running, hesitates for balance when ascending stairs, cannot rise directly from the seated position, but shifts his weight laterally in order to do so, presents with flat feet secondary to tight heel cords, or cannot perform a standing jump. Any of these subtle findings of "soft" weakness requires a serum muscle enzyme determination to confirm or rule out the diagnosis. Strauss Surgical Group, 4640 Marine Drive, Chicago, Illinois 60640, U.S.A.
IRWIN M. SIEGEL
Thus, in view of previous experimental findings, we suggest that alterations in the ST interval of the E.c.G. recorded post partum reveal information about accumulated hypoxic stress to which the newborn child was subjected. Department of Obstetrics and Gynæcology, Sahlgrenska Sjukhuset, and Department of Pœdiatrics, Ostra Sjukhuset, Göteborg, Sweden.
ULTRASOUND MONITORING OF FETAL MOVEMENTS
E.C.G. CHANGES AS SIGN OF HYPOXIA INTRA PARTUM an
SiR,—The fetal electrocardiogram (E.C.G.) is used mainly as indicator of fetal heart-rate in clinical practice. Although
alterations in the pattern of the fetal
have been detected
during labour, these alterations are believed to be preceded by changes of the heart-rate. Our experiments in fetal lambs have shown progressive changes in the ST interval of the fetal E.C.G. (elevation of sT-segment, high and peaked T waves) as an early and constant sign of fetal asphyxia before deterioration of circulatory indices and well in advance of any bradycardia.’1 These changes are signs of myocardial glycolysis.2 We have now investigated in a consecutive series, E.c.. changes in immediately post partum in man. A CR-Iead with the precordial electrode placed between the nipple and the sternum was recorded within the first minute after birth. In twenty-four single births sixteen babies had normal Apgar scores (8-10) at 1 min and normal E.C.G., while in the other eight transient hypoxic altera-
KLAS-HENRY HÖKEGÅRD KARL GUSTAF ROSÉN
al.’ are to be congratulated for their fetal movements. However, their statement that "monitoring of fetal movements as an indicator of normal and abnormal fetal development appears to have been neglected" needs some correction. Also we feel that some of the questions they raised have already been answered. We are surprised that a group studying fetal movements so enthusiastically do not seem to realise that real-time scanning (practised throughout continental Europe) is the method of choice for investigation of fetal movements and are not familiar with work published on this subject.
tions in the E.c.G. were recorded in six. The E.c.G. returned to normal within a few minutes. Three of these babies had an Apgar score of 6 or 7 at 1 min while the other three had normal Apgar scores. In two cases there was an Apgar score of 6 or 7 associated with a normal E.C.G. All newborn children had normal heart-rate. They had a normal neonatal period except for one child who had a mild hypoglycaemia. This baby had had an Apgar score of 7 at 1 min as well as E.c.G. changes (see
figure). 1. 2.
Rosén, K. G., Kjellmer, I. Acta physiol. scand. 1975, 93, Rosén, K. G., Isaksson, O. Biol. Neonate (in the press).
Frequency of fetal movements detected by ultrasound. Shaded area: mean + s.D. for control population. 8
0-0, -8, ae
serial studies et
in fetal death.
Real-time sonar studies of fetal movements were reported in 1971 by Reinold.2 On the basis of 250 examinations done at 18-20 weeks’ gestation Reinold described different types of active movements (strong and slow) and their absence with fetal death. Reinold’s work has also been published in English.3 Since then in most departments ultrasound evaluation of fetal movements with regard to presence or absence, type, and frequency has become the most important single procedure in the management of threatened abortion. Whereas it is easy to detect the presence or absence of fetal movements, evaluation of their type is more difficult. As in other areas of perinatal biophysical monitoring the main problem is quantification. For frequency of movements, our group45has established the normal range in early pregnancy and has demonstrated the prognostic value of abnormal frequencies with impending early fetal death (see figure). QuanK. M., Harris, P. F., Slater, J. H., Porter, G A. Lancet, 1976, i, 719. 2. Reinold, E. Z. Geburtsh. Gynäk. 1971, 174, 220. 1.
Higginbottom, J., Bagnall,
Reinold, E. J. perinat. Med 1973, 1, 65. Haller, U., Rüttgers, H., Wille, F., Heinrich, D., Müller, P , Kubli, F. Gynäk. Rdsch 1973, 13, Suppl. 1, p. 118. Haller, U. Rüttgers, H., Wille, F., Müller, P, Heinrich, D, Kubli, F in Perinatale Medizin, (edited by J. W. Dudenhausen and E. Saling, vol. v, p 30. Stuttgart, 1974.
E.C.G. changes 1, 3, 5, and 7 min post partum in full-term boy with the umbilical cord around the neck and Apgar score 7 at 1 min.
92 tification of
has been done by measuring moveand areas, and correlations have been found with pregnancy outcome.6 We hope that this information will help our colleagues in Manchester in their future research. F. KUBLI Universitats-Frauenklmik, U. HALLER Heidelberg, H. HENNER West Germany ment
PATHOGENESIS OF ESSENTIAL HYPERTENSION
SiR,—A hypothesis in the true sense of the word contains the elements of Zadkine’s Rotterdam statue (see figure): the contours are marked and the core is replaced by clear thought, which can be substantiated by means of empirics. If this definition is correct, one of the latest products’ from the Glasgow M.R.C. workers is not a hypothesis. Instead of a clear outline of hard evidence surrounding a new perspective we observe a familiar pattern of worn-out thoughts punctuated by neologisms. We refer to the terms "integrated pressure", "renal transformation time", and "stepwise interaction". Any investigator who tries to measure bloodpressure in a round-the-clock fashion realises that it is virtually impossible to integrate blood-pressure from the records. It is therefore equally impossible to prove or disprove that it is integrated blood-pressure, rather than basal blood-pressures or maximal pressure, which determines the outcome. The existence of an adrenergic drive in the young hypertensive is easy to think of, but very difficult to prove. According to our experience, plasma-noradrenaline concentrations do not rise in the earliest stages of hypertension (unpublished). We were surprised to find that the time-honoured hypothesis of "baroreceptor resetting"-which may be, and has been, put to the test in the laboratory-has been left out of the picture. "Renal transformation time", which as a vascular phenomenon could partly reflect baroreceptor resetting, is far from being a time-related variable. In fact cortical blood-flow is already appreciably decreased in young "labile" hypertensives.9 We would ask the Glasgow workers to be more specific about their concept of the "renal abnormality". Does it merely consist of a vascular alteration, or is there any evidence of intrinsic abnormality in the nephron? If the hydrostatic and oncotic forces surrounding the nephron are balanced at a higher level, does such a process occur throughout the kidney, or is it limited to the outer cortical area paralleling the hoemodynamic changes? The time is past for any theory to lump together the outer cortical and juxtamedullary nephrons, since a discrimination can be made on the basis of structural and functional properties (e.g., sodium handling). The "renal abnormality" is apparently not reflected in plasma-renin concentrations since these were stated to be normal. We have even evidence that they tend to be reduced.’° This suggests a negative rather than a positive feedback mechanism, the kidney playing the role of counteracting the high blood-pressure. Perhaps, then, "the slower, but reversible effect on urinary sodium excretion" is the real mechanism. However, in the same paper Brown et al. note that exchangeable sodium, plasma volume, and extracellular volume are "unremarkable". It should be added that many investigators have observed reduced plasma volumes, and if the data from different laboratories are pooled, the difference is statistically significant"6. Henner,
H., Haller, U., Wolf-Zimper, O., Lorenz, W. J., Bader, R., Müller, B., Kubh, F. Excerpta med. int Congr. Ser. no. 363. Proc. 2nd Eur. Congr. Ultrason. Med. held in Munich, in May, 1975. 7. Brown, J. J., Lever, A. F., Robertson, J. I. S., Schalekamp, M. A. Lancet, 1976, i, 1217. 8. Alam, G. M., Smirk, F H. Br. Heart J 1943, 5, 152. 9. Kolsters, G. Thesis, Rotterdam, 1976. 10. Schalekamp, M. A. D. H., Birkenhäger, W. H., Kolsters, G, Lever, A. F. in Hypertension. Current Problems (edited by A. Distler and H. P. Wolff, p. 133. Stuttgart, 1974 11. Birkenhäger, W. H., Schalekamp, M. A. D. H. Control Mechanisms in Essential Hypertension. Amsterdam (in the press .
0. Zadkine’s Rotterdam statue,
the elements of
again, therefore, a negative rather than a positive feedback mechanism. Perhaps Brown et al. consider a breakdown of a vasodepressor mechanism. But how would they then visualise "stepwise interaction"? It is to be hoped that they will one day put forward a hypothesis which fully accounts for known facts and which can be tested in the clinical setting.
Department of Internal Medicine, Zuiderziekenhuis, Rotterdam, Netherlands
W. H. BIRKENHÄGER T. L. KHO P. W. DE LEEUW R. VANDONGEN A. WESTER G. A. ZAAL
are surprised by the rather peevish response of friend, Professor Birkenhager, and his colleagues, to our paper (June 5, p. 1217). Even more surprising is their invocation of Zadkine’s statue as a model for scientific hypothesis. The people of Rotterdam more usually regard it as a symbol of indiscriminate aggression.
The criticisms of the Rotterdam workers seem to us to have little substance. We also dislike neologisms, but, with the exception of "renal transformation time", a term we defined, the phrases they object to are already in use. Dealing with more specific points they raise: first, despite their assertions, "integrated pressure" could be derived from continuous measurement of blood-pressure in man.12 Birkenhager has made similar measurements himself. Renal transformation time is also measureable; after 8 weeks, in 50% of rats the kidney is "transformed" and able to maintain
hypertension.4 We are surprised by Professor Birkenhager’s reluctance to accept a role for the kidney in essential hypertension, since this is an idea he has previously proposed5 and defended6 with us.
1. Littler, W A, Honour, A. J, Sleight, P., Stott, F D Br. med J. 1972, iii, 76. 2 Littler, W A , West, M J., Honour, A J, Sleight, P. Proc. 7th Eur Congr. Cardiol 1976, p. 670 abstr. 3. Birkenhager, W H, Houwing, L. A., Van Es, A., Lamers, H. J., Mulder, A H. Clin Sci 1968, 35, 445 4. Floyer, M. A ibid. 1951, 10, 405 5. Kolsters, G., Schalekamp. M A., Birkenhager, W. H, Lever, A. F. in Pathophysiology and Management of Arterial Hypertension (edited by G. Berglund, L. Hansson, and L. Werkö ; p 54, Goteborg, 1975. 6. Birkenhager, W. H, Brown, J J., Lever, A. F, Robertson, J. I. S., Schalekamp, M A. Lancet, 1975, i, 1423