Case descriptions

1. An emergency home called because of an asthma attack wherein a 16-year-old girl was found supporting herself with both hands at the kitchen sink. She was making occasional short, high-pitched noises like a faint hiccup sound, trying to breathe. She then collapsed and became unconscious, with cessation of respiration. Mouth-to-mouth resuscitation failed, even with a clear airway. The patient was turned over on her face in an attempt to use the Schafer method of artificial respiration. Two hands were placed flat over the lower part of the chest, the thumbs over the spine and the fingers around each side of the lower part of the chest using the operator’s body weight to compress the chest against the floor. There was an immediate escape of air from the lungs, suggesting that the reason the mouth-to-mouth respiration had failed was that the lungs were already overinflated and the chest wall was at maximal extension. After four or five compressions, the patient started to breathe on her own. Intravenous hydrocortisone and adrenaline were then administered, as well as oxygen by facemask, and by the time the ambulance arrived 45 min later, she had regained consciousness.

2. A large man having an asthma attack, again with similar faint hiccup-like noises and no air entry into the lungs and no chest movement, was standing with both hands on the back of a settee. Both the operator’s arms were placed round the lower part of the chest, only just being able to link the two hands because of the patient’s size. This also helped to support the patient in an upright posture. Chest compression was performed. 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 physician’s car. This patient had a further attack 2 months later, when no external pressure application was used, and he died.

3. A 59-year-old man who had asthma and chronic bronchitis presented, at a home visit, with severe cyanosis. He was taking very short inspiratory gasps. The operator’s both hands were placed on the lower part of the patient’s chest, squeezing the lower part of the chest inwards and downwards in time with the patient’s expirations. There was immediate and marked improvement in the patient’s condition after even the first compression, and he had recovered by the time he reached the hospital.

Comment

All three patients reported here were resuscitated by manual external chest compression with ease and very little pressure. The first two were of the acute asphyxic asthma type with sudden onset. The third case used to be called “asthma and chronic bronchitis” but now would be called by the perhaps less descriptively accurate “chronic obstructive pulmonary disease” (COPD). If the patient had died in the attack, the death would have been registered as COPD and cor-pulmonale but consequent to the unexpected sudden response of chest compression, “asthma” would appear to be the more accurate primary diagnosis.

Discussion

In addition to the three cases described here and that of Watts, Fisher et al7 described a case of acute sudden asphyxic asthma treated successfully by external chest compression after mechanical ventilation had failed and concluded that “the use of external chest compression will have its greatest impact when initiated in a pre hospital setting among patients with severe sudden onset of asphyxic asthma”. However, Van der Touw et al8 described the effects of compressing the rib cage in four intubated, mechanically ventilated adult patients recovering from acute severe asthma. They concluded that “manual compression of the rib cage during consecutive tidal expirations would be ineffective in reducing pulmonary hyperinflation during the emergency management of asthma”. However, the four patients in that study had survived transfer to hospital and may have had gradual decompensation. This is not the clinical picture of patients with acute asphyxic asthma described here or those described by Watts and by Fisher et al.

There was a rapid rise in deaths due to asthma during the 1960s. Speizer et al9 reported that the death rate from asthma increased annually in England and Wales from 1960 to 1965. Later, together with Strang, they investigated the use of drugs preceding deaths due to asthma and obtained death certificates in which asthma was described as the underlying cause in patients aged 5 to 34 years, registered in England and Wales from October 1966 to 31 March 1967. Surprisingly, 81% of deaths occurred suddenly, outside the hospital, and were frequently unexpected, so much so that 59% were referred to coroners (any other cause of death except asthma was rare at autopsy). Of the 133 patients, 37 died in less than 1 hour. At the time, the only explanation put forward was the introduction and, possibly, overuse of sympathomimetic aerosols and corticosteroids.10

That therapy was not the cause of an increasing death rate is supported by Molfino et al,2 who examined the mechanisms by which patients might die of acute asthma. These authors studied 10 patients who arrived at a hospital in respiratory arrest or developed it soon after admission and concluded that “the near-fatal nature of the exacerbations was the result of severe asphyxia rather than cardiac arrhythmia and that undertreament rather than overtreatment may contribute to an increase in mortality from asthma.” This contrasts with the generally accepted view that the epidemic of deaths due to asthma from 1960 to 1970 was caused by the adverse effects of treatment.9 10

What did change was that mouth-to-mouth resuscitation was introduced as the standard resuscitation technique for respiratory arrest and the previously trusted methods of chest compression were discarded. Up to that time, chest compression of the lower ribs, Schafer’s prone and Holger Neilson’s method were the only techniques used. (Cardiopulmonary resuscitation in which the sternum is depressed to compress the heart chambers is without effect on respiration.) They were easier to use correctly than mouth-to-mouth resuscitation and were widely used in the UK. It is certainly possible that this change in practice was responsible for the increased number of deaths.

There is evidence that there is a separate group of patients with asthma with extremely rapid onset of life-threatening asthma with no earlier signs of deterioration or increase in peak expiratory flow prior to the onset. This group of patients is more difficult to ventilate mechanically but recovers more rapidly and has a higher incidence of respiratory arrest.2 3 4 6

Epidemiological studies have investigated the problem of sudden death in asthma, but none have elucidated a mechanism separating them from asthma in general. The usual explanation is that extreme bronchospasm, rather than mucus plugging, bronchial oedema or vascular bronchial compression, plays the primary role in pathogenesis3 6. During suffocation, there is a powerful urge to expand the chest forcefully, as when a drowning person inhales water into the lungs. In the cases described, this urge to “breathe in” appeared to take over the respiratory response. This hypothesis of a chest wall effect producing sudden asphyxia would explain the following:

1. Why life-threatening asthma can occur without previous warning or a decrease in peak expiratory flow. These patients may account for most of the deaths occurring outside the hospital and are the ones needing first aid before medical help arrives.

2. Why some patients who experience severe asthma attacks recover so rapidly.2 3 A few of these patients may have recurrent attacks and recover before getting to the hospital. These patients stand the risk of being labelled as overbreathing or neurotic. Others have never had previous hospital attendance or even a severe asthma attack.

3. The sudden increase in asthma-associated deaths from 1960 to 1965 previously discussed,9 as patients who died of asthma would be the ones responding best to the frequently used method of artificial respiration prior to 1960

At present, any emergency in asthma is dealt with by the patient getting to the hospital as speedily as possible, and then, if there is no quick improvement, a decision has to made whether ventilation or intubation is necessary. It would take less than a minute of assisted expirations to discover whether chest compression would be effective. In the past, chest compression was performed in the prone position, but it can easily be done with the patient sitting up and by encircling the lower ribs with both arms and hands and exerting pressure inwards and downwards, as in case 3 described above.

Summary

Chest compression to treat respiratory arrest due to asthma is safe and sufficiently simple to be taught to relatives. The results of the chest compression described here were too immediate to leave doubt about its effectiveness. Case 1 clearly demonstrated that the chest wall had been “extended” abnormally. No more air could be blown in by mouth-to-mouth resuscitation, even after respiratory arrest and unconsciousness. This contrasts with the ease with which the overstretched chest wall could be compressed manually. One cannot pump air into overinflated bellows to get them to work, but this is being attempted with mouth-to-mouth resuscitation or even mechanical ventilation. The speedy recovery with chest compression suggests a “chest wall effect” rather than acute bronchial constriction as the cause of the asphyxia. It is likely that the immediate response to chest compression depends on how important a factor this is in any individual asthma attack. It may be a factor in any type of asthma or COPD (case 3), but one will not know unless chest compression is tried. If that patient had died, his death would have been certified (quite correctly) as COPD and cor-pulmonale, but the response to chest compression suggests that it would have been another overlooked asthma death.

Conclusion

Chest compression may be life-saving in acute asphyxic asthma.