Inspiratory impairment in right ventricular performance during acute asthma

F Jardin, O Dubourg, A Margairaz and JP Bourdarias Chest 1987;92;789-795 DOI 10.1378/chest.92.5.789

The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.org/cgi/content/abstract/92/5/789

CHEST is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright 2007 by the American College of Chest Physicians, 3300 Dundee Road, Northbrook IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder (http://www.chestjournal.org/misc/reprints.shtml). ISSN: 0012-3692.

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Inspiratory Performance
Fran#{231}oisJardin, Andr#{233}Margairaz, M.D.; M.D.

Impairment in Right Ventricular during Acute Asthma*

Olivier Dubourg, M.D.
,

FCC.?; M.D.

; andJean-Pierre

Bourdarias,

Right ventricular function was investigated in seven asthmatic patients during an acute attack, using simultaneous bedside right heart catheterization and two-dimensional echocardiography (2DE). Hemodynamic and echocardiographic data were compared during four successive periods of the respiratory cycle: inspiration, early expiration, midexpiration, and late expiration. During inspiration, 2DE showed a significant increase in right ventricular area at both end-systole and end-diastole. This inspiratory right ventricular enlargement coexisted with a significant reduction in 2DE stroke area and pulmonary artery pulse pressure suggesting an inspiratory reduction in right

ventricular stroke output. A transient depression of right ventricular function during deep inspiratory effort in asthma was thus strongly suggested. The negative pressure surrounding the right ventricle at inspiration is advocated as the causative factor enabling reduction in the hydraulic force effecting right ventricular ejection. The highly negative pleural pressure probably holds the right ventricular free wall and restrains its systolic inward motion, as suggested by the finding ofa concomitant inspiratory reduction in right ventricular developed pressure and 2DE fractional area contraction.

T
posed
111

he influence has been several

ofrespiration investigated

on cardiac extensively and clinical for the in dyspneic Pulmonary phasic left ventricular devoted advocated. study and
in

performance the past.4 have prodecline

cardiographic

measurements.

perkrmed

tion,

were and

obtained were data

reference

during

the after

first

hour
patients

in the semisupine posiin the ICU while patients

recovered from their

Numerous

experimental

studies inspiratory

were
attack
provide asthma,

breathing

spontaneous1.
discharged from two
values

All
three previous
concerning

to five
pleural

days. were also included to

acute pressure

explanations observed mT

Additional

studies5

arterial pulse during cardiac

ing,

patientsSb or venous pooichanges afterloadto bronchial dein

in
function

and
suI)jects.

respirators
lhe first

changes
previous

in right
study5 by means

ventricular concerned
pleural nine

in
was

ventricular

interdependence,2

normal Patients
measured

asthmatic

right
ing4 asthma,

ventricular
have

input,
clinical noticed

with comparable
during an acute

age range.
attack

in whom ofan

pressure

esophageal
Using

l)all000,
these
(Fig

successively we have

been

together

with
wedge

right

heart

pressure

measurements.

data,
1). In

In a previous crease despite

in

we plotted
capillary the second

the relationship
pressure right studs.

between
throughout ventricular

pleural
the

pressure
respirator

and pulmonary
cycle

a profound

inspiratory

pulmonary
simultaneous

artery

pulse
suggests ability

pressure.
of right

Occurring
ventricuin

enhancement decrease pumping

health
out
the changes

volunteers
reS))iratOr%
induced

dimensions were evaluated in 12 l)y two-dimensional echocardiographv throughcycle, and used as reference values to assess breath-

a quiet
From

lar filling, this right ventricular efforts. The tricular attack large edly present function ofasthma. negative increased

an impairment during inspiratory

ing.
illustrate

by continuous positive airway pressure this second stud we obtained echocardiographic

the reSI)iratorv (Table changes 1). in right ventricular size StIl)jects Study right heart catheterization

data to
occurring

study
in a

was designed to assess right yengroup of patients during a severe clinical setting is associated and
#{176}

ill normal
Hemodynainic Bedside

This

with mark-

was

perfi)rmed

using

a triple

swings in pleural pressure659 functional residual capacity.

PATIENTS
AND

Table

1-2DE

Measurements

ofRight View)4

Ventricle

METHODS

(Short

Axis

Patients

Inspiration asthmatic were

intensive

Expiration 8.5(2.3) 6.9(2.1) 1.6(0.6) 18.8(5.3)

in young mean adult volunteers

Seven
55 ears)

patients
care

(mean

investigated and the

hospital.

during
unit.

age. 39 years, a severe attack

consent

ranging requiring
was

from

21 to

HVEDAcIn2/In2

9.1(2.7)

manage-

RVESA
RVSA RVFAC *Obtailsed
of

illeIlt ill our each patient,

regulations

Inftrmed

obtained
the
and l)epartment

from
ethical
echo-

cm2/m2 cm2/m2
%

7.4(2.5)
1.7(0.8) 18.7(8)

protocol

was

consistent

with

of our

Simultaneous

hemodynamic

in a
quiet

previous breathing.

study alues

conducted are

*FrI,1

the Respiratory

Intensive

Care

Unit and the

during
ventricular systolic

(SD);
and

RVEDA,
ventricular RVFAC,

right
endright

Cardiology, Ambroise Pare Hospital, Boulogne, France. This work wa.s sup}orted in part by a Grant of UER Paris-Ouest. Manuscript received October 31; revision accepted March 31. Reprint requests: Dr Jardin, Hopital Ambrose Pare, 9 Avenue Charles de Gaulle, 92104 Boulogne Cedex, France

end-diastolic area; RVSA, right

area

area; ventricular
contraction

RVESA, stroke

right area;

ventricular fractional between inspiration

.The

and expiration

were

slight changes Ol)SerVed not statistically significant.

CHEST

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PP mmHg 30

size parallel

of

the to

inferior and inferior initial the

vena rotated

cava. vena

The the cava,

transducer two-dimensional the vessel and

was

placed sector was

in was

subcostal
observed

position
in its

so that

carefully recorded lead recordings analysis and endwas as the cycle. (ie, endof and

abdominal echocardiographic recorder,

portion. examinations together single frame

area

Two-dimensional

were an ECG

20
10
0

. Inspiration #{176}Expiration

PP: 12 #{149}0.85PCWP R 0.89

0

on were
right

a JVC played

video-tape flow. back

with

respiratory
ventricular

Two-dimensional for subsequent

cavity cross-sectional

echocardiographic stop-motion
at end-diastole

systole, defined smallest From diastolic

using by the these area

a previously onset ofthe

described QRS, cavity we area). and area area)

technique.6 end-systole throughout calculated and fractional

End-diastole was the stroke defined cardiac area area

cross-sectional measurements, minus

-10 -20
30/

/
P

end-systolic

contraction

(ie, stroke

area/end-diastolic

-66.0.94

PC WP

Protocol During mitted respiratory the study, cycle: by a systole, beat, followed both the onset occurring of the simultaneously of four (1) an both by defined different beat, during occurring defined inspiratory occurring as a systole beat, a diastole recorded cardiac defined inspiration; occurring at (4) a late by a systole The three value consecutive at each volume the at respiratory beats as in flow per-

individualizing

a whole

a diastole (2) an early the end of of the by beat, just subject

-40 -40
FIGURE

-30

-20

-10

10

20

30

PCWP mmHg

followed expiratory inspiration expiration; a systole, defined before represents cycles. beat the was total

1. Data obtained in nine asthmatic patients during an acute attack.6 Individual values for inspiratory (closed circles) and expiratory (open circles) pulmonary capillary wedge pressure (PCWP) are plotted against simultaneous pleural pressure values (PP), obtained by means of an esophageal balloon. Note that the slope is nearly identical at inspiration and expiration.

onset

(3) a midexpiratory as an expiratory the average Percentage also expiratory Analysis analysis followed the null was hypothesis. calculated diastole next calculated as the

as a diastole

followed occurring

in midexpiration; followed from volume actual inspiration.

expiratory for each

respiratory expiratory divided by

ofexpiratory volume.

achieved expiratory

lumen monary pressures.

transducers

balloon artery

catheter were

permitting capillary measured

at

simultaneous wedge) with and line, level. volume, while with calibrated From pressure pulse
diastolic

recording right and Pressure obtained were a 500 and recordings,

pressure)

of pulquartz

(or pulmonary
positioned

ventricular atmospheric measurerecorder by means breathing The

Pressures was were with used recorded an ECG through

Hewlett-Packard

the zero and

midaxillary reference exhaled

Statistical Statistical variance to exclude

pressure ments together spontaneously

as the on lead

performed test.

using A value

a two-way ofp<0.025

analysis was required

of

a multichannel

photographic patients the nose with

by Scheffes

of a disposable pneumotachograph and rectly

artery

pneumotachograph a mouthpiece was to pulmonary

minus

occluded.

RESULTS

previously a differential artery

succeeding

ml syringe a Hewlettwe and di-

was

connected respiratory

transducer pressure ventricular Right diastolic

All

asthmatic

patients

had

a clinically

detectable

Packard

integrator.

measured
systolic

(ie. pulmonary
right systolic endand of the not had found of if peak ventricular plateau, ofthe

ventricular
minus

developed
preceding

pressure end-diastolic read the as the pressure

(ie, right
pressure). preejection was measured discomfort

diastolic a plateau ECG method. measure previously parallel,6

respiratory

pressure was used. To avoid pleural done.6 the

was Cardiac

paradoxic pulse. They also exhibited a respiratory rate of2l 10 (mean [SD]) breaths per minute, with an I!E ratio at 0.410.16. Mean tidal volume was 541185 ml. Nine 7 percent of this tidal volume was exhaled during an early expiratory beat, whereas 51 4 percent and 85 6 percent was exhaled during a mid and a late expiratory beat, respectively. Heart rate was 12512 beats per minute, and cardiac index 4.150.79 L!min/m2. Respiratory swings in pulmonary capillary wedge pressure with an average wedge pressure ranged between of3O 4 mm Hg. averaged 15.44.5 24 and 33 mm Hg, Pulmonary capillary mm Hg at expira-

was not clear,

at the onset to the changes

wave

output with

by the thermodilution patients, balloon, in esophageal previously the we did as we been magnitude

additional pressure Since

an esophageal pressure to
pressure.

respiratory wedge used

pressure

and pulmonary

capillary latter was

changes

have

approximate

in pleural

Echocardiographic Echocardiographic sector lion During because parasternal cases, surement cycle left was ventricle scanner. is often the period satisfactory short of the obtained short satisfactory In difficult

Study studies asthmatic due ofthe axis right axis view as reference study, views ventricular only from points. the was taken were patients, to the four other could occasionally size using We during the short studied permitting subcostal also were performed markedly using increased patients were recorded visualization whole axis the a phased-array examinalung volume. Even in and view. variations some meaThis of the in if not included

tion, at a time when pleural mospheric in acute asthma inspiration, when pleural mospheric.6 previous and there nary either

pressure is usually supraatand 14.4 5.8 mm Hg at pressure is markedly subat-

echocardiographic

Similar values have study6 at both expiration

(-12.48.3).

been (16 shown

found in our 7. 9 mm Hg) in Figure pulmopressure the slope of the 1,

echocardiograms examination

not be obtained.

inspiration

As

was a strong linear correlation capillary wedge pressure and at inspiration did or expiration. not significantly

between pleural Moreover, affect

respiratory muscles

subcostal

the papillary

respiratory time this relationship.

Right

790

Ventricular

Performance

during

Acute

Asthma

(Jardin

et a!)

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Table

2-2DE

and

Hemodynamic

Measurements

eterization
2. An

in Asthmatic
Early Inspirationt RVEDA cm2/m2 RVESA cm2/m2 RVSA
cm2/m2

Patients4
Mid Expiration Late Expiration

in asthmatic patients are presented in Table example of 2DE examination (subcostal short axis view) is given in Figure 2. A significant increase in right ventricular
was observed

Expiration

size values. artery exhibited fractional

systole
11.7(3.3) 9.6(2.4) 2.1(1.3) 17.4(9) Hg Hg (SD). ventricular RVFAC, pressure. artery 6.3(5.4) 14(7.5) RVEDA, right 10.1(3) 6.2(3.1) 3.9(1.4) 40.1(14.9) 19.3(7) 36.2(8.1) ventricular area; pressure; inspiration 7.1(2.5) 4.5(2) 2.7(1.6) 36.9(16.3) 13.2(4) 26.7(6.9) end-diastolic RVSA, RVDP, versus right area right area; ventricular contraction; ventricular 6.1(1) 4.1(0.7) 2(0.8) 31.9(9.9) 8.8(4.1) 22.3(5.1) RVESA, stroke PAPP, devel-

at both end-diastole at inspiration when Right pulse ventricular pressure were

and endcompared stroke also area signifi-

with and

expiratory pulmonary

cantly
patients ventricular ventricular

reduced
also

at this

respiratory

time.

Asthmatic

a significant reduction in right area contraction and right pressure at inspiration, comparboth paramthe whole of pressure are vena shown cava and in was a

RVFAC % PAPP mm RVDP mm *Mean right area; oped

developed

atively to expiratory values. Furthermore, eters exhibited parallel changes during respiratory cycle. Illustrative examples changes recorded in asthmatic collapse of the patients inferior Figure 3. An inspiratory

end-systolic right ventricular pulse tp<0.025

fractional

pulmonary

expiration.

observed at 2DE examination representative example is given

in all patients, in Figure 4.

Right

ventricular in the study short

measurements axis are view and conducted

using

2DE

exin a was
DISCUSSION

amination
previous

obtained

during
breathing ventricular

quiet

breathing
conditions, size and

in young adult volunteers, given in Table 1. In normal changes minimal in right and not

In the present study, right ventricular assessed by correlating bedside right data with two-dimensional measurements of the right deserve special comments, their use in a group

performance heart catheechocar-

respiratory function were

terization diographic techniques concerning

statistically significant. ments obtained by 2DE

Right ventricular measureexamination and cardiac cath-

ventricle. Both particularly dyspneic

of acutely

FIGURE

subcostal
recorded respiratory

2. An illustrative approach. ED,

respiratory cycle,

example oftwo-dimensional echocardiographic short axis view obtained froln the end-diastole; ES, end-systole; RV, right ventricle; LV, left ventricle. Simultaneously flow permitted to measure right and left cavity sizes at ftur different phases ofthe whole ie, inspiration, early expiration, midexpiration, and late expiration (see protocol section).

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ECG Ii
,

r-r-T-

rr

Jrrrrr7
-Th

patients. During acute asthma, the right heart pressures merely represents

inspiratory fall in the concurrent

fall in intrapleural
more appropriate

IumTT
4Hg

pressure.6 Thus, it would appear for our purpose to use transmural

pressures.

Pleural

pressure

was
a

not measured
previous capillary pleural

in the

present study. demonstrated sure calculate calculation pressures, could be

However, in that pulmonary used instead pressure.

study, we wedge prespressure this mode to of

of

transmural may affect it does not

Although

the absolute value of transmural alter the validity ofthe compari-

son between three reasons, affected to the ing is based changes values; and

inspiratory and expiratory values for as follow: (1) both absolute values are same extent; (2) our subsequent reasonupon measurements of instantaneous and pressure not upon absolute measured pressure in the (3) changes

in pressure

present study occurred almost instantaneously so that they could not be influenced by pleural pressure, which did not change during this short lapse of time. Concomitantly, two-dimensional echocardiography was used to measure right ventricular dimensions in the the short left axis view, ventricle. at the midpapillary Papillary muscles muscle were level used of as

reference points to insure cardiographic views. The ing been 2DE right ventricular

reproducibility reliability of2DE and patients The

of the echofor assesshas of with of

volumes

performance usefulness from those

previously demonstrated.3 in distinguishing normal

ventricular volume overload has also been reported,4 and in a recent study, we found that measurements

FIGURE 3. Two illustrative examples of pressure recordings. pulmonary artery pressure; RV, right ventricular pressure. inspiratory beat; 2 is early expiratory beat; 3 is midexpiratory and 4, late expiratory beat.

PA, 1 is beat;

right ventricular size using thermodilution compared favorably with similar determinations by 2DE In our asthmatic patients, respiratory changes in right ventricular size were determined in the short axis
.

view.

One

may

argue

that

this

approach

could

not

..

..

..-

V..,.

4. An inferior vena inspiration; 2, expiration (A,

FI;i.RE

illustrative example ofvena caval collapse at inspiration. Top, four end-diastolic cava (IVC), receiving hepatic vems (h) and anastomosing with the right early expiration; 3, mid-expiration; 4, late expiration. Bottom, frame-by-frame B) and onset of inspiration (C, D) illustrating the rapidity of IVC collapse.

views
atrium view

o. he
(ra). 1. at end-

792

Right Ventncular

Performance

dunng

Acute

Asthma

(Jardin

et a!)

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provide

an accurate right manner volunteers, in right

estimate ventricle during

of right configuration respiration. et long

ventricular changed However,

yolin an in

sibility.

Thus,

when

functional

residual

capacity additional to reduce

is

umes ifthe eccentric normal changes

markedly increased lung inflation by

as in acute inspiration is expected

Brinker ventricular

al6 found axis and

parallel short axis

dimensions during a loaded inspiratory effort. We thus assumed that changes in right ventricular short-axis area reflected similar changes in right ventricular volume. The ventricular acute asthma. an inspiratory results of the function present is impaired study suggest at inspiration that right during

pulmonary vascular compliance. Accordingly, spiratory reduction in the pulmonary arterial likely reflected a reduction in right ventricular output. This is consonant with inspiratory reduction in right and the finding ventricular by 2DE stroke

the inpulse stroke of an area

fractional area contraction. In a previous study, we postulated that in right ventricular ejection at inspiration from an afterload and

impairment in asthma in the right rela-

On two-dimensional echocardiograms, enlargement of the right ventricular

could result ventricular

inspiratory increase Experimentally, and normal Just the

cavity was noted at both end-diastole and end-systole. It is a well recognized fact that venous return to the right ume.78 heart The is augmented increase increase in in right during right inspiration stroke diastolic with volsize a concurrent ventricular ventricular

tionship between is Ushaped,a conditions, no effect asthma where lung

vascular resistance therefore, in is expected residual resistance.24

lung volume respiratory little or in opposite, is markedly by a tidal vascular

inflation

to have

on vascular functional

capacity

at inspiration observed in asthma to an increased venous return pleural pressure.69 the initial part ofthe inspiratory collapse, inspiratory decrease due to compression
19

might thus be related due to the negative

increased,0 any increase in lung volume breath would sharply increase pulmonary resistance afterload. ventricular which, However, developed in turn, raises right the highest values pressure and 2DE

In fact, in our asthmatic patients, abdominal vena cava exhibited an as already reported.6 A 50 percent in inferior vena caval diameter from the has inspiratory reported of the increase in normal abdominal also be to decaval vessels but still vena in been collapse

ventricular for right fractional

intraabdominal The vena cava observed

pressure inspiratory

area contraction were observed before any substantial exhalation it is likely that a rise of pulmonary mediated through changes in account for the inspiratory decrease lar ejection. The hydraulic force affecting is decreased during inspiration the decline in intrapleural

at early expiration, had occurred. Thus, vascular resistance lung volume cannot in right ventricuejection equal to

in asthmatic inability pressure, In in any case,

patients of collapsible a classic20 abdominal

might

explained transmit bated collapse pleural protect

by the a negative concept.2 is expected pressure the right

left ventricular by an amount pressure.42327

to limit the promoting

effect ofdeep negative venous return and cavity against for the excessive observed impairment reduction in asthmatic suggested at the reduction same in imply a Pulmothe

As a result,

ventricular

enlargement. A second inspiratory

possible increase

explanation in right ventricular

left ventricular stroke volume falls at inspiration. On the opposite, right ventricular ejection is thought not to be affected by this mechanism, since the right ventricle ejects blood into the pulmonary circulation which is presumably subjected However, external to the same inspiratory pleural presfor the right fall in pleural sure actually ventricle, the whole pressure pressure. reflects the if the pressure

end-diastolic

size is that it resulted from in right ventricular ejection. in the patients, a reduction respiratory pulmonary reduction
nary

an inspiratory The inspiratory pulse observed indirectly output

pulmonary and

arterial previously

noticed,6 ventricular

in right time. arterial in right pulse ofthe decrease

it does not reflect the external pressure for pulmonary vascular bed. Changes in pleural or lung volume can modify the size of the

Indeed,

an inspiratory

intraparenchymal present in these the intraalveolar percent

nary

vessels

and

the

amount ways. represent

of

blood

pulse does ventricular

not necessarily stroke output.

vessels in opposite vessels, which

Moreover, about 60

arterial

(compliance)
observed

also depends on the distensibility pulmonary vascular bed. Thus, in pulse pressure at inspiration

of the
circulation,

pressure

but

total vascular resistance of the pulmoare not directly exposed to the pleural are actually exposed to the alveolar When the airways in acute asthma, should be pressure. pressure alveolar are the open to alveolar as atWith the achieved distending value. ejection
1987

could also have in pulmonary lung inflation previously vascular ments

been caused by an inspiratory vascular distensibility. The on pulmonary vascular

increase effects of has

distending pressure.8 the atmosphere, as distending mospheric markedly during pressure Accordingly, pressure pressure negative inspiratory can

distensibility

calculated

been addressed in several reports. The bed ofthe lung was divided into two compartthat responded opposite to inflation. However, the net effect of vascular disten-

minus pleural levels of pleural efforts, reach that

CHEST

the

when the lungs were highly distended, inflation was a major reduction in

indeed we believe

a very positive right ventricular

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can

no longer

be

considered by the

as strictly physiologists,

independent the right

from pleural pressure. As often emphasized ventricle

markedly negative pleural pressure, ated with an increased lung volume, impair right ventricular contraction. could be expected the weak contractile it more vulnerable an external pressure, positive as in cardiac

when it is assocican significantly Such findings

right
for the

acts ventricular ejection

as a bellows. free wall pressure ofa given

The inward is responsible during stroke systole, volume.

motion of the for an increase and in turn, Experimen-

in intracavitary

since the thin compliant wall and power ofthe right ventricle make than the left ventricle to the effect of either negative tamponade. as in asthma, or

tally, there is a direct relation between the magnitude ofthe free wall motion and the level ofright ventricular developed pressure. Thus, changes in right ventricular developed pressure noted in the present study presumably reflected changes in amplitude of the inward motion of the right ventricular free by 2DE changed wall. This amplitude was also directly assessed area contraction. Both parameters lel manner during indicated a marked motion ofthe right tion. This finding the whole reduction ventricular can best be fractional in a paral-

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Lancet

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respiration.

Shoukas

on left ventricular

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HP, JN,

Engel et

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pressure

Clin

44:1882-99 pulmonary asthmatic

S. Relation

acute

an average

pleural swings an inspiratory

by loaded inspiration in pulmonary artery

produced flow. More

Med

recently, similar findings were reported by Olsen et al27 in dogs in whom inspiratory pleural pressure reached an average negative level of 12 m m Hg. However, the levels of negative pleural pressure achieved in these experimental those observed negative pleural tive value apparent reported of25 protocols are far less pronounced than setting, a negafor the in acute asthma. In this clinical pressure currently overtakes mm Hg,6-89 and this can account our data can object

J.

volumes

in exacerbations

Med

41:259-73 Gu#{233}retF, Prost evaluation pressure breathing.

JF, Ozier

Y, Bourdarias during continuous Physiol

JP.
1984;

Echocardiographic

of ventricles

Appl

discrepancy between in other studies. One

and those that similar

13 Watanabe Estimation

F, Katsume

levels ofnegative pleural man during the Mueller noticeable right ventricular ever, during the Mueller Guzman ing ofthe significant et al#{176} produced interventricular right ventricular

pressure could be reached in maneuver,6 without any systolic dysfunction. Howmaneuver, Brinker et al6 and evidence ofa systolic flattenseptum leading to suspect a systolic dysfunction, even which does is a forced inspiration not induce a large alveolar On the an open distending other hand, airway, as in

echocardiography. 14 Bommer dimensional 15 Jardin Bourdarias the using Chest 16 Brinker Permutt right 17 18 19 Brecher 1956 Franklin and Mintz inferior left A. Determination

L, Neumann

thermodilution

a comparative as a reference

two-dimensional

echocardiography

ifthe Mueller maneuver, against a closed airway, pressure pressure gradient and the

5, Weisfeldt

between the pleural pressure. performed with

and Stratton
between

an inspiratory

effort

R, Rushmer Circ W, Res Iskandrian

in acute asthma, alveolar distending In conclusion,

794

results in a significant increase pressure. our present data suggest that

ventricular Katler caval vena

ultrasonography:

Right Ventricular

Performance

during

Acute

Asthma

(Jardin

at a!)

Downloaded from chestjournal.org on September 1, 2008 Copyright 1987 by American College of Chest Physicians

ings 20 Guyton return return 21 22 Lloyd

and

its AC,

use

in assessing AW, right atrial

right-heart Abernathy pressures 1957; on inferior 55:1701-08 D, Riley

function. B, Richardson and the vena

Circulation 26 T normal caval blood Venous venous 27 flow of the Physiol H. Influ29 28

Physiol BudaA, L. ance. Olsen ished MorrisJ, right cardiac Effect

1978; Pinsky N Engl CD, stroke

44:703-09 M, Ingels M, Daughters pressure 1979; Maier during 301:453-59 GW, inspiration: D, Everson relation Cardiovasc inspiration Surg N, Green Davis JW, Rankin JS. Diminpump. a reverse C, Wechsler to chamber 1986; LH. thoracic on G, Stinson left ventricular E, Alderman perform-

1981; 64:1018-25 Lindsey Am Effect at various curve. TC.

of intrathoracic

J
Tyson

Med GS,

Physiol 1983;

189:609-15

of inspiration Physiol parts JL, Mc inflation Physiol N. 5, Proctor

volume 1985;

in dogs. HowellJ, lung 1961; 23 ence 24 25 Murgo arterial Robotham Rabson

Appl Permutt

Circulation R. Effect ofinflation bed. E,

72:668-79
G, Hamm dimension: A. Dynamic volume 91 :879-87 Effects of normal function. Weisfeldt septal Br Heart displaceM, 1981; during

Pellom ventricular cycle.

on different 16:71-76

ofpulmonary Gregor 1960; Input man. M,

vascular Berglund lung 15:878-82 impedance Circ Res 1984; on

J App!
Borst

J
Brown

Thorac

Whittenberger of state resistance.

ScharfSM, and AppI loaded Physiol

R, Saunders

of AppI

of the

pulmonary of the

vascular pulmonary 30

spontaneous 1979; P, Maughan

on cardiovascular L, BrinkerJ, with leftward in man.

J
system

47:582-90
L, Yin F, Weaton gradient maneuver

JP, Westerhof
in normal

Guzman ment

J, Lixfeld J.
Effects

W, Holland

54:666-73 L, McGregor D, Bryan

performance.

et al. Transseptal

pressure the Mueller

C,
App!

during

of respiration

on cardiac

46:657-62

Neural
This Postgraduate contact Medicine, Professor Royal W12 OHS, one-day program M edical

and Endocrine
will School, Po!ak or be held Professor Medical January S. School, R. Hammersmith

System
28, Hospital, Bloom, 1988 London,

of the Lung
sponsored England. of Hospital, by and For at the Royal and information, Histochemistry

J.

M.

Departments

Postgraduate England.

Ilammersmith

l)u

Cane

Road,

London

CHEST

92

/ 5

NOVEMBER,

1987

795

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Inspiratory impairment in right ventricular performance during acute asthma F Jardin, O Dubourg, A Margairaz and JP Bourdarias Chest 1987;92;789-795 DOI 10.1378/chest.92.5.789 This information is current as of September 1, 2008
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