DTIC ADA628225: Hemodynamics Associated with Breathing Through an Inspiratory Impedance Threshold Device in Human Volunteers

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by  Defense Technical Information Center

Hemodynamics associated with breathing through an inspiratory
impedance threshold device in human volunteers
Victor A. Convertino, PhD; Duane A. Ratliff, MS; Kathy L. Ryan, PhD; Donald F. Doerr, BSEE;
David A. Ludwig, PhD; Gary W. Muniz; Deanna L. Britton; Savran D. Clah;
Kathleen B. Fernald; Alicia F. Ruiz; Keith G. Lurie, MD; Ahamed H. Idris, MD
Objective: Increased negative intrathoracic pressure during Measurements and Main Results: Compared with the control
spontaneous inspiration through an impedance threshold device condition,ITDproducedhigherstrokevolume(124(cid:1)3vs.137(cid:1)
(ITD) causes elevated arterial blood pressure in humans. This 3 mL; p (cid:2) .013), heart rate (63 (cid:1) 3 vs. 68 (cid:1) 3 beats/min; p (cid:2)
studywasperformedtodeterminewhethertheacuteincreasein .049),cardiacoutput(7.69vs.9.34L/min;p(cid:2).001),andsystolic
bloodpressureinducedbybreathingthroughanITDisassociated bloodpressure(115(cid:1)2to122(cid:1)2mmHg[15.33(cid:1)0.3to16.26
with increased stroke volume and cardiac output. (cid:1)0.3kPa];p(cid:2).005)withoutaffectingexpiredminuteventilation
Design: Randomized, blinded, controlled trial. (6.2 (cid:1) 0.4 to 6.5 (cid:1) 0.4 L/min; p (cid:2) .609).
Setting: Laboratory. Conclusions:BreathingwithanITDatrelativelylowimpedance
Subjects: Ten women and ten men. increases systolic blood pressure by increasing stroke volume
Interventions:Wemeasuredhemodynamicandrespiratoryre- and cardiac output. The ITD may provide short-term protection
sponsesduringtwoseparateITDconditions:1)breathingthrough against cardiovascular collapse induced by orthostatic stress or
afacemaskwithanITD(impedanceof6cmH O[0.59kPa])and hemorrhage. (Crit Care Med 2004; 32[Suppl.]:S381–S386)
2
2) breathing through the same face mask with a sham ITD KEY WORDS: respiration; blood pressure; heart rate; stroke vol-
(control). Stroke volume was measured by thoracic bioimped- ume; cardiac output; peripheral vascular resistance; shock; hy-
ance. potension; hemorrhage; orthostasis
H
emorrhagicshockremainsa sure and greater organ blood flows in tions raise the possibility that a Starling
leading cause of death hypovolemic, hypotensive humans and effect with a subsequent increase in
worldwide(1–3).Oneofthe animals(6–13).Buildingonthisconcept, stroke volume and cardiac output repre-
challengestoeffectivetreat- an inspiratory impedance threshold de- sents the underlying mechanism associ-
ment is maintenance of vital organ per- vice (ITD) was designed to create a vac- ated with the elevated blood pressure
fusion when intravenous access, intrave- uumwithinthechesteachtimethechest during inspiratory resistance (16). How-
nous fluids, drug therapies, and surgical expandsduringthedecompressionphase ever, stroke volume during resistance
intervention are not immediately avail- of inspiration (9–11, 14). Recent studies breathing with an ITD set at relatively
able(4,5).Greaternegativeintrathoracic have demonstrated that use of an ITD low inspiratory impedance has not been
pressurecanbeproducedbyapplyingre- increases left ventricular end-diastolic reported in animals or humans. We hy-
sistance during spontaneous inspiration volume (9, 15) and end-tidal CO (6, 7, pothesized that the acute relative eleva-
2
(6–10) and has been associated with ele- 13) in conditions of circulatory collapse tioninbloodpressureinducedbybreathing
vations in systemic arterial blood pres- and hemorrhagic shock. These observa- through an ITD would be mechanistically
linked with increased stroke volume and
cardiac output. This investigation is fo-
cused on testing this concept for the first
FromtheUSArmyInstituteofSurgicalResearch, tuteofSurgicalResearchandtheNationalAeronautics timeinhumans.
FortSamHouston,TX(VAC,KLR);BioneticsCorpora- and Space Administration (CRDA DAMD17-01-0112)
tion(DAR),TechnologyImplementationBranch(DFD), andagrantfromtheU.S.ArmyCombatCasualtyCare
and Spaceflight and Life Sciences Training Program ResearchProgram. METHODS
(DLB,SDC,KBF,AFR),NASA,KennedySpaceCenter, Theviewsexpressedhereinaretheprivateviews
FL;GeorgiaPreventionInstitute,DepartmentofPedi- oftheauthorsandarenottobeconstruedasrepre- Subjects.Atotalof20healthy,normoten-
atrics,MedicalCollegeofGeorgia,Augusta,GA(DAL); senting those of the National Aeronautics and Space sive,nonsmokingmen(n(cid:1)10)andwomen(n
Professional Performance Development Group, San Administration,DepartmentofDefense,orDepartment (cid:1)10)servedassubjects.Descriptivedatafor
Antonio, TX (GWM); Advanced Circulatory Systems, oftheArmy. the subjects are presented in Table 1. The
Minneapolis, MN (KGL); Department of Emergency K.Lurieisaco-inventoroftheimpedancethresh-
subjects had not undergone any particular
Medicine, University of Minnesota, Minneapolis, MN olddeviceandfoundedAdvancedCirculatorySystems
type of exercise training. Because of the po-
(KGL); and Department of Surgery and Emergency todevelopthedevice.
tentialeffectsoncardiovascularfunction,sub-
Medicine, University of Texas Southwestern Medical Copyright©2004bytheSocietyofCriticalCare
Center,Dallas,TX(AHI). MedicineandLippincottWilliams&Wilkins jects refrained from exercise and stimulants
Supported,inpart,byaCooperativeResearchand such as caffeine and other nonprescription
DOI:10.1097/01.CCM.0000134348.69165.15
DevelopmentAgreementbetweentheUSArmyInsti- drugs48hrsbeforetesting.Duringanorien-
CritCareMed2004Vol.32,No.9(Suppl.) S381
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1. REPORT DATE 2. REPORT TYPE 3. DATES COVERED
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4. TITLE AND SUBTITLE 5a. CONTRACT NUMBER
Hemodynamics associated with the human hypertensive response to
5b. GRANT NUMBER
breathing through an inspiratory impedance threshold device.
5c. PROGRAM ELEMENT NUMBER
6. AUTHOR(S) 5d. PROJECT NUMBER
Convertino V. A., Ratliff D. A., Ryan K. L., Doerr D. F., Ludwig D. A.,
5e. TASK NUMBER
Muniz G. W., Britton D. L., Klah S. D., Fernald K. B., Ruiz A. F., Idris
A., Lurie K. G., 5f. WORK UNIT NUMBER
7. PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION
United States Army Institute of Surgical Research, JBSA Fort Sam REPORT NUMBER
Houston, TX 78234
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Approved for public release, distribution unlimited
13. SUPPLEMENTARY NOTES
14. ABSTRACT
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Standard Form 298 (Rev. 8-98)
Prescribed by ANSI Std Z39-18
tation period that preceded each experiment, thevalveandtheskinofthesubject’sfacethat the1-mintimeperiod.Tidalvolume(inliters)
allsubjectsweremadefamiliarwiththelabo- was sufficient to eliminate any air leakage wascalculatedbydividingminuteventilation
ratory, the protocol, and procedures. Experi- (Fig. 1A). Because of the greater vacuum byrespiratoryrate.
mental procedures and protocols were re- withinthechest,alargeramountofbloodis Hemodynamic Measurements. Continu-
viewedandapprovedbytheResearchCouncil drawn from the extrathoracic venous system ousHRwasmeasuredwithaHewlett-Packard
and Human Use Committee of the US Army into the chest and heart during inspiration, monitoring system from a standard electro-
InstituteofSurgicalResearchandtheHuman thereby enhancing cardiac preload (6, 9). cardiogram. SBP and DBP were measured
Investigative Review Board of the Kennedy Therefore,useoftheITDresultsinanimme- noninvasivelywithanautomatedsphygmoma-
Space Center for the use of human subjects. diateincreaseinarterialbloodpressure(6,7, nometerbloodpressuremeasurementdevice.
Eachsubjectgavewritteninformedvoluntary 9,12,13,15).Thereislittleresistanceduring Meanarterialpressurewascalculatedbydivid-
consenttoparticipateintheexperiments. exhalation. ing the sum of SBP and twice DBP by three.
Protocol.Eachsubjectcompletedtwotest- Measurement of Ventilatory Response to Beat-to-beat SV was measured noninvasively
ing sessions that entailed measurements of ITDBreathing.Aftertheinitial3minsofITD using thoracic electrical bioimpedance with
arterial blood pressures, heart rate (HR), breathing, minute ventilation (in liters per an HIC-2000 Bio-Electric Impedance Cardio-
strokevolume(SV),andrespiration1)during minute) was measured from the additive in- graph (Bio-Impedance Technology, Chapel
breathing through a face mask with an ITD spiratory flow for 1 min with an Interface Hill, NC). The thoracic electrical bioimped-
(AdvancedCirculatorySystems,EdenPrairie, Associates (model VMM 402, Laguna Niguel, ance technique is based on the resistance
MN)setatapproximately6cmH O(0.59kPa) CA) turbine transducer (Fig. 1B). Inspiratory changes in the thorax to a low-intensity (4
2
and 2) during a control session (breathing impedance was measured during the same mA),high-frequency(70kHz)alternativecur-
throughthesamefacemaskwithashamITD). time interval using an MKS (PDR-C-1C, An- rentappliedtothethoraxbytwoouter-surface
SubjectswereblindedtothetypeofITDused. dover, MA) pressure transducer between the electrodes placed at the root of the neck and
The order of treatment was counterbalanced ITD–patientmaskinterface(Fig.1B).Thean- two surface electrodes placed at the xiphoid
sothattensubjects(fivemenandfivewomen) alogwaveformwasrecordedonaGould(East- processatthemidaxillaryline.TheR-waveof
underwenthemodynamicandrespiratorytest- lake,OH)strip-chartrecorder,andthechange the electrocardiogram was taken as a land-
ingduringactiveITDtreatmentfirstwhilethe in pressure (negative intrathoracic pressure) mark to average dZ/dt waveforms over ten
remaining ten subjects (five men and five wasmeasuredincentimetersofH O.Respira- cardiaccyclesthatwererecordedin20secsat
2
women)underwenttestingwiththeshamITD tory rate (in breaths per minute) was mea- the beginning of minute 4 of each measure-
treatment(controlcondition)first.Therewas sured by counting the negative pressure de- ment period. SV measured during and at 5
approximately 1 wk (mean (cid:2) SD, 7.2 (cid:2) 1.3 flections occurring on the strip chart during mins after ITD breathing was determined as
days)betweeneachexperimentaltestsession.
Both testing sessions were initiated at the
sametimeofdayforanyparticularsubject.
Table1.Subjectgroupdescriptivedata
HR,SV,arterialbloodpressures,andtidal
volumes were measured as subjects breathed Women Men
throughafacemaskwithanITD.Thehemo- (n(cid:1)10) (n(cid:1)10)
dynamic and respiratory measurements were
repeated at 5 mins after completion of the Age,yrs 32(cid:2)4 33(cid:2)4
14-min ITD breathing cycle. This protocol Height,cm 167(cid:2)2 177(cid:2)1
represented a complete experimental session. Weight,kg 63.8(cid:2)2.5 78.8(cid:2)2.9
Avalvesetat6cmH O(0.59kPa)ofcracking Heartrate,beats/min 66(cid:2)3 61(cid:2)3
pressure(i.e.,thepre2ssureatwhichthevalve Systolicbloodpressure,mmHg 110(cid:2)3 120(cid:2)3
Systolicbloodpressure,kPa 14.6(cid:2)0.4 16.0(cid:2)0.4
opened, allowing air inflow) was chosen be-
Diastolicbloodpressure,mmHg 71(cid:2)2 75(cid:2)3
causeimpedancelevelsashighas20cmH O
2 Diastolicbloodpressure,kPa 9.46(cid:2)0.3 75(cid:2)0.4
(1.96 kPa) were previously proven tolerable
and sufficient to increase arterial blood pres- Valuespresentedasmean(cid:2)SE.
sureinhumansubjects(13,17).Eachsubject
hadhisorherowndisposablefacemask.Dur-
ing all experiments, continuous beat-by-beat
HRwasmeasuredfromanelectrocardiogram
and systolic (SBP) and diastolic (DBP) blood
pressures were measured noninvasively by a
sphygmomanometricbloodpressuremonitor-
ing device. Each experimental session was
conductedoveraperiodof(cid:3)60mins.
Breathing with the ITD.At the beginning
of each experimental testing session, each
subject breathed spontaneously through an
ITD for 14 mins. The ITD comprises a valve
thatcloseswhenthepressurewithinthetho-
rax is less than atmospheric pressure and a
second valve (termed the safety check valve)
that opens at a preset negative intrathoracic
pressure (6–8, 14). The ITD was designed to
create inspiratory resistance and to therefore Figure1.Photographsoftheimpedancethresholddevice(ITD)aloneandappliedtoasubject.Left,
increasethemagnitudeofthevacuumwithin illustrationoftheITDplacementonasubjectinstrumentedformeasurementofheartrate(electro-
thechestofaspontaneouslybreathingsubject cardiogram),bloodpressure(cuff),andstrokevolume(electricalimpedanceelectrodesontheneck
duringinspiration.TheITDwasattachedtoa andthorax).Right,illustrationofthevalveconnectedtoafacemaskandsensorsformeasurementof
facemasktoensurethatasealexistedbetween ventilatoryvolume/rateandinspiratorypressure.
S382 CritCareMed2004Vol.32,No.9(Suppl.)
the average SV from the ten cardiac cycles. andbloodpressure,allvalueswerewithin DISCUSSION
VentricularSVwasdeterminedwiththepartly established normal limits.
empiricalformula:SV(inmillilitersperbeat) ITD and Sex Effects. Sex did not in- One of the primary mechanisms that
(cid:1)p(cid:4)(L/Zo)(cid:5)2(cid:4)LVET(cid:4)(dZ/dt)min,where fluence the responses of SBP(F(cid:1)0.348; contribute to severe hypotension and ul-
p(inohm-centimeters)isthebloodresistivity, p (cid:1) .563), DBP (F (cid:1) 0.016; p (cid:1) .902), timatelyshockafteranacutehemorrhage
a constant of 135 ohm-cm (1.35 ohm-m) in
HR(F(cid:1)0.845;p(cid:1).370),SV(F(cid:1)2.894; isthereductionincirculatingbloodvol-
vivo; L (in centimeters) is the mean distance
between the inner pick-up electrodes; Z (in p (cid:1) .106), CO (F (cid:1) 0.321; p (cid:1) .578), umeandsubsequentreductionincardiac
ohms) is the mean baseline thoracic imoped- TPR(F(cid:1)0.030;p(cid:1).864),minuteventi- fillingandSV(19).Therefore,anythera-
ance;LVET(inseconds)istheleftventricular lation (F (cid:1) 0.084; p (cid:1) .776), or tidal vol- peutic approach that is designed to in-
ejection time; and (dZ/dt) (in ohms per ume (F (cid:1) 0.296; p (cid:1) .593) across treat- crease venous return and SV without
min
second) is the height of the dZ/dt peak (Z- mentduringeitherspontaneousbreathing causinghemodilutionshouldbeaneffec-
point) measured from the zero line. Most in- tive therapy for the acute treatment of
through the ITD or control experimental
vestigators who measured SV with thoracic massivebloodloss.Theapplicationofre-
conditions.Women(11breaths/min)had
electrical bioimpedance have reported corre- sistance during spontaneous inspiration
a slightly higher respiratory rate than
lationcoefficientsof0.70–0.93incomparison has been shown to cause an immediate
men (9 breaths/min) (F (cid:1) 5.174; p (cid:1)
withthermodilutiontechniques(18).Cardiac increase in arterial blood pressure when
output (CO) was calculated as the product of .035)duringITDbreathing.Fiveminutes applied in different clinical models asso-
HRandSV.Totalsystemicperipheralresistance after spontaneous breathing on the ITD
ciated with significant life-threatening
(TPR)wascalculatedbydividingmeanarterial was terminated, SBP, DBP, HR, SV, CO,
hypotension(6,7,9–13).Theconceptby
pressure by CO, and is expressed as peripheral and TPR were statistically similar (F val-
resistanceunits(inmmHg·min(cid:5)1·L(cid:5)1). ues of (cid:3)0.415; p values of (cid:6).527) across which the ITD functions to increase
bloodpressureisbasedonthemechanics
StatisticalAnalysis.Thestatisticalanalysis
was a standard two group (men, women) by experimental conditions. Based on these ofproducingagreatervacuumwithinthe
twotreatment(6cmH OITD,control)bytwo analyses,thedatawerecombinedandan- thorax during each inspiration, which
time periods (during,25 mins after) mixed- alyzed as a sample size of 20. subsequentlymayincreasevenousreturn
model analysis of variance. The model was Respiratory Effects of Spontaneous andpreloadtotheheart(6,7,9,10).We
mixed in the sense that subjects were nested Breathing on an ITD. Average peak neg- thereforehypothesizedthattheelevation
within groups by sex and crossed with treat- ative airway pressure of (cid:5)9.4 (cid:2) 0.3 cm in arterial blood pressure induced by ap-
ments and time (i.e., one between-subjects H O ((cid:5)0.92 (cid:2) 0.03 kPa) was generated plication of respiratory resistance (i.e.,
2
factor [sex] and two within-subjects factors during spontaneous breathing on the spontaneous breathing through an ITD)
[treatment and time]). To simplify the statis-
ITD.Therewasnomaintreatmenteffect resultsfromanincreaseinSVandCO.To
ticalanalysisandmakeitmoreinterpretable,
(F (cid:1) 0.271; p (cid:1) .609) on minute venti- test this hypothesis, we measured SV in
separate statistical models were constructed
lation during spontaneous breathing normovolemic, normotensive human
formeasurementstakenduringITDbreathing
and5minsafterthecessationofITDbreath- throughtheITD(6.5(cid:2)0.4L/min)com- subjects during spontaneous breathing
ing. All main effects and subsequent interac- pared with breathing through the sham throughanITD.Ourdataconfirmedthat
tions were analyzed across six dependent ef- device (6.2 (cid:2) 0.4 L/min). However, tidal applicationoftheITDincreasedSBPina
fects (SBP, DBP, HR, SV, CO, TPR). Exact p volumewashigher(F(cid:1)10.05;p(cid:1).005) manner similar to that previously re-
values were calculated for each independent and respiratory rate was lower (F (cid:1) ported (6, 7, 9–13, 15). A new finding of
effect and reflect the probability of obtaining 8.084; p (cid:1) .011) during spontaneous thepresentinvestigationwasthattheel-
theobservedorgreatereffectgivenonlyran- breathingthroughtheITD(0.86(cid:2)0.04L evation in blood pressure induced by
dom departure from the assumption of no
and 9 (cid:2) 1 breaths/min, respectively) spontaneous inspiration on an ITD was
effects. Orthogonal polynomials (i.e., dose-
mechanistically associated with an in-
response modeling) or independent contrasts compared with breathing through the
were constructed in the event of statistical sham device (0.67 (cid:2) 0.04 L and 10 (cid:2) 1 crease in SV and CO.
An increase in SV and CO during
differences associated with the main effect of breath/min, respectively).
spontaneous breathing against high re-
the treatment (i.e., inspiratory impedance Hemodynamic Effects. Mean ((cid:2)SE)
level). Standard errors are raw measures of SBP, DBP, HR, SV, CO, and TPR data sistancepressures(68–88cmH2O[6.67–
variation about the specific treatment group 8.63 kPa]) has been reported previously
duringand5minsafterthecessationof
mean. These standard errors do not reflect (16). Because of the extraordinarily high
spontaneousbreathingthroughtheITD
variabilityspecifictothefactorsbeingtested resistance, Coast et al. (16) suggested
are presented in Figure 2. There was a
or the variability associated with statistical that the increased CO was a result of
tests and subsequent p values given in the large main treatment effect of sponta- greater energy demand required for the
text. neous breathing through the ITD on workofbreathing.Ourdataareuniquein
SBP, HR, SV, CO, and TPR (F values of
demonstrating that a relatively low in-
(cid:6)4.481; p values of (cid:3).049). There was
RESULTS spiratory resistance can increase CO and
no statistically distinguishable treat- blood pressure with no effect on meta-
DescriptiveData.AverageandSEbase- ment effect of spontaneous breathing bolic demand because the average ((cid:2)
line values for age, height, weight, HR, through the ITD on DBP or minute standarderror)oxygenuptakeintensub-
andbloodpressuresforwomenandmen ventilation. Five minutes after sponta- jects during 6 cm H O (0.59 kPa) of ITD
2
arepresentedinTable1.Maleandfemale neous breathing on the ITD was termi- breathing (247 (cid:2) 17 mL/min) was not
groups were matched for age. Subjects nated, all hemodynamic variables were statistically different from that of 228 (cid:2)
showedtheexpectedandwell-established statisticallysimilar(Fvaluesof(cid:3)0.415; 14mL/minduringbreathingonthesham
differences between sexes on height, p values of (cid:6).527) across experimental device (unpublished data). Breathing
weight, HR, and blood pressure. For HR conditions (Fig. 2). throughtheITDwaswelltoleratedbyour
CritCareMed2004Vol.32,No.9(Suppl.) S383
Figure2.Systolicanddiastolicbloodpressures,heartrate,strokevolume,cardiacoutput,andtotalperipheralvascularresistanceduring(Breath)andafter
(5-minRec)spontaneousbreathingontheimpedancethresholddevice(ITV)at0cmHOresistance(shamcontrol,openbars)and6cmHO(0.59kPa)
2 2
resistance(linedbars).Barsandlinesrepresentmean(cid:2)1SE,respectively(n(cid:1)20).bpm,beatsperminute;PRU,peripheralresistanceunits.
subjects. In light of the statistically sim- response relationship to a higher sure, either individually or collectively,
ilareffectsonventilatorymechanics(vol- operating range (20, 21). We also found caused by breathing through an ITD in
umeandrate)andoxygenuptakeduring thattheelevatedHRresponseduringITD our subjects probably reduced sympa-
breathing on the ITD and sham devices, breathingwasassociatedwitharesetting thetic nerve activity to the vasculature.
ourresultssuggestthattheapplicationof of the baroreflex to a higher operating This compensatory response of the pe-
an ITD to patients in a clinical setting range in our subjects (17). Thus, the in- ripheralvascularresistancecouldprovide
could provide a tolerable therapeutic ap- crease in CO elicited by spontaneous twoimportantmechanismsofprotection
proach for acute treatment of life- breathing on the ITD involves mecha- if applied during hemorrhage. First, a
threateninghypovolemiaorhypotension. nisms that contribute to elevations in lower relative vasoconstriction would
InadditiontoanincreasedSV,anun- both SV and HR. functiontoincreaseperfusionofvitalor-
expected elevation in HR during sponta- TPR was significantly lower during gansandsubsequentlydelayischemicin-
neousbreathingontheITDalsocontrib- spontaneousinspirationontheITDcom- jurytotissues.Second,theabilitytorely
uted to higher CO and SBP. Because of pared with the control condition. This on less peripheral vascular resistance for
the elevation of arterial blood pressure may be expected in light of the evidence agivenbloodlosswouldprovideagreater
duringinspiratoryresistance,wehadan- that a linear stimulus-response relation- capacity for vasoconstrictive reserve to
ticipatedabradycardicresponsemediated ship exists between SV and sympathetic defend against hypotension and cardio-
by arterial baroreflex feedback control, nerve activity (22, 23). Thus, as cardiac vascular collapse (24). Future experi-
but ITD breathing actually elicited a filling, SV and blood pressure decrease ments are necessary to test this intrigu-
tachycardicresponseinthefaceofrising underconditionsofcentralhypovolemia, ing hypothesis.
arterial blood pressure. Although this areflexincreaseinsympatheticnerveac- Although modest (7 mm Hg [0.93
tachycardic response seems contraindi- tivity to vascular smooth muscle results kPa]),themagnitudeoftheaverageacute
cated,itissimilartotheconcurrentele- inacompensatoryelevationinperipheral elevationinSBPobservedinoursubjects
vation in HR and arterial blood pressure resistance in an attempt to maintain may be important in that it occurred in
responses observed during physical exer- bloodpressure.Althoughwedidnotmea- healthy normovolemic, normotensive
cise when increased negative intratho- sure sympathetic nerve activity in the subjects in the supine position, which
racicpressuresareassociatedwithreset- present investigation, it is likely that the optimizes venous return. Under these
ting of the cardiac baroreflex stimulus– increases in SV and arterial blood pres- conditions,venousreturnisoptimal.We
S384 CritCareMed2004Vol.32,No.9(Suppl.)

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