Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 120

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189


USA > Ohio > Hancock County > Findlay > Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens > Part 120


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bour whose movements have been calibrated. This plethysmo graph is put into exactly that position in which it allows the heart to lie naturally and then fixed there with a clamped support. Its lower surface is made nearly flat so as not to dislodge the heart nor press upon the great veins." The out- flowing blood is caught in a graduated glass cylinder and a: the level of the blood rises in the cylinder each 10 ce. is re- corded by an electric signal writing on the same drum as the manometers and plethysmograph. All of these pens are ex- actly superposed.


The table, the height of which can be raised or lowered br a screw, is adjusted so that the heart is on a level with the zero of the graduated uprights which run nearly to the ceiling of the room. Pressure is then estimated in centimeters of blood although it is, of course, easy to read it off in milli- meters of mercury from the curves. A Jacquet chronograph accompanies the manometers.


It is clear that a constant error is involved in estimating the total output, because although the subclavian arteries can be ligated, the carotids must be left open. Of course, one might arrange a separate circulation for the head, but the error is constant enough to make little difference in the result obtained. It involves a constant difference between the esti- mated value of the plethysmographic excursion and the measured output per beat. Part of this may be residual bloni. but part is blood escaping into the carotids.


In introducing the canulas into the aorta it has been found advisable to open the subclavian artery and allow free bleeding while the aorta is clamped in order to relieve the strain upar the heart. When the animal is thus arranged, the pressure against which the heart expels blood into the aorta is de- termined by the position of the outflow tube. The pressure of the blood entering the distal portion of the aorta, and conse- quently the amount of blood finally supplied to the heart, de- pends upon the height at which the cistern is placed. If the cistern is maintained at a constant height and the outfor tube moved up and down, it is found that the actual output of the heart through the aorta is changed but little by the al- terations in pressure, as pointed out by Howell and Donaldson. It seems, however, that when the cistern stands far above the outflow tube, a certain amount of blood must run through the animal to the outflow by the force of gravity.


Ordinarily the elevation of pressure in the intact animal i: produced by narrowing the arterioles which would undoubtedly tend to affect the amount of blood entering the veins; but ap- parently this is exactly compensated by the increased forve and consequent rapidity with which the heart sends the blon! through the narrow channels and the circulation proceeds 25


3 Martin: Philos. Trans. Roy. Soc., 1883, p. 663.


' Howell & Donaldson: Philos. Trans. Roy. Soc., 1884, part 1, p. 139.


" Lohmann: Pflüger's Archiv, 118, 1908.


" The tambour of the plethysmograph may be calibrated, of course, by attaching it to a flask into which a burette allows fluid to drop 1 cc. at a time, but it is much more readily and exactly done with a syringe. One cc. or 5 cc. of water is expelled from the syringe into a graduate and the ring on the piston rod then screwed down tight on the top of the syringe. After this the excursion of the piston is 1 cc. or 5 cc. as arranged and it is quite easy to communicate this to the tambour. It can be done rapidly and produces a curve like that obtained from the heart.


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D


K


C


F


B


E


A


A, Heart enclosed in glass and rubber plethysmograph. B. Arch of aorta from which runs C, the artificial aorta with glass outlet tube at the top.


D, The tube leading from the reservoir of defibrinated blood through the coil immersed in warm water, to E, the distal portion of the aorta.


F. Hürthle manometer, and G, mercury manometer connected with the artificial aorta (C).


H. Tambour connected with the plethysmograph (A).


I, Jacquet chronograph. J, Electric signal controlled by the in- terrupter K.


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JOHNS HOPKINS HOSPITAL BULLETIN.


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before. So, too, it is found that if the cistern and outflow tube are kept at the same level, the outflow and inflow are about constant and thus probably resemble more closely the condi- tions in the intact animal than when the inflow is kept con- stant and the level of outflow changed. Nevertheless, both conditions were studied in many curves.


When the level of the cistern and of the outflow were the same, the elevation of these increased the rate of the circula- tion. The amount of blood thrown out of the aorta per beat increases with the elevation ; consequently, the amount of blood handled by the ventricle increases, the ventricle dilates and its excursion increases. It not only relaxes to a greater degree, but it contracts and empties itself completely. Thus the plethysmographic curve not only shows an increased excursion, with heightened pressure of this sort, but occupies a position further below the base line. This is the usual criterion of the tone of the ventricle, but if we disregard the conditions of malnutrition of the myocardium, of which we shall speak later. it seems that such accommodative dilatation, associated as it is with an improved excursion and the easy performance of increased work, should hardly be referred to as a diminution of tone. This, however, is a question of definition, and we hope to say more at another time of the question of tone. In practice, the plethysmograph was opened at each change of pressure so that its excursions, when again closed, were exe- cuted directly about the base line. In this way, calibration is less complicated and the disturbing element of the compres- sion of the air in the plethysmograph was eliminated. When this was not done, however, it was found that at a pressure of 150-200 cm. of blood, the heart would make very great ex- cursions at a level far below the base line, ejecting blood very rapidly, while at low pressures the heart became very small and made small excursions at a level far above the base line with relatively slight output of blood (Curve I). This seems to be chiefly dependent upon the amount of blood handled, for when the cistern was kept at a constant level, the excursions varied far less.


The character of the normal pulse may be studied in the curve of the Hurthle manometer taken from the aorta laterally. It might seem that the substitution of gravity for the re- sistance offered by friction in the arterioles might produce fallacies in the interpretation of the pulse curve, but after all, the elasticity of the arteries, represented here by that of the rubber tube, is the only force which forms the pulse aside from the peripheral resistance and the impulse from the heart. As a matter of fact, experiments were made to test this both in the normal intact animal and in those in which aortic in- sufficiency had already been produced, and it was found that the pulse curve, after the cutting of the aorta and the establish- ment of the new arrangement, was indistinguishable from that of the intact animal of five minutes before, as may be seen in the accompanying curves (Curve IX).


It might be thought that in the intact arterial tree it would be easy for the elastic contraction of the artery to continuously propel blood along into the veins, whereas in the upright rubber tube, the expulsion must depend upon the impulse of


the heart alone; but a moment's reflection will show that with the cessation of the systolic impulse and the escape of blood over the level of the outflow, the level of the blood is still exactly there, and if the elastic tube is overdistended its recoil will drive more blood over, precisely as in the case of the arterial tree with its capillaries.


The pulse curve shows the dicrotic notch and wave precisely as in the intact animal. The position of this notch changes with changes in the level of the outflow, being low on the slop: when the outflow is low and rising toward the summit of the primary wave, as the outflow tube, and consequently the pres- sure and tension of the wall are elevated.


It is difficult for me to believe that the form of the pul wave can be directly dependent upon the rapid escape of the blood from the arteries. If the tube into which the heart eject: blood is elastic, and of any considerable length, even if it le widely open at its end, it will require an appreciable time for the blood to pass along and escape, and it seems probable tho: even in such a case the pulse wave will reach the end of the tube before the actual mass of fluid, the injection of which produced that pulse wave, does so and escapes.


Even if the elastic tube be of uniform caliber throughout, I do not believe that the form of the systolic pulse wave could be affected by the actual escape of the fluid, for it is certainly formed before that, if the tube is of any considerable length. To attain such a condition, the aorta would require to be lis a very short, very widely open straight tube with rigid walls. Far less, then, does it seem possible that the arterial tree 35 it exists could afford such conditions even with the maximal conceivable dilation of the arterioles.


On the other hand, although it cannot be conceded that the systolic quantum of blood could get out of the way rapidly enough to produce a change in the form of that systolic ware (since the wave is an expression of pressure and not of th: movement of fluid), it is obvious that its rapid removal will leave the vessel partly empty with relaxed walls when the time arrives for the next systolic impact; and it is this relaxed con- dition of the wall, I think, which causes the peculiar form ". the pulse in aortic insufficiency.


Stewart has explained, on the basis of the work of Haycraft, Lewis, Roy and others, how the collapsing character of the pulse is dependent upon a low diastolic pressure, high systelie pressure and therefore high pulse pressure not being necessary. I may quote a paragraph : " From the figures given by Roy of the extensibility of the arterial walls at different pressures, twi pulse curves are drawn (Fig. 35). In both instances the er- cess of systolic over diastolic pressure is the same, viz: 60 mn. Hg. but they differ in that in one the diastolic pressure is be- low normal, viz: 50 mm. Hg. while in the other it is some- what above normal, viz: 80 mm. Hg. In the lower curve the amplitude is double that in the upper, the angle between the upstroke and downstroke is more acute, and the dicrotie notch relatively lower. In the upper curve, upstroke and down- stroke are oblique and the angle between them is widened. Iz the curve taken at the low pressure there is more movement of the arterial wall for the same change of pressure. The en:


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It seems that with low pressure the amplitude of the pulse is increased chiefly by the facile yielding of the lax wall of the ncompletely distended artery so that the relative position of the dicrotic notch is due to the increased excursion of the vessel wall above that point in the curve at which the end of the systole is indicated by the dicrotic notch.


It can be readily shown that the actual amount of blood which escapes when the heart is working at a low pressure is ess than that when the heart pumps against a high pressure because the amount supplied to the heart is less. In other words, the rate of the circulation becomes greater at the higher pressure, at least up to a certain optimum, but this seems to have nothing to do with the character of the pulse except in :hat, at the high pressure, the walls of the artery are under high tension while at a low pressure they are lax. At high ension the systolic pressure would not be able to expand the ressel so far by its sudden impulse before the closure of the ralves and therefore the dicrotic notch would appear after only i slight systolic fling, whereas if the pressure during diastole s low and the walls of the vessel lax, the same systolic impulse


150


130


110


100


90


80


70


60


50


Fig. 35 .- Diagrammatic representation of two pulse curves in- 'icating the same pulse pressure, but at different diastolic pres- ures. The horizontal lines indicate the extensibility of the rtery at given pressures (after Lewis).


could produce a considerable fling before the dicrotic notch which would therefore stand relatively low on the downward ope. Measured from the trough of the wave the dicrotic otch might stand equally high in a collapsing and a non- llapsing pulse, but in the collapsing, the excessive excursion Dove this would make the dicrotic notch relatively low. This especially strikingly seen in the tremendous collapsing pulse hich occurs when the heart is dying from inadequate coronary rculation. The slow but violent systoles throw a quantity blood into the relaxed almost empty artery and a great fling sults before the dicrotic notch.


This gives a ready explanation of the change in the char- ter of the pulse when the aorta is compressed or adrenalin ren. These measures increase the tension of the arterial Il by preventing the outflow and it is this increased tension ich changes the form of the pulse. In the case of arterio- erosis in which aortic insufficiency is said not to produce a ical collapsing pulse, it seems more probable that the idity of the artery wall prevents its being distended by the folic impulse even more effectively than a heightened tension


insufficiency produced by tearing the valve the dicrotic notch may be quite high on the downstroke of the curve if the pressure is maintained at a fairly high level, it is often very indistinct and one receives the impression that the imperfection of the valves prevents its proper formation.


In the arrangement of the circulation described, the posi- tion of the outflow tube determines in a way the pressure. As long as the tube is full to the outflow level, that level repre- sents the diastolic pressure. If the valves are intact the heart responds and maintains the level, but if its nutrition suffers, it dilates and the blood leyel falls rapidly in the tube. If the aortic valves are torn, the level is maintained but by more active work on the part of the heart. The systolic pressure rises above this, dilating the tube as shown by the summit of the pulse wave which passes along to the outflow.


If, in the animal with an artificial aorta, the outflow tube be set at any level and aortic insufficiency be produced, the pulse pressure instantly becomes greatly increased. There is noth- ing to represent the supposed accommodative widening of the peripheral vessels here and the outflow from the end of the tube per beat is practically always just what it was before, but still there is greatly increased pulse pressure both from systolic elevation and diastolic fall. The only possible explana- tion of this is the existence of regurgitation. This relaxes the tension of the wall of the vessel which then receives with the next systole the regurgitated blood together with the normal output. Since the amount of the regurgitated blood again sinks back, the actual outflow is the normal; but the impact of the whole mass thrown out by the heart on the relaxed ar- terial wall gives the collapsing character of the pulse wave, and the fall in the diastolic pressure must be due, not to a periph- eral escape, but to an escape into the heart.


If the level of the outflow tube is high and a high systolic tension thus allowed, the systole will take place into a tube already tense-no great fling or sudden distension will be produced before the end of systole and the dicrotic notch will therefore be at the bottom of only a relatively small part of the downward slope. If the outflow tube be at a low level, less blood will reach the heart from the low cistern, less effort will be made to handle it, less will be thrown into the vessels whose size and elasticity are constant, and the lax wall will be given a fling which leaves the dicrotic notch low.


Another possible explanation of the position of the dicrotic wave lies in the fact that when the valves are torn they can hardly give rise to such a sharp wave or notch and that it may well be that the recoil is from the wall of the ventricle rather than from the valve. Indeed, in many of the curves of extreme insufficiency, it is difficult to discern anything of the dicrotic wave at all. This is especially suggested by the auscultation of the murmur, for although, of course, any such method must be inexact, one is much inpressed by watching the formation of the curve in a slowly beating heart with low dicrotic notch or hyperdicrotism following aortic insufficiency with the finger and the stethoscope on the heart. The murmur starts precisely with the end of the systolic heave and persists through the


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downward slope to the trough or notch where it stops-the hyperdicrotic wave is executed in silence and then begins sharply the new systole (Curve VI).


1 On the whole, it seems that the position of the dicrotic notch is chiefly a question of the tension of the vessel wall. Similarly the collapsing quality of the pulse must be a question of the in- complete filling of the aorta just prior to systole and the conse- quent fling of its lax wall by the injection of the systolic quantum.


I can readily understand that long continuance of this con- dition might widen the arteries and thus possibly account for the capillary pulse which would be the more easily brought about by the impulsion of an excessive quantity of blood into the aorta even though that blood never reached the periphery. Indeed it is not hard to believe that with hypertrophy of the ventricle the blood might be sent more rapidly through the veins. But all of these things are the final effects of the changes resulting from aortic insufficiency and not their causes.


By means of the rearrangement of the circulation with the artificial aorta, it is possible to arrive at some mathematical conclusions as to the exact nature of the mechanism of the blood flow in aortic insufficiency, for it is easy to estimate the output from the aorta at each beat of the heart and at the same time to measure the output from the ventricle as cal- culated from the calibration of the plethysmographic tracing. When the valves are intact, these two figures are not far apart. A constant error lies in the escape of blood into the carotids, and nothing more than a comparison of the relations before and after insufficiency is attempted. When the valve is torn, it is found that the systolic pressure as shown by the manom- eters is maintained. The diastolic pressure sinks, the output per beat or at least per minute (for the rate may change and become slower) is about the same, the plethysmographic curve maintains its level or stands a little higher-its excursions are greatly increased in amplitude. These things are true of the artificial aorta and I find them true also of the animal with intact aorta, although Dr. Stewart finds no marked increase in the plethysmographic excursion. In a few experiments made to determine this point I have found an increased plethysmo- graphic excursion exactly as in the cases with the aorta cut.


It must be borne in mind, however, that if there be regurgi- tation into the ventricle, the amount of blood actually circulat- ing round to the heart will tend to be less than normal, while the volume of the left ventricle will be increased by the recep- tion of the regurgitant blood. The volume of the right ventri- cle, will, however, be correspondingly decreased on account of the smaller amount of blood it receives. Such a combination might conceivably proceed without on the whole any en- largement of the heart and in that way account for the high level of the plethysmographic curve.


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Before the insufficiency, the amount expelled per beat from the aorta nearly equals that put out by the ventricle, but im- mediately upon tearing the valve there arises a great discrep- ancy. The excursion of the cardiac plethysmograph becomes much greater, showing a much larger output, while the aortic


delivery remains practically unchanged-undoubtedly there- fore, at each beat a considerable quantity of blood is throw ?! out of the heart into the aorta which never reaches the outflow orifice. It must go back into the heart and be thrown out again in the same futile way at the next systole. Even at such low pressures as 30 mm. Hg. this "residual " blood may be three times as much after the lesion as it was in the norma! heart at pressures of 60 or even 100 mm. Hg.


There is thus a considerable regurgitation, and when a re- gurgitation of 1 or 2 cc. is spoken of in a dog it is by no means insignificant, for repeated studies of the output per beat at normal pressures in dogs show that quantities such as 10-1? cc. per beat are far too great and that the dog's heart actually puts out quantities nearer 2 cc. per beat when the dog weighs 7 or 8 kg.


The estimation of the work of the heart at any given level of aortic pressure as the product of the plethysmographie es- cursion and the rate shows us that there is a sudden great in- crease when the aortic valve is cut. Thus, in one experimen: in which the pressure in the aorta was 120 cm. of blood, the work of the ventricle per minute was represented by 348.4 (f. of blood as compared with 220.9 cc. before the valve was tort. although the actual output from the aorta during this time wa: only 228 as compared with 203 while the heart was intact. This difference is evidently to be accounted for entirely by the regurgitation of the blood and the hypertrophy of the ventrici- is, in the same way, easily accounted for as the result of the excessive amount of useless work put upon the ventricle the imperfection of that mechanism which normally secures and renders permanent the effect of each contraction.'


Positive efforts to make clear the nature of the collapsin: pulse may easily be made with this modified arrangement of the circulation. It seemed possible that the mere excess it blood from whatever source which the ventricle was called upon to handle, might stimulate its walls to more violent contractions and thus heighten the pulse pressure. To te: this, blood was led from another cistern at a rather high! pressure into the left ventricle through a glass tube which was introduced in one instance through the subclavian artery and between the aortic valves in a heart in which no valve hal been torn, and in another experiment on a normal dog the extra blood was brought into the ventricle through the same sort of tube which was introduced through the auricular ap- pendix and the mitral orifice into the ventricle. In both cases the valves closed snugly about this tube and there was no leak- age. In both experiments the result was merely a slight el .- vation of pressure and a considerable increase in the aerti: output (largely due, no doubt, to gravity). Nothing of the collapsing character appeared in the pulse.


On the other hand, when the tube passing into the left ven- tricle was led, not from a separate blood reservoir at a high level, but from any point along the side of the artificial aorta which was tapped with the aid of a "T" tube, the pulse instantly assumed the collapsing character when the artificis! regurgitation was allowed, and as suddenly stopped and re- turned to normal when that tube was clamped. Undoubtedly


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18 Brown in the heart with a torn aortic ilve. In this curve the height of the dicrotic notch will cor- spond roughly with the level at which the aorta is tapped. Again, if in an experiment in which a collapsing pulse. has en produced by tearing the valve, we introduce an artificial ilve into the tube which represents the aorta, the pulse will se its collapsing character, and the more perfectly the valve ts the more nearly will it approach the normal form.


From all this it seems unavoidable to conclude that regurgi- tion plays a predominant part in the whole complex of aortic sufficiency. The ventricle throws out a quantity of blood to the aorta, which is more than naturally emptied and re- xed by the regurgitation of the previous diastole, thus giving great fling to the loose wall. Much of the blood returns to e ventricle being in fact only churned out and back from the Intricle. Still, so great is the new effort that a normal or early normal amount of blood may be discharged from the orta. The great pulse pressure produced in this way is very laracteristic and since it persists at all pressures it would seem constitute a specially good criterion of the condition. The latation of the peripheral capillaries at each pulsation must : due to the same projectile form of systolic filling of the re- xed vessels.


CONCLUSIONS.


1. By means of the arrangement of the circulation de- ribed, it is possible to estimate the work of the ventricle and study the influence of various factors upon it.




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