Noninvasive assessment of central circulatory pressures by analysis of ear densitographic changes during the valsalva maneuver

Noninvasive assessment of central circulatory pressures by analysis of ear densitographic changes during the valsalva maneuver

Noninvasive Assessment of Central Circulatory Pressures by Analysis of Ear Densitographic Changes During the Valsalva Maneuver Luciano Bernardi, MD, R...

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Noninvasive Assessment of Central Circulatory Pressures by Analysis of Ear Densitographic Changes During the Valsalva Maneuver Luciano Bernardi, MD, Riccardo Saviolo, MD, and David H. Spodick, MD, DSC

The ear densitogram was monitored in 21 consecutivepathtswRhvarkusdegreesofmyocardid hc9on(NewYorlchartAssocia9onclassItoIV) thing tbe standanliwd Valsalva maneuver to evdrebtionrbetweentbepattem uatetbequntitative ofrespomandthec&rdciraMorypresuues. Tbeeardensbgraphkifirstd6dvativeconeistenUy t&ring tbe strdn -~-pubepreuve pha8eoftheVdsdva maneuver @eat-to-beat corda9011 [r] range 0.99 to 0.72). The percent decroaseoftbededtograpbkpdsederivativeduring straincotmMedwitbleft-end&stoiiC preuureatrest(r=0.92,p<0.901),butnotwith cmdiaceutput,cadiacbmdexandejec9ontraction. wasusedtotakeinto multipk-m actountmdtlpIeaspects(timeintervabandpulse to the Val~)of~pstternofsalvamaneuver.Asare&t,both~improved rubakntidly (r = 0.97, p
I

n heart failure1-5 and volume overload,6v7 an abnormal pattern of aortic pulse pressure (the “square wave”) occurs during the strain phaseof the Valsalva maneuver.It was suggestedthat this qualitative fmding may be useful to support the diagnosisof myocardial dysfunction.s-*3Recently, in quantifying the pressure pattern during Valsalva strain, we reported that aortic pulse pressure decay correlated with left ventricular end-diastolic pressure and pulmonary wedge pressure, rather than ejection fraction, cardiac output and cardiac index.t4 Becausethe indexes used to define pulse pressure decay were independent of the absolute values of aortic pulse pressure,we hypothesizedthat the Valsalva maneuver could potentially predict invasive parameters noninvasively, if the aortic pressurepattern could be reproduced noninvasively. We showedthat the ear densitographic pulse is consistently and predictably related to the pulse wave of large arteries,15and reliably reflects central circulatory phenomena including ejection time,16 ejection rate,17 stroke volume, ejection fraction and velocity of circumferential fiber shortening.18In this study we recorded the ear densitogram to test its predictive ability for aortic pressuredecay during Valsalva strain, and thus evaluate central circulatory pressuresnoninvasively. MFTHODS

Patknb: We investigated 21 patients with a mean age of 61 years (range 33 to 78). Fourteen consecutive patients were undergoing diagnostic catheterization and 7 patients were in the medical intensive and coronary units for right-sided cardiac pressure monitoring; all gave informed consent.Cardiac disability was classified by New York Heart Association criteria. The diagnoses,hemodynamics,functional class and medications are listed in Table I. QMete&ationr Right-sided heart catheterization, left ventricular angiograms and coronary arteriography were performed according to standard techniques. Swan-Ganz thermodilution catheters were used in the intensive care units. In the catheterization laboratory, right (right atrium, pulmonary artery) and left (puhnonary wedge, left ventricular end-diastolic and aortic) From the Department of Internal Medicine, University of Pavia, Pavia, pressuresand cardiac output were measured. Italy, the Department of Medicine, University of Massachusetts,and The ear densitographic transducer, previously de the Cardiology Division, Saint Vincent Hospital, Worcester,Massachu- scribed in detail,16J9was attached to the pinna. The setts.Manuscript receivedMarch 8,1989; revisedmanuscript received photosensitiveelement is part of a direct current bridge and acceptedJune 34 1989. Addressfor reprints: David H. Spodick, MD, Saint Vincent Hospi- connectedto a differentiating circuit with a 12-HZ cutoff low-passfilter, providing its first derivative. tal, Worcester,Massachusetts01604. THE AMERICAN JOURNAL OF CARDIOLOGY OCTOBER 1.1989

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I II II Ill IV

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1:

8 12 6

9 7 8 7 5 5 30 14

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25

45 26 32 30 25 38

34 27 18 22 21 24

14 11 6 8 11 8 11 18 26 13 22 23 12 18

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134 140 110 130 120 74

130 110 130 150 140 130 115 150 125 155 150 110 155 105 106 65 80

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57 44 56 63 40 69 67 44 51 65 34 49 65 60 -

EF (%)

,9blocker fi bkxker, Ca antagonist fl blocker, nitrates f?blocker, Ca antagonist, insulin ,9 blocker, nitrates fl blocker, Ca antagonist Digoxin, furosemide fl blocker, Ca antagonist, nitrates /3bkxker, nitrates, HCTZ Nitrates fl blocker, Ca antagonist, nitrates fl blocker, Ca antagonist Niiates Ca blocker, nitrates, HCTZ Dopamine, lklocaine, dioxin, procainamide Dioxin, furosemide. nitrates Digotin Insulin, furosemide, nitrates 6 blocker, HCTZ. diabinese Dobotrimine, lidocaine

Last Medications

Ml IDC

MI, CHF AF, CABG AF

ACP Ml MI, CS

ACP Ml

MI MI, COPD MS, CHF Ml

Remarks

ACP - at@al chest pain: AF - atriel fibfil!ation; Aop = eortic diaetolii pressure; AoS = awtic dlC FW+SUre;Ca - Cdkium: CAB0 * after CWo”ary artery bypass graftjng; CAD = corona arte disease; CHF = congetie heart failure; Cl = cardiac index CD - cwdiec output; COPD - chronic ob&ucW e lung disease; CS = cardiogenic she a? = dnbetes ‘, mellitus: EF - ep fra&mr: IDC = idqathk tiated cardiomyopathy; LVEDV - !e% ventrkul ar end-diastolic pressure: MI = myocardii PAS - pulmonery artecy eyMk pressure; PAW P pulmonary &ery wedge pre+ infarction; MS - mitral stenosis; NYHA - New York Heart qssodation functionel dass; PA - mean pulmonary artery pressure; AD - pulmonary artery dW&iic pr-re; sure: RA - f&t atrium pressure; SH = systemii hyperkww 0 = absent; + - present.

16 75, F 17 75, M 18 61,M 1964,F 20 54,M 21 74, M

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2.0 2.5 2.5 2.9 2.4 2.7 2.9 2.3 2.4 2.9 2.4 2.8 2.5 2.1 1.8

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1 67,M 2 52, M 3 43,M 4 51,M 554,M 664,F 7 33,F 8 75,M 9 67, M 10 54,M 11 71,M 12 48,F 13 68,F 14 63,M 15 74,M

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Cl (CO/m?

PAW RA LVEDP AoS AoD CO PAD PAS PA Age F’t &rs), Sex CAD SH DM NYHA (mm Hg) (mm Hg) (mm Hg) (mm Hg) (mm Hg) (mm Hg) (mm Hg) (mm Hg) (liiers/min)

TABLE I Clinical Profile

Rare &nsitogr~@~y: The ear densitogram responds to the blood volume flow between sensing and lightemitting elements, producing a composite signali of pulse waves directly related to and varying with the morphology of central arterial pul~es,~~and of slowly fluctuating componentsdue to phasic differences in venous return. After electronic differentiation, densitographic pulse morphology is even closer to that of arterial displacement and pressurepulses,and equally suitable to precisely identify time intervalsi Valsahfa maneuver: Our patients performed a standardized Valsalva maneuver lying supine and blowing into a manometer to maintain 40 mm Hg of pressure for 10 seconds.The procedure was repeated at least 3 times, or until a satisfactory maneuver was directly observed. Electrocardiogram and ear densitogram derivative were recorded at 50 mm/s simultaneously with continuous right atrial, pulmonary artery and aortic pressures.Medical intensive care and coronary unit patients underwent the same protocol, but with only right-sided heart pressuresand thermodilution cardiac output. One patient received sublingual nitroglycerin after the first Valsalva maneuver and the protocol was repeatedafter hemodynamic stabilization. Only the Valsalva maneuver performed before nitroglycerin was used in the regressionequations; the secondmaneuver tested whether the regressionequation would correctly predict new pulmonary artery wedge pressure. HemodyMmk measuremen& We measured mean right atria1 pressure, mean pulmonary artery pressure, pulmonary artery wedge pressure,left ventricular enddiastolic pressure,systolic and diastolic aortic pressure, thermodilution cardiac output, cardiac index and ejection fraction, computed by planimetry of the end-systolic and end-diastolic cincangiograms.

TABLE II Hemodynamic

RAP (mm Hg) PA (mm Hg) PCWP(mm Hg) LVEDP(mm Hg) AoS (mm Hg) AoD (mm Hg) CO (liters/min) Cl (liters/m? EF (%)

Parameters

at Rest

No. of Pts

Mean f SD

Range

21 21 21 14 21 21 21 21 14

5.7 f 3.4 21.f 16 11.8k6.8 10.8 f 6.2 127f 20 71f9 4.74f0.98 2.58f0.40 55fll

o-11.5 7-w 5-30 3-23 74-155 55-80 2.96-6.76 1.79-2.95 40-67

PCWP = pulmonary capillary wedge pressure: RAP = right at&l standard deviation. Other abbreviatiom as in Table I.

pressure:

SD =

terval; (6) slope of linear fit of RR interval shortening; (7) last beat/first beat percent left ventricular ejection time; (8) longest/shortest percent left ventricular ejection time; (9) slope of linear tit of left ventricular ejection time shortening; (10) last beat/first beat percent diastolic time; (11) longest/shortest percent diastolic time; and (12) slopeof linear fit of diastolic time shortening. In 3 patients with atria1 fibrillation, last/first percent ratios were obtained averaging the first 5 and the last 5 beats, with ratio (2) obtained by averaging the 3 highest amplitude beats at start-strain. Figure 1 shows the ear densitographic signal during the Valsalva maneuver in a normal subject. Statistkal -4s: Statistical analysis was performed by linear regression and linear correlation coefficient. The ability of the ear densitogram to track central aortic pulse responsesto Valsalva strain was assessedby beat-to-beat correlation of the amplitudes of both signals for each maneuver. Multiple stepwise regressionanalysis20was used to evaluate the correlation betweenhemodynamicsat rest and the global Valsalva Quadtative evabath of the Valsahfa maneuver: To quantify the changes occurring during Valsalva effect on the pressure pulse pattern. Significance was strain, the following indexes were obtained from the ear assessedby F ratio of multiple regression analysis of densitographic first derivative and the aortic pulse pres- variance.” sure14:(1) last beat/first beat percent pulse amplitude ratio; (2) minimal/maximal percent pulse amplitude; RESULTS and (3) normalized slopeof linear lit of pulse amplitude Table II lists the hemodynamicsat rest. decay (first pulse amplitude = 100). Also, the following Valsalva maneuver: Typical increasesof right and time indexes were evaluated by using ear densitogram- left ventricular pressureswere observed in all patients derived time intervals: (4) last beat/first beat percent during Valsalva strain. Aortic pressure pulse response RR interval ratio; (5) longest/shortest percent RR in- varied from a square wave to a typical normal decrease

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NONlNVAslVE ASSESSMENT OF CENTRAL CIRCULATORY PRE33URES

in amplitude. Under stable hemodynamic conditions, repetition of the maneuver differed no more than 18% in any parameter. Invasive and noninvasive eorrelQuantitative pulse pressure decay during Valsalva strain correlated closely with the corresponding decay of ear densitographic amplitude (r = 0.70 for minimal/maximal percent pulse amplitude ratio, r = 0.74 for last/first percent pulse amplitude ratio and r = 0.74 for linear slope,

AORTIC

PULSE

p
modynamies ai restr Ear densitographic pulse changes during Valsalva strain correlated significantly with left ventricular end-diastolic pressure(min/max: r = 0.88, p
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wedgepressure(min/max: r = 0.63, p
ations causedby pulsatile flow. A close functional relation between arterial blood volume changesand variations in arterial pressure was first pc&ulated22for intraarterially recorded Valsalva responses,suggestingdiagnostically useful correlations between a photoplethysmographically recorded Valsalva responseand corresponding cardiovascular events.22 The typical normal responseto Valsalva strain is progressivedecay in amplitude of aortic pulse pressure, often preceded by transient augmentation along with progressiveshortening of cycle length, ejection time and diastolic time.21In a typical abnormal response,pulse pressure is almost unchanged while both systolic and diastolic aortic pressuresshift upward (square wave). In a randomly selectedgroup of patients, aortic pulse pressure decay during Valsalva strain showeda wide range of patterns, normal to square wave, correlating with the level of central circulatory pressuresat rest.ii

30 r = 0.973

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THE AMERICAN JOURNAL OF CARDIOLOGY OCTOBER 1.1989

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The densitogram tracked the aortic pressure pulse REFERENCES I. Price HL, Conner EH. Certain aspectsof the hemodynamicresponseto the pattern very closely during strain, beat-to-beat correla- Valsalva maneuver.J Appl Physiot 1953;5:449-456. tions were excellent in all patients, despite some re 2. Stucki P, Hatcher JD, JudsonWE, Wins RW. Studiesof circulation time sponsesapproaching a square wave with small changes during the Valsalva test in normal subjectsand in patients with congestiveheart CircuIation 1955:l I.?WMW. in aortic and densitographic pulse amplitudes. These failure. 3. Sharpey-ShaferEP. Effects of Valsalva maneuveron the normal and failii agree completely with previous studiesr7-I9confuming circulation. Br Med J 1955;19.693695. that aortic pulse morphology during strain can be repro- 4. Burroughs RW, Bruce RA. Signiticance of abnormai phase II responseto Valsalva maneuverin cardiac patients. Circulation X956:14:72-76. duced noninvasively (Figures 2 and 3). 5. Knowles JH, Gorrm R, Storey CF. Clinical teat for puhnonary congestionwith There was excellent correlation betweennoninvasive the use of the Valsalva maneuver.JAMA 1956;160:44-48. data and resting left ventricular end-diastolic pressure, 6. JudsonWE, Hatcher JD, Wiikins RW. Blood pressureresponsesto the Valsalmaneuverin cardiac patimts with and without congestivefaihtre. Circulation and (to a lesser degree) pulmonary artery wedge pres- va 1955:I1:889&V. sure. 7. Wilkinson PL, Stowe DF, Tyberg JV, Parmley WW. Pressure and flow We also found fairly gcod correlations with changes changesduring Valsalva-like maneuversin dogsfollowing volume infusion. Am J Physiol 1977;233:H93-H99. in pulmonary wedge pressure and left ventricular end- 3. Gorlin R, Knowles JH, Storey CF. The Valsalva maneuveras a test of cardiac diastolic pressure,and several indexes derived from the function. Pathologic physiology and cliicai signiiicance. Am J Med 1957;22: specific pressure pulse pattern during strain. Because 197-212. EUshergEL Heart rate responseto the Valsalva maneuwsrasa test of circnlaeach such noninvasive index identified a single aspectof 9. tory integrity. JAMA 1%3:186:200-205. a complex hemodynamic response,it is not surprising 10. Levitt AB. A simpletest of cardiac ftmction baseduponthe heart rate changes that those correlations predict pressure levels at rest induced by the Valsalva maneuver.Am J Cwdiol 1966;18.9&99. Morand P, I.&an&i J, Raffoux P. La manoeuvrede Valsalva: test global de with a rather large error. However, multivariate analy- la11.fonction myocardique.Arch Ma1 Coew 1972,65:1483-1495. sis permitted a more global evaluation of strain re 12. Zema MJ, Reativo B, SOST, Sniderman KW, Kline S. Left ventricular SpOllSeS.

It is unclear why Valsalva hemodynamic responses correlated with left ventricular filling pressuresrather than cardiac output, cardiac index and ejection fraction. Yet these responsesmay reflect resting left ventricular compliance and the pulmonary blood reservoir.14To explain the better correlation obtained with left ventricular end-diastolic and pulmonary artery wedgepressures, it should be considered that end-diastolic pressure re fleets combined myocardii compliance and preload, and wedgepressurereflects left-ventricular end-diastolic pressure changes. The method requires the patient’s collaboration, yet is easy and safe, becausein the failing heart increased intrathoracic pressure may augment cardiac performance.23 The correlations from multiple regression seemstrong enough to reliably predict the status of filling pressuresat rest noninvasively, which is indicated by the low standard error of estimate and narrow comidence limits (Figure 4). Moreover, these results were obtained despite patient inhomogeneity regarding de gree of cardiac impairment, diagnosis,therapy and clinical conditions (Table I).

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dysfmtction-bedsideValsalva manetwer. Br Heari J 198&44:560-569. 13. Zema MJ, CaccavanoM, Khgfield P. Detection of left ventricular dysfunction in ambulatory subjects with the bedside Vahalva maneuver.Am J Med 1983;75:241-248. 14. Bernardi L, Saviolo R, Spcdick DH. Do hemodynamicresponsesto the Valsalva maneuverreflect myomrdial dysfunction? Chest 1989,95:986-991. 15. Bernardi L, Lumina C, Garavani E, Mami B, Fiirdi G. Computerizedstudy to assessmorphological and time relationships between ear densitogram and carotid pulse. Acto Gudiol (Brwr) 1985,0:156-159. 16. Quarry-Pigott V, Chirife R, Spodick DH. Ejection time by ear densitogram and its derivative. Cliical and physiological applications. Cimrlution 1973; 48:239-246. 17. Haffty BG, Singh JB, Spodick DH. Tracking left ventricular performance noninvasively.Responseof the peak ear pulsederivative during cardiac catheterization. Chest 1983:83:543-546. 16. N&mum Y, Haffty BG, Spedick DH, Paladin0D, Moreau K, FRssasAP. Respnses of peakear-pulse derivativeto changingleft ventricular function. Am J Physiol 1980:238:H355-H359. 19. Chirife R Spcdick DH. Densitography: a new method for evaluation of cardiac performanceat rest and during exercise.Am Heari J 1972:83:493-503. 20. Kleinbaum DG, Kupper LL. Applied RegressionAnalysis and Gther Mtdtivariate Mcthads. North Scituate, Maszachusetts:Duxbuty Press,1978:131-180. 21. FkssasAP, Kumar S, Spodick DH. Effects of the Valsalva maneuveron the cardiic systolic interval% beat-t&eat versus time analysis. Am Heart J 1970; 80522-531. 22. Weinman J, Ben-Yaakov S, SapoznikovD. The application of photoplethysmography to the record& of Valsalva maneuver responses.fsr J Med Sci 1%9,5:534-536. 23. Pinsky MR, Summer WR, Wii RA, Permutt S, Bromberger-BameaB. Augmentation of cardiac function by elevation of intrathoracic pressure.J Appl Physiol 1983;54.950-955.