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My son was driving his 1986 Camaro when he saw the temperature gauge soar. There was a loud screech, then a whamity sound up front for a few seconds. This was followed by a bang and thumping low in the front of the car while smoke came out the tail pipe. A mechnanic recorded the words used to describe the symptoms that led to severe dysfunction of my son's beloved car. The mechanic used my son's symptom descriptors to isolate the sequence of events to a loss of oil pressure followed by overheating of the engine cylinders, which led to seizing of the pistons, then breaking of engine metal, and finally total engine failure. In a similar way, during an asthma attack, the patient feels that something in their respiratory system is changing. The symptoms have a temporal information pattern that causes increasing distress. The fundamental question is what physiological processes elicit these symptoms.
Patients with asthma use a variety of descriptors that are related yet different (1). In the study by Binks and coworkers (4) published in this issue (pp. 78-82) they studied two of those symptoms, chest tightness and a sense of effort breathing, to determine the origins of these feelings. They report that patients with asthma can easily estimate the change in their sensation of chest tightness and ventilatory effort when spontaneously breathing during a methacholine bronchoconstriction challenge. They demonstrated that the sensation of chest tightness and effort, while occurring simultaneously, were from separate sensory sources. This was tested by repeating the methacholine bronchoconstriction with the patients mechanically ventilated. This allowed the mechanical ventilator to decrease the need for the inspiratory muscles to ventilate against the bronchoconstricted lung. They could separate these two components of respiratory sensation by a significant decrease in the sense of effort with no change in chest tightness. The fact that chest tightness did not change when the drive and effort of breathing was decreased suggests that the intrinsic changes in afferent activity in the airway epithelium and smooth muscle elicited the sense of chest tightness, separate from the respiratory pump-related sense of effort. Their results, thus, demonstrate both these sensations occur with bronchoconstriction but are of separate physiological origin, that is, the sensation of chest tightness is of airway origin and the sensation of effort is from the respiratory pump.
An asthmatic attack is a temporal process beginning with a stimulus eliciting brochoconstriction and exacerbated airway inflammation (airway sensation). This produces a change in airway mechanics and an increased impediment to ventilation. The patient must breathe against an altered lung mechanical environment to maintain ventilation (respiratory pumping sensation). The changes in airway mechanics subsequently lead to dynamic airway compression resulting in hyperinflation (volume sensation). This can then lead to alveolar hypoventilation, which will result in hypoxia and hypercapnia (chemosensation). Binks and coworkers (4) have studied the sensations produced during the early bronchoconstriction phase of an asthma exacerbation. Their results suggest that the changes in the airway activate afferents that are interpreted by the central nervous system as chest tightness. They also show bronchoconstriction-induced decreases in lung compliance and increases in airway resistance that caused an increase in the work of breathing, expressed as an increased effort to breathe. The primary perceptual change they induced with their experimental protocol was relieving some of the ventilatory work performed by the respiratory pump with mechanical ventilation. This reduced the patient's respiratory pump work and decreased the sense of effort. The ability to sense acute airway inflammation and increased ventilatory load is an essential component for early recognition of an attack of asthma. One difficulty in deciphering the language of a patient experiencing an exacerbation of asthma is the multiple system origin of the sensory information and the changing nature of the symptoms as the exacerbation progresses. Therefore, it is important to determine the self-assessment capabilities of patients, such as their ability to sense their respiratory status (chest tightness and sense of effort) throughout an exacerbation (4), as one component of a self-management program for asthma.
When the patients were placed on mechanical ventilation, Binks and coworkers (4) report a significant decrease in the sense of effort, but the sense of effort does not go to zero. This is under conditions in which the patient has little spontaneous breathing as indicated by the pressure measurements. Thus, the bronchoconstriction effect on the airway producing the sensation of chest tightness is also interpreted as an increased effort to ventilate the lung, even if that ventilation is by an external source. Perhaps the patients cannot completely differentiate between the sense of effort and chest tightness. Alternatively, ventilating the bronchoconstricted lung changes mechanoreceptor activity of the respiratory system in a manner that tells the subject it is more difficult to inflate the lung. This suggests there is an effort component that remains in their sensation of the methacholine-induced bronchoconstriction when they are mechanically ventilated. The perceptual system mediating the sensation of bronchoconstriction receives respiratory information that is dependent on the pattern of breathing (5). With bronchoconstriction, the pattern of the mechanical forces related to ventilation change in a specific manner, producing an associated change in the patterning of sensory information. Using the collage of afferent activity from the respiratory tract and respiratory muscles (8), the central nervous system can then detect a change in ventilatory status, locate the source of the change, determine the type of change occurring, differentiate the quality of the sensation, and apply word descriptors to what they are feeling, that is, chest tightness and effort.
The ability of the patient and physician to sort through the screech, whamity, bang, and thump provides the essential information to diagnose the sequence of events and correlate the symptom description with pathophysiological status. The awareness that early events portend an increasingly severe condition is important for timely treatment. The sensations of chest tightness and an increased effort to breathe are probably of separate physiological origin (4), yet they occur simultaneously during bronchoconstriction and provide essential information early in an exacerbation of asthma for patients to self-assess their respiratory status and seek treatment.
Gainesville, Florida
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Footnotes |
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References |
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1. Simon PM, Schwartzstein RM, Weiss JW, Fencl V, Techtsoonian M, Weinberger SE. Distinguishable types of dyspnea in patients with shortness of breath. Am Rev Respir Dis 1990; 142: 1009-1014 [Medline].
2.
Killian KJ,
Watson R,
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Symptom perception during acute bronchoconstriction.
Am J Respir Crit Care Med
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490-496
3. Manning HL, Schwartzstein RM. Respiratory sensations in asthma: physiological and clinical implications. J Asthma 2001; 38: 447-460 [Medline].
4.
Binks AP,
Moosavi SH,
Banzett RB,
Schwartzstein RM.
"Tightness" sensation of asthma does not arise from the work of breathing.
Am J
Respir Crit Care Med
2001;
165:
78-82
5.
Killian KJ,
Bucens DD,
Campbell EJM.
Effect of breathing patterns on
the perceived magnitude of added loads to breathing.
J Appl Physiol
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52:
578-584
6. Zechman FW, Wiley RL, Davenport PW. Ability of healthy men to discriminate between added inspiratory resistive and elastic loads. Respir Physiol 1981; 45: 111-120 [Medline].
7. Zechman FW, Wiley RL, Davenport PW, Burki NK. Load detection latencies and temporal patterns of added load sensation. Am Rev Respir Dis 1979; 119: 73-75 [Medline].
8. Zechman FW, Wiley RL. Afferent inputs to breathing: respiratory sensation. In: Cherniack NS, Widdicombe JG, editors. Handbook of physiology, Section 3: The respiratory system, Vol. II: Control of breathing, I. Bethesda, MD: American Physiological Society; 1986. p. 449-474.
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