Laryngeal resistance immediately after panting in asthmatic subjects.

The panting manoeuvre may be used during the assessment of airway resistance and in asthmatic patients during bronchial provocation testing or spontaneous asthma. To study whether panting opens the larynx in patients with asthma, laryngeal resistance was examined in six patients with stable asthma before and after methacholine induced bronchoconstriction and in another six patients with spontaneous asthma. Subjects were asked to pant and then to hold their breath immediately afterwards. Laryngeal resistance after panting was compared to that during quiet tidal breathing. Change in laryngeal resistance was estimated by a method using low frequency sound and respiratory resistance by forced oscillation at 10 Hz. Mean baseline respiratory resistance during inspiration was 0.245 and 0.470 kPa/l.s before and after methacholine in the patients with stable asthma and 0.480 kPa/l.s in the patients with spontaneous asthma. In the patients with stable asthma mean laryngeal resistance was lower after panting than during the preceding quiet tidal breathing, both before and after methacholine induced bronchoconstriction (by 0.08 before and by 0.065 kPa/l.s after). In contrast, the patients with spontaneous asthma showed an increase in laryngeal resistance after panting of 0.089 kPa/l.s. The magnitude of change in laryngeal resistance after panting was similar to the change in respiratory resistance in the patients with spontaneous asthma and in the patients with stable asthma after methacholine, but was greater than the change in respiratory resistance in the patients with stable asthma before methacholine. These results suggest that panting may cause different effects on the laryngeal aperture in patients with stable and spontaneous asthma.     

Role of cooling and drying in hyperventilation induced asthma.

Respiratory heat loss has been proposed as a mechanism of exercise induced asthma. Whether the predominant stimulus is airway drying or cooling remains unclear. We have measured changes in FEV1 after isocapnic cold air hyperventilation (CAH) (-23.4 degrees (SD 0.43 degrees) C) and dry ambient air hyperventilation (AAH) (18.7 degrees (0.52 degrees)C) in seven asthmatic patients (mean age 31 (SD 9) years and baseline FEV1 3.2(0.9)1) and in seven normal subjects (age 28(6) years and FEV1 3.6(0.7)1). The inspired water content in both cases was 0.3 mg/l air. The rate of respiratory heat exchange per breath was calculated in watts (W) with microcomputer based equipment. Cold air hyperventilation caused a fall in FEV1 almost twice that of ambient air hyperventilation at each level of ventilation: CAH v AAH (% fall) 8.0 (5.1) v 3.9 (4.0) at 15 l/min, 11.6 (7.8) v 7.0 (4.4) at 30 l/min, and 20.7 (10.9) v 12.4 (6.3) at 60 l/min. Identical latent heat loss (evaporative drying) was imposed on the airway during the two challenges. Sensible heat loss (convective cooling) in cold air hyperventilation was 41 W at 15 l/min, 63 W at 30 l/min, and 114 W at 60 l/min; whereas in ambient air hyperventilation the loss was 6, 13, and 23 W respectively. It is concluded that the rate of cooling of the upper airway is the predominant stimulus in hyperventilation induced asthma.     

Evaluation of a new electronic spirometer: the vitalograph "Escort" spirometer.

BACKGROUND--The "Escort" spirometer is a lightweight, hand held spirometer employing a Fleisch pneumotachograph. Measurements of forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and peak expiratory flow (PEF) are obtained from a single FVC manoeuvre. Results are displayed on a small liquid crystal display, but there is no graphical display. The performance of the Escort spirometer has been compared with that of a wedge bellows spirometer (Vitalograph S model) and a Wright PEF meter. METHODS--One hundred and thirteen subjects performed three FVC manoeuvres on the wedge bellows and Escort spirometers and three PEF manoeuvres on the Wright meter. The best reading for each index was recorded. In 21 of the subjects comparison of a Wright manoeuvre with an FVC manoeuvre on the Escort spirometer was performed, whilst in three subjects the effect of repeated blows was studied. RESULTS--The FEV1 ranged from 0.5 to 5.4 litres, FVC from 1.05 to 6.2 litres, and PEF from 100 to 725 l/min. The mean (SD) difference for the FEV1 was -0.05 (0.15) (95% confidence interval (95% CI) -0.07 to -0.02) litres, for FVC 0.03 (0.28) (95% CI -0.02 to +0.08) litres, and for PEF 1.68 (50.6) (95% CI -7.7 to +11.1) l/min. The differences were positively correlated with the mean reading for PEF and FVC but not for FEV1. The Wright PEF manoeuvre performed on the Escort produced significantly higher PEF readings (mean difference -22.9 litres). There was no significant effect of repeated FVC manoeuvres on any of the indices. CONCLUSIONS--The Escort spirometer compares extremely well with a wedge bellows spirometer for measurement of FEV1 and FVC, whilst yielding results of PEF from an FVC manoeuvre which are comparable to those obtained from a Wright meter. It can be recommended for use as a portable hand held spirometer.     

Effect on histamine responsiveness of reducing airway dimensions by altering posture.

Baseline airway geometry is thought to be an important determinant of the airway response to challenge; this geometry is altered by changing posture. The effect of changes in posture on airway calibre, midtidal lung volume, and the airway response to inhaled histamine was studied in eight healthy subjects (four female; mean (SD) age 29.8 (5.1) years, FEV1 3.54 (0.65) 1). Each subject was studied in both sitting and supine postures on two days; airway calibre was assessed by measuring total respiratory resistance (Rrs) at 6 Hz with a forced oscillation technique applied over 16 seconds of tidal breathing. Appropriate doses of histamine were selected by preliminary experiments and were always inhaled with the subject in the supine posture. Midtidal lung volume was larger in the sitting (2.9 (0.8) 1) than in the supine posture (2.4 (0.5) 1). Baseline Rrs was lower in the sitting than in the supine posture (2.03 (0.44) and 3.12 (0.76) cm H2O.1(-1).s*). The mean absolute increase in Rrs after the same dose of histamine was 1.22 cm H2O.1(-1).s in the sitting position (65.8% increase over baseline) and 1.39 cm H2O.1(-1).s (48.8% increase over baseline) in the supine position. The geometric mean provocation concentration of histamine causing a given percentage increase in Rrs was similar in the sitting (8.26 mg/ml) and supine (8.65 mg/ml) positions. Thus there was no significant increase in responsiveness after the reduction of airway dimensions and extra-airway distending forces that occurs in the supine posture.     

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.     

Evaluation of a non-invasive method of assessing opioid induced respiratory depression

Opioid induced respiratory depression is potentially fatal. The aim of this study was to validate a monitoring system that could be used to assess respiratory depression in postoperative patients. The hypercapnic ventilatory response was estimated non-invasively in 12 volunteers. In two steps, we tested a system which delivered carbon dioxide (CO(2)) challenges through a venturi mask, measuring changes in ventilation with an uncalibrated respiratory inductance plethysmograph (RIP). RIP and pneumotachograph measurements of ventilation, taken at the same time during a CO(2) challenge, were similar; group mean (SD), pneumotachograph 13.9 (3.5) l x min(-1) x kPa(-1), RIP 14.3 (2.9) l x min(-1) x kPa(-1). Bland-Altmann analysis showed the variation between these two methods was +/- 5 l x min(-1) x kPa(-1) (2 SD). Second, we confirmed that the venturi mask is suitable for delivering CO(2) challenges. Despite the variability in RIP measurements, a simple multimodal respiratory monitoring system could be developed that incorporates clinical observation and non-invasive measurement of the ventilatory response to CO(2).     

Effects of propranolol inhalation on the diurnal increase in FEV1 and on propranolol airways responsiveness in atopic subjects with asthma.

BACKGROUND--Propranolol inhalation provocation tests are used to measure indirect airways responsiveness in the investigation of asthma. In this study the effects of repeated propranolol inhalation provocation tests within the same day on normal diurnal variation in the forced expiratory volume in one second (FEV1) and subsequent propranolol airways responsiveness were investigated. METHODS--Fifteen atopic asthmatic subjects were challenged with doubling concentrations of propranolol at 08.00 and 16.00 hours on the same study day and at 16.00 hours on a control day to exclude changes related to normal diurnal variation. RESULTS--Mean (SD) baseline FEV1 at 16.00 hours on the study day was 3.38 (0.23) 1, significantly lower than the value at 16.00 hours on the control day of 3.70 (0.24) 1 (p = 0.001). No differences were found between the geometric mean provocative concentration of propranolol causing a 20% fall in FEV1 (PC20) measured on the study day (08.00 hours, 9.3 mg/ml; 16.00 hours, 11.3 mg/ml) and on the control day (16.00 hours 9.3 mg/ml). CONCLUSIONS--The results suggest that propranolol provocation at 08.00 hours has a long lasting effect on FEV1, thereby counteracting the normal diurnal increase in diameter of the airways. This makes propranolol challenge tests less suitable for studying indirect airways responsiveness in the course of one day. Because the FEV1 does not return to control values, it is not possible to determine whether tachyphylaxis to repeated propranolol challenge with a time interval of up to eight hours occurs.     

Mechanisms of improvement of respiratory failure in patients with restrictive thoracic disease treated with non-invasive ventilation

BACKGROUND: Nocturnal non-invasive ventilation (NIV) is an effective treatment for hypercapnic respiratory failure in patients with restrictive thoracic disease. We hypothesised that NIV may reverse respiratory failure by increasing the ventilatory response to carbon dioxide, reducing inspiratory muscle fatigue, or enhancing pulmonary mechanics. METHODS: Twenty patients with restrictive disease were studied at baseline (D0) and at 5-8 days (D5) and 3 months (3M). RESULTS: Mean (SD) daytime arterial carbon dioxide tension (Paco(2)) was reduced from 7.1 (0.9) kPa to 6.6 (0.8) kPa at D5 and 6.3 (0.9) kPa at 3M (p = 0.004), with the mean (SD) hypercapnic ventilatory response increasing from 2.8 (2.3) l/min/kPa to 3.6 (2.4) l/min/kPa at D5 and 4.3 (3.3) l/min/kPa at 3M (p = 0.044). No increase was observed in measures of inspiratory muscle strength including twitch transdiaphragmatic pressure, nor in lung function or respiratory system compliance. CONCLUSIONS: These findings suggest that increased ventilatory response to carbon dioxide is the principal mechanism underlying the long term improvement in gas exchange following NIV in patients with restrictive thoracic disease. Increases in respiratory muscle strength (sniff oesophageal pressure and sniff nasal pressure) correlated with reductions in the Epworth sleepiness score, possibly indicating an increase in the ability of patients to activate inspiratory muscles rather than an improvement in contractility.     

Resistance of tracheal tubes 3.0 and 3.5 mm internal diameter

The resistance of RAE, Rüsch, Mallinckrodt paediatric and Portex plain nasal and oral tracheal tubes with internal diameters 3.0 mm and 3.5 mm was calculated at air flows of 1 to 10 litres per minute. The flow resistance profiles of RAE and Rüsch tracheal tubes was generally higher than those of Mallinckrodt paediatric and Portex plain tubes. All RAE and Rüsch nasotracheal tubes of size 3.0 mm internal diameter and orotracheal tubes 3.0 mm internal diameter had a flow resistance exceeding 3.0 kPa litres/second at an air flow of 4 litres/minute. It is concluded that these tracheal tubes ought only to be used with assisted or controlled ventilation.     

Effect of breathing circuit resistance on the measurement of ventilatory function

BACKGROUND: The American Thoracic Society (ATS) has set the acceptable resistance for spirometers at less than 1.5 cm H2O/l/s over the flow range 0-14 l/s and for monitoring devices at less than 2.5 cm H2O/l/s (0-14 l/s). The aims of this study were to determine the resistance characteristics of commonly used spirometers and monitoring devices and the effect of resistance on ventilatory function. METHODS: The resistance of five spirometers (Vitalograph wedge bellows, Morgan rolling seal, Stead Wells water sealed, Fleisch pneumotachograph, Lilly pneumotachograph) and three monitoring devices (Spiro 1, Ferraris, mini-Wright) was measured from the back pressure developed over a range of known flows (1.6-13.1 l/s). Peak expiratory flow (PEF), forced expiratory flow in one second (FEV1), forced vital capacity (FVC), and mid forced expiratory flow (FEF25-75%) were measured on six subjects with normal lung function and 13 subjects with respiratory disorders using a pneumotachograph. Ventilatory function was then repeated with four different sized resistors (approximately 1-11 cmH2O/l/s) inserted between the mouthpiece and pneumotachograph. RESULTS: All five diagnostic spirometers and two of the three monitoring devices passed the ATS upper limit for resistance. PEF, FEV1 and FVC showed significant (p < 0.05) inverse correlations with added resistance with no significant difference between the normal and patient groups. At a resistance of 1.5 cm H2O/l/s the mean percentage falls (95% confidence interval) were: PEF 6.9% (5.4 to 8.3); FEV1 1.9% (1.0 to 2.8), and FVC 1.5% (0.8 to 2.3). CONCLUSIONS: The ATS resistance specification for diagnostic spirometers appears to be appropriate. However, the specification for monitoring devices may be too conservative. PEF was found to be the most sensitive index to added resistance.     

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.


     

Positive end-expiratory pressure

The immediate haemodynamic effects of the addition of a positive end-expiratory pressure (PEEP) of 5 cmH2O has been studied in eleven patients undergoing artificial ventilation for respiratory failure. Mean cardiac output fell from 6.0 to 5.5 litres/min. This was due to a similar decrease in stroke volume. Individual patients showed greater, though short-lived, changes. There was also a statistically significant increase in central venous pressure (from 8-9 cmH2O) and peripheral resistance (from 1280 to 1380 dyn sec cm-5) associated with the application of PEEP. Overall changes in heart rate and mean arterial blood pressure were insignificant. Arterial oxygen tension increased in the majority of patients but the mean figure was unchanged. Mean oxygen delivery to the tissues fell from 830 to 780 ml/min.     

Effects of hypercapnia and hypocapnia on respiratory resistance in normal and asthmatic subjects.

The effects of hypercapnia and hypocapnia on respiratory resistance were studied in 15 healthy subjects and 30 asthmatic subjects. Respiratory resistance (impedance) was measured with the pseudo-random noise forced oscillation technique while the subjects rebreathed from a wet spirometer in a closed respiratory circuit in which end tidal carbon dioxide tension (PCO2) could be controlled. Hypercapnia was induced by partially short circuiting the carbon dioxide absorber, and hypocapnia by voluntary hyperventilation. The circulating air was saturated with water vapour and kept at body temperature and ambient pressure. A rise of end tidal PCO2 of 1 kPa caused a significant fall in respiratory resistance in both normal and asthmatic subjects (15% and 9% respectively). A fall of PCO2 of 1 kPa did not cause any significant change in impedance in the control group. In the asthmatic patients resistance increased by 13%, reactance fell by 45%, and the frequency dependence of resistance rose 240%. These findings confirm that hypocapnia may contribute to airway obstruction in asthmatic patients, even when water and heat loss are prevented.     

Relation of fetal growth to adult lung function in south India

BACKGROUND: Follow up studies in Britain have shown that low rates of fetal growth are followed by reduced lung function in adult life, independent of smoking and social class. It is suggested that fetal adaptations to undernutrition in utero result in permanent changes in lung structure, which in turn lead to chronic airflow obstruction. India has high rates of intrauterine growth retardation, but no study has examined the association between fetal growth and adult lung function in Indian people. We have related size at birth to lung function in an urban Indian population aged 38-59 years. METHODS: Two hundred and eighty six men and women born in one hospital in Mysore City, South India, during 1934-1953 were traced by a house-to-house survey of the city. Their mean forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) were measured using a turbine spirometer. These measurements were linked to their size at birth, recorded at the time. RESULTS: In both men and women mean FEV1 fell with decreasing birthweight. Adjusted for age and height, it fell by 0.09 litres with each pound (454 g) decrease in birthweight in men (95% confidence interval (CI) 0.01 to 0.16) and by 0.06 (95% CI -0.01 to 0.13) in women. Likewise, mean FVC fell by 0.11 litres (95% CI 0.02 to 0.19) with each pound decrease in birthweight in men, and by 0.08 litres (95% CI 0.002 to 0.16) in women. FEV1 and FVC were lower in men who smoked, but the associations with size at birth were independent of smoking. Small head circumference at birth was associated with a low FEV1/FVC ratio in men which may reflect restriction in airway growth in early gestation. CONCLUSION: This is further evidence that adult lung function is "programmed" in fetal life. Smoking may be particularly detrimental to the lung function of populations already disadvantaged by poor rates of fetal growth.


     

Nasal ventilation in acute exacerbations of chronic obstructive pulmonary disease: effect of ventilator mode on arterial blood gas tensions.

BACKGROUND--There are no controlled trials of the use of different modes of nasal intermittent positive pressure ventilation (NIPPV) in patients with exacerbations of chronic obstructive pulmonary disease (COPD). This study describes the effect on blood gas tensions of four different modes of nasal ventilation. METHODS--Twelve patients with acute exacerbations of COPD were studied (mean (SD) FEV1 0.59 (0.13) l, PaO2 (air) 5.10 (1.12) kPa, PaCO2 9.28 (1.97) kPa, pH 7.32 (0.03)). Each patient underwent four one-hour periods of nasal ventilation in randomised order: (a) inspiratory pressure support 18 cm H2O; (b) pressure support 18 cm H2O+positive end expiratory pressure (PEEP) 6 cm H2O (IPAP+EPAP); (c) continuous positive airway pressure (CPAP) 8 cm H2O; and (d) volume cycled NIPPV. Arterial blood samples were obtained before each period of ventilation and at one hour. RESULTS--Pressure support, CPAP, and volume cycled NIPPV all produced significant improvements in PaO2; there was no difference between these three modes. The change in PaO2 with IPAP+EPAP did not reach statistical significance. None of the modes produced significant changes in mean PaCO2; patients with higher baseline levels tended to show a rise in PaCO2 whereas those with lower baseline levels tended to show a fall. CONCLUSIONS--Although PaO2 improved in all patients there are differences in efficacy between the modes, while the changes in PaCO2 were variable. The addition of EPAP conferred no advantage in terms of blood gas tensions.     

Evaluation of pulsed dose oxygen delivery during exercise in patients with severe chronic obstructive pulmonary disease

BACKGROUND: Oxygen conserving devices may lead to substantial increases in the duration of oxygen provided. A study was undertaken to compare the performance of a pulsed dose oxygen delivery (PDOD) system with continuous flow oxygen or air during a maximal walking test. METHODS: Fourteen patients with chronic obstructive pulmonary disease (COPD) and arterial oxygen desaturation on exercise (mean (SD) forced expiratory volume in one second (FEV1) 0.83 (0.28) 1, arterial oxygen pressure (PaO2) 8.38 (1.24) kPa, arterial carbon dioxide pressure (PaCO2) 5.95 (0.86) kPa) were randomised to perform a walking test using air administered via a cylinder or continuous flow oxygen at 2 l/min or by a PDOD system. RESULTS: There was no significant difference in the mean arterial oxygen saturation (SaO2) using the PDOD system or with continuous flow oxygen (p = 0.33). Patients showed greatest desaturation whilst walking with the air cylinder (SaO2 79.2 (8.59)%) which was significantly different from the desaturation with both continuous flow oxygen (87.6 (5.85)%, p = 0.001) and PDOD (85.6 (7.36)%, p = 0.004). There was no significant difference between the distance walked using oxygen delivered at 2 l/min by continuous flow or via the PDOD (p = 0.72; CI 0.34 to 1.08). The mean (SD) distance walked on continuous flow oxygen (203.6 (106.1) m) and PDOD (207.9 (109.8) m) was significantly greater than the distance walked with the air cylinder (188.6 (110.02) m); (1.12 fold increase in distance, CI 1.01 to 1.23, p = 0.02, and 1.14 fold increase in distance, CI 1.01 to 1.28, p = 0.03, respectively). CONCLUSIONS: These findings suggest that the pulsed dose oxygen conserving device was as effective as continuous flow oxygen in maintaining arterial oxygen saturation and that the use of this device was associated with similar improvements in exercise tolerance to patients taking continuous flow oxygen therapy.     

Comparison of airway reactivity induced by histamine, methacholine, and isocapnic hyperventilation in normal and asthmatic subjects

In an investigation of a rapid screening test for airway reactivity using isocapnic hyperventilation with room air and cold air the results of this test were compared with the airway response to histamine and methacholine challenge. Twelve non-atopic, non-smoking normal subjects and 11 subjects with stable asthma who had an FEV1 above 74% of the predicted value were studied. In the normal subjects isocapnic hyperventilation with room air (75 l/min; 22 degrees C (SEM 0.2 degrees); 10 mg H2O/l air) and isocapnic hyperventilation with cold air (77 l/min; -10 degrees C (0.9 degrees); 2.4 mg H2O/l air) produced no significant change in FEV1. In the asthmatic subjects, hyperventilation with room air (71 l/min; 22 degrees C (0.8 degrees); 10 mg H2O/l air) caused a mean fall in FEV1 of 11.7%; cold air hyperventilation (70 l/min; -10 degrees C (0.9 degrees); 2.4 mg H2O/l air) caused a mean fall in FEV1 of 20.4%. Cold air hyperventilation produced greater separation between normal and asthmatic subjects than room air. The provocative concentration of histamine required to reduce the FEV1 by 20% (PC20) correlated closely with the PC20 for methacholine (r = 0.95; p less than 0.001). Both tests separated normal from asthmatic subjects. PC20 for both histamine and methacholine correlated with the fall in FEV1 after cold air hyperventilation (r = 0.93, p less than 0.001; r = 0.87, p less than 0.001 respectively). We conclude that the results of a rapid screening test based on hyperventilation with cold air correlate well with a standard pharmacological challenge.     

Respiratory function and ribcage contribution to ventilation in body positions commonly used during anesthesia

Lung function tests are normally performed in the upright position, whereas anesthesia is usually administered with the patient in the supine position, and occasionally in other postures. We therefore compared forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), functional residual capacity (FRC), and ribcage contribution to ventilation by respiratory inductive plethysmography in 13 conscious healthy male volunteers, sitting and in four horizontal positions used during anesthesia. Forced vital capacity and FEV1 were similar in all positions, except for a significant mean increase in FVC of 300 mL (SD 213) when sitting compared with when supine (P less than 0.001). The mean decrease in FRC was 806 mL (SD 293) between the sitting and supine positions (P less than 0.001). A significant increase in FRC occurred (252 mL, SD 329, P less than 0.01) when supine subjects raised their arms above their heads as required for computed tomography. Functional residual capacity in the prone and lateral positions was significantly larger than in the supine position (mean change 350 mL, P less than 0.001), but was still some 450 mL less than in the sitting position. Mean ribcage contribution was similar in all horizontal positions (32%-36%), whereas supine values were significantly different from those of the sitting position (mean 70%, SD 11, P less than 0.001). In conclusion, the various horizontal postures studied have no effect on FVC, FEV1, or ribcage contribution to ventilation. However, FRC in the prone, lateral, and arms-up positions is on average 250 mL larger than in the supine position, an observation that may affect gas exchange during anesthesia in these positions.     

Importance of airflow obstruction after thoracoplasty.

Thirty six patients previously treated for pulmonary tuberculosis by thoracoplasty were studied to determine the prevalence and effect of airflow obstruction. The mean (SD) FEV1 was 1.3 (0.65) 1 and the mean forced expiratory ratio (FER) 64% (12%). FEV1 was less than predicted in every patient whereas FER was less than predicted in 30, being below the lower 98th percentile in 15 (42%). In the 18 patients who complained of breathlessness the means of the standardised residuals (SR) for FEV1, peak expiratory flow (PEF), and FER were significantly lower and that for residual volume/total lung capacity (RV/TLC) significantly higher than those for the 18 patients who were not breathless (all p less than 0.0001). There was no difference in the smoking history of the two groups. Only three of the 23 patients in whom reversibility of airflow obstruction was assessed showed a greater than 25% increase in PEF. None showed an increase in FEV1 of greater than 15%. The 18 who were breathless had significantly lower values of arterial oxygen tension (PaO2) and higher values of arterial carbon dioxide tension (PaCO2) (p less than 0.0001). Thirteen of these patients were in chronic respiratory failure (PaO2 less than 8.0 kPa or PaCO2 greater than 5.9 kPa, or both) compared with only one of the 18 who were not breathless. The indices correlating best with PaO2 and PaCO2 were SR FEV1 and SR PEF respectively. SR FEV1 accounted for 34% of the variance in PaO2 and SR PEF for 29% of the variance in PaCO2. Airflow obstruction has been found to be common in patients with a thoracoplasty and to be associated with hypoxia and hypercapnia.     

Peak intratracheal pressure during controlled ventilation in infants and children

The mathematical relationship between peak ventilator breathing system pressure displayed on the digital meter of the Siemens SV900C ventilator, and peak intratracheal pressure measured at the distal end of the tracheal tube, was defined and incorporated into a computer program. The mean difference between peak airway pressure calculated by the computer and directly measured peak intratracheal pressure was 0.02 kPa (SD 0.10) in 18 infants and children. The mean difference between ventilator breathing system pressure and intratracheal pressure in the same group was 0.82 kPa (SD 0.91). Bench tests established that the decrease in peak pressure displayed by the ventilator (from 1.36 to 0.38 kPa) while inspiratory time was increased from 20 to 80% of the respiratory period, concealed an increase (from 0.2 to 0.38 kPa) in intratracheal pressure which occurs during this process; and that the large increase in pressure displayed by the ventilator (from 0.3 to 6 kPa) while respiratory frequency was increased from 20 to 120 breaths/minute, concealed a small increase in peak intratracheal pressure (0.2-0.3 kPa) which occurs during this process. These changes were accurately predicted by the computer program. The increase in intratracheal pressure associated with prolonged inspiratory times explains the high incidence of barotrauma which has recently been associated with this procedure in infants.