First Aid in Asthma

Chest compression First Aid for Acute Asphyxic Asthma and Respiratory Arrest

Dr. Rex Harrison B.A. M.B. B.Chir.(Cantab) D.L.O. DRCOG

A discussion paper.

This paper describes three cases of sudden severe life threatening asphyxic asthma and their treatment by manual chest compression in primary care. This is followed by a discussion of the mechanisms involved in this condition, treatment by chest compression and its historical context. 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

CASE 1

An emergency home visit called because of an asthmatic attack found a 17 year old girl supporting herself with both hands at the kitchen sink. She was making short high-pitched grunt-like noises like a quiet hiccough trying to breathe. At this point she collapsed unconscious with cessation of respiration. Mouth to mouth resuscitation failed even with the head lifted slightly and a clear airway. The patient was turned over on her face in an attempt to use the Schafer method of artificial respiration with two hands placed flat over the lower chest, thumbs over the spine and the fingers around each side of the lower chest using the operator’s body weight to compress the chest against the floor. There was an immediate satisfying escape of air from the lungs for many seconds suggesting that the reason the mouth to mouth respiration had failed was that the lungs were already over inflated. Following 4 or 5 compression manoeuvres the patient started to breathe on her own. Intravenous hydrocortisone and adrenaline were then administered together with oxygen by mask and by the time the ambulance arrived three quarters of an hour later she was regaining consciousness.

CASE 2

A large man, having a severe asthmatic attack, again with the same faint hiccough like grunting noises and no air entry into the lungs and no chest movement, was standing with both hands on the back of a settee. Forewarned by the previous case the operator placed both arms round the lower part of the patient’s chest a) to support him, and b) to give chest compression at the same time. Because of his size the hands could were only just able to link together. Chest compression was performed by squeezing the operator’s chest against the lower part of the patient’s thorax from the rear. The patient made an immediate respiratory gasp and was encouraged to slow these gasps so that chest compression allowed more prolonged expiration. The patient’s relief was immediate. Chest compression was continued until the patient’s wife had retrieved drugs and emergency oxygen from the doctor’s car. Intravenous hydrocortisone and adrenaline were administered immediately although the acute emergency was over and the patient was fully recovered by the time he arrived in the hospital. This patient had a further attack two months later when no external pressure application was available and he died.

CASE 3

A man of 59, who had asthma and chronic bronchitis, presented at a home visit with severe cyanosis. He was taking very short inspiratory gasps. Both hands were placed in the lower part of his chest squeezing the lower part of the chest inward and downwards in time with his expirations. There was marked and immediate improvement in his condition after even the first compression and he recovered in hospital.

All the patients had used Salbutamol aerosol inhalers and discarded them prior to my arrival. The cases occurred before modern nebulisers were available.

All the patients had used aerosol inhalers excessively and discarded them prior to arrival. The cases occurred before modern nebulisers were available.

Background and discussion

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 1960-65 the mortality from asthma increased annually and went up eight times in seven year,6,7 despite the introduction of new effective treatments. 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 treatment6.

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 pathogenesis3,6 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.

Conclusion

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.

1) Molfino R.N.A., Nannini L.J. , MartelliA.N., & Slusky A.S.. Respiratory Arrest in Near-fatal asthma. New England Journal of Medicine Vol. 34 No.5 285-8 Feb 2004

2) Watts J.I.M Thoracic Compression for Asthma. Chest / 86 / 3 September, 1984

3) Wasserfaller J-B Schaller M-D Feil F, & Perret C.H. Sudden Asphyxic Asthma: A Distinct Entity? Intensive Care Service Depart. of Med. University Hospital Lausanne, Switzerland.

4) Fisher M.M, Whaley A.P, R.R. Pye R.R. External Chest Compression in the Management of Acute Severe Asthma- A Technique in Search of Evidence. Prehospital and Disaster Medicine Vol.16 No. 3 July - Sept 2001

5) Van der Touw T, Mudaliar Y, Nayyar V, Cardiorespiratory effects of manually compressing the rib cage during tidal expiration in mechanically ventilated patients recovering from acute severe asthma. Critical Care Med 1998 August;26(8) :1361-

6) Speizer FE, Doll R, Heaf P. Observations on recent increase in mortality from asthma. BMJ1968;1:335-339

7) Marks G., Burney P. Disease of the Respiratory System

8) M L Burra, B H Daviesb, A Hoareb, A Jonesc, I J Williamsond, S K Holgatee, R Arthurse, I G C Hodges A confidential inquiry into asthma deaths in Wales. Thorax 1999;54:985-989 ( November )

9) Ayres JG, Miles JF, Barnes PJ. Brittle asthma. Thorax1998; 53:315–21.

10) C E Bucknall, R Slack, C C Godley, T W Mackay, S C Wright, on behalf of SCIAD collaborators. Scottish Confidential Inquiry into Asthma Deaths (SCIAD), 1994-6 Thorax 1999;54:978-984 ( November )

11) British Thoracic Association. Death from asthma in two regions of England. BMJ 1992;285;1251-5