Comparison of Respiratory Retraining Techniques in the Treatment of PVFD Deborah J. Matheron, M.S. & Bridget Russell, Ph.D, CCC-SLP Department of Speech Pathology and Audiology, State University of New York at Fredonia Introduction Method Subject Purpose The purpose of this study was to determine if respiratory retraining therapy would result in a reduction in exertional dyspnea and improved ventilatory response during exercise in an athlete with diagnosed PVFD. Background •Paradoxical Vocal Fold Dysfunction (PVFD) is: • The improper closure of the vocal folds during either inspiration and/or expiration in the absence of organic laryngeal pathology (Newman, Mason & Schmaling, 1995; Morrison, Rammage & Emami, 1999) •Possible etiologies: • Excitation of chemoreceptors in the olfactory passages and pharynx due to irritation (Morrison et al,1999) • Psychological stressors including failure to respond to emotional situations, including conversion disorder (Martin, Blager, Gay & Wood, 1987; Andrianopoulos, Gallivan & Gallivan, 2000) • Laryngeal dystonia with neurological basis (Morrison et al, 1999; Treole, Trudeau & Forrest, 1999) • Viral infection (Andrianopoulos et al, 2000; Altman, Mirza, Ruiz & Sataloff, 2000) •Assessment • Often misdiagnosed as exercise-induced asthma (EIA) in athletes (Rundell & Spiering, 2003; Brugman & Simmons, 1998; Landwehr, Wood, Blager & Milgrom, 1996; McFadden & Zawadski, 1996) • Differential diagnosis Direct laryngoscopic observation (Martin et al, 1987) Ventilatory measures (Mathers-Schmidt, 2001; Goldman & Muers, 1991) Patient history (Sandage & Zelazny, 2004; Mathers-Schmidt, 2001; Andrianopoulos et al, 2000) •History of Treatment • Therapy adapted from functional voice disorder protocol (Brugman & Newman, 1993) • Relaxation (Martin et al, 1987) • Inhalation of helium-oxygen mixture (Martin et al, 1987; Christopher, Wood, Eckert, Blager, Raney Southrada, 1983) • Injection of botulinum toxin (LaBlance, Maves, Sullivan & Garibaldi, 1993; Brin, Blitzer, Braun, Stewart & Fahn, 1991 as cited by Altman et al, 2000) • Respiratory retraining: Diaphragmatic breathing (Sullivan, Heywood & Beukelman, 2001; Martin et al, 1987) “Wide-open-throat” breathing (Martin et al, 1987) Concentration on exhalation; timed by count (Gallivan, Hoffman & Gallivan, 1996); on fricative /s/ (Sandage, personal communication, June 15, 2006; Andrews, 2002; Martin et al, 1987) Using sniff, blow or pant techniques, nasal inspiration, lip pursing (Sandage, personal communication, June 15, 2006; Sandage & Zelazny, 2004; Andrews, 2002; Newsham, Klaben, Miller & Saunders, 2002; Weiss, 2001; Altman et al, 2000; Andrianopoulos et al, 2000; Pitchenik, 1991) • 13 year old female athlete • Diagnosed with PVFD by direct laryngoscopy and patient history by an otolaryngologist • Reported episodes of PVFD during sporting events, exposure to certain environmental odors and in high-stress academic situations • Laryngeal examination indicated reflux as evidenced by erythemia of posterior glottis. Prilosec was prescribed Equipment • Vista Mini-CPX System (Vacumetrics Inc./Vacu-Med Division) Tests pulmonary and cardiopulmonary function in exercise Collects timing, flow and gas samples using a turbine connected outside of the facemask • Separate end-tidal CO2 Module (measures end-tidal CO2) • A Hans Rudolph air-cushioned facemask (Vacumed Model KM201) • Vacu-Med Turbofit version 5.05 software analysis program • Schwinn stationary bicycle model DX-900 . VO2 significantly increased in all conditions: A) Baseline vs. Episode w/o Tx B) Episode w/o Tx vs. TxI C) Episode w/o Tx vs. TxII (see figure 1 and contrast table). ETCO2 comparisons: A) Significantly increased B) & C) No significant difference (see figure 2 and contrast table). TI comparisons: A) Decreased significantly B) Increased slightly but not significantly C) Increased significantly (see figure 2 and contrast table) TE comparisons: A) Decreased significantly B) Increased slightly but not significantly C) Increased significantly (see figure 2 and contrast table) How are respiratory timing measures including inspiratory time (TI) and expiratory time (TE), and respiratory rate (RR) affected by respiratory retraining? Is respiratory retraining effective in returning affected measures to pre-episode levels? RR comparisons: A) Increased significantly B) Increased significantly C) Decreased significantly (see figure 3 and contrast table) 9 TxI returned ET CO2 to pre-episode levels 9 TxII returned respiratory rate to pre-episode levels . Figure 2 Figure 1 Procedures Subject Instructions: • During baseline sessions, patient was instructed to: Signal onset of PVFD episode Manage episode in her usual manner during exercise (baseline) • During treatment sessions, patient was instructed to: Signal onset of PVFD episode Initiate respiratory retraining protocol Signal reduction of PVFD symptoms . Equipment Protocol: • Facemask was fitted over subject’s mouth and nose prior to all data collection sessions • Subject was instructed to pedal on stationary bicycle at regulated rate while ventilatory measures were collected Figure 3 . Treatment I (TxI) Respiratory Retraining Protocol: . • Regulated closed mouth/nasal inspiration • Regulated pursed lip expiration • Continued retraining until resolution of PVFD episode Treatment II (TxII) Respiratory Retraining Protocol: • • • • Closed mouth/Deep nasal sniff inspiration Regulated pursed lip expiration through small oral opening Subject instructed to focus expiratory pressure against more tightly closed, pursed lips Continue retraining until resolution of PVFD episode Statistical Analysis • Repeated measures ANOVA for main effect • Tukey-Kramer HSD to compare significant main effect means (post-hoc) Still image of vocal folds taken during inspiration from nasendoscopic examination Results How . are blood gas measures, including oxygen consumption (VO2/ml/kg/min) and end tidal carbon dioxide (ETCO2/mmHg), affected by respiratory retraining? Posterior Glottal Chink Discussion 9 Respiratory rate and inspiratory and expiratory times indicated that during the PVFD episode, the subject began to inspire and expire more quickly and thus breathing frequency increased. Treatment I did not significantly increase inspiratory or expiratory timing, however, the means indicated a trend moving toward increased times. The measures indicate the subject’s attempt to adhere to treatment. (i.e. The subject attempted to change respiratory pattern in accordance with . clinician’s instructions.) Treatment II did significantly increase inspiratory and expiratory timing and respiratory rate. . 9 VO2 nearly doubled between baseline and episode without treatment. This higher cost of breathing indicates increased muscular effort. VO2 also significantly increased in all conditions. The increase during treatment conditions may indicate the subject’s attempt at manipulating the respiratory musculature during the retraining maneuvers and thus further increasing the cost of breathing. 9 The response to Treatment I respiratory retraining was indicated by decreased end tidal CO2 which signaled the return of pre-episode blood gas levels (i.e. homeostatic balance was regained during treatment). However, according to subject report, Treatment II reduced perceived dyspnea more quickly. Conclusion Camera view artifact; True Vocal Folds not part of anatomy Courtesy of Brian Same, MD, Buffalo 9 During a PVFD episode, breathing became more rapid and shallow. Blood gases and oxygen consumption increased, which indicated a state of hypoventilation (i.e. the decreased ability to rid CO2 from the blood) and increased muscular effort . Treatment I returned blood gases to pre-episode levels, returning the system to homeostasis. Treatment II returned respiratory rate to pre-episode level, potentially reducing subject-perceived dyspnea. Subject’s PVFD symptom were relieved through respiratory retraining treatments. This change is reflected in both perceived and measured outcomes. References (Sandage, 2004) Otolaryngological Group, Buffalo, NY Research Questions . 9 How are blood gas measures, including oxygen consumption (VO2/ml/kg/min) and end tidal carbon dioxide (ETCO2/mmHg), affected by each respiratory retraining task? 9 How are respiratory timing measures, including inspiratory time (TI) and expiratory time (TE), and respiratory rate (RR), affected by each respiratory retraining task? 9 Which respiratory retraining task is more effective in returning perturbed ventilation and respiratory timing to pre-episode levels? 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