Volume 69 Number 4 Annotations 569

development of heart black or an independent lower rhythm. In the second instance, do not under- estimate the contribution of bed rest and do not deliberately mask your own observations with unnecessary diuretic agents.

4. You are now armed. Do not acquire extra baggage from the doctrinaires. If you remain both vigilant and skeptical, you can continue to learn from observation from each human being on whom you are called to assay digitalis.

Leo G. Horan, M.D. Nancy C. Flowers, M.D. Department of Medicine

University of Tennessee College of Medicine 858 Madison Avenue

Memphis 3, Term.

REFERENCES

1. Conference on Therapy: The dose of a drug, Am. J. Med. 2:296, 1947.

2. Withering, W.: An account of the foxglove, Birmingham, 1785, C. G. J. and J. Robinson.

3. Gold, H., Cattell, M., Modell, W., Kwit, N. T., Kramer, M. L., and Zahm, W.: Clinical studies on digitoxin, with further observations on its use in the single average full dose method of digitalization, J. Pharmacol. & Exper. Therap. 82:187, 1944.

4. Friedberg, C.: Diseases of the heart, ed. 2, Philadelphia, 1956, W. B. Saunders Company, Chapter 11, p. 263.

5. Rodman, T., and Pastor, B. H.: The hemo- dynamic effects of digitalis in the normal and diseased heart, AM. HEART J. 65:564, 1963.

6. Lown, B., and Levine, S.: Current concepts in digitalis therapy, Boston, 1954, Little, Brown & Company.

7. Batterman, R. C., DeGraff, A. C., Gutner, L. B., Rose, 0. A., and Lhowe, J.: Studies with gitalin (amorphous) for the treatment of patients with congestive heart failure, AM. HEART J. 42:292, 1951.

8. Batterman, R. C., DeGraff, A. C., Gutner, L. B., and Rose, 0. A.: The therapeutic range of gitalin (amorphous) compared with other digitalis preparations, Circulation 5:201, 1952.

9. Gold, H., and Cattell, M.: Status of bioassay of the digitalis group, Science 93:197, 1941.

10. Gold, H.,: Digitalis and some of its derivatives, Science97:125 (A) and 150 (B), 1943.

11. Cattell, M., and Gold, H.: Studies on purified

digitalis glucosides. The relationship between therapeutic and toxic potency, J. Pharmacol. & Exper. Therap. 71:114, 1941.

12. Hejtmancik, M. R., and Herrmann, G. R.: A clinical study of gitalin, A.M.A. Arch. Int. Med. 90:224, 1952.

13. Weiss, A., and Steigmann, F.: Gitalin in the treatment of congestive heart failure: A clinical study, Am. J. M. SC. 227:188, 1954.

14. Gruhzit, C. C., and Farah, A. E.: Determina- tion of the therapeutic range of gitalin in the heart-lung preparation of the dog, J. Pharma- col. & Exper. Therap. 108:112, 1953.

15. Church, G., Schamoth, L., Schwartz, N. L., and Marriott, H. J. L.: Deliberate digitalis in- toxication, a comparison of the toxic and therapeutic effects of four glycoside prepa- rations, Ann. Int. Med. 57:946, 1962.

16. Lown, B., and Levine, S.: Current concepts in digitalis therapy, New England J. Med. 250:771, 819, 866, 1954.

17. Von Capeller, D., and Stern, T. N.: Acetyl strophanthidin used as a measure to evaluate the status of digitalization, AM. HEART J. 55:8, 1958.

18. Bower, J. O., and Mengle, H. A. K.: Additive effects of calcium and digitalis, warning, with report of two deaths, J.A.M.A. 106:1151, 1936.

19. Kohn, R. M., and Kiley, J. E.: Electrocardio- graphic changes during hemodialysis, with observations on contribution of electrolyte disturbances to digitalis toxicity, Ann. Int. Med. 39:38, 1953.

20. Lown, B., and Levine, H. D.: Atria1 arrhyth- mias, digitalis and potassium, Clinton, Mass., 1958, Landsberger Medical Books, Inc.

21. Winsor, T.: Potassium and digitalis intoxica- tion, AM. HEART J. 60:151, 1960.

22. Kay, C. F.: The clinical use of digitalis prepa- rations, Part I-IV, Circulation 12:116, 1955. Part V-IX, Circulation 12:291, 1955.

23. MacKenzie, Sir James: Diseases of the heart, Chapter XXX, Auricular Fibrillation, ed. 32, p. 211, London, 1914. Printed in Classics of Cardiology, edited by F. A. Willius and T. E. Keys, New York, 1941, Dover, p, 769.

24. Kayden, H. J.: The current status of procaine amide in the management of cardiac arrhyth- mias, Prog. Cardiovas. Dis. 3:331, 1961.

25. Sokolow, M., and Perloff, D. B.: The phar- macology and use of quinidine in heart disease, Prog. Cardiovas. Dis. 3:316, 1961.

Population study of arterial pressure

Several attempts have been made to add to knowl- edge of essential hypertension by the study of blood pressure in the general population. It has been shown that arterial pressure is continuously distributed, and that in unselected individuals for whom clinical

or other evidence of associated abnormality is lack- ing, only an arbitrary division can be made between normotensive and hypertensive.‘a2 From this evi- dence it was concluded that essential hypertension is not a disease entity, that the genetic influence on

570 Annotations

pressure is multifactorial, and that environmental in- fluences on pressure must be import;mt.3 Objections were taken to this interpretation on the grounds that it was not in accord with clinical experience, and that bimodality could be demonstrated in dis- tribution of pressures of selected groups-for es- ample, sibs of hypertensive propositi.4,” It was sug- gested, therefore, that essential hypertension is a disease entity, perhaps attributable to a single dominant gene.

A possible reconciliation between these view- points was proposed in the light of evidence con- cerning the distribution of arterial pressure in a large industrial population.6 Here too it was shown that pressure is continuously distributed in unselected males, and reported irregularities of distribution interpreted as bimodality were considered to be due to small numbers. It was suggested that differences of opinion about the nature of essential hypertension arise chiefly from the fact that, defined as “elevation of blood pressure without apparent cause” it must include two different groups of cases: those in which no pathologic condition is present and which can probably be regarded as the upper end of the dis- tribution in the general population; and those in which associated pathologic conditions are present but unrecognized. The proportion of the latter in a series from which recognized “secondary” cases have been removed is probably much greater at very high than at moderately high levels of pressure. It was proposed that patients with raised arterial pressure could usefully be divided into two groups: patho- logic types, in which associated anomalies are present (whether recognized or unrecognized) ; and physiologic types, in which no pathologic condition is present and which can properly be regarded as being at the upper end of the distribution of pressure in the general population.

This distinction throws no light on the significance of high blood pressure (both in respect of subsequent trend of pressure and clinical prognosis) in the absence of associated anomalies (i.e., in the physio- logic types.) Clearly it will be desirable to follow the trend of pressure by continuous observation of the same individuals over a considerable period of time, but some of the difficulties of doing so have been underlined by a recent report based on two British populations.7 Arterial pressures of 833 Birmingham men were measured by eleven general practitioners on two occasions separated by an interval of 3 years. No special precautions were taken, and mean dif- ferences between readings were: systolic, 17.4 mm. ; diastolic, 10.0 mm. Hg. Coefficients of correlation between first and second readings were: systolic, 0.63; diastolic, 0.50. Similar observations were made on 500 men in two surveys in the Rhondda Fach and Vale of Glamorgan after intervals of 4 and 4% years, respectively. All pressures were measured by one observer who took certain precautions, but their effect on consistency of readings was not great. Mean changes in systolic and diastolic pressures were 14.6 and 8.1 mm. Hg, and coefficients of correlation were 0.72 and 0.63, respectively. Not surprisingly, first readings which were low tended to be higher at the second reading, whereas those which were high tended to fall, but the amount of scatter about the mean did not change appreciably.

~l‘hosc discrepancies bctwcen consecutive meas- urcments of blood preysure on the same individuals show the unreliability of the diagnosis of hyper- tension which rests on a single record of casual pres- sure. For example, in Birmingham the proportions of men with systolic pressures over 180 mm. Hg was approximately the same at both surveys. But of 216 men with systolic pressures above this level at the first examination, 85 had pressure below it at the second. Of 617 men with pressures under 180 mm. Hg when first examined, 77 had pressure above that level at the later examination. Similar changes were observed in both Birmingham and South Wales data using other criteria of hypertension.

An anomalous feature of the Birmingham findings was that, although data from each survey showed the expected increase in systolic pressure with ad- vancing age, mean pressure was no higher at the second examination than at the first, although the men were 3 years older. This result could not be attributed to differential mortality, since those who died during the interval were excluded. The South Wales data were more consistent with expectation, the mean of the second measurements of systolic pressure being higher than that of the first, but closer examination showed that this was true only for the Rhondda Fach series. In the Vale of Glamor- gan (as in Birmingham!, mean pressure did not rise. L1 possible explanation for these anomalies was sug- gested by the inverse relationship between tem- perature and arterial pressure. Retrospective euam- ination of Birmingham meteorological records indi- cated that air temperatures were, in general, much higher when the second observations were made than at the first surve)’ (although both readings were made during the summer months). Even greater differences in temperature presumably operated in the Glamorgan surveys, since the ilrst was in the winter and the second in summer. Both Rhondda surveys, on the other hand, were carried out during the winter.

The results of these surveys illustrate some of the difficulties which will confront those who try to pro- vide the much needed evidence on the trend of ar- terial pressure with increasing age in individuals in the general population. In longitudinal study of sub- stantial numbers of subjects (which is needed) it is difficult to do more than record casual pressures. Yet they provide a very unreliable guide to basal pressure, and cannot be much improved by reline- ments of technique which are feasible for use with a considerable random pop~~lation. Perhaps the most practical, although still difficult, procedure would be to take frequent measurements of casual pressure from which mean values for each individual can be estimated

Thomas McKeown, M.D. Medical School

University of Birmingham Birmingham 15, England

REFERENCES

1. Hamilton, M., Pickering, G. W., Roberts, J. A. F., and Sowry, G. S. C.: The aetiology of essential hypertension: (1) The arterial pressure in the general population, Clin. SC. 13:11, 1954.

2. Miall, W. E., and Oldham, P. D.: Factors in-

Volume 67 Number 4

Annotations 571

fluencing arterial blood pressure in the general population, Clin. SC. 17:409, 1958.

3. Pickering, G. W.: The nature of essential hyper- tension, London, 1961, J. and A. Churchill.

4. Platt, R.: The nature of essential hypertension, Lancet fi55, 1959.

5. Morrison, S. L., and Morris, J. N.: Epidemio- logical observations on high blood pressure without evident cause, Lancet 2:864, 1959.

The medical witness

A medical witness may belong to one of three main categories. Firstly, he may give testimony about his own treatment of the litigant, which makes him rather like other factual witnesses, or, secondly, he may be asked to examine the patient solely with a view to qualifying himself to give evidence, either for the litigant or the opposing party. The third type of medical witness is one who does not, or who is unable to, examine the patient personally, but who is prepared to express his opinions on assumed facts and other scientific data.

The first type of witness appears in court often as a result of subpoena and does so with trepidation and reluctance, since he feels quite out of his depth. Perhaps in attempting to guide the answers he gives toward his patient’s interests, he may find that he is given a drubbing by opposing counsel and made to appear rather foolish. With experience, the occa- sional witness, in addition to answering truthfully and promptly, gives the appearance of impartiality which only comes by refusing to be a partisan in the case.

The second type of witness often comes from among the younger specialists who may eagerly seek this class of work because of its good remunera- tion, with few or no bad debts. It is challenging work and keeps a medical witness on his toes by making him delve into the literature in order to be authori- tative in court. The only pitfall here is when a wit- ness goes beyond his speciality. This can lead to a most unhappy scene in court when one’s deficiencies show through under the stress of a punishing viva vote examination by a determined counsel.

The third type of witness is, I believe, becoming rather rare in America, where many specialist physicians and surgeons try to avoid court appear- ances because of painful experiences, and because of divergence of the medical and legal viewpoint on what constitutes the truth. “Even after considerable experience, the physician gains the impression that neither the counsel for the plaintiff, nor the counsel for the defendant has any idea of seeking the truth, and nothing but the truth; but he is only making every effort to win his case.*‘2

This situation has led to the experiment in New York City of having a medical panel from which are chosen impartial medical witnesses. The scheme appears to be operating successfully and spreading.

6. Lowe, C. R., and McKeown, T.: Arterial pres- sure in an industrial population and its bearing on the problem of essential hypertension, Lancet 1:1086, 1962.

7. McKeown, T., Record, R. G., and Whitfield, A. G. W.: Variation in casual measurements of arterial pressure in two populations (Birming- ham and South Wales) re-examined after inter- vals of 3-4&s years, Clin. SC. 24:437, 1963.

Some of the witnesses in this third group are often semiretired specialists, a few of whom polarize them- selves as plaintiff’s or defendant’s men, and their value as witnesses is soon summed up by the judges. Others, because of personal research or because of their writings in a special field, attract work and then run the risk of becoming rubber stamps en- dorsing the viewpoints of insurance company medical officers. Only scientific integrity will protect them from the temptation to endorse all the work that comes from such big insurance clients.

Occasionally, too, much publicity is given to medical witnesses in court, but more often than not, insufficient notice is taken of bizarre opinions ex- pressed by specialist witnesses. Sometimes this is pure venality, sometimes expediency. On very rare occasions we see an innovator at work, weaving attractive theories out of the air and giving scientilic- sounding names to various stages in the process. To prove a particular case and to trace its mecha- nisms from cause to effect, he then proceeds to walk on these fragile steps of verbal imagery as if they were the concrete of reality. Their apparent plausi- bility may convince juries but less often judges, and they operate best where there is a division of opinion among the orthodox. These people do the medical profession a great deal of harm by spuriously in- vesting it with an image of complete confusion over, often fundamental, issues.

The Chief Justice of Australia, Sir Owen Dixon, before his elevation, once sagely remarked, apropos the ease or difficulty with which a medical witness carried out his task of explaining the medical aspect of a case to the court, “That it is not when medical or scientific conceptions are intricate, but when they are vague, that the process is troublesome.” Un- fortunately, in medicine, many conditions have no well-defined etiology, and this allows unlimited scope for legal argument, especially if the services of an “innovator” can be procured.

In the state of New South Wales, in injury cases, or where illness has followed trauma, “the critical matter for investigation in so many cases is whether or not there is any causal connection between a proved trauma and admitted incapacity, or whether trauma has acceIerated, aggravated, or precipitated some pre-existing disability.“1 “Causal” in the legal sense implies attribution of responsibility,