Continuous Negative Airway Pressure Research Articles

Continuous negative airway pressure “CNAP”: Novel nasal foreign body removal

<p class="abstract"><span lang="EN-IN">We report on a novel and innovative method used to extricate nasal foreign bodies in infants and young children– a common presentation in pediatric emergency care that can at times have potentially serious consequences. In the case of a three-year-old girl, ‘continuous negative airway pressure (CNAP)’ using a continuous positive airway pressure (CPAP) mask and a domestic vacuum cleaner, a nasal foreign body was removed quickly and effectively in a simple and painless procedure. While more cases are needed to confirm safety and efficacy, the principles underlying this technique could have great potential for future clinical use due to its simplicity and accessibility, particularly when compared to other techniques currently used in the home and in the emergency department.</span></p>

Intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs

The intrathoracic pressure regulator (ITPR) was created to improve hemodynamics by generating continuous negative airway pressure between positive pressure ventilations to enhance cardiac preload in apnoeic animals. In normovolemic and hypovolemic pigs, we tested the hypothesis that continuous negative intrathoracic pressure set at -5 or -10mmHg, interrupted only for intermittent positive pressure ventilations, would decrease intracranial (ICP) and right atrial (RAP) pressure, and increase mean arterial pressure (MAP). Twelve pigs were anesthetized with propofol and ventilated with a bag. The ITPR was used to vary baseline endotracheal pressures (ETPs) for 5min periods in the following sequence: 0, -5, 0, -10, 0mmHg under normovolemic conditions. Six pigs were bled 50% (32.5+/-mL/kg) of their estimated blood volume and the airway pressure sequence was repeated. Six other pigs were bled 35% (22.75+/-mL/kg) of their estimated blood volume and the same airway pressure sequence was repeated. Intracranial, aortic, right atrial pressures, arterial blood gases, end tidal CO(2) (ETCO(2)), were measured. ANOVA was used for statistical analysis. Linear regression analysis was performed for ETP and ICP. Mean arterial and vital organ perfusion pressures were significantly improved and RA pressure significantly decreased with the use of the ITPR; the effect was greater with the more negative ETPs and lower circulating blood volume. The change of ICP was linearly related to the ETP and blood loss: DeltaICP=[1.22-0.84(1-%blood loss/100)]xETP, r(2)=0.88 (in mmHg), p<0.001. There were no adverse device effects and there was a significant increase of ETCO(2) with the use of ITPR. The ITPR decreased RAP and ICP significantly and improved mean arterial and cerebral and coronary perfusion pressures without affecting acid base balance severely. The decrease in ICP was directly proportional to the reduction in intrathoracic pressure. The effects were more pronounced in severe hypovolemic and hypotensive states with more negative ETP pressure.

Respiratory impedance response to continuous negative airway pressure in awake controls and OSAS

The aim of the study was to determine whether the response of respiratory impedance (Zrs) to decreasing levels of continuous negative airway pressure (CNAP) during wakefulness, differs in controls and subjects with obstructive sleep apnoea syndrome (OSAS). Zrs was measured by the forced oscillation technique (4-32 Hz) in 15 controls and 21 patients with OSAS (apnoea/hypopnoea index >20 per sleep hour) with normal lung function, in the basal state and with application of decreasing CNAP of -5, -10, and -15 hPa. Respiratory resistance was extrapolated to 0 Hz (R0) and estimated at 16 Hz (R16) by linear regression analysis of respiratory resistive impedance versus frequency. Respiratory elastance (Ers) and inertance (Irs) were estimated by multilinear regression analysis of respiratory reactance versus frequency, and resonance frequency (RF) was determined as RF=(1/2pi)(Ers/Irs)0.5. In both groups, R0, R16, Ers and RF significantly increased as the CNAP level decreased (p <0.0001 for all). R0, Ers, and RF increased significantly more in OSAS than in controls (p < 0.01, 0.001, and 0.0001, respectively), independently of the severity of obesity. Receiver operator characteristic curves showed that the parameter which best detected OSAS was RF, with a sensitivity of 81% and 93% specificity for the 13.6 Hz cut-off point. The results of the present study suggest that the response of respiratory impedance to decreasing continuous negative airway pressure levels, might allow detection of obstructive sleep apnoea syndrome in subjects with normal lung function.

Effects of continuous negative airway pressure on lung volume and respiratory resistance.

This study was designed to determine the responses of lung volume and respiratory resistance (Rrs) to decreasing levels of continuous negative airway pressure (CNAP). Twenty normal subjects were studied in the basal state and under CNAP levels of -5, -10, and -15 hPa. Rrs was measured by the forced oscillation technique (4-32 Hz). End-expiratory lung volume (EELV) and tidal volume (VT) were measured by whole body plethysmography. Rrs was extrapolated to 0 Hz (R(0)) and estimated at 16 Hz (R(16)) by linear regression analysis of Rrs vs. frequency. Specific Rrs, SR(0) and SR(16), were then calculated as R(0) (EELV + VT/2) and R(16) (EELV + VT/2), respectively. EELV significantly decreased, whereas R(0), R(16), SR(0), and SR(16) significantly increased, as the CNAP level decreased (P < 0.0001 for all). At the lowest CNAP level, R(0) and R(16) reached 198 +/- 13 and 175 +/- 9% of their respective basal values. The CNAP-induced increase in R(0) was significantly higher than that in R(16) (P < 0.004). Our results demonstrate that the CNAP-induced increase in Rrs does not result from a direct lung volume effect only and strongly suggest the involvement of other factors affecting both intrathoracic and extrathoracic airway caliber.

Deflation-related variability of breathing pattern persists with intact upper airway

In anesthetized, tracheotomized rats continuous negative airway pressure (CNAP) augments breath-to-breath variability of the respiratory pattern compared to that during continuous positive airway pressure (CPAP). To test the hypothesis that loss of airflow regulation by the upper airway was responsible for this increased variability during CNAP we measured respiratory pattern regularity in rats with intact airways subjected to steady inflating and deflating transrespiratory pressures. The coefficients of variation of tidal volume, peak inspiratory flow, and rate of change of flow at end-inspiration were larger during deflation maneuvers than during inflations, whereas the coefficients of variation of inspiratory and expiratory durations were not different. A variable degree of expiratory flow retardation often was observed during deflation. We conclude that breathing through the upper airway does not prevent the increase in variability of the respiratory pattern associated with deflation.

Upper airway collapsibility, and contractile and metabolic characteristics of musculus uvulae

Physiologic, metabolic, and histochemical characteristics of one upper airway (UA) dilator muscle (musculus uvulae; MU) differ between sleep apnea hypopnea syndrome (SAHS) and nonapneic snorers. We hypothesized that these differences in MU characteristics could result from the cumulative effects of the diurnal and nocturnal intermittent contractions of UA muscles in order to compensate for a permanent increase in UA collapsibility. The aim of this study was to determine the influence of UA collapsibility on MU characteristics. Seventeen SAHS and three nonapneic snorers, who underwent an uvulo-palato-pharyngoplasty as a treatment for snoring or SAHS, participated in the study. Awake and sleeping UA critical pressure (Pcrit) was measured during continuous positive or negative airway pressure trials by analysis of the relationship between maximal inspiratory flow and the upstream pressure of flow-limited breathing cycles. Maximum isometric twitch (Pt) and tetanic tension (Po), fatigability measurements, activities of marker enzymes for anaerobic and aerobic-oxidative profile, and fiber type proportions and areas of MU were determined. There was a significant positive relationship between Pt, Po, and Pcrit measured during wakefulness and sleep. The fatigability index was negatively correlated with awake Pcrit values (r = -0.79). Activity level of the anaerobic enzymes as well as the percentage of surface occupied by type I and type IIA muscle fibers as correlated witb awake Pcrit. We conclude that the differences in awake UA collapsibility help to determine the contractile properties and metabolic and histochemical characteristics of MU.

Effects of genioglossal response to negative airway pressure on upper airway collapsibility during sleep

Continuous negative airway pressure (CNAP) trials can be used to measure upper airway (UA) collapsibility. This procedure can be accompanied by an increase in UA muscle activity. The purpose of this study was to evaluate the influence of CNAP-induced increase in genioglossal (GG) activity on UA collapsibility in 10 healthy sleeping men. UA collapsibility was measured on two occasions; each recording was preceded by the administration of a placebo or diazepam (0.15 mg/kg) in a randomized double-blind crossover design. In seven subjects, the decrease in mask pressure (Pmask) was associated with an increase in mean GG electromyographic (EMG) activity during the placebo trial, with a significant negative relationship between these two variables. This relationship was still observed with diazepam. In six subjects, the slope of the relationship between mean EMG and Pmask was less negative with diazepam. This was associated with an increase in critical pressure (Pcrit). With the placebo, a positive relationship was found between Pcrit and the slope of the mean EMG/Pmask relationship. We conclude that Pcrit is influenced by the GG response to the decrease in Pmask during CNAP.

Histamine-induced end-tidal inspiratory activity and lung receptors in cats.

Hyperinflation in acute asthma has been associated with inspiratory muscle activity, which persist during expiration. The main objective of the present study was to evaluate the role of rapidly adapting receptors (RARs), slowly adapting receptors (SARs) and C-fibre endings in generating end-tidal inspiratory activity (ETIA). ETIA was induced by intravenous administration of histamine and continuous negative airway pressure (CNAP) in anaesthetized, spontaneously breathing cats. To differentiate between reflex activities from the three types of lung receptors, both vagus nerves were cooled to eight different temperatures (Tvg) between 4 and 37 degrees C. It is known that CNAP stimulates RARs and inhibits SARs. Histamine was used to stimulate RARs, and this was combined with continuous positive airway pressure (CPAP) to further stimulate SARs. ETIA was evoked in the diaphragm and in parasternal intercostal muscles by both stimuli (histamine and CNAP) in 8 out of 18 cats. After vagotomy, neither histamine nor CNAP evoked ETIA any more. At Tvg = 37 degrees C, CPAP suppressed histamine-induced ETIA; whereas, this suppression was diminished at Tvg between 14 and 8 degrees C. ETIA sharply declined for Tvg between 8 degrees and 4 degrees C, and at Tvg = 4 degrees C ETIA had virtually disappeared. At Tvg = 37 degrees and 22 degrees C values of ETIA during CNAP were larger than those in response to histamine; whereas, at Tvg = 10 degrees C comparable ETIA values were obtained. It was shown that ETIA is a vagal reflex activity in which C-fibre endings are not involved. Histamine-induced ETIA originates from stimulation of RARs, and is inhibited by stimulation of SARs. Mechanical stimulation of RARs is a forceful stimulus to induce ETIA. This suggests that hyperinflation in acute asthma might be due, at least in part, to ETIA resulting from an imbalance between SAR and RAR activity.

Regional Blood Volume Distribution during Positive and Negative Airway Pressure Breathing in Supine Humans

Institute fur Experimentelle und Kiinische Anasthesiologie, Heinrich-Heine-Universitat, Dusseldorf, Germany, and Abeteilung fur Medizin, Kernforschungsanlage, Julich, Germany

Continuous negative airway pressure increases tonic activity in diaphragm and intercostal muscles in humans

The main objective of the present study was to quantify the increase in tonic inspiratory activity (delta TIA) in response to continuous negative airway pressure (CNAP) in humans. TIA represents the activity in inspiratory muscles at the end of expiration. In 20 subjects, electromyograms (EMGs) were recorded from the diaphragm and parasternal intercostal muscles (ICM) with surface electrodes during control and at three different levels of CNAP (-0.3, -0.6, and -0.9 kPa; 1 kPa approximately 10 cmH2O). From these recordings we determined delta TIA and the amplitudes of phasic EMG activities (EMGphas) during CNAP and control. To evaluate the effects of CNAP on functional residual capacity (FRC), respiratory frequency, tidal volume, and minute ventilation, the subjects were connected to a closed breathing circuit. When the pressure at the airway opening was -0.9 kPa, mean values of delta TIA were 53 and 49% of control EMGphas for the diaphragm and ICM, respectively. In addition, EMGphas at airway opening pressure of -0.9 kPa had increased to 195 and 162% of control EMGphas for the diaphragm and ICM, respectively. The concomitant decrease in FRC was on average 18.7% of predicted FRC. Minute ventilation had increased significantly (P < 0.05) at all levels of CNAP compared with control. We conclude that CNAP is a forceful stimulus to increase TIA in humans in both the diaphragm and the ICM.

Influence of lung volume dependence of upper airway resistance during continuous negative airway pressure

To quantify the contribution of lung volume dependence of upper airway (UA) on continuous negative airway pressure (CNAP)-induced increase in upper airway resistance, we compared the changes in supralaryngeal resistance during an isolated decrease in lung volume and during CNAP in eight normal awake subjects. Inspiratory supralaryngeal resistance was measured at isoflow during four trials, during two CNAP trials where the pressure in a nasal mask was progressively decreased in 3- to 5-cmH2O steps and during two continuous positive extrathoracic pressure (CPEP) trials where the pressure around the chest (in an iron lung) was increased in similar steps. The CNAP and CPEP trials were done in random order. During the CPEP trial, the neck was covered by a rigid collar to prevent compression by the cervical seal of the iron lung. In each subject, resistance progressively increased during the experiments. The increase was linearily correlated with the pressure increase in the iron lung and with the square of the mask pressure during CNAP. There was a highly significant correlation between the rate of rise in resistance between CNAP and CPEP: the steeper the increase in resistance with decreasing lung volume, the steeper the increase in resistance with decreasing airway pressure. Lung volume dependence in UA resistance can account for 61% of the CNAP-induced increase in resistance. We conclude that in normal awake subjects the changes in supralaryngeal resistance induced by CNAP can partly be explained by the lung volume dependence of this resistance.

Regional blood volume distribution during positive and negative airway pressure breathing in supine humans

To assess the effects of continuous positive (CPAP) or negative airway pressure (CNAP) breathing (+/- 10-12 cmH2O, duration 25 min) on blood content in the body's capacitance vasculature, regional distribution of labeled red blood cells was evaluated in seven spontaneously breathing supine volunteers. Counts were acquired by whole body scans and detectors overlying the liver, intestine, left ventricle, and lower arm, and arterial pressure, heart rate, calf blood flow and vascular resistance, hematocrit, vasopressin, and atrial natriuretic peptide plasma concentrations were also obtained. With CPAP, thoracic, cardiac, and left ventricular counts diminished significantly by 7-10%, were accompanied by significant increases in counts over both the gut and liver, and remained decreased during CPAP but reversed to baseline with zero airway pressure. Calf blood flow and vascular resistance significantly decreased and increased, respectively, whereas limb counts, arterial pressure, heart rate, and hormone concentrations remained unchanged. With CNAP, in contrast, regional counts and other variables did not change. Thus, moderate levels of CPAP deplete the intrathoracic vascular bed and heart, shifting blood toward the gut and liver but not toward the limbs. No short-term compensation increasing cardiac filling during CPAP was seen. In contrast, CNAP did not alter intrathoracic or organ blood content and, therefore, does not simply mirror the effects evoked by CPAP.

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.

Tonic activity in inspiratory muscles during continuous negative airway pressure

We studied tonic inspiratory activity (TIA) induced by continuous negative airway pressure (CNAP) in anaesthetized, spontaneously breathing cats. TIA in the diaphragm and parasternal intercostal muscles (ICM) was quantified in response to tracheal pressure P tr = −0.3 to −1.2 kPa . To differentiate between reflexes from rapidly adapting receptors (RARs), slowly adapting receptors (SARs) and C-fiber endings different temperatures of the vagus nerves (T vg) were used between 4 and 37°C. at P tr = −1.2 kPa mean TIA values were 41% and 62% of peak inspiratory EMG activity of control breaths for the diaphragm and ICM, respectively. After vagotomy and for T vg < 6° C CNAP did not induce TIA anymore. Changes in inspiratory and expiratory time during vagal cooling down to 4°C confirmed the selective block of conductance in vagal afferents of the three types of lung receptors. We conclude that CNAP-induced TIA results from stimulations of RARs. Our data strongly indicate that stimulation of SARs suppresses TIA, wereas C-fiber endings are not involved in TIA at all. The results suggest that part of the hyperinflation in bronchial asthma may be caused by TIA in response to mechanical stimulation of RARs.

Upper Airway Distensibility and Collapsibility in Patients with Obstructive Sleep Apnea

The present study was performed to evaluate the distensibility and collapsibility characteristics of regional segments of the UA in patients with OSA and in normal subjects in response to changes in airway pressure. Seventeen male patients with moderately severe OSA and 13 normal subjects underwent CT of the UA in the supine position while awake. Axial views were obtained from the level of the hard palate to the hypopharynx under conditions of -5, 0, and +10 cm H2O of CAP. The results indicated that the Amin occurred within 20 mm of the hard palate in the retropalatal region of the UA in 16 (94 percent) of the 17 patients and in 12 (92 percent) of the 13 normal subjects. Continuous negative airway pressure of -5 cm H2O failed to significantly decrease either Amin or Amean in either the patients or normal subjects, suggesting good UA load compensation during wakefulness. Continuous positive airway pressure of 10 cm H2O significantly increased Amin and Amean to a similar extent in both groups. The Amin was significantly smaller by 40 percent, 33 percent, and 37 percent in the patients with OSA, compared to the normal subjects, at -5, 0, and +10 cm H2O of CAP, respectively. In contrast, Amean did not differ between the groups. The CT scan criterion of Amin less than or greater than 1.0 cm2 during tidal ventilation of atmospheric pressure correctly categorized patients with OSA and normal subjects with an accuracy of 70 percent. While the behavior of the UA in response to nasal CPAP and CNAP failed to increase the accuracy of CT scan criteria to a level sufficient for clinical use in the diagnosis of OSA, the results clearly indicate that structural changes in the UA contribute to the development of OSA.

The influence on the breathing pattern in man of moderate levels of continuous positive and negative airway pressure and of positive end‐expiratory pressure during air and CO2 inhalation

The purpose of this study was to determine in man the effect on the breathing pattern of continuous positive (CPAP), continuous negative (CNAP) and positive end-expiratory (PEEP) airway pressure during air breathing and CO2 inhalation. Six subjects were exposed to CPAP, CNAP and PEEP 0.5 kPa, while five subjects were exposed to CPAP and CNAP 0.8 kPa. End-expiratory lung volume increased during CPAP 0.8 kPa and decreased during CNAP 0.8 kPa. CPAP induced more extensive changes in the ventilatory pattern, and the changes in each parameter were larger than observed during CNAP and PEEP at the same pressure level. In contrast to previous reports we found the effect of CO2 inhalation combined with the effect of pressure breathing to be not stronger than additive. Even moderate CPAP induced alveolar hyperventilation with marked reduction in arterial PCO2 (PaCO2) when breathing air. With increasing fraction of CO2 in the inspiratory gas, the difference in PaCO2 between CPAP and no CPAP disappeared. PEEP also affected the breathing pattern in that it induced an increase in mean inspiratory flow and mean expiratory flow and a reduction in inspiratory duration. Occurrence of ventilatory pauses depended on whether mouthpiece or facemask was used. CPAP and CNAP did not influence the occurrence of pauses, while PEEP prolonged post-expiratory pauses. We conclude that CPAP, CNAP and PEEP induce active ventilatory responses in man and that strong mechanisms are involved during CPAP since PaCO2 is markedly reduced.

Upper airway and respiratory muscle responses to continuous negative airway pressure

To determine upper airway and respiratory muscle responses to nasal continuous negative airway pressure (CNAP), we quantitated the changes in diaphragmatic and genioglossal electromyographic activity, inspiratory duration, tidal volume, minute ventilation, and end-expiratory lung volume (EEL) during CNAP in six normal subjects during wakefulness and five during sleep. During wakefulness, CNAP resulted in immediate increases in electromyographic diaphragmatic and genioglossal muscle activity, and inspiratory duration, preserved or increased tidal volume and minute ventilation, and decreased EEL. During non-rapid-eye-movement and rapid-eye-movement sleep, CNAP was associated with no immediate muscle or timing responses, incomplete or complete upper airway occlusion, and decreased EEL. Progressive diaphragmatic and genioglossal responses were observed during non-rapid-eye-movement sleep in association with arterial O2 desaturation, but airway patency was not reestablished until further increases occurred with arousal. These results indicate that normal subjects, while awake, can fully compensate for CNAP by increasing respiratory and upper airway muscle activities but are unable to do so during sleep in the absence of arousal. This sleep-induced failure of load compensation predisposes the airways to collapse under conditions which threaten airway patency during sleep. The abrupt electromyogram responses seen during wakefulness and arousal are indicative of the importance of state effects, whereas the gradual increases seen during sleep probably reflect responses to changing blood gas composition.

Volume, flow, and timing of each breath during negative airway pressure in humans.

We have analyzed the effects of 4-6 min of 5, 10 and 15 cmH2O continuous negative airway pressure breathing (NPB) on steady-state end-expiratory lung volume (delta VR) and breathing pattern. Fourteen healthy adults, seated in a full body box, breathed via a mouthpiece on a bag-in-box. Pressure in the body box was elevated to the desired pressure level. Inspiratory (TI) and expiratory (TE) durations, tidal volume (VT), minute ventilation (VI), mean inspiratory flow (VT/TI), and mean expiratory flow (VT/TE) were calculated from pneumotachometer recordings. The effects of NPB are decreases in delta VR, VT, and VT/TI and increases in VT/TE. The responses to NPB are an increase in breathing frequency, due to a shortened TE, and an increase in inspiratory activity. The decrease in delta VR and the increase in VT/TE are limited by an active retardation of expiratory flow. End-tidal CO2 and VI were not altered significantly during NPB, suggesting no alveolar hyperventilation. Thus multiple components of the human response to NPB are not all engaged at the same levels of NPB. The changes in the timing of respiratory events occur at -5 cmH2O, whereas VT compensation is not seen until -15 cmH2O.

Immediate effects of positive-pressure breathing on the ventilatary response to CO2.

ArticleImmediate effects of positive-pressure breathing on the ventilatary response to CO2.D C Flenley, L D Pengelly, and J Milic-EmiliD C Flenley, L D Pengelly, and J Milic-EmiliPublished Online:01 Jan 1971https://doi.org/10.1152/jappl.1971.30.1.7MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByObstructive sleep apnea syndrome and asthma: the role of continuous positive airway pressure treatmentAnnals of Allergy, Asthma & Immunology, Vol. 101, No. 4Differential Inspiratory Muscle Pressure Contributions to Breathing during Dynamic HyperinflationAmerican Journal of Respiratory and Critical Care Medicine, Vol. 156, No. 2Measurements of PEEP-Induced Changes in Lung VolumeChest, Vol. 112, No. 1The influence on the breathing pattern in man of moderate levels of continuous positive and negative airway pressure and of positive end-expiratory pressure during air and CO 2 inhalationActa Physiologica Scandinavica, Vol. 138, No. 3Breathing Responses to Imposed Mechanical Loads1 January 2011Load compensation during positive pressure breathing in anesthetized manRespiration Physiology, Vol. 65, No. 3Effect of endotracheal continuous positive airway pressure on sensitivity to carbon dioxide and on respiratory timing in preterm infantsPediatric Pulmonology, Vol. 2, No. 2Therapy of Hyaline Membrane DiseaseRESPIRATORY MUSCLES RESPONSE TO LOADINGMuscle activity during chest wall restriction and positive pressure breathing in manRespiration Physiology, Vol. 35, No. 3Current Therapy in Hyaline Membrane DiseaseClinics in Perinatology, Vol. 5, No. 2EFFECT OF CONTINUOUS POSITIVE AIRWAY PRESSURE BREATHING ON CARDIORESPIRATORY FUNCTION IN INFANTS WITH RESPIRATORY DISTRESS SYNDROMEActa Paediatrica, Vol. 66, No. 1Some Steady-State Effects of Respiratory LoadsChest, Vol. 70, No. 1Occlusion pressure as a measure of respiratory center output cm conscious manRespiration Physiology, Vol. 23, No. 2Immediate ventilatory response to elastic loads and positive pressure in manRespiration Physiology, Vol. 18, No. 3A New Stimulant for Ventilatory Failure?The Lancet, Vol. 301, No. 7806The Role of the Intrinsic Properties of the Respiratory Muscles in the Regulation of VentilationChest, Vol. 61, No. 2The role of the vagus nerves in the respiratory response to CO2 under hyperoxic conditionsPfl�gers Archiv European Journal of Physiology, Vol. 336, No. 2 More from this issue > Volume 30Issue 1January 1971Pages 7-11 https://doi.org/10.1152/jappl.1971.30.1.7PubMed4249901History Published online 1 January 1971 Published in print 1 January 1971 Metrics

Airway closure: demonstration by breathing 100 percent O2 at low lung volumes and by N2 washout.

Airway closure - demonstration by breathing pure oxygen at low lung volumes and by nitrogen washout