High frequency diaphragmatic fatigue detected with paired stimuli in humans.

PURPOSE: The purpose of this study was to determine whether high frequency fatigue was present in the diaphragm after intense whole body endurance exercise. METHODS: We used bilateral phrenic nerve stimulation (BPNS) before and during recovery from whole body exercise to detect fatigue in the diaphragm. To detect high frequency fatigue we used paired stimuli at 10, 20, 50, 70, and 100 Hz frequency and determined the transdiaphragmatic pressure (Pdi) response to the second stimulation (T2). RESULTS: The subjects (N = 10) exercised at 93.3 +/- 2.3% of their VO2max for 9.9 +/- 0.5 min. The Pdi response to "twitch" and 10 Hz "tetanic" stimulation was decreased immediately after exercise versus pre-exercise values (-23.4 +/- 3.3%). The T2 amplitude was substantially reduced at all frequencies immediately after exercise (-28.0%), but by 30 min into recovery the T2 amplitude at 70 and 100 Hz was not different from pre-exercise values. In contrast, at 10 and 20 Hz the T2 response was still significantly reduced. CONCLUSIONS: We interpret these data to mean that high frequency fatigue as well as low frequency fatigue were present in the diaphragm after intense whole body endurance exercise.

Automated detection and classification of sleep-disordered breathing from conventional polysomnography data.

Efficient automated detection of sleep-disordered breathing (SDB) from routine polysomnography (PSG) data is made difficult by the availability of only indirect measurements of breathing. The approach we used to overcome this limitation was to incorporate pulse oximetry into the definitions of apnea and hypopnea. In our algorithm, 1) we begin with the detection of desaturation as a fall in oxyhemoglobin saturation level of 2% or greater once a rate of descent greater than 0.1% per second (but less than 4% per second) has been achieved and then ask if an apnea or hypopnea was responsible; 2) an apnea is detected if there is a period of no breathing, as indicated by sum respiratory inductive plethysmography (RIP), lasting at least 10 seconds and coincident with the desaturation event; and 3) if there is breathing, a hypopnea is defined as a minimum of three breaths showing at least 20% reduction in sum RIP magnitude from the immediately preceding breath followed by a return to at least 90% of that "baseline" breath. Our evaluation of this algorithm using 10 PSG records containing 1,938 SDB events showed strong event-by-event agreement with manual scoring by an experienced polysomnographer. On the basis of manually verified computer desaturations, detection sensitivity and specificity percentages were, respectively, 73.6 and 90.8% for apneas and 84.1 and 86.1% for hypopneas. Overall, 93.1% of the manually detected events were detected by the algorithm. We have designed an efficient algorithm for detecting and classifying SDB events that emulates manual scoring with high accuracy.

Simultaneous digitization of upper airway fiber-optic images and respiratory signals.

We developed an inexpensive and efficient method for simultaneously digitizing respiratory signals and fiber-optic images of the upper airway. The main components of the system are a fiber-optic scope, a charge coupled device video camera, and a personal computer equipped with a frame grabber and an A/D board. The frame grabber digitizes images at five frames per second while the A/D board samples six respiratory signals at 25 samples per second. Digitized images are saved only in the event that the user instructs the computer to do so in order to limit disk space requirements. A circular buffering technique provides continuous storage of the most recent 50 frames in frame grabber memory. This feature gives the user up to 10 seconds, following the beginning of a respiratory event, to initiate the saving of images to computer hard disk. A postacquisition program displays the data acquired during the sleep study and allows the user to interactively select images for subsequent upper airway area measurement. This system enables us to observe and quantify the dynamics of the upper airway during different breathing conditions with minimal time and cost. It is also a potential clinical tool to use to determine the site of obstruction during sleep in patients with obstructive sleep apnea.

Role of vagal feedback from the lung in hypoxic-induced tachycardia in humans.

We assessed the cardiovascular responses to systemic normocapnic hypoxia in five normal subjects, five double lung transplant patients with lung denervation and intact hearts, and five patients with denervated hearts. Progressive normocapnic hypoxia was induced over 10-15 min and maintained for 2-3 min each at 90, 87, 84, and 80% arterial O2 saturation (SaO2). Normal subjects showed the most pronounced mean increase in heart rate (dHR/dSaO2 = 0.86 +/- 0.13 beat/min per 1% SaO2). Three lung-denervated subjects had normal tachycardiac responses (1.6, 0.9, and 0.69 beats/min per 1%), whereas the other two had distinctly lower responses (0.34 and 0.39 beat/min per 1%). Most of the lung-denervated subjects also showed a significant tachycardia with even mild hypoxia; none showed a bradycardiac response to any level of hypoxia. In the heart-denervated group, hypoxic tachycardia was significantly lower than normal (0.29 +/- 0.13 beat/min per 1%). We conclude that vagal feedback from the lungs is not required for the normal chronotropic response to hypoxia in humans; however, this mechanism may contribute significantly to the marked variability in hypoxic-induced tachycardia found among human subjects. These data in humans contrast with the progressive bradycardiac response to hypoxia reported in vagally denervated (or nonhyperpneic) dogs and cats.

Respiratory sinus arrhythmia in humans: an obligatory role for vagal feedback from the lungs.

Respiratory sinus arrhythmia (RSA) is used as a noninvasive measure of vagal cardiac input, but its causative mechanisms in humans remain undetermined. We compared the RSA of five lung-denervated double-lung transplant patients with intact hearts to six normal (N) control subjects, five heart-denervated patients, and two liver transplant patients at matched tidal volumes (VT's) and breathing frequencies. In N and liver transplant subjects, RSA was significant during eupnea and increased two- to threefold with increasing VT and inspiratory effort. In heart- and lung-denervated subjects, RSA at eupnea was significant but was only 53% of that in N subjects and was not respondent to changing VT, inspiratory effort, or breathing frequency. We also compared the RSA of N subjects during voluntary (active) and passive positive pressure ventilation at normocapnia. RSA was reduced from 11 +/- 2.2 beats/min during active ventilation to 5.4 +/- 0.8 beats/min during PPV. We conclude that vagal feedback from pulmonary stretch receptors is obligatory for the generation of a neurally mediated RSA in awake humans at normal and raised levels of VT and respiratory motor output. In intact humans, we also hypothesize an important effect for nonpulmonary central and/or peripheral modulation of RSA. It is likely that the key mechanisms for neurally mediated RSA in unanesthetized humans are mutually dependent.