RespiratoO, Medicine (1992) 86, 211-214

Effects on pulmonary function of oral high frequency oscillation in normal and asthmatic subjects M. L. AITKEN*, J. M. VINCENT AND D. J. PIERSON

Division of Pulmonary and Critical Care Medicine, University of Washington Medical Center and Harborview Medical Center, Department of Medicine, University of Washington, Seattle, Washington, U.S.A.

High frequency jet devices are not only used as 'internal percussors' to aid clearance of pulmonary secretions, but are also a mode ofventilatory support. As physical stimuli can cause bronchospasm in asthmatic individuals, we hypothesized that direct airway vibration may induce bronchospasm. To ascertain whether an airway vibration jet device could cause bronchoconstriction, we exposed eight asthmatic and six normal subjects to 5 min of jetinduced airway vibration or placebo treatment with cross-over at 3 h. Subjects breathed spontaneously for 5 min through an open mouthpiece into which either jet (10 Hz, 25 psi) or sham pulsations (same device, pressure vented to room at compressor) were delivered in a double-blind, random order. A constant-volume body plethysmograph measured functional residual capacity and specific airway conductance (SGAw) and a water seal spirometer measured forced expiratory volume in 1 s (FEV~) and forced vital capacity (FVC). These pulmonary function measurements were taken before and at 5, 10, 20, 30, 60, 90 and 120 min after each exposure. In the normal subjects there was no significant change in any pulmonary function. There was no statistically significant change in the pulmonary function in the asthmatic patients. However, the oral high frequency oscillator induced a clinical asthmatic attack in one asthmatic patient. In this one patient, the FEVt fell 35% from its initial value at 5 min following exposure to a maximum of 49% decline from initial value at I h following exposure. We conclude that this airway vibration jet device can cause clinically significant bronchoconstriction in susceptible asthmatic subjects, and suggest that possible effects on airway function be considered when high frequency gas pulsation is used for chest physiotherapy or as a mode of ventilatory support.

Introduction High frequency airway pulsation devices are currently in clinical use not only to support oxygenation and ventilation in the critical care setting, but also as 'internal percussors' for the treatment of retained airway secretions and to increase mucociliary clearance (1-6). Physical stimuli to the airways such as cold air and endotracheal intubation (7) can cause bronchospasm in asthmatic individuals. High frequency oscillatory devices stimulate pulmonary vagal afferent fibers (8), and theoretically oscillatory devices could produce bronchospasm through a neural mechanism. We wondered whether airway vibration from such a device could produce detectable changes in pulmonary function in patients with hyper-responsive airways. This study examines the effect ofan airway vibration jet device on pulmonary function in both normal subjects and clinically stable asthmatic patients. Received I I March 1991 and accepted in revised form 17 September

1991. *To whom correspondence and reprints should be addressed at: Division of Pulmonary and Critical Care, RM-12, University of Washington, Seattle, WA 98195, U.S.A.

0954-6111/92/030211+ 04 $03.00/0

Methods PATIENT SELECTION

We studied six normal subjects and eight asthmatic patients. Normal subjects were recruited personally by one of the investigators, and asthmatic subjects were recruited from the outpatient pulmonary clinics of the University of Washington. Every subject performed spirometry and completed a questionnaire concerning medical history, current medications and smoking history. NORMAL SUBJECTS

In the normal group care was taken in subject selection to avoid inclusion of persons with reactive airways. There was no personal or family history of asthma or exercise intolerance. No subject demonstrated a statistically significant response (9) of any spirometric index [forced vital capacity (FVC), forced expiratory volume in 1 s (FEVt) ], to 20 inspiratory capacity inhalations of 0.6% metaproterenol nebulized by a compressor. None had suffered a respiratory tract infection within the preceding 6 weeks. Three of the normals were former smokers, with 1, 5 and 6 © I992Bailli~reTindaU

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pack-year exposures, but none had smoked in the preceding 4 years. No normal subject used medication of any kind. There were four women and two men with a mean age (_SD) of 3 2 + 6 years (range 25--41 years). They had normal pulmonary function tests. At the time of screening for entry into the study their mean FVC was 4.34- 1.11 (104% predicted) and FEVj was 3.6+0.71 (110% predicted). ASTHMATIC SUBJECTS

Each ofthe eight asthmatic subjects (four male, four female) gave a history of exercise-related bronchospasm and had experienced repeated episodes of cough, dyspnea, and wheezing with intercurrent symptom-free intervals. Heightened airway reactivity was demonstrated in each asthmatic subject by significant response in one or more spirometric indices to isoetharine, delivered undiluted by a compressor driven nebulizer (9). No asthmatic subject had ever smoked. Seven patients regularly used a p2-adrenergic agonist by inhalation, four were taking a xanthine derivative orally and one inhaled beclomethasone. All patients requiring xanthines were using a sustained release preparation. Subjects refrained from taking all forms ofinhated medication for 6 h prior to the study. No asthmatic subject was taking glucocorticoids, orally administered fl sympathomimetics or sodium cromoglycate. The mean age (4-st)) was 2 7 _ 7 years (range 18-39 years). At the initial screening visit for entry into the study, their mean FVC was 4.3 4- 1.01 (93% predicted) FEV l was 3-0 + 0-71 (78% predicted). APPARATUS

The pulmonary vibrator used in this study (Clinijet R, Inspiron Corporation, Rancho

Cucamonga, CA) is a compact unit (9" x 9" x 2.5") that provides small pulses (approximately 25 ml) of gas at a pressure of 30 psi and a frequency of 10 Hz, operating on compressed air or oxygen at 255 psi. Pulsations are delivered via a fenestrated mouthpiece (Fig. 1) through which the subject breathes spontaneously at will. Immediately below the mouthpiece there is a 10-ml reservoir chamber filled with water to provide humidification. The placebo or sham unit has the identical external appearance to the vibrator but its pulsations are directed to the room and no vibrations reach the mouthpiece. PROTOCOL

All subjects were given 5 min of airway vibration using compressed air as the gas source, or placebo treatment, in random order with cross-over at 2 h. Subjects wore noseclips and compressed their cheeks with their hands to minimize attenuation of airway vibrations. FEV~ and FVC were measured with a water-seal spirometer and specific airway conductance (SGAw) was measured with a constant volume body plethysmograph. Measurements were made before each challenge and at 5, 10, 20, 30, 60, 90 and 120 rain after each exposure. Any coughing, wheezing or other adverse effects were noted. STATISTICAL METHODS

Spirometric and $GAW changes were evaluated by plotting a regression analysis for the values of each subject over time. The slope of the regression lines of clinijet and placebo was compared using a Student's paired ttest (10). Statistical significance was determined as P>0.05.

High frequency jet devices and pulmonary function

213

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Fig. 2 Change in SGAw (mean values) from initial measurements over 2 h for the clinijet (

) and placebo (- -) treatments in eight asthmatic patients. There is no statistical difference between the clinijet and placebo (P > 0-05). Bars represent _ s~. Results

All subjects completed both phases of the study. In normal subjects, there were no significant changes in pulmonary function with either placebo or vibration. In the asthmatic subjects there were no statistically significant changes in any of the measured pulmonary functions after the placebo treatment. The mean FEV t and SGAW values were not changed by the vibration device. Before the vibration device, the initial FEVj and FVC were 3.4+0.91 and 4.6__+1.01 with maximal fall seen 60 min following vibration (FEV~ and FVC 3.1_ 1-11 and 4.3-1-0.41, respectively: P>0"05). The mean changes in SGAw in the asthmatic subjects following the placebo and following the clinijet are shown in Fig. 2. One patient had a clinically significant asthmatic attack. She began to cough while the vibrating device was in use and immediately after the completion of the 5-min episode felt wheezy in addition to coughing. On auscultation wheezes were heard and she felt progressively more dyspneic and 'tight' in the subsequent hour, and audible wheezes were apparent. Her FEV Ldropped by 49% of the initial value at 1 h. After completion of the study at 2 h, treatment with a fladrenergic agonist delivered by a nebulizer alleviated her attack. No other subject or patient had any symptoms from either the placebo or the vibration challenges. Discussion

The present study shows that this airway vibration jet device (10Hz, 5 min challenge) does not cause airway hyperreactivity in most subjects, but can cause detectable changes in airway function in some susceptible asthmatic subjects. One of the eight asthmatic patients studied had a clinical asthma attack.

We examined only 14 subjects. Our numbers are too small to determine if this detrimental effect on pulmonary function occurs in the normal population and how frequently it is seen in asthmatic subjects. However, there has been at least one previous clinical report of high frequency ventilation inducing bronchospasm (11). The mechanism by which the vibrator apparatus causes bronchospasm is unclear. There may be a disturbance of irritant receptors analogous to that observed with other physical stimuli (7) producing an immediate vagal response. Man et aL (8) has shown that a different high frequency device (10-30Hz) stimulates vagal afferent nerves in dogs. The vibrator requires pressurized air or oxygen to operate. The pressurized gas is dry and there is a subjective sensation of orophyaryngeal drying. The reservoir in the device is designed to overcome this problem, but it is possible that the patients received a hyperosmolar challenge. Our study, however, was not designed to establish the mechanism by which the bronchospasm occurred but as a pragmatic test of whether this type of airway challenge was able to induce bronchospasm in susceptible individuals, as jets are being used for a variety of applications worldwide (1-6). There was only a 2-h interval between the vibrator and the placebo treatment. The four asthmatics who were randomly assigned to receive the vibrator first may still have been in refractory stage and hence no effect is seen with the placebo treatment which may have otherwise been present. We consider this improbable, however, because any change in pulmonary function with the placebo treatment was small. The individual who experienced a clinically significant asthmatic attack had been randomly assigned to

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receive the sham treatment first. It is unclear why this asthmatic subject responded more than the other seven. This subject was very atopic, but otherwise had no distinguishing features. We conclude that this vibration apparatus, as clinically used to loosen secretions, can cause clinical bronchospasm in some susceptible individuals. Further studies are warranted to determine the incidence of bronchospasm caused by this device in the asthmatic population, and to elucidate the mechanism involved. We caution that clinicians using airway vibrators, whether for ventilation support or for secretion removal, should be aware of the potential for serious bronchospasm. References I. Czech K. Ein Hochfrequenz-Jet System zur post traumatischen pulmonalprotektion. Heft zur Unfallheilkunde, Heft 156, Zusammengeseltt yon G. Schag. Berlin: Springer-Verlag, 1983;289-29 I. 2. George R, Johnson M, Pavia D, Agnew J, Clarke, S, Geddes D. Increase in mucociliary clearance in normal man induced by oral high frequency oscillation. Thorax 1985; 40: 433-437. 3. George R, Pavia D, Lopez-Vidriero M, et al. Oral high

4. 5. 6.

7. 8. 9. 10.

11.

frequency oscillation (OHFO) as an adjunct to physiotherapy (PHYSIO) in cystic fibrosis (CF). Thorax 1986; 41: 235(P). Armengol J, Man S, Logus J, Man G, King E. Effects of high frequency oscillatory ventilation on canine tracheal mucus transport. Crit Care Med 1981; 9: 192A. King M, Philips D, Zidulka A, Chang H. Tracheal mucus clearance in high frequency oscillation. Am Rev Respir Dis 1984; 130: 703-706. McEvoy R, Davies N, Hedenstierna G, Hartman M, Spragg R, Wagner P. Lung mucociliary transport during high frequency ventilation. Am Rev Respir Dis 1982; 126: 452-456. Stauffer J, Silvestri R. Complications of endotracheal intubation, tracheostomy and artificial airways. Respir Care 1982;27: 417--434. Man G, Man F, Kappagoda C. Effect of high frequency oscillating ventilation on vagal and phrenic nerve activities. J Appl Physiol 1983; 54: 502-507. American College of Chest Physicians Committee on Emphysema. Criteria for the assessment of reversibility in airway obstruction. Chest 1974;65: 552-553. O'Brian P, Shampo M. Statistical considerations for performing multiple tests in a single experiment. 3. Repeated measures over time. Mayo Clin Proc 1988; 63: 918-920. Carlton, GC, Kahn RC, Howland WS, Ray Jr C, Turnbull A. Clinical experience with high frequency jet ventilation. Crit Care Med 1981; 9: I-6.

Effects of pulmonary function of oral high frequency oscillation in normal and asthmatic subjects.

High frequency jet devices are not only used as 'internal percussors' to aid clearance of pulmonary secretions, but are also a mode of ventilatory sup...
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