Download The decrease of cardiac chamber volumes and output during

Am J Physiol Heart Circ Physiol 305: H1004–H1009, 2013.
First published July 26, 2013; doi:10.1152/ajpheart.00309.2013.
The decrease of cardiac chamber volumes and output during positive-pressure
ventilation
Kasper Kyhl,1 Kiril Aleksov Ahtarovski,1 Kasper Iversen,2 Carsten Thomsen,3 Niels Vejlstrup,1
Thomas Engstrøm,1 and Per Lav Madsen1,4
1
The Cardiovascular Magnetic Resonance Imaging Group, Department of Cardiology, Rigshospitalet, Copenhagen, Denmark;
Department of Cardiology, Hillerød Hospital, Hillerød, Denmark; 3Department of Radiology, Rigshospitalet, Copenhagen,
Denmark; and 4Department of Cardiology, Hvidovre University Hospital, Copenhagen, Denmark
2
Submitted 8 April 2013; accepted in final form 20 July 2013
Kyhl K, Ahtarovski KA, Iversen K, Thomsen C, Vejlstrup N,
Engstrøm T, Madsen PL. The decrease of cardiac chamber volumes
and output during positive-pressure ventilation. Am J Physiol Heart
Circ Physiol 305: H1004 –H1009, 2013. First published July 26, 2013;
doi:10.1152/ajpheart.00309.2013.—Positive-pressure ventilation (PPV)
is widely used for treatment of acute cardiorespiratory failure, occasionally at the expense of compromised cardiac function and arterial
blood pressure. The explanation why has largely rested on interpretation of intracardiac pressure changes. We evaluated the effect of
PPV on the central circulation by studying cardiac chamber volumes
with cardiac magnetic resonance imaging (CMR). We hypothesized
that PPV lowers cardiac output (CO) mainly via the Frank-Starling
relationship. In 18 healthy volunteers, cardiac chamber volumes and
flow in aorta and the pulmonary artery were measured by CMR during
PPV levels of 0, 10, and 20 cmH2O applied via a respirator and a face
mask. All cardiac chamber volumes decreased in proportion to the
level of PPV. Following 20-cmH2O PPV, the total diastolic and
systolic cardiac volumes (⫾SE) decreased from 605 (⫾29) ml to 446
(⫾29) ml (P ⬍ 0.001) and from 265 (⫾17) ml to 212 (⫾16) ml (P ⬍
0.001). Left ventricular stroke volume decreased by 27 (⫾4) ml/beat;
heart rate increased by 7 (⫾2) beats/min; and CO decreased by 1.0
(⫾0.4) l/min (P ⬍ 0.001). From 0 to 20 cmH2O, right and left
ventricular peak filling rates decreased by ⫺146 (⫾32) and ⫺187
(⫾64) ml/s (P ⬍ 0.05) but maximal emptying rates were unchanged.
Cardiac filling and output decrease with increasing PPV in healthy
volunteers. The decrease is seen even at low levels of PPV and should
be taken into account when submitting patients to mechanical ventilation with positive pressures. The decrease in CO is fully explained
by the Frank-Starling mechanism.
cardiac physiology; positive-pressure ventilation; cardiovascular magnetic resonance; central hemodynamic; mechanical ventilation; FrankStarling relationship
(PPV) with positive end-expiratory
pressure (PEEP) is used during anesthesia and during treatment
of acute critical respiratory failure including pulmonary edema
(25, 28). While PPV usually improves alveolar oxygen diffusion and alleviates atelectasis and hypoxic vasoconstriction,
these positive effects must be balanced against the risk of
compromised cardiovascular function with a decrease in cardiac output (CO) (7, 8, 25) and often also in arterial blood
pressure (18, 25). Studies on the mechanisms that lead to
cardiovascular compromise with PPV have shown that PPV
increases central venous and pulmonary artery pressures (4),
lowers pulmonary artery capillary wedge pressure, and conse-
POSITIVE-PRESSURE VENTILATION
Address for reprint requests and other correspondence: K. Kyhl, The
Cardiovascular Magnetic Resonance Imaging Group, The Heart Centre, Dept.
of Cardiology, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark (e-mail: [email protected]).
H1004
quently also left ventricular (LV) filling pressure (4, 9). Echocardiographic studies suggest that LV contractility remains
unchanged (2, 16, 17). It has been suggested that the reported
changes in cardiac transmural pressures and the associated
changes in abdominal pressure together with changes in LV
afterload may result in compromised cardiac filling (25).
Filling of the cardiac chambers is not unambiguously determined from transmural pressures but can be validated with
cardiac magnetic resonance imaging (CMR) that with steadystate, free-precession sequences is considered the gold standard
of in vivo measurements of cardiac chamber volumes (10, 11,
21). CMR is particularly useful in evaluation of the right side
of the heart, which cannot be reliably measured with echocardiography. CMR phase-contrast sequences are the gold standard for noninvasive measurements of flow in the pulmonary
artery and ascending aorta. We hypothesize that PPV negatively influences the circulation mainly through impaired filling
of the cardiac chambers. To test this hypothesis, we used CMR
to determine cardiac chamber volumes and function during
PPV in healthy subjects with pressure levels applied in the
clinic (up to 20 cmH2O).
METHODS
Eighteen volunteers (18 – 61 yr; 7 women) without a history of
cardiac, metabolic, or pulmonary disease and free of medication
participated in the study after providing oral and written informed
consent. The Copenhagen Ethics Committee approved the protocol
(H-1-2011-073), and the study was carried out in accordance with the
Helsinki Declaration. Exclusion criteria included pregnancy, claustrophobia, contraindications to CMR (pacemaker/ICD-unit and cerebral
clips), and inability to undergo the positive-pressure ventilation procedure.
The protocol consisted of three consecutive periods each lasting
⬃30 min: one period on spontaneous breathing at atmospheric level,
and two periods on noninvasive ventilation with inspiratory pressures
of 12 and 22 cmH20 and expiratory pressures of 9 and 19 cmH2O,
respectively. Thus patients were ventilated with 0 cmH2O (PPV0), 10
cmH2O (PPV10), and 20 cmH2O (PPV20). The pressures were chosen
to match the range of pressures applied in the clinic (29, 32). At each
PPV level volunteers were ventilated for 10 min before a comprehensive CMR scan was performed. Subjects underwent all pressure levels
and were scanned three times. First, the subjects were scanned during
spontaneous respiration (PPV0). Next, PPV10 and PPV20 where applied in random order, as a randomization system secured that an
equal number of subjects started with PPV10 and PPV20, respectively.
In six subjects, systemic blood pressure was measured at the end of
each scan sequence.
Positive-pressure ventilation. The subjects were noninvasively
ventilated on a CMR-compatible respirator (Datex-Ohmeda Aestiva/5
MRI Anesthesia System, GE Healthcare, Madison, WI) set to pres-
0363-6135/13 Copyright © 2013 the American Physiological Society
http://www.ajpheart.org
CARDIAC FUNCTION DURING POSITIVE-PRESSURE VENTILATION
sure-support ventilation mode, a minimal respiratory rate of 2 min⫺1,
and a time of inspiration of 1.3 s. PPV was applied via a tight-fitting
face mask used for postoperative noninvasive ventilation. In the
scanner room, the ventilator was placed as close to the subject and the
300-gauss line (gauss, a measure of magnetic field strength) as
possible, thereby minimizing the length of the inflexible tubes. The
subjects were instructed to breath normally during PPV.
CMR protocol. Retrospectively ECG-gated CMR was performed
on a 1.5-T MRI scanner with phased-array coils (Avanto, Siemens
Medical Solutions, Erlangen, Germany). Following scout imaging,
cine image loops of the heart were obtained with steady-state, free
precession sequences with a parallel imaging acceleration factor of 2
(TRUE-FISP; echo-time 1.5 ms; repetition time 3.0 ms; flip-angle
60°; GRAPPA), a slice-thickness of 8 mm, and a temporal resolution
of 24 – 45 ms (25 phases per cardiac cycle). First, two-, three-, and
four-chamber images were obtained; second, two RV outflow tract
planes perpendicular to each other were obtained; third, a cine
perpendicular to aorta in the three-chamber image was obtained. From
these images, a double oblique stack of the heart including both atria
was obtained (slice thickness 8 mm, no gap, 16 –22 slices). All images
were taken during 6 –10 s end-tidal expiratory breath holds. LV and
RV volumes and ejection fractions were computed from the stack of
double-oblique cine images using dedicated software with semiautomatic edge detection of the endocardial contour (CMR42 v. 4.0.1,
Circle Cardiovascular Imaging, Calgary, Canada). Trabeculation at
the level of the apex was excluded, and the papillary muscles were
included in the myocardium when in continuum with the compacted
myocardium (14, 31). The volumes of each short-axis slice (luminal
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area ⫻ slice thickness) were automatically summed to obtain ventricular and atrial volumes, respectively. The tricuspid and mitral valve
planes were defined according to methods described by Prakken et al.
and others (Fig. 1) (14, 27, 31). Ejection fractions were taken as the
stroke volume divided by the end-diastolic volume. Image analysis
was performed blinded to knowledge of the PPV level. In 10 subjects,
RV and LV volumes were determined for all 25 phases of the cardiac
cycle. Output from the LV and the RV, respectively, were determined
with flow sequences (through-plane phase-contrast sequences; velocity encoding of 200 cm/s) with planes corresponding to the sinotubular junction and the pulmonary artery 1–2 cm distal to the pulmonary
valve.
Statistics. According to published data by Grothues et al. (11) it is
possible to detect changes of 10 ml in LV end-diastolic volume
(LVEDV) with a power of 0.9 (␣ ⫽ 0.05, 2-sided) with only 10 patients.
Reproducibility for RV is slightly lower than for LV (10). To allow for
dropouts and slightly lower changes, we included 18 volunteers. Data
were tested for normality. Changes with treatment (PPV of 0, 10, and 20
cmH2O) were evaluated with a Student’s t-test. A two-sided P value ⱕ
0.05 was considered statistically significant. Data are presented as means
(⫾SE).
RESULTS
All subjects tolerated PPV and completed the protocol. All
cardiac volumes decreased with PPV (Table 1; Figs. 1 and 2).
From PPV0 to PPV20, the total cardiac volume (the sum of both
atrial and both ventricular volumes) decreased from 605 (⫾29)
Fig. 1. A representative example of changes in
cardiac chamber volumes (endocardial borders
semiautomatically drawn with fine lines) during three levels (0, 10, and 20 cmH2O) of
positive-pressure ventilation (PPV) (same cardiac level). A–D: cardiac chambers (shortaxis images) during breathing at an atmospheric level (expiratory phase; end-diastole).
E–H: cardiac chambers during PPV of 10
cmH2O. I–L: cardiac chambers during PPV of
20 cmH2O. The first two images in each series
show the right (RA) and left (LA) atria, and the
last two images in each series show the right
(RV) and left (LV) ventricles. Note the visibly
smaller cardiac chambers with increasing positive-pressure ventilation.
AJP-Heart Circ Physiol • doi:10.1152/ajpheart.00309.2013 • www.ajpheart.org
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CARDIAC FUNCTION DURING POSITIVE-PRESSURE VENTILATION
Table 1. Cardiac chamber volumes and ascending aortic flow with positive-pressure ventilation levels of 10 and 20 cmH2O
in 18 healthy subjects
Absolute Values, Average (SE)
Left ventricle
HR, beats/min
LVEDV, ml
LVESV, ml
LVSV, ml
LVEF, %
CO, l/min
Left atrium
LAEDV, ml
LAESV, ml
LASV, ml
Right ventricle
RVEDV, ml
RVESV, ml
RVSV, ml
RVEF, %
CO, l/min
Right atrium
RAEDV, ml
RAESV, ml
RASV, ml
Flow-phase contrast
Ascending aorta, ml/s
Pulmonary artery, ml/s
Total heart volume
Diastole, ml
Systole, ml
LV function
Peak systolic emptying, ml/s
Peak diastolic filling, ml/s
RV function
Peak systolic emptying, ml/s
Peak diastolic filling, ml/s
Changes, Average (SE)/%
PPV0
PPV10
PPV20
PPV0–10
PPV10–20
PPV0–20
60 (2)
173 (8)
58 (5)
114 (4)
67 (2)
6.8 (0.3)
62 (2)
153 (6)
51 (4)
102 (4)
67 (1)
6.3 (0.3)
67 (2)
138 (8)
51 (4)
87 (5)
64 (1)
5.8 (0.3)
1 (3)/2%
⫺20† (10)/⫺11%
⫺8† (6)/⫺13%
⫺12† (6)/⫺11%
0 (2)/0%
⫺0.6† (0.4)/⫺8%
5† (3)/9%
⫺15† (10)/⫺10%
0 (6)/0%
⫺15† (6)/⫺15%
⫺4† (1)/⫺5%
⫺0.5† (0.4)/⫺8%
7† (3)/11%
⫺34† (11)/⫺20%
⫺7* (6)/⫺13%
⫺27† (6)/⫺24%
⫺3* (2)/⫺5%
⫺1.0† (0.4)/⫺16%
86 (5)
49 (3)
37 (3)
70 (4)
42 (3)
28 (2)
⫺16† (7)/⫺15%
⫺1* (4)/⫺2%
⫺14† (4)/⫺28%
⫺16† (6)/⫺19%
⫺7† (4)/⫺15%
⫺9† (4)/⫺24%
⫺32† (6)/⫺31%
⫺8† (4)/⫺16%
⫺23† (4)/⫺45%
198 (10)
82 (6)
115 (5)
59 (1)
6.9 (0.3)
178 (8)
77 (5)
100 (4)
57 (1)
6.1 (0.3)
157 (11)
69 (6)
88 (6)
56 (2)
5.7 (0.3)
⫺20† (13)/⫺10%
⫺4 (8)/⫺5%
⫺15† (6)/⫺13%
⫺2† (1)/⫺4%
⫺0.7† (0.4)/⫺11%
⫺21† (14)/⫺12%
⫺8† (8)/⫺11%
⫺13† (7)/⫺13%
⫺0.4 (2)/⫺1%
⫺0.4* (0.4)/⫺7%
⫺41† (15)/⫺21%
⫺12† (9)/⫺15%
⫺27† (8)/⫺24%
⫺3† (2)/⫺5%
⫺1.1† (0.4)/⫺16%
132 (8)
75 (6)
57 (5)
100 (8)
62 (6)
38 (3)
81 (9)
51 (6)
30 (4)
⫺32† (11)/⫺24%
⫺13† (9)/⫺18%
⫺19† (6)/⫺33%
⫺19† (12)/⫺19%
⫺11† (9)/⫺18%
⫺8* (5)⫺⫺20%
⫺51† (12)/⫺39%
⫺25† (9)/⫺33%
⫺27† (6)/⫺47%
112 (4)
121 (6)
95 (4)
103 (6)
79 (5)
87 (6)
⫺17† (6)/⫺15%
⫺18† (8)/⫺15%
⫺16† (6)/⫺17%
⫺17† (8)/⫺16%
⫺33† (6)/⫺29%
⫺34† (8)/⫺28%
605 (29)
265 (17)
517 (25)
245 (16)
446 (29)
212 (16)
⫺88† (38)/⫺15%
⫺21* (23)/⫺8%
⫺71† (38)/⫺14%
⫺32† (23)/⫺13%
⫺159† (41)/⫺26%
⫺53† (23)/⫺20%
512 (39)
517 (32)
501 (26)
429 (33)
519 (56)
371 (42)
⫺11 (28)/⫺2%
⫺88† (17)/⫺17%
18 (59)/4%
⫺58 (36)/⫺14%
7 (47)/1%
⫺146† (32)/⫺28%
611 (43)
516 (60)
581 (35)
387 (32)
583 (63)
328 (38)
⫺30 (46)/⫺13%
⫺128* (54)/⫺25%
⫺2 (47)/⫺0.2%
⫺59 (48)/⫺15%
⫺29 (76)/⫺5%
⫺187* (64)/⫺36%
102 (5)
50 (3)
52 (3)
SE, standard error of the mean; PPV, positive-pressure ventilation; PPV10, PPV of 10 cmH2O; PPV20, PPV of 20 cmH2O; HR, heart rate; LV, left ventricle;
RV, right ventricle; LVEDV and RVEDV, LV and RV end-diastolic volume, respectively; LVESV and RVESV, LV and RV end-systolic volume, respectively;
LVSV anad RVSV, LV and RV stroke volume, respectively; LVEF and RVEF, LV and RV ejection fraction, respectively; LA, left atrium; RA, right atrium;
LAEDV and RAEDV, LA and RA end-diastolic volume, respectively; LAESV and RAESV, LV and RA end-systolic volume, respectively; LASV and RASV,
LA and RA stroke volume, respectively; CO, cardiac output. †P ⬍ 0.01. *P ⬍ 0.05.
to 446 (⫾29) ml (26%, P ⬍ 0.001) during ventricular diastole
and from 265 (⫾17) to 212 (⫾16) ml (20%, P ⬍ 0.001) during
ventricular systole, respectively. Heart rate increased by 7 (⫾3)
beats/min, and blood pressure was not affected by the procedure performed with average blood pressure being [124 (⫾9)]/
[81 (⫾8)] mmHg at PPV0, [121 (⫾7)]/[82 (⫾7)] mmHg at
PPV10, and [122 (⫾9)]/[82 (⫾11)] mmHg at PPV20. We did
not observe shifting of the interventricular septum in any
subjects.
During PPV20, LVEDV, LV end-systolic volume (LVESV),
and LV stroke volume (LVSV) decreased by 20, 13, and 24%,
respectively (Table 1), and with little increase in HR, LVCO
decreased by 16%. LVEDV decreased to the same extent with
each increase in PPV (11 and 20%, respectively), while
LVESV decreased 13% between rest and PPV10, but did not
decrease between PPV10 and PPV20. As a consequence, LVSV
decreased with a near-linear relation to increasing levels of PPV
(Fig. 3). Right ventricular end-diastolic volume (RVEDV), endsystolic volume (RVESV), and stroke volume (RVSV) demonstrated the same absolute and relative changes as seen for the
LV. Both diastolic and systolic atrial volumes decreased in
relation to PPV, with atrial volumes decreasing relatively more
than the ventricular. The RA volumes decreased absolutely and
relatively more than the LA volumes. The RA stroke volume
(RASV) and LA stroke volume (LASV) decreased by almost
50% between rest and PPV20.
No difference between flow in aorta and LVSV or flow in
pulmonary artery and RVSV was found during any of the test
settings. Flow in the aorta decreased by 33 ml/s (28%, P ⬍
0.001) between rest and PPV20, and flow in pulmonary artery
decreased by 34 ml/s (29%, P ⬍ 0.001) between rest and
PPV20. With increasing PPV, both left and right ventricular
peak-filling rates decreased, whereas the peak-emptying rates
remained constant (Table 1; Fig. 4).
DISCUSSION
We applied magnetic resonance imaging to measured cardiac chamber volumes and right and left ventricular output
during noninvasive positive-pressure ventilation to understand
and quantitate the influence of the latter on the heart and central
circulation. We hypothesized that positive-pressure ventilation
negatively affects the circulation via the Frank-Starling mechanism; i.e., that cardiac output is lowered through lowered right
AJP-Heart Circ Physiol • doi:10.1152/ajpheart.00309.2013 • www.ajpheart.org
CARDIAC FUNCTION DURING POSITIVE-PRESSURE VENTILATION
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Fig. 2. End-diastolic cardiac chamber volumes with
increasing positive-pressure ventilation of 0 (PPV0),
10 (PPV10), and 20 cmH2O (PPV20) in 18 healthy
subjects. †P ⬍ 0.01.
and left ventricular end-diastolic volumes. We found that, in
healthy subjects, increasing airway pressure to 10 and 20
cmH2O decreases total heart volume, all four individual chamber volumes, and output of both atria and both ventricles
equally and progressively. Left and right ventricle end-diastolic volumes and peak filling rates decreased progressively
with an increasing positive inspiratory pressure. Heart rate
increased little and consequently the decrease in ventricular
stroke volumes lowered cardiac output significantly (by 8 and
16%, respectively, at 10 and 20 cmH2O).
While PPV improves alveolar gas diffusion and reduces
atelectasis and hypoxic vasoconstriction, these positive effects
should be balanced against compromising cardiac function to
the extent of arterial hypotension with higher PPV levels (18,
25, 28). A compromised circulation has been related to changes
in intrathoracic pressure, circulating blood volume, autonomic
tone, and endocrine response (25). In the acute setting mainly
the influence of positive intrathoracic pressure on RV and LV
pre- and afterload and diastolic interventricular interdependence have been considered important although their precise
interplay has not been determined (25). With heart and lung
interactions during PPV, volume displacements have been
inferred from measurements of intrathoracic pressures and
transmural chamber pressures, but such can be misleading
estimates of chamber filling and myocyte stretch (12, 19, 25).
Myocardial stretch is best reflected by chamber volumes, but
RV and LV volume changes are not reliably determined with
echocardiography (1). We therefore studied cardiac filling and
output during PPV with CMR, the gold standard for precise
and reproducible cardiac chamber volume measurements.
In this study, HR and arterial blood pressure did not change
significantly and hence important adrenergic and parasympathetic influences can be ruled out. Also, we do not hold it likely
that other hormone changes affect this setting significantly.
During spontaneous inspiration, the intrathoracic pressure becomes subatmospheric (26), but during PPV it increases to
positive values. The atria have more compressible walls than the
ventricles, and the RA and LA end-diastolic volumes decreased
by 31 and 39%, respectively, while the RV and LV end-diastolic
volumes decreased by only 20 and 21%. In accordance with the
Frank-Starling relationship, the lowered RVEDV decreases
RVSV; and the reduced RVSV results in comparable changes in
LVSV (2, 24), especially so in the setting of increased intrathoracic pressure when the pulmonary blood volume decreases and
any buffering function of the pulmonary circulation is limited
(30). It has been suggested that only PPV above 10 cmH2O lowers
cardiac filling (4, 5, 22), but in our study even a PPV of 10 cmH2O
was demonstrated to lower the volume and output of all four
cardiac chambers.
Even without a positive pressure applied to the airways, it is
difficult to relate intracardiac pressure to central blood volume
and venous return. One has to estimate transmural pressures,
which is difficult as the pressure applied to airways is transferred differently to different parts of the thoracic cavity (19,
26). If pulmonary hyperinflation compresses the LA and pulmonary veins, pulmonary venous resistance, pulmonary artery
pressure, and hence RV afterload must increase (13). With
respect to LV afterload, PPV decreases the transmural pressure
of the LV by increasing the outside pressure on all structures of
the thorax (19). Thus, if mean arterial pressure is unchanged,
PPV lowers LV afterload (3, 6, 23). We found the decrease in
LVEDV/-SV to match the decrease in RVEDV/-SV and our
data are best explained by the Frank-Starling mechanism without significant influences from changes in afterload. Diastolic
ventricular interdependence has been implicated for depressed
cardiac function during PPV (26). In our subjects, however,
RV volume was always lowered, and never increased, and
hence the interventricular septum was not left shifted. Thus, in
our study, ventricular interdependence does not provide an
explanation for the decrease in CO (2, 15, 16, 20). Unchanged
arterial pressures, end-systolic volumes, and ventricular peakemptying rates argue against significant changes in RV and LV
contractility. As shown by the analysis of changes during the
cardiac cycle, the main change seen with positive-pressure
AJP-Heart Circ Physiol • doi:10.1152/ajpheart.00309.2013 • www.ajpheart.org
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CARDIAC FUNCTION DURING POSITIVE-PRESSURE VENTILATION
ventilation is a significant decrease in ventricular peak filling
rate in line with the notion that changes are mainly consequences of the Frank-Starling relationship.
With cardiovascular magnetic resonance imaging, we have
in healthy subjects conclusively demonstrated a negative correlation between the applied level of positive airway pressures
and decreases in right and left ventricular filling and output.
The influence of positive airway pressure on the cardiac function is fully explained by the Frank-Starling relationship. These
changes should always be taken into consideration during treatment of patients with positive-pressure ventilation, as cardiac
volumes and output are shown to diminish significantly even at a
Fig. 4. Time-volume curves from mean values of the left (A) and right (B)
ventricle during positive-pressure ventilation at 0 (PPV0), 10 (PPV10), and 20
cmH2O (PPV20) in 10 normal subjects. Graphs are constructed from 25 cardiac
phases.
positive pressure of 10 cmH2O. At a positive-pressure level of 20
cmH2O, the cardiac volume decreases by an average of 26%.
GRANTS
P. L. Madsen and K. Kyhl were both supported by the Danish Heart
Foundation.
DISCLOSURES
No conflicts of interest, financial or otherwise, are declared by the author(s).
Fig. 3. Stroke volume (SV; top) and cardiac output (CO; bottom) during
positive-pressure ventilation at 0 (PPV0), 10 (PPV10), and 20 cmH2O (PPV20)
for the right (broken line) and left (solid) ventricles in 18 healthy subjects. For
both ventricles the same decrease in filling is seen relative to an increment in
positive-pressure ventilation level. †P ⬍ 0.01, *P ⬍ 0.05 compared with
previous level of PPV.
AUTHOR CONTRIBUTIONS
Author contributions: K.K., K.A.A., K.K.I., C.T., N.G.V., T.E., and P.L.M.
conception and design of research; K.K., K.A.A., C.T., and N.G.V. performed
experiments; K.K., K.K.I., and P.L.M. analyzed data; K.K., K.A.A., K.K.I.,
C.T., N.G.V., T.E., and P.L.M. interpreted results of experiments; K.K. and
AJP-Heart Circ Physiol • doi:10.1152/ajpheart.00309.2013 • www.ajpheart.org
CARDIAC FUNCTION DURING POSITIVE-PRESSURE VENTILATION
P.L.M. prepared figures; K.K., N.G.V., and P.L.M. drafted manuscript; K.K.,
K.A.A., K.K.I., N.G.V., T.E., and P.L.M. edited and revised manuscript; K.K.,
K.A.A., K.K.I., C.T., N.G.V., T.E., and P.L.M. approved final version of
manuscript.
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