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THE AUSCULTATORY GAP.
919 disease is life-long, it is hoped that the protection obvious are rapid vibrations in the arterial wall this prophylactic treatment will prove and eddies in the blood stream. Vibrations in the The preparation and preservation arterial wall depend, first, on the tension and structure durable. equally of the vaccine still present difficulties and the need for of the wall, and, secondly, on the form of the pulse-
following
a living dose to complete the immunity is an undesirable complication. This is especially disconcerting since the dose of living virus though not causing any overt symptoms of distemper has appeared in some instances to have caused the animal to become a carrier for a time. A further paper describing the results of experiments with dogs along similar lines is promised in the near future.
Annotations. "
Ne quid nimis."
THE AUSCULTATORY GAP.
i estimating blood pressure by the method the orthodox procedure is to raise the pressure I in the armlet to about 200 or 250 mm. of Hg and then allow it to fall slowly until the characteristic sounds can be heard over the brachial artery immediately below the point of compression. As the pressure continues to fall the sounds change both in quality and intensity. At first they are clear but faint; later, they are accompanied by a rushing murmur; then they once more become sharp, at first increasing in intensity and then diminishing. Finally, the sharp sounds are abruptly replaced by a dull thud, and when the pressure has fallen another
auscultatory
IN
few millimetres the sounds die away.
The first appearance of the sounds marks the systolic, and the sudden transition from sharp to dull sounds the diastolic pressure. In most subjects the arterial sounds conform fairly well to this description, and the determination of systolic and diastolic pressures is easy. Sometimes, unfortunately, this is not so ; the transition from the sharp sounds of the third phase to the dull sounds of the fourth phase, instead of being abrupt, is gradual, and extends over a range of 20 mm. or more, affording no satisfactory diastolic end-point. The determination of the systolic pressure generally presents less difficulty, but a possible source of error, first pointed out by French and American workers some ten years ago, may occasionally lead to a wrong reading. In certain cases the normal sequence of the Korotkow sounds heard during decompression is interrupted by"a zone of complete silence. This silent interval or auscultatory gap," as it has been termed, usually replaces, in part or whole, the sounds of the second phase-i.e., those which are accompanied by a murmur. From a diagnostic point of view this is of some importance, since it may lead to an under-estimation of the systolic pressure, the sounds preceding the auscultatory gap being missed and their reappearance being taken as the systolic reading. Such a mistake can easily be avoided by first estimating the systolic pressure by palpation, a technique which is to be recommended, since it eliminates the necessity for submitting the patient to the needless discomfort of a high initial compression when his blood pressure is within normal limits. The " auscultatory gap " was first noticed in cases of aortic stenosis, but subsequent observations have shown that it is not confined to that condition, but is frequently associated with hyperpiesis. Such was the common factor in a series of four cases recently reported in this journal by P. C. Gibson,! and in 28 out of 30 cases reported in America by S. G. Mudd and P. D. White.2 Various hypotheses have been put forward as to the mechanism of production of the " auscultatory gap," and an explanation of its presence is to be sought in considering the different factors concerned in the production of the Korotkow sounds. Of these the first and most 1 THE LANCET, 1927, ii., 1012. 2 Arch. Int. Med., 1928, xli., 249.
The steep wave-front of the typical Corrigan aortic incompetence produces a sudden shock which excites violent vibrations in the artery, whereas the slow-rising anacrotic pulse of aortic stenosis can slip through almost unnoticed. It is like a finely tapered wedge which glides quietly and smoothly into place. The sphygmogram in hyperpiesis is not unlike that of aortic stenosis, the upstroke rising gradually to a well-sustained plateau. Conse quently, in both these conditions the force acting upon the arterial wall is such as to excite but little commotion. To turn now to the second factorthe condition of the wall on which these forces act. Decompression is divisible into three stages. During the first stage the compressing pressure is considerably higher than the diastolic pressure. During the second stage it is only slightly higher, and during the third stage the compressing pressure is lower than the diastolic. It is therefore only during the third and last stage of decompression that the effective internal pressure is sufficient to keep the arterial wall on the stretch throughout the whole cardiac cycle. During the first two stages the artery collapses more or less completely in diastole. Further, during the first stage of decompression the external is so much greater than the internal pressure that the passage of the pulse-wave cannot stretch the artery sufficiently to produce violent vibrations, such as occur during the second stage, which corresponds to the maximal oscillations as recorded by Pachon’s or Erlanger’s instruments, and to the sharp loud third phase sounds heard on auscultation. It is easy to understand why the slow rising pulse of aortic stenosis, or of hyperpiesis, may fail to produce rapid vibrations in the artery during the earlier stages of decompression, but it is more difficult to explain why the sounds, having once made their appearance, should afterwards die away as the compressing pressure falls. The most likely explanation of this curious phenomenon appears to be that the accumulation of residual blood in the artery during the second stage of decompression acts as a damper which further limits the vibrations of the arterial wall. wave.
pulse of
RESEARCH ON POLIOMYELITIS. field of medical practice is new knowledge in that of the neurotropic more urgently desired than viruses. The necessity of employing monkeys for the experimental study of these viruses has impeded progress by reason of the heavy cost involved, and although it is nearly 20 years since Landsteiner showed that the virus of poliomyelitis could be transmitted to monkeys, it is doubtful if the knowledge we have since gained of this and other neurotropic viruses has materially clarified the preventive and therapeutic outlook. On the practical side little has been discovered about the prevention and control of infantile paralysis in spite of the intensive study which has been given to the problem. The present is a favourable time for a new attack on the problem, for the last decade has witnessed considerable developments in our knowledge of virus diseases and their methods of attack. The medical profession will therefore welcome the formation of an international committee for the study of poliomyelitis under the distinguished chairmanship of Dr. William H. Park, director of the Bureau of Laboratories of the New York City Health Department. Arrangements have been made for a concerted three-year attack on the difficult problems of prevention and therapy presented by this formidable and crippling disease. To enable research to be carried out at a number of centres, both in the United States and in Europe, a sum of $250,000 has been given by Mr. Jeremiah Milbank, a prominent New York financier who takes an active personal interest in hospitals and charities. The following are the centres which have been chosen IN
no
following
a living dose to complete the immunity is an undesirable complication. This is especially disconcerting since the dose of living virus though not causing any overt symptoms of distemper has appeared in some instances to have caused the animal to become a carrier for a time. A further paper describing the results of experiments with dogs along similar lines is promised in the near future.
Annotations. "
Ne quid nimis."
THE AUSCULTATORY GAP.
i estimating blood pressure by the method the orthodox procedure is to raise the pressure I in the armlet to about 200 or 250 mm. of Hg and then allow it to fall slowly until the characteristic sounds can be heard over the brachial artery immediately below the point of compression. As the pressure continues to fall the sounds change both in quality and intensity. At first they are clear but faint; later, they are accompanied by a rushing murmur; then they once more become sharp, at first increasing in intensity and then diminishing. Finally, the sharp sounds are abruptly replaced by a dull thud, and when the pressure has fallen another
auscultatory
IN
few millimetres the sounds die away.
The first appearance of the sounds marks the systolic, and the sudden transition from sharp to dull sounds the diastolic pressure. In most subjects the arterial sounds conform fairly well to this description, and the determination of systolic and diastolic pressures is easy. Sometimes, unfortunately, this is not so ; the transition from the sharp sounds of the third phase to the dull sounds of the fourth phase, instead of being abrupt, is gradual, and extends over a range of 20 mm. or more, affording no satisfactory diastolic end-point. The determination of the systolic pressure generally presents less difficulty, but a possible source of error, first pointed out by French and American workers some ten years ago, may occasionally lead to a wrong reading. In certain cases the normal sequence of the Korotkow sounds heard during decompression is interrupted by"a zone of complete silence. This silent interval or auscultatory gap," as it has been termed, usually replaces, in part or whole, the sounds of the second phase-i.e., those which are accompanied by a murmur. From a diagnostic point of view this is of some importance, since it may lead to an under-estimation of the systolic pressure, the sounds preceding the auscultatory gap being missed and their reappearance being taken as the systolic reading. Such a mistake can easily be avoided by first estimating the systolic pressure by palpation, a technique which is to be recommended, since it eliminates the necessity for submitting the patient to the needless discomfort of a high initial compression when his blood pressure is within normal limits. The " auscultatory gap " was first noticed in cases of aortic stenosis, but subsequent observations have shown that it is not confined to that condition, but is frequently associated with hyperpiesis. Such was the common factor in a series of four cases recently reported in this journal by P. C. Gibson,! and in 28 out of 30 cases reported in America by S. G. Mudd and P. D. White.2 Various hypotheses have been put forward as to the mechanism of production of the " auscultatory gap," and an explanation of its presence is to be sought in considering the different factors concerned in the production of the Korotkow sounds. Of these the first and most 1 THE LANCET, 1927, ii., 1012. 2 Arch. Int. Med., 1928, xli., 249.
The steep wave-front of the typical Corrigan aortic incompetence produces a sudden shock which excites violent vibrations in the artery, whereas the slow-rising anacrotic pulse of aortic stenosis can slip through almost unnoticed. It is like a finely tapered wedge which glides quietly and smoothly into place. The sphygmogram in hyperpiesis is not unlike that of aortic stenosis, the upstroke rising gradually to a well-sustained plateau. Conse quently, in both these conditions the force acting upon the arterial wall is such as to excite but little commotion. To turn now to the second factorthe condition of the wall on which these forces act. Decompression is divisible into three stages. During the first stage the compressing pressure is considerably higher than the diastolic pressure. During the second stage it is only slightly higher, and during the third stage the compressing pressure is lower than the diastolic. It is therefore only during the third and last stage of decompression that the effective internal pressure is sufficient to keep the arterial wall on the stretch throughout the whole cardiac cycle. During the first two stages the artery collapses more or less completely in diastole. Further, during the first stage of decompression the external is so much greater than the internal pressure that the passage of the pulse-wave cannot stretch the artery sufficiently to produce violent vibrations, such as occur during the second stage, which corresponds to the maximal oscillations as recorded by Pachon’s or Erlanger’s instruments, and to the sharp loud third phase sounds heard on auscultation. It is easy to understand why the slow rising pulse of aortic stenosis, or of hyperpiesis, may fail to produce rapid vibrations in the artery during the earlier stages of decompression, but it is more difficult to explain why the sounds, having once made their appearance, should afterwards die away as the compressing pressure falls. The most likely explanation of this curious phenomenon appears to be that the accumulation of residual blood in the artery during the second stage of decompression acts as a damper which further limits the vibrations of the arterial wall. wave.
pulse of
RESEARCH ON POLIOMYELITIS. field of medical practice is new knowledge in that of the neurotropic more urgently desired than viruses. The necessity of employing monkeys for the experimental study of these viruses has impeded progress by reason of the heavy cost involved, and although it is nearly 20 years since Landsteiner showed that the virus of poliomyelitis could be transmitted to monkeys, it is doubtful if the knowledge we have since gained of this and other neurotropic viruses has materially clarified the preventive and therapeutic outlook. On the practical side little has been discovered about the prevention and control of infantile paralysis in spite of the intensive study which has been given to the problem. The present is a favourable time for a new attack on the problem, for the last decade has witnessed considerable developments in our knowledge of virus diseases and their methods of attack. The medical profession will therefore welcome the formation of an international committee for the study of poliomyelitis under the distinguished chairmanship of Dr. William H. Park, director of the Bureau of Laboratories of the New York City Health Department. Arrangements have been made for a concerted three-year attack on the difficult problems of prevention and therapy presented by this formidable and crippling disease. To enable research to be carried out at a number of centres, both in the United States and in Europe, a sum of $250,000 has been given by Mr. Jeremiah Milbank, a prominent New York financier who takes an active personal interest in hospitals and charities. The following are the centres which have been chosen IN
no