Respiratory muscle fatigue is a loss in the capacity of respiratory muscles to develop force and/or velocity under load, finally resulting in exhaustion or task failure which is reversible on rest (NMkBIWoikshop...i1990). Various mechanisms are possible: failure to generate force because of reduced central motor output (central fatigue), failure to transmit the neuronal message (transmission fatigue), or failure to generate force within the respiratory muscles (peripheral fatigue). About half the reduction in diaphragmatic force can be attributed to reduced central motor drive. However, it remains unclear whether this is a primary or a secondary mechanism (i.e. vital adaptation on a lower level).
Central fatigue is considered to be present when maximum voluntary contraction generates less force than maximum electrical stimulation (diaphragmatic force tested by the twitch occlusion test). In contrast, the existence and relevance of transmission fatigue (i.e. neuromuscular function failure) is still questionable. Peripheral (i.e. muscular) fatigue is beyond the scope of this chapter.
Intermittent (nocturnal) non-invasive mechanical ventilation appears to be efficacious in some groups of patients with chronic respiratory failure. However, it is still not clear whether this benefit is due to 'resting' (unloading) fatigued muscles by the intermittent mechanical ventilation or to preventing the neural control system from adapting to high CO2 levels. Breathlessness and dyspnea
Breathlessness is the recognition of an inappropriate relationship between respiratory work and total body work ( Burdon..ef...a/: 19.94). It is a subjective symptom whose origin is not completely understood. In addition to the mechanics of breathing (i.e. work and lung volume), many other factors are involved. Perception depends on subjective experience: 'normal' (after exercise) or 'abnormal' (not related to adequate activity). The threshold of perception may vary. Some patients tolerate severe respiratory loads with little or no complaint of breathlessness; this may occur because of individual characteristics or because of temporal adaptation.
Temporal adaptation allows a significant disability to be tolerated with a reduction or absence of symptoms. This can be clinically dangerous, since it may result in underestimation of actual risk. About 25 per cent of the change in lung volume is necessary in acute asthma before any change in symptoms is noticed. Thus larger changes in background load are required in patients with abnormal pulmonary mechanics, i.e. patients with chronic background load (e.g. chronic inadequately treated asthma), before changes in sensation occur. However, if the change in background load is recent, smaller changes in sensation are noticed. There are considerable variations between individuals. Identification of the subgroup of patients who have impaired perception of breathlessness (e.g. external loading) is clinically important.
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.