functional characteristics of the left ventricular inflow...

Functional Characteristics of the LeftVentricular Inflow and

Outflow TractsBy Donald V. Priola, B.S., Charles E. Osadjan, M.D., and

Walter C. Randall, Ph.D.

• The heart chambers contract sequential-ly1 and any significant alteration in spreadof the electrical activity may bring about achange in sequence. While recording con-tractile force from multiple sites on a singleventricle, it was noted that different portionsof the ventricular myocardium showed con-secutive onset of systole.2 Puff employedhigh-speed cinematography to study changesin ventricular configuration during systole.3-4

He reported that the inflow and outflowtracts contract consecutively, simulating aperistaltic wave along the main blood path-way through each ventricle. His observationssuggest that, during ventricular systole, theoblique tracts of fibers twist and the papil-lary muscles become opposed in such a wayas to produce physical separation of the in-flow and outflow tracts.

While studying synchrony of ventricularcontraction,125 we observed that the inter-vals between initial pressure elevations in dif-ferent chambers were influenced by the po-sition of the catheters within the chambers.We also noted that the wave form of forcerecordings from the ventricular muscle de-pended strongly upon the placing of thestrain gauges relative to the orientation ofthe muscle layers. We examined therefore theinflow and outflow tracts of the left ventricleto learn whether these are simply convenientanatomical terms or represent functional car-

From the Department of Physiology, StritchSchool of Medicine and the Graduate School, LoyolaUniversity, Chicago, Illinois.

Supported by Crants HE-02705 and HE-08682from the National Institutes of Health, U. S. PublicHealth Service.

Accepted for publication January 4, 1965.

diac chambers. This report describes the re-sults of these investigations.

MethodsMongrel dogs were anesthetized with phen-

cyclidine HC1* (2 mg/kg IM) and a-chloralose(60 to 80 mg/kg iv). Thoracotomy was per-formed in the left fifth interspace and the entiresixth rib was removed. The animals were main-tained on positive-pressure respiration. All pres-sure and force data were recorded on an Offnertype R ink-writing oscillograph at a paper speedof 250 mm/sec. Both the force and the pressuresignals were capable of faithful recording (out-put > 90% of input) to 125 cycles/sec.

In order to record multiple intraventricularpressures, specially constructed intraventricularcannulas0 were inserted into the inflow and out-flow tracts of the left ventricle (fig. 1). Theinflow tract cannula was inserted through thelateral portion of the free wall about 1 cm belowthe A-V groove. Outflow pressure was obtainedfrom a similar cannula in the anterior wall situat-ed midway between the base and apex andabout 1 cm lateral to the interventricular septum.The inflow tract extends from the mitral valveto the apex of the ventricle, and is boundedlaterally by the free wall and medially by theanterior and posterior papillary muscles. Dimen-sions of the interpapillary space appear to varyconsiderably during the cardiac cycle. The out-flow tract extends from the apical region to theaortic valve, and is bounded by the interventric-ular septum and the papillary muscles. Care wastaken to avoid placing the cannulas in intra-ventricular "pockets" at the base of the papillarymuscles. Catheter placement was confirmed bypostmortem observation and all data from ex-periments with questionable placement were dis-carded. Each of the cannulas was connected toa Statham P23Db transducer via identical lengthsof PE50 polyethylene tubing, calculated to givea slightly underdamped recording.

*Sernylan, generously furnished by Parke, Davisand Company.

Circulation Research, Vol. XVU, Auguii 1965 123

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124 PRIOLA, OSADJAN, RANDALL

FIGURE 1

Diagrammatic representation of interior of the leftventricle showing positions of cannulas in inflow andoutflow tracts, hypothetical boundaries of the twotracts, and direction of flow (arrows). LA: left atrium,A and P: anterior and posterior papillary muscles, RAand RV: right atrium and ventricle.

Direct recordings of the instantaneous pressuredifferentials between the inflow and outflow tractswere obtained by connecting the inflow and out-flow cannulas to a Pace P21D differential pres-sure transducer. Because this transducer measuresthe pressure differential across a single dia-phragm, the possibility of error resulting fromphase differences between two transducer dia-phragms was eliminated. The Pace transducerhas a frequency response that is flat to 600cycles/sec.

Force recordings of inflow and outflow tractcontractions were obtained by suturing BaldwinSR4 strain gauges (modified Walton gauges) di-rectly to the ventricular surface. The stitcheswhich fixed the gauges in position penetratedto a depth of about 5 mm.

In order to determine the interior configura-tion of the ventricle during systole and diastole,plaster of Paris was injected into the ventriclevia the left atrium: (a) in the heart of a freshly-sacrificed animal, (b) immediately before theheart was stopped in diastole following the in-fusion of KC1, or (c) before the heart wasstopped in systole following the infusion of CaCl2.The entire heart was then excised and immediate-ly immersed in liquid nitrogen. After the heartwas completely frozen, it was cut transverselyand each section photographed.

Results

Simultaneous pressures from the inflow andoutflow tracts of the left ventricle were suc-cessfully recorded in 14 animals. Faithfullyrecorded pressure tracings from both inflowand outflow tracts showed the characteristiccomponents of a ventricular pressure curve.The presystolic or atrial filling wave was fre-quently prominent in both traces. In 10 ofthe 14 experiments, the first elevation of intra-ventricular pressure, measured from the onsetof the entrant phase7 occurred in the inflowtract. This was followed 4 to 18 msec laterby the beginning of pressure rise in theoutflow tract (fig. 2). In the upper panel arethe intraventricular pressure recordings fromthe inflow (top) and outflow (bottom) tractsof the left ventricle. The interval betweenthe beginning of the entrant phases of systolein the two tracts is indicated by the twovertical lines and measures 12 msec. Thelower panel shows a record taken from thesame animal a few minutes later with ampli-fier gain increased by a factor of ten andwith the pen excursions electronically limited.This amplified the diastolic and entrantperiods but truncated the pressure curve be-

ftwn

* LV PRESSURE- INFLOW TRACT

3.FIGURE 2

Pressure pulses recorded directly from the inflow(top) and outflow (bottom) tracts of the left ventricle.Upper panel shows recordings at one-tenth the am-plifier gain of those in lower panel. Pen excursionswere electronically limited at the higher gain. Verti-cal coordinates are simultaneous.

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VENTRICULAR INFLOW AND OUTFLOW TRACTS 125

tween early and late systole. The entrantphases were more sharply defined andmeasurement of the inflow-outflow intervalfacilitated. This interval measured 17 msecas denoted by the two vertical ordinates. Inthe remaining four animals of this series, thepressure elevations in the inflow and outflowtracts were simultaneous or only slightlyasynchronous. On rare occasions, and partic-ularly during arrhythmias, outflow tract pres-sure rose slightly before inflow tract pressure.

Direct recordings of the instantaneous in-flow-outflow pressure gradients in the left ven-tricle were obtained in 12 additional animals.In 10, the differential pressure trace indicatedearliest pressure development in the inflowtract (fig. 3). The initial small downwarddeflection is presumably related to left atrialcontraction. The differential pressure ap-proaches zero during the development of theT wave of the ECG, and in late systole thetracing indicates a higher outflow tractpressure. This is the type of curve whichwould be expected if the two intraventrieularpressures are similar in form, amplitude andduration but displaced in time.

Thus, it appeared that the mechanical con-traction of the inflow tract preceded that ofthe outflow tract. This was explored in fouranimals with strain gauges applied to the

left ventricular myocardium in the sameareas in which the inflow and outflow tractcannulas were inserted routinely (fig. 4). Theinflow tract force recording showed a definiterise 20 msec before the initial increase offorce in the outflow tract. When the straingauges were moved closer together, thisasynchrony became less apparent and it wasexaggerated if the gauges were moved far-ther apart. This confirmed the suggestion2-3

that mechanical contraction proceeds in awave-like fashion across the ventricle.

The apparent asynchrony of pressurechanges in the inflow and outflow tracts isdifficult to explain if the ventricle is truly asingle, openly communicating chamberthroughout systole. If this were the case, pres-sure in such a system should be transmittedrapidly to all parts of the chamber, and adifferential could not exist except for thebrief period required for the transmission ofpressure. This required a measurement ofconduction velocity of a pressure wave acrossthe ventricle.

Catheters were inserted into the inflow andoutflow tracts of the left ventricle as describedabove. An impact of essentially constantforce and rate of application was deliveredto'; a small area on the external surface ofthe heart as close to the inflow tract cannula

ECG I

LV0-LViI—2 50 msec H

BP150

75

0FIGURE 3

Simultaneous recordings of pressure pulses in the left atrium (LA) and mammary artery (BP),lead II of the ECG, and differential pressure trace from inflow and outflow tract cannulas inthe left ventricle (LVO-LVJ. Note simultaneous ordinates at right of figure.




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as possible. The resulting pressure wavewas easily detectable in the ventricular re-cordings. Assuming the distance between thetwo catheters to be constant, the apparent

conduction velocity of the superimposedpressure wave was calculated during suc-cessive portions of the cardiac cycle (fig. 5).The straight line distance between the cath-

LV FORCE-OUTFLOW TRACTI 250 MSEC -

mmHGISO

roo-

sto

LV PRESSURE-OUTFLOW TRACT '

FIGURE 4

Strain gauge force recordings from muscle overlying the inflow (top) and outflow (middle)tracts of the left ventricle. Bottom trace shows left ventricidar pressure pulse recorded fromthe outflow tract.

mm HG MID-DIASTOLE

EARLY SYSTOLE.

LATE DIASTOLE

/ \

velocity • 14m/eec^' \

1 i»Mt

MAXIMUM SYSTOLE

LV PRESSURE

-—INFLOW TRACT

LV PRESSURE

.OUTFLOW TRACT

H

EARLY OIA!

velocity • ? velocity* 5 5m/sec

FIGURE S

Impact pressure waves are shown superimposed upon pressure pulses recorded from the leftventricular inflow (top) and outflow (bottom) tracts at successive periods of the ventricularcycle. Each panel shows impact waves delivered in the inflow tract and recorded simultane-ously in both traces. Apparent conduction velocity of the impact wave between the tracts isshown.

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eters was measured postmortem and foundto be 5.5 cm. The upper record in each panelrepresents inflow tract pressure and the lowerpanel outflow tract pressure. In mid-diastole,the transmission time was 4 msec and theapparent conduction velocity was calculatedto be 14 M/sec. In late diastole, the trans-mission time was unchanged and the ap-parent velocity again was 14 M/sec. However,in early systole, transmission time lengthenedabruptly to 8 msec and the apparent con-duction velocity decreased to 6.9 M/sec.During maximum systole, the impact wavewas markedly attenuated and could not beclearly detected in the outflow tract pressuretracing. When the impact was delivered inearly diastole, apparent conduction velocitywas reduced to 5.5 M/sec. Delivery of theimpact to the ventricular wall over the out-flow tract revealed comparable alterationsin velocity of transmission.

In order to visualize the internal configu-ration of the ventricle in the various stagesof the cardiac cycle, three techniques wereused: 1) Hearts were excised from freshly-sacrificed animals, filled with plaster of Pariswhich was allowed to set, and then sectionedand photographed. 2) Hearts were arrestedin diastole by intracoronary or intravenousinfusion of KCI, filled with plaster of Paris,frozen in liquid N«, sectioned and photo-graphed. 3) Hearts were arrested in systoleby CaClo infusion via the left atrium orfemoral vein and treated in a manner identi-cal to the second group. A photograph of amacrosection of a heart arrested in diastoleby KCI is illustrated in figure 6A. It is clearthat the left ventricle consisted of a singlechamber with the papillary muscles widelyseparated. Hearts from freshly-sacrificed ani-mals showed similar internal configuration.

Hearts which were sectioned and examinedafter arrest in systole by CaCl2 exhibited acompletely different appearance (fig. 6B).The left ventricular cavity was discontinuous,the inflow and outflow tracts being separatedby the apposition of the anterior and posteriorpapillary muscles. Basilar sections of heartsin the CaCl2 series showed partitioning of


FIGURE 6

Photographs of macrosections through the apical por-tions of two dog hearts injected with plaster of Parisand frozen instantaneously in liquid nitrogen. A:heart stopped in diastole; arrows indicate the widelyseparated papillary muscles in the left ventricle. B:heart stopped in systole. Shows close apposition ofthe anterior and posterior papillary muscles in theleft ventricle completely separating the inflow (right)from the outflow (left) tract.

the ventricle by the dependent mitral valveleaflet.

Discussion

The terms "inflow tract" and "outflowtract" are not new. They have been usedclinically for many years to relate ventricularanatomy to the functional pathway of bloodthrough the working heart. However, the de-scription of the sequential and reciprocalcontractions of the two tracts offered by Puffemphasizes this functional relationship.3-4 Hedescribes an initial contraction of the inflowtract which causes expansion of the outflowtract, and is followed by contraction of theoutflow tract beginning with the subaorticrecessus. During contraction the obliquetracts of fibers in the inflow tract twist and



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the papillary muscles become intertwined,closing the interpapillary space. Thus a newwall, nonexistent in diastole, is formed by thepapillary muscles and the contracted recessus.If this hypothesis is correct, a distinct intra-ventricular pressure gradient may be pre-dicted during systole. Examination of differ-ential pressure recordings from inflow andoutflow tracts (fig. 3) revealed precedencein the inflow side, giving functional verifica-tion of the motion picture analysis of Puff.

If the straight-line distance between therecording catheters is assumed to be constantthroughout the cardiac cycle, apparent con-duction velocity can be computed, as in figure5. The apparent decrease in conduction veloc-ity during systole might be explained: 1) bydifferences in the physical properties of themyocardium during systole and diastole, 2) byalterations of the intercatheter distance as aresult of the change in systolic intraventriculardimensions, 3) by interposition of some in-traventricular structure between the tracts.A decrease in pressure wave velocity wouldbe expected if the distensibility of the systolicmyocardium increased. We have no specific-information concerning this. However, duringthe isovolumetric phase of systole, the in-crease of myocardial tension is great for/ anegligible change of fiber length and there-fore, a decrease of distensibility should beexpected. If data derived from striated musclecan be applied to cardiac muscle, the experi-ments of Buchthal and Rosenfalck8 should berelevant. These workers found that the elasticmodulus (reciprocal of distensibility) ofstriated muscle was higher in contractingmuscle than in relaxed muscle. Distensibilityof the myocardium would thus decreaseduring systole, resulting in increased conduc-tion velocity rather than reduced velocity. Inthis context the decrease in apparent conduc-tion velocity during systole results probablyfrom something other than a change in thephysical characteristics of the myocardium.Increased intercatheter distance would alsocause the apparent conduction velocity to de-crease. However, Hawthorne has shown9 thatthe internal diameter of the ventricle de-

creases during systole. It must be concluded,therefore, that the effective path length ofthe pressure wave increases, or transmissionof the wave is impeded by the interpositionof some intraventricular structure betweenthe inflow and outflow tract catheters. Theseconclusions are made tenable by the anatomi-cal studies that compare the heart arrestedin diastole with the heart arrested in systole.

It is believed generally that the papillarymuscles and the trabeculae carneae are thefirst areas of the ventricles to enter mechanicalcontraction.10 By their contraction, the papil-lary muscles tend to increase their diameter,pull the edges of the mitral valve cusps down-ward and cause a decrease in the longitu-dinal dimension of the ventricle. All thesechanges tend to separate the ventricularcavity into an inflow and outflow tract. Ifthis hypothesis is correct, the separation ofthe ventricle into inflow and outflow tractsshould not occur when the papillary musclesare not allowed to come into apposition witheach other during systole. Two preliminaryexperiments have demonstrated that, whenthe ventricular volume is increased by partialocclusion of the aorta, the inflow-outflowasynchrony disappears.

Severe subendocardial hemorrhages havebeen reported on the papillary muscles afterprolonged stimulation of the stellate ganglionor after catecholamine infusion.11 It is be-lieved that this results from increased car-diac contractile force and greater systolicejection with direct mechanical impact be-tween the anterior and posterior papillarymuscles. The incidence of these lesions de-creases during partial aortic occlusion or in-fusion of large amounts of fluid which main-tain systolic volume at a high level.

Summary

Simultaneous pressures were recorded fromthe left ventricular inflow and outflow tractsin 14 dogs. In 10 the inflow tract enteredsystole 4 to 18 msec before the correspondingoutflow tract. In 12 additional animals, dif-ferential pressure recordings from the twotracts confirmed precedence in the inflowtract. In four animals, strain gauge recordings




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from the epicardial surfaces of the inflow andoutflow tracts exhibited asynchrony with pre-cedence in the inflow tract.

Hearts excised from freshly-sacrificed ani-mals or hearts stopped in diastole by KC1infusion showed a single, openly-communi-cating ventricular chamber. In contrast, heartsarrested in systole by infusion of CaCl2 re-vealed a separation of the left ventricle bythe apposition of the anterior and posteriorpapillary muscles and the dependent mitralvalve leaflet.

The apparent conduction velocity of an im-pact pressure wave from inflow to outflowtract depended upon the portion of the car-diac cycle during which it was delivered.From a maximum of 14 M/sec in mid andlate diastole, it decreased to 6.9 M/sec in earlysystole and 5.5 M/sec in early diastole. Com-plete attenuation of pressure wave transmis-sion often occurred during maximum systole.

These data support the concept that theleft ventricle may become separated, duringsystole, into an inflow and outflow tract. Itappears that the division is accomplished bya change in the systolic ventricular architec-ture, with apposition of the anterior and pos-terior papillary muscles and the downwardmovement of the mitral valve leaflets. It isprobable that this phenomenon is functionalin hearts working near the lower limits oftheir systolic reserve.

References1. PHIOLA, D. V., AND RANDALL, W. C : Alterations

in cardiac synchrony induced by the cardiac

sympathetic nerves. Circulation Res. 15: 463,1964.

2. OSADJAN, C. E., AND RANDALL, \V. C : Effects

of left stellate ganglion stimulation on leftventricular synchrony in dogs. Am. J. Physiol.207: 181, 1964.

3. PUFF, A.: Systemumstellungen der Muskelfasern

im Kontraktionsvorgang an der rechten Herz-kammer. Verh. Anat. Ges. Anat. Anz. 105:355, 1958.

4. PUFF, A.: Die Morphologie des Bewegungsa-

blaufes der Herzkammern (Eine Untersuch-ung iiber die wechselseitige Beeinflussung desKontraktionsablaufes im rechten und linkenVentrikel). Anat. Anz. 108: 342, 1960.

5. RANDALL, W. C, AND PHIOLA, D. V.: Influence

of cardiac sympathetics on synchrony of ven-tricular contraction. Proc. Soc. Exptl. Biol.Med. 115: 46, 1964.

6. RANDALL, W. C, AND KELSO, A. F.: Dynamic

basis for sympathetic cardiac augmentation.Am. J. Physiol. 198: 971, 1960.

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ventricular pressure curve on the basis ofrapidly summated fractionate contractions.Am. J. Physiol. 80: 1, 1927.

8. BUCHTHAL, F., AND ROSENFALCK, P.: Elastic

properties of striated muscle. In Tissue Elas-ticity, ed. by J. W. Remington, Baltimore,Waverly Press, 1957, p. 73.

9. HAWTHORNE, E. W.: Instantaneous dimensional

changes of the left ventricle in dogs. Circula-down ward 9: 110, 1961.

10. RUSHMER, R. F.: Cardiovascular Dynamics,

t Philadelphia, W. B. Saunders Company, 1961,p. 48.

11. KAYE, M. P., MCDONALD, R. H., AND RANDALL,

W. C : Systolic hypertension and subendo-cardial hemorrhages produced by electricalstimulation of the stellate ganglion. Circula-tion Res. 9: 1164, 1961.




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DONALD V. PRIOLA, CHARLES E. OSADJAN and WALTER C. RANDALLFunctional Characteristics of the Left Ventricular Inflow and Outflow Tracts

Print ISSN: 0009-7330. Online ISSN: 1524-4571 Copyright © 1965 American Heart Association, Inc. All rights reserved.is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Circulation Research

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