A mathematical model to detect inspiratory flow limitation during sleep. (73/770)

The physiological significance of inspiratory flow limitation (IFL) has recently been recognized, but methods of detecting IFL can be subjective. We sought to develop a mathematical model of the upper airway pressure-flow relationship that would objectively detect flow limitation. We present a theoretical discussion that predicts that a polynomial function [F(P) = AP(3) + BP(2) + CP + D, where F(P) is flow and P is supraglottic pressure] best characterizes the pressure-flow relationship and allows for the objective detection of IFL. In protocol 1, step 1, we performed curve-fitting of the pressure-flow relationship of 20 breaths to 5 mathematical functions and found that highest correlation coefficients (R(2)) for quadratic (0.88 +/- 0.10) and polynomial (0.91 +/- 0.05; P < 0.05 for both compared with the other functions) functions. In step 2, we performed error-fit calculations on 50 breaths by comparing the quadratic and polynomial functions and found that the error fit was lowest for the polynomial function (3.3 +/- 0.06 vs. 21.1 +/- 19.0%; P < 0.001). In protocol 2, we performed sensitivity/specificity analysis on two sets of breaths (50 and 544 breaths) by comparing the mathematical determination of IFL to manual determination. Mathematical determination of IFL had high sensitivity and specificity and a positive predictive value (>99% for each). We conclude that a polynomial function can be used to predict the relationship between pressure and flow in the upper airway and objectively determine the presence of IFL.  (+info)

A reevaluation of the validity of unrestrained plethysmography in mice. (74/770)

Presently, unrestrained plethysmography is widely used to assess bronchial responsiveness in mice. An empirical quantity known as enhanced pause is derived from the plethysmographic box pressure [P(b)(t), where t is time] and assumed to be an index of bronchoconstriction. We show that P(b)(t) is determined largely by gas conditioning when normal mice breathe spontaneously inside a closed chamber in which the air is at ambient conditions. When the air in the chamber is heated and humidified to body conditions, the changes in P(b)(t) are reduced by about two-thirds. The remaining changes are thus due to gas compression and expansion within the lung and are amplified when the animals breathe through increased resistances. We show that the time integral of P(b)(t) over inspiration is accurately predicted by a term containing airway resistance, functional residual capacity, and tidal volume. We conclude that unrestrained plethysmography can be used to accurately characterize changes in airway resistance only if functional residual capacity and tidal volume are measured independently and the chamber gas is preconditioned to body temperature and humidity.  (+info)

Phonospirometry for noninvasive measurement of ventilation: methodology and preliminary results. (75/770)

We measured tracheal flow from tracheal sounds to estimate tidal volume, minute ventilation (VI), respiratory frequency, mean inspiratory flow (VT/TI), and duty cycle (TI/Ttot). In 11 normal subjects, 3 patients with unstable airway obstruction, and 3 stable asthmatic patients, we measured tracheal sounds and flow twice: first to derive flow-sound relationships and second to obtain flow-volume relationships from the sound signal. The flow-volume relationship was compared with pneumotach-derived volume. When subjects were seated, facing forward and with neck rotation, flexion, and standing, flow-volume relationship was within 15% of pneumotach-derived volume. Error increased with neck extension and while supine. We then measured ventilation without mouthpiece or nose clip from tracheal sounds during quiet breathing for up to 30 min. Normal results +/- SD revealed tidal volume = 0.37 +/- 0.065 liter, respiratory frequency = 19.3 +/- 3.5 breaths/min, VI = 6.9 +/- 1.2 l/min, VT/TI = 0.31 +/- 0.06 l/s, and TI/Ttot = 0.37 +/- 0.04. Unstable airway obstruction had large VI due to increased VT/TI. With the exception of TI/Ttot, variations in ventilatory parameters were closer to log normal than normal distributions and tended to be greater in patients. We conclude that phonospirometry measures ventilation reasonably accurately without mouthpiece, nose clip, or rigid postural constraints.  (+info)

Transient mechanical benefits of a deep inflation in the injured mouse lung. (76/770)

The lasting effects of a recruitment maneuver (RM) in the injured lung are not well characterized. We speculated that the reduction in respiratory elastance (H) after a deep inflation (DI) is transient in nature and should be sustained longer at higher positive end-expiratory pressure (PEEP). Thirteen ventilated mice were given 2 DIs at various levels of PEEP before and after saline lavage. Forced oscillations were used to measure H periodically over 7 min after the DIs. Time constants (tau) were estimated for the post-DI recovery in H. Values for tau before lavage (80-115 s) were reduced after lavage (13-30 s) at all levels of PEEP (P = 0.0001). PEEP did not significantly influence tau before or after lavage. The plateau level and total recovery in H after a DI were significantly influenced by PEEP and lavage (P < 0.0001). Our results suggest that for a DI to be beneficial in the injured mouse lung, it may have to be applied several times a minute.  (+info)

Detection of inspiratory resistive loads in double-lung transplant recipients. (77/770)

The afferent pathways mediating respiratory load perception are still largely unknown. To assess the role of lung vagal afferents in respiratory sensation, detection of inspiratory resistive loads was compared between 10 double-lung transplant (DLT) recipients with normal lung function and 12 healthy control (Nor) subjects. Despite a similar unloaded and loaded breathing pattern, the DLT group had a significantly higher detection threshold (2.91 +/- 0.5 vs. 1.55 +/- 0.3 cmH(2)O. l(-1). s) and Weber fraction (0.50 +/- 0.1 vs. 0.30 +/- 0.1) compared with the Nor group. These results suggest that inspiratory resistive load detection occurs in the absence of vagal afferent feedback from the lung but that lung vagal afferents contribute to inspiratory resistive load detection response in humans. Lung vagal afferents are not essential to the regulation of resting breathing and load compensation responses.  (+info)

Magnitude estimation of inspiratory resistive loads by double-lung transplant recipients. (78/770)

The purpose of this study was to investigate the role of afferent input from the lung and lower airways in magnitude estimation of inspiratory resistive loads (R). To assess the role of lung vagal afferents in respiratory sensation, sensations related to inspiratory R, reflected by subjects' percentage of handgrip responses (HG%), were compared between double-lung transplant (DLT) recipients with normal lung function and healthy control (Nor) subjects. Perceptual sensitivity to the external load was measured as the slope of HG% as a function of peak mouth pressure (Pm), and the slope of HG% as a function of R, after a log-log transformation. The results showed that the DLT group had a similar HG% response, as well as the slopes of log HG%-log Pm and log HG%-log R, compared with the Nor group. Furthermore, the ventilatory responses to external loads were also similar between the two groups. These results suggest that lung vagal afferents do not play a significant role in magnitude estimation of inspiratory resistive loads in humans.  (+info)

Determinants of long-term facilitation in humans during NREM sleep. (79/770)

Long-term facilitation (LTF) is a prolonged increase in ventilatory motor output after episodic peripheral chemoreceptor stimulation. We have previously shown that LTF is activated during sleep following repetitive hypoxia in snorers (Babcock MA and Badr MS. Sleep 21: 709-716, 1998). The purpose of this study was 1) to ascertain the relative contribution of inspiratory flow limitation to the development of LTF and 2) to determine the effect of eliminating inspiratory flow limitation by nasal CPAP on LTF. We studied 25 normal subjects during stable non-rapid eye movement sleep. We induced 10 episodes of brief repetitive isocapnic hypoxia (inspired O(2) fraction = 8%; 3 min) followed by 5 min of room air. Measurements were obtained during control and at 20 min of recovery (R(20)). During the episodic hypoxia study, inspiratory minute ventilation (Vi) increased from 6.7 +/- 1.9 l/min during the control period to 8.2 +/- 2.7 l/min at R(20) (122% of control; P < 0.05). Linear regression analysis confirmed that inspiratory flow limitation during control was the only independent determinant of the presence of LTF (P = 0.005). Six subjects were restudied by using nasal continuous positive airway pressure to ascertain the effect of eliminating inspiratory flow limitation on LTF. Vi during the recovery period was 97 +/- 10% (P > 0.05). In conclusion, 1) repetitive hypoxia in sleeping humans is followed by increased Vi in the recovery period, indicative of development of LTF; 2) inspiratory flow limitation is the only independent determinant of posthypoxic LTF in sleeping human; 3) elimination of inspiratory flow limitation abolished the ventilatory manifestations of LTF; and 4) we propose that increased Vi in the recovery period was a result of preferential recruitment of upper airway dilators by repetitive hypoxia.  (+info)

Effect of inspiratory muscle strength training on inspiratory motor drive and RREP early peak components. (80/770)

This study investigated the effect of inspiratory muscle strength training (IMST) on inspiratory motor drive [mouth occlusion pressure at 0.1 s (P(0.1))] and respiratory-related evoked potentials (RREP). It was hypothesized that, if IMST increased inspiratory muscle strength, inspiratory motor drive would decrease. If motor drive were related to the RREP, it was further hypothesized that an IMST-related decrease in drive would change RREP latency and/or amplitude. Twenty-three subjects received IMST at 75% of their maximal inspiratory pressure (Pi(max)) with the use of a pressure threshold valve. IMST consisted of four sets of six breaths daily for 4 wk. P(0.1) and the RREP were recorded before and after IMST. Posttraining, Pi(max) increased significantly by 36.0 +/- 2.7%. P(0.1) decreased significantly by 21.9 +/- 5.2%. The increase in Pi(max) was significantly correlated to the decrease in P(0.1). RREP peaks P(1a), N(f), P(1), and N(1) were identified pre- and post-IMST, and there was no difference in either amplitude or latency for those peaks. These results demonstrate that high-intensity IMST significantly increased Pi(max), decreased P(0.1), but did not change the RREP.  (+info)