Online ISSN: 1524-4539 Copyright © 1958 American Heart Association. All rights reserved. Print ISSN: 0009-7322.

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1958;18;1125-1130 CirculationARTHUR W. FEINBERG, HENRY LAX and William Urban

Studies of the Arterial Pulse Wave

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Studies of the Arterial Pulse WaveARTHUR W. FEINBERG, M.D. AND HENRY LAX, M.D.

With the technical assistance of William Urban

Previous studies have shown abnormalities of the arterial pulse wave in hypertensivesubjects of all age groups. The major change has been diminution to disappearanceof the dicrotic wave. The pharmacologic differences between epinephrine and norepi-nephrine offer a means of studying the mechanism of this change in the dicrotic wave.In the present study, normotensive subjects have had transient hypertension inducedby the infusion of epinephrine and norepinephrine. The different effects of these drugson their arterial pulse waves have been recorded.

I N A previous report,' describing observa-tions on the arterial pulse wave in human

subjects, a new technic was introduced forrecording the pulse wave without intra-arte-rial puncture. The method has been shown tobe sensitive and to give reproducible results.The accuracy of the recordings has been dem-onstrated by the similarity of simultaneousintra-arterial and extra-arterial tracings.

Figures 1 and 2 show typical instances ofnormal and abnormal arterial pulse waves asrecorded by this technic. The major differencein the abnormal cases appears to be diminu-tion to disappearance of the dicrotic wave.These changes in the dicrotic segment of thearterial pulse wave have been found in hyper-tensive subjects of all age groups as well asin patients with generalized arteriosclerosis,coronary arteriosclerosis, and diabetes melli-tus.The dicrotic wave has been ascribed to a

reflected wave from the recoil of the bloodcolumn against the closed aortic valve. Morerecent studies2-7 indicate that peripheral fac-tors also play a role in the formation of thedicrotic wave. The technic described hereinseemed to offer another means of studying themechanism of the dicrotic wave.

From the Research Service, First (Columbia Uni-versity) Division, Goldwater Memorial Hospital, De-partment of Hospitals, New York, N.Y., and theDepartment of Medicine, College of Physicians andSurgeons, Columbia University.

Supported in part by grants from the Albert andMary Lasker Foundation and the New York HeartAssociation and by a grant from George and MoniqueUzielli.

The pharmacologic studies of Goldenbergand his group8 have shown that although bothepinephrine and norepinephrine produce com-parable degrees of hypertension, they do so indifferent ways. The hypertensive action ofepinephrine in man is due primarily to alarge increase in cardiac output that over-balances a decrease in total peripheral resist-ance. On the other hand, hypertensioninduced by norepinephrine is produced inman by a striking increase in peripheral re-sistance with little or no change in the cardiac

FIG. 1. Normal arterial pulse waves recorded fromthe third digit of a healthy 25 year old man. Thevertical lines are time signals 0.1 second apart and thehorizontal lines represent pressure increments of 10inmn. Hg in the cuff applied about the finger. Thecuff pressure (P) is recorded simultaneously but inde-pendently of the components of the pulse wave. Noteinitial wave (I) and well defined dicrotic wave (D).

Circulation, Volume XVIII? December 195125

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FEINBERG, LAX

output. It, al))eared that investigation of theeffeet of these 2 drugs, with their differenicentral and peripheral actions, Light help toexplain the inode of origin of the dicroticwave. Accordingly, the present study hasbeen carried out on the effect of intravenousinfusions of epinephrine and norepinephrine,iii quantities sufficient to produce signifieainthypertension, on the dicrotie wave of pre-sumai11.bly healthy, normotensive individuals.

METHOD AND TECHNIC

Ai sensitive rubber cuff with an inelastic backingis applied to the external surface of the limb orligit. The cuff consists of a thin rectangularineiabrane 11/2 by 3 inches cemented at the edgesto a backing piece of rubberized cloth. A 1/8inch I.D. nipple attached at the (enter of the clothis connected to a 3 foot length of 1/8 inch rubbertubing. This tubing serves the dual purpose ofinflating the cuff and connecting it to the recordingchamber of a differential pressure transducer. Thecuff is attached by an inelastic strap to the cx-treinity to be examined.

The differential pressure tramnsducer consists ofa circular beryllium copper diaphraemn 0.006 inchthick and 11/2 inches ill diaimieter separating 2air chambers. Air pressure required to inflate thecuff is introduced to both chambers, causing nodeflection of the diaphragm. Pressure disturbancesoriginating at the cuff, however, are conducted tothe recording chamber only. These disturbances

cause tile (liaplirlaglii to (lefect according to theirintensity and direction.

Deflections of the diaphragm are transmitted bymechanical linkage either to a Statham absolutepressure strain gage or to a piezo-electric crystalcartridge that generates electric energy accordingto the mechanical motion imposed upon it. Thecrystal unit (Astatic inicrophone cartridge D-104)has an output of -45 db. referred to 1 volt permicro bar. Output from the crystal is amplifiedwith a class A balanced push-pull amplifier withcontinuous variable gain from 0 to 16 db. max.The amplifier feeds a dual-coil string-type mirrorg(alvanometer.Permanent recordings are made on 12 ciii. wide

electrocardiographic paper, with a Cambridge 3-speed camera. Camera speeds are 121/2, 25, or50 inma. per second. Timning. marks appear asequally spaced vertical lines. Recordings can alsobe mna(le intra-arterially amiAd takeni on (lireet-writ-ing electrocardiograph papem.

The frequency response of the entire systemifrcomn cuff to galvanometer shows the response tole substantially flat to 40 cps., which is well abovethe 5 to 6 cycle range encountered in studyingarterial pulse waves.

Continuously variable gain control enables theoperator to standardize the amplitude of record-inlgs without affecting the conmfiguratiomi of thearterial pulse wave. This feature is of value incomparative studies over a period of time on thesame subject. Recording at the same basic ampli-tude permits standardized conditions insofar as theinstrument itself is concerned. The only variablesthen lie with the patient.

FIG. 2. Left. Abnormal arterial pulse wave. Note diminished size of dicrotic wave (D).The cuff pressure (P) is also recorded. Right. M1ore severely albnormal arterial pulse wave

sliowiiig aI complete albesenee of the dicrotic wave.

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STUDIES OF ARTERIAL PULSE WAVE

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MIX*. ATRN.UP.N3_N_STOPPEDFIG. 3. Effect of intravenous infusion of norephiinephlrine on the arterial pulse wvave of a

32 year old normotensive male subject. Note the diminution of the dicrotic wave (D) in .dand its virtual disappearance in 3. It startsreturned to control levels.

All arterial pulse wave tracings during thisstudy were recorded intra-arterially. A Cour-nand needle (18 gage, 2 3/64 inch. no. 488LNR) was introduced into a brachial artery.

Pulse pressure waves were transmitted to a

Statham P-23A absolute pressure strain gage

and a continuous intra-arterial pulse wave

tracing was begun. After a control periodlasting from 2 to 5 minutes, a previously in-troduced infusion of glucose and water was

changed to an infusion containing either nor-

epinephrine (Levophed) or epinephrine (Sii-prarenin, Winthrop). The blood pressure was

taken by cuff at 1 minute intervals and insome cases was also recorded on the tracing.After 3 minutes of sustained elevation of sys-

tolic and diastolic pressures, the intravenousinfusion was discontinued but the continuousintra-arterial pulse wave recording was main-tained until the configuration of the pulsewave had about returned to its control ap-

pearance. This usually took 10 to 15 minutes.The blood pressure invariably fell to its base-line levels before the control pulse w*ve con-

figuration was restored.

to return in 4 after the blood I)ressure has

RESULTS

IVith iNorepiie phrinieNine normotensive, presuniably healthy

subjects were given norepinephrine by intra-venous infusion. In all individuals, as theblood pressure rose, the well defined dieroticwave of the control intra-arterial pulse wave

became smaller and finally disappeared comn-pletely. Upon discontinuing the norepineph-rine, the dicrotic wave reappeared within mini-utes of the return of the blood pressure to

control levels.Figure 3 is. illustrative of these ehlatges.

The subject was a, 32 year old male hospitalporter with no (clinical evidences of vasculardisease. His resting blood pressure was

120/80, and a well defined dicrotic wave isseen on his initial pulse tracing. The bloodpressure rose to 170/110 after 1 minute ofintravenous norepinephrine in doses of 0.4 1Lg.per Kg. per minute and the dicrotic wave be-came markedly smaller. The double peakingof the anaerotie wave has been seen ins othersubjects with hypertension, whether natural

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F1INBERG, LAX

XPI NEPBRIN TLS

3.S. B.P.145/80

I.BeUOS 1 MIN. OF

ImJsion EMIN PHIRINE

m~~~~~~~~~~~~~~~~~~~. . .

5 MIN.O SMIN. OFFG4.NfeeRINE ePINErINeOI

FIG. 4. Effect of intravenous infusion of epinephrine oil

amplitude of the entire ws-ave increases with riseelearly seen at all times.

or induced. Its cause remains unexplained.After 3 mitiutes of sustained hypertension, thedierotic wave completely disappeared. Fiveminutes after stopping the norepinephrine in-fusion, the blood pressure had returne to itscontrol level of 120/80 and the dicrotic wave

had started to become evident agaiin. Thestudy was discontinued in this patient beforethe dicrotic wave had recovered its full height.

WVith EpincephrineCFour normotensive, presumably healthy

subjects were givens epinephrille intravenous-lv. Despite elevations of the systolic anddiastolic blood pressure comparable to thoseseemi ini the experiments with norepinephrine,no basic chamrge was noted in the conifigurationiof the dicrotic wave. Specifically, the di-crotic wave was neither diminished nor haddisappeared in amiy of the subjects studied,even though the over-all amplitude of thepulse wave increased as the blood pressurerose.

Figure 4 illustrates these changes in a 21year old female hospital technician. Epineph-rine was infused intravenously in doses of 0.4

iII bloc

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2PINEFPRINE

6 MIN. AFTEREPINEPHINE STOPPED

arterial pulse wave. Although theod pressure, dicrotic wave (D) is

,ug. per Kg. per minute for a total of 8 mimn-utes. During this time the blood pressurerose from 122/80 to a sustained peak of 220/110. Although the form of the arterial pulsewave reflected this chanige ini the blood pres-

sure, the dicrotic wave remainled clearly de-fined in all tracings.

In one of the normotensive iubjects (a 30ear old male technician) epinephrine and

norepinephrine were given consecutively, witha 15 minute interval betweeni the administra-tion of the 2 drugs to permit return of thecontrol pattern. The typical difference be-tween the effects of epinephrine and norepi-nephrine are demonstrated in this case (fig.5). Both drugs produced approximately thesame elevation of blood pressure. Norepineph-rime caused a complete disappearance of thedicrotic wave, whereas the dicrotic wave was

undisturbed after the administration of epi-nephrine.

DISCUSSION

The mode of origin and propagation of thedicrotic wave has been investigated for yars

but remains incompletely understood. The

S.S. B.P.122/80

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STUDIES OF ARTERIAL PULSE WAVE1

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FIG. 5. Effect of epinephrine and norepinephrine given consecutively to the same patientafter a 15 minute interval. Note persistence of the dicrotic wave (D) in the epinephrinetracings and its disappearance after norepinephrine. Both drugs gave comparable elevationsof blood pressure.

classic theory explains the dicrotic peak asa reflected wave initiated by the recoil of thearterial blood column against the closed aor-tic valve. The studies of Hamilton, Reming-ton, and Dow,2-5 Wiggers,6 and Alexander7`have shown that the arterial pulse wave is.progressively transformed in its passage downthe aorta and its arterial branches, suggestingthat the physiologic state of the peripheralvessels may play an important part in influ--encing the appearance of the dicrotic wave..Our initial studies' also suggested thatchanges in the peripheral arteries determinethe presence or absence of the dicrotic waveof the arterial pulse. It was found, for exam-ple, that the dicrotic wave was markedly ab-normal in hypertensive subjects of all agegroups, in patients with peripheral arterio-sclerosis, and in diabetic patients as young as14 years of age.The results of the present study would seem

to support this view. In the 4 subjects givenepinephrine, the dicrotic wave was not basi-cally altered although the blood pressure rosesignificantly. On the other hand, in all 9 pa-

tients who received norepinephrine, the di-crotic wave was abolished or markedly re-duced in size, despite a similar rise in bloodpressure. These findings are well explainedby what is known of the pharmacologic differ-ences between the 2 drugs. Goldenberg andothers8 have shown that the actions of epi-nephrine and norepinephrine in man are sim-ilar only in that they both produce significantelevations of blood pressure. The hyperten-sive effect of norepinephrine is due to an in-crease of total peripheral resistance, with nosignificant change in cardiac output. Epi-nephrine, on the other hand, raises the bloodpressure predominantly by a central actionon the heart, iiicreasing the rate and force ofcardiac contractions and the cardiac output.The peripheral resistance actually decreases,because of an over-all vasodilating action.The marked difference between the effects of

epinephrine and norepinephrine on the di-erotic wave thus support the hypothesis thatchanges in the tonus of the arterial wall havesignificant effects on the configuration of thedistinctive waves seen in arterial pulse trac-ings.

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3FEINBERG, LAX

SUMMARYPrevious studies have shown a diminution

to disappearance of the dicrotic wave in thepresence of clinical evidences of arteriosclero-sis, diabetes mellitus, and hypertensive vas-cular disease.

Transitory hypertension was induced in 13normotensive subjects by intravenous infusions of either norepinephrine or epinephrine.A continuous intra-arterial pulse-wave tracingwas recorded from the brachial artery before,during, and after the infusions in most in-stances.The pulse waves of all 9 subjects given nor-

epinephrine demonstrated disappearance ofthe dicrotie wave as the blood pressure rose.The dicrotic wave reappeared as the bloodpressure returned to normal. Contrariwise,4 subjects given epinephrine had no changein the dicrotic wave despite comparable ele-vation of the blood pressure.The different effects on the dicrotic wave

may be related to the pharmacologic differ-ences between the 2 drugs. Epinephrine hy-pertension is produced by an increased car-diac output in spite of a reduced totalperipheral resistance; norepinephrine hyper-tension is caused by an increased peripheralresistance with little or no change in cardiacoutput.The evidence presented lends support to

the theory that peripheral factors play animportant role in the production of the di-erotic peak of the arterial pulse wave.

SUMMARIO IN INTERLINGUAPrevie studios ha monstrate un diminution

o dispariton del unda dicrotic in le presentiade manifestationes clinic de arteriosclerosis,diabete mellite, e hypertensive morbo vascu-lar.

Hypertension transitori esseva inducite in13 subjectos normotensive per infusiones intra-venose de norepinephrina o de epinephrina.Un registration continue del unda del pulsointra-arterial esseva effectuate pro le arteriabrachial ante, durante, e post le infusiones(in le majoritate del casos).Le undas de pulso del 9 subjectos recipiente

norepinephrina exhibiva disparition del unda

dicrotic in association con le augmento delpression de sanguine. Le unda dicrotic re-appareva quando le pression de sanguine re-tornava a nivellos normal. Del altere latere,4 subjectos recipiente epinephrina exhibivanulle alteration del unda dicrotic in despectode comparabile augmentos del pression de san-guine.Le differentia inter le effectos exercite super

le undas dicrotic es possibilemente relationateal differentias pharmacologic inter le duo dro-gas. Hypertension a epinephrina es produciteper un augmento del rendimento cardiac indespecto de un reducite total resistentiaperipheric. Hypertension a norepinephrinaes causate per un augmento del resistentiaperipheric con pauc o nulle alteration delrendimento cardiac.Le datos presentate supporta le theoria que

factores peripheric ha un rolo importante inle production del culmine dicrotic que charae-terisa le unda del pulso arterial.

REFERENCES1. LAX, H., FEINBERG, A. W., AND COHEN, B. M.:

Studies of the arterial pulse wave. I. Thenormal pulse wave and its modification inthe presence of human arteriosclerosis. J.Chron. Dis. 3: 618, 1956.

2. HAMILTON, W. F., AND Dow, P.: An experi-mental study of the standing waves in thepulse propagated through the aorta. Am.J. Physiol. 125: 48, 1939.

3. -: The patterns of the arterial pressurepulse. Am. J. Physiol. 141: 235, 1944.

4. -, REMINGTON, J. W., AND Dow, P.: Thedetermination of the propagation velocityof the arterial pulse wave. Am. J. Physiol.144: 521, 1945.

5. REMINGTON, J. W., AND HAMILTON, W. F.:The construction of a theoretical cardiacejection curve from the contour of theaortic pressure pulse. Am. J. Physiol. 144:546, 1945.

6. WIGGERS, C. J.: Physiology in Health andDisease, Ed. 5. Philadelphia, Lea & Febiger,1954, chaps. 37 and 38.

7. ALEXANDER, R. S.: Factors determining thecontour of pressure pulses recorded fromthe aorta. Fed. Proc. 2: 738, 1952.

8. GOLDENBERG, M., PINES, K. L., BALDWIN, E.D. F., GREENE, D. G., AND ROH, C. E.: Thehemodynamic response of man to nor-epi-nephrine and epinephrine and its relationto the problem of hypertension. Am. J. Med.5: 792, 1948.

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