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American Journal of Respiratory and Critical Care Medicine Vol 167. pp. 101-102, (2003)
© 2003 American Thoracic Society


Editorial

Je Peux Parler!

Jeannette D. Hoit, Ph.D.a and Robert B. Banzett, Ph.D.b

a Department of Speech and Hearing Sciences University of Arizona Tucson, Arizona
b Physiology Program Harvard School of Public Health Harvard University Boston, Massachusetts

I can speak! Imagine the relief of hearing your own voice after months, or perhaps years, of being silenced by an inflated tracheostomy tube cuff. This is the relief experienced by the ventilator user whose cuff has just been deflated and whose power of speech has just returned. This relief may soon change to disappointment and frustration, however, when speech is found to be a poor approximation of what it used to be before the ventilator. Fortunately, there are ways to improve ventilator-supported speech, one of which is described by French authors Prigent and colleagues (1) in this issue of AJRCCM (pp. 114–119).

For patients who use invasive positive-pressure ventilation, the essential step to establishing speech is deflation of the tracheostomy cuff (or insertion of a fenestrated tracheostomy tube). This allows airflow to reach the larynx so that the vocal folds can vibrate. Most patients who are chronically ventilated for neuromuscular disease can tolerate having the cuff deflated throughout the waking hours (2, 3). Many patients with acute conditions also can tolerate cuff deflation, though generally for shorter periods. But even with the cuff, deflated speech is usually far from normal.

Common problems with ventilator-supported speech include long pauses, short phrases, uneven loudness, and poor voice quality (4, 5). These problems can be explained in large part by examining the tracheal pressure waveform. During normal speech production, tracheal pressure is relatively low (usually 5 to 10 cm H2O, depending on loudness) (6, 7), but it must be at least 2 cm H2O for the vocal folds to vibrate (8, 9). Pressure is also relatively steady, so that loudness and voice quality can be relatively stable (10, 11). This steady pressure requires careful coordination of chest wall muscles to compensate for the changing elastic recoil throughout expiration. During invasive positive-pressure ventilation, the tracheal pressure waveform looks strikingly different from the normal waveform. It is common to see the pressure rise to 30 cm H2O or higher, then fall rapidly to zero. This fast-changing pressure causes noticeable variability in loudness and voice quality. Also, the pressure remains below the minimum required to vibrate the vocal folds for prolonged periods. This leads to long, awkward pauses between spoken phrases.

As previously shown, speech can be improved by modifying the tracheal pressure waveform to better meet the requirements of speech production (5, 12). Realizing this, one need only use knowledge of respiratory physiology and ventilator function to alter the pressure waveform in ways that improve speech yet maintain adequate pulmonary gas exchange. The approach used by Prigent and coworkers (1) succeeded in doing just that. They used bilevel positive-pressure ventilation, a combination of pressure support ventilation (in which the ventilator supplies a target pressure) and positive end-expiratory pressure to improve speech in their subjects. These authors realized that pressure-support ventilation would compensate for flow lost through the larynx during speech production, and that the steady and prolonged inflation pressure would be beneficial to speech. Also, the positive end-expiratory pressure would prolong speech during the deflation phase (because the tracheal pressure remained above the minimum pressure required to vibrate the vocal folds). With bilevel positive-pressure ventilation, speaking time per respiratory cycle essentially doubled compared with their subjects' usual mode of ventilation. Our laboratory has made similar speech improvements with volume-controlled positive-pressure ventilation (5, 12). By lengthening inspiratory time and applying positive end-expiratory pressure, speaking time increased, pause time decreased, and loudness, voice quality, and other perceptual features of speech improved.

The work of Prigent and coworkers (1) and earlier work by the present authors (5) has demonstrated how easy it is to improve speech by merely adjusting the ventilator to modify the tracheal pressure waveform. These studies have also shown that patients are generally more comfortable with improved-speech settings, and that gas exchange is seldom measurably affected. Although these findings may not seem earth shaking at first glance, consider the clinical implications. First, simple adjustments to the ventilator can dramatically improve communication for people whose circumstance makes normal human interaction difficult. Second, using a ventilator-adjustment approach to improve speech can avoid the use of a one-way speech valve. By avoiding use of a one-way valve, patients do not have to risk potentially fatal errors (such as placing the valve in the ventilator line while the tracheostomy tube cuff is still inflated). They now have several safer and less expensive options.

The efficacy of these ventilator-adjustment interventions is now well documented in patients ventilated for neuromuscular failure. This approach may also help patients who are ventilated for other reasons, but this has not been researched. Adjustments other than those already described may also benefit speech. For example, switching from volume-controlled ventilation to pressure-controlled ventilation may improve loudness and voice quality because a pressure-targeted pressure waveform is "flatter" than a volume-targeted waveform. This, however, has not been formally tested.

The message of Prigent and coworkers (1) and that of related work is: deflate the cuff, let your patient speak, and adjust the ventilator to improve speech by using the tracheal pressure waveform as your guide. Your patients will almost certainly shout a resounding "Merci!"

REFERENCES

  1. Prigent H, Samuel C, Louis B, Abinun M-F, Zerah-Lancner F, Lejaille M, Raphael J-C, Lofaso F. Comparative effects of two ventilatory modes on speech in tracheostomized patients with neuromuscular disease. Am J Respir Crit Care Med. 2003;167:114–119.[Abstract/Free Full Text]
  2. Bach JR, Alba AS. Tracheostomy ventilation: a study of efficacy with deflated cuffs and cuffless tubes. Chest 1990;97:679–683.[Abstract/Free Full Text]
  3. Tippett DC, Siebens AA. Preserving oral communication in individuals with tracheostomy and ventilator dependency. Am J Speech-Lang Pathol 1995;4:55–61.[Abstract/Free Full Text]
  4. Hoit JD, Shea SA, Banzett RB. Speech production during mechanical ventilation in tracheostomized individuals. J Speech Hear Res 1994;37:53–63.
  5. Hoit JD, Banzett RB. Simple adjustments can improve ventilator-supported speech. Amer J Speech-Lang Pathol 1997;6:87–96.
  6. Netsell RW. Subglottal and intraoral air pressures during the intervocalic contrast of /t/ and /d/. Phonetica 1969;20:68–73.
  7. Murry T, Brown WS. Subglottal air pressure during two types of vocal activity: vocal fry and modal phonation. Folia Phoniatr (Basel) 1971;23:440–449.
  8. Draper MH, Ladefoged P, Whitteridge D. Expiratory pressures and air flow during speech. BMJ 1960;1:1837–1843.
  9. Lieberman P, Knudson R, Mead J. Determination of the rate of change of fundamental frequency with respect to subglottal air pressure during sustained phonation. J Acoust Soc Am 1969;45:1537–1543.[CrossRef][Medline]
  10. Bouhuys A, Proctor DF, Mead J. Kinetic aspects of singing. J Appl Physiol 1966;21:483–496.[Free Full Text]
  11. Hixon TJ, Mead J, Goldman MD. Dynamics of the chest wall during speech production: function of the thorax, rib cage, diaphragm, and abdomen. J Speech Hear Res 1976;19:297–356.
  12. Hoit JD, Banzett RB, Brown R. Improving ventilator-supported speech. TELEROUNDS #39 Live Satellite Transmission, December 10, 1997, National Center for Neurogenic Communication Disorders, Tucson, Arizona (videotape available).



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