Surgery and the respiratory muscles.
Explore the source record for details and available documents.
Abdomen↗
Biomedical subjects
D Georgopoulos
Publications and source records attributed to D Georgopoulos.
Proportional assist ventilation: an alternative approach to wean the patient.
Explore the source record for details and available documents.
Humans↗
Effects of pulmonary and intercostal denervation on the response of breathing frequency to varying inspiratory flow.
In mechanically ventilated awake and sleeping humans, it has been shown that increasing inspiratory flow rate (V'I) exerted a reflex excitatory effect on respiratory output. Mechanoreceptors located in intercostal muscles or within the lung have been suggested as possible pathways that may mediate the excitatory effect of V'I. To test this, five patients with bilateral lung transplantation (LTP) and eight quadriplegics with spinal cord transection at the level of C6-C7 (QP) were studied. Patients were connected to a volume cycle ventilator in the assist volume-control mode and V'I was randomly changed. V'I pattern was square and all breaths were patient-triggered. V'I values of 30, 60 and 90 L x min(-1) were studied. Each level of V'I was sustained for 15 breaths. Airway pressures, end-tidal partial pressure of carbon dioxide (PCO2), airflows and volumes were measured breath by breath. Thirty seven trials in LTP and sixty in QP, where V'I was randomly changed between 30 and 90 L x min(-1), were analysed. In both groups of patients, minute ventilation increased and total breath duration decreased significantly as V'I increased. These changes were complete in the first breath after V'I transition, without evidence of adaptation of the response. The magnitude of the response did not differ between the two groups of patients and was comparable to that observed previously in conscious normal subjects. We conclude that the excitatory effect of inspiratory flow rate on breathing frequency persists in patients who have pulmonary or intercostal denervation. These results do not favour receptors located within the lung (below the resection lines) or in the intercostal muscles to mediate the response of breathing frequency to flow rate.
Denervation↗
Bronchodilator delivery by metered-dose inhaler in mechanically ventilated COPD patients: influence of end-inspiratory pause.
The delivery of bronchodilators with a metered-dose inhaler (MDI) and a spacer in mechanically ventilated patients has become widespread practice. However, the various ventilator settings that influence the efficacy of MDI are not well established. Application of an end-inspiratory pause (EIP) during drug delivery has been suggested as one of the factors that might increase the effectiveness of this therapy. To test this, the effect of EIP on the bronchodilation induced by beta2-agonists administered with MDI and a spacer in a group of mechanically ventilated patients with chronic obstructive pulmonary disease (COPD) was examined. Twelve patients with COPD, mechanically ventilated on volume-controlled mode, were prospectively randomized to receive six puffs of salbutamol (100 microg x puff(-1)) either with or without EIP of 5 s duration. Salbutamol was administered with an MDI adapted to the inspiratory limb of the ventilator circuit using an aerosol cloud-enhancer spacer. After a 6 h wash-out, patients were crossed over to receive salbutamol by the alternative mode of administration. Static and dynamic airway pressures, minimum (Rmin) and maximum (Rmax) airflow resistance, the difference between Rmax and Rmin (deltaR), static end-inspiratory respiratory system compliance (Cst,rs) and cardiac frequency (fc) were measured before and at 15, 30 and 60 min after salbutamol administration. Salbutamol caused a significant decrease in dynamic and static airway pressures, Rmin and Rmax. These changes were not influenced by application of EIP and were evident at 15, 30 and 60 min after salbutamol. With and without EIP, Cst,rs,deltaR and fc did not change after salbutamol. In conclusion, salbutamol delivered with a metered-dose inhaler and a spacer device induced significant bronchodilation in mechanically ventilated patients with chronic obstructive pulmonary disease, the magnitude of which was not affected by an end-expiratory pause of 5 s. These results do not support the use of end-inspiratory pause when bronchodilators are administered in adequate doses during controlled mechanical ventilation.
Aged↗
Effects of inspiratory muscle unloading on the response of respiratory motor output to CO2.
Inspiratory muscle output is downregulated when the mechanical load is reduced in awake humans. It is not known whether this is related to reduction in PCO2 or to removal of load-related neural responses. To address this issue, we did Read CO2 rebreathing tests in 13 normal subjects with and without unloading and compared respiratory output at identical end-tidal PCO2 (PET(CO2)) levels. Unloading was carried out with proportional assist ventilation (flow assist = 2 cm H2O/L/s plus volume assist = 4 cm H2O/L, representing approximately 50% reduction of the normal resistance and elastance). Ventilatory output (n = 13), total pressure of respiratory muscles (Pmus, n = 8), and transdiaphragmatic pressure (Pdi, n = 5) were computed at different PET(CO2) levels. Pmus was computed from esophageal pressure (Pes) using the Campbell diagram, and Pdi was measured from the difference between gastric pressure and Pes. Unloading caused an increase in ventilation (VI) and tidal volume (VT) at all PET(CO2) levels with no significant effect on slope (VI/PET(CO2) or VT/PET(CO2)) or respiratory rate. At low PET(CO2) (50 mm Hg), Pdi and Pmus waveforms did not differ with and without unloading. At high PET(C02) (59 mm Hg), peak Pdi and Pmus decreased by only 18.8 +/- 8.3% and 13.8 +/- 9.5%, respectively (NS, p > 0.05). Using a model that allows nonlinearity in the pressure-volume relation and for intrinsic muscle properties (force-length and force-velocity relations), we estimated the expected changes in mean VT and VI when the level of assist used in this study was applied in the absence of any change in neural output response to CO2. The predicted and observed changes in VT and VI were similar. We conclude that when chemical stimuli are rigorously controlled, unloading does not result in downregulation of respiratory muscle activation.
Adult↗
Respiratory response to CO2 during pressure-support ventilation in conscious normal humans.
The respiratory response to CO2 during pressure-support ventilation (PSV) was studied in 16 conscious normal humans. The subjects breathed through a mouthpiece connected to a ventilator in PSV mode, with pressure set to the highest comfortable level for each subject (10.1 +/- 0.6 cm H2O, mean +/- SE). Compared with breathing spontaneously through the ventilator (CPAP mode with zero positive end-expiratory pressure), with PSV, tidal volume (VT) increased significantly (1.16 +/- 0.1 versus 0.85 +/- 0.04 L), whereas breathing frequency (f) remained stable (16.0 +/- 0.9 versus 15.6 +/- 1.1 breaths/min). As a result, the subjects hyperventilated, decreasing significantly end-tidal PCO2 (PETCO2, 23.5 +/- 1.2 versus 35.5 +/- 1.1 mm Hg). Fraction of inspired CO2 (FICO2) was then increased in steps, and changes in respiratory motor output were quantitated from changes in f, VT, ventilation (VI), peak inspiratory flow (Vpeak), and muscle pressure (Pmus). Pmus was calculated by the equation of motion, based on respiratory system mechanics, which were measured previously by airway occlusion at end-inspiration, VT, VI, and Pmus increased significantly with increasing PETCO2, and the response was detectable even below eupneic levels; f remained relatively stable over a wide range of PETCO2 (23 to 45 mm Hg) and increase significantly only when PETCO2 approached 50 mm Hg. These results indicate that in conscious normal humans during PSV, CO2 responsiveness extends well into hypocapnia and is expressed principally as an increase in intensity of respiratory motor output with little change in respiratory rate.
Adult↗
Long-term alterations of respiratory function in adolescents wearing a brace for idiopathic scoliosis.
STUDY DESIGN: This is a prospective study. OBJECTIVE: The authors investigated the effects of continuous bracing for idiopathic scoliosis on lung function variables at three consecutive time points over a 2-year period. SUMMARY OF BACKGROUND DATA: Only short-term results regarding lung function impairment caused by bracing exist. METHODS: Thirty adolescents (aged 13.6 +/- 1.8 years) with primary idiopathic thoracic scoliosis of 28.7 degrees +/- 4.1 degrees and primary lumbar scoliosis of 26.5 degrees +/- 10.4 degrees were treated with a Boston brace. All patients underwent pulmonary function studies at the beginning of brace treatment and 12 and 24 months after treatment initiation. The examinations were always performed while the patients were sitting, in and out of the brace. Patients removed the brace for 1 hour before the measurements for non-brace-wearing were performed. Vital capacity, forced expiratory volume in 1.0 second, and minute ventilation were determined with a low inertia, low resistance bell spirometer. Lung volume, including total lung capacity and functional residual capacity, was recorded. RESULTS: The primary thoracic scoliosis was corrected to 14.5 degrees +/- 4.0 degrees and the primary lumbar scoliosis to 13.0 degrees +/- 6.0 degrees. The values of the following parameters taken while the brace was worn were significantly lower than those taken without the brace at all time points (one-way analysis of variance); vital capacity (P < 0.02), forced vital capacity (P < 0.03), functional residual capacity (P < 0.02), and residual volume (P < 0.05). Furthermore, the predicted negative residual volume and negative functional residual capacity values differed significantly in all time points from negative residual volume and negative functional residual capacity values of patients while wearing the Boston brace (P < 0.01 and P < 0.02, respectively). CONCLUSIONS: The results suggest that brace wearing for mild idiopathic scoliosis does not harm adolescent lung function over a 2-year period and is recommended for treatment of idiopathic scoliosis in early adolescence when the generally accepted criteria for bracing are fulfilled.
Adolescent↗
Effects of breathing route, temperature and volume of inspired gas, and airway anesthesia on the response of respiratory output to varying inspiratory flow.
The determinants of the response of the respiratory output to inspiratory flow rates (VI) were examined in awake normal subjects. Subjects were connected to a volume-cycle ventilator in the assist/control mode, and VI was increased in steps from 30 to 90 L/min and then back to 30 L/min. VI pattern was square, and all breaths were subject-triggered. In six subjects the effects of breathing route (nasal or mouth) and temperature and volume of inspired gas (Protocol A) and in 8 subjects the effects of airway anesthesia (upper and lower airways; Protocol B) on the response of respiratory output to varying VI were studied. In Protocol B, in order to calculate muscle pressure during inspiration (Pmus), respiratory system mechanics were measured using the interrupter method at end-inspiration. Independent of conditions studied, breathing frequency increased significantly and end-tidal concentration of CO2 decreased as VI increased. The response was graded and reversible and not affected by breathing route, temperature and volume of inspired gas, and airway anesthesia. With and without airway anesthesia (Protocol B), neural inspiratory and expiratory time and neural duty cycle, estimated from Pmus waveform, decreased significantly as VI increased. At all conditions studied, the rate of change in airway pressure prior to triggering the ventilator tended to increase as VI increased. The changes in timing and drive were nearly complete within the first two breaths after transition, with no evidence of adaptation during a given VI period. We conclude that VI exerts an excitatory effect on respiratory output which is independent of breathing route, temperature and volume of inspirate, and airway anesthesia. The response most likely is neural in origin, mediated through receptors not accessible to anesthesia, such as those located in the chest wall or below the airway mucosa.
Adult↗
Effects of non-REM sleep on the response of respiratory output to varying inspiratory flow.
It has been shown in mechanically ventilated awake normal humans that increasing inspiratory flow rate (VI) exerts an excitatory effect on respiratory output. It is not known if this effect persists during sleep. To test this, seven normal adults were studied during wakefulness and non-rapid eye movement (non-REM) sleep. Subjects were connected through a nose mask to a volume-cycled ventilator in the assist/control mode, and VI was increased in steps (3 to 4 breaths each) from 30 to 70 L/min and then back to 30 L/min. VI pattern was square, and all breaths were subject-triggered. Forty-one trials during non-REM sleep and 10 during wakefulness were analyzed. Both during sleep and wakefulness minute ventilation increased and total breath duration (Ttot) decreased significantly in a graded and reversible manner as VI increased. These changes were complete in the first breath after VI transition. The response was significantly less during sleep than during wakefulness (p < 0.050; at 30 L/min Ttot, expressed as percent of that at 70 L/min, was 110.2 +/- 1.3% during sleep and 127.8 +/- 3.9% during wakefulness. During wakefulness, the rate of change in airway pressure before triggering the ventilator (dp/dt), an index of respiratory drive, increased significantly (p < 0.05) with increasing VI. During sleep dp/dt was not affected by VI changes. In four sleeping subjects the increase in VI was sustained for 1.5 to 2 min. There was no evidence for adaptation of the response; Ttot, averaged over the last three breaths, did not differ from that obtained with VI was sustained for only 3 to 4 breaths. We concluded that VI exerts an excitatory effect on respiratory output, mediated by a reflex neural mechanism, and the gain of this reflex is attenuated by sleep.
Adaptation, Physiological↗
Control of breathing in mechanically ventilated patients.
During mechanical ventilation, the respiratory system is under the influence of two pumps, the ventilator pump and the patient's own respiratory muscles. Depending on the mode of mechanical ventilatory support, ventilation may be totally controlled by the ventilator or may be determined by the interaction between patient respiratory effort and ventilator function. In either case, compared to spontaneous breathing, the breathing pattern is altered and this may influence: 1) force-length and force-velocity relationships of respiratory muscles (mechanical feedback); 2) chemical stimuli (chemical feedback); 3) the activity of various receptors located in the respiratory tract, lung and chest wall (reflex feedback); and 4) behavioural response (behavioural feedback). Changes in these feedback systems may modify the function of the ventilator, in a way that is dependent on the mode of mechanical ventilatory support, ventilator settings, mechanics of the respiratory system and the sleep/awake stage. Thus, the response of ventilator to patient effort, and that of patient effort to ventilator-delivered breath are inevitably the two components of control of breathing during mechanical ventilation; the ventilatory output is the final expression of the interaction between these two components. As a result of this interaction, the various aspects of control of breathing of the respiratory system may be masked or modulated by mechanical ventilation, depending on several factors related both to patient and ventilator. This should be taken into consideration in the management of mechanically ventilated patients.
Behavior↗
Effects of breathing patterns on mechanically ventilated patients with chronic obstructive pulmonary disease and dynamic hyperinflation.
OBJECTIVE: To examine the circulatory and respiratory effects of breathing pattern in patients with chronic obstructive pulmonary disease (COPD) and dynamic hyperinflation (DH) during controlled mechanical ventilation. DESIGN: Prospective, controlled, randomized, non-blinded study. SETTING: Respiratory intensive care unit of a university hospital. PATIENTS: Nine patients with acute respiratory failure and DH due to acute exacerbations of COPD. INTERVENTIONS: Keeping tidal volume and total breath duration (TTOT) constant, patients were ventilated at six different values of expiratory time (TE). TE changes were randomly induced by alterations of constant inspiratory flow (VI) and/or end-inspiratory pause (EIP). Patients were studied at three levels of VI(0.93 +/- 0.08, 0.72 +/- 0.06 and 0.55 +/- 0.04 l/s, mean +/- SE), with and without EIP (10% of TTOT). MEASUREMENTS AND RESULTS: Lung volumes, airflows, airways pressures, oxygenation indices and dead space were measured. Alveolar pressure and airway resistance (Rmin), as well as the additional resistance (delta R) due to viscoelastic pressure dissipation and time-constant inequalities, were estimated by rapid airway occlusion during inflation. In seven out of nine patients, right-heart catheterization was performed and hemodynamic parameters were obtained at each value of TE. A significant decrease of intrinsic positive end-expiratory pressure (PEEPi), end-inspiratory static and mean (mPaw) airway pressures, end-expiratory lung volume above passive FRC (Vtrap), delta R and venous admixture and a significant increase of peak airway pressure, Rmin, stroke volume index and mixed venous PO2 (PvO2) were observed when VI increased. At each VI, the addition of EIP significantly decreased iso-volume expiratory flows and PvO2 and increased Vtrap and mPaw. CONCLUSIONS: We conclude that in mechanically ventilated patients with COPD, the pattern of lung inflation and TE alteration have a significant impact on respiratory system mechanics, gas exchange and hemodynamics. Addition of EIP in patients with COPD may be detrimental.
Acute Disease↗
Ventilatory post-stimulus potentiation in patients with brain damage.
In normal humans when a brief hypoxic ventilatory stimulus is terminated abruptly by breathing 100% O2, ventilation during hyperoxia gradually declines to baseline prehypoxic levels without an undershoot. This has been interpreted as evidence of decay of short-term potentiation (STP), a mechanism located in the brainstem and not dependent upon higher center inputs. STP decay may be important in preventing periodic breathing by damping ventilatory responses to cyclic stimuli. Patients with brain damage commonly have periodic breathing that may be caused partly by impairment of STP activation. To test this 12 tracheostomized patients with severe brain damage (Glasgow score 9.9 +/- 0.6) were studied. Breathing stability was estimated by at least 6 h of capnography and from these records apnea index (AI, episodes/hour) and cyclic changes of end-tidal CO2 (c-PETCO2, cycles/hour) were derived. STP activation was examined by brief exposure to hypoxia (45 s, end-tidal O2 = 50 mm Hg) followed by hyperoxia. Forty-four hypoxic-hyperoxic runs were analyzed and compared with 19 normoxic-hyperoxic trials. At the end of the hypoxia ventilation (VI) increased 39.5 +/- 5.8% and PETCO2 decreased 2.7 +/- 0.6 mm Hg to 91.5 +/- 2.2% of baseline value. When hypoxia was terminated abruptly by hyperoxia VI dropped immediately to 63.2 +/- 7.2% of baseline, remaining for 35 s significantly lower than the corresponding values acquired during hyperoxia after normoxia. After hypoxia, apneas occurred in 19 of 44 hyperoxic runs. There was a negative relationship between nadir hyperoxic ventilation after hypoxia and both AI and c-PETCO2.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Effect of hypoxic sensitivity on decay of respiratory short-term potentiation.
In normal conscious humans, when a brief hypoxic ventilatory stimulus is followed immediately by breathing 100% O2, ventilation during hyperoxia gradually declines to baseline prehypoxic levels without an undershoot. During the decline, ventilation is greater than baseline in the absence of hypoxia and hypercapnia. This has been interpreted as evidence of decay of short-term potentiation (STP) or afterdischarge. It is not known whether the intensity of the stimulus that activates STP influences the time course of its decay. Therefore we studied STP decay in nine normal adults after administration of placebo (P) and almitrine (A) in a single-blind manner on 2 separate days. On each day, three runs consisting of 45 s of isocapnic hypoxia (end-tidal PO2 = 55 mm Hg) followed by 2 min of hyperoxia were conducted while ventilation (VI) was measured breath by breath. Baseline VT did not differ between A and P, but at the end of hypoxia, VI with A was 169 +/- 14% (SE) of baseline while VI with P was 132 +/- 7% of baseline (p < 0.05). Immediately after hyperoxia was instituted, VI fell abruptly, the fall being 36% of baseline for A and 15% for P. This probably represented the withdrawal of peripheral chemoreceptor input. Thereafter, VI declined slowly toward baseline, and the time course of this decline did not differ between P and A. Our results indicate that within the limits we studied, the increase of the intensity of the discharge of the peripheral chemoreceptors during hypoxia does not influence STP decay.
Adult↗
Factors determining lobar emptying during maximal and partial forced deflations in nonhomogeneous airway obstruction in dogs.
The partial expiratory flow-volume (PEFV) maneuver has been proposed as a sensitive test to detect nonuniform airway disease. We tested this hypothesis in seven dogs in an open-chest preparation in which the right upper lobe (RUL) bronchus was partially obstructed. Alveolar capsules were placed on the obstructed RUL and nonobstructed right lower lobe (RLL) to measure respective alveolar pressures (Palv) during PEFV and maximal expiratory flow-volume (MEFV) maneuvers. PEFV curves were initiated at about 75% of the whole-lung vital capacity (VC). A Pitot static tube was placed into the airway to identify sites of flow limitation (choke-points [CP]), frictional pressure losses to CP (Pfr), CP area (A*), and compliance (K*). Results were analyzed at 45% VC, where a central tracheal CP was identified, and at 29% VC, where lobar CP were identified. At both lung volumes, the results showed that during PEFV, Palv and flows of the obstructed RUL decreased, whereas Palv and flows of the RLL increased compared with values obtained during MEFV. However, total maximal expiratory flow (Vmax) did not change between maneuvers. At 45% VC, although Pfr decreased during PEFV, this decrease was not large enough to result in an increase in A* and hence total Vmax because CP were identified in the noncompliant trachea. At 29% VC, offsetting changes in lobar A* and flow occurred between maneuvers: during PEFV, RLL A* and flow relatively increased while RUL A* and flow decreased. This study describes the mechanisms that explain why the PEFV maneuver is not useful in the detection of nonhomogeneous airway obstruction.
Animals↗
Effects of extrinsic positive end-expiratory pressure on mechanically ventilated patients with chronic obstructive pulmonary disease and dynamic hyperinflation.
OBJECTIVE: To examine the circulatory and respiratory effects of extrinsic positive end-expiratory pressure (PEEPe) in patients with chronic obstructive pulmonary disease (COPD) and dynamic hyperinflation during controlled mechanical ventilation. DESIGN: Different levels of PEEPe were applied randomly in mechanically ventilated patients with COPD and dynamic hyperinflation. SETTING: Respiratory Intensive Care Unit of a University Hospital. PATIENTS: 9 patients with acute respiratory failure and dynamic hyperinflation due to acute exacerbation of COPD. INTERVENTIONS: PEEPe 35%, 58% and 86% of intrinsic PEEP (PEEPi) were applied. MEASUREMENTS AND RESULTS: Using flow-directed pulmonary artery catheters hemodynamic measurements were obtained, while simultaneously lung volumes, airflows and airway pressures were recorded. In order to estimate alveolar pressures (Palv), rapid airway occlusions during passive expiration were also performed. At no level of PEEPe were significant changes in cardiac output, gas exchange variables, dead space, airways inflation resistances and respiratory system static end-inspiratory compliance observed. At high level of PEEPe central venous, mean pulmonary arterial and pulmonary capillary wedge pressures were increased significantly. All but one patient were flow-limited during passive expiration. PEEPe 86% of PEEPi caused a significant increase in end-expiratory lung volume and total PEEP. Iso-volume pressure-flow curves showed volume-dependence expiratory flow limitation in 2 patients, while in 8 patients volume-dependence of critical driving pressure (Palv-mouth pressure) that decreased flows was also observed. CONCLUSIONS: The effects of PEEPe on iso-volume flow and hence on lung mechanics and hemodynamics, depend on many factors, such as airways resistances, lung volumes and airway characteristics, making the patient response to PEEPe unpredictable.
Aged↗
Respiratory short-term potentiation (after-discharge) in elderly humans.
During a ventilatory stimulus, respiratory short-term potentiation (STP, after-discharge) develops, so that ventilation after the stimulus is greater than that before the stimulus. When the stimulus is withdrawn STP gradually decays, tending to prevent hypoventilation and therefore stabilizing breathing pattern. STP has been demonstrated in young humans after brief hypoxic stimuli. Since respiratory arrhythmias increase with age, we examined the decay of STP in normal elderly humans (mean age 62), comparing them with young normals (mean age 27). Resting subjects were exposed to 35-50 sec hypoxia (end-tidal PO2 = 55 Torr) followed by hyperoxia and breathing analyzed during the hyperoxic period, when the subjects were also hypocapnic. With hypoxia, ventilation increased to 152% of control in both the older and younger subjects while end-tidal CO2 fell to 92.0% of control in the older subjects and 94.7% of control in the younger. In both groups the hypoxic increase in ventilation was almost entirely due to an increase of tidal volume. During hyperoxia, ventilation and tidal volume declined over 20-25 sec to control, pre-hypoxic levels, without an apparent undershoot, and there were no consistent differences between the older and younger subjects. Prolonging the hypoxic exposure to 90 sec had no influence on STP in the older subjects. We conclude that neither age nor prolonging the hypoxic stimulus from 50 to 90 sec influenced STP.
Adult↗
Buspirone effect on breathlessness and exercise performance in patients with chronic obstructive pulmonary disease.
Buspirone is an anxiolytic agent that appears to have no sedative effects. The aim of this study was to assess the effects of buspirone on breathlessness and exercise tolerance in patients with chronic airway obstruction. Sixteen patients, age 56.9 +/- 17.0; forced expiratory volume in 1 s (FEV1) 1.15 +/- 0.42 l; FEV1/forced vital capacity (FVC) 50.7 +/- 15.0%; PaCO2 42.2 +/- 5.5 mm Hg; and PaO2 57.6 +/- 10 mm Hg, underwent a 6-min walking test, an incremental cycle ergometer test, an incremental treadmill walking test with self-assessment of dyspnea on Borg's scale during exercise and an assessment of respiratory drive (P 0.1), timing [inspiration time (TI)/total breathing time (Ttot)], PaO2, PaCO2, FVC, FEV1, following oral administration for 14 days of placebo or buspirone (20 mg daily) in a double-blind, cross-over randomized way. We also used the symptom check list-90-R for the assessment of subjective complaints and symptomatic behavior. A significant improvement in anxiety, depression and obsessive symptoms and complaints was noted after buspirone treatment. The P 0.1, TI/Ttot, arterial blood gases and respiratory mechanics did not change after drug treatment. There was an improvement in exercise tolerance and in the sensation of dyspnea during the buspirone period. Thus, as given in this study, oral buspirone has therapeutic potential in the treatment of dyspnea in patients with chronic lung disease.
Adult↗
Ventilatory response to hypoxia in elderly humans.
In young adults the ventilatory response to 25 min of isocapnic hypoxia (SaO2 = 80%) is characterized by an initial increase in ventilation followed by a decline. The increase and decline are proportional. Because older adults have been reported to have reduced initial ventilatory responses to hypoxia, we compared responses to hypoxia in 14 older (mean age 62) and 15 younger (mean age 29) subjects. There was no difference. Both groups demonstrated a similar initial increase in ventilation with hypoxia and a similar subsequent decline due to a decline in tidal volume. In both groups the size of the initial increase was proportional to the subsequent decline. In both groups hyperoxia immediately after 25 min of hypoxia transiently depressed ventilation, while hyperoxia after room air breathing did not. We conclude that the ventilatory response to 25 min of hypoxia is independent of age in normal humans.
Adolescent↗