The Arterial Pulse Wave and Vascular Compliance

Original Paper

The Arterial Pulse Wave and Vascular ComplianceJoseph P. Noon, RN, PhD

This review will highlight the im-portance and relevance of pulse

wave analysis (PWA) that encom-passes pulse wave velocity (PWV)and augmentation index (AIx)—bothare measures of arterial compliance.This tool is particularly useful wheninvestigating patients who are at riskof, or who have established, cardio-vascular disease. The reason for adopt-ing this noninvasive technique is thatit provides central hemodynamic in-formation that is unobtainable fromconventional brachial artery (periph-eral) recordings of blood pressure (BP)using a cuff sphygmomanometer. Inaddition, it assesses arterial ‘‘stiffness’’as an independent risk factor for car-diovascular disease. Indeed, traditionalrisk factors all lead to the end result ofarterial stiffness. In a preventative sit-uation, PWA can detect early arterialstiffness, which can be halted or evenreversed by appropriate intervention.In this paper, a historical backgroundof mechanics and blood flow willbe presented, followed by a review ofPWA for monitoring arterial compli-ance and central hemodynamics. Theaccumulated evidence that emphasizesthe importance of PWA in clinicalpractice will be addressed.

HISTORICAL BACKGROUNDPalpation of the arterial pulse is a fun-damental sign in clinical practice,providing more information thanmerely the heart rate. In fact, theterm ‘‘pulse’’ has been used incorrectlyto denote the frequency of the heartbeat. When the left ventricle ejectsblood into the aorta, the elasticity ofthis vessel allows it to stretch. This isthe start of the pulse wave, and is whatis palpated during an assessment of the

pulse. If the heart generates the occa-sional ineffective beat, it may not bedetected at the radial artery. Likewise,if a major heart irregularity is present,palpation of heart beat frequency atthe radial artery may not correspondto the actual rate of the heart. Now-adays, we assume the importance ofhypertension in relation to cardiovas-cular disease. As long ago as 1827,William Bright diagnosed high BP onthe ‘‘hardness’’ of the pulse.1 A morescientific method for assessing thepulse called sphygmography2 was de-veloped by Dr Frederick Akbar Ma-homed (Figure 1a). Sphygmographyprovided a qualitative illustration ofthe effects of medication on the arte-rial pulse, as well as providing a pic-ture of the arterial waveform inhypertension and other diseases.Mahomed also used sphygmographyto describe the effects of aging on ar-

terial degeneration.3 These effectswere of great interest to the insurancecompanies, and were included in theirestimation of risk.4 Although the tech-nique of sphygmography became wellestablished in medical practice of theday, reported in journals and text-books (Figure 1), it went out of favorwith the introduction of the cuffsphygmomanometer in the early 20thcentury.5,6

Because diastolic, systolic, and pulsepressures (PP) are related to the physicalproperties of the elastic arteries, currentattention has been redirected towardarterial stiffness, PWV, and alteredwave reflection as independent riskfactors for cardiovascular disease.7–10

Comparable with Mahomed’s 1874work,3 recent studies have shown anassociation between normal agingand arterial stiffness,11,12 and betweenarterial stiffness and coronary artery

For just over 1 century, we have relied on cuff sphygmomanometry to measure bloodpressure at a peripheral (brachial) site. This measurement provides a quantitativesnapshot of hemodynamic activity at 1 part of the arterial tree. Because the heart andbrain are exposed to central (aortic) and not peripheral (brachial) pressure, it mightbe timely for nurses to start looking at alternative techniques to provide moremeaningful information on central hemodynamics. The noninvasive technique ofapplanation tonometry allows such measurements to be performed quickly in thenursing clinic. By analyzing the pulse wave and calculating pulse wave velocity, thetechnique also assesses arterial ‘‘stiffness.’’ This method of cardiovascular assessmentfurther enables nurses to monitor the central effects of antihypertensive, lipidlowering, and other drug therapy over time. Prog Cardiovasc Nurs. 2009;24:53–58. &2009 Wiley Periodicals, Inc.

From the Devonshire Care Center, Edmonton, AB, CanadaAddress for correspondence:Joseph P. Noon, RN, PhD, Devonshire Care Center, 1808 Rabbit Hill Road,Edmonton, AB, T6R 3H2, CanadaE-mail: [email protected] received August 29, 2008; revised December 26, 2008; acceptedJanuary 14, 2009

June 2009 Progress in Cardiovascular Nursing

53r 2009 Wiley Periodicals, Inc.

I:/Bwus/Pcv/31/[email protected]

disease,10,13 myocardial infarction,14

heart failure,15 hypertension,16,17

stroke,18,19 diabetes mellitus,20–23 renaldisease,24 hypercholesterolemia,25 chil-dren with chronic kidney disease,26 en-dothelial function,27 inflammation,28

and all-cause cardiovascular mortal-ity.16,29 Vascular damage is commonto all of these conditions, with inflam-mation being a prerequisite, and leadingto arterial stiffness. The central patho-logical processes involved are mainly

structural, as we shall see, with endo-thelial dysfunction also playing a role.The focus on sphygmomanometry asdeveloped by Mahomed and others atthe beginning of the 20th centurywaned until about 50 years ago whenMacDonald’s seminal work on bloodflow in arteries and arterial mechanicswas published.30 Since then, the adventof the microcomputer allowed Profes-sors Michael O’Rourke and WilmerNichols to develop a 21st-century ver-sion of sphygmography.31

THE METHOD OF PWA ANDPWV BY APPLANATIONTONOMETRY TO ASSESSARTERIAL COMPLIANCEThe technique of PWA using theSphygmoCors Cardiovascular Man-agement System (AtCor Medical,Sydney, Australia), which determinescentral aortic pressure and AIx and-PWV, has been used in many studiesover the past decade.7,30–32 Other de-vices are being manufactured increas-ingly, e.g., the oscillometric andcapacitive method described by Cohnand colleagues.33 PWA is used in-creasingly by nurses in the clinic andby research nurses in the research lab-oratory. Central (aortic) pressure canbe measured and the AIx calculated, toyield an index of arterial stiffness.Gating or synchronizing the signals attwo sites of the electrocardiogram(ECG) allows PWV to be measured.Thus, PWA provides an accurate,noninvasive, easily applied methodwith which to measure central pres-sures and two indices of stiffness, i.e.,PWV and AIx. In applying the tech-nique to a clinical situation, a high-fidelity micromanometer (SPT-301;Millar Instruments, Houston, TX)can be used to flatten but not occludethe artery in question, using gentlepressure. Because of its very high-fre-quency ultrasound specifications, thismanometer is highly accurate andcomparatively inexpensive. Other ‘‘ar-ray’’ micromanometers are available byMillar Instruments and other compa-nies (e.g., model N-500, Nellcor Inc.,Boulder, CO); however, these ma-

Figure 1. The figures depict the evolution of sphygmography technology in the late1800s to the early 1900s, before the advent of the modern sphygmomanometer. (a)Sphygmomanometry instrument developed by Dr Mahomed in 1872 (Courtesy:University of Manchester Medical School Museum, 2008); (b) Sphygmomanometrydevice developed by Dr Dudgeon and used by Sir James MacKenzie in 1902(Courtesy: Homeopathe International, 2001); and (c) Sphygmograph with arterialwaveform recorded by a pen-recorder developed by Dr Marley in 1914 (Courtesy:Letzte Anderung: June 21, 2007).

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nometers are costly. When the arteryunderlying the skin surface is flattenedusing gentle pressure of the manom-eter, circumferential pressures withinthat point of the artery are equalizedand an accurate pressure waveform canbe recorded; this technique is termedapplanation tonometry (Figure 2).Data are collected directly into a lap-top computer. After 20 sequentialwaveforms are acquired, the integralsoftware is used to generate an aver-aged peripheral and correspondingcentral waveform, which was thensubjected to further analysis: determi-nation of either AIx or PWV.

Physiological variations in the pulsewave and in PWV are seen at differentsites of the arterial tree. Because thevelocity of wave travel is faster instiffer and smaller vessels, this struc-tural alteration causes a progressive in-crease in the PWV along the arterialtree.34 There is also a progressive in-crease in PP from the central aorta tothe peripheral sites. This PP amplifica-tion is less evident with aging,32 prob-ably due to the increased aortic PWV,which is secondary to aortic stiffness. Inhealthy adults, the PWV is approxi-mately 7.3 m/s from the heart to theradial artery and 8.0 m/s from the heartto the femoral artery.32 The incident(forward) wave is reflected backwardalong the arterial system from periph-eral reflection sites to the ascendingaorta. A high level of arterial stiffness(decreased compliance) causes an in-crease in PWV and earlier return of thereflected wave to the ascending aor-ta.34,35 Early return of reflected pressurewaves adds to the amplitude of the in-cident wave during the systolic phase(Figure 2b). Thus, the augmentation inthe systolic part of the ascending aorticpressure further increases systolic pres-sure and ventricular afterload. A PWV48.5 to 9.0 m/s would be indicative ofarterial stiffness.

RELIABILITY AND VALIDITY OFTHE INSTRUMENTIt is important to determine the mea-surement of PWA and PWV withprecision if they are used as indicators

of arterial compliance. In other words,considerable reliance is placed on asingle instrument, and we must besure of its reliability and reproducibil-ity, irrespective of the operator. Thesystem’s internal mathematical trans-fer factor, which converts peripheraldata to corresponding central pressuredata, has been shown to equate wellwith many invasive studies, and foundto be highly accurate and reproduc-ible.9,36,37 The system has a built-inquality control that calculates the co-efficient of variation (CV) for multiplewaveforms, and will not accept sam-pling with a preset CV value of be-tween 41% and 45%. In addition,before each patient is studied, the ma-chine engages in self-calibration based

on the input of BP measurementstaken with another device (our labo-ratory uses the well-validated OmronHEM-705CP semiautomated sphyg-momanometer; Omron Corporation,Kyoto, Japan, but many other vali-dated devices are available). AIx isdefined as the difference betweenthe first and the second peaks of thecentral arterial waveform, expressed asa percentage of the PP (Figure 2b). Todetermine PWV, pressure waveformsare recorded at 2 sites: the carotid andradial, or carotid and femoral arteries.Using the R wave of a simultaneouslyrecorded ECG as a reference frame,the wave transit time is calculated bythe system software. The surface dis-tance between the 2 recording sites is

Figure 2. (a) Diagrammatic representation of the artery being ‘‘applanated’’ betweenthe ultrasound sensor and the underlying hard structure—in this case, a bone. Actualapplanation of the radial artery, with the wave form from the laptop screen shownbelow. Compare this with the more cumbersome devices in Fig. 1. (b) Definition ofthe augmentation index (AIx). The inflection point (P1) identifies the merging pointof the propagated and reflected waves (the reflected wave arriving back sooner ifarterial stiffness is present). AP, augmentation pressure; PP, pulse pressure; SBP,systolic blood pressure; and DBP, diastolic blood pressure.


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then measured, thus allowing PWV tobe determined (velocity 5 distance/time). Like many other medical in-struments, reliance on the accuracyand validity of this device is importantif clinical decisions are made on thebasis of its measurements.

WHY IS LARGE-ARTERYCOMPLIANCE OF CLINICALIMPORTANCE?Historically, elevated peripheral vascularresistance is associated with essentialhypertension. Reduced arterial compli-ance or distensibility and arterial stiff-ness are often used interchangeably byresearchers. Mathematically and con-ceptually, they are different.36 Compli-ance of an arterial segment representsthe increase in its crosssectional volumefor a given increase in pressure, whichdoes not account for the diastolic di-mension before distension begins. Dis-tensibility is compliance normalized byarterial diameter. Stiffness is the recip-rocal of distensibility.34,38 Recently, thishas been challenged because it ignoresthe pulsatile component,PP, of arterialpressure.39 Arterial compliance is aprincipal determinant of BP. Compli-ance is pressure dependent, subject toarterial structural mechanics,38,39 andalso relies on the function of the vas-cular endothelium.27 Ventricular ejec-tion, interacting with the elasticity ofthe large arteries and the viscosity of theblood and wave reflection are 2 majordeterminants of the pulsatile compo-nent of BP. An increased PP reflectsdecreased arterial compliance (i.e., in-creased stiffness). Thus, elevated systolicblood pressure (SBP) and PP are nowconsidered to be more reliable indica-tors of cardiovascular risk than diastolicblood pressure (DBP).37,39–46 An in-crease in large-artery stiffness and aconsequent increase in the amplitude ofwave reflection result in a dispropor-tionate increase in SBP and arterialpulsatility. This disproportionate in-crease in SBP increases PP, producingthe phenomenon known as isolatedsystolic hypertension (ISH).47 ISH ischaracterized by a widening PP, due toincreased SBP and a normal DBP.44,47

We know that arterial stiffness increaseswith aging,3,11,12,38 which may accountfor ISH in the elderly. Given the chang-ing demographics, especially the emer-gence of an increasingly aging popula-tion, we should be aware of PP inall patients, as elevations may pointtoward ISH.

THE CHARACTERISTICS OFLARGE ARTERIES ANDPULSATILE FLOWA reevaluation of these hemodynamicindicators of cardiovascular risk can beconceptualized by viewing large arteriesas simple passive conduits. Large arteriescushion pulsatile flow generated by ven-tricular contraction during each cardiaccycle, transforming intermittent flow intoa steady flow of blood in the peripheryand reducing the pressure oscillationscaused by the intermittent ventricularejection.38,45,46,48 The viscoelastic prop-erties of the arterial wall determine theartery’s ability to perform this cushionfunction. During systole, large arteries(e.g., the proximal aorta) expand toaccommodate stroke volume (SV) andrebound during diastole to facilitateforward blood flow. When arterial com-pliance is decreased, less cushioning ofSV occurs in the arterial bed during sys-tole, and so a greater proportion of SV isforwarded to the periphery. Conse-quently, the amplitude of the arterialpulse wave during systole increases anddiastolic pressure declines.38,48

One way to think about this reser-voir or cushioning capacity is illus-trated in the Windkessel model, whichdescribes the recoiling of large arteries(Windkessel vessels). Windkessel inGerman means elastic reservoir.49 Thewalls of large arteries (e.g., aorta, com-mon carotid, subclavian, and pulmo-nary arteries and their larger branches)contain elastic fibers in their walls.These arteries increase their diameterswhen the BP increases during systoleand decrease their diameters when theBP declines during diastole. Thediameter changes result in the largearteries containing more blood duringsystole than during diastole. This ad-ditional blood is discharged peripher-

ally during the next diastole. Thiscompliance effect of the Windkesselprevents excessive increases in BP dur-ing systole. One result is a lower fluidmechanical load on the heart thanotherwise would have occurred. Pres-sure wave reflections in the arterialsystem (a distributed system, as con-trasted with a lumped system) can anddo alter this effect.

The mechanical properties of thelarge arteries, the viscosity of theblood, the volume of blood beingejected from the heart, and the forceof ventricular ejection are all impor-tant because impairments of or inter-ruptions to any of these processes canlead to heart failure. We can detectpossible anomalies by measuring arte-rial stiffness at an early stage in thedisease process so that effective treat-ments can be considered.

COMPLIANCE AND THEARTERIAL TREEThis cushioning effect of large arteriesis affected by their structural mechan-ics, such as compliance. Arterial com-pliance also determines pressure wavetravel and reflection in the rest of thearterial system. Thus, increased resis-tance in the periphery due to arterialstiffness causes earlier reflection of thepulse wave.50 The incident wave, gen-erated by ventricular ejection, movesaway from the heart at a finite speed.The speed of pulse wave propagation(PWV) increases as arterial compliancedecreases. The proximal aorta is rela-tively compliant to accepting the SV.As the aorta extends distally, it be-comes less compliant. The complianceof the arteries also decreases with dis-tance from the heart. Indeed, the ob-servation was made 450 years agothat BP varies throughout the arterialtree.51 Systolic BP in the peripheralbrachial artery is approximately 5 to30 mm Hg higher than in the centralaorta. This keeps blood flowing in theforward direction as diastolic andmean pressures are slightly lower inthe periphery. This is important be-cause the heart and brain are exposedto aortic, not brachial, pressure. While


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autoregulation of blood flow is a con-tributing factor to BP, it may be lessresponsive with high BP. This point isparticularly pertinent to nurses whorecord the brachial BP routinely. Inthe management of cardiovascular pa-tients, quick and easy measurementsof central hemodynamics made byPWA (central PP, central BP, centralAIx, ejection duration, subendocardialviability ratio [SEVR or Buckberg ra-tio], etc.,) may be of more value in theclinical setting, whether in the cardio-vascular risk reduction clinic or in theheart failure unit.

CLINICAL TRIAL EVIDENCEFOR THE USE OF PWAIt has been generally accepted over theyears that lowering of BP, irrespective ofthe particular antihypertensive agentused, results in better cardiovascularoutcomes. However, there has been arecent paradox surrounding b-blockersthat do lower BP, but that do not im-prove outcome.52–55 Even in loweringBP, the selective b1-adrenoceptor an-tagonist, atenolol, seems less effectivethan other agents,54,55 despite an equiv-alent effect on brachial pressure, whichmay also explain why it also fails toimprove outcome.56 An explanation forthe b-blocker inconsistency emergesfrom the recent Conduit Artery Func-tion Evaluation (CAFE) study.57 In thisstudy, both brachial and aortic BPswere measured in a subset of 2199 pa-tients from the Anglo-Scandanavian

Cardiac Outcomes Trial (ASCOT)study.58 Systolic and PPs in the aortawere 4.3 and 3.0 mm Hg lower, re-spectively, in patients randomized to acalcium-channel blocker (CCB) and anangiotensin-converting enzyme (ACE)inhibitor (amlodipine/perindopril) thanthose on a b-blocker and thiazide di-uretic (atenolol/bendroflumethiazide),despite virtually identical reductions inbrachial pressure. In addition, aortic PPwas a significant independent determi-nant of total cardiovascular and renalevents, even after adjusting for differ-ences in brachial pressure. Thus, inhypertensive patients, having centralhemodynamic information is more im-portant than knowing about brachialpressure, taken with a conventional cuffsphygmomanometer. These results inthe CAFE study may in part explain theresults in the main ASCOT study: thatpatients assigned to atenolol/bend-roflumethiazide did not do as well be-cause they had higher aortic pressuresthan those receiving the CCB/ACE in-hibitor treatment. However, most ofthe BP data from the randomized-con-trolled trials over the years have beenbased on brachial artery measurements.Reductions in brachial pressure havecertainly led to improved patient out-comes. Nevertheless, CAFE is a start,and shows the value in assessing centralpressures and of measuring arterial com-pliance in targeting specific, more effec-tive treatment to individual patients.Serial assessment of arterial applanation

tonometry also monitors the effect oftreatment on compliance over time,showing, for example, that statins may‘‘normalize’’ impaired distensibility,i.e., make stiff arteries more compliantagain.59 This is important for nursesin making the actual measurements,and also important in influencing whichtreatment to use, in accordance withthe evidence-based clinical guidelines.Changes in arterial compliance havealso been seen in patients with other,nonpharmacological treatments, such ashemodialysis60 and renal transplant.61

SUMMARYIn summary, as arterial compliancedecreases (stiffness increases), both theamplitude of the pressure wave gener-ated by ventricular ejection and PWVincrease, causing early return of thereflected pressure wave from the pe-riphery to the aorta. The importanceof applanation tonometry has beenhighlighted throughout this paper,and can be summarized by reiteratingthat it allows assessment of not onlyarterial stiffness by measuring pulsewave reflection and PWV, but it alsoprovides more information on centralhemodynamics than conventionalbrachial artery sphygmomanometry.Thus, the simple, noninvasive tech-nique of applanation tonometry couldbe adopted more by nurses as part ofthe overall cardiovascular risk assess-ment in our hypertension, lipid, andrisk-reduction clinics.

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The Arterial Pulse Wave and Vascular Compliance