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·CIRCULATORY DYNAMICS

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·MODERN MEDICAL MONOGRAPHS
4
CIRCULATORY DYNAMICS
Physiologic Studies
By CARL J WIGGERS, M D , Sc D, FACP
Professor of Physiology and Director Department of Physiology School
of Medicine 11 estern Reserte Unuersity Cleeland Ohio
GRUNE & STRATTON
New York
1952

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GRL E & STRATTON IN
341 Fourth Avenue
New York City 16
Printed in USA for Grune Stratton

·Contents PAGE PREFACE 111 1 2 3 5 I Basic IL VODYNAVIC PRINCIPLES IN THE INTERPRETATION OF CIRCULA CORY DISORDERS Elementary Hemodynamics Hemodynamics of pulsating streams The aortic compression chamber The Pressure Pulse and Its Transformation in Trans Inis lon l'he phrnomena of damping and ware summation lluman Systolic and Diastolic Pressures I actors afiecting systohc and diastolic pressures The Clinical Importance of Irterial Pul e Tracings Clinical information derived from central pules Clinical salue of radial and femoral pulses Reconstructer pressure pulses in man I stimation of stroke volume and cardiac output I he Dynamics of Ilypertension The concept of peripheral resistance The concept of total peripheral resist ince Units of resistance The interpretation of change in pressure pules and pule pressure of hypertension Summary References 8 10 14 18 19 21 21 23 24 24 26 28 28 30 32 34 30 36 II DETERMINANTS OF CARDIAC PERFORMANCE Three Classic Discoveries The Law of Uniformity of Behavior The Applicability of Laws of Initial Tension and Length to Vammalian Hearts Intrinsic Cardiac Factors Summary References 37 17 48 49 ·CONTENTS TII DINAMICS OF TEVTRICULAR CONTRACTION UYDER AD NORMAL CONDITIOS 53 The Interpretation of Ventricular Pressure Pulses 53 Succssic Myocardial and Dynamic Fients during the Cardiac Cycle 56 Determinants of Iyocardial Responses 60 Pericardial Effusion 03 Ilyperv olemia 0.) Oligema 07 Arterial Hypertension of Peripheral Origin OS lortic Coarctation 70 Tortic Stenosis 71 Pulmonary Stenosis 73 Idioventricular Rhythms 73 Ventricular Alternation 78 Coronary Occlusion--Myocardial Ischemia 82 The Importance of Cardiac Valves 83 Aortic Regurgitation 86 Mitral Insufficiency 90 Mitral Stenosis 96 Summary 98 References 101 INDEX 10) ·Preface DURING the past year it has been my privilege to deliver several lectures on phases of circulatory physiology to which I have contrib uted during the past forty years Whenever necessary the original interpretations of experimental results were re evaluated in the light of subsequent work Three of these discourses dealt with experi mental aspects of circulatory dynamics and it was thought that their collection in book form would prose useful to intestigators and pro gressive practitioners interested in human circulatory dynamics The original lectures then have been reca t as chapters here The first chapter begins with a simple exposition of heriodynamic laws analyzes the practical information which can be gained from arterial pressure rendings and arterial pulse registrations and shows by wav of illustration hon information so gained enhances our under standıng of the dynamics of hypertension The second chapter concerns itself with the phy-lological mecha nisms by which the ventricles adapt themseli es to altered circulatory states in health and disease Theories are di orced from factual data an integration of successive new discos eries with classic lans of the heart leads to a modern concept of cardiac adaptation The third chapter is devoted to interpretations of ventricular con traction patterns by means of critical analyses of ventricular pressure curves The discussions include alterations which take place as a result of pericardial effu ion hypprvolemia oligemia arterial hyper tension aortic coarctation aortic and pulmonary stenosis Idioven tricular rhythms ventricular alteration coronary orclusion myocardial ischemia and valvular lesions CJ11 Cleveland Ohio April 1952 11

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·CHAPTER I Basic Hemodynamic Principles in the Interpretation of Circulatory Disorders* DISEASES are experiments performed by nature on animals and human beings It is one of the responsibilities of physicians to under stand the character of the human experiment going on to the end that it may be terminated or that natural compensatory mechanisms may be aided Physicians can gain assistance in these tashs in several ways (1) They can apply available information gained through an orderly solution of problems regardless of their apparent practical value (2) They can be guided by information accumulated through careful climcal studies of disease (3) They can benefit from considera tion of animal experiments in which nature s disorders have been reduplicated or simulated (1) They can by experience and continued practice improve their capacity to assess the significance of signs and symptoms They can through the use of laboratory apparatus and technics translate phenomena which are undetectable by the un arded senses into forms which the mind can grasp The measurement of human blood pressures and the registration of arterial pulses are currently giving a great deal of information in the diagnosis of cir culatory disorders But in my opinion the cardiologist in his every day practice is still not using all the information that the e procedures could vield for this reason it appears desirable to restes a number of busic prinuples which may enliance the value of available infor matron In substance lectures del ered before the lashington State Heart 18 a ciation Spokan Washington Sept 9 1900 and the Postgraduate Symposium on Heart Disease California Ileart Association San Francisco Oet w 1950 ·2 (IRCULATORI DINAMIC Flementary llemodynamics Hemodynamics is concerned with the fore(4 operative in the pro pulsion of blool around the circulaton 450m The physical forces com crned have been partlı derned from hydroxly namıy such as are conca meel in supplying water to dwellings is illustrated in figure 1 1 water flow, from a high re xers oir through a series of pipes to faucis located at varving distances above ground lesel The cleve A cleric Fig 1 –Two diagrams illustrating the hydro lynamic principles determin ing the Box of water from faucets 1 constant pressure reservoir and rigid pipe system Brhythmic pump system through elastic hose tion of the water surface above ground level (P) constitutes the mo tuve force and the difference between this les el and that of any faucet bay Pl is an important determinant of the greatest possible flow from the tap If the pressure in the central reseri or fixes or fall or if respective taps are located at higher or lower levels of a tall buld ing the maximal flou from a fully opened tap will inercase or decrease in proportion to the differences in elevation (or pressure) botueen the surface of the reservoir and the faucet ·BASIC HEMODYNAMIC PRINCIPLES 3 Again if two faucets (P) at the same elevation in a near and far dwelling are successively opened the rate of water deliver from the near one exceeds that of the far one only slightly This shows that the loss of pressure due to friction in the main delivery pipes is rather slight Of course the narron er and longer the pipe the greater the pressure drop due to resistance Now it is a common experience that the volume of water delivered by any faucet can be regulated widely between a small drip to a full gush by the extent to which it is opened ie by the degree of friction or resistance encountered within the faucet In other words the great est and most variable resistance is in the stopcochs Similarly the arterioles in the body represent stopcocks which hy altering their caliber meter the volume of blood which enters the capillaries All of this is common sense or shall we say it borders on the moronic Expres ed mathematically the rate of flow (F) varies directly with the pressure difference (P - Pi) and inversely with the resistance (R) mainly at the outlets of the system Such a formulation P - P is the essence of Poiseuilles law with one exception R viz a viscosity factor (V) It is obuous that if such a supply system were suddenly filled with a highly viscid fluid such as mola ses the rate of flow from any faucet would be greatly decreased despite the fact that pressure differences and apertures of faucets (resistance) did not vary Since the viscosity of blood is approximately five times that of water and may vary under different conditions the full Poiseulle equation becomes 4 FPP x or transposing Resistance (h) = ? Pax 1 Hemodynamics of Pulsatıng Streams while such physical principles are exceedingly useful in formulating elementary concepts of hemo dynamics they describe the forces which more blood through the arterial tree and into the capillaries iery incompletely This is prin cipally due to the fact that the conduits are elastie not rigd tubes and that a pulsating not a constant pres ure is created by the ven tricular pump The situation could be compared to a hypothetic ·1 CIRCUL ITOF) DY\AICS Hitat upp stem such 75 13 allu trateri figure 1 B, in which no Hon besition is attainable later can be lifted from 1 deep well to 16 palce and placed under pre sure b a combination lift and pi uure pump If such water were pumped through a rigid system * ter would flow out of opened faucets m & perexlie fashion accel (ritm with uh stroke of the pump and rapidly decelerating to 2010 during the period that water 18 bing lifted into the pump If however the conducting system were elastic as in the allustration it would expand and accommodate a part of the liquid during the trude and rucol durmg the filling time of the pump thus maintain Ing 1 constant flon from the faucets at a higher level While this illustrates the mechanism of the mammalian circulation in an elementary au preche theoretical hemodynamic deductions have proved difficult owing to the physical effects of vascular branch ing the variable caliber and distensibility of mu cular arteries the rcverberating pressure waves set up the change in viscosity which takes place through filtration o mosis or secretion in passage of blood through capillaries For the e rca ony theoretical deductions must still be tested by experimental studies on animals Experimental work has established the conditions which are oper tue in the normal mimmalian circulation With cach ventricular systole a certam volume of blood i iriously called the strohe solume systolic discharge or pulse i olume is expelled brusquely into the aorta In man this equals approximately 60 or 70 cc and the whole period of cjcction lasts only o 20 second or less Tully two thurds of the total trohe volume (about to c ) 19 displaced into the ascending nortn and arch within 0 1 second and sery little during the last Ou second of ejection since the ascending aorta and arch are already di tended under a pressure of 70 to 80 mm Hg it is obvious that space for wome 1) cc of blood must be made in an interu al of time which would be called instantaneous in photography This is accomplished partly by the forward mos ement of blood (hinctic energy of Sou) and partly by distention of the elastic aortic arch through an increase in pressure (potential energy of pressure) The pressure change thus creital is transmitted as 7 ne over the entire aorta and its many lirinchies down to the capillaries and causes sucre le expan one of mori penipheral segments of the arten al tree Olx souls this progresite expansion of the arterial wall from the aorth to the periphery must ·BASIC HEVODIC PRICIPI ES be accompanied by a forward mouement of blood so that arteries as far away as the donalis pedis are expanding before ventricular systole has terminated This pressure ware thus tranmitted at a rate of 8 to 15 meters per second and the evpansion and elongation of the ar terial wall which it induces constitute the palpable or recordable arterial pule Vore precisely the velocity with which this pressure wave is trans mitted penipherally depends on the distensibility characteristic of the vessels and on their degree of distention by internal pre sures According to Sands and Bazett et al ? the normal velocity is les in the more distensible aorta (about 3 to 4 meters 'sec ) than in the mus cular arteries of the limbs (about 7 to 14 meters/sec ) It thus point it is well to be reminded of another estabh hed fact Whereas the pressure wave normally travels at a rate of 3 to 14 meters per second and produces an arceleration of blood flow along the whole arterial tree the actual velocity with which corpuscular elements move is much slower for evample it averages only 18 cm et in the abdominal aorta and 14 or 15 cm/s in the femoral arteries In other words whereas the pressure wave reaches the vessels of the foot within 02 to 0 3 second it requires 2 5 seconds (or several heart beats) for the corpuscles ejected into the aorta during any heart beat to reach the foot The rea on for this may be clarified by the aid of the diagram in figure? Is in licated in the crosshatched area all of the blood ejerted during any systue is accommodated in the aortic réservoir This moves the blood within this segment to a more distal part of the arterial tree as indicated by the black area This in tum translocates blool to a third segment and so on The relation between the proparation of pressure and movement of the arterial blood rol umn has been aptly compared to the rapid transmission of force throu,h a row of billiard balls and the relatively slight onward move ment which the row of balls undergoes The Aortic Compression Chamber It is obous that the elastic aorta and to a le er extent the arteney derized from it constitute a continuous elastic chamber which takes up icon iderable volume of blood under pressure during systolic ejection With the clo ure of the semilunar valves at the end of ventricular systole the pres ure energy thus tored is gradually used to press blood out of the larger arteries through their branches and sub branches into the capillanes ·6 CIRCUI ATORY DYNAMICS Since the potential pressure energy 14 gradually conscried into kineti energy of flow the arterial pren lire slowly declines cluring clustole It is for this reason that the clastic rescrvoir which Insures a continu ous capilları flow has been designated as the compression chamber of the arterial system FIG -Diagram illustrating the translocation of blood in the aorta and some of its branches during three heart beata The Pressure Pulse and Its Transformation in Transmission By connecting highly response types of calibrated pressure re corders to vanous points in the arterial system 18 chematically indicated in figure 3 the details of the pressure changes during systole and diastole (an be recorded at vanous points of the arterial system In such records the tctual pressure existing at any moment of the cycle can be calculated and the rate of pressure transmision deter mined Figure 3 also illustrates the character and magnitude of the ·BASIC IIFVODYVAVIC PRINCIPLES pressure changes thu re orded from an aorta a radial and a femoral artery of the dog The whole pressure cure is designated the pres sure pulse The maximal pressure reached during sy stole is the sys olic pressure the minimal pressure realized at the end of diastole is the diastolic pressure and the numerical difference between these represents the pulse pressure The expansion of the ves cls which the pressure pulse produces in any part of the arterial s tem is the pulse 42 Fro 3-Diagram illustrating the principles of recording lateral pressure pulses from the aorta radial artery and femoral artery by optical manometers and the configuration of pressure pulses in these regions Insert diagram indı cates procedure for recording pulsatile changes of arteries A clear comprehension of these different terms and especially the differentiation between pressure pulse and pulse pressure is of the utmost importance in hemodynamic considerations to follow A glance at illustrations such as shown in figure 3 makes it apparent that the pressure pulses differ both a regards contour and systolic and dia stolie values m different parts of the artenal trec Under normal conditions the aortic pressure pul e n es sharply ·8 CIRCUL ITORI DINAVICS (a-b) and after a high anat rotic shoulder (b), gradually ri es to a rounded summit (b-c) The pressure then declines slightly during the latter third of sy stolie ejection (-1) until closure of the semi lunar valies which is signaled by a sharp shaped inasura (e) During diastole (0-1) the pressure declines asymptotically except for a slight Wave (1-8) A pressure pulse recorded simultaneously from a peripheral artery such as the radial reveals a different form of pre ure pulse The bo ginning of the pulse is delayed it rises less abruptly to 1 peaked and carlier summit (a b) The sy stolic pressure tihen nt this point docs not devate greatly from that in the porta but it may be a little higher depending on the state of contraction of the mu cular artcncs Jaung passed the park the pressure fills smoothly to a lower level (luring late stole (1-c) and early chastole (c) to the dicrotic notch (d) and thereafter acquires a prominent dıerotic wave (e-f) superimpo ed on its slow diastolie decline The ene drustolic pressure ad un is nearly equal to that of the aorta Similar changes tahe place in the femorul pressure pule but the rise 19 much more abript the peak is sharper ind the systolic pres sure reached crccedls that of the aorta, often by as much as 20 or 30 mm Hg The diastolic decline of pressure during late apstole (h-e) and early dastole (c-d) is also morc ibript and the decrotic notch and wave become more conspicuous than in records from the radial artery It may be added that similar pres ure pulses recorded from still more peripheral arteries such as the dorsalis pedis shou (sen greiter augmentation of the sistolic pres inc Obuously a hemoly namic explanation is required which enables us to comprehend how an onward movement of blood can take place during sy stole when pres sure is higher in the femoral artery than it 1in the aorta An inser I found in the fact that the pressure penh is reached Inter in the peripheral than in the central i essels aortic pressure exceeds femoral pressure significantly during the early portion of systole but 1 re versc pressure gradient temporarily superi enes during the latter part of systole which actually allows a backflow of blood toward the aorta : The Phenomena of Damping and II ate Summation I clear under standing of the problem demands an inalysis of the hemodynamic phenomena which bring about temporal distortions of pressure pulses ·BASIC HETODISI RISCIPLES in different arternes lhe transformation of the central to the peripheral pul take place chiefly through the operation of two major fartorgum champing und wate summation 1 The 51st bloodi m the clasſic compression Chamber acts as & liquid sboch absorber by virtue of which minor abrupt pressure changes are smoothed away and the rates of pressure see and fall are retarded This phenomeOn 18 (alled damping is a result the 0 02 03 04 05 06 07 100- Ts 4 Dagram eltu trating the ringspl s of daming and wave summa tion in the arterial selem sortie pressure pule B changes in contour and amplitude due to dam se mature of rebound wave D surmation of currey Bani( Ordinate prey ure in mm llg Ilse 49 ac in 0 I Bec contour of the central pressure wave 1 sschinged to that of wate B 331 figure + ? The forward impulse of tlie centrifugal prosaure uale causes the hloost column to rebomst from regions of suddenly increzsing re exstance thus guy ny to n decrementing diphase centnpetal wale *xxh as illustrated in curie ( of figure ! Sme both of these 1&109 are procent in the saint item of tubes thes sumate and cause a resultant preasure pusier such as shown w eurie D of figure Th ·10 CIRCI I \TORY DIVAMICS obviously has all the distinguushing charuturistics of px ripheral pulses exhibited in figure 3 the pressure continues to the so that in the radial artery sj stolu pre cure agum equals that in the aorta and in the femoral and dorsalı» peclis urtaries it exceeds aorta pressure by 20 to 30 mm Hg Similarly a summation of the two mies causes the di crotic notch and ware It is at present the consensus that the induced oscillation is a stationary pressure ware in the aorta proluced by a positive rebound or reflection of the blood column from a point of rapidly increasing peripheral resi tance which in effect reproduces the phenomena physically recognized in a clo ed tube but the locus of reflection is not agreed upon Rerent ob criations indicate that certainly under abnormal conditions and perhaps even under normal conditions the induced oscillation muy begin with a negative instead of a positive phase Summarizing the sudden uptake of blood by the aorta during a tole and the gradual reconversion of pressure energy to flow during diastole give rise to a characteristic pressure pulse in the norta In its progressive transmission to peripheral branching arteries damping of this fundamental ware tends to obliterate the finer oscillations to retard the rate of pressure clevation and to reduce the pressure pcal attained However the sudden impact causes a reflected pres sure ware wluch summates with the fundamental nase in such a way that the peak pressure is restored to aortic systolic les cls as m the radial or exceeds it as in the femoral In addition the diastolic limb is distorted by the accession of a negatn e dicrotic notch and a positive di rotic wave As a result of the changes in the systolic portion of the peripheral pressure pulse a large volume of blood is first moved on ward in the femoral artery during early sy stole but a part of this blood flows bach during the latter period of ystole lluman Systolic and Diastolic Pressures The maximal and minimal pressures temporarily present in any artery-by definition the systolic and diastolic pressures--can now he recorded from accessible arteries by use of calibrated hypodermic manometers and they have even been recorded from the norta through rrec of intra arterial catheters The e momentary preasures ran of course be more con eniently measured by means of modern sphyg momanometers with the aid of proper teclinic? Comprison of in ·BASIC IIEVODINAVIC PRIVCIPLES 11 direct and direct methods for determining arterial pressure in the brachial artery induates that systolic and diastolic pressures can be determined with reasonable accuracy when the respective cuff pres sures are rend at the time that ounds appear and disappear in the cubital artery ? The theoretical principles which underlie the use of these sound phenomena as enteria of systolic and diastolic pressures can be illustrated as in figure 5 Ov 1 120 SOUNDS 100 988 00. $0 PRO IM L GRACMIAL PRESSURE PRO MA BAACHIA P 5 20 DITAL BAN IA MARIS NG WITH OCCIDIC PR R DSTA BRACH PRO SU SWTH WI ATCE PRI BIG 5-Diagrams ind cating theoretical foundation for determination of systolic and diastolic arterial pressures by palpation and auscultation To right dynamic con litions during comų lete occlusion of a compressed segment Tol ft dynamic conditions in proximal an ldistal arteries including intensity of auscultatory 8 un 14 during s rial decompresson of artery Ordinates indt cate intra arterial pressure except last column of numerals which indicates cuff pressures As long as extra arterial pressure exceeds intra arterial stolic pres ure (left diagram) the artenal segment under the compression cuff remains collapsed The arteries distal to the cuff empty and at tain equilibrium with capıllary and venous pressures at approxi mately 20 mm Hg Systolic pressure in the provim ul artery rises a trifle above its normal value owing to an impact and reflection of pressure from the orcluded vessel (Walthy and liiggers') When pressure in the cuff is allowed to fall progressively to or below intra arterial diastolic pressure (nght diagram of fiz 5) larger and larger segments of the proximal pressure pul e penetrate the com pressed segment with the result that the distal arteries fill and the ·12 CIRCUL 'TORI DIVVICS peripheral pulse increases up to its normal amplitude Simultaneously hy drulic disturbances and, or changes in the irtenl walls the place which are responsible for the sharp ppm auscultitory younds of increasing thien diminishing intensity (145) The dynamic mechanisms which create the horothoff sounds and the factory which determine their mis and u mmg ay extra ar terial pressure falls to diastolic les els are not wholly understood The sharp snapping character of the sounds manifested althe on auscultation and registration would com to pret lude their cauration by turbulence peripheral to the cult for turbulence usually gne rre to murmurs not snapping wounds However turbulence may be a scuondary factor when a distinct murmurish phase desclops In 1919 Frlangerl presented experimental evidence whichu icon on int with the view that a water hammer effect is induced as blood rushes into the opening artery at high velocity Subsequent observations": on the movements of an related artery in a compres ton chamber brought to light evidence which seemed incompatible with such an cxplanation I he fuct that sounds arise in the distal end of the com pressed vessel and start as soon as the compreened segment contains a small diastolic residuum led Irlanger to the conclusion that a vibratory state develope as soon as the tr insmitted wire pisses through a partially filled in treti lied resel It increases as the diz stolic residuum augments during decompression it diminishes when the vessel comes under tension and disappears completely when the vessel is fully opened Simultaneous registration of pulses peripheral to the compression chamber while an artery wis being compressed revealed the existence of a series of harp was clets the most prom ment of which was usually negative immediately ahead of the rising limb of the pulse The first horothoff sound became audible in the artery beyond the compression chamber simultaneou ly with the des elopment of these wasclets is decompres ion proceeded the re corded wavelets increased in amplitude and compleuty mounting on the anacrotic limb The snapping sounds were thus attributed to this so called pre anacrotic phenomenon later ascribed by Bram well' to the breaking of a ware front In 1931 I runk and lezler's re described the phenomenon and concluded that it is produced by long tudinal stretching of the arterial walls Hoseier Franger in 1910 showed that this is not a necessary condition for dei clopment of the anacrotic phenomenon ·BASIC I VODYEIC PUI CIPLES 13 The appearance of the pre anacrotic vibrations superimposed on the pulse waves at various stages of decompression are shown in fig ure 6 \umerals have been arbitrarily assigned to indicate the relation of cuff pressures to assumed intra aftersal systolsc/diastolic pressures of 120/80 As illustrated in the lonest curse one of the early pulses to traserse a compressed segment of artery is characterized by a small negatne dip and a very steep positive eles ation followed by another dsp and a fex after ubrations These probably represent the first snapping sound which is heard the pre anncrotic ubratrong are 80 90. 100 110 118 Fit Gerses of actual pre sure pulse showing pre anacrotic phenomena folloxetty pt suure palar during various cuff pressures a hea arterial mustale and diastolic pressures are a sumei tole 1 and 80 mm Hx respersively Discussion in text succeeded in a non pressure wave of small amplstude As decompres 4109 proceeds (un es at 110 100 mm Ilgestra artersal pressure) the initial sharp negative oscillation is follonel by streper rices and larger after vibratione apparently related to the increasing intensity of Dawsusitatory simde They are followed by progre suely farger pulsce which start from hayher and her mtial lessis is extra stenal prevure (at al mit 90 mm W) approu big mitra arterial dsastola pressure the vibratios krome (varser and mount luglier on the pecuning limbs 1 resumably when extra arterial pressure at so mm Hg equals intra arterial diastolic pressure the sharp sound nurutions ·CIRCULITORY DIGICS disappear and a pure pul o sarcis recorded That stich registrations actually incorporate both the transmitted puke wasc and the sounds heard on auscultation cannot be questioned Their interpretation is still subject to personal opinion The author is not wholly satisfied with Bramwell s breaker hypothesis !? The cry steep rise of pressure displayed is certainly suggestic of a water hammer effect Factors Afccling Systolic and Diastolic Pressures In normal indu viduals having a systolic pressure of approximately 120 mm Hg and a diastolic pressure of about 80 mm IIg the equilibrium of the arterial system is such that the rhythmic discharges of the left ventricle main tain a small rescrie volume in the arterial compression chamber «lule the outflors from the arteries into the capillaries during systole and diastole equals the stroke volume 11 henever this equilibrium is disturbed by changes in heart rate strohe volume peripheral re sistance or arterial distensibility the peripheral outflow us dispro portionate to the input until a new state of equilibrium has been established When this has been attained the normal relation of sys tolic to diastolic pressure is altered The nature of the changes is studied to best advantage in artificial circulation schemes in which one factor can be altered at a time Such studies illustrated in figure y have shown that an increase in heart rate elevates diastolic pres sure more than sy stolic thus reducing the pulse pressure incrcase in strohe volume raises sy stolic pressure more than diastolic thereby in creasing the pulse pressure Augmentation of peripheral resistance elevates diastolic pressure more than sy stolic until diastolic distensi bility begins to dimmish drastically then systolic pressure rises pro gressively faster than diastolic until the pul e pressure actually er cceds the normal As illustrated by the solid lines in figure 8 the change in trend normally occurs approximately at levels of 100 mm Hg of diastolic pressure but considerable elevation of drustolic pres sure (to approximately 150 mm lig) is required before the pulse pres sure exceeds that existing at normal diastolic let els If however the destensibility of the arterial system is reduced by pathologic processes (as in arteriosclerosis and perhaps through functional changes in arterial walls) the pulse pressure amplitude begins to increase at lower diastolic pressure levels This 19 illustrated by the solid plus the dotted lines in figure 8 The dynamic changes responsible for the relative changes in sy stolic ·BASIC HEVODIYAVIC PRINCIPLF 15 and diastolic preasure and therefore in pul e pressure amplitude deserve a more complete analysis Comprehensible theoretical ex A B Fie 7-Records ol tained from artifieial circulation model illustrating ef Sects on systolic and lia. tolic pressure during and after (v y) alteration of van ous factors separately t effect of increasing heart rate B effect of increasing stroke volume C effect of increasing peripheral resistance within constant ranges of arterial distensibility D effect of re lueing distengt ility of arterial Bystem planations can be ha ed un postulations which in olie balanıcs be tween the systolic input into the aorta under different degrees of dis tention and the relatie outfion from all branches of the arterial tree ·16 CIRCULATORY DIIVICS during sy stolt and diastole In illu tration to which such an analysis fortuitously applice may be guien Suppose the heart beating at 7) bcats per minute delners strohe volumes of 70 cc cach into an clastic aorta Sufficient blood is moi ed along so that we may assume a run NORMAL ARTERIES комн SCLEROTIC ARTERIES PULSE PRESSURE AMPLITUDE wa 50 100 150 200 DIASTOLIC PRESSURE FIO 8-Diagram illustrating the anticipated changes in pulse pressure am plitude at different diastolic pressures in normal arterres (solid lines) and 10 sclerotic arteries (solid plus dash lincs) Discussion in text off from the whole arterul tree of u ce during systole and 15 cc during diastole If strohe volume peripheral resistance and cortic distensibility remun the same while the heart rate increases to 90 beats per minute the reserte volume in the arterial system becomes greater and diastolic pressure 1» eles ated when an equilibrium 1118 been attained relatuely more blood leaves the peripheral arterial ·BASIC FEHODYNAMIC PRINCIPI ES 17 sistem during sy stole owing to the elevation of mein systolic pres sure and less runoff during diastole oming to the abbreviation of this period Since more energ is converted to flow dunng systole and less proportionately during diastole a stolic pressure is raised less than diastolic pressure Hemodynamic studies have shown however that this type of logical analysis does not hold in the case of other deter minants of systolic and diastolic pressures and indeed is not the basic explanation for effects produred by heart rate changes The dynamic considerations even fail in simple circulation schema in which dow from a single tube with a controllable terminal resistance is uued For example when heart rate stroke volume and artenal distensi bihty all remain constant an increase in peripheral resistance causes a relatively greater elevation of diastolic pressure and a smaller pulse pressure Secording to thus concept one would need to postulato a redistribution of peripheral efflux so that a stolic outflow beromes relatively greater and diastolic outflow relatively less than under control conditions It has been shown in circulation models that contrary changes occur si stolic runoff 18 relatisely reduced a trifa and diastolic runoff corre pondingly increased The situation becomes even more complicated when the runoff from the arterial tree occurs through numerous branches with widely differing lengths and dif ferent coefficients of elastirity A better explanation is based on the relation which exists between the total volume of the arterial tree and the systolic uptake during ventricular contraction As long as the volume elasticity coefficient remains relatively constant this is expressed by the formula dp dp in which is the actual volume of the einstic arterial system di the sudden increment in its volume and dp the udden increment of pre sure proluced Translateri the formula can be written pulse pressure Y diastolic volume rem uns constant stroke volume During cardiac acceleration the stroke volume remains unrhanged but since the diastolic volume of the artenal system merea es pule pre sure must necesunly decrer e to balance the equation With increind systolic di charge the strohe volume increases more ·18 CINCUL 4TORY DINAMICS than the diastolic volume of the arterial system and pulse pressure must necessarily increase to balance the equation With augmented peripheral resrtance to outflon the diastolic volume increases while the systolic discharge remains constant As long as the coefficient of clasticity remuns unchanged the pulse pres gure decreases Under greater degrees of distention the distensibility of the arterial system decreases rapidly so that greater pressure in crements are required to stretch the walls and accommodate the normal systolic discharge Therefore systolic pressure mounts pro gressively with increasing peripheral resistance until the pulse prea sure exceeds the normal (tig 8) Similar supernormal pulse pressures can however develop at considerably lower diastolic pressures when the distensibility of arteries has been reduced When pulse rate stroke volume and peripheral resistance remain unchanged reduction in aortic distensibility per se auscs a slig! decline of diastolic pressure and a considerable nic of systolic pressure with pronounced increase in pulso pressure (fig 7) The Clinical Importance of Arterial Pulse Tracings The pulse represents the changes in diameter of vessels produced by internal changes in pulse pressure Sincc a lay in the response of arterial walls to internal pressures called hysteresis has been obseried ex perimentally in excised arterial strips 18 and in the aorta in situ follow ing protracted and drastic changes in diastolic distention the ques tron arises whether the pulse recorded from large arteries faithfully depicts the form and magnitude of the pressuire pulse There is no good evidence that hysteresis operates under stabilized conditions Simul taneous registrations from the interior and cxterior of a vessel gne curies which are identical within the limits of measurement the finer vibrations which occur during isometric contraction and during closure of the semilunar alves are accurately inscribed on central pulse tracings at proper pressure les els Arterial pulses can be recorded accurately from wuperficial arteries by firmly pressing a small funnel over an artery and connecting this with an optical recorder (see insert fig 3) Registration from deeper arte res such as the radial requires the use of special instruments called sphygmographıs the principles and operation of wuch are de scribed elsew here 18 ·BASIC NEMODYA 431C PRINCIPLES 19 Typical subclavian and radial pulses from a normal subject are reproduced i figure 9 It will be noted that their contours conform essentially to that of pressure pulses depicted in figure 3 Clinical Information Derned from Central Pulses The durations of systole and diastole and of the whole cycle but information regard ing temporal events of the cardiac cycle Normally, a definite and almont constant linear relationship eusts between total systole and cycle length This is the so called S/C ratio Graplis and formulae 120 100 80 De pod Ma F10 9 --IIuman subclavian and radısl pulses showing correspon lence of con tours with those of intra arterial pressure pulses Compare letters a hint re records with those in Sgure 3 By placing systolic and diastolic pressures deter mine i by ept ygmomanometry to top and bottom of euch curven an ordinate Bcale on left can be constructed Discussion in text for the expected average durations of systole at different kart rates have been constructed by different intestigators 18 ** Deviations fro the normal standard can be measured A permanent increase in the period of sy stole more than 0 2 second beyond the figure diar acteristic for a gn en heart rate suggests that the diastolic size of the ventricle is increased This may be caused by a greater senous se turn or through accumulation of blood during compan ataul path logic conditions Excessive abbrevntion of systole when the hes rate is rapid is frequently indicatne of a predominant acrelers nervous or adrenergic humoral influence Systole is al decreto ·20 CIRCULATORI DI AMICS during myocardial failure such as super enes during anoxia atrial fibrillation valvular insufficiency or hypertension In such cases abbreviation of cjection is usually associated with an elevation of venous pressure and increase in diastolie size The contour of the central puke gives useful information with re gard to the discharge process of the left ventricle under abnormal conditions Sescral typical deviations from the normal are shown in figure 10 When peripheral resistance is high and the aorta is normally distensible the pulse exhibits an initial steep risc followed by a rising plateau until the incisura When aortic re istance is low while the HIGH LOW LOW AORTIC RESISTANCE AORTIC RESISTANCE SYSTOLIC DISCHARGE NORMAL CENTRAL RADIAL CENTRAL À RADIAL MILD SEYERE DIMINISHED AORTIC DISTENSIBILITY STENOSS AORTIC INSUFFICIENCY Fro 10 - Illustrations of changes in contour and amplitude of subclavian and radial pulses under abnormal cardiovascular conditions Discussion in text Tote changes in transmission rates stroke volume remains good the pulse curve displays a preliminary peak due to a momentary fling of blood in the lax arterial system This is followed by a lower systolic summit succeeded by a rapid de cline and a deep incisural drop to a low diastolic level When the stroke volume is small the pulse displays a smooth rounded curte during systole and a los flat segment during diastole Diminished distensi bility of the aorta is characterized by a rapid ascent of a large pulve Have a high incisura and a gradual asymptotic decline during dia stole Lesions of the aortic valves cause distinctie pulse patterns Aortic stenosis results in a small pulse initiated by a brief sharp risc which is succeeded by a sharp anacrotic inchura This in turn is followed by a slowly rising systolic plateau upon which murmur vibra ·BISIC HEWODYNAMIC PNINCIPLES 21 tions are superimposed ortic regurgitation is always accompanied by a large pulse for the diastolic pre sure is low and the pulse pressure large The magnitude of the regurgitation is generally reflected in the diastolic decline in small lenks the declmc occurs gradually during diastole m large leaks it takes place immediately after the incisura The reasons for these changes tre discussed in Chapter III Clinical I aluc of hadial and l'emoral Pulses While the registration or palpation of these pul ps offers a convenient method for estimating heart rate and for discovering or even adentifying arrhythmias it should be apparent that their value an estimatmg performance of the left ventricle is decidedly reduced by virtue of physical changes in transmission of the pressure puls levertheless significant changes accompany some of the conditions discussed above l'or example in arteriosclerosis the approach to a more rigid state allows a more rupul and faithful transmision of pre ure to the periphery so that as illustrated in figure 10 a definite and istra may be present in states of high peripher il resistance or reduced cardiac output the cures are chiefly characterized by changes m their amplitude In aortic stenosis the rise of the ascending limb is very much retarded ind may display an inacrotic notch the chief churcteristics of severe aortic insufficiency consist of a rapid ri с of pressure to a hi,h miximum gung rive to the palpatory sensation deseribed as water hammer and a rapid decline of pre sure with abolition of the dicrotic ware decribed as the palpatory scusation of cullap The water hammer and collap ing features together constitute the Corrigan pule Reconstructed Pressure Pulecs in Van Obviously the pul e curies just describe give only the contour of pres ure variations within an artery they are devoll of orclinate values If at the time that central pulse trulingirc recorded systolic and diastolic pressures are meas ured in the brachial artery no great error 15 incurred in placing these values at the summit and foot of an arterial puke and subdividing thesc pre sure value proportionately over the spin This procedure 18 ahonn m figure 11 In this bly a pressure pul c such as could be recorded ductly from tlıc interior of in artery can be recon tructed with a reasonable degree of fidelity Trom such recon fructions in which the ordinate ale is projected to zero it is posible to make a number of constructions from which important dynami informition can be derived For instance a pres ·22 CIRCULATORI DYN 131ICS sure pulse (schematically shown in figure 11) may be integrated to determine mean pres ure (P.) during an (dle by measuring the pressure area under such a cure and determining its 11 crage height Since «uch integration takes cogniz ince of the contour of the pres surt pulse the mean pressure so determined is more reliable than ir nous propo el formulations wuch arbitrarily estimate I. as one half systolic + duistolit pressure or diastolic pres ure + pulse pressure etc Obviously uch mein pressure 19 only a theoretic one mm Hg 150 B C Psm 100 F x Pm Pam E 50 0 A D G FIG 11 - Diagram allustrating the integration of a central pressure pulse for accurate determinations of mean cyclic pressure (I.) mean systolic pres sure (Pm) mean diastolic pressure (Pon) and the fractions of systolic mean pressure which represent static effort (?) and dynamic effort (V) Discussion in text (After CJ Wiggers Physiology of Shock courtesy of the Common wealth Fund) out it is highly important in calculating peripheral resistance (see belon) It is also possible to determine the mean pressure which er ists during systole (Pm) or diastole (Pam) respectively by converting the pressure curse during these phases into two theoretic rectangles (ABC D and DEFG) Under certain conditions a knowledge of the systolic and diastolic mean pressures is very important The mean diastolic pressure is a dominant determinant of coronary flow whereas the mean sy stolic pressure (P.) rather than the mean cyclic pressure (Pm) should be used in calculations of cardiac Work In arteriosclerosis aortic insufficiency and hyperten ion P - greatly exceeds Pån indi ·BASIC HELIODYNAVIC PRI\CIPLES 23 area 1 cating that the runoff from the arterial system is much greater during systole than during diastole The capillary pulse often observed in these conditions is thus explained by the altered dynamics of the cir culation Unfortunately changes from normal P./Pam ratios cannot be used as a quantitative index of the relative influx into capillaries during systole and diastole Apparenth different lengths and diame ters of arteries leading from the rorta to capillaries affect regional outflows through variable damping and peripheral pressure chamber effects 15 The pressures during systole can again be divided into components illustrated by the areas I and Y of figure 11 The total pre ure energy represented by area I equals the pressure energy that the left ven tricle is required to expend as static effort in maintaining pressure at a diastolic level If the ventricle should develop only sufficient pres sure for this purpose as frequently happens in early premature con tractions no ejection could occur (see Chapter III) The pressure de veloped over and above this (area 1) on the contrary is expended in the forward movement of blood Consequently the quotient area Y can be recorded as an index of the economy of effort during ejection (Wiggers and Katz") While such a quotient is not equivalent to the mechanical efficiency of the left ventricle (work energy total energy studies on the energetics of muscular contractions suggest that it may under varying dynamic conditions alter directionally if not quan titatively as the mechanical efficiency Estimation of Stroke I olume and Cardiac Output Vany attempts have been made to utilize data supplied by pres ure pulses for esti mation of stroke volume and through multiplication by heart rate of cardiac output per minute The simplest criterion involves the use of pulse pressure In 1904 Erlanger and Hooker?? suggested that the pulse pressure is dominantly affected by changes in stroke volume thus the product of pulse pressure and heart rate should serve as + furr index of directional changes in cardiac output \l'hile this criterion muv have some predictive value when its use is limited to the sturls of changes in cardiac output in the same subject the current conscti u is that it is not reliable in comparing the cardiac outputs of different individuals because the arterial distensibilits encountered in differ ent individuals i unes so greatls : Attempts to take cogniz ince of the ·21 CIRCULATORY DIAVICS distensibility characteristic of the aorta by relating pul-c pressure to PP PI dastolic mcan or some arbitrary value (eg Pd + (P) (P) PP Pd+P p) have also not proved sticcessful ? I number of investigators hue made serious efforts to cmplo: other information supplied by pres lire pul-es in the calculation of stroke volume I discussion of the e procedures would curry us tou far afield 1 summirs can be found elsewhere? The technic requires specialized training to av ord pitfalls Vost important comprisons of cardiac output by these methods and use of the Fich principle have not been found consistently fuorable Those who report consistent results admit that the integration procese innot be applied to ab normal types of pressure contours and finally the procedure 19 as yet not applicable to human beings 23 (See also llexandler ) 1 hc Dynamics of Ilypertension Clinical studies strongly support the view that essential hyperten sion is not basically accounted for through increase in heart rate stroke volume or blood visconty hence the infcreme based on Poreuilles luthit increased peripheral resistance must necessarily be the primary fructor The (oncept of Peripheral Resistance Resistance to Now of blood is encountered throuliout the arterial tree To judge from the decline in mean (y clic pressure from thic aorta to the termin il branches of the arterial tree in normal subjects this resistance according to I runk amounts to about 20 per cent of the total resistance lIowever the minute vessel including arterioles metarterioles and capillarica constitute the chief areas of changmg peripheral resistance The adjective peripheral therefort rcfers solely to the minute distal vos els of the arterial tree regardless of whether they are located in the interior or on the surf uc of the body Some confu ton on this point occasionally arises because in mu pristine circulation in superfiul vessels is also referred to as the peripheral arculation Peripheral resistance is determined by all factors which tend to impede the flow of blood from branches of the arterial tice Tlieve in clude (a) passive factors such as the equlibrium between intra and extravascular pres ures and the resistance offered by venous pres ·BASIC HEMODINAVIC PRINCIPLES sure di tal to capillaries and (b) active factors such as changes in the calher of arterioles produced by 59somntor action Physically and Hcording to Poreulles las resistance is determmed by the char acteristic of the tube (length diameter and blood viscosity (1)) In applying loreules lzu der al from the study of flows through rigid tubes to put atmg floud m distic systems such as the arteries A numlys of re ervations must be made a caletrations Eccording to formulation peripheral resistance is u ually treatel as though the chiameter and length of minute vessele remzi1} (entially constant with moreang pre ure ind turmgchinges of pressure in the cardise, cycle Ictually diret MEFON OPIC ob ration, andate that is els expand and retract passively with chwgrs in prossure They have alo revealed that the minute ses cly of many regions undergo 113 termittent change in size-sometimes to the point of complete ob literation The fact that this intermittence or curs out of phasc in different regions probably are out for the relatnely con tant arterial pressure mamtamedi in the larger arteries 11 hen there arations be come synchronized they give me to the well knonn vasomotor or Traube lerng 12ves of urter pressure In order to simplify hemouls nomir an aly 19 mall arteries and arterioles huic generally been treated 24 though thses brauched di chotomously into spillaries and the remistince has been computex from the respective lengths and lumeters of sucre ne linear met ments such a welion fuls to tzke kegu zance of large and small Arteriovenoue pluunts the irpillary hunts de rest by Chambers and 7cfarb ver the rumorous 1919 o the pleen) hver and heist ets the possosbity houlet tse hept in mind that closure of arter enous situath and contraction of precapıllar: phincters rather than active change in the arterioles leuling directly into capillaries constitute the true topy och of the Orculation The Uscouty factor whub enters into l visculle 4 canation 19 4 truhs component to eval trate 191 the buds The si soesty of blood pretermined 133 trois entirely different from that of the came blood flowing througit capil laries of an ang 111 1hre : !!! pitt due to effects that the soul! x) ameters « manillaries luule (1360 it ud in purt to the inter range of pie ma w takes place on the region A}o the real Corpus les alter is slet their pt age through eapıllarien as a result of the interchange of g The concentration of corpuscles ulzzed ·26 CIRCULATORI DI VICS takes place particularly in the lunes after extraction of the glomeru lar filtrate 18 ? 111d example of changes in 114cosity which take place within the capillaries themselves It is therefore not surprising that most observers have failed to find a linear relation between pre sure and flou in most organs stud ied including sheletal muscle kidney and lungs (I or references see liggers ") According to Green the minute vessels may dilate pissively or new capillaries and I-T anastomoses may open as arterial pressure eles ates from low to high levels The effect which these pissive changes have on calculations of peripheral resistance must be established before vasomotor action can be mfcrred from pressure/flox relations The foregoing discussion should make it obvious that changes in peripheral resistance many region cannot be derived from simple application of Poiseuilles las Tor con estimates of changes in vis cosity be deduced bjuggling the factors in Poiseuilles equation Vany tyros in hemody nimic investigation have fallen into the e traps The Concept of Total Peripheral Resistance The re istance of the arterial system cannot be calculated as in a branching and rebranch mg tube in which all of the liquid flous through a single ct of terminal ve scls of mmute size 1 he architecture of the arterial tree is such that organs and tissues are supplied through many parallel urcuits each with its own resist inee A mechanical concept of such shunts each with its own resistance (Trg etc ) is schematized in the diagram of figure 12 The term total peripher il resistance (1 PR) translated from the German Gesamt 1l zderstandt signifies the resultant resistance to efflux from mins parallel circuits such as exist in the borly Theoreti cally such a total resistance may be calculated as in electric circuits 1 1 1 + IPR ri Since, under stabilized conditions the cfflux from ill of these circuits over a certain time interval equals the cardiac output over the same period TPR cu be expressed as men aortic pressure duided by cardiac output Such calculations have been used extensively in at tempts to differentiate changes in arterial pres ure due to cardiac 1 + r3 Is

·27
BASIC IIFVODINAVIC PRINCIPLES
1
or total peripheral resistance factors They must however be used
with a keen recognition of their limitations The resultant resistantes
ODNE
ORGAN
KINDLIMas
FIG 19-Diagram illustrating the rinciple of parallel resistances in the
circulatory system (After CJ Wiggers Bull 1 Icad Vied courtesy of
New York Academy of Medicine )
in numerous parallel circuits do not indicate that similar directional
changes are nece arily taking plare in all vascular terntories or or
gans the resistance my indeed increa e in some regions and decrease

·28 CIHCL L4TORI DEVAMICS B all others il lule it is the consensus that alth calculations of FPR in the present of moler itu ch uges on mein arterial pressure do mdicate directioual changes it is not a necessir inference that such changes are occ1110ned by iromotor action walls the fuct that I'R (an be cipressed in numeri ulumits perhaps gives a fal carnst of quantita tion which does not cust I nuts of hrustaner In electrical plitsus the ritio of clectromotre force to current flow is designated by a unit known as the ohm It has cemed destrable to have similar hydraulic units of resistanc The most widely used formula reduces all values to cge units 1 PR = merun pressure v mm Hg 13 6 x 980 cardiac output (cc /sec) me un pre sure v 1332 cardiac output (cc/«cc) dy nes scc/cm The author las designated this as the ab olute unit (nu) but oning to its small magnitude a lirge ab olute unit (1 l)equalıng 1000 a u seems more serticeable in the study of territorial resistances In order to avoid calrulation of mm llg into absolute units Green and huis associates suggested is a unit PRI an abbreviation for the term peripheral resistance imit this defined as mean arterial pressure (mm Hg) flow in cc/min This unit is hones er so large that TPR would cqual approximatels 1 00 PRU Bizett has suggested the formula R = 3 mean arterial pressure (mm Ilg) cardiac index which gives a normal value of about 100 However it has been ques tioned whether it is desirable to mtroduce surface area into such equi tions A unit suitable for all occasions has so far not been es oli ed (See discussion Iliggers) The Interpretation of Changes in Pressure Pulses and Pulse I ressure of llypertension If as 13 generally concelled hypertension is chiefly occasioned by increase in peripheral resistance, the pulse pres ure would be expected to diminish at least until diastolic pressure er ·BASIC HEMODY MIC PPINCIPLES 29 ceeds 100 mm Hg Ictually clinical studies have revealed that sua tolic pressure 15 elevated comparatuely more than diastolic and that the pul e pressure exceeds normal values The explanation would appear to be that the proceses which cause contraction of the ar terioles also act to reduce the extensibility of larger arteries com prising the compression chamber and thus virtually art as milder forms of arterio clero is The following evidence has been brought forward on previous occasions to support this theory (1) If we compute total peripheral resistance (TPR) in normal subjects and in patients with varying degrees of hypertension the curve of TPR and mean bloor pressure are not parallel many discrepancies exist between the degree of hypertension and calculated CPR Thus cases are found in which a high mean pressure is associated with a nearls normal TPR and others m which a relatively slight eles ation of mean pressure shows a lugh TPR (2) If the rentral and peripheral arterial pul es are recorded from patients having diastolic pre- ures over 90 mm Hg and a high systolic pressure they fail to show the contour changes characteristic of an increase in peripheral resistance alone All have earmarks of pres ures transmitted over less distensible tubes as ollu trated in figure 10 (3) Experimental evidence has been adduced that acute hypertension produced by va ocon trictor drugs is accompanied by a reduction in the caliber and disten ibility of the aorta If these hemodynamic considerations are correct the common in terpretation of the significance of diastolic pressure reading in hy pertensie states requires revision It is a common impression that elevation of systolic pressure even though considerable ) not too Serious as long as diastolic pressure remains lon According to hemodynamic lans and the evidence which has been submitted it would seem to indicate a reduction of arterial distensibility ie either de velopment of arteriosclerotic changes or diminution of aortic dis tensibility due to functional mechanisms The real reason why a high diastolic pre sure is apparently more unfavorable for the left sentricle can be clanied by again referring to figure 11 It is obvious that the higher the diastolic preure the greater the static effort (1) which must be de eloped before blood is ejected into the aorta Con equently the question presents it elf whether the left ventrcle contracting against a higher dia tolic pren 1 ·30 CIRCULATORY DY\AVICS sure operates less efficiently than under normal conditions lo study this problem ll right and his associites** compared the cconomy of effort in hearts of 81 normal and 51 hypertensie subjects hi determin ing the ratio of the static and dynamic components accordmg to the method outlined Their survey rei erled that the economy of effort in hearts of normal medical students instructors and attendants ranges from 0215 to 0 880 with a median of 0 428 Ils pertensive patients showed a wider range of the index namely from 0 220 to 1 030 However 70 per cent had an index above 0 428 the median of the normal group The encouraging fact emerges from such studies that a large proportion of hypertensies display an economy of effort inder which equals or exceeds that of normal subjects Analyzed with respect to age persons 50 years of age or more tend to have a better economy of effort inder than younger hypertensives Summary 1 The factors concerned with the flow of blood in the arterial sys tem are basically expressed by Poiseuille s law but this formulation describes the dynamics of pulsating streams in elastic vessels only partially 2 Each ventricular sy stole forces blood into an already filled and stretched aorta partly by moving the existing column peripherally and partly by further distension of the aorta and its branches Dur ing diastole the gradual recoil of the elastic w ulls causes the flow of blood to continue out of the arterial system through arterioles into capillaries The steady flow through capillaries is thus achieved by the compression chamber funcion of the aorta and the volume of capillary flow is determined by vasomotor changes in arterioles which act as the stopcochs of the circulation 3 The phasic changes of pressure during systole and diastolodirectly recordable from the arterial system-are called the pulse pressure The highest and lowest pressures momentarily reached dur ing systole and diastole respectu ely arc by definition the systolic and diastolic pressures and their difference is the pulse pressure The changes in the diameters of large arteries which conform to internal pressure changes constitute the pulse 4 The contour of the central pressurt pulse is altered in its trans mis on to peripheral arteries such as the radial and femoral by ·BASIC HEMODYNAMIC PRINCIPLES 31 (a) damping of the basic transmitted pressure ware and (b) by summa tion with a diphasic reflected wave The former tends to reduce and the latter to raise systolic pressure over that in the aorta 5 The mechanism of the Korotkoff sounds commonly employed as criteria in the estimation of human arterial pressure is discussed 6 The relative changes in systolic and diastolic pressures often allow inferences as to the cause of blood pressure readings which des rate from normal standards Thus assuming a normal state of arterial distensibility pule pressure increases as a result of augmented strohe volume it is reduced by cardiac acceleration and up to dia stolu pres ure of approximately 100 mm Hg by increased peripheral resistance Above this diastolic pressure and at louer pressures when aortic distensibility is reluced pulse pressure increases steadily The reasons for these effects are given 7 Properly recorded pulses from central arteries permit important deductions regarding cardiac behavior (a) by calculation of the tem poral relations of sy stole to cycle length (S/C ratio) and (b) by dis tinctne changes in pulse contours The latter are described and il lustrated 8 Central pulses ein be converted to central pressure pulses with rcasonable accuracy by placing systolic and diastolic pressure read ings obtained from the brachial artery as ordinates for the summits and troughs of pres ure curies Through integration of such curven mein cyclic mean systolic and mean diastolic pressures can be esti mated The value of each of these in hemodynamic analysis is dis cused Peconstructed pressure pul es also enable one to evaluate the economy of left ventricular effort 9 The architecture of the arterial system is such that many shunt circuits are derived from the aorta before its bifurcation into the aliac arteries Each of these circuits has its vanable regional re istance The resultant or so called total peripheral resistance (TPR) 1» de termined by ianations in the various regional resistance A number of units of resis nce are defined and cautions are gren the possibility of drawing unwarranted interpretations from numerical data thus dernied 10 The hemodynamie principles discussed are applied to the prob lein of human hypertension This condition is not satı factorily char acterized as a di order of augmented total peripheral resistance ·32 CIRCEL ITORI DI NABIICY reduced distensibility of large arteries organic or functional in nature, must be assumed to account for the characteristic changes in arterial pules and pulse pressures ? he encouraging fact emerges that a large proportion of hypertensies particularly in the older age groups mamtain an economy of effort of the left ventricle which equals or exceeds that of normal subjects REFERENCES SIND JAVE Studies in pulse wave velocity II I ulse velocity in patho logical conditions im J Physiol 71 519 19% * BAZETT H C COTTON FS LAPLACE L B AVD Scott JC Calculation of cardiac output and effective peripheral resistance from blood pressure measurements with an appendis on the size of the aorta in man Am J I hy siol 113 312 1933 WRIGHT GW AND I HELPs Comparison of procedures for increising blood flow to limbs using improved optical plethysmograph J Clin In vestigation 19 273 1910 HIPLEY RL GREGG DE AND SCITROEDER TT An experimental study of flow patterns in various peripheral Arturica Am j Physiol 138 (18 1913 WAITTLESEY R T Dynamic changes in arterial pre sure pulses produced by simulated saccular aneurysm Am J I hy 810168 192 19.? • \LEXANDER RS Factors determining the contour of pre sure pulses re corded from the aorta Federation Proc 1957 (in press) * BORDLEY JAMES III Corvon CHARLES 4 RJAVILTON 1 F JERR WJ AND WIGGERS CJ Recommendations for human blood pressure determinations by sphygmomanometers Circulation 4 503 1951 • VALTBY ALICE B AND WIGCERS C J Studies in human blood pressure criteria and methods | Effect of partial and complete occlusion on actual pressures in compressed arteries Am J Physiol 100 601 1939 LOR'S IM The nature and time relations of the compression sounds of horothoff in man Am J Ihysiol 76 217 1996 " I'RLANER J Studies in blood pressure estimatton by indirect methods Il Vechanism of the compression sounds Am J Physiol 10 8 1916 I - Studies in blood pressure estimation by indirect methods III Vove ments in the artery under compression during blood pressure determina trons Am J Physiol 55 84 1921 12 BRANN ELL J C The change in form of the pul e nave in the course of transmission Heart 1 23 1925 1) FRANKO AND WEZLER K Die Bestimmung des Blutdruchs beim Vien schen 2tschr í Biol 91 439 1931 14 ] RLANGER J Relation of longitudinal ten ion of an artery to the prcana crotic (breaker) phenomenon Am Heart J 19 399 1910 1* WIGGERS C J Influence of yoseular factors on mean pressure pulse preg sure and phasic peripheral flow Am J I hy stol 123 614 1935 ·BASIC HEVODYNAMIC PRINCIPLES 33 19 ][ ANILTON HF REVICTOX J W 410 Dow P Determination of the propagation selocity of the arterial pulse wave Am J Physiol 144 591 1915 IVICCERS CJ AND WECRIA R Active changes in size and distensibility of the aorta during acute hypertension Am J Physiol 124 603 1934 Circulation in Health and Di ease ed I hiladelphia Les and Felger 1993 Pp 190 FT I OMBARD HP AND COPE O V Duration of the systole of the left ven tricle of man im J Physiol 77 263 1996 2 WICCERS CJ I hygiology in Health and Disease ed 5 Phila lelphia Lea and Febiger 1949 Pp 6 9 and As and haiz L \ The static and dynamic effort of the heart during ejection Am J Phy8:01 85 297 1998 HOOKER DRAND ERLANGER J An experimental study of blool pressure and of pulse pressure Johns Hopkins Hosp Rep 12 145 1904 I EMINGTON JW TOBACX CR HAMILTOY W F AND GOLD JJ Volume elasticity characteristics of the human aorta and prediction of the stroke volume from the pressure pulse 4m J Physiol 159 99 1948 WICCER C J Peripheral circulation Ann Rev Physiol 990 191, GREEN HD LEN IS RACER O N D AND HELJER A L Blood flon penipleral re istance and vascular tonus with observations on the relationship between I lood flow and cutaneous temperature Am J I hys 101 141 519 1914 16 WIGGERS C J Physical and physiological aspects of arteriosclerosis and hypertension Ann Int Med 6 19 1937 The dynamics of hypertension Am Heart J 16 515 1938 WRIGHT GW HALLARAY WR AND WIGGERS CJCconomy of effort index for hearts of normal and I ypertensive subjects Am J Physiot 1'6 89 1939 ·CHAPTER II Determinants of Cardiac Performance* - DURIAG the past 50 years progress in the study of heart di case has been achici ed over different pathuais! {mong these in the elin ical application of instrumentations and technics originally designed in and limited to physiologie laboratories Since my entn into med ical school in 1901 I have witnessed the succesulle employment of sphygmographs phlebograplis apex beat recorders sphygmomanom eters plethysmogr roentgenographs electrocardiographs and phonocardiographs Some of these have not suruned the dictates of experimental fashions and are known to the present generation only as muscum preces or text figuren? if at all They were retired from the armamentarium of clinicians because the information gained did not appear commensurate with the time and effort iequired for their proper use with the development of high fidelity pressure recorders in laboratories and the demonstrited safety of arterial punctures and cardiac catheterization in hospitals we have entered an era in which circulatory dering ments are being intensii cly studied through the interpretation of cardiac outputs and of pressure pulses recorded directly from the cirdine chambers and large vessels The interpreta tion of circulatory dynamics by such procedures requires not only a comparison of data from human subjects in health and discuse but also the utilization of information derned from more controllable experiments on animals lle can obviously not hope to comprehend the processes through which organisms die unless we understand the mechanisms which keep them alre The purposes of this review are (1) to restate briefly some important cxperimental results on cardiae performance (2) to re examine con cisely the deductions theories and concepts of cardiae behavior to Communication presented before tlpha of Kentucky tipha Omega Alpha Louisville hy Vay 18 19,1 and at Section Pathology & Physiology Ameri can Medical Association Atlantic City J June 13 1951 31 ·DETERMINANTS OF CARDIAC PFRFORVAVCE 35 which they have given rie and (3) to attempt a resynthesis of evi dence into a modern physiologic concept of myocardial regulation Such a process of modernization nyols es a di orcement of factual data from theories and the integration of successive discoveries with classical ones of the past when this is done it frequently happens as in this instance that very old laws of cardiac behavior have merely been given more extended applications rather than that essentially new ones have been discovered Three Classic Dıscoreries 1 In 1869 a young American Dr H P Bow ditch undertook the study of physiology in Ludwigs faboratory in Leipzig His investi gation on the apex of the frog s ventricle publi hed in 1871% has be come a classic in physiology He showed that if the condition of the heart muscle rernains unaltered the contrartions remain equal re gardless of the strength of stimuli applied 4s Ranvier expressed at the heart s motto is all or none The paradox that the ventricles can obviously alter the vigor of their contractions under normal as well as pathologic conditions was explained by another observation in the same investigation namely that excitation of the resting frog s ventricle by successaie shocks of the same intensity at short in terials results in a progressive increase in amplitude of contractions The phenomena called treppe or staircase is obviously occasioned by the fact that each stimulus exerts a beneficial after-effect on the responsiveness of cardiac mu cle Summarizing the lan of all or none implies that cardiac muscle either does not contract at all or responds to the fullest extent but the magnitude of the all or none response is determined by the in herent condition of the muscle 2 In 1884 Honell and Donaldson' presented unequivocal evidence that the dog s heurt has intrinsic mechanisms by which its output is nicely adju ted to the venous input Using the \ewell Martin heart lung preparation it was found that augmentation of venous inflow to a beurt weighing 76 Gm caused the cardiac output to increase from 480 to 1964 cc per minute the strohe volume from 52 to 21 6 cc and the right trial pressure from 10 to 60 cm of blood The compen sation for increasing olumes of venous retum was not quite perfect however incre ises in output of the left ventricle laggerl progressrely ·36 CIRCULATORY DYNAMICS behind the available supply of blood in the cnous reservoirs lpon reducing i cnous inflon so that atrul pressure ſell to the original les el of 10 cm of blood cardırc output dropped to 400 cc and the stroke volume to 238 ce which indicated that the performance had de teriorated slightly after a short period of strain 3 In 1895, O Frank' published his miestigations on the di 119mics of heart muscle Hus object was to rorrelate as far as possi ble the mechanical reactions of cardiac muscle with the well known responses of sheletal musele previously established by Fick J von brey and Blix It should be recalled that these investigators had established a relationship between the force of contraction and the degree of stretch and tension under which heletal muscles were placed previous to stimulation that 19 the so called initial length and tension Frank recorded isometric and isotonic contractions of the frog s atrı and ventricle during various degrees of diastolic filling and pressure He found that within limits stepwise increases in da stolic volume and pressure just before contraction-hcrcufter called the presystolic iolume and pressure-etermme the magnitude of the all or none response These studies emphasized that the cardiac re Sponse to artificial or natural cxcitation is determined wholly by hemodynamic events which precede excitation Years of experimentation have not only confirmed the basic laws of cardiac behavior founded upon these observations but they have also elucidated the many variables whuch tend to obscure their opera tion in the control of the mammalian heart under normal and patho logic conditions The Lart of Uniformity of Behavior In 1906 | Henderson succeeded in improving previously u ed p'ethysmographic technics sufficiently to establish patterns of ven tricular filling and emptying under different circulatory conditions I study of cardiometric records led Henderson and his assouates' to the conclusions (1) that the sentricles haic a fixed pattern of re laxation which delermines their diastolic capacity as long as the cnous supply is at normal levels and (2) that further increase in senous supply cannot augment ventricular filling and systolic di chare Such a concept set an extremely low limit to the cardiac re spon e to increasing initial tension and length Iccording to this vex ·DIT: RUINATS OF CARDE IC PERFOR\C} 37 aino the only nay in which greater volumes of venous bloul Could Ic pumped to the aorta nould be through an in/rene in heart rate lccording to buy lass of uniformitz of behavior cardic output in creases progresssicht up to rates of 180 per mupute thereafter be coming stationary and durms extreme tachycardia dimuahing rap I rapprar al or llentler ons sorh indicates that his analysis of entricular volume <uri(9 gives a valuable geometrie plan for eval atmg the effert of Ge'e length on ystolic discharge and cardiac output but his conclusion that increased venous return cannot aug ment sentru ular filling does not seem to have been supported by vel experimental en lence Blenderson was unquestionably correct in his deduction that ventricular filling occurs largeli in early chastole as a result of ! i pressure differences but he underestimated the additional quantity of blood that the atra snject into the sentnotes partly bustuse the slouer beats in his experiments were obtained during agus cumulation and therefore associated with depre son of atrial contrartion The Applicability of Laus of Initial Tension and Length to Mammalian Ilearts In 1914 the ster" reported xperiments which demonstrated that etcry increas or lesttase iti volume of blood returning to the right utrum simultaneousls uiters the instial tension besght ai contour of the right intras entrưular presure ure These experiments nere the first to demonstrate that the rent trons established for the frog verstrale are also applicable to the naturally beating right ventrarle of dogs In brief the con due nas reached that the gradient of the Bometr pressure nie and the peak se stoler pressure are determine by changes in the preuz sl olie tension as long as marhed changes ??? usherent contractility are not omultaneoush produced by experimen tal proredures (oncurrently and quite independently other itirators notably Stirling and kin umocrates wnel Stru” sextigated the effert of cha Mary in presy stolse tuisonand longthons ponysoft ofitelbenrts Since the work of Stirling and lus group has found the greatest at fentsa in ration ti thual studies a reapprstul of their 193 eetrga tions anil kuncion* atkl be of timeli interest The e mrestigators ·38 CIRCULATORI DI VAVICS utilized their well known heart lung preparation' which w 19 designed to control heart rate mean arterial pressure and enous inflox, and to vary any one of these factors at a time This was of signal im portance despite the facts that the individual factors cannot be con trolled as independently as the British ini estigators believed and that the dynamic conditions under sluch the heart operates deu ate some what from those which eust in the body 4-7 The important results and conclusions pertinent to our discussion can be summanzed as follons 1 When arterial resistance and scnous inflow were hept constant -within limits of the preparation-ariations in heart rate from 60 to 100 per minute caused no significant changes in cardiac output per minute (Viru alder and Starling") a conclusion diametrically op posed to that of Henderson and his associates. The inference was drann- and later it was supported in a measure by registrtion of olume curves--that ventricular filling is not dominated by a fixed pattern of relaxation and elastic resrst ince to filling pressures (Pat terson Piper and Starling!) 2 At constant heart rate and mean arterial pressure progresante augmentation of venous inflow (nused progressive increases in dia stolic size (stretch) systolic discharge and cardiac output per minute up to a critical atrial pressure (compensation) Beyond this a stolic discharge and cardiac output decreased (derompensation) These results were interpreted as follows I compensatory increase in stroke volumes takes place as long as the icntrcles can undergo additional distcntron I hen no further distention 19 possible owing to limitations imposed by the elastic ventricular stretch or the restruning action of the pericardium 'S the rapidly increasing presystolic tension exerted on individual fibers hinders the lei clopment of contractile force and systolic discharge diminishes (Patterson Piper and Starling') 3 During the compensatory state that is while cardınc output in creased with augmenting venous supply ---pre sures rose pari passu in both atria slowly at first and thereafter at a progressively increas ing rate During the stage of decompen ation (when cardiac output of the left scntricle began to declinc) pres ure ro e rapidly in the right atrium but fell in the left (right heart failure) (Patterson and asso ciatest1) The fatigued or depressed heart could have an output equal to ·DETERILISANTS OP VRDIC PERFORACE that of a fresh fitart but required a higher atrial prensure and greater press stolic ventricular distention The corollary follows that at com trolled heart rates the competence of the my arardium may be tested hat comparing the ststole discharge at equivalent venous pressures or by determing the 1 enous pressure requrcd to produce equna font stroke volumes 1 his procedure kas been used by hrajert in the heart ſung preparation and by the authorlt in the mtact animal In some experiments in which simultaneous volume and pressure cuney from the ventricles were recorded it appeared that consider able increase in preszatole sentrular ssze took place while the prees stolic or mutal tension in the left ventricle remained uncanged or actually fell (Patterson Psper and Starling') Joweter at the time theve investigators worked it was not realized that slight shifts in the entire pressure cure cannot be excluded unless a base line for optical pressure curses is simultaneously recorded from their observations the intereace seemed warranted that the presystolte size (stretch) of the ventricles 19 not determmed solely by actual fillsag pressures (mean atral proesures) but 13 affected also by inherent vanations in ther rate of relatation and elastic or tosue resistance to stretchmy On the whole they believed that the mammalsan ventricle unlike that of the frog studied by Trank rarely reaches & state of statie iclaxation before the succeeding best super enes From these osservations Starling soft quoted fat of the heart * is derived 20 There is a general apresion that the graphic repre sentation of the lus often reproduced was ba ed on data from these experiments The careful reader will discover the frank statement that the published curves are reproductions of graphs previously published by Blue and by 0 Frank (Patterson Piper and Starling') So far our analy 613 of the mechanical conction of the heart & contraction does not differ fasentially from Frank s classical exposition of the mechanical espoły affecting contraction of the frog a heart In this work honerer Frank as dealing stth contractile tissue skich had long periods of diastole so that it had resebid a static condition before the beginning of systole and he found that the energs set free in the exciter condition (te mersured by the tensson ket up) 543 proportional to the initial se dil tolic tension on the muscle But in this case it is sot easy to decide nliether the determinus factor is read the initial tension of the syst: a) length of the muscle fibres In the manualan heart ne ore dealing with an org in bets a contract ·10 CIRCUL410R DINAMICS ing ripidly and rhythmicalls such contraction being a nece iry condition for the preservation of its functional activit: The condition of the heart thercfore as to both tension and length of its muscle fibres is altering con tinuously during diastole from one leat to the next In Franks experiments on the frogs herrt the initial length 1&9 proportional to the initial ten jon so that the augmentation of energet free on contraction might have been due either to the increa el ten on or to the increased length In nur experiments we have found that it in length rather than ten ion which determines the energy of contraction We thus find no constant connection between the dinstolic tension and the succeeding contraction though as a rule the e tro quantities will be altered together But we do find a direct proportion between the diastolic volume of the heart (ie the length of its muscle fibres) and the encro et free in the following systole The law of the heart is therefore the sune 23 thint of skeletal mu cle namely that the mechanical energy set free on pa ange from the re ting to the contracted tate depends on the area of chemically actne surfaces, re on the length of the mu cle fibies This simple formula scrics to explair the whole behavour of the isolated mammalian heart -18 mouenient poucrs of aulaptahon to carying demands made upon il lchamour to fatigue and the influence of its neries or chemical agencies such as acid rons or adrenalin (Author s Itales ) The basic idea underlying Starling slun of the heart nimelt that myocardial sesponse is determined basically in the degree to unch fibers are stretched has been supported with one exception 2? Loy all ubsequent ini estigators ™-1 Honcier attention may be directed to the fact that all investigators have as umed the existence of a linear relation between presystolic ventruulir captats and length of fibers and between presy stolie intracardiac pressure and initial ten ion on muscle fibers The validity of this assumption for the mimmaluan ventricles compo ed of complicated superimposed muscle bands ar ranged to pull in different directions has neier been adequately cs tablished In 1922 Wiggers and hatza restudied the mechani m of adaptation to increasing venous return by means of cardiometric technic in a controlled circulation preparation The preparition, as progressively improved in subsequent re earches is diagrammatized in figure 13 The heart of a lights anesthetized dog is exposed under artificial re piration just enough for the vnimal to retain natural diaphragmatic ·CUT YAG: DI TERVISI VTS OF CANDIC PERFORMACE moi ennents This offers a simple indication that blood gases remain e sentially normal The cardiat neries are severed The heart rate is controllable within wide ranges it ss reduced to 10 or per minute by clamping the sur node and then dating the heart by electra hochs applied to the night atrium \ enous return can be decreaser through grader compression of the inferior vena cala or increased by an mfusion of wann suline into a jugular vein the redurtion in blood Visoity which accompanies surh infusion is ac antageous dynamic Vinta CLAMP FI 13 Diagram australing the controlled circulati i preparation for studying art arate determinants of ventricular reason D se 10 text alls for it has prosel just about suflu sent to mamtain a constant als ewtoint pressure drepite muie sing stroke solumey Irterial rementance 14 lse (extrolled by tightening or lou cheng 83 ajustable clamp plaseul around the lonest portion of the thotjoc aorta Volume (unes of the sentree are recorded optically together with Arterial pressure pules is de enike dekher ? 5 Typical curses are *** 11 figure 1! The solume frings descend with dimmution of veutri ular volume during stole and rise during dia tolic filling Changes in slope (1-3) indicate changes in the rate of sentricular ·CIRCULITORI DY\AVICS emptying and filling During the pha c of sometric contraction (2-3) the curies erther rise or fall slightly Ihesc variations arc unavoidable artefacts created by slight shift of the cardiac base with respect to the rubber diaphragm During systolic cjection (3-7) several changes in rate of emptying corresponding to inflections of the aortic pressure cune are indicated by vertical lmes lhe rapid ejection rate from 3-6 and the marked reduction from 6-7 are particularly noteworthis Systole ceases at 7 and the interval 7-8 demarcates the isometric FIG 14 ---Simultancously recorded volume curve of ventricles (uprer) and aortic pressure (lower) shoning corresponding inflection during phases of ejection and division of systole and diastole into commonly accepted phases (1 2) atrial systole (2-3) isometric contractron (3 5) period of maximal sys tolic ejection (5-7) period of reduced systolic ejection (7) end of evstole (7-8) isometric relaxation (8-9) rapid diastolic filling (9-1) retarded diastolic inflow (diastassa) (After J Wiggers Physiology in Health and Disca e courtesy of Les and Febiger Philadelphia) relaxation phase of the ventricles ventricular fillmg occurs rapidly at first (8-9) and then more gradually (9-1) dividing the filling into phases of ripid inflow and drastasis This is followed by atral systole (1-2) The results obtained by hatz and myself in the main confirmed those of Starling and his group but some amplification and certain differences were found I During the compensatory stage of increreed venous re turn (com pare curses A and B in fig 15) ventricular filling proceeded more rapidly throughout diastole that is during the succes ne periods of rapid inflon dastasis, and atral contraction The larger systolic ·DETERMIN LXTY OF CARDIAC PERFORMACE 43 discharge was accomplished by a greater velocity of ejection a pro longation of the ejection period (compare a and b) and occasionally even more complete emptying It is obvious at a glance that such curves are not superimposable as regards uither their systolic or dia stolic limbs Optical pies ure curses from the right ventricle (lower series fig 15) demonstrated that the presy stolic intraventricular HIG 15-Changes in configuration of ventricular volume curves (upper series) and right ventricular pressure pulses (loner series) during progres ive increas in rate of venous return 41) curves matched at beginning of ventricu Iar systole a b c denote ends of systole and illustrate changes in relative durations of systoles (4) control (B) during compensatory stage (C) during decompensatory stage (After CJ Wiggers Physiology in Health and Disease courtesy of I ea and Fehiger Philadelphis) pressure (initial lension) increased steadily the gradient of pressure before ejection (isometric phase) was steeper and the curves reached higher peaks The larger volumes ejected by the right ventricle under higher pressure necessarily caused an elevation of left atrial pressure Contrary to Starling s observations, Opdy he and his associates have recently demonstrated that the increa e in pressure was much larger in the left than in the right atrium osing to a les er distensi Wilty of the left atrium and its tnbutsy sexy ·11 CIRCUL 4 TORY DINAVICS 2 Contrary to interpretations by Starlıg and his associates 10 found that reduction in stroke volume with ercussive rates of cnous inflou may not conditioned by the fact that the ventricles had reached their detention limits decompensation des cloped while the process of diastolic distention w 19 actually accelerating (fig 15 B () In other word, it appears that beyond a intical degree of stretch addı tional extension either has a rei erscd effect on the rele. c of mechan ical energy or contraction is hindered by the greatly mcreasing dia stolic tension This also accords with Frank s observations on frog hearts and with those of I undin" on stretched moicties of ventricu lar muscle Inalysis of volume and right ventricular pressure cures (fig lo C) indicated that despite a large increase in diastolic size and in initial tension the mechanism of discharge changed the entre les emptied themselses less forcibly and completely indeed the systolic size was sometimes smaller than the normal diastolic size in onor mous increase in residual volume was apparent (sce a and c curves I and C) indicating that a considemble effective solume of blood stagnated in the heart during progressive decompensation the sky tolic pressurc» in the night I entricle and pulmonary artery decreased and consonant with Starlings resulta pressure in the left atrium fell 3 llith constant venous return and 15ht atunl presures the car diac output s as found to be far from constant at different heart rates as the British investigators claimed Inder carefully controlled trial pres tire the alterations in strohe volume with progresulte acceleration followed the predictions of I Ilenderson rither better than the er perimental results of Starling and his group IIoneter unless arterial and venous pressures were readjusted with every change in herrt rate the beats were not superimposable and accurate predictions as to the relation of cardiac output to heart rate could not be made Thic reasons for the variable effects of heart rate changes on stroke volume and cardiac output per minute have gradually become clearer from the study of a large number of ventricular volume cures The integration of a large number of phy s tl and physiolo, determin unt on ventricular filling are im oled in attempts made to dissociate the chain of events with the aid of the diagram in figure 16 The hcar y curie (V) represents a sentricular volume curve unler normal conditions at a heart rate of 7) per minute The record is then in such a manner that ventricular empty ing is indicated by the donjistrohe ·DETERVIANTS OF CARDIAC PERFORMANCE 45 and filling by the upstrohe The residual volume is indicated without ordinate values The phases of systole and diastole for this beat are numbered as in figure 14 An acceleration of the heart approximately to 120 per minute would according to l Henderson & scheme merely cut into the filling curte as indicated by the are A This however is an oversimplification of N N A B 7 B -- RESIDUAL VOLUME Fra 16 - Heavı curve (N) typical volume curse for leart cycle 0 8 second (15 per minute) \umerals same as in figure 14 Assembly of superimposed ven tricular volume curses illustrate variable factors that may influence stroke volume when heart rate increases to 120 per minute (A) 41 ridgement of natural filling and reduction of stroke volume according to lenderson (B) Turther reduction in systolic discharge owing to coincident se luction in atrial pressure and reduced filling rate słown at F and dimiaisted force of atrial systole at (C) Restoration of strohe volume to eontrol of curve A by greater effectiveness of an atrial systole (1) which supervenes immediately after or Juring rapid inflow (D) Increa in stroke volume to that of a beat with long cicle (N) as a re ult of accelerator nerve action or adrenergic humoral effects which increase force of atrial contraction and more completely empty the ventricles (re luction of residual volume) (L) Further augmentation of systolic discharge through simultaneous increase in venoug return and more rapid fill ing as in exercise Lines on right (N I) indicate at a glance comparative stroke volumes for corresponding volume curves chunges that actually take place In the first place despite constancy in returning blood volumes such acceleration very quickl reduces the pressure and volume of bloocł in the tra in a mechanical way Simply stated morc blood 1pumped per minute than is recen cd Is a result the rite of falling during the rapid inflow phase tends to become more gradual as in the cun e labeled I Smce the atria start their contractions at a shorter initial length the vigor of their contrac ·40 CIRCUL ITORI DYNAMICS tions would be diminished and it might be expected that their con tribution to cntricular filling would be reduced as indicated in the wave However this diminishimg effect of atrial contraction appears to be offset by the fact that atrial contractions coming at the time of incomplete ventricular filling are more effective than those that occur after a long diastasis as in the solid line curve Is i result the incre ment becomes somewhat greater as indi nted in the wave I which may restore the systolic stroke C approximately to that of stroke i \ccessarily the diastolic filling curies are not superimposable but the net effect on strohe volume approximates Ilenderson s predlutions If in addition the increase in heart rate is induced by activation of the accelerator mechanism and release of the vagis mechanism the force of atrial systole may be increased significantly and the contri bution to ventricular filling may be represented by wave 2 Under such hypothetic conditions the strohe volume D muy almost equal that of the control bent for the accelerator mechanism al o acts directly on the ventricles to reduce their resudnal volumes Such an approximate proportionality of cardiac output to heart ratc can obviously be maintained only as long as the volume of ve nous return cquals the cardiac output If as a result of many condi trong--hemorrhage and shock for example, this is not a complı lcd these compensatory reactions cannot be muutuned If on the other hand venous return augments at the same time that the heart ac celerates 7 in exercise the strohe volumes can defimtely excred the normal as illostrated in curve [ This analysis of the many coeffi cients which affect ventricular filling explains why insestigators have differed (1) as to the contribution of atrial sy stole to ventricular filling and (b) as to the effect of heart rate changes on cardıc output per minute It seems apparent now that the constant cardiac outputs obtainer! by Starling and his associates over wide ranges of heart rates were due to a fortuitous balance between these variable factors The British investigators failed to recognize that the available supply and pres sure of blood in the right atrnım is determmed as much by chinges in cycle length as by the pressure head in a scnous reservoir Further more as Krayer has pointed out these inicstigators altered heart rate through changes of temperature of the inflowing blood uluchers ·DETERVISI VTS OF CARDI IC PERFORMACE 17 certainly not without influence on the inherent contractuty of the ventricles Intrinsic Cardiac Factors Our analysis of the relationship between atrial volume and pres sures duration of the inflow periods and force of atrial contractions on the one hand and systolic discharge and cardiac output per minute on the other accord basically with the law of initial length The re sultant effect of filling pressure, atrial activity and the available fill ing time regulate the degree of ventricular distention (initial length) realized at any given cycle length and this in turn determines the velocity volume and duration of the systolic discharges However this is only a first approximation to reactions of the heart muscle at a given initial length in the body As Starling and his group pointed out at equivalent initial lengths a heart in good condition responds with a larger strohe volume than a fatigued heart Also as Wiggers and Katz: pointed out the pattern of ventricular emptying 18 not solely governed by presystolic billing but it is also affected by reduction in coronary flow Hearts stimulated or depressed by drugs chemical changes in the blood or through nerve actions show similar variations in a study of the dynamics of drug actions I pointed out in 1927' that the voor and pattern of sentricular contraction and consequently its systolic discharge can be influenced (a) by agents which primarily affect the contractilits of the myocardium as well as (b) by those which sec ondarily affect contractility through changes in initial tension or length such as are induced by ulterations in venous return arterial resistance and heart rate To the latter may be added hydrody namuc effects produced his such pathologic conditions as coronary insuffi ciency valvular le sons anomalous cardiovascular circuits pulmonary vascular changes and pericardial effusions In short the ventricles do not obey the law of all or nothing at any given degree of fiber stretch their magnitude of response depends on the physiologic state of myocardial reactivity Starling was certainly aware of the impor tince of the condition of the heart muscle but did not include this in phrasing the lin of the heart I would suggest therefore that to 11 od ambiguity or misin ·18 CIRCL LITORI DINAMICS terpretation the last of the heart be amended omen dat as follows The lau of the heart is thus the same as the law of muscular tis ue generally that the energy of contraction hoxe er measured in a function of the length of the muscle fiber under equilalent stales of responsueness Within recent years the operation of the law of initra! length has seriously been questioned on the basis of studies of the human heart by cathcterization technics $6 We may predict with con fidence that when we are able to overcome the technu al difficulties that still impair the accuract of pressure determinations in catheter ization studies 27 a creful cu aluation of results will demonstrate the alxdity of the law of cardiac performance Moncler 1 predu i that complete assessment of the regulation of cardini performance is not likely to succeed from anal es of hemodynamic data during health and discase alonc because innumerable anables ue bound to be concerned The multiple factors which can separately influence the response of the myocardium at equivalent initial lengths must be submitted to intensive cıperimental studies of a basit sort i wide new field awaits exploration Sothing would give me greiter plez ure than to attach the many fucets of this interesting problem However since I am approaching the end of my cıperimental career I cun per haps best serve the cause of cardiac re eirch inc horting a new genera tion of investigators to accept the challenge of their exccution Summary Three classi discos cries--- 3 Bon ditch in 1869 by Howell and Donaldson in 1884 and bi o franh in 1899- Jard the foundation for the basic laus which govern the regulation of ventricular re ponses Years of further experimentation have not only hown that the mim malian heart operates according to these basic laws but have al o elucidated the many variables which sometimes obscure the evidence that these basic lans are important under normal and pathologic conditions In 1906 ) Henderson er olsed a law of uniformity of cardiac behavior which offered a geometric plan for roughly ex aluating the relation of ventricular filling at different cycle lengths to sy stolic dis charge and cardiac output but his conclusion that the systolic dis charge at any given heart rate cannot be increased above its normal value has not been supported by further studies In 1914 Straub and the writer independently reported experiments ·DETERMINANTS OF CARDI4C PERFORMANCE 19 on mammalian hearts which appeared to show that the reactions of the mammalian ventricles to changes in senous return and arterial resistance harmonized with laus derived by Frank from studies on frogs hearts These experiments like those of O Frank were unable to determine whether changes in presy stolic pressure (initial tension) or volume (initial length) fundamentally regulate the degree of re spon lencs, however measured Shortly after the publication of these researches Starling and his associates on the basis of experiments on the heart lung preparation which were hghly suggestre but not quite conclusite concluded that in the reaction of the heart to increased inflow and increased resistance the only factor which constantly varies with the respon e of the ventricle is the volume of the heart that is the length of its muscle fibers The law of the heart was thus reduced to the formula that the mechanical energy et free on passage from the resting to the constricted state depends on the area of chem ically actu e surfaces le on the length of the muscle fibers This basic concept has uh equently been validated by nearly all iniesta gators In 1922 the writer and hatz delineated the detailed changes in the patterns of ventricular filling and emptying occasioned by alterations in venous return arterial resistance and heart rate and analyzed their relation to presı stolic ventricular volume It was concluded that Starlings interpretations required some morlification For instance the rate and degree of ventricular filling are a resultant of the atrio ventricular pre sure gradient the variable effect of atrial systole and the time interval available for ventricular filling Furthermore these and subsequent studies by the writer liave revealed that while the mode duration and extent of ventricular emptying are in a measure determined by the preystolic size primary factors which affect the respon leness of the my orardum are likewi e of great importance These include such fuctore as coronary blood suppls humoral agents and nervous artions on the ventricular muscle It is suggested that the operation of the law of initial length will ako bc found valid in the human heart under equivalent states of myocardial responsivenes REFERE\CFS HIGGERS CJ Path 813 of me lical progres Science 91 23 1910 Circulation in Ilealth and Di Leel. Thiladelptua Les ani Febiger ·50 CIRCULATORY DIVIVICS * JIURTER Untersuchungen am arteriellen menschlichen Blute Deutsche Arch ( klin Med 103 1 191? STADIE VC Oxygen of arterial and venous blood is preumonia and ita relation to cj anonis J I xper Med 30 215 1919 * COURYADI ATD RANGES III Catheterization of right auricle in man I roc Soc 1 eper Biol (Ned 4 462 1911 . BOW DITCH HIP Ueber die ligenthumlichkeiten der Reizbarkeit wrlche die Muskelfasern des Ilerzens zeigen Berichte d math phys each (c sellsch d \19sensch Leipzig 1871 P 66% RANSIER L 1 Leçons d anatomie générale faitre au Collège de France 1877-1818 Ipp nerv term des muscles de la vie organique etc I aris Ballıere et This ISSO I 1.5 HOWELL WH AND DONALDSON Frank JR I xperiments upon the heart of the dog with reference to maximum volume of blood sent out by left Ventriele in a single beat Philosophical Tr London Pt 1 151 1881 • FRANK 0 Zur Dynamik des llerzmuskels Ztschr ( Biol 3 30 195 .IIENDERSON I Volume curve of the ventricles of the mammalian heart and the significance of this curve in espect to the mechanics of the heart beat and the filling of the ventricles im J I hisol 16 395 1906 Icapnia and shoch II principle underlying the normal variations in the volume of the blood stream and the deviation from this principle in shock Am J Physiol 23 315 373 1909 --- AND BAARINGER T B JR The conditions determining the volume of the arterial blood stream Am J I 1910) 31 988 1913 The relation of venous pressur to cardiac efficiency Ibıl 1 3,2 1913 WICERS CJ Some factors controlling the shape of the pres urc curyc in the right ventricle Am J Physiol 93 397 1914 IVAREN ALDER J AND STARLING T On the constancy of the systolic output under varving conditions J Physiol 48 315 1914 PATTERSOV SW AND STARLING I II On the mechanical factors hich determine the output of the ventricles J Physiol 48 357 1911 I INFR HI AND STARLING S 1 Regulation of the brart beat J Phys 101 48 497 1914 EVANS CLAVD VATSLOKA I Lffect of various mechanical conditions on the ga cous metabolism and efficiency of the mammalian heart J 1 hysiol 49 319 1914 12 STRAUB II Dynamik des Saugeticsherzens I Deutsche Arch fhlin Med 115 531 1914 II Ibid 116 409 1914 howLTOY FI AND STARTING I 1 Influence of variations in tems era ture and blood pressure on the performance of the 1sulated mammalian heart J I hysiol 44 906 1912 11 WIGGERS C J The present status of cardiodynamic studies on normal and pathologic hearts (llarves I ccture) Arch Int Ved 27 410 191 11 LATZ IN Observations on the dynamics of ventricular contraction in the heart lung preparation im J I hy310) 80 40 1997 ·DETERVA A\TS OF CARDIAC PERFORMANCE 1 16 RAYER 0 Versucbe Am ipsuffizienten Herzen Arch f Exper Pathu Pharmakol 16' I 1931 17 h NEBEL R Clastizitatsserhaltnr se des arteriellen Systems am Starling schen Herzlungenpraparat Ireb f exper Path u Pharmakol 197 48 1941 Uber den Einflus des elastischen Widerstandes auf die hrei lauf verhaltnisse am Herzlungenpraparat Ibid 197 196 1941 * MEEK 11 J AD EYSTER JAF Effect of į lethora and variations in venous pressure on diastolic size and output of heart Am J Physiol 61 196 1977 WILSON J A A\D VEEK W J Effect of pericardium on cardiac distention 28 determined by tray Am J Physiol 84 34 19% WIGGERS C J The Physiology of Shock New York The Commonwealth Fund 1930 STARLING EH The La of the Heart Beat New Iorh an London Long mans Green 1918 "Di PALMA JR AND REISS R 4 Miographic study of the cats beart Am J Physiol 155 327 1918 " WIGCERS CJ Pressure Pulses 12 tbe Cardiova cular System New Work and I ondon Longmans Green 19.8 hatz L M Relation of initial volume and initial presgure to the dynamics of ventricular contraction 4m J Physiol 8 319 1999 STRL GHOLD HUBFRT Cinematographic study of systolic and diastolıc heart Bize with special reference to the effects of anova Am J Physiol 94 611 19,0 *BRAMS WA AND KATZ LT Studies on the overd stepded heart I Effect of venesection Am J l hygio) 98 506 1931 * SULZER R Die mechanischen Eigenschaften des Herzmuskels Ztschr! Biol 99 515 193 * VOLDON SKY LF AND VIS HER VI B Analysis of the factors concerned in the automatic adjustment of the ventricle to increa, ed load 1 A study of the importance of contraction rate and filling pressure in pro lucing alterations in diastolic volume by Variations in arterial pressure Am J Phys101 106 39 1233 WIGGERS CJ The dominant eontrol of mammal an ventricular dynamics by initial length Rey de la Soc argent de Biol Suppl 10 516 1934 19 JOHNSON AND LATZ LITone in the mammalian ventricle Am J Phy 10) 118 76 1931 habar II AD ISSCHER VI B I lastic properties of the beating tortor e ventricle with particular reference to busteresis {m J Physiol 1 5 43 1939 Voss ( AND JOHiso Differential effects of stretch upon stroke volume of right and left ventricles Im J Physiol 139 59 1943 HIGGFRS CJD | 4tz L Contour of the ventneular volume curves under different con latins Am J Physiol 58 439 ign OPDYKP D F DUOMARCO J DILLON 1 H SCHREIBER I LITTLE PC ANE SEELT I DStudi of imultaneous nght and left atral pres M622 ·52 CIRCLL ATOR) DYNAVICS sure pulses under normal and experimentallı altered conditions im J Physiol 164 258 1918 LITTLF ROBERT C Volume elastic properties of the right and left atrium Am J Physiol 158 237 1919 * LUNDIG Vlechanical properties of cardiac muscle Icta physiol scan dinsv 7 Suppi \o 1914 *TVIGCERS CJ Studies on the cardiody namic actions of drugs I The ap plications of optical methods of pressure registration in the study of car diac stimulants and depressants J Pharmacol Exper Therap 30 217 1927 II The mechanism of cardiac stimulation by epinephrine Ibid 30 233 1927 ** STEAD EI JR AND WARREN JY Cardiac output in man analysis of mechanisms varying cardiac output based on recent clinical studies Arch Int Ved 80 237 1917 WARREV JI BRANNAN ES WEEYS HIS AND STEAD EA JR I ffect of increasing blood volume and right atrial pressure on circulation of nor mal subjects by intravenous infusions Im J Med 4 193 1918 17\Vicders C J Peripheral circulation Inn Rev Physiol 9 255 1917 ·CIIAPTER III Dynamics of Ventricular Contraction under Abnormal Conditions Vm the past two decades clical and esperimental studies of cardiac outpit per minute and per beat-save yielded much im portant uformation ron, crung the nature of cardiovasuclar chis orders Howryor basic understanding of such conditions also re quires a comprehension of the wars and means by which ardzac output is either mantained or altered The dynamics of ventricular contraction which concerns itself aath the mechanism through shrich cardsac output is altered can be er aluated to a considerable extent by a riga analı 58 of pres ure pul es recorded from the ventricular (atten non it happens that durig inrious periods onre 1912 I have used such pressure pulses to study the basit changes in cardic Eyelinor produced during abnormal circulatory conditions in experimental anmalce this work 11.99 published largely in journals of physi lo pressous to the anahening of clinical interest in cardiods nantis much of it probably tres dormant on library shelics In 1 sess of the current restes a interest the time cms appropriate for recall mg some of the studies and suggestmg that experimental work of this Bature be gen ronsideration in the evaluation of human cardio vascular problems It rem uns mi considered judgmerst thiet dedue tsons regarding carby belassor derned from controllable acute expriments on the dogs heart can be transferred to human hearts provided that proper rescrie and caution are exercid The Interpretation of ventricular Pressure Pulses In inventigator who attempts to Irau conclusions from records of kontrulur pren ute peel as must exorci iertan prenutions if he The Henry Jackson Memorial Lecture d Ivered before the Massachu etis lleatt ha ocrat 18 Inc Bostan Vass June 4 19al ·CIRCULATORI DYNAMICS wishes to avoid the formulation of wrong deductions Recorded eunes should always be examined and evaluated as to their reliability that is to say, whether they truly depict pressure fluctuations or are dis torted by artefacts of registration The latter are more easily intro duced than avoided Distortion of ventricular pressure curves results from the use of inadequate manometer systems 1 : Theoretic physical formulations and practical tests have demonstrated that reliable curves can be recorded only by a manometer system which has an adequate frequency and proper damping characteristics expressed Fro 17 -Two graphs of a truc left ventricular pressure pulse (N) and the game deformed through artefacts (A) In the latter the delayed rise the super imposed vibration (1) the dip and aftervibrations (Y) following relatation are artefacts common to undamped low frequency aj stems The late systolic rise (7) which can generally be abolished by changing position of intracardiac sound is probably produced by location of sounds in pochets by the logarithmic decrement of its free vibrations There have been and still are investigators u ho maintain that curies with high fre quency components can be inscribed with properly damped lon ire quency manometers Such a task appears to resemble one which would require a bass fiddle player to perform a musical score written for flute or piccolo Artefacts are also produced through periodic obstruction of manom eter tubes or through displacement of a catheter and the leart in relation to one another during contraction and relaxation but these are usually recognizable and when present must be discounted i fer common distortions of ventricular pressure curies are shown in ·EXTRICE LA CONTRACTIOT UNDER HVORYAL CONDITIONS the assembly of records in figure 17 The leavy curse () represents the actual pressure fluctuations the other cun e (a) combines vanous distortions which mas appear singly or in combination in records Curses recorded by manometers of low frequency are characterized by retardation of the pressure nse (cune ) the production of vibra trons at the onset of ejection (x) and a negative dip and/or after vibration shona aty Location of a trocar or sound in intraventric A Fid 18 -Identical ventriculas pressure pulses recor le l with mapometers of different sensitivity (4 B) an ion paper fravekng at different speeds (B C) ular pockets eg beluid pupillar mu cles or 1 aliae probably gives 118€ to rurses with a secondary peak at the end of stole as shown 2t 7 Tantrirular grewure cun es muy di plas apparent rather than real <ifferences in their patterns depending on the sensitrusty of the manom tttts employed and the speed at which cures are recorded on mor ing pur Thus curie lun hgure 181) a typical normal curse If the same pressure pulse is recordel hy # manometer hang inne the ·56 CIRCULATORY DINAMICS sensitnity curve B emerges and if tis record be taken at half the puper speed curte ( deselops It is apparent that important in flections tend to be obscured in curte ( and that artefacts might not be recognizable if in aldition the amplitude of such a cure is re duced to 10 cm bi u e of direct recorders contour changes cannot be inferred A judicious balance between ordinate and abscissal values 19 obuously important in the regntration of pressure pulses Successive myocardial and Dynamu Eients during the Cardiac Cycle A proper interpretation of myocardial activity through analı sis of the ventricular pre sure pulse requires a knon lease of its relationship to other cardiodynamic events the relation of sentrculer pressure variations during alle sive phases of the heart (vole to pressure changes in the aorta ind left atrium to a surfare my ogram to ACOUS tic phenomena to volume changes of the sentricles and to an elect10 cardiogram (standard lend II) are shou n m figure 19 The persistence with which curses of inaccurate contours and erroneous time relations continue to appear in papers and textbooks mahes publication of such a chart desirable comprehension of correlated escnts expressed in mh a series of tries was once regarded as an academu exercise in the current era of hemodynamic studies it becomes an mest apable requirement The subdomion of the cardine cicle whech I uggested in 1921 194 apparently gamed rather general acceptanec Iccording to thi scheme systole begins with the rise of ventricular pressure at 1 and ends with the release of ten ion in all muscle umts at (fig 19) It is divided into phases of sometric contraction (1-C) marimum chee tron (CD) and reduced ejection (D-F) The subsequent period of drastole is divided into phases of prolodtastole representing the time required for closure of the semilunar talers (F-G) isometric relara tron (G-H) rapid uentricular filling (-1) drastasis (I-1) and filling hy atrial contraction (1-1) Abnormal patterns of ventricular contraction cannot be inferred from ventricular pressure pulses unless an investigator or reader pousesses the capity for translating the tracings into mental | tures of proct wees shah tafe place in the heart anel vascular sistem during the period of the heart cycle outlmed by the sentricular press sure curse lle may therefore relleu briefly the main muscular and ·1 VTRIC LA CONTATTI L\DER BJORNAL CONDITIOTS 57 01 ot bs 06 07 OB 09 10 HYOGRAM LIO AORTIE. PRESSURE K 90 LEO 170 160 50 40 VENTHICULARI PRESSURE 120 IATRIALI PRESSURE LIO LO Hot HEART WOUNDS CC VOLUME CLAVE OF xNTRCLE 50 60 ECG 1r 19-Clart slowing correlation of various is namic mc int tary toc an ciectrical events dunha cul cicle hemom eients nm na Slutren the pas of 10 metrır (utrition tolic contron the i ometrie relaturit preluck to suh date it son the day effort of the lart dur ng ·8 CIRCUI \TORI DYNAMICS the e re poctisc phu es may be compared to the task of (1) raising a pail of water from the ground to a high level (2) holding it at this level while most of its contents are thrown with some force over a wall and (3) bringing the pail back to the ground for refilling It the onset of mechanical sy stole at A the entire myocardium of the left uentricle has been ciuted This is er denced by its comedence with the peak of R of a standard or direct electrocardiographic lead : Owing to a latency honen er, onks the initially cruted fractions have started to contract As more and more contractile fractions summate the pressure rises slowly at first (A-B) but very rapidly as soon 23 all fractions participate in the summation process (B-C) Since the mitral and milunar valves are closed during the interval 1-C and blood neither enters nor leaves the left ventricle contraction is es sentially isometric that 1 energy of contraction is converted to tension Ictually however a little energy is lost through a slight yielding of the valvular structures and in readjustments in the form and position of the heart In the development of a ngid muscular state the entricles rotato assume a more globular shape and excrt a trac tion on the atrı ind large resuels Vyogrims recorded from the left ventrcular surfact such as are reproduced in ligure 19 res cal that the surface layers may even lengthen as a result of changes in form of the ventricle However reduction in the base to apex aus demon strates that the rept al fibers undergoi hortenin. Thus altcrlonded mode of ventricular contruction has the adı ntage that sufficient vis a tergo is de cloped to stert quickly and contmie a brusque and forceful cjection of blood into the nort 1 against a relatively lugh aortic resistance The ejcction of blood takes place within a relatively short period (C-F) it is about 0 20 second in man and less in lower animals Reference to volume curves of the cntrcles (fig 19) reveals that two thirds of the whole stroke volume is ejected during the first half of this period (C-D) and 1 compamtisely small faction during the latter half (D-F) Since efflux of blood from aortic branches cicerds uptake from the ventricles during the latter half of ejection the pres qurts in the aorta and left ventricle decline (D-I) Thus the summits of the sentricular and aortic pressures demarcate the tran ition from rapid to reduced systolic ejection Vore than this, the inflections of th ventricular as well as of the aortic pres. ure curice from C to F ·VITPICULIP COSTRICTIO U PER BORVIL CONDITIONS 59 refiert mmor changes in the rate of ystolic ejection This is clearly illustrated by comparing changes in ventricular volume with pressure Tariauons in the root of the aorta in figure 20 The mutial steep nice of aortic pressure (3+) 15 accompanied by a brusque mosement of only a small volume of blood into the norta The continued elevation of Aortic pressure from # to 513 attended by a rapid empts mg of the ventricle During the slower ri e of aortic pre sure to a ummit (5-6) the rate of entricular emptying diminishes progressively and during the systolic decline of pres ure (6-7) 1t stery lon It is apparent that 4 Fru - Simultaneous records of changes in & normal ventricular volume (us per) and sortic pre ure (loxer) demonstrating the corre pon leece of in Me tions (1) during systolic ejection Volum curve is inscribed 8) that enptung of ventrics is recor led as d va troke filling 49 upstrohe (After C 151ggers Phys Jogi in Health an Diege courtes Lea snd Febiger 1 htadelphia) de pite the variable efflux from the ports the configuration of the aorle (and ventricular pressure pelses is dominated log the changing rates of ventricular emptying I rom a dynamic standpont mechanical ni tole terminates at F (hig 19) for ul mu cle fractions have reased to dei clop ter ion The completion of the T deflection t the time indicates that rc polirtion has been completed.lones er theoretic conade ratrons and the re pouse to electrical stimuh' trongh fan or the ver that me hhers have sea el to de elop ten on earher for evample at F Il dope pol mean that a Jengthening of my ord.) nhers has com ·8 CIRCULITORI DI AMICS the e rupectre phases mat be compared to the task of (1) riising a pail of water from the ground to a high level 2) holding it at this level while most of its contents are thrown with one force over a wall and (3) bringing the pail back to the ground for refilling It the onset of mechanical systole at the entire myocardium of the left ventricle has been cated This is evidenced by its coincidence with the peak of R of a standard or direct electrocardiographic lead * Uning to a latency honcter only the initially cruited fmctions have started to contract is more and more contractile frictions summate the pres ure ni es slowl at first (1-B) but very rapidly as soon as all fractions participate in the summation proces (B-C) Since the mitral and semilunar valves are closed during the interval 1 and blood neither enters nor leaves the left ventricle contraction is ex sentilly isometric that i energy of contraction is converted to ten. 1on Actuall however a little energy is lost through a light yielding of the valvular structures and in readjustments in the form and position of the heart in the desclopment of a rigid mu (ular stite the ventricles rotate assume a more globular hape and exert tru tion on the atm and large (cls Vyogrims recorded from the left ventricular surface such as are reproduced in figure 19 reveal that the surf uceluyers may even len, then as a re ult of druges in fom of the ventricle However recluction in the base to Up aus demon strates that the cptul fibers undergo 1 shortening Ilus afterloaded mode of ventriculır contraction has the ads intage that sufficient 1 is a tergo is developed to start quichli and continue a bru que and forceful ejection of bloul anto the tort1 A, ta relatach lugh aortic resistance The ejection of blood takes place within 1 relately shiort period (C-F), it is about 0 23 second in man and less in lower animals Reference to volume curves of the sentricles (fig 19) rei culs that two thirds of the whole stroke volume is cjected dunng the first half of this period (C-D) and 1 comp iratneli small fraction during the latter half (D-F) Since eflux of blood from aortic branches encerel uptahe from the ventricles during the latter half of ejection the prem ures in the aorta and left ventricle decline (D-F) Thus the summits of the sentricular and aortic pres ures demarcate the transition from rapid to reduced systolic ejection Vore than this, the inflections of thentncular as well as of the aortic pressure curies from C to I ·FYRICL L41 COYTACTION UDFR BIORY IL CONDITIONS 59 reficit minor changes in the rate of systolii ejection This is clearly illustrated by compuing changes in ventricular volume with pressure Xariations in the root of the corta s figure 20 The instsal steep rise of aortic pres ure (3-7)accompamed by a brusque movement of only a mall volume of blood into the aorta The continued elevation of aortic pressure from 4 to 5 is attendeil by a rapid emptying of the sentricle During the slower rise of aortic pres ure to a „ummit (5-6) the rate of entricular emptying dimım hes progressneh anni durmg the systoli decline of pressure (6-7) it 18 1ery low It is apparent that 9 8 Ho 0 Simultaneous re ords of changes in ar mal ventricular volusse (upper) and aortic pre sure nerd monstrating the correspon leace of in #ccions (1) during systolic ejection lolume eurve as inscribed so that mptı ng of ventricles is recorded as dou nstrohe filling as upstroke (Alter clligcerg Physiol is a Health an) Di esse courtesy Lea and Febiger Child lclus) di pite the variable efflus from the aorta the configuration of the sortit (and ventricular) pirs are pul rs is dominated by the changing rates of ventnmlar empty ng From a dinamic standpoint mechanical sistole terminates at F (Hg 19) for ill mu cle fractions have ceaed to develop ten ion Ilor completion of the T deflection by this time indicates that repolarization las tarn completed.lones er theoretic con ideration and the response to electrical tumuli strongli favor the view that time filter haecca ed to develop tension earlier for example at F They do not mean that a lengthening of myocardial fibers has com ·60 CIRCI LATORY DISTICS menced On the contrary my onlams reproduced in figure 19 and 21 demonstrate that the ventricular relaxation starts with a reduction of tension for 08 second or longer (G-HI) before the fibers lengthen (HI-I) and ventricular filling begins: It has been tempting to relate the gradient of pressure decline and the duration of the isometric relaxation pha es (G-H) to physiologie differences in the relaxation process Flowever the effects of physical forces cannot be wholly excluded Thene mclude (1) the reflling of coronary resuels (2) the volume of residual blood remuning after ejection (3) the pressure M Tir 21 - Simultaneous records of the changes in length of a small area of the left ventricular surface (upper curve) related to a ventricular pre sure pulse (lower curve) AC isometric contraction CD matimal systolic ejec tron D F reduced ejection and protodiastole I H isometric relaxation Vote that shortening of surface fibers begins at C and terminates at II Time 0 second at the onset of isometric relaxation and (4) the atrial pressure which determines the time at which curies intercept at H It may be added however that my ograms such as are reproduced in figure 21 offer no support for the view that refilling of the coronary vessels during 1sametric relaxation stretches the myocardium Determinants of Myocardial Responses The contraction pattern of the ventricles is determined by factors that affect the physiologic condition of the heart muscle directly and by those that art through changes in input and output loads The ·VE TRICULAR CONTRICTION UNDER BVORIAL (OVDITIO former have been termed primary and the latter selondary coefficient (ree Chapter II) Primary coefficients include the direct myocardial effects of local metabolites fatigue abnormal chemical constituents of the blood including drugs coronary insufficiency and nervous impulses Through these true cardiac stimulation or depression 18 produced Secondary coefficients cause alterations in cardiac vutput bg molifying the diastolic filling or arterial resistance In pathologic conditions tertiary coefficients can significantly modify the ventric ular contraction patterns in mechanical ways These include such factors as an abnormal sequence or deletion of fractionate contractions and valvular lesions which cause the ventricles to contract in a loaded or isometric rather than an afterloaded manner As Starling and his associatesto inferred from studies on a heart lung preparation the responses of a ventricle under many normal and pathologic conditions are determined by its presystolic size or the Initial length from which fibers start their contraction Personal ex perience has confirmed Frank s earlier postulate that with exceptions to be noted later changes in initial length are produced by alterations in ventricular pressure at the onset of contraction namely by the initial ten ion Such changes though small are usually discernible in optical records of sufficient amplitude Honet er controlled conditions are required for studying the effects of such a secondary coefficient These conditions are that the heart rate remains constant and that the myocardial reactions are not simultancously affected by primary or tertiary factors enumerated above In Chapter II experimental procedures were described by which heart rate can be kept constant in the intact circulation while enous inflow and arterial resistance are independently adjustable (see fig 13 p 41) Basic studies on such controlled circulation preparation have revealed that alterations in the pattern of sentricular contrac tions produced by primary and secondary coefficients can be dis tinguished by the relation that the amplitude form and duration of contractions bear to initial tensioni 1 hus as illustrated by curics 1 and 2 of figure 221 progres ise elevations of nitral ten ion at A are accompanied by increasing force and duration of contractions up to a critical level After the critical degree of stretch has been exceeded initial tension increases more rapidly and is folloned by contractions hayang a more gradual ni e a lower amplitude and a shorter duration ·02 CIRCULATORY DYNAMICS as depicted in curie 3 of figure 221 These changes from a normal curie illustrate compensation ind decompensation with increasing mput lords It may be added that the decompensatory responses must probably be assigned to some innate effect on the myocardium, L240 210 2 8 L180 B L150 B! L120 N N 90 2 60 B L30 I I Trg 22 -- Asgemblies of transcribed ventricular pressure pulses comparing the effect of progressive increase lo initial length and tension (secondary cocffi cients) and the effects of primary myocardial coefficients I normal curve 1 2 compensatory responses to increasing initial ten sron following rapid sahne infusion 3 decompensating response from over sistention by a large infusion Note progressive increase in initial tension at and lengthening of systole AB II N normal curve 1 augmentation of contraction with fall an initial ten4ion (1) and shortening of systole (A B) following a donc of epinephrine in 1 preparation with controlled heart rate 2 depression of contraction with elevation of initial tension slower gradient and abbreytation of contraction (1 B) following a small dose of chloral bydrate heart rate controlled perhaps a fatigue process The effects of primary coefficients are al lustrated by the curies of figure 2211 If the myocardium is stimu Jated as hy epinephrine or accelerator nervous impulses while heart rate and venous return tre hept constant the contractions lx come larger steeper and shorter un duration the stroke olume increa eu and consequentls the initial tension declines Such a response is shokn ·VLYTRCIUR CONTRACTION LADER {BNORUIL CONDITIONS in care 1 If on the contrary the ventricular muscle is depressed 29 by chloral hidrate or Pitreseint the ventricular contrartions te come more graduad rerch a louer summt und are abbrevated the strohe volume is reduced and antial toyon s elevated through de velopment of a larger reserie volume From these olisen ations the rule can be deduled (1) that secondary chuges in ventricular response ran be mferred from sentricular pris aure curses when initial tension and amplitude of contraction alter in the same direction and (2) that primary changes m i entricular re sponse are characterized by opposite changes in initial tension and amplitude of contraction It must be recognized of course that the body primary and secondary factors frequenth operate at the we time Thurs even when tertiary factors are not mrolu ed st often he cames difficult f not impossible to determine the basic mechanisms <fx govern ventricular performance Is was emphasized in Chapter Il such a dilenama arises n hen compurntne observations are muck at uffering kreart rates for the duration of dustohe filling affects tsal tension and length and therefore the magnitude rigor udruation of sentrsular contrai trong The advantages of studying the mecha urm of al»ormal xardiac re pones m cıperimental animals in huh heart rate asuell as input and output lords are controllable rather thun in human subjects when this cannot be achiesed should Isa ob 1019 With this brief orientation ne lrall prorced to inalyze the mech 1119 Whuth determine entne ular contraction patterns in 2 mm dyer of experimental conditions which wmulate hocal (sta ulatory disorders l'ericardial Efusion The ds siamic changes produced bs degrees of perirar al effuxion wosh significantly interfere with sentri ular filling and thereby a ruke reduction in cardiae output hare heen thoroughly worked out by number of mestigators 1- Onr xustom 18 aduceli Umstel ton consideration of the support that studies 0 33rdt effenn fase falses to the thesis that chan 31 tral lumth rather than mural fusson 14 the irist serontlans deliminant of sentricular re nie hinee initial tension and length generally alter in the same direction it hry pro eu diffruit to drin inferences as to much of the vartbles ·CI CIRCULITORI DIWAJIICS basically affects myocardial te ponse lle deduction of Starling and his associates that the energy of contraction honei er measured is determined by changes in initial length of the muscle fibers has been since confirmed by numerous studies in which a dissociation of intral 120 80 A 40- 120 80- C D 40 0 120- 80- E F 40 0 Fio 23-Series of left ventricular pre sure curves showing how progressive Increases in pericardial fluid and pressure stcarlls clevate initial tension in relation to a bae line but decrease maximal ventricular pressures and grali ents of contraction I ericardial pressures expres ed in mm Hg &* follou s Curve \ = 15 mm B - 75 mm C00 mm D - 100 am C = 135 mm F very high reading doubtful length and tension was achieved by experimental expedients (for bibliography see refs 22-31 page 51 ) When the volume of liquid with the pericardium exceeds the natural avaslable spate the mtrapericardial struttures are compressed by increasing pressure around them " The artial tension within the ventricles rises almost proportionally with trapen inbral pres ure but their diastolic size decreases oking to the impairment of filling ·VETRICELIN COVTRACTION LIDT AVONAL CONDITIO Oy The fact that changes in imtul tension and length we dissociated thus afforded 11 opportunity to determine experimentally which of these factors dommates carac response Some of the changes found in cntrcular pressure puls are llustrated by records of higuse 23 Cach sme rease in perkardial and intial ventricular tension is accom panied by development of less pre sure and sloner gradients The durations of isometsie contraction and ejection decrease despate some lengthens of the heart rycle of these reartsons are obuously the opposite of those normally 15500 121rd 11th mreise in initial tension hereas they becord with changes resulting from reduction in presys tolic size or initial length of ms orardal hbers Ilyper olema The basic renetions uhrh al compam an mercast in plasmr rol ume can be reduplaated experimentally by senous infusions of salıne solutions or plasma Briefly recapstulated the followmgrhamn of events takes place the greater output of the right ventricle not only ele watcs left atrı il pressure at the moment when the mitralia es open but also induces more vigorous atrial stoles Through these tuo mcchansms the left sentrale is more completels filled and mitial tension an elevated Me ventrcular responses are thove exemplified In unes I and II of figure 22 (haru teristic effects consist of steper sometru gradient cher use of pressure to a higher peak (1133518 (jertion and a prolongations of systole The larger stroke cum whubs arromp 1315€) these pressure changes is achieved through the commoned effects of a higher velocity of ejection me prolongation of the Czectron phi pid kute production of policy themie hyper olemia erches similar response Isgure 24 hou s representatie curves recorded by Gregs and my arif" after injertion of sadlimented matched corpuseks on r a peruel of fire minutes Comparison of curves 1 and B res cats an cleration of mul ten-ion a steeper metre gradient a higher vt stofir prekare and an extenson of su stole 11 are typical changes stesures by concordant Brescs in initial tension and length The Nie persist for a cousserable time is shown in curses and D 11 le respectis el 80 and } } } mutes after the infusion of cry th hulcea ed in malı 4 of aortie pirnsure pulses led to the an that the augmented peripheral te : tante otiusione} by

·66
CIRCUI TORI DIMICS
greater scosity of the blood and the strain of a higher input load
were less important determnants of left ventricular re ponse Hon
بینی
А
B
nun
с
D
FIC 21 -Four left sentricular pressure curves i control B shortly after
infusion of 00 cc sedimented matched corpuscles in 5 minutes C$ minutes
later D 115 minutes later Observe elevation of initial tengon at a and higher
pressure maxima Duration of systole as follons in seconds 1 0 172 B 0 1
C010 D 0 1/2
cver it may be noted in these records that whereas sy stole 14 some
whal prolonged in curie B It shortens again in cunes C and I)
suggesting an influence of the higher output load (sce later)

·VLVTRICULAR CONTRACTIOY LYDEN ABSORMAL CONDITIONS The recently reported obsery ations from Gregg s laborators that following blood transfusion no consistent relationship was found he tueen strohe volume and presy stolte pressure in the left ventricle do not necessanly negate the preceding conclusion They could equally well be interpreted as evidence for the limitations of the dse dilution method employed Olugemia Reduction in blood solume such as erists after a severe hemorrhage hag reversed effects on ventricular pressure curves lloeier af a state of hypotension is maintained for long intervals the my orardum 20 40 O- Fir 15 49gemblage of transenbed curves ahoning pressure changes in the right ventricle after hemorrbage and transfusion Discussion in text (After Oper ke and Waggers is depressed presumably through defectue coronary flon Is a result the ventricles cupel smaller strohe volumes their residual volume bxec omes larger and intial tension selurny to normal levels Since pressure and resistance decline less in the pulmonary arten than in the aorta the base effects of prolonged diminution in 1 enous retum are exhibited better in the right heart Some changes in right ventricul ir behavor reported luz Opel he and my elfts are reproduced in figure 25 Cune 1 represents 3 right ventricular preset re surse taken as a control Curse 2 was recorded shortis after artırsai mei pressure had been reduced to 6) mm lig by a sesere hemorrhage The sometne uscent remains steep despite a fall in initial ten von but watole as typically abridged and the storie summit a loner (ure 3 x98 recorded after a state of hypoten ion at a 50 mm 15 ·68 CIRCULATORY DIVAMICS le el had persisted for 88 minutes the closer re of pressure to a lower summit and a further abbreviation of sistole regardless of the sight recovery of initial tension are obvious Cunet was recorded immediately after a further reduction of arterial pressure to 30 mm IIg and curie 5 minutes later Initial tension is elevated above that of the control curse 1 but the gradie its and summits of the pressure curses are decidedly reduced Such deterioration of contrac tion with sing initial tension strongly suggests that a primary mo cardial depression has superi ened (For further discussion se refer ence 2) Arterial Ilypertension of Peripheral Origin The effects of increa ed peripheral resistance on ventricular con traction patterns can be analyzed best by applying a mechanu al constrictor to the aorta just above the diaphragm' "Even so adaptu tion occurs in two stages The first stage illustrated by curves labeled 2 and 4 figure 26 persists only for the first two to five bcats after 1 sudden constriction The changes in the ventricular pressure pulses are solely attributable to increased aortic resistance for the initial tension remains unaltered Since ventricular pressure must be ele vated to higher les els before the semilunar vales open Isometrie contraction (1-C) is slightly prolonged the isometric pressure gra dient is not affected because the ventricle is not exposed to the higher aortic pres. ure during this period In response to a higher aortic pres. ure the systolic ejection penod (C-F) Ly typically abridged to and to such an extent that sy stole as a whole (A-F) is al o shorter The pressure ni es to a higher summit (D) These immediate reactions are important in demonstrating that the basic re ponse to a sudden increase in aortic resistance consists in developracnt of greater tension with abbreviation of contraction However with each contraction the strohe volume is not quite nor mal a small amount of blood is retained and with a normal inflow volume quickly increases the pris tolic size and initial tension The second stage then super enes Curic 10 of figure 26 illustrates the e secondary effects in the tenth beat following aortje rompre con Inital tension is slihtly elevated the i ometne gradient 19 steeper the period of sometric contraction decreases and the cjection phase C-F is now prolonged The reactions ·VENTRICULAR CONTRACTION IDEA 18YORSAL CONDITIONS 89 of the ventricle to increques instial ten on and length or tously he come dominant Changes in the contour of the pressure summits reveal that the pattern of su tolir ejection bas changed Responses of a similar nature follos generalized augmentation of arlerolar resistance such as can be updured by stimulating the cen 180 160 1140 In 120 C N 80 60 40 20 A blembase of tran cribed curves ta beating changes o lest ven tricular p escur from normal {) during the second fourth and tenth beats After audden com 4 109 of th forts just al ove the diaphragm In beats 2 and 4 note same inual tension prolongation of isometric contraction (A C) dualarepent of summs (D) later in sistole and earlier termiation of systole att in i eat 10 aote additional effects of increngiag Bittat tension at I such *1 ateeper sometric gradient higher systohc pressure (D) and prolongation of systole (4F) (13) ends of the guy neries The myocardial reponses are complı ttel hoseser by the greater enous retum wlich folloss displace munt of blool from minute peripheral 104, and the pleen and by ugmentation of coronars flou Con equentis the output of the night heart parkly increases and larger volumes of blood are delivered to the left heart . The ne of instsal presure and the liſt ventncular ·70 CIRCULATORI DINAMICS responses art thus accentuated to such an extent that the stroke olume actually exceeds the normal Aortic Coarctation Clinical types of aortic coarctation can be simulated by stepwise constriction of the aorta proximul to the left subclavan arteri Re Cent studies by Gupta and my self"' hue shown that the lumen of the torta must be reduced by 55 to 60 per cent before an elevation $180 1160 140 120 L100 80 160 L40 -20 CN Catfc A Fja, - Assemblage of transcribed records showing deviations from a normal left ventricular pressure curve (V) folloning reduction in aortic lumen just peripheral to gubclavian artery by 60 per cent in curve 1 and by 87 per cent in curve 2 Note abbreviation of the 1sometric phase (A C) the delayed summit (D) and the abbreviation of contraction (4 F) curve 1 Also observe the htgher initial tension (A) the higher rounded summit (D) and lengthening of øjstole (A F) in curve 2 of aortic and left ventricular pressures ensues Figure 27 shons some consequences of effective degrees of couri tation Comparison of the e curics with those of figure 26 reveals many similarities but there are two important differences in the former aortic diastolic pressure rises in the latter it declines Conscquentis in corrctation isometre con traction is terminated earlier as indicated at C, and C, on curies of figure 27 liso initial tension (A) fails to increase until the aorta has been constricted to 80 per cent of its natural diameter As soon 29 initial tension increases systolic ventricular pressure 18 cleated still ·SESTRICE L4R COSTRITION DER BIORUAL CONDITIO more as shown in curier of figure 27 anrl the ssstole discharge al o becomes frenter hinte augmented strokt solumes are realized depute & marked re durtion an aortu pressure below the coarclation and hence a drastk tecrcate in inferior caval for the interenie lodows that total 1 enous return 19 tebalanced through corresponding augmentation in superior caval and coronary fons The correttness of this deduction had bech previously demonstrated in simlar expenmenis performed in son Junction with hatz 18 shsh indicated that night atral and ventricular presures may cien cleiate slightly owing to s somewhat greater total venous return It has been amph 1817el that the augmented pulse pressure central 10 a corretation 19 associated with ? decline of diastolrr pressure Such hemodynamic effects (annot be attributed to an increase in aortic resistance at the site of narrowing or to an augmented stroke volume It bereme ois sous to however that when an effective construction exw the capacits of the aorticompression chamber becomes vers kmall and ita volume elasticity cocfficient (dP I ) 19 greatly more sed low it can be demoustrated on artificial circuta tion models that when ersus alent stroke volumes need to be taken up ma compression chamber w fuck is less distensible (increase in dP I ) the mean pressure alters sery little trut systolic pressure re and diastolic prouzre fal4* Menxe ( upta and cers' con uded that the entral elfects of aortic rose tation are sot skol's due to murea pressstanse at the lor tis of retation but that they alomon credu tron in rapuity and duten bilty of the compression chamber The latter 19 wholly re ponssble for the rainction of diastole prostire and contnbutes to the elesation of ssstolic pressure m the aorts and left sentru le Aortic Stenosis This patholog condition is usually studied experimentally by tightening a cor around the corta in close proximity to the aortic orfire Such & stenosis differs physically from that presented by co ir tatsusm that the aortie compres son chamber kentirely abolished! and airiulator <hzels proximal to the steno is return less blood to the right heart 11 spatigators grex tltat 9. in the case of aorti corretation the aortic onfice mu the narronai to beturen A and Ser far 7D page 13 ·72 CIRCULITORY DYAVICS 70 per cent of its original diameter before cardiac output per heat or per minute is reduced (Tor bibliography sec reference 21) leier theless narrowing of 1, to 30 per cent suffices to create audible and recordable mumurs The changes in left ventricular contraction depend on the degree of aortir narrowing in mild degrees of stenosis exemplified by curie L220 3 F L140 N -80 -С A L20 FIG 9 --Transcribed left ventricular pressure curves showing effects of ditt rent degrees of aortic stenosis N normal curve 1 = 2 per cent constric tion curve 2 = 45 per cent constriction curve 3 = $5 per cent construction Lettering as in previous figures Description in text 1 of figure 28 the ventricular pressure curves resemble those produced by moderate augmentation of aortic resistance shown in figure 26 initial tension and the isometric pressure gradient remain unaltered but the pressure summit is higher and displaced to a later moment of svstole Isometric contraction (A-C) is prolongedi slightly but the duration of total sy stole (A-D) 18 not affected De Heer 25 who re corded similar curves believed that slich reactions typils the effects of aortic stenosis augmentation of aortic resistance was considered ·VTRICUL.4L CUTRITIOIDER NORUL CONDITION 73 to be the chef determinant of myocardial response However hatz 233d his associates found that the ventricular presure curies are more pealed as soon as the degree of steno-s becomes dynamicalls gmficut The pressure summit is reached earlier not later w systole Such contraction patterns are shown in the transenbed curses 2 and 3 of figure 27 When ventricular certion 19 seriously impeded the ventricles approach an isometric type of contraction in which the sncreasent residual olume and mashed elevation of stað tension contribute to the production of very high stolt ventri ular pressure It should be kept m mund that the reactions of the left ventricle may be more favorable in experimental than in clinical stenosis In the former the constru lion 14 peripheral to the roronary orefices and coronary hlood flow is decidedly enhanced in the latter the narrou ing is proumal to the coronary ostia and coronary fou 18 unquestion abils recured In order to determine whether superposstion of roro nary insufficiency alters the mechanism of ventricular response the effects of seere pulmonın stenosis may be analyzed Pulmonary Stenosis Figure 29 contains segments of rerords obtained by Funeberg and my self during pro,ressie circular compression of the pulmo nary artery segments 1 to 3 shon teady increases in mital tension higher stol susunits and contoure kisslar to those obseried pt mus pas se ansti stenosis It may be noted that the aorta prywatnes istuin to be afferted in segment } in sheh 12 per cent rerlur tre 12 in the lumen of the pulmonan trien had been produced ! ghth greater constrution initiatrs « greater declme of arterial pressure ?y shonn h egments 4 - and 6 which repertn els repre went «onstrictions of wl J9 and 63 per cent of the lumen 1}xe right sentricular pressure curses all display contours typical of an kometrar mule of contraction Honeser as shown in segments 5 and the sy stolte summit rapidly falls with increring steno-23 ustead of n ng further as in aortic stenosis (Fig 28) Simee ich leclme of pres ut Basociated with marke elevation of inttial tenson « a logical mfuence that myocardial depression due to a lectuate coronary flow hi stipenciler! ummarizing the abilits of the night or left ventru le to overcome 13) re 1tune of a nutroned aortic orifice depende as murh upon the

·130
18
C
2
0
Drex
A 3
3
Ea
4
SA
0
F
0 43
-
+Ae
A-20
5
6
Fio --Srgments of records showing changes in aortic preveure (urtir)
and right ventricular pressures (lower) following steparse increases of rul
monary steaost8 1 control ' - 20 prr cent constriction 3 - 52 per rent con
atriction + 56 per cent constriction 5 = 59 per cent constriction 6 - 63
THT cent constriction Discussion in test

·VE VTRICI LAR COYTRACTION TYDER AR\ORIAL CONDITION 73 ability of the myocardium to compensate as upon the actual degree of narrowing The te pongiveness of the myocardnim in turn depend on the adequacy or insufficiency of coronary blood flow The abnormalities of ventricular contraction so far con dered ! lustrate conditions in which primary and secondary factors separately or together determine the nature of ventricular responses e tum now to consideration of a few conditions in which tertiary factors play Important roles PH 13 07 wwwwwwww Fra 30 -- Tortic (upper) and left ventricular (loner) curves depicting changes during an effective premature contraction / ometric pha e E ejection phase Time 02 second Di cu ion un lett Idiouentricular Rhythms It is well establıslied that premature sentricular contrartions or a succession of such beats during sentricular tachycardia are charac terized by delivery of smaller stroke volumes The contraction patterns of a normal and a premature entricular systole can be comparel in the ventricular pre sure curses shown in figure 30 The premature beat differs from the preceding normal one in several nais namely the lower systolic pres ure summit the changes in contour the prolongation of 1 ometric contraction (I) and an abbres nation of the ejection period (C) suffictent to shorten sy tole as a whole (I + F) The reduced force and duration of contraction are related to the shorter period of filling in the antecedent beat and consequenth a ·76 CIRCUL 4TORY DYNAMICS reduction in presystolic size and initial length Attention mas be directed to the fact that the premature contraction starts at a higher initial tension because it begins before relaxation of the previous I II F CA H н 029 135 098 074 06.159 105 073 065 025 015 .03) oss Ox) oss od 015 035 Fra 31 --Coraparison of left ventricular pressure curves of same cycle length when excited over normal pathways (I) and from a ventricular focus (IT) The diagrams below compare the approximate order time and direction of the excitation process during excitation from a supraventricular (I) and ven tricular focus (II) Letterng as before Vote prolongation of sometric con traction (A C) and ejection (CF) in 11 Time 02 second Discussion in tcut beat has been completed This is another illustration of a condition in which initial tension and length change in opposite directions and as prej jou ly explained the reactions scem to follow changes in intial ·VENTRICULAR CO\TRICTION LIDER ABNORVIL MODITIONS 77 length not those in initial tension Hovercr the shorter initial length 18 not the dominant factor which determmes the impurment of ven tricular contraction The basic factor concerned was di coi cred in 1922' by comparing beats of the same cycle length excited from supraventricular and ven triculır foci Such records are shown in figure 31 The idioventricular beats (right) ari e from the same initial tension as normal beats thereby excluding scuondary reactions to initin length Nevertheless beats due to direct ventricular stimulation display a longer Isometric contraction (1-C) a prolongation of systolic ejection (C-F) and a conspicuously lower systolic stimmit Thiene changes are due to the abnormal order and spread of ventricular excitation from an idio ventricular pacemaker The concept des elopel 18 illustrated by the aid of the diagrams beneath the pressure curves of figure 31 During normal excitation (I) impulses are conducted with great speed to all fractions of the myocardium hence a rapid summation of fractionate contractions takes place When impul es ari e from a ventricular focus (II) they spread more slowly at first and m a random fashion with the result that the phasic entry of contractions is delayed is analyzed elsewhere? thus results in prolongation of contraction and des clopment of less maximal ten ton In addition the order and direc tion of sprend of the ventricular cutation proese determines the mechankal officiency of contraction During normal excitation over bundle branches the interventricular septum 19 primarily excited and contracts first i rigid fixation is thus provided around which the ventricular muscle scrolls can contract and empty the ventricles efficiently lthen cxcitation usises from the ventricular focus im pulacs et cntually reach the bundle branches but they travel in a reverse direction the septum is excited last and from aper to be The resulting contraction of the ventricle as a whole would appear to bele y eficient and may contribute to the loner pres ure des eloper during sy stolic ejection lo summarize idioi entricular leats are less efficient than normal ones beciu e the sentncular pattern of contraction is affected by fuo factors (a) the abnormal sequence in which fractionate contrac tions develop and (b) the changes in ventricular filling which occur when the diastole of a preceding beit sabridge! The former retards the rate of pressure development and prolonge contraction but re ·78 CIRCUL {TOR: DYNAMICS duces the maximul pressure developed The latter contributes to the slos de clopment of tension and lower systolic pressure through changes in initial length but reduces the period of contraction to such an extent that the lengthenmg effect due to aberrant excitation 19 overbitinced hence the ejection phase shortens Ventricular Alternation It appears to be the currensus that sentricular alternation is # primary licorder ini olumg abnormal excitation and or contraction of myocardial fractions In 1914 Wenchebach' adianced cogent a priori re lines for the concept that some types of alternation may loc I IN Fra 39 -Transcribed curves of left ventricular pressure I control curve before alternation II larger beat and III smaller leat of an alternating couple Lettering as before L, I, and I s indicate the effect that different levels of atrial pressure may fase on the time when ventricular inflow begins induced and sustained by hemodynamic mechanisms which auc alterations of ventricular filling in alternate berts The question there fore arose whether there are two types of ventricular alternation myogenic and dynamic and if so whether means cut for their differentiation One of the first questions that interested the writer in the study of alternation $115 whether the large as well as the m2) beat of an alternans couple is abnormal then records were fortu tously obtained at the moment en alternation stuted spontane ously the surprising discostry was made that the larger beat of an alternins couple is never maller than the precedut, lormal one anci frequently is even larger (fig 32 curtes I II) In such supernormal beats the gradient of sometrie contra£tion is a trille steeper and ·IF TRICLLAR CONTRACTION LNDI RARIORVAL (OVDITION) 79 systolic ejection and total systole are both a trifle longer than in pic ceding normal beats It would appear that the large alternans Feat involies no fewer contractin, frictions than a procedm, normal une Several explanations for such supernormal beats ure possible (1) state of potential alteration may have existed in the beats rewarded as normal that is to say an equal number of contracting trutt10115 may be deleted in every beat (2) The incre i ed umplitucle and dura tion may be secondary to a slight increase in presy stolicize und in tial tension which for some rer on a comp imies the on et of alterna tion (fig 32 curve II) The dynamic differences between large and small beats of an alter nans couple tre illustrated by curves II and III of figure 32 The smaller beat starts from a slightly loner presystolic pre ure it als Fra 33 — Aortic (upper) and left ventricular (lower) pres ure curves show ing the development of temporary alternation (1 2 3 +) after a compensatory pause (C) following a premature contraction (1) is normal leat Time 04 second plays a more gradual i ometric gradient 1 longer isometric phase (a-c) a shorter systolic ejection pha e () and a shorter period of total systole (a-d) These changes were attributed » I am to dele tion of contracting fractions Since pressure also degrades more slowly during isometric relaxation (d-e) Straub lad greater tre son chiffer ences in relaxation concluding that alternans develops only when the heart rate is so fast or the contour of the pres ure curies o broad that the pressure does not have sufficient time to decline before the next ventricular excitation superi enes During an mestigation of premature ventricular systole the ob Acriation was made that a temporary altcmation often follows a long diastolic pau pt # A typical re pon-e is shown in figure 33 A premature Nistole (P) succeeds a normal contraction () The long compensatory pruse (C) allows greater filling of the sentricies and elevates initial ten ion lightly This could account for the larger ·SO CIRCULATORI DYT 410CS and prolonged post compensatory beat lonever it is not at once onuous why beat 2 is so much smaller and why alternation persisted in beats 3 and 4 and in two more beats not included in the record Further studies rei caled that similar reactions follow brief 12631 U N N wwwwwwwww Fio 31 -Two sets of aortic pressure pulses and ventricular volume curves systolic emptying indicated hy downstrohe in the latter Upper set normal beats lower set changes in larger beat (1) and spiller leat (S) after develop ment of alternation The strohe volume of smaller I eat (S) 18 less complete and is followed by more gradual filling (UV) The stroke volume of the larger beat exceeds that of normal ones shonn in the upper set Discussion in text Time 002 second (\fter CJ Wiggers Pressure I ulges in the Cardiovascular System courtesy of Longmang Green London ) stimulation or a temporary block Volume CUTS ES of the son tricles such as are reproduced in figure 34 demonstrate that the rate of diastolic inflow is slower in the maller beat but since the entricu lar expulsion is less complete the presystolic volume and initial length preceding the larger ixat are greater 1 On the basis of such ·VI VTRICULIR CONTRIOTION UDIR AB\ORYAL CO DITIONS 81 results it was obvious that alternition enn arise dunng the period of 10djustment from a momentary inercase in diastolic size It was emphuized however that much alternation is temporary and tahes place only when the heart beats rapulls It is therefore pos able that a tendency to alteration exists previous to the disturb ince of ven tricular filling Summarizing my content viens it appears Inghly probable that entricular alternation always my olscy the defection of some fric tionate contractions durin, the smaller bcat However changes in the intensity of alternation do not necessarily signify quantal variations in the deletion of fractionate contractions They can be induced by accondary dynimie factors which alter diastolic distention and initial tension For example of the residurl volume of blood 19 suddenly increased during a smaller contraction the addition of a normal in flow volume during sucreeding relaxation leads to a larger presystolic Volume and initial ten ion with the result that the amplitude of the larger contraction is augmented It is for uch dynamic reason that a casual irregulinity muy intensify in eusting alternation While ventricular alternation u ually involves deletion of fructions distributed throu hout the myocardium it may be caused by alter nate changes of contraction in only one region The fact that periodic interruption of blood flow in a coronary ramus frequently re-ults in alternatim of the ventricle as a whole affordded (reen" an opportunity to study the dynamics of alternation accompanying coronary in uf ticiency Vyrographic records from the region of impured blood sup ply revealed that three types of alternation may ocur (1) The region my shorten les dummg the smaller than during the larger beat (2) It may shorten Juring the larger and actually stretch during the muller be it indicating, alternate ab rnce of contractions (3) It may cyprind in both the small and the large beats but to a fewer extent in thic latter (rern" al o found that the surface fibers in an ischemic arri ar stretched to a greater extent before inception of the smaller bezts than previous to the onset of the larger one te interpreted this as proving that alternation following coronari in lei nav due to perioclie deletion of contractile units anil not to alternate responsey to chinken in initial length Turther upport for the localized ource of ternating luts in my ocardial ischemia 114 recentis offered in the ·82 CIRCULATORI DYAMICS observations of llellerstein and I ebox * They reported that the ST segment and T wart more rarely the QRS complex alter in epi cardial leads from regions overlying the ini oled area These discussions of alternation following coronary insufficiency offer a natural transition to our next topic Coronary Occlusion-Myocardial Ischemia The immediate dynamic effects following experimental coronary occlusion were first analyzed by Oriasand have recently been con firmed by Kupfer Representative immediate effects are shown in FROM B X Y Z Fig 35 -- Aortic (upper) and left ventricular (lower) pressure curves show ing the immediate and dela; ed effects follosing occlusion of the ramus descen dens anterior A control B one minute after coronary Occlusion (compensa tion four minutes after occlusion I control from another experiment effect two minutes after coronary ocelusion Z decompensation 15 minutes after occlusion Discussion in tert segment B figure 3, 1 and B Within a minute after interruption of coronary ffoir aortic pressures and pulse pressure are reduced and the form of the aortic pressure pule 19 altered tro phenomena that definitely indicate immediate reduction in systolic discharge the left ventricular pressure cures furnish the explanation for such ventricu lar impairment The Hometric pressure rise is slower but since the semilunar valses open at a lower pre ure this phase may not be ·LEYTHICULAR CONTRACTION UNDŁR 1BVOR SAL CONDITIONS 83 prolonged The period of sy stolic ejection is abbreviated considerably and the pressure summit is lover and more rounded Oras " applying busic information guined from previous studies inferred that these immediate changes are caused by a deletion or impaiment of con tractions in the block of myocardium within the territory of the oc cluded resel In 1932 Tennant and liggers' demonstrated objec 2 27 fro 30 -Tno record of my ograms from the anterior surface of the left ventricle (upper curve) with sortic pressure sul ea sud an electrocardiogram (lead II) I & normal control al records obtaireitno minutes after occluding the ramus descendens ante for Note that in 1 shorteding of the area 13 in cated by an unsard deviation of the curve shule in Il marked etpansson 18 demonstrated by a downward movement teine otheti a vertical line titely by myographer tracings that this interpretation is correct is shown in figure 3611 approximately within a minute after coronary Occlusion the chemic area no longer shortens but expınds brusque during isometric contrretion and either remains ao during the re mainder of my stole or tindergoes a slight hortenng Cucn such a lunt through experimental oli ersation a number of investir tor # hare uh cuently launlı mein of fuormitopu rentg4110 ·81 CIRCULITORY DIICS graphic and clectrokimographic technics that the infarcted area in human cascs expands in a similar fashion Such defective contraction in the potentially infarcted arci reduces the total myocardial force for raising intraventricular pressuire In addition some of the pre sure created by still viable portions of the myor arduum 15 punt in stretch ing the ischemic area and is thus untı ulable for expelling blood into the aorta Is shown in segment of figure 35 taken four minutes after coro nary occlusion the heart has compensatory mechanisms by means of wuch dynamic conditions cin be quickly restored to normal pro uded the remaining myocardium is in good condition 11 hile this interpretation accords with the general clinical opinion the experi ments just quoted are to my knowledge the only ones on record which really demon trated that compensation occur not through improve ment of collateral circulation in the affected area " but through en hanced action of the unmvolied myocardium Lyperiments such as these also clucidate the mechanisms by which the rest of the mu cle respondly promptly and componentes through nua e martolo size and elevation of tral tension " Bricfis the following cham of etenis tahes place During hy podynamic beats such as are cubiteri in segment B the sentricle expe) le s blood the accumulating is tolic remainders addeel to oncomng blood progressively in a c the presystolic volume and pressure in the left ventricle and stretch the viable muscle this muscle in accordance with the lau of initial ten sion and length contracts more viborou ly thereht restormg card output and arterial pressures to normal Such compensation is illus trated in segment C If on the contrary the wable yantra ular muscle is not in food ze poustic condition promis ir dotcuoration uperoxy See mort 1 and 7 of figure 3 taken from another e pamant mustrito this type of response The ventriculu pies uic summit louers ntr ulls sstole 19 shortened and arterial pul « presures full prorech despite the fact that initial tension ni es steadily As far as my expert mental cu dence goes the circulatory failure which follos , utirely due to myocardial decompensation there has ncier bien endence in our studies such udirates that peripheral fictors are involved in the circulatory failure * " Cinulatory imbalance mit houmier super sent through the development of cardiac irregularitie for instance, repeated premature contractions or athul fibrillation de place blood ·VVZRICULAR COSTRICTION UNDEP BORIL (OVDITIONS 6) from the arterial to the venuus de and to the pulmonary vesels with the result that a significant hypotens2011 may develop uhuh 19 often confused with a true state of hork The Importance of Cardiac I ales Handell Henderson pomtel out that the land chilun ir Valyes clust the ventricles to contract and relax in a manner imilir to that of a keletal muscle attached to an instrument devised by SL AV Tir 31 - Dingranı illu trating tic rinciple ir ch s korhadder D scrip tion in text (1fter Ilen lers in curley Am J I hys ol ) Mich and known as a work addir íslustrated in figure 37 the upper end of a muscle is attached to a stiff pring wluch rzi be arranged to record the muscular tension before and during contraction The lower end of the muscle is attached to a movable lever on which a small kent is hung Tlus soight which correspond to the mput loud of the ventricles lengthens the muscle lightly and creates a small ten $ion picuous to contruction (utsal length and ton ion) ratchet 11 upon the tootheel wheel of the work diler comparable to the 1-1 alice presents the leier from mosing until sufficept to jon las ·86 CIPCULATOI I DYAMICS been developed to or crcome the furce of a larger weight attached to the toothed sheel This height which corresponds to the output load of the ventrı le 19 supported during the phases of sometri contrac tion and relaxation by a second ratchet SL which corresponds to the cemilunar valies Such an arrangement causes the muscle to contract in an after loaded minner If we release the ratchet L the large loud acts upon the mu cle before contraction starts and a loaded type of contraction re ults 1 similar stuntion might be expected when the aortic valves are grossis incompetent If we reerse the ritchet 41 no connection clists with the large vhcel to which the heavier weight is attached Hence contraction of the muscle would merels raise and lower the small weight and never move the large one similar situation might be postulated during gross mitri incompetencs nimely that blood would merely be moi ed back and forth between the left atrium and ventricle without any discharge into the aorta Obviously neither of these postulated effects artually takes place in the heart which can still propel blood after deletion of all valves The phyical and physiologic reactions which make this possible need to be considered Aortic Regurgitation The dynamics of the valvular lesion which has interested me since 1915 involves three problems (1) the mechanisms by which systoliu discharge is essentially restored to normal (2) the time of regurgita tion during diastole and (3) the factors which determine the regurgi tated volume (for bibliography sce references 24 46 47 ) The immediate effect of an hortie leak is a retłuction in the net stroke volume a smaller aortic pulsc pressure and an mirease in the dia tolic ventricular olume When the myocardrum is in good con dition it responds at once to the greater initial length and tension with a more vigorous contraction is a result the tidal volume ex pelled from the ventricle increase considerably The lo s of pres ure which arcurs during diastole results in a cry lou end diastolic pres sure in the aorta Since si stolte pressure is Lenerally clevated through the augmented systolic discharge the aortic pul c presstipe is extremely large Thc e changes are illustrated in figures 38 and 39 Iliggers and Maltby 's di covered that the reaction patterns of the left ventricle depend to a considerable extent on the size of the aper ·FYTRICULAR CONTRACTION UNDER ABNORMAL CONDITIOV8 S7 ture The effects produced by small leaks are shown in figure 38 The initial tension is increased at A and the isometri contraction phase (A-C) is shorter because expulsion of blood starts at a lower aortic pressure (C) The increased durations of ejection (C-F) and of total sy stole (A-F) are reactions to the higher initial tension The WMWMWWww Fir 39 - Upper records normal aortic and left ventricular pressure pulses Lower recor is same after production of a comparatively small aortic valvular leah 1 C isometric contraction C-F ejection ph9904 F I relaxation to l asic pressure levels summit of the pressure curse is reached carlier bec use the ventricle empties itself more completely unng the early portion of ejection when aortic pres ure 19 still ubnormal Summaning the pattern of ventricular contraction as cxhibited by the form of left ventricular pressure curves 18 a re ultant of (1) the lowered aortic re istance dur ing the early part of contraction and (2) the compen atory effect ·88 CIRCUI \TORY DININCS produced by a greater presistolie stretch and elevation of initial tension When the nortir leaflets are spread wide apart so as to illou mau mum reflux during diastole the pattern of ventriculat contraction 19 further changed because the full aortic load plays on the left ven Wiwwwwwwwwwwwwwww Fio 39 - Upper records normal aortic and left sentricular pressure pula lower records same after production of a nia inium aortic valvular nulli ciency Lettering as in figure 39 tricle and it contracts in a lorded manner Such continctions tend to be of shorter duration than isometric types of contraction Tlic effects on left ventricular pressure (uris an illustrated in fiqure 39 Ilie elevation of initial tension is unquestionablı re pottuible for the ck velopment of a higher systolic pre sure and the cjection of larger trdal volumes into the aorta The latter (alt Ix inferred directly from ·IL TRICULAR CONTRACTION DER BYORVAL CODITIONS 89 the large aortic pulse pressure which starts from a lower diastolic pressure However, in the majority of cases the expected lengthening of total ay stole is neutralized by the loaded manner of contraction It might be expected that an isometric contraction period could not exist in a londed contraction Actually records that are reproduced in figure 39 indicate that a brief ri e of ventricular pressure (1-C) still occurs before aortic presure starts to rise This delay 19 ex plained by the facts that the current of blood in the sentricle must be reversed and that aortic duastohe pressure slightly exceeds that in the ventricles The records of figures 38 and 39 show clearly that the time of dia stolic regirgitation depends on the size of the aortic orifice With openings of small and moderate size (fig 38) the gradient and dura tion of sometric rclaration remains unaltered the chief decline of aortic pressure occurring after completion of isometrie relaxation at Illence the inference that significant regurgitation does not take place until relaxation has progres ed to a pressure level at which the mitral vakey open In this was a dynamic situation is created in which flow from the left atrium competes for ventricular spare with that through a leaking aortic vale (See also fig 10 Chapter I) On the contrary when the emilunar valses are widely eparated aortic pressure falls abruptly to a los fer el during the time the left ventricle relaxes (fig 39 F-I) and consequently declines compara trely little during the remainder of diastole The inference follous logically that in very large leaks regurgitation takes place immedi ately during the decrease of ventricular tension It may be addeci parenthetically that this period corresponds to sometric relaxation in the normal heart but cannot be de ignated as such since the von tricle contracts as a loaded not as an afterloaded muscle The slow clevation of tension after I in figure 39 18 attributable to ventricular filling from the left atrium The influence that the ize of the leaking aortic orifice has on the regurgitant volume has been studied from physical and engineering standpoints on molels as well as on dead hearts (For bibliography sce references 24 4 +7) Typerimental work convinces us however that the magnitude of regurgitation depends as much on the ticcelle pressure chfferences as on the size of the Icahing orifice Is a matter of fart for purelt phs al rei ons the total presure difference du ·90 CIRCUL {TORY DYVAMICS minishes as the size of the leading orifice increases the hydraulic principles can be gleaned from the allustration in figure 10 in which aortic pre sure curies simulating those obtained after large and small leahs are superimpo ed on a common sentricular pressure cure The stuccessmediastolic gradientsintheciseof smallerleahs are represented by the sea Cy and those on the case of larger laks by the area (x + Cr In former curs I defended the vien preu jously suggested by Stew art that the percentage of the tidal volume which regurgitates ro mains relatively small esen when salses are grosely deficient Sub c quent observations in our ounio 17 and other laboratorica demon 160 120 180 40 Fra 10-Diagram elowing that the diastolic preeguro differential between aorta and left ventrcle 19 less in the case of small sized sortic orifices (CY) than in large ones (Cx + Cy) strated however that regurgitation solume may increasc up to 60 per cent of the tidal volume with large aortic opemings Mitral Insufficiency It is generally conceded on the basis of animal experiments that the reduction in sy stolic discharge which results from reflux of blood into the left atrum is somchos compensated bt mobilization of a larger tidel olumIn 1922 Wiggers and rel's clucidate the com pensatory mechanisms concerned through sestration of prresure pulves from the left atrium and entriele Our studies indicated that the sudden creation of 1 mitral leak 18 succeeded by the following trun of cuents By urtue of the systolic backflow through incompe tent sales the volume of blood discharged wto the aorta elung eich sy stole is reduced As illustrated a figutt 11 maximal ventricular ten son is louered immediately, but it increases gradually as initial ·VI.XTRICL LAR CO TRACTIO\ W\DIR VORU AL CONDITION 01 pressure res It the same time the pres ure in the left atrum in creuses and the cures show a marhe sistolic elevation with mumur ubrations superimpose! Inder the greater head of prea ure at F the left ventricle fills more completels and the effects of augmented initial tension and press stolte volume come into play Vaximal intra Tentricular pressure increases steadily and the duration of tole as slightly prolonged u Л r **WMNM'LA...? 612 return wu. Fic 41 — Pressure curves in left atnum (upper) and left ventricle (lower) illustrating immediate and stabilize i effect of rendering the mutral valves suddenly insufficient AB atnal systole B-C 1sometric ventncular contrac tion CD ejection phase E From tric relaxation Time 09 second lote superposition of systolic murmur vibrations on atral curve Description in tert (After Wiggers an: Feil courtesy of Shaw and Sons London.) The records of figure 41 shou other interesting details Compani ons of phasic presure changes in the left atrium and ventrcle demon strate that even when a statut equilibrium has been reached left atrial pres ure ri es onls to a minimal extent during i ometric con traction indicating that no significant regirgitation takes place dur ing this phase The main elevation of left atrial pres ure and the real regurgitation or cur simultaneously with di charle of blooil into the aorta Furthermort regurgitation does not terminate preti ch with Rystole for atral pressure continues to my at a relucel rate during the period of isometric relaxation These t mes of regurgitation and corroboratel by registration of solume changes of the left atrium Special forms of cardiometers Such records are lont in figure 42 When regurgitation cyrsts the left atral volume deerd en during atral A stole (A-B) increases very little during i metrie sentorular ·92 CIRCULATORI DIN IVICS contraction (B-C) augments rapidly and con iderably during the period of sy stole ejection (C-D), and continues to increase for 108 second durmg isometric relation of the rentricle (D-E) During the succeeding rapid inflow phase (F-1) the uolume of the left atrium decreases rapidly as it empties into the left ventricle Physical factors alone account for such a time course of regurgita tion Since the isometric contraction phase is very short (004 to 00 necond) and the pressure mcreases roughly from 1 to 70 mm llg the inertia of blood within the sentricle cannot be quuchly overcome and the blood is not set in backward motion until the aortic al es lave opened Thus any considerable reflux is dynamically impossible even #hen openings of con iderable size exist in the contrary systult ejection lasts from 0 15 to 023 econd and the mtraventricular pres sure ranges from 70 to 160 mm Ilg The continuance of such pres»ures over a longer time interval determines the considerable backflow dur ing systolic ejection Finally since ventricular pres ure still exceeds intre atrial during isometric tclaration equal to 0 08 to 009 second regurgitation continues despite the fact that diastole is actually m progress That the e types of regurgitation do not in olie mechunisms pe cular to the heart but are determined by play si al factors can be demonstrated successfully by simple apparatus llustrated in figure 43 The device consists of a chamber (1) to which an optim) musom eter (MI) recording the pres ure within it is attached The pressures increased by rapid compression of large bulb (A) I land is thus des placed either through a valveless tune into a boitlt (C) ag unst a Aurd column varying from 0 to 10 mm H20 or bx a larver tube through a valie mto a sceond receptacle (F) contine a mercuri column equal to 60 or 80 mm Hg Time relations of regirgstation to pressure de elopment, is well as the volume actually regurgitatel into the bottle (0) under different pressure condicions may be op tically recorded by connecting the bottle (C) to a tambour (1) at tached to an optical capsule (T) Figure 4 shows a record in which the pre urc sariations in the stem simulate those in the fue irt is pressure is rapidly to a point corresponding approximately to the scometre phase (1-B) thx regurgitation indit ated by the iluker curie serccerlingly hight During the subsequent nie and fall of pressure (B-6) corrr poudang ·FNTRICULAR CO TF ACTION INDIR ABNOVIL (\DITO )3 w TIC 42 - 1 olume change of the left atrium relate to a lift ventricular 8 ure curye Uri r volume curves during tral Artion ( 11 valve Lower volume curves adju tel to Hilme vontricular premaure curve 1 ut taken aſter production of mitral inruil ciency A B recrrae ir atpalvolim luring atral 818) B-C Blight inCTCA an volune during is metric contraction in both curves CD mrr marhei inere ein volume aluring #stoli cjection in lower curyr Di continuand volume increa during 180mmire rraratin in wer curve II mote mathel reluction in atrial volume during rajil infx planc in lower curve (Vter 1188 so an 1 cl" courte > Sham at Song I ondon )

·91
CIRCULTON DYINICS
D
H20
C
M
А
B
TIG 43 - Physical model to demonstrate regurgitation and forward move
ment or a liquid Description in text (After Wiggers and Feil courtesi Shaw
and Song London )
Fic H-Records of pressure (hghter curse) and periods of returgration
obtained when bulb of aprarstus shown in figure #1 18 compresse I to simulate
Ventricular pr gure clang a 1 B isometrie n e of pressure BC pri of
ontput into piercury chamler CD relaration of bull Description in text
(Alter Baggers And Feil courte jol Shaw and hory Isnion

·FVTRICULAR CONTRACIJO UPŁR BORILAL COVDITIONS 9) roughly to the ejection phase a larger olume is regurgitated 4c in the heart this backflow does not cease when compression is stopped at C but continues until D It can al o be denionstrated that such a physical phenomenon is conditioned upon a rapid compression of the hulb If the bulb is squeezed very lowly and the pressure elevated Very gradually backflow starts at once and regurgitation becomes large during the isometric period which is there by al o prolonged The bulb may indeed be compre sed so slowly that its entire contents are emptied into the bottle The inference is clear the volume of re gur,itation is conditioned not onls by the size of the leak and the mean pressure in the rentricle but also by the velocity of tension development during isometric contraction Given the same orfice more blood regurgitates when ventricular contractions become hypo dynamic HIerein lies the real compensatory importance of good muscular action during mitrul insufficiency Filure of the myocarduum to respond adequately to the increase in initial ten ion results in a series of es ents which end in decompen ation The seriousnes of the valvu lar lesion consists in the fact that the patient or anım al with incom petent mitral values has lost a factor of safety by which slight cardiac depression can be readily with tond Vitral msufficiency i dangerous pumarıls not by virtue of the circulatory changes induced through Valyul ır deficiency but on acount of the constant hability to de compensation from any iau e which weakens ventricular contraction Inally attention may be duected to the fact that since the rate of pressure increase is surh an important determin unt of the volume re gurgitater calıulation of the ize of leaking orifices from laus ba ed on static equations do not necess zrely apply to the heating heart Mitral Stenosis It has been recognized for centuries on a priori reasoning (Vieus ens 1715) that arros of the mitral orifice introduces 1 resistance to the flow of blood from the left atrium into the ventricle thereby impairin, its filling and stolic output This was confirmed by care ful studie on artifiual models and by earls experimental work it was generally agreed that marked degrees of mitral n irron ing cause a reduction in stroke olume , decline of arterial pre ure and a decreu od enous retum to the right heart The con i lent a c of left ·90 CIRCULATORY DIA AMICS atrial pressure (auses pulmon irt congestion and according to most observers an increa e in pulmonary arterial pre sure The con ensus has been that right atrial and systolic right intricular pressures fall (For revicus ec referosxe 24) In 1931 Katz and Siegels properly called attention to the difficulty of producing this lesion cyperimentally without introducing secondary changes in the circulation Usmg the purse string suturc method however they constently found an immediate reduction in sy tolle left ventricular and aorta pressures with a reduction in aortic pulc pressure and a pronounced elevation of left atrial pressure The um pitude of the atrial contraction wave increased markedly The efforts on pulmonary arterial and right veutri ulir pressures agurn proved variable probably dependmg on the condition of the arculation at the time of observation In some cyperiments systolic pressure rose M the right ventricle and pulmonary artery pulse pressure increasi in other experiments hoseier it decreed and with it the systoli and pul e pressures in the pulmonary artery fell In restucı mg the interrelations of right and left atru il pressure Brecher and Opulykes found that right atrial pressure shows a sight mean elevation chefly due to an une renc m the atrial contraction ware for the pressure at the time the tricuspid alie opens was slightly reduced It is improlırble therefore that results indicating a decreased force of right entricular contraction represent stundard dynamic consequences of mitral stenosis Current studies by Inkene os reveal that pulmonary (apılları pressure also rises but the pulmonary vascular resistance presents the transmission of phase pressure Change as claimed by some mi estigators The dynamic effects of extreme mitral stenosis arc of course de termmed by the wsze of the mutral orifire for it is obvious that suffi cient pres urc cannot be des eloped in the left atrium to overcome the Great resistance to flow through a very gl} sht or banging funnel When the stenosis is not too extreme honcker the dynamic conc quences are governed as much by the effectii ne suf compen atori mechanisms as by the size of the mitral orifice hutz and Stegels last three important mechanisms by which a varable improccat in ventricular influx can be brought about (1) the elevation of left atrial pres ure during the earli nastofie period of sestreitar fillage (2) the cou i tent abbreuition of ventricular systole and curre pond ·PEVTRICUL IN CONTRACTION UNDER 18 VORVAL CONDITIONS 97 ing extension of the diastolic filliug period (3) the augmentation of left atrial contraction as a result of its greater diastolic stretch and the consequent development of a high atrial pressure further suc Instel meehan m has not stood the test of time When these com pensatory mei hanisms are abrogated as during tachyardia or atrial fibrillation cireulatory decompensation ran develop suddenly In view of the relation of compensatory mechant ms to the size of the mitral orifire a number of attempts have been made to determine the maximum degree of stenosis const tent with approximately nor mal cardiac output during rest and exercise Ily drodynamic studies hy Allan" on artificial values in a physical system led to the conclu bion that a reduction of urface area by 7 per cent can take place Hithout marhed increa e in resistance Simple tests by the writeri on encued hearts of recently hilled dogs eemed to confirm the e findings for the valvular orifiee could be occluded by sounds equal to 01 per cent of the orifice without impeding flow from the left atrium under a pressure of only 14 cm H,0 The problem has recently been attached in a more thorough manner by Corlin and Gorlin * They developed a formula which permits calculation of the size of the mi tral orfice by means of information now obtainable from patients viz Vatral area = mitral value flow 31 V pulmonary capillary pressure minus 5 mm Hg Patients with mitral orifices of 25 sq cm compensated well Thone with orifices of 13 to 164 cmcperiences limitation of actius Subject with valic areas of 0 0 to 11 srp in hailory limited ar tivity and tho e in which reduction to 0 4 to 09 q cm existed were confined to bed or chair In ont lu ion it is apparent that experimental work has not as yet Hati factorily estabh hed the dynamic reactions of the right ventrick to various grades of mitral steno is The common oh«eration that initial tension and systolic preure are reluced in the night sentricle Is duhuult to quit with the frequent des clopment of night ventricular hy sx rtrophy flourier it hould be remembered that clinical fomº of picre mitrat touo is al o lead to alterations in the pulmonar Vascular es stem thie uperimpove effects of such liave not as yet been 1eproduced experimentally for these reasons the clinical study ·98 CIRCULITORI DYNAMICS of the dynamics of mitral stenosis continues to remain a fruitful field for further exploration Summary Selected types of experiments carried out in our laboratory during the past 33 years relevant to the interpretation of clinical disorders are reviened from an analysis of ventricular pressure pulses infer cnces were drawn as to basic determinants of cardiac performance in experimental conditions simulating those which arisc clinically The analysis included alterations in sentricular contraction patterns produced by pericardial effusion hypers olemia oligemia arterial hypertension of peripheral origin and that due to coarctation of the aorta aortic and pulmonary stenosis idioventricular rhythms ven tricular alternation coronary occlusion and myocardial ischemia aortic regurgitation and mitral insufficiency 1 The following prine iples were emphasized for gudance in inter preting ventricular pressure kurtes Investigators who attempt to analyze the mechanisms of cardiac adaptation from ventricular prex sure pulses should first satisfy themselves that the recorded curves accurately depict the pressure changes 10 that they are not de formed by artefacts or that when present these can be di counted They must be able to translate changing pressure salues gradients and inflections presented by ventricular pressure curses into mental pictures of dynımıc processes the integration of pressure pulses from the left atria i entriele and aorta with my ographic and acoustic phenomena volume chanyes in the ventricles and electrical pheno mena once considered as ac ademic exercise, has become an inescup able requirement in the curient era of hemodynamic intestinations 2 As Starling has pointed out the responses of the myocardium under many normal and pathologie conditions are determined in changes in the presy stolic size of a sentricle that is the initial length of its fibers Per onal experience has confirmed Frank s carlter postu late that under ordinary conditions changes in initial length are po duced by alterations in ventricular pressure at the on et of con tractions, that is the initial tension 3 The laws of initial length and tension so formulated assumes the existence of controlled conditions Con equently their determinat effect on force magnitude and duration of contraction can be sats ·VENTRICULAR CONTRACTIO UNDER B\ORMAL CO\DITIONS 99 factorily studied only when the following conditions ohtiin (a) the (cle length must remain constant (b) the ba ic condition of the myorardıum must remain the same otherwie its te ponse varies at identical initial tension and length and (c) conditions which change the mode of ventricular contraction in mechanical ways must not be operative + Under such controlled conditions changes in the force ampli tude and duration of ventricular pressure curies accompanied by an elevation of imtul ten ion can be referred to the beneficial effects of tretch Such a dominant rontrol of the contraction patterns is al lustrated by re ponses to increased and decrea.cd venous return dur ing respective states of hy pers olemia and olgemia When the reactivity of the myocardium is enhanced or depressed throu, h local metabolites fatigue humoral agents nervous actions or inadequate coronary fox the ventricular re pon es alter without changes in initial tension or more commonly with changes in an op po ite direction Thus following the up of cardiac depressant drugs or prolonged hypotension such as occurs in hock the forre magni tude and duration of ventricular contractions decrea e through pri mar myocardial depression and this leads to elevation of initial length and tension 6 Inder special conditions initial ten ion and length may deviate in opposite directions in which case the reactions are determined by changes in initial length This happens during large pericirdial effu sons for the elevated pericardial pre ure is transferred to the ven tricular cruity at the same time that diastolic filling is hindereul The ventricles develop ley pressure and their contraction i abridged de pite an elevation of initial tension | imilar dissociation of initial tenson and length fupervenes when a premature sentricular systole starts before the preceding beat has relaxed completely Vlechanical impairment of filling al o operates to dissociate initial tension and pren ure in ventricular tachy canlia and alternation but it is not basically important in determining the contraction pattern 7 The slower and smaller contractions ch played by xats of sen tricular origin are procluced by a slower entry of fractionate contrar tjona combined with failure to fix the septum primanly Similarly the apprrent depression of myocardial contraction exhibited bs the smaller beat of an altem ins couple is caused by deletion of ome frac ·100 CIRCULATORI DY 4 IL tionate contrictions There is no evidence that the inherent reactivity of muscle fractions participating in contraction is changed There is food evidence that they re pond to secondary changes in initial ten sion and length which may either augment or counteract the effect of aberrant myocardial contractions Depression of sentrulur con traction which follows coronary occlusion almost immediately is like mase due to enfeeblement or absence of contraction in the mifarcted area but complete compensation may result from response of stable muscle to increase in initial tension and length On the other hand myocardial depression may supervene and intensify the hypodynamil response of the left ventricle leading to circulatory failure 8 It must be obvious from data so far annlyzed that the establish ment of concordant or discorçlant changes m intal tension (or atrial pressures, and contraction patterns in uncontrolled or abnormal con ditions cannot be cited to validate or invalidite the operation of the las of initial tension and length 9 A careful study of left ventricular pres ure curse has revealed that the law of intial tension and length determines the ventricular responses under grossly abnormal conditions but the resulting con traction patterns are modified more or less through operation of other coefficients (a) In aortic hypertension due to increased periph eral resistance the force of contraction is enhanced and its duration tends to be curtailed through action of a greater output loud (b) In aortic coarctation the ventricular effects of increa ad rei tance and rise of initial tension tre decidedls moclified by the fact that the left ventricular contents must be displaced into a smaller and less des ten ble compression chamber (c) in aortic steno is the effects of increased initial length ind augmented re istance on santricular con traction are modified by the shift from an afterlorded to a more nearly isometric type of contraction (d) In aci cre aortic insufhmency the increased initial length and tension are responsible for the compensa tory increase in force of contraction but their effects on the ventritt lar contraction pattern are modified through a sluft from an after loaded to a loaded type of contraction (e) Existence of incompetent mitral salie modifies the sentricular re pone thrould change m inscal tension but the sentricular contraction pattern in modifiel becau e a part of the tidal olume regurgitates into the left atrium ·VENTRICULAR COATRICTION UNDER ABSORVIL CODITIOS 101 ( While the dynamic effects of mitral stenosis are dominantly deter mined by the size of the mitral orifice in the case of very severe lesions they are largely a result of the effectiveness or ineffrctiveness of compensatory reactions when lesions are not extreme 7 REFERENCES * \ICCERS CJ Pressure Pulses in the Cardiovascular System Nen lorh and London Longmans Green 1999 - Physiology of Shock New York The Commonnealth Fund 19.0 (Cambridge Vass Harvard University Press) Studies on the consecutive phases of the cardiac cycle I The duration of the consecutive phases of the cardiac cicle and the criteria for their precise determination Am J Physiol 56 415 1971 The electrocardiogram its relation to cardiodynamic events Arch Int Ved O93 1917 The independence of electrical and mechanical reactions in the mam malan beart Am Heart J 1 173 1925 Interpretation of the intraventricular pressure curve on the basis of rapidly summated fractionate contractions im J Physol 80 12 1997 The muscular reactions of the mammahan ventricles to artifcial sur face stimuli im J Physiol 3 316 1995 TENANT RAND NICGERS CJ The effect of coronary occlusion on myo cardial contraction im J Physiol 11 331 1933 WICCER4 CJ Studies on the card odynamic actins of drugs I The ap plications of optical metl ods of pressure registration in the study of cardiac stimulants and depres ants J Pharmacol (Exper Therap $0 217 19.7 LATTERSON SY I IPER HAND STARLING II The regulation of the heart I eat J l hyeol 48 465 1914 CAVYO BAND CATTFLI Vich I xperimental traumatic shock critical Ivel na falling hl od pressure irch Surg 4 300 19» Kino As Mechanical effect of fluti in the pericar lium on the function the leart J I hatol 51 >1 191" Hilson J1 AND VfFkk #J I ffect of the pericarilium on carlac din tent tas determine 1 by the rat Am J 11, tol 8 31 197 ITSEBETC M11 Tunctional capre ty of the normal pericardium Am Fleart Tu 749 1936 * \WIGGFRS CJ The dominant control of mammalian ventriculat ly nam 1. utal length Rev Sc argent de Bol Sur 1 10 516 1934 14 — and LATE L \ Ti e contour of the ver tricular volume curves under Jifferent con lotions Am J Pl ys101 58 439 190 (RHD I AND \ICCFR C j The circulatory effects of acute experi mntall spervolemia Am J P 8100 101 193 1933 ·102 CIRCITLATORI DITAUICS 17 FEROL S01 TB SH4DLE O AND GREGO DB Effect of blood Ipľu910 on left ventricular pressure and stroke volume in the closed chest dog Federation Proc 11 46 1903 IS OPDTKE DF AND WIGGERS CJ Studies of night and left ventricular activity during hemorrhagic hypotension and shock Am J Ph1810l 187 270 1946 IOGERS CJ Studies on the consecutive cases of the cardiac cicle II The laws governing the relatne durations of entricular aystole and di Astole Am J Phys101 56 439 1991 harz L N AND TRIGGERS CJ The influence of high systemic bloo i preu gures on the right ventricle and pulmonary circuit Im J Phyer ) 8? 01 1997 11 GUPTA TC AND HIGGERS J Basic hemodynamic changes produced by aortic coarctation of diferent degrees Circulation 17 1957 ** VGCERS CJ The influence of vascular factors on mean pressure pulac pressure and phasic peripheral fou im J I'by stol 129 614 175 *--- Physiology in Health and Digesse ed 5 Philadelphia Lea ( Febrger 1919 --- Dic pathologische I hy stologie des hreislauls ber hlappenerkrankungen des Herzens Ergebn d Physiol 29 250 1999 " DE HEER JL Die Dynamik des Saugetierherzens im Kreislauf an der Aorm bet Aortenutenose und nach Strophanthin Irch fd ges Phys101 148 1 1912 ? harz L V RALL I AD CIFER SI The cardio lynamic changes in the aorta and left ventricle due to steno is of the aorta J Chn Investiga tion 5 9 1929 2) FINEBERG VI AND III G} R3 CJ Compensation and failure of the right ventricle im licart J 11 %35 1930 ?WENCKEB CH IF Di Unregelmassigo Fierztätigkeit und ihre klinische Bedeutung Berlin Englemann 1914 19 WIGCERS CJ The dynamics of ventricular alternation Ann Cho Med 6 102 1921 LASIN RII Zum Problem des llerzalternans Arch fd ges Physiol 181 6. 1920 41 STRAOB I Dynaruk der lietzalternans Deutsch Arch f Win Med 13 403 1917 7711GGERS CJ The cause of temporary rentncular alternation fouinc a long diastolic pause Proc Soc Exper Biol & Ved 2 396 1997 The cause of temporary ventricular alternation following a long dia stolic pause Contributions to Viedical Science dedicated to Atar the Aan Irbor George Wahr 1927 P 60 ** GRET II D The nature of sentricular alternation resulting from se luce! coronary blood flow im J Phy stol 114 407 1936 35 ITELLFRSTE I AND I IFROM I V lectrical Alternation in expert mental coronary artery seclusion m ) hysso) 160 366 19,0 ·VENTRICULAR CONTRACTIO UWDER ABNORMAL CONDITIONS 103 *ORIAS OSCAR The dynamic changes in the ventricles folloning ligation of the ramus de cendens anterior Am J Phys101 100 6 193? IT KUPFERS Can experimental shock be induced by coronary occlusion? Proc Soc Exper Bol & Ved 76 137 1951 GBSER R AND CRAWFORD J Roentgenkymographic studies of myo cardial infarction Am Heart J 18 8 1939 "Su$s3AN VIL DACK S AND VLASTER AV The roentgenkymogram in myocardial infarction I The abnormalities in left ventricular contraction Am Heart J 19 453 1910 ** MASTER AV GUBER R DACK S AND JAFFE II L The diagnos 3 of coronary occlusion and myocardial infarction by fluoroscopre examination Am Heart J DO 45 1910 DACE S PALET D H AND SUSSMAN VIL A comparison of electrokymog taphy and roentgenkymography in the study of myocardial infarction Circulation 1 551 1950 SCHWEDEL JB SANET P AND VEDVICE II Electrokymographic studies of abnormal left ventricular pulsations Am Heart J 40 410 1900 WIGGERS C J The problem of functional coronary collaterals Exper Med & Surg 8 40% 1950 * The functional importance of coronary collaterals Circulation 6 609 1952 Tb functional consequ nces of coronary occlusion Ano Int Med 83 158 1915 TIENDERSON I The volume curve of the ventricles of the mammalian beart and the significance of tt 18 curve in respect to the mechanics of the heart beat and the filling of the ventricles Am J Physiol 16 395 1906 "Waagers C J The magnitude of regurgitation thaortic leaks of different Bizes J AM A 97 1359 1931 " AND GREEN ID Experimental aortic insuff crenev I Regurgitation maximum and mechanisms for its accommodation within the mammalian ventricle Proc Soc Exper Biol & Ve 1 07 599 1930 THFISEN H AVD WILLIA395 H 1 Further observations on experi mental aortic insuficiency II Cinematographic studies of changes in ventricular size and in left sentricular discharge J Clin Investigation 9 215 1930 AND VIALTBT AB Further of servations on experimental aortic in aufficiency IV Hemodynamic factors determining the characteristic changes in aortic and ventricular pressure pulses Am J Physiol 97 619 1931 TIe 4 LYS A FRIEDELL IL CARLAND I HAND VADRAZO VF alvular effciency in mitral and aortic insufficiency 4m J Physiol 129 397 1910 AVD FEIL II Cardiodynamics of mutral tosuff crency Flearto 149 19 ho STRAUB II Die Dynamik der happenfeller des Inken Herzens Deutsche Arch f blin Ved 1915 1917 7 b

·101
CIRCULATORI DYTICS
5 LATZ L AND SIFGEL VII The cardiodynamic eflects of scute mitral
stenosis Am Heart J 6672 1931
* OPDYXF D F AND BRECHER GA Vodifying effects of interatrial septal
defect on the cardiodynamics of mitral stenosis im Jihssio) 10. 53
1931
41 NEVEY JI In preparation
1 schema of the circulafion with experiments to determine
the a Iditional load on the apparatus pro luced by cnn litians repre enting
vals ular lesions Ileart 12 181 1996
* GORLIN R AND GORLIN SG Bisdraulic formula for calculation of the
area of the stepotic mitral valve other cardiac salses sod cen sal circula
tory shunts Am Ileart J 41 I 1991

·Subject Index 111-or none law 317 valves importance of su Alternation of ventricular tents "S Circulatory disorders basic hemo Aortic conretation 70 dynamic principles in 1 comprension chamber 5 Compression chamber 5 regurgitation 86 Controlled circulation preparation effect of on aystolte and diastolic 40 41 pressure SG Coronary occlusion effect of on arterial pulses % 86 Corrigan sulse 21 stenosis iſ arterial pul ce in Daming of pressure pulse 8 9 volume elasticity coefficient 17 71 Dicrotic wave 8 10 interat Durstelic pressure 7 (see also lly typertension of peripheral origin pertension) GRS factors affecting 14/ pressure (8) human meisurement of 10 factors affecting 11/ Destensibility of arteries 16 17 human 10 in lypertension 16 " / mean calculation of ? Drugs ag intrinsic cardiac factors 41 pulse() 5 7 Dynamics of hyp stension clinical importance of 14 86 Dynamics of ventricular contraction femoral 891 31 GOS radial 8 19 21 un ler al normal conditions 53 Arteriosclero 19 effect of on systolic and lastolic pre sure Le nomy of cur liac cffort inder 3 15 16 18 9 in 1 y pertens on 30 on arter al pul og ng I lectrocardiogram and dynamic Atrial contraction an! ventriculr car 119c events 5% filling 37 41 Itrial , t ssures and augmente 1 ven Femoral pulse 8 ?1 ous return 375 Frank & studies of cardio lynamics 36 41 61 Bloo il ressure S e Arterial Diastole and Systolic reasures leart ompenentory mel in sps of 38 Cardise (sec al o leirt ollen 49 61 tricles) after c ronary occlu con S? in aortic circlation cycle dyosmic eve te during R performance leterminants of 3 in aortic regurgitation in sortie stenosis 1 O 1 ·106 SUBJFCT I DET 6 Heart Continued applicability of to mammalian compensatory mechanisms of Con hearts 37/ 60 finued I osewille 3 25 26 in hypertension 68 uniformity of behavir 36 in mitral insufficiency 90 in mitral stenosis 96 Vitral insufficiency SOS in pulmonary stenosis 73 Vitral stenosis 96 decompensation of 38 41 Myocardial ischemia 8 fatigue of 38 40 62 Myocardium (see Heart and Ven lung preparation 38 tricles) muscle condition of 40 47 Vyograms of ventricle 57 60 dynamics of 394 47/ after coronary Occlusion 83 performance determination of 314 rate and cardiac output 37 38 41/Oligemia 671 rate and arterial pressures 14 15 Ilemodynamic(s) elementary 1/ Pericardial effusion 63 64 of hypertension ? I eripheral resistance 3 blood pressure 10% (see also concepts of 245 Arterial pres ure Hyi rten units of 28 sion) Poiseuille s lax 3 25 principles in determination of 105 Polycythema 65 Ilypertension Pre anacrotic phenomenon 12 dynamics of 245 I remature ventricular beats dy of peripheral origin 68f namics of 758 pressure pulse and pulse pressure Pressure(s) in 16 20 27 arterial (see Arterial Syatolic IIypervolemia 655 Diastolic and Pulae pres sure) Idioventricular rhythms dynamics atrial 371 of 5f curves (see Aortic Atrial Ven locisura 8 tricular and I ressure Pulsea) Initial length and tension 36 37 43 pulse(s) 49 61 63 68 Su definition of 7 Instrumentation in study of heart in hypertension 20 disease 34 reconstructed in man 19 21 Isometric contraction and relaxation ventricular interprctation of of ventricles 42 56 72 53f Presystolic volume and pressure See lorotkoff sounds mechanism of 12 Initial length and tension Pulmonary stenosis 73 Pulse(8) all-or none 35 4 clinical significance of 18 heart Starlings 39 61 femoral 8 21 amendment of 47 43 fadial 8 19 21 initial tension and length 36 39 pressure 7 Law ·107 SL BJECT IDEX factors affecting 19/ In hypertension 28 Velocity S Volume See Strobe volume Pusus alternans Sec Ventricular alteraation Tachycardia dynamics of 4a 46 ? Total peripheral resistancc (TIA) * 3333 of 3 Traube Ilering ayrs 25 Unsformity of Tehty or low Nacial pulse & 19 21 Renstance See Total and Pennisera! Tagsstances R/C ratio 19 Starlings las of heart 39 fi amendment of 4 19 Stationary wave compres9101 chamber 10 Stenosis sortie 71/ mitral 961 olmonary 734 Stroke volume (tee also lenticular volume curves) effect on ajalolic and tastolic Dregure !! 15 eatination of by pul venoug return and 399 49 Summation of W&VCS arterial >>stem 30 Syatotic discharge Se Strohe vclume Systolic pres ure (see ala Uy po tension: factors affecting 345 human 10 Velocrt of pulse wave 5 Senous return and stroke volum 35 428 Tentriculas alternation is contraction aft rloaded and loadette of & 86 coefficients affecting dynamics of 345 under at normal cond son mograms 5 60 83 por ssure pulacy int fpretation 1 531 stede en stole phas a 305 4 124 by cardsa l munics of 4 pressure 23 an v lume arves hats 814 Ilume Jassie corffcrent of yor tre cou) res non chat or 1 3 1 15 ter a mi

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