was no significant relationship between VT and Ptot in the total group nor in the two subgroups, indicating some length-tension inappropriateness in both groups. CONCLUSIONS: In patients with distinctive pulmonary disease who are normocapnic or hypocapnic the mechanical load (delta TTIi) and length-tension inappropriateness (LTI) on ventilatory muscles seem to be the main determinant of exertional dyspnoea. As soon as hypercapnia occurs, this seems to override all other inputs for dyspnoea.     

The effects of thoracic epidural analgesia with bupivacaine 0.25% on ventilatory mechanics in patients with severe chronic obstructive pulmonary disease

Optimal analgesia is important after thoracotomy in pulmonary-limited patients to avoid pain-related pulmonary complications. Thoracic epidural anesthesia (TEA) can provide excellent pain relief. However, potential paralysis of respiratory muscles and changes in bronchial tone might be unfavorable in patients with end-stage chronic obstructive pulmonary disease (COPD). Therefore, we evaluated the effect of TEA on maximal inspiratory pressure, pattern of breathing, ventilatory mechanics, and gas exchange in 12 end-stage COPD patients. Pulmonary resistance, work of breathing, dynamic intrinsic positive end-expiratory pressure, and peak inspiratory and expiratory flow rates were evaluated by assessing esophageal pressure and airflow. An increase in minute ventilation (7.50 +/- 2.60 vs 8.70 +/- 2.10 L/min; P = 0.04) by means of increased tidal volume (0.46 +/- 0.16 vs 0.53 +/- 0.14 L/breath; P = 0.003) was detected after TEA. These changes were accompanied by an increase in peak inspiratory flow rate (0.48 +/- 0.17 vs 0.55 +/- 0.14 L/s; P = 0.02) and a decrease in pulmonary resistance (20.7 +/- 9.9 vs 16.6 +/- 8.1 cm H(2)O. L(-1). s(-1); P = 0.02). Peak expiratory flow rate, dynamic intrinsic positive end-expiratory pressure, work of breathing, PaO(2), and maximal inspiratory pressure were unchanged (all P > 0.50). We conclude that TEA with bupivacaine 0.25% can be used safely in end-stage COPD patients. IMPLICATIONS: Thoracic epidural anesthesia with bupivacaine 0.25% does not impair ventilatory mechanics and inspiratory respiratory muscle strength in severely limited chronic obstructive pulmonary disease patients. Thus, thoracic epidural anesthesia can be used safely in patients with end-stage chronic obstructive pulmonary disease.     

Evaluation of amplified spontaneous pattern ventilation in postoperative patients. Comparison with pressure support]

HYPOTHESIS: Amplified spontaneous pattern (ASP) ventilation is a new method for giving partial support by reproducing, in an amplified manner, the patients' own spontaneous flow wave form, thereby optimizing patient adaptation to support. OBJECTIVES: To study clinical use of ASP ventilation for the first time in terms of flow wave form, patient synchronization, ventilation pattern, work of breathing (WOB), and inspiratory effort by transpulmonary pressure (TPP) and to compare ASP and pressure support ventilation applied in a similar clinical setting. PATIENTS AND METHOD: We studied 20 patients after heart surgery during weaning from controlled ventilation. Each patient was ventilated during 4 phases of 15 min each with two similar levels of support using ASP and PS applied successively and randomly. Maximum support (ASPmax and PSmax) was that which was set to give the same respiratory frequency (F) and tidal volume (VT) as that recorded during the earlier period of controlled ventilation. Half support (PEA1/2 and PS1/2) was set for half the aforementioned levels. At the end of each phase we obtained gas measurements and flow (V) curves and VT and pressure in airways and esophagus (Pes) to measure F, VT, the ratio of inspiratory to total time (TI/TTOT and TPP, as well as the VT/Pes loop with a mechanical ventilation monitor. The WOB was determined by measuring area under the curve (Campbell's method). RESULTS: We observed no significant differences between the two modes, with similar levels of support, with regard to ventilation (PaCO2) or ventilatory pattern (F, VT, TI/TTOT). De-adaptation occurred, however, eight times with PS (25%) but never with ASP. WOB and TPP decreased with PS when level of support increased, whereas with ASP these variables were constant regardless of level of amplification within the normal range. CONCLUSIONS: Adaptation to support is better with ASP than with PS during postoperative weaning and causes no significant respiratory work overload.     

Physiological effects and optimisation of nasal assist-control ventilation for patients with chronic obstructive pulmonary disease in respiratory failure

BACKGROUND: A study was undertaken to investigate the effects of non- invasive assist-control ventilation (ACV) by nasal mask on respiratory physiological parameters and comfort in acute on chronic respiratory failure (ACRF). METHODS: Fifteen patients with chronic obstructive pulmonary disease (COPD) were prospectively and randomly assigned to two non-invasive ventilation (NIV) sequences in spontaneous breathing (SB) and ACV mode. ACV settings were always optimised and therefore subsequently adjusted according to patient's tolerance and air leaks. RESULTS: ACV significantly decreased all the total inspiratory work of breathing (WOBinsp) parameters, pressure time product, and oesophageal pressure variation in comparison with SB mode. The ACV mode also resulted in a significant reduction in surface diaphragmatic electromyographic activity to 36% of the control values and significantly improved the breathing pattern. SB did not change the arterial blood gas tensions from baseline values whereas ACV significantly improved both the PaO2 from a mean (SD) of 8.45 (2.95) kPa to 13.31 (2.15) kPa, PaCO2 from 9.52 (1.61) kPa to 7.39 (1.39) kPa, and the pH from 7.32 (0.03) to 7.40 (0.07). The respiratory comfort was significantly lower with ACV than with SB. CONCLUSIONS: This study shows that the clinical benefit of non-invasive ACV in the management of ACRF in patients with COPD results in a reduced inspiratory muscle activity providing an improvement in breathing pattern and gas exchange. Despite respiratory discomfort, the muscle rest provided appears sufficient when ACV settings are optimised.


     

Effect of salmeterol on respiratory muscle activity during exercise in poorly reversible COPD

BACKGROUND: Some patients with irreversible chronic obstructive pulmonary disease (COPD) experience subjective benefit from long acting bronchodilators without change in forced expiratory volume in 1 second (FEV(1)). Dynamic hyperinflation is an important determinant of exercise induced dyspnoea in COPD. We hypothesised that long acting bronchodilators improve symptoms by reducing dynamic hyperinflation and work of breathing, as measured by respiratory muscle pressure-time products. METHODS: Sixteen patients with "irreversible" COPD (<10% improvement in FEV(1) following a bronchodilator challenge; mean FEV(1) 31.1% predicted) were recruited into a randomised, double blind, placebo controlled, crossover study of salmeterol (50 micro g twice a day). Treatment periods were of 2 weeks duration with a 2 week washout period. Primary outcome measures were end exercise isotime transdiaphragmatic pressure-time product and dynamic hyperinflation as measured by inspiratory capacity. RESULTS: Salmeterol significantly reduced the transdiaphragmatic pressure-time product (294.5 v 348.6 cm H(2)O/s/min; p = 0.03), dynamic hyperinflation (0.22 v 0.33 litres; p = 0.002), and Borg scores during endurance treadmill walk (3.78 v 4.62; p = 0.02). There was no significant change in exercise endurance time. Improvements in isotime Borg score were significantly correlated to changes in tidal volume/oesophageal pressure swings, end expiratory lung volume, and inspiratory capacity, but not pressure-time products. CONCLUSIONS: Despite apparent "non-reversibility" in spirometric parameters, long acting bronchodilators can cause both symptomatic and physiological improvement during exercise in severe COPD.     

Effets ventilatoires d’une hypothermic modérée (36° C–28° C) chez le chien anesthésie à l’halothane

Changes in systemic haemodynamic variables (mean arterial pressure, MAP; heart rate, HR; cardiac output, Qc), in oxygen consumption, VO2, and in ventilation (minute ventilation, V; respiratory frequency, f; tidal volume, VT; and arterial blood gases) with particular attention to respiratory times (duration of inspiration, TI; duration of expiration, TE; duration of the breathing cycle, TTOT), to respiratory timing (TI/TTOT) and respiratory drive (VT/TI) were studied during moderate progressive hypothermia (36 degrees C to 28 degrees C) during stable halothane anaesthesia (MAC = 1.5) in six dogs. MAP, HR and Qc decreased; V and f decreased, the decrease in f being correlated with that in temperature (r = 0.66; P < 0.01). Tidal volume did not change. The PaO2 and pHa decreased while PaCO2 increased slightly. The decrease in ventilation was related to changes in respiratory times (TI and TE) which increased (TE more than TI) and in respiratory drive (VT/TI which decreased due to the increase in TI). The relation between VT/TI and TI/TTOT changes was not constant during cooling. Changes in respiratory times and drive could be due to the effect of cold on medullar respiratory control.     

Assessment of spontaneous ventilation in anesthetized children with use of a pediatric circle or a Jackson-Rees system

To compare respiratory workloads, inspiratory efforts were evaluated in 11 children anesthetized with halothane while breathing through a pediatric circle or a Jackson-Rees system. All underwent urogenital surgery and received caudal analgesia after tracheal intubation. Anesthesia was maintained with O2/air at an end-tidal halothane concentration of 0.8%. A pediatric circle system at a fresh gas flow (FGF) of 0.5 and 1.5 x min ventilation (VE) (C0.5 and C1.5, respectively) and a Jackson-Rees system at FGF of 1.5 and 3.0 x VE (JR1.5 and JR3.0, respectively) were used in each patient in a random order. Tidal volume (VT), mean inspiratory flow (VT divided by the duration of inspiration TI, VT/TI), and the initial fast slopes of the airway occlusion pressure phase (delta P degrees/delta t FAST) were significantly lower (P less than 0.05) with the Jackson-Rees than with the circle system, indicating greater impedence to spontaneous breathing with the Jackson-Rees system. The Jackson-Rees system also required a greater peak transpulmonary pressure (PtpMAXe) than did the circle system to achieve the same peak expiratory flows (VMAXe, P less than 0.05), again suggesting an increased resistance with the Jackson-Rees system. These results are most likely explained by the difference in elastic loads (two to three times more with the Jackson-Rees systems) between the two systems. The pediatric circle system appears to be a reliable alternative to the Jackson-Rees system.     

Respiratory effort perception at rest and during carbon dioxide rebreathing in patients with dystrophia myotonica.

BACKGROUND--Breathlessness appears to be closely related to the perception of the outgoing motor command to breathe and should be increased in the presence of muscle weakness. However, breathlessness is not a common symptom in patients with chronic muscle disease who have weak respiratory muscles. The factors that determine the perception of respiratory effort in such patients have not been examined. METHODS--The inspiratory effort sensation during resting breathing and progressive hypercapnia was investigated in 12 patients with dystrophia myotonica with weak respiratory muscles (nine men and three women of mean (SD) age 41.1 (10.5) years; maximum inspiratory pressure 43.1 (17.2) cm H2O) and an age and sex matched control group of normal subjects of mean age 39.6 (10.6) years and a maximum inspiratory pressure of 123 (15.2) cm H2O. RESULTS--During resting breathing with a mouthpiece no differences were seen in inspiratory effort sensation, mouth occlusion pressure, or tidal volume, but inspiratory time and cycle duration were significantly shorter in the patients with dystrophia. Minute ventilation (VE) was significantly higher in the patients (15.8 (4.0) l/min v 12.5 (2.6) l/min), while resting breathing was no more variable in the patients than in controls. The ventilatory response to carbon dioxide (VE/PCO2) was not significantly lower in the patients (14.9 (6.9) l/min/kPa) than in the controls (17.4 (4.3) l/min/kPa). Effort sensation responses to carbon dioxide driven breathing were similar in the control subjects and the patients. With regression analysis of pooled data neither maximum inspiratory pressure nor disease state contributed to perceived inspiratory effort during hypercapnia. CONCLUSIONS--Moderately severe global respiratory muscle weakness does not appear to influence the ventilatory response to rising carbon dioxide tension or the perception of inspiratory effort in patients with dystrophia myotonica.     

Hypercapnia due to rupture of the unidirectional valve in the inspiratory limb of the breathing system after induction of general anesthesia--a case report

Malfunction of either inspiratory or expiratory check valve in a breathing circuit system may allow carbon dioxide (CO2) rebreathing and result in hypercapnia. The subsequent increase of PaCO2 may entail increased sympathetic activity which in turn causes serious problems such as tachyarrhythmia and myocardial ischemia, particularly in patients who have history of coronary artery disease (CAD). Here, we report an incident of rupture of the inspiratory valve in the breathing circuit which happened to a patient during induction of general anesthesia and eventuated in markedly heightened end-tidal CO2 (EtCO2) of the patient. The recognition, related complications and management of the inspiratory valve malfunction are discussed.