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PubMed1984

Respiratory function of hyoid muscles and hyoid arch.

The position of the hyoid arch suggests that it supports soft tissue surrounding the upper airway (UA) and can act to maintain UA patency. We also suspected that muscles inserting on the hyoid arch might show respiratory patterns of activity that could be affected by respiratory stimuli. To test these possibilities, we moved the hyoid arch ventrally in six anesthetized dogs either by traction on it or by stimulation of hyoid muscles. UA resistance was decreased 73 +/- (SE) 6% and 72 +/- 6% by traction and stimulation during expiration and 57 +/- 15% and 52 +/- 8% during inspiration. Moving averages of the geniohyoid (GH) and thyrohyoid (TH) obtained in six other dogs breathing 100% O2 showed phasic respiratory activity while the sternohyoid (SH) showed phasic respiratory activity in only two of these animals and no activity in four. With progressive hypercapnia, GH and TH increased as did SH when activity was already present. Airway occlusion at end expiration augmented and prolonged inspiratory activity in the hyoid muscles but did not elicit SH activity if not already present. Occlusion at end inspiration suppressed phasic activity in hyoid muscles for as long as in the diaphragm. After vagotomy activity increased and became almost exclusively inspiratory. Activity appeared in SH when not previously present. Duration and amplitude of hyoid muscle activity were increased with negative UA pressure and augmented breaths. We conclude that the hyoid arch and muscles can strongly affect UA flow resistance. Hyoid muscles show responses to chemical, vagal, and negative pressure stimuli similar to other UA muscles.

Airway Resistance↗
PubMed1984

Model analysis of tidal volume response to inspiratory elastic loads.

Based on experimental inspiratory driving pressure waveforms and active respiratory impedance data of anesthetized cats, we made model predictions of the factors that determine the immediate (first loaded breath) intrinsic (i.e., nonneural) tidal volume compensation to added inspiratory elastic loads. The time course of driving pressure (P) was given by P = atb, where a is the pressure at 1 s from onset of inspiration and represents the intensity of neuromuscular drive, t is time, and b is an index of the shape of the driving pressure wave. For a given active respiratory impedance, tidal volume compensation to added elastic loads decreases with increasing inspiratory duration and decreasing value of b but is independent of a. We have also assessed the validity of the "effective elastance" (Lynne-Davies et al., J. Appl. Physiol. 30: 512-516, 1971) as a predictor of tidal volume responses to elastic loads. In absence of vagal feedback, the effective elastance appears to be a reliable predictor, except for short inspiratory duration and a very high intrinsic resistance.

Airway Resistance↗
PubMed1985

Ontogeny of respiratory control and pulmonary mechanics in newborn rabbits.

Maturation of the respiratory pattern and the active and passive mechanical properties of the respiratory system were assessed in 19 tracheotomized rabbits (postnatal age range: 1-26 days) placed in a body plethysmograph. With maturation both minute ventilation and tidal volume significantly increased, whereas respiratory frequency decreased. When normalized for body weight (kg) both the passive (Rrs X kg) and active (R'rs X kg) resistances of the respiratory system significantly increased with age, whereas the corresponding passive (Crs X kg-1) and active (C'rs X kg-1) compliances significantly decreased. At any given age R'rs X kg only slightly exceeded Rrs X kg, whereas C'rs X kg-1 was significantly lower than Crs X kg-1. Moreover, the maturational increases in Rrs X kg and R'rs X kg exceeded the corresponding decreases in Crs X kg-1 and C'rs X kg-1, resulting in significant age-related increases in both the passive (tau rs) and active (tau'rs) time constants of the respiratory system. Due to the age-related increases in tau'rs, producing a delayed volume response to any given inspiratory driving pressure, the relative volume loss obtained at any time during inspiration was greater in the maturing rabbit. On the other hand, because of concomitant compensatory changes in respiratory pattern, evidenced by increases in inspiratory duration with age, the end-inspiratory tidal volume loss in the maturing animal was maintained generally less than 10% at all postnatal ages. Thus maturational changes in respiratory pattern appear coupled to changes in the active mechanical properties of the respiratory system. The latter coupling serves to optimize the transduction of inspiratory pressure into volume change in a manner consistent with establishing the minimum inspiratory work of breathing during postnatal development.

Age Factors↗
PubMed1985

Effects of breathing pattern on inspiratory muscle endurance in humans.

Endurance of the inspiratory muscles was measured in normal volunteers using a threshold resistance that produced a relatively constant mouth-pressure load, independent of inspiratory flow rate (VTI). Breathing pattern was controlled by visual feedback from an oscilloscope. Endurance was measured as the length of time (Tlim) a target VTI could be maintained with maximum effort. Effects of changes in breathing pattern on Tlim were compared with control measurements made the same day. Increases in VTI or in duty cycle (inspiratory time/total period) shortened Tlim, whereas decreases lengthened Tlim. However, effects of changes in VTI were less than equivalent changes in tidal volume produced by alterations in duty cycle. Furthermore, when two breathing pattern changes were altered simultaneously to keep the rate of external inspiratory work (Winsp) constant, significant effects due to changes in duty cycle were still observed. In conclusion, 1) both VTI and duty cycle have significant effects on measurements of inspiratory muscle endurance and 2) the effects of VTI are less than the effects of duty cycle for the same Winsp.

Adult↗
PubMed1986

Ventilatory response to sustained hypoxia in normal adults.

We examined the ventilatory response to moderate (arterial O2 saturation 80%), sustained, isocapnic hypoxia in 20 young adults. During 25 min of hypoxia, inspiratory minute ventilation (VI) showed an initial brisk increase but then declined to a level intermediate between the initial increase and resting room air VI. The intermediate level of VI was a plateau that did not change significantly when hypoxia was extended up to 1 h. The relation between the amount of initial increase and subsequent decrease in ventilation during constant hypoxia was not random; the magnitude of the eventual decline correlated confidently with the degree of initial hyperventilation. Evaluation of breathing pattern revealed that during constant hypoxia there was little alteration in respiratory timing and that the changes in VI were related to significant alterations in tidal volume and mean inspiratory flow (VT/TI). None of the changes was reproduced during a sham control protocol, in which room air was substituted for the period of low fractional concentration of inspired O2. We conclude that ventilatory response to hypoxia in adults is not sustained; it exhibits some biphasic features similar to the neonatal hypoxic response.

Adult↗
PubMed1989

Aminophylline effects on ventilatory response to hypoxia and hyperoxia in normal adults.

In 10 normal young adults, ventilation was evaluated with and without pretreatment with aminophylline, an adenosine blocker, while they breathed pure O2 1) after breathing room air and 2) after 25 min of isocapnic hypoxia (arterial O2 saturation 80%). With and without aminophylline, 5 min of hyperoxia significantly increased inspiratory minute ventilation (VI) from the normoxic base line. In control experiments, with hypoxia, VI initially increased and then declined to levels that were slightly above the normoxic base line. Pretreatment with aminophylline significantly attenuated the hypoxic ventilatory decline. During transitions to pure O2 (cessation of carotid bodies' output), VI and breathing patterns were analyzed breath by breath with a moving-average technique, searching for nadirs before and after hyperoxia. On placebo days, at the end of hypoxia, hyperoxia produced nadirs that were significantly lower than those observed with room-air breathing and also significantly lower than when hyperoxia followed normoxia, averaging, respectively, 6.41 +/- 0.52, 8.07 +/- 0.32, and 8.04 +/- 0.39 (SE) l/min. This hypoxic depression was due to significant decrease in tidal volume and prolongation of expiratory time. Aminophylline partly prevented these alterations in breathing pattern; significant posthypoxic ventilatory depression was not observed. We conclude that aminophylline attenuated hypoxic central depression of ventilation, although it does not affect hyperoxic steady-state hyperventilation. Adenosine may play a modulatory role in hypoxic but not in hyperoxic ventilation.

Adenosine↗
PubMed1989

Increased chemoreceptor output and ventilatory response to sustained hypoxia.

In adult humans the ventilatory response to sustained hypoxia (VRSH) is biphasic, characterized by an initial brisk increase, due to peripheral chemoreceptor (PC) stimulation, followed by a decline attributed to central depressant action of hypoxia. To study the effects of selective stimulation of PC on the ventilatory response pattern to hypoxia, the VRSH was evaluated after pretreatment with almitrine (A), a PC stimulant. Eight subjects were pretreated with A (75 mg po) or placebo (P) on 2 days in a single-blind manner. Two hours after drug administration, they breathed, in succession, room air (10 min), O2 (5 min), room air (5 min), hypoxia [25 min, arterial O2 saturation (SaO2) = 80%], O2 (5 min), and room air (5 min). End-tidal CO2 was kept constant at the normoxic base-line values. Inspiratory minute ventilation (VI) and breathing patterns were measured over the last 2 min of each period and during minutes 3-5 of hypoxia, and nadirs in VI were assessed just before and after O2 exposure. Independent of the day, the VRSH was biphasic. With P and A pretreatment, early hypoxia increased VI 4.6 +/- 1 and 14.2 +/- 1 (SE) l/min, respectively, from values obtained during the preceding room-air period. On A day the hypoxic ventilatory decline was significantly larger than that on P day, and on both days the decline was a constant fraction of the acute hypoxic response.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Breathing during sleep with mild hypoxia.

To investigate ventilatory response to mild hypoxia during non-rapid-eye-movement sleep, we administered approximately 16% O2 (which corresponds to concentrations found in commercial high altitude air craft) to 12 normal subjects by using a Venturi mask, which did not alter the breathing pattern during this study. Under mild hypoxia, inspiratory minute ventilation during sleep showed an initial rapid increase (P less than 0.001) but then declined significantly (P less than 0.001) and stabilized. Stable levels differed among individuals and, compared with those measured before hypoxia, were significantly lower in some subjects, higher in one, and essentially unchanged in the others. The initial rapid increase in minute ventilation after mild hypoxia during sleep correlated with the respective values of hypoxic ventilatory response during the awake state (P less than 0.01), but the final lowered levels did not. We conclude that the ventilatory response after mild hypoxia during sleep is biphasic and hypoxic depression exerts considerable influence on ventilation under mild hypoxia during sleep. So we should take hypoxic depression into consideration to evaluate the response to hypoxia during sleep.

Adult↗
PubMed1989

Naloxone alters the early response to an inspiratory flow-resistive load.

In a previous study in unanesthetized goats, we demonstrated that cerebrospinal fluid levels of beta-endorphin were significantly elevated after 2.5 h of inspiratory flow-resistive loading. Naloxone (NLX) (0.1 mg/kg) administration partially and transiently reversed the tidal volume depression seen during loading. In the current study, we tested the hypothesis that endogenous opioid elaboration results in depression of respiratory output to the diaphragm. In six studies of five unanesthetized goats, tidal volume (VT), transdiaphragmatic pressure (Pdi), diaphragmatic electromyogram (EMGdi), and arterial blood gases were monitored. A continuous NLX (0.1 mg/kg) or saline (SAL) infusion was begun 5 min before an inspiratory flow-resistive load of 120 cmH2O.l-1.s was imposed. Our data show that the depression of VT induced by the load was prevented by NLX as early as 15 min and persisted for 2 h. At 2 h, Pdi was still 294 +/- 45% of the base-line value compared with 217 +/- 35% during SAL. There was no difference in EMGdi between the groups at any time. However, the augmentation of Pdi was associated with a greater increase in end-expiratory gastric pressure in the NLX group. We conclude that the reduction in VT and Pdi associated with endogenous opioid elaboration is not mediated by a decrease in neural output to the diaphragm, but it appears to be the result of a decrease in respiratory output to the abdominal muscles.

Airway Resistance↗
PubMed1990

Sensation of inspired volumes and pressures in professional wind instrument players.

Previous studies have failed to show consistent differences in pulmonary function between wind instrument musicians and normal controls. In this study, respiratory sensation was assessed in 13 professional wind instrument players and 13 age-matched controls. Psychophysical techniques were used to assess magnitude estimation and reproduction of lung volumes and inspiratory pressures. The exponent for volume magnitude estimation was not different in musicians and controls (1.17 +/- 0.11 vs. 1.16 +/- 0.11), but volume reproduction was more accurate in musicians. The mean exponent for pressure magnitude estimation was 1.34 +/- 0.14 and 1.06 +/- 0.09 (P = 0.057) in musicians and controls, respectively. There was no difference between groups for absolute or constant error for pressure reproduction. Professional wind instrument players appear to have some inherent or acquired differences in respiratory perception and ventilatory neuromuscular control compared with other normal subjects.

Adult↗
PubMed1993

Modulation of maximal inspiratory airflow by neuromuscular activity: effect of CO2.

To determine how maximal inspiratory airflow (VImax) is modulated by changes in airway neuromuscular activity, we analyzed pressure-flow relationships obtained during inspiration and expiration in isolated upper airways of anesthetized hyperoxic dogs at different levels of CO2. Inspiratory airflow (VI), hypopharyngeal pressure (Php), pharyngeal pressure at the flow-limiting site (FLS), and alae nasi (AN) and genioglossus (GG) electromyographic (EMG) activity were recorded while VI limitation was produced by rapidly lowering Php until VI plateaued at VImax. VImax and its mechanical determinants, pharyngeal critical pressure (Pcrit) and nasal resistance (Rn) upstream to the FLS, were measured. During hypercapnia (high CO2), VImax increased significantly during inspiration (217.3) and expiration (184.1%). These increases were associated with significant increases in phasic but not tonic AN and GG activity. They were also associated with decreases in Pcrit from -6.2 +/- 1.6 (SE) at hypocapnia to -9.3 +/- 3.0 and -11.8 +/- 3.4 cmH2O at high CO2 during expiration and inspiration, respectively. No significant changes in Rn occurred. When phasic neuromuscular activity was abolished by complete neuromuscular blockade in three dogs, these increases in VImax and decreases in Pcrit at high CO2 were eliminated. When phasic EMG activity was accentuated in four vagotomized dogs, significant increases in VImax and decreases in Pcrit were demonstrated during inspiration vs. expiration at high CO2. These findings indicate that upper airway neuromuscular activity increases VImax in the isolated upper airway by decreasing collapsibility (Pcrit) at the FLS site when neuromuscular activity is stimulated by hypercapnia.

Animals↗
PubMed1993

Expiratory flow limitation and regulation of end-expiratory lung volume during exercise.

To investigate the impact of expiratory flow limitation (FL) on breathing pattern and end-expiratory lung volume (EELV), we imposed a small expiratory threshold load for a few breaths during exercise in nine volunteers (29-62 yr): six were healthy and three had mild-to-moderate airflow obstruction (67-71% predicted forced expiratory volume in 1 s). Six subjects showed evidence of FL, i.e., tidal expiratory flow impinging on maximal forced expiratory flow, at one or more exercise levels. Whenever an expiratory threshold load was imposed, mean expiratory flow decreased (P < 0.02) in association with an increased expiratory time (TE; P < 0.05). When the load was imposed during non-FL conditions, TE increased less than expiratory flow decreased and EELV tended to increase. In contrast, during FL, with the load, TE increased more than expiratory flow decreased, subjects did not achieve maximal expiratory flow until a lower volume, and EELV decreased (P < 0.001). Under both FL and no-FL conditions, unloading reversed the changes associated with loading. These data indicate that the increase in EELV during exercise is linked to the occurrence of FL. We suggest that compression of airways downstream from the flow-limiting segment may elicit a reflex mechanism that influences breathing pattern by terminating expiration prematurely, thus increasing EELV.

Adult↗
PubMed1993

Effects of continuous negative airway pressure-related lung deflation on upper airway collapsibility.

Continuous negative airway pressure (CNAP) causes a decrease in lung volume, which is known to increase upper airway resistance by itself. We studied how this lung volume change could modify upper airway collapsibility with five normal awake subjects. In a first trial, pressure in a nasal mask (Pm) was progressively decreased in 3- to 5-cmH2O steps (CNAP). In a second trial, changes in lung volumes resulting from CNAP were prevented by applying simultaneously an equivalent level of negative extrathoracic pressure into a poncho-type respirator [isovolumetric CNAP (CNAPisovol)]. For each trial, we examined the relationship between the maximal inspiratory airflow of each flow-limited inspiratory cycle and the corresponding Pm by least-squares linear regression analysis and determined the critical pressure. We also determined the Pm threshold corresponding to the first Pm value below which flow limitation occurred. Flow limitation was observed in each subject with CNAP but in only two subjects with CNAPisovol. In these two subjects, the Pm threshold values were -20 and -9 cmH2O with CNAP and -39 and -16 cmH2O with CNAPisovol, respectively. Critical pressures for the same two subjects were -161 and -96 cmH2O with CNAP and -202 and -197 cmH2O with CNAPisovol, respectively. We conclude that CNAP-induced decreases in lung volume increase upper airway collapsibility.

Adult↗
PubMed2002

Determinants of exercise performance in normal men with externally imposed expiratory flow limitation.

To understand how externally applied expiratory flow limitation (EFL) leads to impaired exercise performance and dyspnea, we studied six healthy males during control incremental exercise to exhaustion (C) and with EFL at approximately 1. We measured volume at the mouth (Vm), esophageal, gastric and transdiaphragmatic (Pdi) pressures, maximal exercise power (W(max)) and the difference (Delta) in Borg scale ratings of breathlessness between C and EFL exercise. Optoelectronic plethysmography measured chest wall and lung volume (VL). From Campbell diagrams, we measured alveolar (PA) and expiratory muscle (Pmus) pressures, and from Pdi and abdominal motion, an index of diaphragmatic power (W(di)). Four subjects hyperinflated and two did not. EFL limited performance equally to 65% W(max) with Borg = 9-10 in both. At EFL W(max), inspiratory time (TI) was 0.66s +/- 0.08, expiratory time (TE) 2.12 +/- 0.26 s, Pmus approximately 40 cmH2O and DeltaVL-DeltaVm = 488.7 +/- 74.1 ml. From PA and VL, we calculated compressed gas volume (VC) = 163.0 +/- 4.6 ml. The difference, DeltaVL-DeltaVm-VC (estimated blood volume shift) was 326 ml +/- 66 or 7.2 ml/cmH2O PA. The high Pmus and long TE mimicked a Valsalva maneuver from which the short TI did not allow recovery. Multiple stepwise linear regression revealed that the difference between C and EFL Pmus accounted for 70.3% of the variance in DeltaBorg. DeltaW(di) added 12.5%. We conclude that high expiratory pressures cause severe dyspnea and the possibility of adverse circulatory events, both of which would impair exercise performance.

Adult↗
PubMedDate not supplied

Ventilatory care in status asthmaticus.

Asthma continues to pose a significant medical problem in terms of both morbidity and mortality. A number of patients with a severe exacerbation of asthma fail medical therapy and require urgent intubation and mechanical ventilation. New modalities of ventilatory support, including noninvasive ventilation, have been shown to provide effective ventilation even in the presence of severe bronchoconstriction. An intrinsically high level of auto positive end-expiratory pressure in these patients requires a precise balance between respiratory frequency, tidal volume and inspiratory flow rates. Pressure support ventilation reduces the risk of barotrauma and lowers the work of breathing in these patients. Adjuvant therapy with inhaled anesthetics and bronchoalveolar lavage may also be indicated in patients requiring high pressures to achieve adequate ventilation.

Anesthetics, Inhalation↗
PubMed2001

Assessment of maximum inspiratory pressure. Prior submaximal respiratory muscle activity ('warm-up') enhances maximum inspiratory activity and attenuates the learning effect of repeated measurement.

BACKGROUND: The variability of maximal inspiratory pressure (PImax) in response to repeated measurement affects its reliability; published studies have used between three and twenty PImax measurements on a single occasion. OBJECTIVE: This study investigated the influence of a specific respiratory 'warm-up' upon the repeated measurement of inspiratory muscle strength and attempts to establish a procedure by which PImax can be assessed with maximum reliability using the smallest number of manoeuvres. METHODS: Fourteen healthy subjects, familiar with the Mueller manoeuvre, were studied. The influence of repeated testing on a single occasion was assessed using an 18-measurement protocol. Using a randomised cross-over design, subjects performed the protocol, preceded by a specific respiratory warm-up (RWU) and on another occasion, without any preliminary activity (control). Comparisons were made amongst 'baseline' (best of the first 3 measurements), 'short' series (best of 7th to 9th measurement) and 'long' series (best of the last 3 measurements). RESULTS: Under control conditions, the mean increase ('baseline' vs. 'long' series) was 11.4 (5.8)%; following the RWU, the increase (post RWU 'baseline' vs. 'long' series) was 3.2 (10.0)%. There were statistically significant differences between measurements made at all 3 protocol stages ('baseline', 'short' and 'long' series) under control conditions, but none following the RWU. CONCLUSIONS: The present data suggest that a specific RWU may attenuate the 'learning effect' during repeated PImax measurements, which is one of the main contributors of the test variability. The use of a RWU may provide a means of obtaining reliable values of PImax following just 3 measurements.

Adult↗
PubMed2001

Is there a need for another inhalative beta(2)-agonist besides formoterol in patients with asthma?

Formoterol can substitute the rapid- and short-acting beta(2)-agonists as well as the slow- and long-acting salmeterol. Therefore formoterol in a fixed combination with an inhalant steroid reduces the aerosol devices necessary for asthma control to only one, to be used for regular "controller" and, as needed, "rescue therapy". The side effect profile of formoterol is comparable to the short-acting beta(2)-agonists which makes the combination with a topically active glucocorticoid applicable in patients of any asthma severity as long as they are able to perform an inspiratory vital capacity maneuver

Administration, Topical↗