NEW TRANSDUCER FOR DETECTING FETAL HEART SOUNDS: USE OF COMPLIANCE MATCHING FOR MAXIMUM SOUND TRANSFER

426

thalassaemia in the areas studied. There are, however, several reasons why this is unlikely. The migratory and centrifugal spread of the trans-New-Guinea language throughout mainland New Guinea about 10 000 years ago not only gave rise to the closely related upland languages of groups 4-6 (see table) but also to the lowland languages of Madang Province (group 1)." Thus, the groups with the highest and lowest levels of a thalassaemia are linguistically

This work

a

more

closely

related than the other lowland groups.

Council,

Wellcome Trust.

Correspondence should be addressed to S. J. 0., Department of Tropical Paediatrics, Liverpool School of Tropical Medicine, Pembroke Place, Liverpool L3 5QA. REFERENCES 1. Curtain

2.

Furthermore, with triaxial mapping ofABO and MNS blood

frequency, the New Guinea populations fall into four slightly overlapping groups. 12 On two-dimensional representation, the Madang and Sepik populations are separated from the Austronesians by the Highlanders. Thus, group

it also appears from blood group data that the groups with high prevalence of a thalassaemia are more closely related to the group with the lowest prevalence than they are to each other. A possible relation has been reported between altitude and the prevalence of (3 thalassaemia and glucose-6-phosphate dehydrogenase deficiency, two other red-cell disorders thought to afford heterozygous protection against P falciparum malaria, in Papua New Guinea. 1,13 If more extensive population studies of the type reported here demonstrate a similar relation for a thalassaemia, it may be possible to explain why this single-gene disease is so common throughout the world.

was supported by the Wellcome Trust, the Medical Research and the Rockefeller Foundation. S. J. 0. is supported by the

3.

CC, Kidson C, Gajdusek DC, Gorman JG. Distribution pattern, population genetics and anthropological significance of thalassemia and abnormal hemoglobins in Melanesia. Am J Phys Anthropol 1965; 20: 475-83. Beaven GH, Fox RH, Hornabrook RW. The occurrence of haemoglobin-J (Tongariki) and of thalassaemia on Karkar island and the Papua New Guinea mainland. Trans Roy Soc Lond (Biol) 1974; 268: 269. Booth K. Cord blood survey for haemoglobin Bart’s. Papua New Guinea Med J1981;

24: 264-66. 4. Weatherall DJ, Clegg JB. The thalassaemia syndromes, 3rd ed. Oxford: Blackwell Scientific Publications, 1981. 5. Old JM, Higgs DR. Gene analysis. In: Weatherall DJ, ed. The thalassaemias. Edinburgh: Churchill Livingstone, 1980: 74-102. 6. Wurm SA, Hattori S, eds. Language atlas of the Pacific area. Part I: New Guinea area, Oceania, Australia. Pacific Linguistic Series C: 66. Canberra: Australian Academy of Humanities, Japan Academy, 1981. 7. Higgs DR, Weatherall DJ. Alpha thalassemia. Curr Topics Hematol 1983; 4: 37-97. 8. Brittenham G, Lozoff B, Harris JW, et al. Alpha globin gene number: population and restriction endonuclease studies. Blood 1980; 55: 706-08. 9. Vines AP. An epidemiological sample survey of the highlands, mainland and island regions of the territory of Papua New Guinea. Port Moresby: Department of Health, Papua New Guinea, 1970. 10. Peters W, Christian SH, Jameson JL. Malaria in the highlands of Papua and New Guinea. Med J Aust 1958; ii: 782-87. 11. Wurm SA, ed. Papuan linguistic prehistory and past language migrations in the New Guinea area. In: New Guinea area languages and language study, vol 1. Papuan languages and the New Guinea linguistic scene. Series C, 38. Canberra: Australian National University, 1975; 935-56. 12. Booth PB, Simmons RT. Some thoughts on blood genetic work in Melanesia. Papua New Guinea Med J 1972; 15: 10-14. 13. Gorman JG, Kidson C. Distribution pattern of an inherited trait, red cell enzyme

deficiency in New Guinea and New Britain. Am J Phys Anthropol 1962; 20: 347-56.

which has sufficient inertia not to move significantly at the lowest frequencies measured. This mass is supported on the surrounding area of the mother’s skin by a ring platform of such an area that the fetal heartbeat sound waves in the skin underneath it are insufficient to move the mass. "Compliance-matching" gives the additional advantage that airborne noise would now interfere with the heart-sound signal only if it could enter the mother’s body. The skin-to-air interface is now working to the advantage of the system. The signal-to-noise ratio, defined as peak-to-peak valve-closure signal amplitude compared to baseline peak-to-peak signal, lies typically between 10:1and 100:11 (20-40 dB) when the fetal heart lies up to 7 cm below the mother’s skin surface (depth measured in 20 mothers at 30-41 weeks’ gestation with a Kontron Sigma 10 real-time ultrasound scanner). The residual "noise" appears to be physiological-ie, murmurs in blood vessels and valves and abdominal-muscle tremor (fig 2). The signal is well (>60 dB) above electrical noise. Nevertheless unwanted sound can still arise from cable movements; and in the prototypes this has been avoided by fitting a radiotelemetry transmitter. The fetal heartbeat was found to have frequency compo1 nents well outside the previously monitored band of 80-110 Hz.l and The improved signal-to-noise ratio wider bandwidth (20-250 Hz) reveals, in addition to the occurrence of the first and second fetal heart sounds, other details of valve function. Fetal heart-sound signals, abdominal electrocardiographic (ECG) signals, and a 60 Hz clock signal were simultaneously recorded in 8 mass

Methods and Devices NEW TRANSDUCER FOR DETECTING FETAL HEART SOUNDS: USE OF COMPLIANCE MATCHING FOR MAXIMUM SOUND TRANSFER

D. G. TALBERT JOHN D. P. SOUTHALL

DEWHURST

Department of Obstetrics and Bioengineering, Institute of Obstetrics, Queen Charlotte’s Hospital, Goldhawk Road, London W6 0XG THE

signal energy available from fetal heart sounds is greater than

commonly supposed, and the vibrations produced within the heart have a low frequency and contain components that are not audible with a simple stethoscope. A new transducer has been developed to "feel" these vibrations as well as to detect those at audible This high-energy signal with low-frequency components has not been previously exploited, largely because the vibrations are reflected at the boundary between the mother’s skin and the air. This is well known in ultrasound, where it is described as a mismatch of impedance. At the low frequencies associated with heart sounds a similar effect occurs, and it depends largely on the "compliance" (hardness) on either side of the surface. Air is very much "softer" than the mother, and little sound energy escapes to be picked up by a microphone. Moreover, the piezo-electric crystals within microphones that are used to convert these weak pressure waves into an electrical signal are "hard", and so placing them directly on the mother’s skin is also ineffective. This difficulty has been overcome by using a piezo-electric element in the form ofabar clamped at one end and effectively resting on the mother’s skin at the other (fig 1). Pressure waves from the fetal heart press on one end of the bar, causing it to bend and produce an electrical output. The force required to deflect the end varies as bar length -3 , and so by adjusting the length of the bar the force/displacement relationship can be varied. Sound transfer is maximum when this relationship is the same for the end of the bar as for the mother’s skin. The other end of the bar is attached by silicon-rubber clamps to a reference

frequencies.

Fig

I-Section

through the transducer.

The total weight is 100 g.

427

Fig 2-Fetal

heart sounds.

Upper panel: comparison of timing of fetal ECG from the surface of the maternal abdomen (middle trace) and fetal heart-sound signals (upper trace). The lower trace represents a 60 Hz clock signal. Lower panel: a longer recording of the fetal heart sounds. MT=mitralltricuspid valve closures. AP = aortic/pulmonary valve closures. F fetal and M maternal ECG signals. mothers (gestational age 35-41 weeks) on to an instrumentation tape recorder (Hewlett Packard 3964A and printed at 250 mm/s on an ink-jet chart recorder (Siemens Mingograf) (fig 2). Heart-sound zero-crossing intervals are typically around 10 ms in length. Sections of recording in which consecutive heart sounds were similar in shape were used for direct manual comparison between 10 fetal QRS intervals and 10 heart-sound intervals (from three positions on each recording). There were no detectable differences in intervals measured (to within ±11 ms-the limits of resolution with this technique). Fetal QRS-to-QRS intervals could not be measured accurately when, as often happened, they coincided with the larger and wider maternal ECG complexes. The complexes associated with the pressure-wave mitral/tricuspid valve closures (M/T) were usually larger and longer-lasting than those associated with the aortic/pulmonary valve closures (A/P) (fig. 2). The first heart sound usually started shortly after the zero crossing of the fetal QRS signal. This is similar to the timing described by Luisada and Portaluppi2 for adult hearts. However, unlike the adult, the right ventricular muscle weight in the fetal heart exceeds the left,3 it pumps at similar pressures, and it can contribute signals of equal or greater amplitude. Discontinuities could be discerned in both first and second heart sounds, but those in the M/T complex were the most clear-cut. It was possible to make ambulatory recordings of the fetal heart sounds for periods of up to 6 h (the maximum so far attempted). Adequate signals were obtained only during times when mothers were stationary; artefact occurred during movement. The new transducer allows non-invasive long-term monitoring of fetal heart rate and may provide accurate measurements of shortterm variability from suitable segments of data. The pressure-wave signals contain sufficient energy to give good signal-to-noise ratios when the sensing device is compliance-matched to the mother’s skin surface, and their bandwidth of 20-250 Hz may reveal changes in the timing of valve closures, which can be related to changes in fetal

systemic or pulmonary pressures. Prof R. H. Anderson, Mr N. Abraham, and Dr A. J. Wilson gave invaluable advice on this report, and Miss N. Patel helped with the recordings. D. P. S. is a senior research fellow of the British Heart Foundation.

Correspondence should be addressed to D.

P. S.

REFERENCES 1. Hewlett Packard GMBH. Operatingandservicemanualmodel8020A cardiotocograph.

Hewlett Packard GMBH, Boblingen, West Germany, 1970. 2. Luisada AA, Portaluppi F. The heart sounds. New York: Praeger Scientific. 1982. 3. Emery JL, Macdonald MS. The weight ofthe ventricles in the later weeks of intrauterine life. Br Heart J 1960; 22: 563-70.

Reviews of Books Respiratory Physiology Physiological Principles in Medicine Series. John Widdicombe, St George’s Hospital Medical School, London, and Andrew Davies, Massey University, Palmerston North, New Zealand. London: Edward Arnold. 1983. Pp 118.4.95.

Respiratory Disorders Physiological Principles

in Medicine Series. Ian R. Cameron and N. T.

Bateman, St Thomas’s Hospital Medical School, London. London: Edward Arnold. 1983. Pp 134. 5.95. THESE two small paperbacks aim, as do others in this series, to help pre-clinical students relate physiology to disease, and conversely to explain clinical symptoms and signs in terms of disturbances of function. This admirable purpose highlights a major problem in British medical education, where physiology is taught by physiologists, who rarely have day-to-day clinical experience, and where in later years the student’s legitimate concern with acquiring clinical skills may cause him to overlook the physiological basis of his practice. Like many clinicians who quantitate disordered function in their daily practice, I have a sneaking suspicion that I too could teach much of the physiology which is relevant to my clinical practice-if only I had the time. This illusion might be dispelled, however, if I were to attempt to write as clear and concise an account of modern respiratory physiology as John Widdicombe and Andrew Davies provide in their book. Their wide background in both human and animal physiology is the basis of much accurate information, presented in a pleasingly didactic fashion, without the encumbrance of detailed references which would be needed for a more critical scientific audience, but with an up-to-date reading list at the end of each chapter, where the sleepy student may be awakened by a brisk recital of what he should have learned in the preceding pages. Line-diagrams are liberally used, and most add to clarity, but it seems sad that there is no diagram relating the components of acid-base balance to each other, for many clinicians and students find this one of the more baffling areas to interpret for bedside use. The section on control of breathing and respiratory reflexes is authoritative, but I find it a little disturbing to be told that "intrapleural pressure can be measured by introducing an air filled needle into the intrapleural space"-with the implication that the oesophageal balloon, usually used for this purpose, is preferred merely because it is less unpleasant. This and other minor points (eg, fig 8.7, which implies that hypoxic