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(Chest. 1999;116:1646-1652.)
© 1999 American College of Chest Physicians

Route of Breathing in Patients With Asthma*

Kristina Kairaitis, MBBS; Sarah R. Garlick, BSc, (Hons); John R. Wheatley, PhD and Terence C. Amis, PhD

* From the Department of Respiratory Medicine, Westmead Hospital, Sydney, NSW, Australia.

Correspondence to: Kristina Kairaitis, MBBS, Department of Respiratory Medicine, Westmead Hospital, Westmead NSW, 2145 Australia; e-mail: kristinak{at}westgate.wh.usyd.edu.au


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Study objectives: To measure route of breathing in chronic asthmatic patients during and after an acute severe exacerbation.

Patients or participants: Thirteen asthmatic patients were studied during hospital admission for acute asthma and, in 9 patients, again when asymptomatic. Nine healthy subjects were also studied.

Interventions: Spontaneous route of breathing was qualitatively assessed using oral and nasal thermistor probes, and was then quantified using a dual compartment face mask with attached pneumotachographs.

Measurements and results: All asthmatic patients had severe bronchoconstriction initially (FEV1, 46 ± 3% of predicted) that had resolved at follow-up (FEV1, 91 ± 6% of predicted). No healthy subject had evidence of bronchoconstriction (FEV1, 102 ± 5% of predicted). During acute asthma, 11 asthmatics were spontaneously breathing oronasally, as assessed using thermistor probes, while all 13 breathed oronasally via face mask. When assessed using thermistor probes, seven of nine asymptomatic asthmatic patients studied were breathing exclusively via the nose; however, all breathed oronasally via face mask. In contrast, while eight of nine healthy subjects were also breathing exclusively via the nose when assessed using thermistor probes, all breathed nasally only via face mask.

Conclusions: Thus, when asymptomatic and at rest, asthmatic patients breathe exclusively via the nose. However, during acute exacerbations of asthma, these patients switch to oronasal breathing. Unlike healthy subjects, chronic asthmatic patients also switch to oronasal breathing when wearing a face mask, irrespective of the degree of bronchoconstriction. We speculate that asthmatics may have an increased tendency to switch to oral breathing, a factor that may contribute to the pathogenesis of their asthma.

Key Words: asthma • mouth breathing • route of breathing


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Asthma is a common chronic respiratory disease that is characterized by acute exacerbations of bronchoconstriction associated with airway inflammation and airway smooth muscle hyperresponsiveness. Inhaled allergens and other stimuli, eg, cold dry air, can precipitate acute bronchoconstriction in susceptible asthmatic patients.1 The nasal passages play an important role in the defense of the respiratory system against these environmental insults. In particular, the heat exchange, humidification, and filtration functions of the nose protect the lower airway from inhaled particles and from drying and cooling of mucosal surfaces. When the nasal airway is bypassed (eg, during inspiration via the mouth), much of this protective benefit is lost.2 The importance of this concept is well known in relation to exercise-induced asthma, where it has long been appreciated that nasal breathing provides a protective influence.3 However, virtually nothing is known about the route of breathing employed by asthmatic patients during an acute attack. Indeed, it is not known whether the route of breathing employed by such patients differs from that of healthy subjects, even when they are relatively well.

Many asthmatic patients suffer from concomitant allergic nasal disease (eg, nasal polyps, allergic rhinitis),4 which may increase the nasal resistance to airflow and the work of breathing (WOB) through the nose. During episodes of acute bronchoconstriction, asthmatic patients may not be able to sustain the extra work associated with nasal breathing and may, therefore, switch breathing routes to the potentially lower resistance oral pathway. Consequently, we hypothesize that during acute exacerbations, asthmatic patients will breathe oronasally. Furthermore, oronasal breathing may worsen bronchoconstriction because of increased exposure of the lower airways to a higher inhaled antigen load and to cooler, drier air.

Recognition of a role for breathing route in the pathogenesis of asthma has a number of potential therapeutic applications. For example, should asthmatics be trained to use the nasal route and avoid oral breathing? Should nasal and sinus disease in asthmatics be treated aggressively in order to promote nasal breathing, and does this have any influence on the natural history of asthma in such patients?

Therefore, the aims of the present study were to test the first part of our hypothesis by examining the following: (1) the route of breathing utilized by asthmatic patients, both during and after an acute episode of bronchoconstriction; and (2) the route of breathing employed by asthmatic patients compared to the route of breathing used by healthy subjects.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Conclusion
 References
 
Subjects
We studied 13 nonsmoking, asthmatic patients who were experiencing an acute exacerbation requiring hospital admission (the initial study). All patients were receiving oral prednisolone, 50 mg qd, and salbutamol, 5 mg every 4 h, via a nebulizer. Nine patients were studied again between 6 weeks and 16 weeks later, when they had recovered and were relatively asymptomatic (the follow-up study). At the follow-up study, all patients were receiving regular inhaled corticosteroids and salbutamol on an "as required" basis. In addition, some patients were receiving inhaled long acting ß2-agonist therapy. Anthropometric data for the patients are shown in Table 1 .


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  		Table 1.. Anthrompometric Data for Asthmatic Patients and FEV1 at the Initial (Symptomatic) and Follow-up (Asymptomatic) Study*

 
On a separate occasion, we studied nine healthy subjects (five females and four males; mean ± SEM age, 26 ± 1 years old; height, 169 ± 4 cm), none of whom had any current respiratory symptoms, except for two subjects who had slight nasal congestion, one of whom also had a history of mild intermittent hay fever. None of the healthy subjects had any history of asthma. All of the subjects, both asthmatic and healthy, were naive to the purpose of the study, and all gave written consent. The only information that was given to the prospective subjects was that their breathing was to be measured. No instructions were given regarding the route of breathing. The protocol was approved by the Western Sydney Area Health Service Ethics Committee.

Measurement of Route of Breathing
All studies were performed during tidal breathing with the subject in an upright seated posture. The spontaneous route of breathing adopted by subjects was assessed using three different approaches. First, and least invasively, with the subject unaware and sitting quietly in the laboratory while waiting for the study to commence, a visual observation was made for approximately 2 min to assess whether each subject had their mouth open or closed. Second, oral and nasal thermistor probes (model F-ONT2A; Grass Instrument; Quincy, MA) were attached to the subject’s face and were used to qualitatively assess oral (O) and nasal (N) airflow (without the connection of the subject to any breathing mask) during 2 min of steady-state breathing. Last, and most invasively, oronasal airflow partitioning was then quantified during 2 min of steady-state breathing by measuring O and N using two pneumotachographs (model 770590; Collins; Sydney, Australia). For this phase of the study, the subjects wore a dual compartment face mask (model 669091; Hans Rudolph; Kansas City, MO) that was sealed to the face using a glycerin-based polymer gel (Ultimate Seal; Hans Rudolph) and tested for leaks prior to each measurement. Microbial filters (MicroGard; SensorMedics; Sydney, Australia) were attached to the nasal and oral pathways. The total dead space of the apparatus was approximately 275 mL and 420 mL for the nasal and oral pathways, respectively. The larger dead space for the oral airway was related to the inclusion of additional apparatus (a three-way tap and an interrupter valve), with which it was originally intended to measure lower airway resistance. However, because of technical problems, these data were not included in the final analysis. The airflow resistance of the apparatus was 0.80 cm H2O/L/s and 2.82 cm H2O/L/s (at 0.6 L/s) for the nasal and oral pathways, respectively. Data were digitized at 400 Hz (MacLab 1/16S; AD Instruments; Sydney, Australia) and stored on a personal computer for later analysis.

Measurement of Asthma Severity
The degree of bronchoconstriction was assessed in the asthmatic patients and healthy subjects by measuring FEV1 (the largest value recorded from three consecutive measurements) at the commencement of each study. For this measurement, subjects performed a standard oral-route maximum forced expiratory vital capacity maneuver through a microbial filter (MicroGard; SensorMedics) while expiratory flow was recorded with a spirometer (Autospirometer AS-800; Minato Medical Science; Osaka, Japan).

Data Analysis
Thermistor probe measurements of O and N were analyzed by scoring airflow as being present or absent for each route. Thus, nasal breathing was defined as being present if > 90% of breaths during the observation period showed an oscillating signal (in phase with respiration) on the nasal thermistor channel only; oral breathing was defined as being present if > 90% of the breaths showed an oscillating signal on the oral thermistor channel only; and oral plus nasal breathing was defined for the remainder of the breaths recorded.

For the partitioned face mask data, nasal and oral peak tidal inspiratory and expiratory airflow (PTIF and PTEF, respectively) expressed in liters per second were also measured as the mean of all breaths recorded (up to 60 consecutive breaths) during a 2-min period. Nasal PTIF and PTEF fractions (nasal PTIF/nasal PTIF and oral PTIF, and nasal PTEF/nasal PTEF and oral PTEF, respectively) were then calculated for each breath analyzed. Data for individual subjects were averaged, and group mean (± SEM) results were calculated. In the asthmatic patients, numeric results obtained during the initial study were compared to results obtained at the follow-up study using a paired t test. Data obtained for asthmatic patients were compared to those obtained in healthy subjects using an unpaired t test. A p value < 0.05 was considered significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Conclusion
 References
 
Healthy Subjects
The FEV1 in the healthy subjects was 102 ± 5% of predicted values. All of the healthy subjects were observed breathing with their mouths apparently closed during the initial observation period. However, analysis of the thermistor probe signal revealed that while eight of the subjects were breathing exclusively via the nasal route, one subject was breathing oronasally (Table 2 ). When the dual compartment face mask and measurement apparatus was in place, all healthy subjects were breathing exclusively via the nasal route, such that nasal PTIF was 0.50 ± 0.03 L/s and nasal PTEF was 0.38 ± 0.02 L/s. Since O was zero in all subjects, the nasal inspiratory and expiratory peak tidal airflow fractions were both 1.0.


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  		Table 2.. The Route of Breathing in Normal Subjects Observed Visually and With the Thermistor and Dual Compartment Face Mask*

 
Asthma Patients
Initial Study: At the time of the initial study, the asthmatic patients were severely bronchoconstricted, with a group mean FEV1 of 46 ± 3% predicted (Table 1) . In contrast to the healthy subject group, eight subjects were observed to have their mouths open throughout the initial observation period, two subjects had their mouths apparently closed, and observations were not recorded for three subjects. The thermistor data showed that 11 of the patients were breathing via both the nasal and oral pathways, including 1 of the patients who was initially observed to be breathing with the mouth apparently closed. The thermistor was not functioning in one study (in a subject who was observed to have a closed mouth at initial observation), and the remaining subject was breathing exclusively via the nose (Table 3) . When breathing via the double compartment face mask and measurement apparatus, and in marked contrast to the healthy subjects, all patients were breathing oronasally. During this phase of the study, nasal PTIF was 0.45 ± 0.06 L/s and nasal PTEF was 0.39 ± 0.07 L/s; neither of these values were significantly different from the corresponding values obtained for the healthy subjects (p > 0.56 for both). However, in the patients there was additional airflow via the mouth, such that the oral PTIF was 0.58 ± 0.05 L/s and oral PTEF was 0.57 ± 0.04 L/s. The nasal inspiratory and expiratory peak tidal airflow fractions in the asthmatic patients ranged from 0.11 to 0.67 and from 0.05 to 0.66, respectively, with group mean values of 0.41 ± 0.04 and 0.34 ± 0.04, respectively, both of which were significantly less (p = 0.0001) than the fractions in the healthy subjects.


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  		Table 3.. The Route of Breathing in 13 Asthmatic Subjects at the Initial (Symptomatic) and Follow-up (Asymptomatic) Study*

 
Follow-up Study: Only 9 of the 13 asthmatic patients were available for follow-up studies. All reported a marked resolution of their symptoms, and FEV1 values had increased substantially in all but one patient (Table 1) . The group mean FEV1 was 91 ± 6% of predicted (range, 61 to 120%) and was significantly greater than at the time of the initial study (p = 0.0001). All except three patients were now observed to be breathing with a closed mouth, while the thermistor data showed exclusive nasal route breathing in all but two patients. However, when the double compartment face mask and measurement apparatus was applied, all patients were found to be breathing via both the mouth and nose (Table 3) . During this phase of the study, nasal PTIF was 0.35 ± 0.05 L/s and nasal PTEF was 0.27 ± 0.04 L/s, while oral PTIF and PTEF were 0.39 ± 0.05 L/s and 0.32 ± 0.04 L/s, respectively. In these nine patients, nasal PTIF, oral PTIF, and oral PTEF (but not nasal PTEF) were all significantly less at follow-up than at the initial study (p < 0.04 for all; Figure 1 , A-D). Furthermore, total (oral plus nasal) peak tidal airflows for the asthmatic patients at follow-up were significantly greater than the corresponding values obtained in the normal subjects (p < 0.03 for all).



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  		Figure 1.. Peak inspiratory (Nasal PTIF; top, A) and peak expiratory (Nasal PTEF; bottom, B) tidal airflow via the nose, together with peak inspiratory (Oral PTIF; top, C) and peak expiratory (Oral PTEF; bottom, D) tidal airflow via the mouth in nine asthmatic patients who were studied both during an acute exacerbation (the initial study) and when asymptomatic (the follow-up study). The different symbols represent individual subjects. Horizontal bars indicate mean values. *p < 0.04.

 
The nasal inspiratory and expiratory peak tidal flow fractions ranged from 0.11 to 0.69 and from 0.06 to 0.69, respectively, with group mean values of 0.47 ± 0.07 and 0.46 ± 0.07, respectively. These values were not significantly different from those obtained from the same patients at the initial study (p > 0.10 for both), but were significantly less than those obtained in the healthy subject group (p < 0.0001 for both).


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Conclusion
 References
 
The principal findings in the present study were the following: (1) during acute exacerbations, most asthmatic patients spontaneously breathe via both the nose and the mouth; (2) when not acutely bronchoconstricted, most asthmatic patients breathe via the nose, but switch to oronasal breathing when breathing via a face mask and measurement apparatus; (3) peak tidal inspiratory and expiratory flow rates in asthmatic patients are higher during an acute exacerbation than when they are asymptomatic; and (4) healthy subjects usually breathe exclusively via the nasal route, both with and without a face mask.

This is the first study to characterize the route of breathing that is spontaneously adopted by asthmatic patients during an acute exacerbation, and it is also the first study to evaluate the influence of a face mask on route of breathing in asthma. There has been only one previous study of route of breathing in asthma, and that was in asymptomatic asthmatic patients wearing a modified scuba mask.5 Furthermore, this latter study did not include any data obtained without a face mask.5 The main finding was that in normal subjects and patients with allergic rhinitis and asymptomatic asthma, all asthmatic patients and most subjects with allergic rhinitis were observed to be breathing oronasally at rest, while normal subjects were breathing exclusively via the nasal route. This finding is consistent with results in the present study.

In addition, the present study has shown that, in the absence of a face mask, asthmatic patients spontaneously breathe exclusively via the nasal pathway when asymptomatic, but switch to oronasal breathing during an acute asthma attack. The use of the oronasal route of breathing during acute exacerbations of asthma may relate to potentially increased flow resistive work associated with nasal vs oral route breathing. An increase in the flow resistive work of nasal route breathing (expressed as nasal power) associated with increasing N has been shown to be a major determinant of the switch from nose-only to oronasal breathing in normal subjects who are exercising.6 Similarly, during an acute exacerbation of asthma, the presence of higher total airflow rates may mean that exclusive use of the nasal route for breathing is not sustainable because of the increased flow resistive work, especially in the setting of an increase in the WOB associated with bronchoconstriction.7 Correspondingly, when patients are asymptomatic and peak tidal airflows are lower, there is a decrease in nasal power combined with lower total WOB (less bronchoconstriction), and this may then result in a return to exclusive nasal route breathing. The total of the peak tidal airflow through the mouth and the nose in symptomatic asthmatic patients, however, was less than the peak tidal N that have been reported to result in a switch to oronasal breathing in exercising healthy subjects.8

The presence of nasal disease in asthmatic patients may also influence the route of breathing via an increase in the flow resistive work of nasal breathing. The presence of a higher nasal resistance in asthmatic patients is related to the presence of nasal disease.9 The incidence of allergic rhinitis in asthmatic patients is, however, between 60% and 78%.10 Epidemiologic studies have shown an increased association of upper airway disorders, such as rhinitis, sinusitis, and hay fever, with both bronchial hyperresponsiveness and asthma.11 Reducing nasal resistance in asthmatic children who are chronic mouth breathers results in a reduction in mouth breathing and exercise-induced asthma.12 This latter study also found a direct relationship between mouth breathing and N obstruction.12 Thus, the presence of nasal obstruction during an acute asthmatic exacerbation may contribute to the development of oronasal breathing.

The presence of bronchoconstriction itself may result in worsening of the nasal airway obstruction, a phenomenon that has been shown to occur with histamine-induced bronchoconstriction,13 although exercise-induced bronchoconstriction does not result in an increase in nasal resistance in asthmatics.14 Consequently, during acute allergic exacerbations of asthma, the presence of bronchoconstriction per se may contribute to an increase in nasal resistance and, potentially, a switch to the oral breathing route.

The change to the oral route of breathing during an acute asthmatic attack may not happen because the mouth represents a lower resistance pathway, but because the resistance of the oral pathway can be more readily manipulated through use of the lips and teeth. Expiratory glottic narrowing has been shown to occur during induced bronchial asthma,15 thus helping to maintain hyperinflation, and thereby contributing to a reduction in total respiratory muscle work.16 This is analogous to expiration through pursed lips as practiced by patients with chronic airflow limitation. However, none of the asthmatic patients were observed to be breathing through pursed lips, suggesting that the change to the oral route is not necessarily for the purpose of providing further expiratory flow braking.

Alterations in the route of breathing may be important in the pathogenesis of asthma, since the nose protects the lower respiratory tract from environmental insults by filtering, warming, and humidifying air. Exercise-induced asthma can be modified by altering the breathing route.3 The breathing route used during exercise has been shown to determine the degree of bronchoconstriction and airway cooling that occurs in asthmatic patients with exercise-induced asthma.17 Indeed, modification of heat loss from the airways using heat and water exchangers18 and face masks19 has been shown to be protective against exercise-induced bronchoconstriction. Nasal breathing also filters inspired air, thus protecting the lower respiratory tract from inhaled particles. The nasal route of breathing has been shown to protect against bronchoconstriction in asthmatic patients who are sensitive to cat allergens20 and in asthmatic patients who are exposed to sulfur dioxide during exercise.21 Thus, nasal breathing has a role in the protection of the lower airway against environmental insults, and bypassing this route may be an initiating factor in exacerbations of asthma.

The finding that, in contrast to healthy subjects, asymptomatic asthmatic patients without evidence of bronchoconstriction change from nasal-only to oronasal breathing with the addition of a face mask and measurement apparatus was surprising and may be related to various factors. Technical factors such as the resistance of the circuit or the dead space may have influenced the route of breathing. However, the resistance of the oral pathway apparatus was greater than the resistance of the nasal pathway apparatus (ie, the subjects breathed via the oral pathway despite the higher apparatus resistance). The presence of a large dead space may have resulted in carbon dioxide rebreathing and an alteration in route of breathing. However, there is no difference in carbon dioxide sensitivity between asthmatic and normal subjects,22 and normal subjects do not alter their breathing route on the face mask. Chronic asthmatic patients have often been exposed to therapeutic interventions utilizing masks for many years and may alter their route of breathing as a result of conditioning. However, all of the asthmatic patients in the present study altered the route of breathing while wearing the face mask, suggesting that either all of the subjects were conditioned to oral-route breathing when wearing a face mask, or that conditioning per se is not an explanation for the alteration in breathing route.

Altered sensitivity to added nasal resistive loads may also explain the alteration in breathing route in asymptomatic asthmatic patients wearing a face mask. Over the physiologic range of background total airway resistance, the nose has been found to have no role in resistive load detection in normal subjects,23 but if the background resistance is outside the physiologic range, the nose may have some influence.23 Thus, the asthmatic patients who were studied when asymptomatic may have all had high background nasal or pulmonary resistance, so that the addition of the apparatus resistance of 0.8 cm/H2O/L/s was sufficient to result in an alteration in breathing route. However, it seems unlikely that all patients had high background pulmonary resistance, as most subjects had a normal FEV1. It also seems unlikely that all patients had a nasal resistance so high that the small apparatus load resulted in an alteration in breathing route, especially since all but two patients were spontaneously breathing via the nose alone prior to application of the face mask. Alternatively, there may be an intrinsic difference in the sensitivity of asthmatic patients to nasal resistive loads compared to normal subjects. However, several studies have shown that asthmatic patients have the same sensitivity as normal subjects to resistive loads at the mouth,24 25 and the resistance in our circuit was similar to loads that can be detected orally by asthmatic patients.24 25 The response to nasal loads in asthmatic subjects, however, has not been tested. Thus, the alteration in breathing route in asymptomatic asthmatic subjects wearing the face mask may be due to altered nasal load sensitivity, possibly in combination with, or because of, a higher background pulmonary or nasal resistance.

The predominant use of the oral route during acute exacerbations of asthma and the increased tendency of asthmatic patients to change their route of breathing to the oronasal route from the nasal route may be important in the pathogenesis and maintenance of exacerbations of asthma. Treatment of chronic sinusitis in asthmatic children reduces the need for regular bronchodilators,26 and ethmoidectomy for nasal polyps in a group of asthmatics decreased bronchial hyperresponsiveness.27 Nocturnal asthma may also be related to breathing route, since mouth breathing during sleep (perhaps related to posture-related increases in nasal resistance) may expose the lower airways to nonspecific irritants (eg, cold dry air) and allergens resulting in an acute exacerbation. Improving nasal breathing with an external mechanical nasal dilator has been shown to reduce nocturnal asthma in a group of asthmatic patients.28 In addition to treating nasal disease in asthmatic patients, it may also be important to consider the temperature, humidity, and delivery route of therapeutic interventions such as oxygen and nebulized salbutamol.


   Conclusion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
References
 
We conclude that during acute exacerbations, asthmatic patients switch breathing route from the nasal route to the oronasal route. Furthermore, even when not acutely bronchoconstricted, asthmatic patients switch to oronasal breathing when wearing a face mask, a phenomenon that does not tend to occur in healthy subjects. We speculate that this may represent increased sensitivity to resistive loading, possibly related to a high nasal airflow resistance. As asthmatic patients appear to switch more readily to oral route breathing than healthy subjects, this instability of oronasal airflow partitioning may constitute a contributing risk factor for the pathogenesis and maintenance of acute exacerbations of their disease. This may have important implications for the management of acute attacks of asthma.


   Acknowledgements
 
The authors wish to thank Emily Di Somma for technical assistance.


   Footnotes
 
Abbreviations: PTEF = peak tidal expiratory airflow expressed in liters per second; PTIF = peak tidal inspiratory airflow expressed in liters per second; N = nasal airflow expressed in liters per second; O = oral airflow expressed in liters per second; WOB = work of breathing

Supported by the National Health and Medical Research Council of Australia and the Westmead Hospital Research Institute.

Received for publication March 16, 1999. Accepted for publication June 2, 1999.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 

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