Breathing pattern and carbon dioxide retention in severe chronic obstructive pulmonary disease.

BACKGROUND: The factors leading to chronic hypercapnia and rapid shallow breathing in patients with severe chronic obstructive pulmonary disease (COPD) are not completely understood. In this study the interrelations between chronic carbon dioxide retention, breathing pattern, dyspnoea, and the pressure required for breathing relative to inspiratory muscle strength in stable COPD patients with severe airflow obstruction were studied. METHODS: Thirty patients with COPD in a clinically stable condition with forced expiratory volume in one second (FEV1) of < 1 litre were studied. In each patient the following parameters were assessed: (1) dyspnoea scale rating, (2) inspiratory muscle strength by measuring minimal pleural pressure (PPLmin), and (3) tidal volume (VT), flow, pleural pressure swing (PPLsw), total lung resistance (RL), dynamic lung elastance (ELdyn), and positive end expiratory alveolar pressure (PEEPi) during resting breathing. RESULTS: Arterial carbon dioxide tension (PaCO2) related directly to RL/PPLmin, and ELdyn/PPLmin, and inversely to VT and PPLmin. There was no relationship between PaCO2 and functional residual capacity (FRC), total lung capacity (TLC), or minute ventilation. PEEPi was similar in eucapnic and hypercapnic patients. Expressing PaCO2 as a combined function of VT and PPLmin (stepwise multiple regression analysis) explained 71% of the variance in PaCO2. Tidal volume was directly related to inspiratory time (TI), and TI was inversely related to the pressure required for breathing relative to inspiratory muscle strength (PPLsw, %PPLmin). There was an association between the severity of dyspnoea and both the increase in PPLsw (%PPLmin) and the shortening in TI. CONCLUSIONS: The results indicate that, in stable patients with COPD with severe airflow obstruction, hypercapnia is associated with shallow breathing and inspiratory muscle weakness, and rapid and shallow breathing appears to be linked to both a marked increase in the pressure required for breathing relative to inspiratory muscle strength and to the severity of the breathlessness.     

Effects of fenoterol on ventilatory response to hypercapnia and hypoxia in patients with chronic obstructive pulmonary disease

BACKGROUND: It has previously been shown that fenoterol, a beta 2 adrenergic agonist, increases the ventilatory response to hypoxia (HVR) and hypercapnia (HCVR) in normal subjects. The effects of beta 2 adrenergic agonists on chemoreceptors in patients with chronic obstructive pulmonary disease (COPD) remain controversial. This study was designed to examine whether fenoterol increases the HVR and HCVR in patients with COPD. METHODS: The HCVR was tested in 20 patients using a rebreathing method and the HVR was examined using a progressive isocapnic hypoxic method. The HCVR and HVR were assessed by calculating the slopes of plots of occlusion pressure (P0.1) and ventilation (VE) against end tidal carbon dioxide pressure (PETCO2) and arterial oxygen saturation (SaO2), respectively. Spirometric values, lung volumes, and respiratory muscle strength were also measured. The HCVR and HVR were examined after the oral administration of fenoterol (15 mg/day) or placebo for seven days. RESULTS: Fenoterol treatment increased the forced expiratory volume in one second (FEV1) and inspiratory muscle strength. In the HCVR the slope of P0.1 versus PETCO2 was increased by fenoterol from 0.35 (0.23) to 0.43 (0.24) (p < 0.01). Moreover, the P0.1 at PETCO2 of 8 kPa was higher on fenoterol than on placebo (p < 0.05) and the VE was also greater (p < 0.01). In the HVR fenoterol treatment increased the P0.1 at 80% SaO2 from 0.90 (0.72) to 0.97 (0.55) kPa (p < 0.05) while the slopes of the response of P0.1 and VE were not changed. CONCLUSIONS: Fenoterol increases the ventilatory response to hypercapnia in patients with COPD, presumably by stimulation of the central chemoreceptor. The hypoxic ventilatory response is only slightly affected by fenoterol.


     

Histamine induced changes in breathing pattern may precede bronchoconstriction in selected patients with bronchial asthma.

BACKGROUND--In asthmatic patients methacholine or histamine challenge may result in more rapid and shallow breathing. Bronchoconstriction can also be associated with changes in the pattern of breathing. However, few studies, particularly in patients with asthma, have investigated the possibility that changes in the pattern of breathing may precede the onset of bronchoconstriction. METHODS--Eight subjects were selected from 34 consecutive asthmatic patients who had previously exhibited a significant increase in respiratory frequency (Rf) and decrease in tidal volume (VT) accompanying a 20% or greater fall in FEV1 during a histamine bronchial provocation test. These patients also had bronchial hyperresponsiveness (histamine PC20FEV1 0.1-0.25 mg/ml). VT, Rf, and the ratio of VT to Rf were evaluated breath by breath under control conditions and two minutes after inhalation of either saline or each of a series of progressively increasing concentrations of histamine. In each subject the coefficient of variation (CV) for each breathing pattern variable was calculated under control conditions and at each histamine concentration over at least 30-40 breaths. For FEV1, VT and Rf step by step coefficients of variation were averaged and the mean (2SD) CV was considered to represent a threshold value in each patient. RESULTS--Histamine challenge resulted in increased Rf and Rf/VT, and decreased VT and FEV1. In all but one subject change in Rf and Rf/VT beyond the threshold value preceded change in FEV1 beyond the threshold value. The threshold concentrations of histamine for Rf and Rf/VT did not correlate with the threshold value for FEV1. CONCLUSIONS--In selected asthmatic patients a change in breathing pattern occurs prior to a change in FEV1. These results suggest that narrowing of the airways, in terms of decrease in FEV1, does not play a major part in the initial change in the pattern of breathing. This may be caused by direct stimulation of vagal airway receptors.     

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.     

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.     

Effect of halothane on diaphragmatic muscle function in pentobarbital-anesthetized dogs

The mechanism underlying the decrease in minute ventilation (VE) observed under halothane anesthesia was investigated in nine spontaneously breathing dogs. Anesthesia was induced with pentobarbital sodium and was maintained with halothane. Inspired fraction of halothane (FIhal) was increased every 30 min, from 0.005 to 0.02. VE decreased from 8.1 +/- 0.9 to 4.8 +/- 0.4 l . min-1 (P less than 0.001), as FIhal increased from 0 to 0.02. This resulted from a decrease in both mean inspiratory flow (VT/TI) and the duty ratio (TI/TTOT). Transdiaphragmatic pressure (Pdi) and the integrated electrical activity of both hemidiaphragms (Edi) were measured during normal breathing, and during breathing against closed airways (P0di, E0di), in order to obtain an index of the inspiratory neuromuscular output of the diaphragm. With increasing FIhal, there was a significant decrease in Pdi, P0di, Edi, and E0di. The authors measured Pdi and Edi generated during supramaximal stimulation of the two phrenic nerves (PSdi, Esdi) at frequencies of 10, 20, 50, and 100 Hz, in order to eliminate in this decrease the role played by a decrease in the neural drive to breathing. PSdi and ESdi decreased significantly with increasing FIhal, and had not returned to the control values 30 min after discontinuation of halothane administration. The authors conclude that, in pentobarbital-anesthetized dogs, halothane is responsible for a diaphragmatic dysfunction, which may be located either at the neuromuscular junction, on the contractile processes of the muscle, or on both, and for a decrease in the activation time of the inspiratory muscles. Both of these effects contribute to the decrease in VE observed under halothane anesthesia.     

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.     

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.     

Quantal ventilatory variability during spontaneous breathing anaesthesia

Background. Cardioventilatory coupling is the triggering ofinspiratory onset by preceding cardiac activity. We have observedtwo forms of coupling with a bimodal (‘quantal’)variation of respiratory period. Methods. We investigated the variables of inspiratory duration(TI), expiratory duration (TE), and tidal volume (VT) whererespiratory period variation was bimodal. In 25 anaesthetizedspontaneously breathing subjects we took 11 samples of recordingwhere the variation of respiratory period was quantal. Results. In eight of these epochs the variation in respiratoryperiod was associated with fluctuations in the number of heartbeats per breath (entrainment ratio) with a constant time intervalbetween inspiration and the immediately preceding heart beat(coupling interval), which we define as pattern II coupling.During pattern II coupling, the quantal variations in respiratoryperiod were entirely caused by variation in TE, with no associatedchanges in either TI or VT. The other three epochs with quantalvariations in respiratory period were observed in pattern IIIcoupling, where an alternating fluctuation in both entrainmentratio and coupling interval occurs. During pattern III coupling,quantal fluctuations were observed in TE, TI, and VT. Implications. Cross correlation analysis suggested that whenpattern III was present, TI was dependent upon the precedingTE, which differs markedly from traditional views on the interactionbetween inspiratory and expiratory duration. VT was linearlyrelated to TI, and so could also be determined by the precedingTE during this type of coupling. Br J Anaesth 2003; 91: 184–9     

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.     

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.     

Pattern of breathing during exercise in patients with interstitial lung disease.

The responses to exercise were studied in 41 patients with pulmonary fibrosis, in whom vital capacity (VC) was reduced to 62% of predicted normal values. Maximum power output (POmax) was 53% predicted; there was a significant relationship between POmax and VC (r = 0.564). The maximum ventilation achieved during exercise was also related to VC (r = 0.614). Although arterial oxygen saturation (SaO2) fell by more than 5% in 13 of 31 patients, there was no relationship between either SaO2 at POmax or the exercise related fall in SaO2 and POmax. Heart rate responses were higher than normal predicted values in seven patients, all of whom showed a low POmax (36% predicted); this finding was due only in part to a fall in SaO2. The ventilatory response to exercise was within normal limits for the patients as a whole; those subjects with the lowest POmax showed relatively higher ventilatory responses to exercise but the difference was not significant. The pattern and timing of breathing was studied in 32 patients and compared with control subjects matched by sex, age, and size. Tidal volume (VT) was low in the patients; maximum VT was related to VC (r = 0.761), but at low values of VC VTmax was higher than in healthy subjects with comparable VC. The total breathing cycle time (Ttot) fell with progressive exercise in patients and controls; Ttot for a given ventilation was shorter in the patients. Inspiratory time (Ti) was shorter in patients than controls, as was Ti/Ttot. In most patients with diffuse pulmonary fibrosis exercise is limited by a reduced ventilatory capacity, despite the adoption of a short Ti and high inspiratory flow rate, both of which serve to optimise tidal volume and breathing frequency and presumably reduce both the force developed by inspiratory muscles and the sensation of breathlessness.     

Effect of continuous positive airway pressure (CPAP) in patients with chronic obstructive pulmonary chsease (COPD) depending on intrinsic PEEP levels

The application of continuous positive airway pressure (CPAP) is known to reduce inspiratory work of breathing in intubated patients with chronic obstructive pulmonary disease (COPD). This effect is caused by a decrease in elastic work related to a reduction in intrinsic PEEP. The aim of this study was to relate the decrease in inspiratory work due to CPAP to the intrinsic PEEP levels obtained during spontaneous breathing without positive pressure. Ten intubated patients with COPD who had been ventilated for acute respiratory failure were studied. Intrinsic PEEP was determined during tracheal occlusions performed at end-expiration when the patient was breathing without positive airway pressure. Inspiratory work was computed during breathing through a circuit with a CPAP of 0.5 kPa and the same circuit without positive pressure. Intrinsic PEEP-levels ranged from 0.26 to 1.31 kPa. Compared to spontaneous breathing without positive pressure, CPAP reduced the total inspiratory work per liter of ventilation (Wltot) from 1.42±0.48 to 1.24±0.50 J·1^-1 (means±SD P <0.01). This decrease was found to be related to the intrinsic PEEP-levels: the largest reductions were found in the patients with an intrinsic PEEP-level close to the CPAP-level applied. In intubated patients with COPD, the decrease in Wltot due to a CPAP of 0.5 kPa was found to be related to the intrinsic PEEP-levels present when no positive airway pressure was applied. The intrinsic PEEP measured during tracheal occlusions could be used to estimate the effect of CPAP in these patients.     

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.     

Effect of domperidone on the ventilatory response to transient hyperoxia in patients anaesthetized with isoflurane

We have studied the ventilatory responses to transient hyperoxia in two groups of patients (n = 10) anaesthetized with isoflurane (0.3 MAC); patients were allocated randomly to receive either domperidone or placebo orally before anaesthesia. In each patient, five two-breath oxygen tests were averaged and minute ventilation (VEinst) or mean inspiratory flow rate (VT/TI) for each post-test breath was compared with the mean values for these variables during baseline ventilation. A decrease to less than the 95% confidence limits of mean baseline values was considered a definite response. According to this definition, transient hyperoxia decreased VEinst in nine of 10 patients in the placebo group and in all patients in the domperidone group. Similar changes occurred in VT/TI, with eight of 10 definite responses in the placebo group and 10 of 10 in the domperidone group. Compared with placebo, in the domperidone group there were larger changes in VEinst (0.30 vs 0.55 litre min-1 (P = 0.05) and VT/TI (8.5 vs 26.6 ml s-1 (P = 0.02)) from respective baselines. Peripheral chemoreceptors appeared to be active during isoflurane anaesthesia and domperidone pretreatment enhanced this activity by increasing respiratory drive.      

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.     

Pattern of carbon dioxide stimulated breathing in patients with chronic airway obstruction

The pattern of stimulated breathing during carbon dioxide inhalation was studied in a group of 21 patients with severe irreversible airways obstruction (mean FEV1 = 0.9 litre, mean FEV1/FVC% = 50%). Carbon dioxide rebreathing experiments were performed, the ventilatory response being defined in terms of total ventilation (V) and CO2 sensitivity (S). Breathing pattern was defined by the changes in tidal volume (delta VT) and respiratory frequency (delta f) and the maximum VT achieved (VTmax). Contrary to some previous studied no significant relationship could be demonstrated between the severity of airway obstruction (FEV1/FVC%, Raw) and the ventilatory response to rebreathing (V, S, delta VT, delta f, VTmax). However, measurements of dynamic lung volume (FEV1, FVC, IC) were found to be significantly correlated with the breathing pattern variables (delta VT, delta f, VTmax). Resting PaO2 and PaCO2 were significantly correlated with delta VT but not delta f. Results indicate that the degree of airway obstruction does not dictate the ventilatory or breathing pattern response to carbon dioxide induced hyperpnoea. In contrast it is the restriction of dynamic lung volume, by limiting the VT response, that appears to determine the ventilatory and breathing pattern response in patients with severe airway obstruction.     

Effect of simulated commercial flight on oxygenation in patients with interstitial lung disease and chronic obstructive pulmonary disease

BACKGROUND: Commercial aircraft cabins provide a hostile environment for patients with underlying respiratory disease. Although there are algorithms and guidelines for predicting in-flight hypoxaemia, these relate to chronic obstructive pulmonary disease (COPD) and data for interstitial lung disease (ILD) are lacking. The purpose of this study was to evaluate the effect of simulated cabin altitude on subjects with ILD at rest and during a limited walking task. METHODS: Fifteen subjects with ILD and 10 subjects with COPD were recruited. All subjects had resting arterial oxygen pressure (PaO2) of >9.3 kPa. Subjects breathed a hypoxic gas mixture containing 15% oxygen with balance nitrogen for 20 minutes at rest followed by a 50 metre walking task. Pulse oximetry (SpO2) was monitored continuously with testing terminated if levels fell below 80%. Arterial blood gas tensions were taken on room air at rest and after the resting and exercise phases of breathing the gas mixture. RESULTS: In both groups there was a statistically significant decrease in arterial oxygen saturation (SaO2) and PaO2 from room air to 15% oxygen at rest and from 15% oxygen at rest to the completion of the walking task. The ILD group differed significantly from the COPD group in resting 15% oxygen SaO2, PaO2, and room air pH. Means for both groups fell below recommended levels at both resting and when walking on 15% oxygen. CONCLUSION: Even in the presence of acceptable arterial blood gas tensions at sea level, subjects with both ILD and COPD fall below recommended levels of oxygenation when cabin altitude is simulated. This is exacerbated by minimal exercise. Resting sea level arterial blood gas tensions are similarly poor in both COPD and ILD for predicting the response to simulated cabin altitude.     

Influence of Dornier HM3 system on respiration during extracorporeal shock-wave lithotripsy

Patients undergoing extracorporeal shock-wave lithotripsy (ESWL) for renal stones in the Dornier HM3 apparatus are immersed to the clavicles in water and anchored by abdominal and leg restraining straps. The respiratory effects of this system and sedation with midazolam were studied in 70 awake patients anesthetized with epidural blockade. On immersion, surface abdominal pressure and respiratory frequency (f) increased. Tidal volume (VT) and arterial saturation (SaO2) decreased. After intravenous midazolam 0.045 mg/kg body weight, VT decreased further to 35% below pre-immersion values and stone excursions measured by fluoroscopy diminished by more than 50%; reduction of VT and stone excursions were linearly correlated (R = 0.45). SaO2 declined sharply to 6.1% (range -1.5-13.8%) below pre-immersion values, whereas end-tidal CO2 (PETCO2) increased more slowly and f remained above the pre-immersion rate. In three patients, SaO2 decreased to below 85% but was rapidly restored to 98-100% by oxygen administration. The respiratory effects of sedative drugs are exaggerated by the Dornier HM3 system, and continuous monitoring of gas exchange and appropriate oxygen administration are recommended in patients receiving regional anesthesia and sedation.     

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.