Deane Hillsman, M.D.
University of California at Davis, USA
Numerous mechanical and chemical feedback mechanisms are the dominant force controlling respiration and breathing patterns. However, it must be questioned whether these normal control mechanisms are always operating correctly if lung structure and physiology has been altered by disease.
This paper postulates the ventilatory response to dynamic hyperinflation (DH) in chronic obstructive pulmonary disease (COPD) and acute asthma is both inappropriate and counterproductive.
Hyperventilation is the probable initiating event in DH, and "relative hyperventilation" in COPD is a vicious circle phenomenon exacerbating DH and/or preventing DH correction.
DH has been recognized for many years. A seminal 1958 paper by William F. Miller (Amer. J. Med. 24; 929-940, 1958) showed an example of hyperventilation in COPD producing 1200 cc of air trapping within only seven breaths.
Tragically, interest in cognitive DH control in COPD waned in the 1970's. There has been a resurgence of interest in DH. This is exemplified by a decade of study by Denis O'Donnell and colleagues in COPD (AJRCCM 164;770-777, 2001) and acute Asthma (Am. Rev. Resp. Dis. 148;1452-1459, 1993).
Their COPD data demonstrated almost identical respiratory rates in exercised patients with DH and normal subjects, revealing the COPD rate as one of "relative hyperventilation," which must therefore be considered pathologic. Their induced acute DH asthma data, lacking a control group, is likewise highly suggestive.
The natural escape from DH in COPD is frequently distressing exhaustion with probable secondary inefficient upper tidal volume reduction and slowing of the respiratory rate.
Cognitive ventilatory strategies to prevent and/or resolve the DH lesion are required. These include rate slowing, expiration prolongation and/or cautious forced exhalation (to minimize dynamic bronchial compression), and transient inspiration volume limitation.
Conclusion: The "relative hyperventilation" response in COPD (and probably acute asthma) to DH generates a vicious circle response and is therefore corrupt. Cognitive breathing pattern control is required to efficiently resolve DH.
From Denis O'Donnell et al, AJRCCM 164; 770-777, 2001
Exercising normals versus patients with severe COPD (average FEV1 = 0.94 lps). The COPD patients were stable and not in a state of Asthmatic bronchospasm at the start of exercise.
Note the COPD patients have an increased Functional Residual Capacity, and that immediately on beginning to exercise they start to "Air Trap" and develop progressive Dynamic Hyperinflation. This is a classic example of a "vicious circle" pathophysiologic lesion, with increasing respiratory rate making the Dynamic Hyperinflation problem progressively worse.
It is apparent these patients are in a state of Dynamic Hyperinflation at rest and/or just bordering on same, and they are therefore extremely vulnerable to any degree of "relative hyperventilation."
It is clear from this data the multiple traditional mechanical / sensory / neural / chemical feedback mechanisms that regulate breathing control have failed in these COPD patients.
It follows therefore that breathing control techniques are mandatory to prevent and/or correct the Dynamic Hyperinflation lesion as described. Rescue bronchodilators would not likely be able to influence this lesion significantly.