Bladder contractions alter inspiratory termination by superior laryngeal and intercostal nerve stimulation.

Gradual distension of the urinary bladder evokes spontaneous bladder contractions (SBCs), which are associated with reduced inspiratory activity in the phrenic and other inspiratory motor nerves. We examined the influence of isovolumetric SBCs on the threshold for termination of phrenic inspiration by electrical stimulation of superior laryngeal and/or mid-thoracic intercostal nerves (ICN) in decerebrate, vagotomized, paralyzed, ventilated cats. Although SBCs reduced phrenic inspiratory activity, the threshold for inspiratory termination by nerve stimulation was increased. The results emphasize the complexity of the synaptic connections among brain stem neurons governing micturition and breathing.     

Inhibitory and excitatory effects on respiration by phrenic nerve afferent stimulation in cats

Respiratory effects of electrical stimulation of phrenic nerve afferents were studied in anesthetized cats, either spontaneously breathing or paralyzed and ventilated. The type of phrenic afferent fibers activated was controlled by recording the evoked action potentials from dorsal root fibers. In both preparations, stimulation at a strength sufficient to activate small diameter myelinated phrenic nerve afferents induced a biphasic response. The first phase lasted a few respiratory cycles and was inhibitory and consisted of a decrease in tidal volume (VT) or phrenic activity (NA), inspiratory time (TI), respiratory duty cycle (TI/Ttot) and instantaneous ventilation (VE) or minute phrenic activity (NMA). Expiratory time (TE) increased and breathing frequency (f) and mean inspiratory flow (VT/TI) or mean inspiratory neural activity (NA/TI) did not change. This short-term response was suppressed in animals pretreated with bicuculline. The second phase was a long-term excitation in which VT or NA, f, VE or NMA and VT/TI increased whereas both TI and TI/Ttot decreased and TE did not change. Unlike published data, our results suggest that small-diameter myelinated phrenic nerve afferents are involved in these responses. These phrenic fibers, like afferents from other muscles, affect respiratory output and may play a role in the control of breathing.     

Estimation of intrapleural pressure in the newborn

We examined the changes in esophageal (Pes), proximal airway (Paw), and direct intrapleural (Ppl) pressure measurements following end-expiratory airway occlusion in anesthetized spontaneously breathing newborn piglets. Simultaneous occluded pressure measurements were obtained during resting ventilation, inspiratory resistive loaded (IRL) breathing, and bilateral transvenous phrenic nerve stimulation. During spontaneous resting ventilation, occluded Paw/Ppl averaged 104 +/- 4% and occluded Pes/Ppl averaged 89 +/- 3%. Similar values were found for occluded spontaneous breaths with IRL. During phrenic nerve stimulation at end-expiratory lung volume, occluded Paw/Ppl averaged 104 +/- 6% while occluded Pes/Ppl decreased to 70 +/- 22%. We conclude that proximal airway pressure more accurately reflects intrapleural pressure than esophageal pressure with occlusion in newborn swine. During phrenic nerve stimulation, esophageal pressure measures are grossly inaccurate estimates of intrapleural pressure with occlusion.     

Ventilatory effects of the interaction between phrenic and limb muscle afferents.

We studied the effects on ventilation and ventilatory muscle activation of stimulation of the central ends of the left phrenic and gastrocnemius nerves separately and concurrently in 10 spontaneously breathing, alpha-chloralose anaesthetized dogs. The nerves were stimulated for 1 min, at a frequency of 40 Hz and pulse duration of 1 ms. The phrenic nerve was stimulated at 20 and 40 times twitch threshold (TT). During these stimulation periods ventilation increased by 39% and 79% of control values, respectively. The gastrocnemius nerve was stimulated at 20 times TT. This produced a 90% increase in ventilation. Stimulation of either nerve resulted in increases in the activity of the right diaphragm, parasternal intercostal and alae nasi muscles comparable in magnitude to the increase in tidal volume. The activities of the genioglossus and transversus abdominis muscle increased to a much greater extent than did the other muscles under all conditions. In contrast, triangularis sterni activity remained unchanged during stimulation of either nerve. The phrenic nerve was then stimulated at 40 times TT for 1 min with superimposed gastrocnemius nerve stimulation (20 times TT) during the last 30 s. Ventilation had risen by 66% after 30 s of phrenic nerve stimulation. With the addition of gastrocnemius nerve stimulation, ventilation rose by a further 84% for a total increase of 150% of the control value. Mathematical summation of the responses to individual nerve stimulation at these intensities predicted a 156% increase in ventilation. Similar degrees of summation were found with respect to respiratory muscle activation. We conclude that the interaction between phrenic and limb muscle (gastrocnemius) afferent is additive with respect to their effects on ventilation.     

Hypothyroidism presenting with respiratory muscle weakness

A 58-yr-old woman presented with recurrent chest infections, breathlessness, and orthopnea. She complained of nonspecific tiredness and aching limbs. A chest radiograph showed an elevated right hemidiaphragm. Thyroid function tests showed her to be severely hypothyroid (T4 = 23 nmol/L; TSH greater than 50 mU/L). Measurement of maximal respiratory mouth pressures (expiratory: 50 cm H2O, normal, 94 +/- 33; inspiratory: 15 cm H2O, normal, 71 +/- 27) suggested global respiratory muscle weakness. Severe bilateral diaphragm weakness was demonstrated by a greatly reduced maximal transdiaphragmatic pressure (Pdi) (Pdi Pimax = 0, normal, 65 +/- 31 cm H2O; sniff Pdi = 25 cm H2O, normal, 121 +/- 25). No Pdi was detectable on stimulation of the right phrenic nerve, whereas, on the left, it was 11 cm H2O (normal 7 to 15 cm H2O). Phrenic nerve conduction time was prolonged to both sides (right, 12 ms, left, 10 ms; normal, less than 9.5 ms). The relaxation rate of Pdi after a maximal sniff and after bilateral phrenic nerve stimulation was abnormally slow (7.4%/10 ms, 6.3%/10 ms, respectively). Three months after starting treatment with thyroxine she had become euthyroid, and phrenic nerve conduction times and Pdi relaxation rates had returned to normal. Maximal respiratory pressures, vital capacity, and maximal voluntary ventilation improved progressively on treatment, although maximal respiratory pressures still had not reached the normal range after six months. We conclude that hypothyroidism may present with breathlessness due to respiratory muscle weakness and/or phrenic nerve neuropathy and is reversible with treatment.     

Transmission fatigue of the rabbit diaphragm

This study evaluates the role of transmission fatigue of the diaphragm in rabbits subjected to inspiratory resistive loading (IRL) sufficiently severe to increase peak tidal airway pressure to about 50% of that elicited by 100 Hz phrenic nerve stimulation. After 58 +/- 14 min of IRL, the transdiaphragmatic pressure (Pdi) responses to phrenic nerve stimulation at 20, 60, and 100 Hz were reduced by approximately one third. In contrast, IRL induced no significant change in the response to direct diaphragm stimulation (in the presence of transient neuromuscular blockade). Although respiratory acidosis occurred during IRL (pH 7.04 +/- 0.04, PCO2 90 +/- 10, PO2 131 +/- 38), it was not sufficient to explain the reduced contractility. In a separate series of experiments, the diaphragm compound action potential elicited by unilateral phrenic nerve stimuli was recorded by implanted diaphragm electrodes and the Pdi elicited by contralateral phrenic nerve stimulation at 100 Hz was measured. Both action potential amplitude and Pdi declined during IRL and both improved after 10 min of recovery. These findings demonstrate that transmission fatigue plays a major role in rabbit diaphragm fatigue induced by spontaneous breathing against inspiratory resistance.     

Properties of inspiratory termination by superior laryngeal and vagal stimulation.

Electrical stimulation of two respiratory afferent nerves, the vagus and the internal branch of the superior laryngeal, was used to terminate inspiration. The short latency responses of phrenic motoneurones to these stimuli were studied to determine if inspiratory termination was preceded by a characteristic phrenic motoneurone discharge pattern, reflecting changes in brainstem inspiratory neurone discharge and inspiratory terminating mechanisms. Stimulus trains of sufficient intensity delivered to the superior laryngeal nerve terminated inspiration within 50 ms and were preceded by a stereotyped pattern of phrenic motoneurone discharge. This consisted of a short latency (disynaptic), predominantly contralateral excitation in response to the first shock of the train, followed by a marked and long lasting inhibition. In contrast, vagal stimulation typically terminated inspiration hundreds of milliseconds after the onset of the stimulus train and was not preceded by a stereotyped pattern of phrenic motoneurone responses to single shocks. Transient short latency responses were obtained but were extremely small, requiring considerable excitation followed by a moderate bilateral depression of activity. Inspiration could be terminated with or without the presence of these short latency responses. These results indicate that superior laryngeal and vagal (presumably pulmonary stretch receptor) afferents have different projections to brainstem inspiratory neurones and may exert their effects on inspiratory duration through different, but as yet undefined, neural mechanisms.     

Diaphragm strength in chronic heart failure.

Reduced respiratory muscle strength has been reported in chronic heart failure (CHF) in several studies. The data supporting this conclusion come almost exclusively from static inspiratory and expiratory mouth pressure maneuvers (MIP, MEP), which many subjects find difficult to perform. We therefore performed a study using measurements that are less dependent on patient aptitude and also provide specific data on diaphragm strength. In 20 male patients and 15 control subjects we measured MIP and MEP as well as esophageal and transdiaphragmatic pressure during maximal sniffs (Sn Pes, Sn Pdi) and cervical magnetic phrenic nerve stimulation (Tw Pdi). In a subgroup the response to paired phrenic nerve stimulation (pTw Pdi) at interpulse intervals from 10 to 200 ms (5 to 100 Hz) was also determined. As expected, MIP was significantly reduced in the CHF group (CHF, 69.5 cm H(2)O; control, 96.7 cm H(2)O; p = 0.01), but differences were much less marked for Sn Pes (CHF, 95.2 cm H(2)O; control, 104.8 cm H(2)O; p = 0.20) and MEP (CHF, 109.1 cm H(2)O; control, 135.7 cm H(2)O; p = 0.09). Diaphragm strength was significantly reduced (Sn Pdi: CHF, 123.8 cm H(2)O; control 143.5 cm H(2)O; p = 0.04. Tw Pdi: CHF, 21.4 cm H(2)O; control, 28.5 cm H(2)O; p = 0.0005). Paired phrenic nerve stimulation suggested a trend to increased twitch summation at 5 to 20 Hz in CHF, although this did not reach significance. We conclude that mild reduction in diaphragm strength occurs in CHF, possibly because of an increased proportion of slow fibers, but overall strength of the respiratory muscles remains well preserved.     

Distribution of motor activity to expiratory muscles during sciatic nerve stimulation in the dog

The present study examined the effect of increasing sensory input from the lower limbs (assessed from the response to electrical stimulation of the sciatic nerve) on the distribution of electrical activity to the expiratory muscles. Expiratory muscle response to sciatic nerve stimulation (SNS) was compared to the response of the inspiratory muscles, and to their response to hypercapnia. In 16 anesthetized dogs afferent SNS increased ventilation and augmented the integrated EMG of all six expiratory muscles studied. Increases in abdominal muscle electrical activity were not uniform, being greater in the transversus abdominis and external oblique as compared to the internal oblique and the rectus abdominis. Increases in thoracic expiratory and inspiratory muscle activity during SNS were similar in magnitude. SNS performed while dogs were breathing 7% CO2, produced increased neural activity similar to those observed during O2 breathing. During CO2 rebreathing, at equal levels of minute ventilation, expiratory muscle responses to SNS and to CO2 were similar. In contrast, the rate of rise of the inspiratory muscle EMGs was greater during SNS. The present study indicates that the abdominal muscles participate in the respiratory response to afferent neural drive from skeletal muscles. The magnitude of their response is independent of their pre-stimulation level of activity and is similar to that observed during CO2 stimulated breathing.     

The effect of treatment on diaphragm contractility in obstructive sleep apnea syndrome

In untreated obstructive sleep apnea syndrome (OSAS) inspiratory efforts are made against an occluded airway and diaphragm fatigue might therefore complicate OSAS. To test this hypothesis we measured twitch transdiaphragmatic pressure (Tw Pdi) in response to bilateral cervical magnetic stimulation of the phrenic nerve roots in nine patients with OSAS before and one month after successful therapy with nasal continuous positive airways pressure (nCPAP). The mean Tw Pdi before therapy was 23.2cm H2O and after therapy was 22.8cm H2O (P = 0.59); the mean change after initiation of nCPAP was 0.4cm H2O with 95% confidence intervals of -1.3cm H2O and +2.1 cm H2O. We conclude that low frequency diaphragm fatigue does not complicate untreated OSAS.     

Vocal cord closure. A cause of upper airway obstruction during controlled ventilation.

Studies of vocal cord function were undertaken in a quadriplegic patient requiring ventilatory assistance, and in 2 normal subjects during controlled ventilation in a tank-type respirator. When the patient and the normal subjects relaxed and made no conscious effort to assist the respirator, the vocal cords were observed to close during inspiration and a large pressure gradient (12 to 19 cm H2O) developed across the cords. When the subjects made a slight inspiratory effort ("assist" mode), the cords opened widely during inspiration. There were large increases in flow and tidal volume in the "assist" mode compared with passive ventilation. Measurements of transdiaphragmatic pressure and esophageal pressure showed that these variables did not increase with the slight assist. Thus, increase in ventilation during the "assist" mode appeared to be due to alleviation of inspiratory obstruction at the level of the vocal cords. The same phenomenon was observed in the patient during phrenic nerve pacing. A pacemaker was designed to be triggered by the electromyographic impulse from an accessory muscle of respiration. In this manner, vocal cord opening could be coordinated with the mechanical assist given by the phrenic nerve pacer.     

Stimulus parameters for phrenic nerve pacing in infants and children

Phrenic nerve pacing has been used since 1966 to support breathing in quadriplegics and patients with central hypoventilation syndrome (CHS). Recently, using low-frequency, long-inspiratory-time (T_i) stimulation, phrenic nerve pacing has been used successfully to support breathing 24 hours per day in adults and older children. However, no similar experience exists for infants and young children. Therefore, in 27 studies in 14 infants and children we determined the effects of changing T_i and interpulse interval (the inverse of stimulus frequency) on ventilation. Diaphragmatic action potentials, airflow, tidal volume, P_ACO2 and Sa_O2 were measured during sleep. Phrenic nerve pacing proved useful in 13 of 14 patients to support breathing either during wakefulness (n = 7) or during sleep (n = 6). We found that adequate ventilation could be achieved at significantly longer interpulse intervals, 95 ± 25 (mean ± SD) ms, and shorter T_i, 580 ± 80 ms, than previously reported. At an average respiratory rate of 21 ± 8 breaths/min it was thus possible to maintain adequate ventilation despite a marked reduction in the number of phrenic nerve stimuli. Theoretically, these reductions in phrenic nerve stimulation should minimize the chance of pacing-induced diaphragmatic damage. These results suggest that 24 hour per day phrenic nerve pacing may be a realistic goal in selected infants and children.     

Spontaneous recovery of diaphragmatic strength in unilateral diaphragmatic paralysis

The aim of the present study was to evaluate diaphragmatic strength in patients with unilateral diaphragmatic paralysis and to determine whether patients with recent diaphragm paralysis develop lower inspiratory pressure than patients with longstanding diaphragmatic paralysis. Twenty patients (16 men and 4 women, 62+/-12 years) and six control subjects were included (4 men and 2 women, 53+/-15 years) in the study. Esophageal pressure during sharp sniff (Pes,sniff), bilateral cervical phrenic nerve magnetic stimulation (Pes,cms) and unilateral phrenic nerve stimulation (Pes,ums) (in nine patients) were measured. Sixteen patients presented right diaphragmatic paralysis and four, left diaphragmatic paralysis. Pes,sniff was higher in control subjects than in patients with diaphragmatic paralysis (respectively 110+/-22 cmH2O and 82+/-24 cmH2O, P<0.05). There was no difference in Pes,cms between patients with diaphragmatic paralysis and control subjects (14+/-7 cmH2O vs. 16+/-4 cmH2O; ns). Pes,ums after stimulation of the affected phrenic nerve was less than 4 cmH2O, was 8+/-2 cmH2O after stimulation of the intact phrenic nerve and was correlated to Pes,cms (R=0.87, P<0.01). There was a positive correlation between Pes,cms, Pes,ums of the intact hemidiaphragm, Pes,sniff and the time from the onset of symptoms and the diaphragmatic explorations (respectively R=0.86, P<0.0001; R=0.72, P<0.05; R=0.48, P<0.05). In conclusion, diaphragmatic strength after unilateral diaphragmatic paralysis seems to improve with time.     

Inspiration Induced by Phrenic Nerve Stimulation Increases Internal Defibrillation Energy Requirements

INTRODUCTION: The purpose of this study was to systematically evaluate the effects of active inspiration induced by phrenic nerve stimulation on the energy required for 50% successful defibrillation (E50). METHODS AND RESULTS: Shocks (95-microF biphasic waveform) were delivered after 10 seconds of ventricular fibrillation between a right ventricular coil and left pectoral test can in ten anesthetized pigs (25 to 37 kg). Using a 1-J step size, the E50 was determined with an up/down, three-reversal method. Positive-pressure ventilation was halted just before fibrillation, and shocks were delivered during expiration or at the end of 2 seconds of bilateral phrenic stimulation (50 Hz, 0.3 msec, 5 to 6 V). Phrenic stimulation produced inspiratory volumes that were 15.3 +/- 1.7 mL/kg (mean +/- SD). The E50 was 9.8 +/- 1.9 J during expiration and increased to 13.0 +/- 1.7 during inspiration (P = 0.001). The leading-edge voltage at the E50 was 451 +/- 46 V during expiration and 519 +/- 33 V during inspiration (P = 0.001). The leading-edge current at the E50 was 9.7 +/- 1.0 A during expiration and increased to 11.3 +/- 1.4 A during inspiration (P = 0.002). The average impedance was 47.8 +/- 2.7 omega during expiration and 47.3 +/- 3.3 omega during inspiration (P = 0.12). CONCLUSION: Inspiration induced by phrenic stimulation results in a 31% increase in the E50 compared with expiration. The decrease in shock efficacy occurs in the absence of a change in impedance. Active inspiration may alter the distribution of the electrical field leading to a decrease in shock efficacy.     

The effects of hypercapnia and hypoxia on single hypoglossal nerve fiber activity

The respiratory related modulation of hypoglossal nerve activity has been studied at the single fiber level in cats under hyperoxic hypercapnia and hypoxic conditions and their conduction velocities determined. Changes in fiber activity were compared to simultaneous changes occurring in phrenic activity. Three different kinds of discharge patterns were observed: (a) inspiratory, (b) phasic activity during both inspiration and expiration, and (c) continuous random activity with no respiratory modulation. These fibers could be grouped into three categories according to their pattern of discharge during CO2 breathing. Type I fibers, mean conduction velocity of 30.0 m/sec, exhibited only an inspiratory phasic discharge during 100% O2 breathing. Their discharge frequency increased rapidly with higher levels of CO2 and hypoxia. Type II fibers, mean conduction velocity of 36.7 m/sec, had three different kinds of inspiratory-expiratory discharge patterns during 100% O2 breathing. With increasing hypercapnia or hypoxia fibers of this group discharged phasically during inspiration and discharge at low frequency during expiration. Type III fibers had a non phasic discharge pattern at 100% O2 breathing and at all levels of CO2 tested (up to 10%). Discharge frequency rose during CO2 rebreathing and hypoxia, but the rate of increase was much less than Type I and Type II fibers. Their mean conduction velocity was 41.3 m/sec. The inspiratory activity of Type I and II fibers increased their activity more than the phrenic during hypercapnia and hypoxia. Type II and Type III fibers are responsible at least in part for the tonic activity of the nerve.     

Twitch airway pressure elicited by magnetic phrenic nerve stimulation in anesthetized healthy children

Children with diaphragm dysfunction may be unable to maintain adequate ventilation. Accurate diagnosis is important, but can only be achieved using an appropriate test and reference range. The aim of this study, therefore, was to measure diaphragm contractility and examine the influence of age and maturation, using magnetic phrenic nerve stimulation in healthy children. Anterolateral magnetic stimulation (MS) of the phrenic nerves was performed using a 43-mm figure-eight coil in 23 children (14 male; mean age, 7.8 years; range, 1.8-15.7) anesthetized for minor surgery with sevoflurane gas. The airway was maintained with a cuffed laryngeal mask airway (LMA) which was briefly occluded during MS. Diaphragm contractility was assessed by measuring the airway pressure (TwPaw) elicited by MS. TwPaw responses were obtained in all subjects, with mean (SD) TwPaw 18.2 (6.8) cm H2O bilateral, 7.3 (3.2) cm H2O left unilateral, and 8.6 (3.1) cm H2O right unilateral. Subgroup analysis was performed in 17 of the children who were prepubertal. Their mean (SD) TwPaw was 17.3 (6.8) cm H2O bilateral, 7.1 (3.7) cm H2O left unilateral, and 8.3 (3.3) right unilateral. The mean (SD) intrapatient coefficients of variation for bilateral and left and right unilateral TwPaw were 8.4% (5.2), 6.7% (3.5), and 11.7% (10.3), respectively. Bilateral and left and right unilateral TwPaw were significantly related to age (P < 0.05). In healthy prepubertal children, diaphragm contractility is primarily influenced by age.     

Respiratory resetting induced by activation of inspiratory bulbo-spinal neurons

The respiratory effects elicited by spinal (C2-C3) stimulation at the level of descending inspiratory axons were studied in paralysed, non-vagotomized and artificially ventilated cats anaesthetized with urethane-chloralose. The activation of inspiratory bulbospinal axons in the ventrolateral quadrant was confirmed by recording the ipsilateral phrenic excitation following a single pulse. Brief stimulus trains delivered at the same locus during expiration elicited short- and long-term phrenic activations. The short-term activation consisted of a tetanic orthodromic response. The long-term activation, of central origin, exhibited the same pattern as a spontaneous inspiration and consisted of an inspiratory resetting which necessitated weak anaesthesia and light hypocapnia. Control experiments (restricted lesions of the medulla and the cervical cord, recording of afferent activity in thalamic sensory nuclei, medullary stimulation) revealed that this inspiratory resetting could not be related to appreciable activation of either non-respiratory efferents or spinal afferent pathways studied but was likely to depend on the activation of the descending inspiratory axons. We conclude that the respiratory resetting obtained by spinal stimulation resulted from mass antidromic activation of the inspiratory bulbospinal neurons which thus appear to be involved in the generation of the respiratory rhythm.     

The effect of the phase relationship between the arterial blood gas oscillations and central neural respiratory activity on phrenic motoneurone output in cats

The aim of the present experiments in artificially ventilated, anesthetized cats was to investigate in which circumstances the timing of the arterial blood gas oscillations within the respiratory cycle can be of importance in determining phrenic motoneurone output. The phase relationship phi was defined as the relative position of the peak of the phrenic bursts within the current continuously measured PaO2 oscillations. It was judged breath by breath whether there was a relationship between phi and neural tidal volume, and neural inspiratory and expiratory duration. Within cats, PETCO2 was kept constant at about 1.5-2% above apneic threshold. It was found that phi indeed partly determined these ventilatory parameters provided the oscillations were large enough. This was evident in normoxia; in moderate hypoxia the influence of phi was demonstrable more easily, i.e. at smaller oscillation amplitudes. In both conditions the effect of phi on neural tidal volume was most pronounced. Neural tidal volume was maximal when peak inspiration coincided with the expiratory trough of the PaO2 oscillations. A 1:1 phase lock between phrenic activity and the ventilatory only occurred when the pump frequency was close to the cats own breathing frequency. Bilateral carotid sinus nerve section abolished the effects of phi.     

Influence of immersion in water on muscle function and breathing pattern in patients with severe diaphragm weakness

STUDY OBJECTIVE: Dyspnea is a common symptom in patients with diaphragm weakness or paralysis. In particular, dyspnea may be aggravated by immersion. We hypothesized that immersion to the neck in water would decrease vital capacity and consequently increase the demand/capacity ratio of the respiratory muscles. DESIGN: Case series study. SUBJECTS: Seven patients with profound diaphragm weakness or paralysis proven by phrenic nerve stimulation, and seven normal control subjects. Intervention and measurements: We measured land-based and water-based spirometry, breathing pattern, and mouth occlusion pressures. RESULTS: We found that the patients could preserve minute ventilation despite a fall in vital capacity from a mean of 2.3 to 1.3 L, but this required an increased respiratory rate (RR) [21.4 to 26.7 breaths/min, p = 0.018]. We used mouth occlusion pressure 100 ms after the start of inspiration (P(0.1)) as an estimation of the drive to breath; P(0.1) increased from 1.4 to 3.9 cm H(2)O (p = 0.018) without significant change in tidal volume. CONCLUSIONS: Relative to control subjects, patients with diaphragm weakness have augmented drive to breathe in order to attempt to defend gas exchange. This conclusion is implied by the presevered minute ventilation with immersion, the augmented RR, and elevated P(0.1) relative to maximum static inspiratory pressure.     

Diaphragm pacing and continuous positive airway pressure

The effect of changes in continuous positive airway pressure (CPAP) on the tidal volume generation by the diaphragm during electrical stimulation of the phrenic nerves in a quadriplegic patient is presented. Measurements of tidal volume, end-tidal PCO2, arterial PCO2, oxygen consumption, physiologic dead space to tidal volume ratio, diaphragm length, and thoracic and abdominal dimensions were made at values of CPAP from 0 to 20 cm H2O during periods of diaphragm pacing. Total respiratory compliance (TRC) was measured during controlled ventilation with incremental positive end-expiratory pressure (PEEP) from 0 to 20 cm H2O. A significant negative correlation was found between increasing CPAP and generated tidal volumes. This correlation was seen to occur even when TRC was constant at degrees of CPAP from 0 to 7.5 cm H2O. When phrenic nerve stimulation was commenced, oxygen consumption rose significantly from values obtained during controlled ventilation, but there was no significant correlation between changes in CPAP and the rise in oxygen consumption. Using inductance methods, thoracic and abdominal diameters were seen to rise as CPAP was increased. As suggested by the decrease in the length of the vertical and horizontal portions of the diaphragm in the chest roentgenogram, the conformation of the diaphragm also changed. It is suggested that the operating length and conformation of the diaphragm are principal factors affecting tidal volume generation during electrical stimulation of the phrenic nerves.