American Journal of Respiratory and Critical Care Medicine

Many patients with respiratory failure related to neuromuscular disease receive chronic invasive ventilation through a tracheostomy. Improving quality of life, of which speech is an important component, is a major goal in these patients. We compared the effects on breathing and speech production of assist-control ventilation (ACV) and bilevel positive-pressure ventilation (BPPV) in nine patients with neuromuscular disease. Ventilator-delivered flow was measured using a pneumotachograph, and respiratory rate, inspiratory time, and ventilator-delivered volume were measured on this flow signal. Gas exchange was assessed using oxygen saturation and end-tidal carbon dioxide measurement. Microphone speech recordings were subjected to quantitative analysis. At rest, ventilatory parameters were similar with both modes. Speech induced an increase in inspiratory time during BPPV, with a greater increase in the volume released by the ventilator during speech as compared with ACV (172 ± 194 versus 26 ± 31 ml). Consequently, speech duration was longer during inspiration with BPPV. Moreover, BPPV allowed speech production to extend into expiration, and three patients could speak continuously during several respiratory cycles while receiving BPPV. Blood gas exchange was not modified by speech with BPPV or ACV. This study shows that BPPV provides better speech duration than ACV with no detectable short-term deleterious effects.

Invasive ventilation through a tracheostomy is widely used in patients with severe neuromuscular respiratory failure (13) or spinal cord injury (4). Improving quality of life in these patients is a central concern and includes attention to optimizing speech production (58). Ventilation is usually given through a cuffless or fenestrated tracheostomy tube that allows speech by creating an air leak (5). During inspiration, part of the ventilator-delivered volume (Vi) is diverted toward the upper airways, elevating subglottic pressures and allowing speech production (911). Thus, with the volume-targeted mode, competition may occur between the airflow needed to produce speech and the airflow needed to achieve a tidal volume large enough to ensure adequate gas exchange (11). Moreover, speech in ventilated patients is dependent on the ventilatory cycle and is possible only during inspiration and a short part of expiration (911), whereas normal speech occurs only during expiration (12, 13).

Hoit and Banzett (10) studied the effect on speech production of simple adjustments of ventilator parameters under a controlled mode. They most efficiently increased speech production by prolonging inspiration and adding positive end-expiratory pressure (PEEP) showing that these adjustments offered a simple, inexpensive, and safe way of improving ventilator-supported speech. The use of a ventilatory mode allowing the combination of both these modifications during speech could therefore allow us to obtain an improvement of speech production.

Pressure support ventilation (PSV) is a form of pressure-targeted mechanical ventilation activated by the patient's inspiratory effort. Once activated, a flow of gas sufficient to meet the patient's inspiratory demands enters the circuit as the expiration valve closes, allowing the pressure to rapidly approach the set level. A pressure plateau is established and maintained until the inspiratory flow decreases to a ventilator-specific minimal level, at which time exhalation occurs. The widespread use of PSV, especially for noninvasive ventilation (14), has made it clear that leakage causes ventilatory pattern changes, including increases in inspiratory time (Ti) and Vi (1518). PSV may allow compensation for leakage, thereby improving speech production. Adding PEEP may keep the expiratory subglottic pressure at a sufficiently high level to allow speech during expiration (9, 10). To investigate these hypotheses, we compared the effects on speech production and ventilation of assist-control ventilation (ACV), which is the most widely used technique in our neuromuscular disease unit, and of bilevel positive-pressure ventilation (BPPV), which combines PSV and PEEP.

Nine subjects with stable neuromuscular respiratory failure treated with ventilation through a cuffless tracheostomy were studied from December 2000 to April 2001. The study protocol was approved by our institutional review board, and written informed consent was obtained from all patients.

To ensure that inspiratory pressure triggers were comparable in all patients with both modes, we used the same ventilator model (Onyx'plus; Mallinckrodt, Les Ulis, France) for all experiments. On the day before testing, patients were familiarized with the Onyx'plus ventilator in both modes. Maximal trigger sensitivity without autotriggering was used. Care was taken to ensure that Vi, Ti, and backup rate were similar to those used during conventional mechanical ventilation. During BPPV, PEEP was 5 cm H2O, and Vi and Ti were adjusted by modifying both the level of inspiratory pressure support and the level of expiratory flow trigger.

The ventilation modes were used in random order. With each mode, the subject was asked to continuously utter the [a] sound for 1 minute, to repeat [ta] as many times as possible for 1 minute, and to read a standard text passage.

At rest and during speech trials, ventilator-delivered flow was measured using a pneumotachograph (Fleisch #2, Switzerland), tracheal pressure was measured at the proximal end of the tracheostomy tube using a differential pressure transducer (MP 45 ± 100 cm H2O; Validyne, Northridge, CA), patient gas exchange was assessed based on oxygen saturation measured using pulse oximetry (Ohmeda Biox; BOC Healthcare, Boulder, CO), and end-tidal carbon dioxide pressure (PetCO2) was measured using a capnograph (Capnogard 1265; Novametrix, Wallingford, CT) placed at the proximal end of the tracheostomy tube. To avoid leaks during PetCO2 measurement, we performed the measurements during the first cycle after the end of speech and took care to close the upper airway during this measurement. Respiratory rate, Ti, Vi, and ventilator-delivered volume per minute were measured on the computerized flow signal.

Acoustic speech signals were recorded using three methods. The signals recorded from a microphone (DM202, MDE; Pierron, Sarreguemines, France) positioned 15 cm from the patient's lip were routed to a microcomputer with an AD converter (MP150 and Acqknowledge; Biopac system, Goleta, CA) that synchronized respiratory (ventilator flow, tracheal pressure, oxygen saturation, and PetCO2) and acoustic data. The AD converter digitized respiratory signals at 128 Hz and speech signals at 2,000 Hz. The acoustic signal was also routed to a computerized speech lab (Evaluation Vocale Assistée; license: CNRS – URA 261 Speech and Language, Version: 2.0; 1995; Soremed, Aix en Provence, France) where the bandwidth of the signal was between 20 and 15,000 Hz to allow assessment of fundamental frequency and speech signal sound pressure level. Finally, the acoustic speech signal was recorded on an audiotape (Sony Walkman Professional, bandwidth 10–16,000 Hz) for possible subsequent qualitative analysis by speech therapists.

Speech was evaluated by measuring three parameters: mean time spent speaking above 40 dB sound pressure level during the respiratory cycle, syllable frequency in the speech portion of the breathing cycle, and time needed to read the passage. Subjects evaluated subjective comfort of speech on a 10-cm horizontal visual analog scale. A qualitative analysis of the audiotape recording samples of the reading trials was also performed by two listeners who were blinded to ventilatory mode. The listeners were both speech-language pathologists. Samples were presented in pairs (BPPV versus ACV) in random order. The listeners were asked to indicate which sample of each pair they preferred and to state the main reason for their preference. Disagreement in interpretation occurred only once and was resolved by consensus.

Statistical Analysis

All results are expressed as means ± SD. Differences between the two ventilatory modes were assessed by repeated measures ANOVA with two factors: (1) the between-subjects factor was the order of the ventilatory modes administration and (2) the within-subjects factor (repeated measures) was the ventilatory mode (ACV versus BPPV). p Values less than 0.05 were considered statistically significant.


Demographic and ventilatory characteristics of the nine study subjects are reported in Table 1

TABLE 1. Characteristics of the nine patients studied





Duration of
 Invasive Ventilation

Time on Ventilator
 Per Day

Type of
 Tracheostomy Tube

 (L, % pred)

 (cm H2O)

 (cm H2O)

Prescribed VI
1M/32 DMD54150524Tracoé # 90.310 (7)NANA0.750
2F/36 UM33158518Tracoé # 70.360 (11)−8100.400
3M/53 BD821751024Rusch # 90.470 (12)−10150.740
4M/24 DMD60163624Tracoé # 70.370 (9)NANA0.500
5M/24 DMD61161518Tracoé # 80.440 (9)−10100.500
6M/36 UM661671520Tracoé # 100.530 (12)−25150.650
7M/36 BD50160323Tracoé # 80.360 (9)−850.400
8M/78 C7T73180518Tracoé # 90.360 (9)−15150.700
Rusch # 8
0.370 (8)

Definition of abbreviations: BD = Becker dystrophy; C7T = tetraplegia caused by C7 spinal cord injury; DMD = Duchenne muscular dystrophy; F = female; M = male; NA = not available; Pemax = maximal expiratory pressure; Pimax = maximal inspiratory pressure; % pred = percentage of predicted value; Prescribed VI = ventilator prescribed-volume; Rusch = unfenestrated tracheostomy tube of the Rusch type (Rüsch Europe Médical, Lefaget, France); Tracoé = unfenestrated tracheostomy tube of the Trachoé type (Pouret Médical, Clichy, France); UM = unidentified myopathy; VC = vital capacity.

. Mean age was 42 ± 20 years. The subjects had severe neuromuscular respiratory failure (vital capacity, 9.6 ± 1.6% of predicted) with marked ventilator dependency (21.4 ± 2.8 hours per day). Eight subjects had myopathy and one had C7 tetraplegia related to a spinal cord injury. Mean duration of invasive ventilation was 6.7 ± 3.6 years. All subjects used a cuffless tracheostomy tube and received ACV as their main ventilation mode.

Ventilator Parameters at Rest

The ventilatory parameters provided by ACV and BPPV at rest are displayed in Table 2

TABLE 2. Ventilation characteristics at rest



ACV versus BPPV
VI, ml599 ± 174635 ± 237NS
RR, min−118.5 ± 2.119.0 ± 2.9NS
V̇I, L/min11.0 ± 1.011.9 ± 1.4NS
TI, s1.15 ± 0.161.15 ± 0.18NS
TI/TTOT0.35 ± 0.020.36 ± 0.09NS
SpO2, %96.7 ± 1.497.3 ± 1.3< 0.05
PETCO2, mm Hg
29.3 ± 4.2
27.3 ± 4.5

Definition of abbreviations: ACV = assist-control ventilation; BPPV = bilevel positive-pressure ventilation; NS = not significant; PETCO2 = end-tidal PCO2; RR = respiratory rate; SpO2 = oxygen saturation; TI = inspiratory time; TTOT = total respiratory time; VI = ventilator delivered-volume; V̇I (L/min) = volume per minute delivered by the ventilator.

. The mean level of inspiratory pressure support required with BPPV to produce a similar Vi as with ACV at rest was 16.5 ± 5.8 cm H2O. The mean level of expiratory flow trigger required with BPPV to produce a similar Ti as with ACV at rest corresponded to a fall in inspiratory flow by 65 ± 20% of the peak flow.

Effect of Speech (Reading) on Ventilator Parameters and Gas Exchange

The effects of speech (reading) on ventilatory parameters during both modes are reported in Table 3

TABLE 3. Changes in ventilation characteristics during speech



ACV versus BPPV
VI, ml+26 ± 31+172 ± 194p < 0.05
RR, min−1+3.7 ± 4.7+2.3 ± 4.0NS
V̇I, L/min+2.6 ± 2.9+5.0 ± 4.4p < 0.05
TI, s−0.01 ± 0.01+0.23 ± 0.26p < 0.02
TI/TTOT+0.06 ± 0.08+0.13 ± 0.07p < 0.02
SpO2, %+0.1 ± 0.3−0.1 ± 0.6NS
PETCO2, mm Hg
+0.3 ± 2.3
−0.3 ± 1.0

For definition of abbreviations, see Table 2.

, and an example of breathing at rest and of sustaining [a] is given in Figure 1 . Ti increased during speech with BPPV but not with ACV. The increase in Vi induced by speech was significantly greater with BPPV than with ACV. Respiratory rate during speech was similar with both modes. Consequently, ventilator-delivered minute volume during speech was significantly higher with BPPV. Gas exchange parameter changes during speech were negligible and similar with the two modes of mechanical ventilation.

The order of use of the two modes had no significant effect on ventilator parameters.

Speech Production
Speech parameters were not affected by the order of use of the ventilatory modes.

Speech sound pressure level was measured as the average of overall signal and was similar with the two modes (74 ± 8 dB with ACV and 76 ± 5 dB with BPPV, not significant). With both modes, the microphone signal amplitude declined progressively during expiration with the decrease in airway pressure. This decline was quicker with the ACV mode. Fundamental frequency was significantly higher with BPPV but remained within the values usually observed in adults (1921) (122 ± 36 Hz with ACV and 127 ± 38 Hz with BPPV, p < 0.05).

Speech production per cycle was longer with BPPV than with ACV (Table 4)

TABLE 4. Speech evaluation



ACV versus BPPV
 p Value
Maximal [a] holding time/respiratory cycle, s1.05 ± 0.162.05 ± 0.47 0.0002
Silent period/respiratory cycle, s1.76 ± 0.530.79 ± 0.66< 0.002
MSD/TTOT, %38.7 ± 10.273.7 ± 20.3< 0.0005
Number of [ta] syllables/respiratory cycle5.44 ± 1.948.74 ± 4.36< 0.01
Number of [ta] syllables/s4.54 ± 1.314.73 ± 1.18NS
Text reading time, s107.3 ± 55.571.0 ± 32.7< 0.01
Number of respiratory cycles for text reading39.2 ± 17.726.7 ± 13.6< 0.005
Syllables/s5.50 ± 1.534.19 ± 0.98< 0.01
Speech comfort, VAS score on a 0–10 scale
4.8 ± 1.8
7.2 ± 2.5
< 0.005

Definition of abbreviations: ACV = assist-control ventilation; BPPV = bilevel positive-pressure support ventilation; MSD = maximal speech duration per respiratory cycle; NS = not significant; TTOT = total respiratory time; VAS = visual analog scale.

Speech comfort was evaluated with a VAS graded from 0 to 10 (0: not comfortable; 10: very comfortable).

as shown by the typical recordings of sustained [a] production with the two ventilatory modes shown in Figure 1.

During the syllable repetition trial, the number of [ta] repetitions per respiratory cycle was significantly higher with BPPV, whereas the number of syllables pronounced per second of speech production was similar with both modes. Moreover, during the text reading trial, both the time and the number of respiratory cycles needed to read the text were significantly shorter with BPPV. Although syllable number per second of speech production was smaller during reading with BPPV, less time was needed to read the standard text passage. Accordingly, as compared with ACV, speech duration was longer with BPPV during both inspiration (by about 0.4 seconds) and expiration (by about 0.6 seconds), as shown in Figures 1 and 2

. The longer inspiratory speech duration was ascribable to the increase in Ti and to a nonsignificant reduction in time from inspiration initiation to speech initiation (280 ± 9 milliseconds with ACV versus 195 ± 12 milliseconds with BPPV).

Figure 3

shows the percentage of the total respiratory cycle used for speech. This percentage was higher in all patients with BPPV than with ACV. Four patients used more than 80% of their respiratory cycle for speech with BPPV, whereas all nine patients used less than 60% of their respiratory cycle with ACV. Moreover, three patients were able to speak continuously during several respiratory cycles with BPPV.

The analysis of speech comfort with a visual analogic scale showed that comfort score was significantly better with BPPV than with ACV (Table 4). The listeners, who were blind to the ventilatory mode, preferred speech produced with BPPV in seven subjects. The reason for this preference was always timing, not loudness or voice quality. In all the patients, speech remained intelligible during the reading test.

Mechanical ventilation has improved life expectancy of many patients presenting respiratory failure especially of restrictive origin (1, 2, 4). It has therefore become of increasing interest to address these patients' quality of life (2225). Speaking is of major importance in the population of tracheostomized patients (6). Speech production is profoundly modified in patients receiving invasive mechanical ventilation through a cuffless tracheostomy tube even with patients who do not present a specific voice disorder related to neurologic or mechanical impairment of the glottis. Indeed, subglottic pressure, which is usually negative during inspiration, becomes positive in these patients after ventilator pressurization. Moreover, while subglottic pressure is positive during expiration in normal subjects and allows voice production, it decreases drastically in invasively ventilated and tracheostomized subjects after the onset of expiration because the upper airway is bypassed by the tracheostomy tube. The effects of these changes on speech production have been described in detail (911). With the conventional volume-control mode, patients use the pressures and flows provided by the ventilator to speak. Ventilator-supported speech is therefore mainly produced during the inspiratory phase of the ventilator cycle and can only be continued during the initial part of the expiratory phase, as it stops when the tracheal pressure falls below the threshold value allowing speech. Accordingly, Hoit and Banzett (10) explored the effects of ventilator adjustments on ventilator-supported speech on six subjects. They showed that the increase of Ti and adding PEEP were most efficient measures in improving speech production and that the combination of these two adjustments allowed the obtainment of best results in speech quality in a subjective and objective evaluation of speech quality. To pursue this line further, we investigated speech produced with a BPPV mode. BPPV combines PEEP and PSV, thus providing an increase in Ti and Vi during speech, which would allow us to obtain the combination of beneficial effects on speech production observed by Hoit and Banzett (10) without manual adjustments. This automatic adjustment is mainly ascribable to the characteristics of the expiratory trigger and to the flow modification observed with the pressure-targeted mode during leakage. Most pressure-support devices, including the one used in our study, terminate inspiration when inspiratory flow falls below a set percentage of the inspiratory peak flow. It has been well demonstrated that the expiratory flow trigger is less easily attained when leakage occurs and that this results in Ti prolongation and in partial compensation for the leakage by an increase in Vi (17). Ti prolongation by leakage has been considered a disadvantage because it can produce desynchronization between the patient and the ventilator (16) and can make the expiratory time too short (17). Adverse effects have been reported in the absence of a time limit for inspiration when constant volume delivery at the pressure-support level created high continuous positive airway pressure levels (15). A time limit for inspiration is now featured in most devices. In contrast to previous studies, we found that a ventilation mode characterized by an increase in Ti in response to an increase in leakage may be beneficial: the result is a rise in the Vi when leakage increases, which allows prolongation of speech production during inspiration.

Furthermore, with both PSV and PEEP, three of our patients were able to speak continuously during several respiratory cycles. Thus, their speech became almost completely independent from their respiration. The effect of PEEP on speech has been investigated by Hoit and coworkers (9), who found that patients were able to speak during a greater percentage of the expiration time when PEEP was set at 4 cm H2O or more. This result is in accordance with physiologic knowledge of voice aerodynamics: most studies report that during normal speech subglottic airway pressure is between 2 and 14 cm H2O (26, 27). Accordingly, we used a PEEP of 5 cm H2O to strike an acceptable compromise between pressure-related side effects and speech improvement.

It is difficult to determine which of the two adjustments (pressure support or PEEP) was the most important for speech improvement. Although they were only asked to evaluate overall speech comfort with the visual analogic scale, all patients signaled a difference in speech production on the different parts of the respiratory cycle and reported more stable and powerful speech production during inspiration than during expiration. As sound pressure level decreases with the subglottic pressure (28, 29), we consistently observed and heard a decrease in microphone signal amplitude (see Figure 1) and sound level during expiration. Nevertheless, in all patients, speech remained intelligible to the experimenters during expiration. In addition, all patients appreciated the ability to extend speech into expiration. Finally because speech duration was significantly increased with BPPV as compared with ACV during both inspiration and expiration (Figure 2), we can conclude that both pressure support and PEEP contributed to increase speech duration. As shown in Figure 2, this increase almost doubled the speech time per respiratory cycle.

An alternative to PEEP could be the use of a one-way speaking valve positioned at the entrance of the tracheostomy tube (30, 31). Air flows through the valve into the tracheostomy tube during inspiration, whereas during expiration, the valve closes, directing exhaled air through the upper airway. This method is widely used during spontaneous breathing to allow speech during expiration and has been proposed more recently during mechanical ventilation (30, 31). However, during mechanical ventilation, the patient, who is usually ventilated with a large tidal volume, must expire all the available air through the upper airway within a generally limited expiratory time. The expiration occurs between the tracheal wall and the tracheal tube that creates substantial additional resistance (32). This additional resistance, which may produce a dynamic hyperinflation (i.e., an end expiratory volume above the functional residual capacity), is not easily foreseeable or adjustable. It is also very different from one patient to another because it depends on the anatomic characteristics of the trachea as well as on the characteristics and the position of the tracheal tube. In contrast, with PEEP, air can be shared between the upper airway and the tracheostomy tube, and although PEEP may also induce hyperinflation, it is easily adjustable according to patient tolerance.

One characteristic of the ventilator used in this study is that with the ACV mode, inspiratory pressure is constant and flow decreases progressively during inspiration, whereas the classic ACV mode generally delivers a constant flow. However, pressure is usually constant in ACV mode with the new generation of polyvalent home ventilators, where a compressor and/or turbine is substituted for the conventional piston or bellows (33). This constant pressurization may be beneficial for speech. Indeed, if the patient cannot control subglottic pressure, which is important for speech modulation, keeping this pressure relatively constant may allow better dynamic adjustment of the vocal fold recoil force, therefore permitting a better control of phonation. Moreover, because subglottic pressures during speech are relatively flat in normal subjects (34), the use of constant pressure during inspiration produces a flow waveform closer to the one observed in normal speech than the peaked waveform obtained with classic ACV (33). However, this possible advantage for speech of the pressure plateau generally observed with pressure-targeted modes was not evaluated in this study.

Given that during normal speech, the mean upper airway airflow rate is between 50 and 300 ml/seconds (3537), it is clear that during release of air by the ventilator, speech is obtained by diverting part of the delivered air toward the larynx. Therefore, the airflow required for speech competes with the airflow required for gas exchange, particularly when the patient uses the volume-targeted mode, with which no compensation for leakage is expected. In a study with a volume-targeted and controlled mode, Shea and coworkers (11) used a pneumotachograph and a face mask to show that leakage ranged from 15 to 38 ml and that tidal volume loss and minute ventilation loss were about 15% during speech. Although we did not evaluate leakage, the absence of a PetCO2 increase during speech suggests that minute ventilation was not significantly affected by speech. This may be ascribable to the increase in respiratory rate observed with both controlled/assisted modes used in our study. An additional explanation may be the larger volume delivered per cycle by the ventilator with the BPPV mode during speech; this additional volume may explain the increase in speech duration observed with BPPV as compared with ACV, with no significant difference in PetCO2.

The subjective experience of patients with mechanical ventilation is of major importance to their psychologic well-being. Social interactions improve when patients are more comfortable with their ventilatory assistance and when they can control the length of their sentences. All nine subjects felt more comfortable during speech with BPPV than with ACV. In addition, the syllable number per second during reading was smaller with BPPV, despite the shorter reading time, suggesting that reading was less hurried. Although most of the study subjects appreciated the improvements provided by BPPV, changing ventilator brands and habits acquired by the patient with the previous brand is difficult. Ventilators of different brands vary in size, weight, safety features, battery autonomy, and wheelchair fixation devices and cannot fulfill all the requirements for ensuring maximal autonomy of these patients.

In summary, our study demonstrates clearly that BPPV allows better speech duration than ACV during both inspiration and expiration. In addition, all subjects felt more comfortable with BPPV. Further studies are needed to confirm that these beneficial effects, and the absence of deleterious effects on ventilation observed during a single test, persist over time.

1. Bach JR, Ishikawa Y, Kim H. Prevention of pulmonary morbidity for patients with Duchenne muscular dystrophy. Chest 1997;112:1024–1028.
2. Raphael JC, Chevret S, Auriant I, Clair B, Gajdos P. Long-term ventilation at home in adults with neurological diseases. Rev Mal Respir 1998;15:495–505.
3. Chailleux E, Fauroux B, Binet F, Dautzenberg B, Polu JM. Predictors of survival in patients receiving domiciliary oxygen therapy or mechanical ventilation: a 10-year analysis of ANTADIR observatory. Chest 1996;109:741–749.
4. DeVivo MJ, Ivie CS III. Life expectancy of ventilator-dependent persons with spinal cord injuries. Chest 1995;108:226–232.
5. Bach JR, Alba AS. Tracheostomy ventilation: a study of efficacy with deflated cuffs and cuffless tubes. Chest 1990;97:679–683.
6. Bach JR. A comparison of long-term ventilatory support alternatives from the perspective of the patient and care giver. Chest 1993;104:1702–1706.
7. Leder SB. Importance of verbal communication for the ventilator-dependent patient. Chest 1990;98:792–793.
8. Miller JR, Colbert AP, Schock NC. Ventilator use in progressive neuromuscular disease: impact on patients and their families. Dev Med Child Neurol 1988;30:200–207.
9. Hoit JD, Shea SA, Banzett RB. Speech production during mechanical ventilation in tracheostomized individuals. J Speech Hear Res 1994;37:53–63.
10. Hoit J, Banzett R. Simple adjustments can improve ventilator-supported speech. Am J Speech-Lang Pathol 1997;6:87–96.
11. Shea SA, Hoit JD, Banzett RB. Competition between gas exchange and speech production in ventilated subjects. Biol Psychol 1998;49:9–27.
12. Bunn JC, Mead J. Control of ventilation during speech. J Appl Physiol 1971;31:870–872.
13. Hoit JD, Lohmeier HL. Influence of continuous speaking on ventilation. J Speech Lang Hear Res 2000;43:1240–1251.
14. Mehta S, Hill NS. Noninvasive ventilation. Am J Respir Crit Care Med 2001;163:540–577.
15. Black JW, Grover BS. A hazard of pressure support ventilation. Chest 1988;93:333–335.
16. Calderini E, Confalonieri M, Puccio PG, Francavilla N, Stella L, Gregoretti C. Patient-ventilator asynchrony during noninvasive ventilation: the role of expiratory trigger. Intensive Care Med 1999;25:662–667.
17. Highcock MP, Shneerson JM, Smith IE. Functional differences in bi-level pressure preset ventilators. Eur Respir J 2001;17:268–273.
18. Mehta S, McCool FD, Hill NS. Leak compensation in positive pressure ventilators: a lung model study. Eur Respir J 2001;17:259–267.
19. Wedin S, Ogren JE. Analysis of the fundamental frequency of the human voice and its frequency distribution before and after a voice training program. Folia Phoniatr 1982;34:143–149.
20. Xue SA, Fucci D. Effects of race and sex on acoustic features of voice analysis. Percept Mot Skills 2000;91:951–958.
21. Hollien H, Shipp T. Speaking fundamental frequency and chronologic age in males. J Speech Hear Res 1972;15:155–159.
22. Bach JR, Campagnolo DI, Hoeman S. Life satisfaction of individuals with Duchenne muscular dystrophy using long-term mechanical ventilatory support. Am J Phys Med Rehabil 1991;70:129–135.
23. Garrod R, Mikelsons C, Paul EA, Wedzicha JA. Randomized controlled trial of domiciliary noninvasive positive pressure ventilation and physical training in severe chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000;162:1335–1341.
24. Schonhofer B, Von Sydow K, Bucher T, Nietsch M, Suchi S, Kohler D, Jones PW. Sexuality in patients with noninvasive mechanical ventilation due to chronic respiratory failure. Am J Respir Crit Care Med 2001;164:1612–1617.
25. Raphael JC, Dazord A, Jaillard P, Andronikof-Sanglade A, Benony H, Kovess V, Charpak Y, Auriant I. Assessment of quality of life for home ventilated patients with Duchenne muscular dystrophy. Rev Neurol (Paris) 2002;158:453–460.
26. Ladefoged P, McKinney NP. Loudness, sound pressure, and subglottal pressure in speech. J Acoust Soc Am 1964;35:454–460.
27. Tanaka S, Gould WJ. Relationships between vocal intensity and noninvasively obtained aerodynamic parameters in normal subjects. J Acoust Soc Am 1983;73:1316–1321.
28. Stathopoulos ET, Weismer G. Oral airflow and air pressure during speech production: a comparative study of children, youths and adults. Folia Phoniatr 1985;37:152–159.
29. Finnegan EM, Luschei ES, Hoffman HT. Modulations in respiratory and laryngeal activity associated with changes in vocal intensity during speech. J Speech Lang Hear Res 2000;43:934–950.
30. Passy V, Baydur A, Prentice W, Darnell-Neal R. Passy-Muir tracheostomy speaking valve on ventilator-dependent patients. Laryngoscope 1993;103:653–658.
31. Manzano JL, Lubillo S, Henriquez D, Martin JC, Perez MC, Wilson DJ. Verbal communication of ventilator-dependent patients. Crit Care Med 1993;21:512–517.
32. Hussey JD, Bishop MJ. Pressures required to move gas through the native airway in the presence of a fenestrated vs a nonfenestrated tracheostomy tube. Chest 1996;110:494–497.
33. Lofaso F, Fodil R, Lorino H, Leroux K, Quintel A, Leroy A, Harf A. Inaccuracy of tidal volume delivered by home mechanical ventilators. Eur Respir J 2000;15:338–341.
34. Murry T, Brown W. Subglottal air pressure during two types of vocal activity: vocal fry and modal phonation. Folia Phoniatr (Basel) 1971;23:440–449.
35. Holmberg EB, Hillman RE, Perkell JS. Glottal airflow and transglottal air pressure measurements for male and female speakers in soft, normal, and loud voice. J Acoust Soc Am 1988;84:511–529.
36. Bard CM, Slavit DH, McCaffrey TV, Lipton RJ. Noninvasive technique for estimating subglottic pressure and laryngeal efficiency. Ann Otol Rhinol Laryngol 1992;101:578–582.
37. Keilmann A, Bader CA. Development of aerodynamic aspects in children's voice. Int J Pediatr Otorhinolaryngol 1995;31:183–190.
Correspondence and requests for reprints should be addressed to Dr. F. Lofaso, Service de Physiologie—Explorations Fonctionnelles, Hôpital Raymond Poincaré, 92380 Garches, France. E-mail:


No related items
American Journal of Respiratory and Critical Care Medicine

Click to see any corrections or updates and to confirm this is the authentic version of record