, Julie Burkin1, Catherine Moffat1 and Anna Spathis1
(1)
Department of Palliative Care, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK
Abstract
The successful management of any symptom requires an understanding of its cause. The aetiology of breathlessness is particularly complex, and pathophysiological and clinical models have been developed in an attempt to explain the underlying mechanisms. This chapter outlines two such models, including the Breathing, Thinking, Functioning model, which explains how breathlessness is perpetuated and can be helpful in guiding symptom assessment and management.
Introduction
The successful management of any symptom requires an understanding of its genesis. Breathlessness is no exception, and an appreciation of the underlying mechanisms can help direct both effective assessment and treatment. Unlike other symptoms, however, the aetiology of breathlessness is particularly complex, and this occurs for a number of reasons.
Respiration is the only body system vital for survival that is under both volitional and automatic control. There is no advantage in other major organs, for example cardiac or renal function, being under conscious influence. Breathing, however, needs to be controlled precisely when undertaking activities, such as swallowing, speaking or swimming. This means that the neural circuitry must involve higher cortical pathways. The perception of breathlessness is a complicated process that is, as yet, not fully understood.
Further complexity occurs at a clinical level. A vast number of pathological processes can have an impact on respiratory function and cause breathlessness. Diseases of the lung parenchyma and chest wall, neuromuscular and cardiac pathology, as well as a myriad of metabolic conditions, can all influence respiration.
The acute and distressing sense of breathlessness is very useful when there is an immediate threat to survival, such as suffocation or inhalation of a noxious substance. A homeostatic threat needs to generate a rapid emotional response, such as terror, that leads in turn to an adaptive behaviour, such as increasing respiratory effort and running away. However, once the symptom becomes chronic, its perception is less helpful and, indeed, can cause maladaptive emotions and behaviours that actually perpetuate the breathlessness.
Pathophysiological and clinical models have been developed in an attempt to explain these complex processes. This chapter sets out two such models, and outlines how an understanding of these mechanisms can closely guide symptom assessment and management.
Models for Understanding the Genesis of Breathlessness
Pathophysiological Model (Parshall et al. 2012)
The mostly widely accepted theory underpinning the perception of breathlessness is the ‘mismatch’ theory.
Breathlessness is experienced when there is mismatch between the demand for ventilation and feedback on actual ventilation. It occurs when ventilatory demand increases or the mechanical process of ventilation is impaired.
The demand for ventilation generates central respiratory motor activity that drives respiration. It is thought that a copy of this efferent information is sent centrally allowing the brain to predict the sensory feedback that should occur. This ‘corollary discharge’ is compared with the peripheral afferent signals that actually arise, and any mismatch between the two leads to the feeling of breathlessness. This integration appears to occur in the limbic-related cortex, in particular the anterior insular region (Schon et al. 2008). This deep inner layer of the brain cortex is involved in awareness of homeostatic threats, and generates emotional and behavioural responses. It can be thought of as an ‘internal alarm centre’, and appears to play a key role in the genesis of breathlessness. This model is represented schematically in Fig. 2.1.
Although complex and theoretical, there are a number of clinically relevant implications of this model:
The large number of afferent inputs into the perception of breathlessness leads to a broad range of potential ways of modulating the symptom.
The close relationship with parts of the brain involved in emotions and thoughts can help clinicians and patients understand the importance of psychological influences on the perception of breathlessness.
It gives a potential explanation for how other unpleasant sensations, such as pain, extreme heat or negative emotions, can influence breathlessness, as all such threats are perceived in a similar area of the brain.
Mr James: Part A
Mr James had to retire early from his work in the building industry as his health was deteriorating. He knew he had COPD, and his breathing was becoming a real problem, even walking about slowly. He also had bad hip, knee and back pain from arthritis, and had been told that he could not have surgery because of his poor chest. Over the last year he had become completely house bound, and was afraid to leave the house even for medical appointments. His GP told him he was agoraphobic, and arranged for him to see the local mental health services, as well as referring him to you for breathlessness management.
At the first meeting, Mr James expresses his anger about being ‘thought of as a loony’. He explains that he is terrified of having a panic when out of the house. This has happened on two occasions; he was terrified and thought he was dying. On detailed questioning he identifies that his breathing is worst on the days when his arthritis is really playing up. His wife says that he sometimes ‘shouts out’ in pain when he first tries to move after sitting for a while.
You explain to Mr and Mrs James that the part of the brain that feels the breathlessness also deals with other unpleasant feelings like pain. This area is like an ‘internal alarm’ to the body, and automatically leads to a number of feelings (like fear) and behaviours (like staying still to try to avoid the breathing or pain problems). When you state that it is ‘all part of the hardwiring of the brain’, and a completely normal response to what is happening, he is visibly relieved and becomes briefly tearful.
Case continued in part B on page…
Breathing, Thinking, Functioning (BTF) Perpetuation Model
This model is the clinical key to the successful management of breathlessness. It both gives an explanation for the perpetuation of the symptom, and leads directly to potential ways of managing it.
In evolutionary terms, there is a clear survival advantage for the perception of a threat to lead to an immediate negative emotion. This in turn motivates behavioural changes to avoid the danger. Once the threat becomes chronic, however, these emotions and behaviours are no longer helpful. Indeed, they can become maladaptive and inadvertently perpetuate the problem.
In chapter 1, the three facets of breathlessness management were introduced: ‘breathing’, ‘thinking’ and ‘functioning’ (or BTF). In each of these, specific unhelpful emotions or behaviours develop. These then lead to three inter-related vicious cycles that prolong and worsen the symptom (Fig. 2.2).
Figure 2.2
Perpetuation of breathlessness by vicious cycles
1.
Breathing vicious cycle
Patients who are breathless often develop an inefficient breathing pattern. They perceive they need to take big breaths in, ‘to get more air’, and usually imagine the air coming into the upper part of their chest. Ask any child to take a big breath in, and it usually involves upper chest movement with hunched shoulders. Patients tend to pant, with a small tidal volume shunting air within the respiratory dead space. Accessory muscles of respiration are used in an attempt to pull air into the upper chest. This all greatly increases the work of breathing and reduces its efficiency. Breathlessness worsens and the vicious cycle has developed.
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