BACKGROUND AND DISCUSSION
This paper describes three cases of sudden severe life threatening asphyxic asthma and their treatment by manual chest compression in primary care. External chest compression has been used for respiratory arrest in asthma but because of the improbability of a medical assistant being present within minutes of the arrest there is only anecdotal evidence of its effectiveness. This is unlikely to change because the duration of sudden asphyxic asthma attacks is extremely short and patients usually die outside hospital often before medical help can arrive.1,3,8,10,11
The first mention of chest compression for asthma in the literature was by J. I. M. Watts2 in 1984. Later M. Fisher et al described a case of acute sudden asphyxic asthma treated successfully by external compression after mechanical ventilation had failed4. He now has trained paramedics in New South Wales to use the technique in spontaneous breathing patients during transfer to hospital and he concludes that the use of mechanical external chest compression (MECC) will have its greatest impact when initiated in a prehospital setting in patients with severe sudden onset asphyxic asthma. This enthusiasm contrasts with and differs dramatically from, the results of a study of the effects of compressing the rib cage in four intubated, mechanically ventilated adult patients recovering from acute severe asthma by T. Van der Trouw et al., who concluded that “manual compression of the rib cage during consecutive tidal expirations would be ineffective in reducing pulmonary hyper inflation during the emergency management of asthma”5 The four patients in the study had survived transfer to hospital, may have had gradual decompensation, or, a few days of unstable conditions over several days prior to admission. This is not the clinical picture of the cases described here of acute asphyxic asthma and this may account for the difference between Trouw’s results and those described here and those of Watts and Fisher.
From 1959-66 the increase (in asthmatic deaths) has been substantial at all ages, but most pronounced in adolescence and young adult life. Between 1959 and 1966 the death rate increased three times at ages 5 to 34 years and nearly eight times at ages 10 to 14 years 6B. At that time the only explanation to account for the increase was the introduction and use of corticosteroids (in 1952) and the use of pressurised aerosols containing sympathomimetics (used increasingly after 1960). These conclusions about the cause of the increase in mortality were and still are widely held7 and were arrived at simply because no other explanation could be found.
There is however an alternative explanation for this steady but dramatic increase in the death rate. Prior to 1960 if anyone stopped breathing the universal response was a chest compression type of artificial respiration (eg the Holger-Neilson method.) Mouth-to-Mouth resuscitation was introduced in 1960 and rapidly replaced the old methods. This could have had a significant effect on the death rate in sudden severe asthma.
That introduction of new treatments was not the cause of the increased death rate is supported by Molfino et al1 who examined the mechanisms by which patients might die in acute asthma. He studied 10 patients who arrived at hospital in respiratory arrest or developed it soon after admission. He concluded that “the near -fatal nature of the exacerbations was the result of severe asphyxia rather than cardiac arrhythmias and that undertreatment rather than overtreatment may contribute to an increase in mortality from asthma.” this contrasts with the generally accepted view that the epidemic of asthma deaths 1960 -1970 was due to adverse affects of treatment6A
There is increasing evidence that there is a separate group of asthma patients with extremely rapid onset of life threatening asthma with no earlier signs of deterioration or change in Peak Flow prior to the onset. This group of patients are more difficult to ventilate mechanically but recover more rapidly and have a higher incidence of respiratory arrest.3,4
A large number of previous studies, many epidemiological, have investigated the problem of sudden death in asthma9, but none have elucidated a mechanism separating them from asthma in general. The usual explanation is that extreme bronchospasm plays the primary role in pathogenesis3,6A rather than mucus plugging, bronchial oedema or vascular bronchial compression but perhaps there is another factor involved.
There is an irresistibly powerful urge to expand the chest very forcefully during suffocation as when a drowning man inhales water into his lungs. What triggers this urge is unknown but may be chemical or neural, presumably acting on a primitive part of the brain associated with the fight and flight mechanism. In acute asphyxic asthma this desperate urge to breathe in appears to take over totally the respiratory response, the inspiratory muscles being driven with increasing frequency and uselessly to expand the chest wall with no time for any expiration. This results in shorter and shorter inspiratory gasps until they cease altogether because extension of the chest wall is limited. This hypothesis suggests that the sudden asphyxia is due to the chest wall being driven to ever increasing expansion even when fully expanded causing ultimate failure of the inspiratory muscles.
One would not pump air into an over inflated bellows to get the bellows to work but this is what one is doing with mouth to mouth resuscitation, or for that matter mechanical ventilation, without first emptying the over distended chest. This report has been written to provide further evidence of the usefulness of manual external chest compression in cases of sudden asphyxic asthma and encourage the importance of including this method in teaching first aid to paramedics, first-aiders and relatives of asthmatics. Chest compression in respiratory arrest from asthma is simple enough to be taught to relatives and safe. This may be the only way that the death rate from such patients can be significantly affected.
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