Clinical Use of Respiratory Changes in Arterial Pulse

Pressure to Monitor the Hemodynamic Effects of PEEP

FRDRIC MICHARD, DENIS CHEMLA, CHRISTIAN RICHARD, MARC WYSOCKI, MICHAEL R. PINSKY,
YVES LECARPENTIER, and JEAN-LOUIS TEBOUL
Service de Ranimation Mdicale et Service de Physiologie Cardio-Respiratoire, Hopital de Bictre, AP-HP, Universit Paris-Sud,
Le Kremlin-Bicetre; INSERM U451-LOA-ENSTA-Ecole Polytechnique, Palaiseau; Service de Ranimation Polyvalente, Institut
Mutualiste Montsouris, Paris, France; and Division of Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania

In ventilated patients with acute lung injury (ALI) we investigated whether respiratory changes in ar-
terial pulse pressure (DPP) could be related to the effects of PEEP and fluid loading (FL) on cardiac in-
dex (CI). Measurements were performed before and after application of a PEEP (10 cm H2O) in 14
patients. When the PEEP-induced decrease in CI was . 10% (six patients), measurements were also
performed after FL. Maximal (PPmax) and minimal (PPmin) values of pulse pressure were deter-
mined over one respiratory cycle and DPP was calculated: DPP (%) 5 100 3 {(PPmax 2 PPmin)/
([PPmax 1 PPmin]/2)}. PEEP decreased CI from 4.2 6 1.1 to 3.8 6 1.3 L/min/m2 (p , 0.01) and in-
creased DPP from 9 6 7 to 16 6 13% (p , 0.01). The PEEP-induced changes in CI correlated with DPP
on ZEEP (r 5 20.91, p , 0.001) and with the PEEP-induced increase in DPP (r 5 20.79, p , 0.001). FL
increased CI from 3.5 6 1.1 to 4.2 6 0.9 L/min/m2 (p , 0.05) and decreased DPP from 27 6 13 to
14 6 9% (p , 0.05). The FL-induced changes in CI correlated with DPP before FL (r 5 0.97, p , 0.01)
and with the FL-induced decrease in DPP (r 5 20.85, p , 0.05). In ventilated patients with ALI, DPP
may be useful in predicting and assessing the hemodynamic effects of PEEP and FL. Michard F,
Chemla D, Richard C, Wysocki M, Pinsky MR, Lecarpentier Y, Teboul J-L. Clinical use of respi-
ratory changes in arterial pulse pressure to monitor the hemodynamic effects of PEEP.
AM J RESPIR CRIT CARE MED 1999;159:935939.

In ventilated patients with acute lung injury (ALI), positive
end-expiratory pressure (PEEP) may improve pulmonary gas
exchange. However, it may also decrease cardiac output and
thus offset the expected benefits in terms of oxygen delivery.
The PEEP-induced decrease in cardiac output is assumed to
be mainly due to a decrease in systemic venous return second-
ary to the increased pleural pressure (13). Impairment of
right ventricular (RV) ejection related to increased transpul-
monary pressure (i.e., alveolar minus pleural pressure) could
also play a role in some patients (4, 5). The adverse hemody-
namic effects of PEEP are not easily predictable in clinical
practice, although they have been shown to be more likely to
occur in patients with low left ventricular (LV) filling pressure
(68).
Mechanical ventilation induces cyclic changes in LV stroke
volume (SV) characterized by a lower LVSV during expira-
tion than during insufflation (912). This respiratory pattern is
mainly explained by the expiratory decrease in LV filling that
followed after a delay (caused by the long pulmonary transit
(Received in original form May 22, 1998 and in revised form October 20, 1998)
Presented in part at the American Thoracic Society International Conference,
1998, Chicago, IL, USA.
Correspondence and requests for reprints should be addressed to Pr. Jean-Louis
Teboul, Service de Ranimation Mdicale, Hopital de Bictre, 78, rue du Gnral
Leclerc, 94275, Le Kremlin-Bictre Cedex, France.
Am J Respir Crit Care Med Vol 159. pp 935939, 1999
Internet address: www.atsjournals.org
time of blood) the decrease in RVSV occurring during insuf-
flation (10). The inspiratory decrease in RVSV has been
shown to result essentially from a decrease in RV filling
caused by the effects of increased pleural pressure on systemic
venous return (9) and from transient impairment of RV ejec-
tion related to increased transpulmonary pressure on pulmo-
nary circulation (13, 14).
Interestingly, the decrease in mean cardiac output induced
by PEEP and the decrease in RVSV induced by mechanical
insufflation share the same mechanisms, i.e., the negative ef-
fects of increased pleural pressure on RV filling and of in-
creased transpulmonary pressure on RV ejection. Thus, it is
reasonable to expect that the magnitude of the expiratory de-
crease in LVSV would correlate with the PEEP-induced de-
crease in mean cardiac output.
Finally, the negative effects of increased pleural pressure
on RV filling should be more pronounced in patients with low
cardiac preload (15, 16). Thus, the beneficial effect of fluid
loading on cardiac output might be expected to correlate with
the magnitude of the inspiratory decrease in RVSV and hence
of the expiratory decrease in LVSV before fluid loading.
Aortic pulse pressure is directly proportional to LVSV and
inversely related to aortic capacitance (17). Respiratory changes
in peripheral pulse pressure (DPP) during mechanical ventila-
tion have been shown to closely reflect the variations in LVSV
during the respiratory cycle (10). Thus, the aim of our study
was to examine the relationships between DPP and the hemo-
dynamic effects of PEEP and fluid loading in ventilated pa-
936 AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 159 1999

tients with ALI. We hypothesized that the higher the DPP on
ZEEP, the higher the PEEP-induced decrease in cardiac out-
put. In patients who received fluid while on PEEP, we also hy-
pothesized that the higher the DPP before fluid loading, the
higher the fluid-loading-induced increase in cardiac output.
corded throughout the respiratory cycle and measured at end-expira-
tion. Cardiac output was calculated as the mean of five measurements
obtained by injecting 10 ml of dextrose solution randomly during the
respiratory cycle. The CI was calculated as the ratio of cardiac output
to body surface area.

METHODS Arterial Pressure Variations

The protocol was approved by the institutional review board for hu-
man subjects (Comit Consultatif de Protection des Personnes dans la
Recherche Biomdicale, Cochin Hospital), and written informed con-
sent was obtained from all the patients next of kin.
Patients
We studied 14 mechanically ventilated patients in whom ALI was di-
agnosed. This group consisted of 10 men and four women 37 to 83 yr
of age (mean age, 58 6 16 yr).
Inclusion criteria were as follows: (1) ALI defined by the combina-
tion of recent bilateral pulmonary infiltrates on chest radiograph, a
PaO2/FIO2 ratio , 300 mm Hg, and a pulmonary artery occlusion pres-
sure (Ppao) below 18 mm Hg; (2) all patients had to be instrumented
with indwelling arterial (radial or femoral) and pulmonary artery
catheters; (3) and all patients had to be hemodynamically stable, as
defined by a variation in heart rate, blood pressure, and CI of less
than 10% over the 15-min period before starting the protocol. Pa-
tients were excluded if they had arrhythmias or any contraindication
to the use of PEEP.
Hemodynamic Measurements
Patients were studied while supine, and zero pressure was measured
at the midaxillary line. Right atrial pressure (PRA) and Ppao were re-
We used the analog output from the monitor (H-P Monitor M1092A;
Hewlett-Packard, Les Ullis, France) via an A-T-D converter to record
the arterial pressure and airway pressure curves over at least 10
breaths simultaneously onto a computer (Toshiba 3200 SX). Record-
ing was performed at a sampling rate of 500 Hz using customized ac-
quisition software. Pulse pressure (PP) was calculated on a beat-to-
beat basis as the difference between systolic and diastolic arterial
pressure. Maximal PP (PPmax) and minimal PP (PPmin) values were
determined over a single respiratory cycle. To assess the respiratory
changes in PP, the percent change in PP was calculated as:
PP ( % ) = 100 { ( PPmax PPmin ) ( [ PPmax + PPmin ] 2 ) }
An example of our data and their analysis is shown in Figure 1.
Respiratory Measurements
Airway pressures were measured by using a pressure transducer (Uni-
flow 43-600; Baxter Edwards Crit Care, Irvine, CA) connected close
to the proximal end of the endotracheal tube. Plateau airway pressure
(Pplat) was measured after an end-inspiratory (2 s) occlusion. Tidal
volume (VT) was measured by means of the ventilator transducer.
The static compliance of the respiratory system (Cst,rs) was calculated
as follows: Cst,rs 5 VT/(Pplat 2 PEEP).

Study Protocol
All patients were sedated and mechanically ventilated in a volume-
controlled mode with an I/E ratio of one-half to one-third. Six patients
were therapeutically paralyzed according to the attending physician.
In three of the eight remaining patients, spontaneous breathing activ-
ity was detected by visual inspection of the airway pressure curve. To
ensure that DPP reflected only the effects of positive pressure ventila-
tion, these three patients were temporarily paralyzed. Measurements
were performed in duplicate, first during 0 cm H2O PEEP (ZEEP)
and then 15 min after the addition of 10 cm H2O PEEP (PEEP). In
patients in whom PEEP induced a decrease in CI of at least 10%, fluid
loading using 500 ml Hetastarch was performed over 30 min and a
third set of hemodynamic measurements was then obtained. Except
for PEEP, ventilatory settings and dosages of inotropic and vasopres-
sive drugs were held constant.

TABLE 1
MAIN CHARACTERISTICS OF THE PATIENTS

Patient Age PO2/FIO2 Crs,st VT

No. Cause of ALI (yr) LIS (mm Hg) (ml/cm H2O) (ml/kg)

1 Bacterial pneumonia 38 2.75 76 27 12

2 Drowning 37 2.5 157 32 12
3 Bacterial pneumonia 37 1.5 266 39 12
4 Bacterial pneumonia 55 2.5 145 30 11
5 Septic shock 58 2.75 56 31 10
6 Aspiration pneumonia 45 1.75 193 42 8
7 Septic shock 71 2.5 75 19 7
8 Bacterial pneumonia 83 1.75 219 32 10
Figure 1. Simultaneous recording of systemic arterial and airway 9 Bacterial pneumonia 82 2.75 56 23 9
pressure curves in one illustrative patient with large pulse pressure 10 Bacterial pneumonia 53 1.75 220 34 9
(PP) variations. Pulse pressure was calculated on a beat-to-beat ba- 11 Bacterial pneumonia 52 1.75 224 34 9
sis as the difference between systolic and diastolic arterial pressure. 12 Septic shock 71 2 192 24 10
Maximal (PPmax) and minimal (PPmin) values for PP were deter- 13 Peritonitis 59 1.5 238 32 12
mined over a single respiratory cycle. Respiratory pulse pressure 14 Bacterial pneumonia 70 1.5 256 31 10
variations (DPP) were calculated as: DPP (%) 5 100 3 {(PPmax 2 Definition of abbreviations: ALI 5 acute lung injury; Crs,st 5 static compliance of the
PPmin)/([PPmax 1 PPmin]/2)}. respiratory system; LIS 5 Lung Injury Score; VT 5 tidal volume.
Michard, Chemla, Richard, et al.: Pulse Pressure Variations and PEEP 937

Statistical Analysis sure on RV filling (9) and of increased transpulmonary pres-

Results were expressed as means 6 standard deviation. The effects of sure on RV ejection (13, 14). In conventional ventilatory
PEEP and fluid loading were assessed using Wilcoxons nonparamet- conditions, this should result in a minimal LVSV during expi-
ric rank sum test (18). Correlations were tested using Spearmans rank ration because of the phase lag between RV output and LV
test. A p value less than 0.05 was considered statistically significant. filling caused by the long blood pulmonary transit time (9, 10,
21). Other mechanisms might also contribute to the increase in
RESULTS LVSV at insufflation, particularly in patients with congestive
The main characteristics of the 14 patients studied are listed in heart failure: (1) a further LV filling caused by squeezing of
Table 1. Our patients had no history of heart failure, and CI blood out of alveolar vessels (20, 27), and (2) a decrease in LV
during ZEEP ranged from 2.9 to 7.0 L/min/m2. All patients ex- afterload caused by the increased pleural pressure (11, 28).
hibited maximal PP during insufflation and minimal PP during In fact, the main mechanisms that induce the inspiratory
the expiratory period. The effects of PEEP on the hemody- decrease in RVSV and hence the expiratory decrease in LVSV
namic parameters are presented in Table 2. are identical to those whereby PEEP decreases mean cardiac
On ZEEP, DPP correlated both with PRA (r 5 20.62, p , output. Accordingly, we found a strong correlation between
0.05) and with Ppao (r 5 20.64, p , 0.05). However, DPP on
ZEEP did not correlate with VT and Crs,st.
PEEP induced a decrease in CI from 4.2 6 1.1 to 3.8 6 1.3
L/min/m2 (p , 0.01) and an increase in DPP from 9 6 7 to
16 6 13% (p , 0.01). The PEEP-induced changes in CI corre-
lated both with DPP on ZEEP (r 5 20.91, p , 0.001) and with
the PEEP-induced changes in DPP (r 5 20.79, p , 0.001)
(Figure 2). The PEEP-induced changes in CI also correlated
with Ppao on ZEEP (r 5 0.75, p , 0.01) but were not signifi-
cantly correlated with PRA on ZEEP (r 5 0.48, p 5 0.08).
Six patients demonstrated a decrease in CI . 10% with the
application of PEEP. In these patients, fluid loading increased
CI from 3.5 6 1.1 to 4.2 6 0.9 L/min/m2 (p , 0.05) and de-
creased DPP from 27 6 13 to 14 6 9% (p , 0.05). The fluid-
loading-induced changes in CI correlated with DPP on PEEP
before volume expansion (r 5 0.97, p , 0.01) and with the
fluid-loading-induced changes in DPP (r 5 20.85, p , 0.05)
(Figure 3).

DISCUSSION
Our results demonstrate strong relationships between DPP
and the effects of both PEEP and fluid loading on cardiac out-
put in ventilated patients with ALI.
All of our patients exhibited a maximal PP during mechan-
ical insufflation and a minimal PP at expiration. These find-
ings are consistent with the respiratory pattern of arterial
pressure previously described in animal and clinical studies
during positive pressure ventilation (912, 1926). The respi-
ratory changes in PP have been shown related to the cyclic
changes in LVSV that followed after a delay the respiratory
changes in RVSV (10). At insufflation, RVSV is minimal be-
cause of the negative effects both of increased pleural pres-

TABLE 2
EFFECTS OF PEEP ON HEMODYNAMIC PARAMETERS*

ZEEP PEEP

HR, beats/min 114 6 16 117 6 17

Pa, mm Hg 81 6 12 73 6 14
PRA, mm Hg 864 9 6 3
Ppa, mm Hg 24 6 6 26 6 5
Ppao, mm Hg 964 12 6 3
CI, L/min/m2 4.2 6 1.1 3.8 6 1.3
DPP, % 967 16 6 13

Definition of abbreviations: CI 5 cardiac index; HR 5 heart rate; Pa 5 mean arterial

pressure; PRA 5 right atrial pressure; Ppa 5 mean pulmonary arterial pressure; Ppao 5 Figure 2. (Upper panel ) Correlation between respiratory pulse
pulmonary artery occlusion pressure; DPP 5 respiratory changes in arterial pulse pres- pressure variations (DPP) on ZEEP and the PEEP-induced changes
sure.
* Values are means 6 SD.
in cardiac index (CI). (Lower panel ) Correlation between PEEP-

p , 0.05. induced changes in DPP (DPP on PEEP 2 DPP on ZEEP) and the

p , 0.01 PEEP versus ZEEP. PEEP-induced changes in CI.
938 AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
Figure 3. (Upper panel) Correlation between respiratory pulse pres-
sure variations (DPP) on PEEP before fluid loading (FL) and the fluid
loading-induced changes in cardiac index (CI). (Lower panel) Cor-
relation between fluid loading-induced changes in DPP (DPP after
FL 2 DPP before FL) and the fluid loading-induced changes in CI.
DPP on ZEEP and the PEEP-induced decrease in CI. This
finding suggests that DPP may be useful in predicting the he-
modynamic effects of PEEP.
The expiratory decrease in LVSV caused by reduced LV
preload should be greater when the left ventricle operates on
the steep rather than on the flat portion of the Frank-Starling
curve (15, 16). Similarly, the inspiratory decrease in RVSV
would be greater in the case of low RV filling (15, 16). These
combined phenomena have been proposed to explain why re-
spiratory changes in arterial pressure are either increased by
hemorrhage (22, 23) or decreased by fluid loading (23, 25) and
why they correlate with LV preload indices such as Ppao (24)
and LV end-diastolic area (25). We also found that DPP corre-
lated with PRA and Ppao. Furthermore, in the six patients who
VOL 159 1999
received fluid, the increase in CI correlated both with DPP be-
fore fluid loading and with the fluid-loading-induced decrease
in DPP. These findings suggest that DPP may be useful for
monitoring the hemodynamic effects of fluid loading.
No correlation was found between DPP and tidal volume.
This result could be due to the small range of VT and to the
fact that, in contrast to others studies (19, 23), we did not mod-
ify VT throughout the study.
When our patients were transfered from ZEEP to PEEP,
the changes in DPP strongly correlated with the changes in CI.
These results were in accordance with those of Pizov and col-
leagues (26) who found that systolic pressure variations in
dogs increased mostly when cardiac output decreased with
PEEP. In preload-sensitive subjects, it may be assumed that
the further increase in pleural pressure with PEEP would have
produced a greater decrease in both expiratory LVSV and
mean cardiac output. However, because our study was not de-
signed to elucidate why DPP increased with PEEP, we cannot
exclude the possibility that mechanisms affecting RV after-
load may also have occurred: an additional increase in RV af-
terload during insufflation on PEEP, related to the extension
of Wests Zone 1 or 2 (13) cannot be excluded. Conversely,
PEEP-induced improvement in functional residual capacity
and/or a decrease in hypoxic pulmonary vasoconstriction might
have resulted in a lower RV afterload during insufflation on
PEEP than on ZEEP.
It must be underlined that arrhythmias and spontaneous
breathing activity may result in misleading interpretation of
DPP. Finally, since our study concerned patients with ALI, the
results cannot be extrapolated to patients with chronic respi-
ratory disease or congestive heart failure.
In summary, our findings suggest that (1) DPP could be
used at the bedside to predict adverse hemodynamic effects of
PEEP, (2) changes in DPP from ZEEP to PEEP could be used
to assess changes in CI that occur when PEEP is applied, (3) in
patients with ALI ventilated with PEEP, DPP and its changes
induced by fluid may be helpful in predicting and assessing the
effects of fluid loading on hemodynamics. Because the poten-
tial risk of using pulmonary artery catheters is currently a sub-
ject of debate (29), the use of DPP to monitor hemodynamics
in ventilated patients with ALI may be an attractive alterna-
tive approach.
Acknowledgment : The writers thank Dr. A. Mercat for technical assistance.
They also thank the physicians and nursing staff of the ICU for their valu-
able cooperation.
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