1323
patient was conscious 1 minute later. The efficiency of massage " was demonstrated by the presence of palpable peripheral pulses, of a systolic blood-pressure of 80 mm. Hg, of a normal electroencephalogram and by the rapid return of consciousness. This demonstrates the efficacy of chest percussion in ventricular asystole due to complete "
heart-block.
Summary Saddle embolectomy after 22 hours’ ischxmia in a patient with cardiomyopathy, cirrhosis of liver, and complete heart-block is described. 100 mEq. of sodium bicarbonate solution (8-4%) given after the circulation was restored did not prevent cardiac arrest and more than 500 mEq. of acid may have been released from the ischaemia region. The evidence suggests that acidosis is the cause of cardiac arrest which sometimes follows restoration of the circulation to an ischxmic region. Very large quantities of bicarbonate may be necessary to prevent acidosis shock and acidosis arrest in similar cases. Requests for reprints should be addressed to Mr. J. S. S. Stewart, Nuffield Department of Surgery, The Radcliffe Infirmary, Oxford. REFERENCES
Baue, A. E., McClerkin, W. W. (1965) Ann. Surg. 161, 41. Burton, G. W., Holderness, M. C., John, H. T. (1964) Lancet, ii, 782. Don Michael, T. A., Stanford, R. L. (1963) ibid. i, 699. Engler, H. S., Ellison, L. T., Moretz, W. H., Simpson, J. G., Gleaton, H. E., Freeman, R. A. (1963) Archs Surg., Chicago, 86, 791. Fry, W. J., Keitzer, W. F., Kraft, R. O., Weese, M. S. (1963) Surgery, Gynec. Obstet. 116, 301. Gross, R. E. (1945) Surgery, St. Louis, 18, 673. Glenn, F., O’Sullivan, W. D. (1952) Ann. Surg. 136, 770. Hohf, R. P., Sutton, G. C. (1960) Surgery, Gynec. Obstet. 110, 693. John, H. T., Peacock, J. H. (1963) Bristol med.-chir. J. 78, 43. Johnstone, J. H., Lawson, N. J., Mucklow, R. G. (1965) Br. med. J. ii, 974. Kenyon, J. R., Cooper, K. E. (1956) Lancet, i, 543. Lishman, I. V. (1964) cited by Stewart (1965b). Mehl, R. L., Paul, H. A., Beattie, E. J. (1964) Lancet, i, 1419. Mavor, G. E., Davidson, L. D., Clark, C. G. (1959) Br. J. Surg. 47, 292. Milstein, B. B. (1963) Cardiac Arrest and Resuscitation; p. 52. London. Peretz, D. I., McGregor, M., Dossetor, J. B. (1964) Canad. med. Ass. J. 90, 673. Rader, L. E., Jr., Keith, H. B., Campbell, G. S. (1961) Surg. Forum, 12, 265. Schweizer, O., Howland, W. S. (1964) Anesth. analg. 43, 420. Stewart, J. S. S. (1964) Br. med. J. i, 476.
(1965a) J. R. Coll. Surg. Edin., 10, 85. (1965b) ibid. p. 228. Stewart, W. K., Morgan, H. G., McGowan, S. W. (1965) Br. Heart J. 27, 490. Tibbs, D. J. (1962) Proc. R. Soc. med. 55, 593. Watkins, E. (1947) Surgery, St. Louis, 22, 530. —
—
—
IMPROVEMENT IN BRONCHIAL ASTHMA NOT REFLECTED IN FORCED EXPIRATORY VOLUME ANN
J. WOOLCOCK
M.B. Adelaide RESEARCH FELLOW
JOHN READ M.D.
Sydney, F.R.A.C.P.
ASSOCIATE PROFESSOR IN MEDICINE
DEPARTMENT OF MEDICINE, UNIVERSITY OF SYDNEY
THE primary disability in patients with bronchial asthma is increased airways obstruction; and measurement of forced expiratory volume in one second (F.E.V.I) is widely used as an index of this airways obstruction. Serial measurements of F.E,V’1 are, at present, the commonest and most useful method in clinical practice of assessing objectively the response of individual patients with asthma to therapy, and of controlling the dosage of powerful agents such as corticosteroids. We have found, as have other workers, that some patients claim a notable subjective benefit to their breathing during the administration of steroids, which is not matched by commensurate improvements in F.E,V’1 nor indeed, in
instances, by any significant improvement in F.E.V’l all. During a detailed long-term study of lung-volumes and lung mechanics in 30 patients with asthma during remissions and relapses of symptoms (Woolcock and Read 1966), we obtained data in 7 patients which provide a functional basis for the clinical improvement seen in a number of these patients. some
at
Methods The 7 patients were aged 23-59 years, and had been under regular observation and study in our department for periods of up to 3 years. In some, airways obstruction was completely reversible; in others, there was a background of chronic irreversible obstructive lung-disease (see accompanying table). All patients were admitted to hospital with a severe exacerbation of dyspnoea. After the start of therapy, daily measurements of lung-volumes and F.E.v.i were made, from the first day on which the patient was sufficiently well to be brought to the laboratory. This varied from the 2nd to the 5th day after admission. F.E.V’l and vital capacity (v.c.) and its subdivisions of inspiratory capacity and expiratory reserve volume, were measured using a standard low-resistance 9-litre spirometer. Functional residual capacity (F.R.C.) was measured by a closedcircuit helium-dilution technique (Read 1958). All volumes were expressed at room temperature and pressure, saturated with water vapour. Results
Results of lung-volume and F.E.V’l measurements at the time of first study and before discharge from hospital are shown in the accompanying table. The 7 patients were selected on the basis of a constant pattern of lung-volume change. Total lung-capacity (T.L.C.), F.R.C., and residual volume (R.v.) were all much increased at the time of admission to hospital, and all diminished during clinical recovery; in each case F.R.c. during the episode of asthma was greater than T.L.c. after recovery. In other words, tidal breathing during the episode of asthma was taking place at a level higher than the point of maximal inspiration after recovery. This situation is represented diagrammatically for 2 patients in figs. 1 and 2. In 4 patients (nos. 1,2,4, and 5), R.v. during the episode of asthma approached or exceeded the T.L.c. measured after clinical recovery-i.e., the lung-volume reached by maximal expiration during the asthma was of the same order as the lung-volume reached by maximal inspiration after recovery (fig. 2). All patients experienced notable subjective clinical improvement as a result of treatment (which included bronchodilator therapy orally and by inhalation, and corticosteroids and antibiotics where they were thought to be indicated by the attending physician). F.E.V., increased notably in 3 patients (nos. 5, 6, and 7) and slightly in 2 others (nos. 2 and 4). The increase in F.E.V’l in the other 2 patients (nos. 1 and 3) was negligible. The " best " F.E.V’l recorded for each patient (see table) shows that in 4 patients (nos. 4-7) the airways obstruction was completely reversible; the remaining 3 patients (nos. 1-3) showed varying functional degrees of irreversible obstructive lung-disease. But clinical improvement, from a state of acute respiratory distress (requiring hospital admission) to one of normality or mild to moderate dyspnoea of effort, was notable in each case in the group, even in those patients where the changes in F.E.V’l were very small. Discussion
Apart from Engstrom’s (1964) studies in children, there is a dearth of serial studies of lung-volumes in patients with asthma, followed from the stage of severe dyspnoea
1324 LUNG-VOLUMES
*
AND F.E,V.,
DURING ASTHMA AND AFTER CLINICAL RECOVERY
Values of a.E.v.l equalling
clinical recovery. The accompanying table and figs. 1 and 2 illustrate that in 7 adult patients the lungs became hyperinflated to such a degree during episodes of asthma that their resting-volume (F.R.C.) was greater than the patient could reach by voluntary effort after recovery. Hyperinflation of the chest is well recognised in patients with asthma clinically and on X-ray; our data indicate that the acute or subacute changes in individual lungvolumes may reach 4 or 5 litres. Fig. 3 illustrates the mechanisms which we believe determine the increases in F.R.c. and R.v. in patients with asthma. Fig. 3A shows diagrammatically a cross-section of normal lung and airway. In fig. 3B, partial obstruction of the airway has been produced (in this illustration by intraluminal mucus). The effects of this obstruction are greater in expiration when the bronchi normally narrow, than in inspiration. This will lead to failure to expel the normal tidal volume in the time available for expiration; while the lesser inspiratory resistance allows a normal tidal volume to be inspired in the time available for inspiration. The level of F.R.c. will rise accordingly. A new point of equilibrium will finally be reached (E). This increased lung-volume will provide a greater elastic recoil of lungs and chest wall to aid expiration and an increased elastic traction on the airways, increasing their intrinsic calibre. The relative effect of a given quantity of intraluminal mucus or mucosal swelling on airway resistance to
will thus be diminished (E).
or
exceeding predicted values.
In the
patient with asthma (D) airway occlusion becomes complete during expiration at a higher lungvolume than in a healthy person (C), because of the intraluminal material. Residual volume is thus increased. The notable elevations of T.L.C. shown by the patients support the view of Mead et al. (1963) that inhibitory reflexes normally limit the degree of voluntary lunginflation. To this we would add that these reflexes must be modified in asthma, perhaps by the increased equilibrium volume (F.R.C.) of the chest and lungs. Increase of F.R.C. then is advantageous or " com" pensatory to the extent that the increased elastic forces associated with the increased lung-volume increase bronchial calibre. This point is illustrated in figs. 1 and 2. In fig. 1, for example, tidal breathing during the episode of asthma took place on an F.R.c. of 9-2 litres. Had the F.R.c. not increased from its usual level of 4-1litres in that patient, there could have been no tidal exchange at all; since this level of 4-1litres was at that time deep in residual volume. The mechanically determined increase of F.R.c. at least " stretched " the bronchi to the point where tidal breathing was possible. A similar situation can be seen in fig. 2 where, had F.R.c. not increased, breathing would have ceased because no air-flow was possible at the usual F.R.C. of 5-5 litres. Indeed, similar considerations apply to each patient represented in the accompanying table; the induced increase in F.R.c. was " compensatory " (indeed lifepreserving) in that no air-flow was possible at the usual F.R.C. in any of them.
Fig. I-Diagrammatic representation of lung-volumes and F.E,V’l in patient 1 during episode of asthma and following clinical recovery.
The resting-level at the end of each tidal breath represents F.R.C.; the points of maximal inspiration and expiration represent T.L.c. and R.v. respectively. The final segment of each tracing represents the F.E.V.}
Fig. 2-Diagrammatic representation of lung-volumes and F.E.V., in patient 7 during episode of asthma and following clinical recovery. Conventions as in fig. 1.
Fig. 3-Inter-relation of lung-volumes, airway calibre, and airway resistance in patients with asthma. See text for explanation.
1325 The compensatory aspects of the increases of lungvolume are, however, not obtained without cost to the patient. As lung-volume increases, even in a healthy person, lung compliance falls. In other words, as the lungs become more and more stretched, it becomes progressively harder to stretch them further during the process of inspiration. At resting-lung-volumes well above normal maximal inspiratory position, such as patients in the present group demonstrate, the elastic work of inspiration is enormous. This greatly increased elastic work must make a major contribution to the patient’s sensation of dyspnoea, and may explain the fact that many patients with severe asthma, if they are prepared to offer any opinion at all, complain that they find it subjectively harder to breathe in than out. Reasoning along these lines for recovery from an episode of asthma indicates why the change in F.E,V’1 may be negligible or small compared with the clinical improvement. With the situation as shown in fig. 3E, if therapy simply reduced the amount of obstruction within the airway and finally removed it completely, there would be a notable increase in airway calibre and a fall in airway resistance. But, as the airway resistance begins to diminish, lung-volume begins to return towards the usual levels. This falling lung-volume will, because of lessening elastic forces, be associated with a diminishing bronchial calibre. The combined effects of diminishing obstruction within the airway and diminishing bronchial calibre will be such that unobstructed bronchial cross-sectional area will increase less rapidly than would be expected from clearing of obstruction alone. Thus in patient 1, a fall of T.L.c. and F.R.c. during recovery was associated with no real change in airways obstruction (as judged by the F.E,V’I) at all (fig. 1). The diminution of acute airways obstruction due to asthma was roughly matched by the increase produced by the lesser elastic distension of airways as lung volumes fell. The undoubted clinical improvement resulted from a major reduction of elastic work associated with the fall of lung-volume. Similar comments apply to patient 3. In patients 2 and 4, the increase of F.E.V’1 during recovery was less than 1 litre, a relatively small improvement compared with the notable clinical improvement they experienced. In each case, a major contribution to improvement is reflected by the decreased elastic work of inspiration associated with the reported falls of F.R.C. Patients 5, 6, and 7 reflect the order of F.E.V’1 change (1-2 litres) that is commonly recognised in improvement from severe asthma. In these 3 patients, changes in flowresistive work alone could be held to account for major clinical improvement. But in these patients also falls of F.R.c. ranging from 2-8 to 3-8 litres must have been associated with notable decreases of elastic work as well. Fig. 2 illustrates how, for example, in patient 7, even the notable increase in F.E.V’1 does not show the real extent of the improvement. Starting from a lung-volume of 8-1 litres (the post-recovery level of T.L.C.) it is doubtful whether the patient could have forcibly expired 0-2 litre in one second during the episode of asthma. The real improvement of F.E.V’1 should perhaps be regarded as being from about 0-2 to 2-4 litres. It is obvious that, in many patients, objective assessment of improvement following the institution of therapy (including steroid therapy) requires the measurement of lung-volumes as well as the more readily performed F.E.V’l measurements.
The data and interpretations of this paper should not be held to suggest that increased airways obstruction is not the primary disturbance in asthma. But we would emphasise that the major secondary changes in lungvolumes here demonstrated have three important roles. allow respiration to continue by their secondary on bronchial calibre. They contribute to dyspnoea by producing a gross increase in the elastic work of inspiration. They obscure (sometimes completely) the extent of the F.E.v.i changes during recovery.
(1) They
effects
(2)
(3)
Summary
Lung-volume changes are reported in 7 patients during recovery from episodes of severe asthma. In these 7 patients, functional residual capacity (F.R.C.) during the episode was greater than total lung capacity (T.L.C.) after recovery. In 4 patients, residual volume during the episode approached or exceeded T.L.c. after recovery. The mechanically induced increases of F.R.C. were " advantageous to these patients, in that air flow was no longer possible at the usual levels of F.R.c. in any of "
them. Increased elastic forces associated with the greater lung-volumes increased bronchial calibre to the point where tidal breathing was possible. The increased lungvolumes must, however, be associated with gross increases in the elastic work of inspiration and contribute to the sensation of dyspnoea. This factor probably also accounts for the common complaint by patients with asthma that inspiration is more difficult than expiration. The diminution of lung-volumes during recovery obscures the real extent of the improvement in forced expiratory volume in one second (F.E.v.i). In some patients, notable objective improvement in functional status is associated with no significant change in F.E.V., at all. This work was supported by a research fellowship and a grant-inaid from the Asthma Foundation of New South Wales. Requests for reprints should be addressed to Dr. John Read, Department of Medicine, University of Sydney, Sydney, Australia. REFERENCES
Engstrom, I. (1964) Acta pœdiat. Stockh. suppl. 155. Mead, J., Milic-Emili, J., Turner, J. M. (1963) J. appl. Physiol. 18, 295. Read, J. (1958) Australas. Ann. Med. 7, 179. Woolcock, A. J., Read, J. (1966) Am. J. Med. (in the press).
PSEUDOMONAS AERUGINOSA CROSS-INFECTION Due to Contaminated
Respiratory Apparatus
IAN PHILLIPS M.A., M.B. Cantab. LECTURER IN MEDICAL MICROBIOLOGY, THOMAS’S HOSPITAL MEDICAL SCHOOL
ST.
GEOFFREY SPENCER Lond., F.F.A. R.C.S.
M.B. ST.
CONSULTANT ANÆSTHETIST, THOMAS’S HOSPITAL, LONDON, S.E.I
CROSS-INFECTION in hospital wards continues to be a serious problem and often hinders otherwise successful advances in treatment. In many forms of therapy the risk of infection is increased, either as a direct result of the treatment itself, or because the patients whose lives are saved by such treatment are already seriously ill and therefore more susceptible to infection. Cross-infection by gram-negative organisms, especially Pseudomonas aeruginosa (pyocyanea), has already received much attention (Williams et al. 1960, Barber 1961, Lancet 1961,