Function of the diaphragm during exercise]

We evaluated the effect of global inspiratory muscle fatigue (GF) on respiratory muscle control during exercise at 30%, 60%, and 90% of maximal power output in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. Respiratory pressures, breathing pattern, and perceived breathlessness were measured. Induction of GF had no effect on the ventilatory parameters during mild and moderate exercise. It altered, however, ventilatory response to heavy exercise by increasing breathing frequency and minute ventilation, with minor changes in tidal volume. This was accompanied by an increase in perceived breathlessness. GF significantly increased both the tonic and phasic activities of abdominal muscles that allowed 1) the diaphragm to maintain its function while developing less pressure, 2) the same tidal volume with lesser shortening of the rib cage inspiratory muscles, and 3) relaxation of the abdominal muscles to contribute to lung inflation. The increased work performed by the abdominal muscles may, however, lead to a reduction in their strength. GF may impair exercise performance in some healthy subjects that is probably not related to excessive breathlessness or other ventilatory factors. The respiratory system is remarkably adaptable in maintaining ventilation during exercise even with impaired inspiratory muscle contractility.     

Respiratory muscle function and control of breathing in patients with acromegaly

Increase in lung size has been described in acromegalic patients, but data on respiratory muscle function and control of breathing are relatively scarce. Lung volumes, arterial blood gas tensions, and respiratory muscle strength and activation during chemical stimulation were investigated in a group of 10 patients with acromegaly, and compared with age- and sex-matched normal controls. Inspiratory muscle force was evaluated by measuring pleural (Ppl,sn) and transdiaphragmatic (Pdi,sn) pressures during maximal sniffs. Dynamic pleural pressure swing (Ppl,sw) was expressed both as absolute value and as percentage of Ppl,sn. Expiratory muscle force was assessed in terms of maximal expiratory pressure (MEP). In 8 of the 10 patients, ventilatory and respiratory muscle responses to hyperoxic progressive hypercapnia and to isocapnic progressive hypoxia were also evaluated. Large lungs, defined as total lung capacity (TLC) greater than predicted (above 95% confidence limits), were found in five patients. Inspiratory or expiratory muscle force was below normal limits in all but three patients. During unstimulated tidal breathing, respiratory frequency (fR) and mean inspiratory flow (tidal volume/inspiratory time (VT/tI)) were greater, while inspiratory time (tI) was shorter than in controls. Minute ventilation (V'E) and mean inspiratory flow response slopes to hypercapnia were normal In contrast, four patients had reduced delta(VT/tI)/arterial oxygen saturation (Sa,O2) and three had reduced deltaV'E/Sa,O2. Ppl,sw(%Ppl,sn) response slopes to increasing end-tidal carbon dioxide tension (PET,CO2) and decreasing Sa,O2 did not differ from the responses of the normal subjects, suggesting normal central chemoresponsiveness. At a PET,CO2 of 8 kPa or an Sa,O2 of 80%, patients had greater fR and lower tI compared with controls. Pdi,sn and Ppl,sn related both to deltaV'E/deltaSa,O2 (r=0.729 and r=0.776, respectively) and delta(VT/tI)/deltaSa,O2 (r=0.860 and r=0.90, respectively). Pdi,sn also related both to deltaV'E/deltaPET,CO2 (r=0.8) and delta(VT/tI)/deltaPET,CO2 (r=0.76). In conclusion, the data suggest the relative independence of pneumomegaly and respiratory muscle strength. Peripheral (muscular) factors appear to modulate a normal central motor output to give a more rapid pattern of breathing.     

Effect of elastic loading on mouth occlusion pressure during CO2 rebreathing in man

In 7 normal subjects, mouth occlusion pressure was evaluated as an index of neural drive to the respiratory muscles during CO2 rebreathing, with and without the addition of 2 degrees of elastic loads. During control and loaded rebreathing, changes in both mouth occlusion pressure and ventilation were linearly related to changes in end-tidal PCO2. With elastic loading, the slope of occlusion pressure versus end-tidal PCO2 response consistently increased from control values in all subjects and was greater with the higher load in 6 of 7 subjects. The ventilatory response to elastic loading was variable and inconsistent owing to the variable increase in frequency of breathing, the tidal volume always being diminished. In normal subjects, both mouth occlusion pressure and ventilation appeared to assess neural drive to the respiratory muscles in response to CO2 rebreathing; with elastic loading, only occlusion pressure continued to reflect neuromuscular output. This increased pressure response could have been mediated by neural reflex and/or intrinsic muscle mechanisms. The data suggest that mouth occlusion pressure may be a useful parameter for evaluating neuromuscular control mechanisms under conditions of increased lung elastance.     

Respiratory muscles and ventilatory failure: 1993 perspective

Some conditions that predispose to ventilatory failure increase the work of breathing (chronic obstructive pulmonary disease [COPD], obesity, kyphoscoliosis), whereas others cause severe respiratory muscle weakness. Specific reasons for muscle weakness include critical illness (electrolyte imbalance, acidemia, shock, sepsis), chronic illness (poor nutrition, cachexia), and neuromuscular diseases. Inspiratory muscle weakness from mechanical disadvantage to the diaphragm is characteristic of asthma and COPD. The increased work of breathing combined with muscle weakness increases the pressure needed to inspire a breath and decreases maximal inspiratory pressure. When this pressure exceeds 0.4, dyspnea and inspiratory muscle fatigue ensue. One way to lower this pressure and avert fatigue is to lower the tidal volume. Ventilatory drive is high, not low, in ventilatory failure. Concomitant shortening of inspiration and breath duration cause the small tidal volume and increased respiratory rate. Gas exchange is compromised by ventilation/perfusion imbalance, and the ratio of dead space to tidal volume is also increased by rapid, shallow breathing. Reduction in tidal volume minimizes dyspnea, but the small tidal volume is inadequate for gas exchange. Acute treatment of respiratory muscle failure involves respiratory muscle rest through mechanical ventilation and removal of noxious influences (infection, metabolic disarray), whereas chronic treatment involves rebuilding the contractile apparatus by nutritional repletion and training.     

Breathing patterns in infants and children under halothane anesthesia: effect of dose and CO2

We studied the amplitude, timing, and shape of the airflow waveform at the mouth of spontaneously breathing children under two sets of conditions: 1) in 30 children aged 9 wk-4.5 yr at 2, 1, and 0% inspired halothane concentration and 2) in 22 children aged 5 mo-7 yr during hyperoxic CO2 rebreathing while recovering from anesthesia. Compared with control values, the relative changes in breath parameters at 1 and 2% halothane were, respectively, as follows: total cycle time -19 and -31%, tidal volume (VT) -30 and -44%, minute ventilation -11 and -17%, and VT/inspiratory time (TI) -16 and -20%. Parameters of timing and breath shape did not change except for the significant but small increase in TI/total cycle time (by 6 and 8%, respectively). With CO2 rebreathing, parameters reflecting inspiratory drive increased significantly in all patients as shown by the slopes of the regressions of these parameters against end-tidal PCO2. Mean slopes expressed in %control value per millimeter of mercury CO2 were 12.1 for minute ventilation, 8.3 for VT, and 10.67 for VT/TI. Parameters reflecting the timing and breath shape remained essentially unchanged. Our results suggest that, in children under halothane anesthesia, the amplitude, timing, and shape of the breathing pattern are controlled independently. In particular, the amplitude and timing of the breath may vary widely without any significant change in the shape.     

Comparative physiologic effects of noninvasive assist-control and pressure support ventilation in acute hypercapnic respiratory failure

STUDY OBJECTIVE: To compare the effects of noninvasive assist-control ventilation (ACV) and pressure support ventilation (PSV) by nasal mask on respiratory physiologic parameters and comfort in acute hypercapnic respiratory failure (AHRF). DESIGN: A prospective randomized study. SETTING: A medical ICU. PATIENTS AND INTERVENTIONS: Fifteen patients with COPD and AHRF were consecutively and randomly assigned to two noninvasive ventilation (NIV) sequences with ACV and PSV mode, spontaneous breathing (SB) via nasal mask being used as control. ACV and PSV settings were always subsequently adjusted according to patient's tolerance and air leaks. Fraction of inspired oxygen did not change between the sequences. MEASUREMENTS AND RESULTS: ACV and PSV mode strongly decreased the inspiratory effort in comparison with SB. The total inspiratory work of breathing (WOBinsp) expressed as WOBinsp/tidal volume (VT) and WOBinsp/respiratory rate (RR), the pressure time product (PTP), and esophageal pressure variations (deltaPes) were the most discriminant parameters (p<0.001). ACV most reduced WOBinsp/VT (p<0.05), deltaPes (p<0.05), and PTP (0.01) compared with PSV mode. The surface diaphragmatic electromyogram activity was also decreased >32% as compared with control values (p<0.01), with no difference between the two modes. Simultaneously, NIV significantly improved breathing pattern (p<0.01) with no difference between ACV and PSV for VT, RR, minute ventilation, and total cycle duration. As compared to SB, respiratory acidosis was similarly improved by both modes. The respiratory comfort assessed by visual analog scale was less with ACV (57.23+/-30.12 mm) than with SB (75.15+/-18.25 mm) (p<0.05) and PSV mode (81.62+/-25.2 mm) (p<0.01) in our patients. CONCLUSIONS: During NIV for AHRF using settings adapted to patient's clinical tolerance and mask air leaks, both ACV and PSV mode provide respiratory muscle rest and similarly improve breathing pattern and gas exchange. However, these physiologic effects are achieved with a lower inspiratory workload but at the expense of a higher respiratory discomfort with ACV than with PSV mode.     

Effect of upper airway cooling and CO2 on diaphragm and geniohyoid muscle activity in the rat

Upper airway (UA) reflexes play an important role in regulating breathing and UA patency, but the effects of UA CO2 and cooling on ventilation and UA muscle activity are controversial. Diaphragm and geniohyoid electromyographic activities were recorded in anaesthetized rats, breathing spontaneously through a low-cervical tracheostomy. Warmed, humidified air containing 0 or 10% CO2 and cooled, room humidity air were applied at constant flow to the UA through a high- cervical tracheostomy. Spontaneous tracheal airflow, UA airflow and temperature, blood pressure, and rectal temperature were recorded. In all animals, the geniohyoid muscle had phasic inspiratory activity, which slightly preceded diaphragmatic activity. CO2 had no effect on mean peak integrated diaphragmatic activity and variable effects on geniohyoid activity. The coefficients of variation of these activities were unaffected by CO2. Similar results were obtained following bilateral mid-cervical vagotomy. Cool air decreased respiratory frequency (78+/-8%) (mean+/-SD % of control), peak inspiratory flow (78+/-5%) and diaphragmatic activity (77+/-4%), and increased geniohyoid activity (149+/-11%). Cutting the superior laryngeal nerves abolished these effects. In conclusion, whilst moderate upper airway cooling inhibits breathing and excites geniohyoid muscle activity, upper airway carbon dioxide has minimal effect.     

Effects of nasal continuous positive airway pressure on breathing pattern and respiratory drive in patients with obstructive sleep apnea syndrome

To examine the influence of continuous positive airway pressure (CPAP) therapy on respiratory center drive in patients with obstructive sleep apnea syndrome (OSAS), 20 normocapnic OSAS patients (group 0) and 20 simple snoring patients were studied. In the first night, diagnostic polysomnography (PSG) was performed. Before and after PSG monitoring, mouth occlusion pressure (P0.1), tidal volume (VT), minute ventilation (VE), respiratory rate (RR), inspiratory time (Ti), expiratory time (Te), total cycle duration (Ttot), inspiratory duty cycle (Ti/Ttot), mean inspiratory flow (VT/Ti) and effective inspiratory impedance (P0.1/VT/Ti, Ieff) were measured while they were breathing room air. In the following night the OSAS patients were treated with nasal CPAP and PSG monitoring and the above mentioned measurements were repeated. The results showed that pre-PSG values of P0.1, RR and P0.1/VT/Ti in the OSAS patients were significantly higher than those in the snoring patients, while VT, Ti, Te and Ttot values were lower. In the first night, the post-PSG P0.1 value in the OSAS patients increased markedly as compared with the pre-PSG. After overnight nasal CPAP therapy, the respiratory disorder index in the OSAS patients decreased markedly, the nadir SaO2 increased markedly, but the post-PSG P0.1 value did not increase significantly. It is concluded that, before sleep, OSAS patients exhibit a higher respiratory drive and a shallow and frequent breathing pattern as compared with simple snoring patients. After nocturnal sleep, the respiratory drive of OSAS patients increases significantly, the breathing pattern becomes more shallow and frequent. Nasal CPAP may effectively relieve the sleep apnea and hypopnea as well as the resulting hypoxemia and therefore correct the changes in breathing pattern and respiratory drive through nocturnal sleep in patients with OSAS.     

Physiological determinants of inspiratory effort sensation during CO2 rebreathing in normal subjects

1. The physiological basis of inspiratory effort sensation remains uncertain. Previous studies have suggested that pleural pressure, rather than inspiratory muscle fatigue, is the principal determinant of inspiratory effort sensation. However, only a limited range of inspiratory flows and breathing patterns have been examined. We suspected that inspiratory effort sensation was related to the inspiratory muscle tension-time index developed whatever the breathing pattern or load, and that this might explain the additional rise in sensation seen with hypercapnia. 2. To investigate this we measured hypercapnic rebreathing responses in seven normal subjects (six males, age range 21-38 years) with and without an inspiratory resistive load of 10 cm H2O. Pleural and transdiaphragmatic pressures, mouth occlusion pressure and breathing pattern were measured. Diaphragmatic and ribcage tension-time indices were calculated from these data. Inspiratory effort sensation was recorded using a Borg scale at 30s intervals during each rebreathing run. 3. Breathing pattern and inspiratory pressure partitioning were unrelated to changes in inspiratory effort sensation during hypercapnia. Tension-time indices reached pre-fatiguing levels during both free breathing and inspiratory resistive loading. 4. Stepwise multiple regression analysis using pooled mechanical, chemical and breathing pattern variables showed that pleural pressure was more closely related to inspiratory effort sensation than was transdiaphragmatic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Phrenic motoneuron discharge during sustained inspiratory resistive loading

I determined whether prolonged inspiratory resistive loading (IRL) affects phrenic motoneuron discharge, independent of changes in chemical drive. In seven decerebrate spontaneously breathing cats, the discharge patterns of eight phrenic motoneurons from filaments of one phrenic nerve were monitored, along with the global activity of the contralateral phrenic nerve, transdiaphragmatic pressure, and fractional end-tidal CO2 levels. Discharge patterns during hyperoxic CO2 rebreathing and breathing against an IRL (2,500-4,000 cmH2O.1-1.s) were compared. During IRL, transdiaphragmatic pressure increased and then either plateaued or decreased. At the highest fractional end-tidal CO2 common to both runs, instantaneous discharge frequencies in six motoneurons were greater during sustained IRL than during rebreathing, when compared at the same time after the onset of inspiration. These increased discharge frequencies suggest the presence of a load-induced nonchemical drive to phrenic motoneurons from unidentified source(s).     

Respiratory mechanics in patients with tense cirrhotic ascites

Lung volumes are decreased by tense ascites and increase after large volume paracentesis (LVP). The overall effect of ascites and LVP on the respiratory function is poorly understood. We studied eight cirrhotic patients with tense ascites before and after LVP. Inspiratory muscle force (maximal transdiaphragmatic pressure (Pdi,max), and the lowest pleural pressure (Pp1,min)) was assessed while the patients were seated. Rib cage and abdominal volume displacements, as well as pleural and gastric pressures were measured during quiet breathing while the patients were supine. Pdi,max and Ppl,min were normal and did not change after LVP (from 84.2+/-19.7 to 85.2+/-17.0 cmH2O and from 68.3+/-19.7 to 74+/-15.9 cmH2O, respectively). The abdominal contribution to the generation of tidal volume was greater than that of the rib cage (79 vs 21%), a pattern which did not change after LVP (73 and 27%). Before LVP, tidal swings both of pleural pressure (Ppl,sw) and transdiaphragmatic pressure (Pdi,sw) were large (15.3+/-4.3 and 18.5+/-3.9 cmH2O, respectively) and the load on inspiratory muscles was increased as a consequence of elevated dynamic elastance of the lung (El,dyn) (11.4+/-2.6 cmH2O x L(-1)) and ("intrinsic") positive end-expiratory pressure (PEEPi) (4.3+/-3.5 cmH2O). LVP reduced the load on the inspiratory muscles, as shown by the significant decrease in Ppl,sw (10.6+/-2.0 cmH2O), Pdi,sw (12.8+/-3.0 cmH2O), El,dyn (10.0+/-2.0 cmH2O x L(-1)) and PEEPi (1.1+/-1.3 cmH2O). The amount of fluid removed was closely related to changes in Ppl,sw and PEEPi. We conclude that the strength of the inspiratory muscles is normal or reduced in seated cirrhotic patients. In the supine position, tense ascites results in an increase in lung elastic load and development of positive end-expiratory pressure, with a consequent overload and increased activation of inspiratory muscles. Large volume paracentesis decreases overloading and activation, but does not change the strength of the inspiratory muscles.     

Carbon dioxide spirogram (but not capnogram) detects leaking inspiratory valve in a circle circuit

Expiratory valve incompetence in the circle circuit is diagnosed by using capnography (PCO2 versus time) when significant CO2 is present throughout inspiration. However, inspiratory valve incompetence will allow CO2-containing expirate to reverse flow into the inspiratory limb. CO2 rebreathing occurs early during the next inspiration, generating a short extension of the alveolar plateau and decreased inspiratory downslope of the capnogram, which may be indistinguishable from normal. We hypothesized that CO2 spirography (PCO2 versus volume) would correctly measure inspired CO2 volume (VCO2) during inspiratory valve leak. Accordingly, a metabolic chamber (alcohol combustion) was connected to a lung simulator, which was mechanically ventilated through a standard anesthesia circle circuit. By multiplying and integrating airway flow and PCO2, overall, expired, and inspired VCO2 (VCO2,br = VCO2,E - VCO2,I) were measured. When the inspiratory valve was compromised (by placing a wire between the valve seat and diaphragm), VCO2,I increased from 2.7 +/- 1.7 to 5.7 +/- 0.2 mL (P < 0.05), as measured by using CO2 spirography. In contrast, the capnogram demonstrated only an imperceptible lengthening of the alveolar plateau and did not measure VCO2,I. To maintain effective alveolar ventilation and CO2 elimination, increased VCO2,I requires a larger tidal volume, which could result in pulmonary barotrauma, decreased cardiac output, and increased intracranial pressure. Implications: Circle circuit inspiratory valve leak will allow CO2-containing expirate to reverse flow into the inspiratory limb, with subsequent rebreathing during the next inspiration. This CO2 rebreathing causes imperceptible lengthening of the alveolar plateau of the capnogram and is detected only by using the CO2 spirogram (PCO2 versus volume).     

Immediate response to inspiratory resistive loading in anesthetized patients with kyphoscoliosis: spirometric and neural effects

In kyphoscoliosis (KS), lung volumes are reduced, respiratory elastance and resistance are increased, and breathing pattern is rapid and shallow, attributes that may contribute to defense of tidal volume (VT) in the face of inspiratory resistive loading. The control of ventilation of 12 anesthetized patients about to undergo corrective spinal surgery was compared to that of 11 anesthetized patients free of cardiothoracic disease during quiet breathing and the first breath through one of three linear resistors. Mean forced vital capacity (FVC) of the KS group was 48% that of the controls (C). Passive elastance (Ers) and active elastance and resistance (E'rs and R'rs, respectively) were computed according to previously described techniques (Behrakis PK, Higgs BD, Baydur A, Zin WA, Milic-Emili J (1983) Active inspiratory impedance in halothane-anesthetized humans. J Appl Physiol 54: 1477-1481). Baseline tidal volume VT, inspiratory duration Tl, expiratory duration TE, duration of total breathing cycle TT, and inspiratory duty cycle TI/TT were significantly reduced, while VE was slightly decreased in the KS. Ers, E'rs, and R'rs, were, respectively, 72, 69, and 89% greater in the KS. Driving pressure (Pmus) was derived from the equation of motion, using active values of respiratory elastance. With resistive loading, there was greater prolongation of TI in the C, while percent reduction in VT and minute ventilation VE was less in KS. Compensation in both groups was achieved through three changes in the Pmus waveform. (1) Peak amplitude increased. (2) The duration of the rising phase increased. (3) The rising Pmus curve became more concave to the time axis. These changes were most marked with application of the highest resistance in both groups. Peak driving pressure and mean rate of rise of Pmus were greater in the KS. Increased intrinsic impedance, Pmus, and differences in changes in neural timing in anesthetized kyphoscoliotics contribute to modestly greater VT defense, compared to that of anesthetized subjects free of cardiorespiratory disease.     

Tracheal pressure triggering a demand-flow continuous positive airway pressure system decreases patient work of breathing

OBJECTIVES: Triggering a ventilator "ON" at the carinal end of the endotracheal tube decreases imposed work of breathing by bypassing the resistance imposed by the breathing circuit and the endotracheal tube. We compared work of breathing during spontaneous ventilation between three methods of triggering the ventilator "ON": a) conventional pressure triggering from inside the ventilator; b) flow-by triggering; or c) tracheal pressure triggering at the carinal end of the endotracheal tube. We hypothesized that the work of breathing would be substantially decreased with tracheal pressure triggering compared with conventional pressure and flow-by methods in patients receiving continuous positive airway pressure. DESIGN: Clinical, prospective study. SETTING: University teaching hospital. PATIENTS: Fourteen adults diagnosed with acute respiratory failure. INTERVENTIONS: All patients were breathing spontaneously at an FIO2 of 0.30 to 0.40 and received 5 cm H2O of continuous positive airway pressure. Three different methods of triggering the ventilator while set in the continuous positive airway pressure mode were administered in random order. MEASUREMENTS AND MAIN RESULTS: Real-time measurements of esophageal pressure and tidal volume were integrated with a respiratory monitor (CP-100, Bicore, Riverside, CA) that uses the Campbell diagram to calculate total work of breathing. Imposed work of breathing was calculated by integrating tidal volume with the pressure at the carinal end of the endotracheal tube. Physiologic work of breathing was calculated by subtracting imposed work of breathing from the total work of breathing. Breathing frequency, the index of rapid shallow breathing (breathing frequency/tidal volume), peak inspiratory flow rate demand, exhaled minute ventilation, and the duration of respiratory muscle contraction assessed by the ratio of inspiratory time to total cycle time were also measured. Data were analyzed by Friedman's repeated-measures analysis of variance on ranks. Alpha was set at .05 for statistical significance. Imposed work of breathing decreased to approximately zero during tracheal pressure triggering. As a result, total work of breathing decreased by approximately 40% compared with the flow-by and conventional methods. During tracheal pressure triggering only, airway pressure increased above baseline pressure to approximately 11 cm H2O, which resembled pressure-support ventilation. Also, during tracheal pressure triggering, tidal volume and peak inspiratory flow rate were significantly increased, while the pressure-time product and the index of rapid shallow breathing were significantly decreased. Hemodynamic status and oxygen saturation were not clinically affected. CONCLUSIONS: The tracheal pressure triggering of a demand-flow continuous positive airway pressure system creates an effect similar to pressure-support ventilation that significantly decreases imposed work of breathing and, thus, total work of breathing. We recommend moving the triggering site of the ventilator to the carinal end of the endotracheal tube.     

Non-invasive assessment of inspiratory muscle performance during exercise in patients with chronic heart failure

AIMS: The aim of this study was to assess inspiratory performance at rest and during exercise in patients with chronic heart failure in comparison with healthy controls using a non-invasive index: the tension-time index of inspiratory muscles (TTMUS). METHODS: We studied 13 patients with chronic heart failure (57 +/- 7 years) and 10 control subjects (58 +/- 6 years) at rest and during an incremental maximal exercise test. Measurements included breathing pattern (inspiratory time, total time of respiratory cycle, minute ventilation, tidal volume and respiratory frequency), mouth occlusion pressure and mean inspiratory pressure (calculated as follows: 5 x mouth occlusion pressure x inspiratory time). The maximal inspiratory pressure was measured at rest. TTMUS was calculated from the equation: TTMUS = PI/PIMAX x TI/TTOT, where PI/PIMAX is the ratio of mean inspiratory pressure to maximal inspiratory pressure and TI/TTOT is the ratio of mean inspiratory time to total time of the respiratory cycle. RESULTS: At rest, the results in patients showed non-significantly higher mouth occlusion pressure, lower maximal inspiratory pressure (P < 0.001), and a higher ratio of mean inspiratory pressure to maximal inspiratory pressure (P < 0.01). There was no difference in the breathing pattern. TTMUS was thus significantly higher in the patients with chronic heart failure (P < 0.001). At maximal exercise (77 +/- 16 W for patients with chronic heart failure vs 142 +/- 27 W for controls, P < 0.001), the ratio of mean inspiratory time to total time of respiratory cycle, the mouth occlusion pressure and the ratio of mean inspiratory pressure to maximal inspiratory pressure were not different. TTMUS was thus comparable in the two groups. During exercise, at comparable workloads (20, 40 and 60 W), the patients showed higher mouth occlusion pressure (P < 0.01) and a higher ratio of mean inspiratory pressure to maximal inspiratory pressure (P < 0.001), whereas the ratio of mean inspiratory time to total time of the respiratory cycle was similar. TTMUS was thus higher in the patients at each workload (P < 0.05). CONCLUSION: This study shows that the determination of TTMUS at rest and during exercise allows the observation of alterations in inspiratory muscle performance as a result of both reduced inspiratory strength, as measured by the maximal inspiratory pressure, and increased ventilatory drive, as reflected by the mouth occlusion pressure in patients with chronic heart failure. The non-invasiveness of this new index is an additional argument for its use in a clinical setting.     

Reduced inspiratory effort during intermittent mandatory ventilation with PEEP

The use of intermittent mandatory ventilation (IMV) and positive and expiratory pressure (PEEP) may demand the patient mount an inspiratory pressure equivalent to the pressure level of the PEEP for spontaneous breathing. During respiratory failure, ineffective inspiratory muscles may be unable to consistently meet such demands, especially if high levels of PEEP are used. A technique which reduces the required inspiratory effort was devised for use in patients being treated with IMV and PEEP. Using this technique, isovolume inspiratory time was dramatically reduced and less inspiratory effort was required. This maneuver may assist spontaneous breathing in patients with respiratory failure on high levels of PEEP.     

Changes in maximal exercise ventilation and breathing pattern in boys during growth: a mixed cross-sectional longitudinal study

The aim of this mixed cross-sectional longitudinal study covering a total age range of 11-17 years, i.e. the entire pubertal growth period, was (1) to specify the changes in maximal breathing pattern during incremental exercise; (2) to determine what parts of the changes are due to anthropometric characteristics, physical fitness and inspiratory or expiratory muscle strength; and (3) to determine if the role of these variables is identical before, during and after pubertal growth spurt. This study was conducted in 44 untrained schoolboys separated into three groups, with an initial age of 11.2 +/- 0.2 years for group A, 12.9 +/- 0.25 years for group B, and 14.9 +/- 0.26 years for group C. These children were subsequently followed for 3 years, during the same time period each year. The maximal inspiratory and expiratory pressures (PI max and PE max) were used as an index of the respiratory muscle strength. During an incremental exercise test, maximal ventilation (VE max), tidal volume (VT max), breathing frequency (fmax), inspiratory and expiratory times (tI max and tE max) and mean inspiratory flow (VT/tI max) were measured at maximal oxygen uptake (VO2max). Our study showed that there was a marked increase with age in VE max, VT max, and VT/tI max, and no significant changes in fmax, tI max and tE max. PI max and PE max showed a general trend towards an increase between 11 and 17 years. The study of the linear correlations between maximal breathing pattern and the anthropometric characteristics, physical fitness and inspiratory or expiratory muscle strength showed that, in the three groups of children, (1) lean body mass was the major determinant of VE max, VT max and VT/tI max and the relationships were significantly different before, during and after the pubertal growth spurt; (2) physical fitness was the main determinant of tI max, tE max and fmax before and after the pubertal growth spurt; and (3) maximal respiratory strength did not play a significant role. In conclusion, this mixed cross-sectional longitudinal study showed, at maximal exercise, a significant increase in VE max during growth due only to a significant increase in VT max and VT/tI max, and that the relationships of anthropometric characteristics and physical fitness with maximal breathing pattern change during growth.     

The effect of vagal blockade on the variability of ventilation in the awake dog

The present study examined the variability of breathing in five (5) awake tracheostomized dogs with the vagi intact and during complete vagal blockade produced by cooling exteriorized cervical vagal loops (VC). Breath by breath variations in both respiratory timing (assessed from the airflow signal) and the drive to the respiratory muscles (as assessed from the rate of inspiratory airflow (VI/TI) and occlusive pressure (P100) were examined. The degree of variability in the parameters characterizing breathing was evaluated from frequency distribution histograms and by calculation of the standard deviation. VC increased the mean values of VT, TI, TE, TI/TTOT, and decreased VT/TI and occlusion pressure, but had no consistent effect on the mean value of VE. The variability of VE, PACO2, VT, TI, TE, TI/TTOT was greater during VC in 4 of the 5 dogs. The increased variability of VE and PACO2 during VC appeared to be due to a poorer correlation between TI and TE. The present study suggests that vagal mechanoreceptors, presumably pulmonary stretch receptors, minimize breath by breath fluctuations in both the level and pattern of ventilation by controlling respiratory timing. An explanation, based on the model of inspiratory off-switching proposed by Beadley et al. (1975) is invoked.     

Occlusion pressures in men rebreathing CO2 under methoxyflurane anesthesia

The effect of general anesthesia on control of breathing was studied by CO2 rebreathing and occlusion pressure measurements in six normal human subjects under methoxyflurane anesthesia. CO2 was found to increase the amplitude of the occlusion pressure wave without changing its shape, so that CO2 responses in terms of the occlusion pressure developed 100 ms after the onset of inspiration (Po/0.1) gave results equivalent to the responses in terms of Po/1.o or any other parameter of the pressure wave. Methoxyflurane depressed the ventilatory response to CO2 but not the occlusion pressure response, implying that the most important action of the anesthetic was to increase the effective elastance of the respiratory system rather than to depress the respiratory centers. The elastance was further increased by CO2, and this mechanical change had the effect of shifting the "apneic threshold" extrapolated from the ventilatory response curve to a lower PAco2. Frequency of breathing, inspiratory and expiratory times were not altered by CO2 in anesthetized subjects.     

Effects of inspiratory flow waveforms on arterial blood gases and respiratory mechanics after open heart surgery

The clinical usefulness of inspiratory flow pattern manipulation during mechanical ventilation remains unclear. The aim of this study was to investigate the effects of different inspiratory flow waveforms, i.e. constant, sinusoidal and decelerating, on arterial blood gases and respiratory mechanics, in mechanically ventilated patients. Eight patients recovering after open heart surgery for valvular replacement and/or coronary bypass were studied. The ventilator inspiratory flow waveform was changed according to a randomized sequence, keeping constant the other variables of the ventilator settings. We measured arterial blood gases, flow, volume and pressure at the proximal (airway opening pressure (Pao)) and distal (Ptr) ends of the endotracheal tubes before and after 30 min of mechanical ventilation with each inspiratory flow waveform. We computed breathing pattern, respiratory mechanics (pressures and dynamic elastance) and inspiratory work, which was then partitioned into its elastic and resistive components. We found that: 1) arterial oxygen tension (Pa,O2) and arterial carbon dioxide tension (Pa,CO2) were not affected by changes in the inspiratory flow waveform; and 2) peak Pao and Ptr were highest with sinusoidal inspiratory flow, whilst mean Pao and Ptr and total work of breathing were least with constant inspiratory flow, mainly because of a concomitant decrease in resistive work during constant flow inflation. The effects of the inspiratory flow profile on Pao, Ptr and total inspiratory work performed by the ventilator were mainly due to the resistive properties of the endotracheal tubes. We conclude that the ventilator inspiratory flow waveform can influence patients' respiratory mechanics, but has no impact on arterial oxygen and arterial carbon dioxide tension.