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ABSTRACT |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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In ventilated patients with acute lung injury (ALI) we investigated whether respiratory changes in arterial pulse pressure (
PP) could be related to the effects of PEEP and fluid loading (FL) on cardiac index (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 determined over one respiratory cycle and PP was calculated: PP (%) = 100 × {(PPmax 
PPmin)/ ([PPmax + PPmin]/2)}. PEEP decreased CI from 4.2 ± 1.1 to 3.8 ± 1.3 L/min/m2 (p < 0.01) and increased PP from 9 ± 7 to 16 ± 13% (p < 0.01). The PEEP-induced changes in CI correlated with PP
on ZEEP (r = 0.91, p < 0.001) and with the PEEP-induced increase in PP (r = 0.79, p < 0.001). FL
increased CI from 3.5 ± 1.1 to 4.2 ± 0.9 L/min/m2 (p < 0.05) and decreased PP from 27 ± 13 to
14 ± 9% (p < 0.05). The FL-induced changes in CI correlated with PP before FL (r = 0.97, p < 0.01)
and with the FL-induced decrease in PP (r = 0.85, p < 0.05). In ventilated patients with ALI, PP
may be useful in predicting and assessing the hemodynamic effects of PEEP and FL.
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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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 secondary to the increased pleural pressure (1). Impairment of right ventricular (RV) ejection related to increased transpulmonary pressure (i.e., alveolar minus pleural pressure) could also play a role in some patients (4, 5). The adverse hemodynamic 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 (6).
Mechanical ventilation induces cyclic changes in LV stroke volume (SV) characterized by a lower LVSV during expiration than during insufflation (9). This respiratory pattern is mainly explained by the expiratory decrease in LV filling that followed after a delay (caused by the long pulmonary transit time of blood) the decrease in RVSV occurring during insufflation (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 ejection related to increased transpulmonary pressure on pulmonary 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 effects of increased pleural pressure on RV filling and of increased transpulmonary pressure on RV ejection. Thus, it is reasonable to expect that the magnitude of the expiratory decrease in LVSV would correlate with the PEEP-induced decrease 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 (PP) during mechanical ventilation 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 PP and the hemodynamic effects of PEEP and fluid loading in ventilated patients with ALI. We hypothesized that the higher the PP on
ZEEP, the higher the PEEP-induced decrease in cardiac output. In patients who received fluid while on PEEP, we also hypothesized that the higher the PP before fluid loading, the
higher the fluid-loading-induced increase in cardiac output.
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METHODS |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The protocol was approved by the institutional review board for human subjects (Comité Consultatif de Protection des Personnes dans la Recherche Biomédicale, Cochin Hospital), and written informed consent was obtained from all the patients' next of kin.
Patients
We studied 14 mechanically ventilated patients in whom ALI was diagnosed. This group consisted of 10 men and four women 37 to 83 yr of age (mean age, 58 ± 16 yr).
Inclusion criteria were as follows: (1) ALI defined by the combination of recent bilateral pulmonary infiltrates on chest radiograph, a PaO2/FIO2 ratio < 300 mm Hg, and a pulmonary artery occlusion pressure (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. Patients 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 recorded throughout the respiratory cycle and measured at end-expiration. 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.
Arterial Pressure Variations
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). Recording was performed at a sampling rate of 500 Hz using customized acquisition 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:
![ΔPP (%)=100×{(PPmax−PPmin)/([PPmax+PPmin]/2)}](/content/vol159/issue3/fulltext/935/img001.gif)
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An example of our data and their analysis is shown in Figure 1.
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Respiratory Measurements
Airway pressures were measured by using a pressure transducer (Uniflow 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 = VT/(Pplat 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 activity was detected by visual inspection of the airway pressure curve. To
ensure that PP reflected only the effects of positive pressure ventilation, 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 vasopressive drugs were held constant.
Statistical Analysis
Results were expressed as means ± standard deviation. The effects of PEEP and fluid loading were assessed using Wilcoxon's nonparametric rank sum test (18). Correlations were tested using Spearman's rank test. A p value less than 0.05 was considered statistically significant.
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RESULTS |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The main characteristics of the 14 patients studied are listed in Table 1. Our patients had no history of heart failure, and CI during ZEEP ranged from 2.9 to 7.0 L/min/m2. All patients exhibited maximal PP during insufflation and minimal PP during the expiratory period. The effects of PEEP on the hemodynamic parameters are presented in Table 2.
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On ZEEP, PP correlated both with PRA (r = 0.62, p < 0.05) and with Ppao (r = 0.64, p < 0.05). However, PP on
ZEEP did not correlate with VT and Crs,st.
PEEP induced a decrease in CI from 4.2 ± 1.1 to 3.8 ± 1.3 L/min/m2 (p < 0.01) and an increase in PP from 9 ± 7 to
16 ± 13% (p < 0.01). The PEEP-induced changes in CI correlated both with PP on ZEEP (r = 0.91, p < 0.001) and with
the PEEP-induced changes in PP (r = 0.79, p < 0.001)
(Figure 2). The PEEP-induced changes in CI also correlated
with Ppao on ZEEP (r = 0.75, p < 0.01) but were not significantly correlated with PRA on ZEEP (r = 0.48, p = 0.08).
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Six patients demonstrated a decrease in CI > 10% with the
application of PEEP. In these patients, fluid loading increased CI from 3.5 ± 1.1 to 4.2 ± 0.9 L/min/m2 (p < 0.05) and decreased PP from 27 ± 13 to 14 ± 9% (p < 0.05). The fluid-loading-induced changes in CI correlated with PP on PEEP
before volume expansion (r = 0.97, p < 0.01) and with the fluid-loading-induced changes in PP (r = 0.85, p < 0.05)
(Figure 3).
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DISCUSSION |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Our results demonstrate strong relationships between PP
and the effects of both PEEP and fluid loading on cardiac output in ventilated patients with ALI.
All of our patients exhibited a maximal PP during mechanical insufflation and a minimal PP at expiration. These findings are consistent with the respiratory pattern of arterial pressure previously described in animal and clinical studies during positive pressure ventilation (9, 19). The respiratory 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 because of the negative effects both of increased pleural pressure on RV filling (9) and of increased transpulmonary pressure on RV ejection (13, 14). In conventional ventilatory conditions, this should result in a minimal LVSV during expiration because of the phase lag between RV output and LV filling caused by the long blood pulmonary transit time (9, 10, 21). Other mechanisms might also contribute to the increase in LVSV at insufflation, particularly in patients with congestive heart failure: (1) a further LV filling caused by squeezing of blood out of alveolar vessels (20, 27), and (2) a decrease in LV afterload caused by the increased pleural pressure (11, 28).
In fact, the main mechanisms that induce the inspiratory
decrease in RVSV and hence the expiratory decrease in LVSV
are identical to those whereby PEEP decreases mean cardiac
output. Accordingly, we found a strong correlation between
PP on ZEEP and the PEEP-induced decrease in CI. This
finding suggests that PP may be useful in predicting the hemodynamic 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 respiratory 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 PP correlated with PRA and Ppao. Furthermore, in the six patients who
received fluid, the increase in CI correlated both with PP before fluid loading and with the fluid-loading-induced decrease
in PP. These findings suggest that PP may be useful for
monitoring the hemodynamic effects of fluid loading.
No correlation was found between PP 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 modify VT throughout the study.
When our patients were transfered from ZEEP to PEEP,
the changes in PP strongly correlated with the changes in CI.
These results were in accordance with those of Pizov and colleagues (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 designed to elucidate why PP increased with PEEP, we cannot
exclude the possibility that mechanisms affecting RV afterload may also have occurred: an additional increase in RV afterload during insufflation on PEEP, related to the extension of West's 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
PP. Finally, since our study concerned patients with ALI, the
results cannot be extrapolated to patients with chronic respiratory disease or congestive heart failure.
In summary, our findings suggest that (1) PP could be
used at the bedside to predict adverse hemodynamic effects of
PEEP, (2) changes in PP 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, PP and its changes
induced by fluid may be helpful in predicting and assessing the
effects of fluid loading on hemodynamics. Because the potential risk of using pulmonary artery catheters is currently a subject of debate (29), the use of PP to monitor hemodynamics
in ventilated patients with ALI may be an attractive alternative approach.
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Footnotes |
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Correspondence and requests for reprints should be addressed to Pr. Jean-Louis Teboul, Service de Réanimation Médicale, Hopital de Bicêtre, 78, rue du Général Leclerc, 94275, Le Kremlin-Bicêtre Cedex, France.
(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.Acknowledgments: The writers thank Dr. A. Mercat for technical assistance. They also thank the physicians and nursing staff of the ICU for their valuable cooperation.
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References |
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ABSTRACT
INTRODUCTION
METHODS
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DISCUSSION
REFERENCES
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M. Feissel, F. Michard, I. Mangin, O. Ruyer, J.-P. Faller, and J.-L. Teboul espiratory Changes in Aortic Blood Velocity as an Indicator of Fluid Responsiveness in Ventilated Patients With Septic Shock Chest, March 1, 2001; 119(3): 867 - 873. [Abstract] [Full Text] [PDF]
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F. MICHARD, S. BOUSSAT, D. CHEMLA, N. ANGUEL, A. MERCAT, Y. LECARPENTIER, C. RICHARD, M. R. PINSKY, and J.-L. TEBOUL Relation between Respiratory Changes in Arterial Pulse Pressure and Fluid Responsiveness in Septic Patients with Acute Circulatory Failure Am. J. Respir. Crit. Care Med., July 1, 2000; 162(1): 134 - 138. [Abstract] [Full Text]
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T. G. Janz, R. Madan, J. J. Marini, W. R. Summer, G. U. Meduri, R. M. Smith, G. R. Epler, and J. Schnader Clinical Conference on Management Dilemmas: Progressive Infiltrates and Respiratory Failure Chest, February 1, 2000; 117(2): 562 - 572. [Full Text] [PDF]
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