Asthma breathing pattern

2.3.2.1 Changes to respiratory physiology in asthma

The condition of asthma is not a single entity. Rather, it is likely to be a heterogeneous condition that can be sub-divided into different phenotypes based on clinical, aetiological, physiological or pathophysiological features (Polosa, 2008). There is also no gold standard diagnosis for asthma, with diagnosis usually based on clinical symptoms (BTS, 2009). Asthma is characterised by airway hyperresponsiveness (Brown et al., 2006), airway inflammation (Pascual & Peters, 2005) and episodic or chronic air flow limitations (Stirling & Chung, 2001). It is believed that many of the observed pulmonary function changes, such as lung function decline (Pascual & Peters, 2005), premature airway closure (Tantucci et al., 2011) and airway

hyperresponsiveness (Brown et al., 2006) are due to remodeling of the airways. Changes in the airway structures lead to a marked increase in airway

resistance, which in turn leads to increased work in the process of breathing. As the degree of airway obstruction worsens expiration becomes active rather than passive, which further increases the work of breathing. As airway walls reduce elasticity and fail to recoil, airway collapse on expiration, resulting in air trapping and hyperinflation (Cormeir, 1990).

It is currently unclear exactly how airway remodeling may affect breathing pattern. However, it is hypothesised that airway hyperresponsiveness may result in bronchoconstriction and hyperventilation, which in turn lead to an increase in tidal volume and respiratory rate. Premature airway closure may also result in reduced expiration time.

Changes in breathing mechanics in asthma

Asthma is an obstructive disease characterised by increased airway resistance. High airway resistance from the airways, along with hyperinflation, will increase the load on the respiratory muscles (Laghi & Tobin, 2003). Hyperinflation often forces the respiratory muscles to operate at non-optimal lengths (Ratnovsky et al., 2008), meaning that respiratory muscles are required to generate higher forces with each breath (Hill, 2004). One of the adaptations to this increase in workload is the persistent use of accessory respiratory muscles to generate additional inspiratory force (Holley & Boots, 2009; Grover et al., 2011; Shaw & Shaw, 2011; Lavietes et al., 1988). In an early study by Martin et al. (1983) the activities of the respiratory muscles of seven asymptomatic asthma patient were studied. Progressive bronchoconstriction was induced with inhaled aerosolized histamine, and the results indicated a relative increase in the recruitment of intercostal/accessory muscles with a progressive increase in

bronchoconstriction. The abdominal muscles, did not demonstrate such an increase, however, suggesting that the recruitment of intercostal/accessory muscles exceeds the recruitment of the diaphragm during acute

bronchoconstriction.

The persistent use of the accessory muscles is referred to as apical breathing (Clifton-Smith & Rowley, 2011) and creates further expansion of the rib cage primarily in the cephalad direction (De Troyer & Kelly, 1984). Apical breathing is not as efficient as diaphragmatic breathing due to the higher lung compliancy of the basal area of the lung, which provides more surface area for gas exchange. The increased use of accessory muscles leads to increased work in breathing and consequent energy wastage (Gorini et al., 1999). The greater recruitment of the rib cage muscles also places them at risk of fatigue as their threshold for fatigue is lower than that for the diaphragm (Zocchi et al., 1993).

In patients with obstructive respiratory disorders such as asthma, paradoxical or asynchronous motion of the rib cage and abdomen have often been reported (Gilmartin & Gibson, 1984; Hammer & Newth, 2009; Aliverti et al., 2009). The

during breathing at rest (Hammer & Newth, 2009). An asynchronous breathing motion refers to non-coordinated motion of the rib cage and abdomen

compartments. It is often characterised by a lag between the two

compartments, or one compartment moving in the opposite direction to the other. The likely contributing factors for chest wall asynchrony in adults include diaphragm weakness (Hammer & Newth, 2009) and hypertrophy of the

accessory muscles (Lavietes et al., 1988). Hyperinflation of the lung can also contribute to asynchronous motion. This is because as lung volume increases, the inspiratory muscles are passively shortened, placing then at a mechanical disadvantage (De Troyer, 1997). Therefore, patients with obstructive respiratory disorders frequently have a reduction of diaphragmatic mobility and its relative contribution to thoracoabdominal motion.

2.3.2.2 Literature on asthma breathing pattern

Published studies on the mild to moderate asthma population have reported no statistically significant differences in breathing pattern during the asymptomatic phase. A study by Delvaux et al. (2002) examined the breathing pattern in eighty mild to moderate asthma patients, according to the American Thoracic Society’s criteria (1993). The mild to moderate asthma patients were aged between 16 and 60 years old and had asthma symptoms at the time of

recruitment. A further forty healthy individuals, matched with the experimental group on the basis of sociodemographic characteristics, were recruited as a control group. The breathing parameters of tidal volume and respiratory rate were monitored by pneumotachograph in a seated position over three-minute recording periods. The difference between the groups was analysed using t- tests. The results showed that mild to moderate asthma patients had higher tidal volume and higher respiratory rate than healthy controls. However, the differences were very small (100ml difference in tidal volume, one breath per minute difference in respiratory rate) and did not reach statistical significance. This study appears to suggest that there is very little difference in tidal volume and respiratory rate between mild to moderate asthma groups and the healthy

population. However, the lack of significant differences may be due to a lack of power calculations for sample size, with the possibility that the sample did not have sufficient power to detect any differences. The recording period was short, and it is doubtful that such a short period of recording would be sufficient to capture the true extent of differences in breathing patterns.

Similar results were also reported in another study by Osborne et al. (2000). These authors investigated breathing pattern in mild to moderate asthma

patients during the stable phase of the condition. Twenty-three participants with a history of asthma were recruited, and a further seventeen healthy participants with matching age, gender and height were recruited as controls. Breathing patterns were recorded via a laboratory standard heated pneumotachograph for five minutes, during which time tidal volume, inspiration time, expiration time, breathing rate and end tidal carbon dioxide were monitored. The differences between the healthy controls and the mild to moderate asthma patients were assessed by t-test.

The results showed that the patient group had a higher tidal volume, shorter inspiration and expiration times and a higher breathing frequency than the healthy controls. This finding seems to support the hypothesis that asthma patient groups may have different breathing patterns in comparison with healthy individuals. However, the observed differences did not reach statistical

significant levels. Because a power calculation was not carried out, the lack of statistical significant difference in respiratory parameters between the two groups may be due to the sample size, which may not have been sufficiently large to have the power to detect small differences. The findings therefore remain inconclusive as to whether there is any difference in respiratory parameters between healthy controls and mild to moderate asthma patients. The recording period was short, consisted of only five minutes of recording. Also, given the complex nature of breathing patterns (Fiamma et al., 2007a), it is doubtful whether the short recording period would be sufficient to capture the true picture of the participants’ breathing patterns, and subtle differences may not have been captured.

Another study by Tobin et al. (1983b) measured breathing pattern in

‘symptomatic’ and ‘asymptomatic’ asthma. The authors defined symptomatic asthma as having dyspnoea at rest or during moderate exertion, accompanied by wheezing. The exact measurement of dyspnoea or wheezing was not

documented in the study. Seventeen asymptomatic asthma patients and fifteen symptomatic asthma patients were recruited, and their breathing patterns in a supine position were monitored by a respiratory inductive plethysmograph over a period of fifteen minutes. The results showed that the breathing rates were 16.6 breaths per minute in the asymptomatic asthma group and 16.0 breaths per minute in the symptomatic asthma group. However, the group mean tidal volume in the symptomatic group was markedly higher (679ml ±275) than in the asymptomatic group (386ml ±133). However, the mean tidal volume of the asymptomatic asthma group was not statistically significantly different from the mean tidal volume recorded from a healthy population (383ml±91). The mean inspiratory drive (defined as inspiration time divided by the total of inspiration and expiration time) of the symptomatic asthma group was also statistically significantly higher than for the asymptomatic group and the healthy group.

This study suggests that symptomatic asthma patients may have a larger mean tidal volume and a stronger inspiratory drive than either healthy individuals or asymptomatic asthma patients. The asymptomatic asthma patients, however, did not demonstrate differences in respiratory parameters in comparison with healthy individuals. The results for this study should be interpreted cautiously since there was no clear definition for inclusion within the asthma population. Given the wide presentation of clinical symptoms and the high incidence of co- existing conditions in asthma (BTS, 2009), it is difficult to draw conclusions from these results without a description of the sample population.