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ABSTRACT |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In mechanically ventilated patients with acute circulatory failure
related to sepsis, we investigated whether the respiratory changes
in arterial pressure could be related to the effects of volume expansion (VE) on cardiac index (CI). Forty patients instrumented with indwelling systemic and pulmonary artery catheters were
studied before and after VE. Maximal and minimal values of pulse
pressure (Ppmax and Ppmin) and systolic pressure (Psmax and Psmin)
were determined over one respiratory cycle. The respiratory changes in pulse pressure (
Pp) were calculated as the difference between Ppmax and Ppmin divided by the mean of the two values and
were expressed as a percentage. The respiratory changes in systolic pressure (Ps) were calculated using a similar formula. The
VE-induced increase in CI was 
15% in 16 patients (responders)
and < 15% in 24 patients (nonresponders). Before VE, Pp (24 ± 9 versus 7 ± 3%, p < 0.001) and Ps (15 ± 5 versus 6 ± 3%, p < 0.001) were higher in responders than in nonresponders. Receiver
operating characteristic (ROC) curves analysis showed that Pp
was a more accurate indicator of fluid responsiveness than Ps.
Before VE, a Pp value of 13% allowed discrimination between responders and nonresponders with a sensitivity of 94% and a specificity of 96%. VE-induced changes in CI closely correlated with Pp
before volume expansion (r2 = 0.85, p < 0.001). VE decreased Pp
from 14 ± 10 to 7 ± 5% (p < 0.001) and VE-induced changes in
Pp correlated with VE-induced changes in CI (r2 = 0.72, p < 0.001). It was concluded that in mechanically ventilated patients
with acute circulatory failure related to sepsis, analysis of Pp is a
simple method for predicting and assessing the hemodynamic effects of VE, and that Pp is a more reliable indicator of fluid responsiveness than Ps.
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Volume expansion (VE) is the first-line therapy proposed in septic patients in an attempt to improve hemodynamics (1). Both the increase in microvascular permeability and venous pooling induce inadequate cardiac preload such that a large amount of fluid is usually needed during the early phase of resuscitation (1). However, excessive VE leads to interstitial fluid accumulation, which may worsen gas exchange, decrease myocardial compliance, and limit oxygen diffusion to the tissues (2). Therefore, in septic patients with acute circulatory failure, reliable predictors of fluid responsiveness are needed at the bedside.
By increasing pleural pressure and transpulmonary pressure, mechanical insufflation may respectively decrease systemic venous return, i.e., right ventricular (RV) filling (3), and
transiently impair RV ejection (4, 5). Therefore, RV stroke
volume may decrease during the inspiratory period, leading to
a left ventricular (LV) preload reduction occurring during the
expiratory period because of the long pulmonary transit time
of blood (6). These respiratory changes in LV preload may induce cyclic changes in LV stroke volume (6, 7). Aortic pulse
pressure (systolic 
diastolic pressure) is directly proportional
to LV stroke volume and inversely related to aortic compliance (8). Thus, the respiratory changes in LV stroke volume
have been shown to be reflected by changes in peripheral
pulse pressure during the respiratory cycle (6).
Interestingly, the cyclic changes in RV preload induced by
mechanical ventilation should result in greater cyclic changes in RV stroke volume when the right ventricle operates on the
steep rather than on the flat portion of the Frank-Starling
curve (9, 10). The cyclic changes in RV stroke volume and
hence in LV preload should also result in greater cyclic
changes in LV stroke volume when the left ventricle operates
on the ascending portion of the Frank-Starling curve (9, 10).
Thus, the magnitude of the respiratory changes in LV stroke
volume and hence of the respiratory changes in pulse pressure
(Pp) should be an indicator of biventricular preload dependence. Consistent with this hypothesis, we have recently demonstrated in mechanically ventilated patients with acute lung
injury that Pp could be used to monitor the adverse hemodynamic effects of PEEP, which are mainly related to a decrease in systemic venous return (11).
The cyclic changes in peripheral systolic pressure induced by
mechanical ventilation have also been studied in animals (12) and in critically ill patients (13, 14). These changes have been
shown to be influenced by the volume status (12) and have been proposed as an indicator of fluid responsiveness (13, 14). Respiratory changes in systolic pressure (Ps) result from changes in aortic transmural pressure (mainly related to changes in LV stroke volume) and from changes in extramural pressure (i.e., from changes in pleural pressure) (7). In contrast, Pp depends only on changes in transmural pressure, because changes in
pleural pressure should affect both systolic and diastolic pressure. Accordingly, Pp is expected to be more reliable than Ps
as an indicator of the respiratory changes in LV stroke volume
and hence of biventricular preload dependence.
Thus, in mechanically ventilated patients with acute circulatory failure related to sepsis, we investigated (1) whether
Pp could predict the hemodynamic effects of VE, (2) whether
changes in Pp could be used to assess changes in cardiac index (CI) induced by VE, and (3) whether Pp might be a
more reliable indicator of fluid responsiveness than Ps.
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METHODS |
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TOP
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, Bicêtre Hospital) and written informed consent was obtained from all the patients' next of kin.
Patients
We studied 40 mechanically ventilated patients diagnosed with acute circulatory failure related to sepsis. This group comprised 32 men and eight
women, aged between 18 and 81 yr (mean age, 55 ± 16 yr). Inclusion criteria were as follows: (1) sepsis defined by the criteria of the American
College of Chest Physicians/Society of Critical Care Medicine Consensus Conference (15); (2) acute circulatory failure defined by a systolic
blood pressure < 90 mm Hg or the need of vasopressive drugs (dopamine > 5 µg/kg/min or norepinephrine); (3) instrumentation with indwelling radial (n = 15) or femoral (n = 25) arterial and pulmonary artery
catheters; (4) hemodynamic stability, defined by a variation in heart
rate, blood pressure, and cardiac output (
) of less than 10% over the
15-min period before starting the protocol. Patients were excluded if
they had arrhythmias, severe hypoxemia (ratio of arterial oxygen pressure to fraction of inspired oxygen [PaO2/FIO2] < 100 mm Hg), or a pulmonary artery occlusion pressure (Ppao) 18 mm Hg.
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. The correct position of the pulmonary artery catheter in West's
zone 3 was checked using a method previously described (16). was
calculated as the mean of five measurements obtained by injecting 10 ml
of dextrose solution randomly during the respiratory cycle. CI, stroke
volume index, and systemic and pulmonary vascular resistances were
calculated using standard formulas.
Respiratory Changes in Arterial Pressure
We used the analog output from the monitor (Monitor M1092A;
Hewlett-Packard, Les Ullis, France) via an analog-to-digital converter to record the arterial pressure and airway pressure curves over at least
3 breaths simultaneously onto a computer (Toshiba 3200 SX, Tokyo,
Japan). Recording was performed at a sampling rate of 500 Hz using
customized acquisition software. Systolic and diastolic arterial pressure were measured on a beat-to-beat basis and pulse pressure (Pp)
was calculated as the difference between systolic and diastolic pressure. Maximal and minimal values for systolic (Psmax and Psmin, respectively) and pulse pressure (Ppmax and Ppmin, respectively) were
determined over a single respiratory cycle. Pp was calculated as previously described (11): Pp (%) = 100 × (Ppmax Ppmin)/[(Ppmax + Ppmin)/2]. Ps was evaluated using a similar formula: Ps (%) = 100 × (Psmax Psmin)/[(Psmax + Psmin)/2]. An example of our data and their
analysis for one subject is shown in Figure 1. Pp and Ps were evaluated in triplicate over each of three consecutive respiratory cycles.
The mean values of the three determinations were used for statistical
analysis.
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Study Protocol
All patients were sedated and mechanically ventilated in a volume-controlled mode with a tidal volume of 8 to 12 ml/kg and an inspiratory/expiratory (I/E) ratio of one-third to one-half. Thirty-two patients were ventilated with a positive end-expiratory pressure (7 ± 4 cm H2O). Nine patients were therapeutically paralyzed on the decision of the attending physician. In eight of the 31 remaining patients, spontaneous breathing activity was detected by visual inspection of the airway pressure curve. To ensure that the respiratory changes in arterial pressure reflected only the effects of positive pressure ventilation, these eight patients were temporarily paralyzed. Measurements were performed in duplicate, first before VE and then 30 min after VE using 500 ml 6% hydroxyethylstarch. Ventilatory settings and dosages of inotropic and vasopressive drugs were held constant.
Statistical Analysis
The effects of VE on hemodynamic parameters were assessed using a
nonparametric Wilcoxon rank sum test (17). Patients were divided in
two groups according to the percent increase in CI in response to VE.
According to Stetz and coworkers (18), we assumed that a 15%
change in CI was needed for clinical significance. Therefore, patients
with a CI increase induced by VE 15% and < 15% were classified
as responders and nonresponders, respectively. The comparison of
hemodynamic parameters before VE in responder and nonresponder
patients was assessed using a nonparametric Mann-Whitney U test.
Results were expressed as mean values ± SD. Receiver operating characteristic (ROC) curves were generated for Pra, Ppao, Pp, and
Ps, varying the discriminating threshold of each parameter. The areas under the ROC curves (± SE) were calculated for each parameter
and compared (19). Linear correlations were tested using the Spearman rank method. A p value less than 0.05 was considered statistically significant.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The 40 patients studied had clear evidence of sepsis (bacterial pneumonia: 30 patients; abdominal sepsis: eight patients; meningitis: two patients). Thirty-two patients received vasopressor support (norepinephrine: 20 patients; dopamine: 12 patients) and the eight remaining patients had severe hypotension (systolic blood pressure = 81 ± 7 mm Hg). Underlying diseases included chronic obstructive pulmonary disease (n = 11), diabetes mellitus (n = 9), ischemic cardiopathy (n = 8), hypertension (n = 8), peripheral vascular disease (n = 5), and chronic renal failure (n = 3). Echocardiography was performed in 22 patients and revealed LV systolic dysfunction in 12 patients. Twenty-two patients survived.
In all patients, maximal pulse and systolic pressures were exhibited during the inspiratory period and minimal pulse and systolic pressures during the expiratory period. The difference between Ppmax and Ppmin ranged from 1 to 20 mm Hg (mean difference: 5 ± 4 mm Hg) and the difference between Psmax and Psmin ranged from 1 to 27 mm Hg (mean difference: 8 ± 6 mm Hg). In all patients, the difference between Ppmax and Ppmin was smaller than the difference between Psmax and Psmin. Hemodynamic parameters before and after VE are presented in Table 1.
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Before VE, Pp ranged from 1 to 44% and Ps from 1 to
28%. Before VE, Pp and Ps were not correlated with either
Pra or Ppao.
VE increased CI from 3.6 ± 0.9 to 4.0 ± 0.9 L/min/m2 (p < 0.001). Sixteen patients were responders (CI increase 15%)
and 24 were nonresponders. Before VE, Pp (24 ± 9 versus 7 ± 3%, p < 0.001) and Ps (15 ± 5 versus 6 ± 3%, p < 0.001) were
higher in responder than in nonresponder patients, whereas Pra
(9 ± 3 versus 9 ± 4 mm Hg) and Ppao (10 ± 3 versus 11 ± 2 mm
Hg) were not significantly different between the two groups.
The areas under the ROC curves (± SE) were as follows: 0.98 ± 0.03 for Pp, 0.91 ± 0.04 for Ps, 0.51 ± 0.12 for Pra, and 0.40 ± 0.09 for Ppao (Figure 2). The area for Pp was significantly
greater than the area for Ps (p < 0.01), Pra (p < 0.01), and
Ppao (p < 0.01). The threshold Pp value of 13% allowed discrimination between responder and nonresponder patients with
a sensitivity of 94% and a specificity of 96%.
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A positive and close linear correlation (r 2 = 0.85, p < 0.001) was found between Pp before VE and VE-induced
changes in CI such that the higher Pp before VE, the greater
was the percent increase in CI [changes in CI (%) = 1.01 × Pp 1.46] (Figure 3). Ps before VE was also significantly
correlated with the VE-induced changes in CI (r 2 = 0.69, p < 0.001), although less strongly than was Pp (Figure 3). Conversely, Pra and Ppao measured before VE were not correlated in any way with VE-induced changes in CI.
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VE decreased both Pp (from 14 ± 10 to 7 ± 5%, p < 0.001) and Ps (from 9 ± 6 to 6 ± 4%, p < 0.001). VE-induced
changes in Pp (Pp after VE minus Pp before VE) were
correlated with VE-induced changes in CI (r 2 = 0.72, p < 0.001) such that the greater the decrease in Pp, the greater
the increase in CI induced by VE (Figure 4). VE-induced changes in Ps (Ps after VE minus Ps before VE) were also
correlated with VE-induced changes in CI (r 2 = 0.64, p < 0.001) (Figure 4).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In mechanically ventilated patients with acute circulatory failure related to sepsis, our results demonstrate a close relationship between Pp and the effects of VE on . These results
strongly suggest that Pp before VE accurately predicts the
effects of VE on and that Pp is a more reliable indicator of
fluid responsiveness than Ps. They also suggest that changes
in Pp induced by VE can be used in assessing contemporaneous changes in .
Pra and Ppao have been proposed for identifying patients who would benefit from VE (20, 21). In the present study, Pra and Ppao before VE were not significantly different between responders and nonresponders and did not correlate with the VE-induced changes in CI. Moreover, the area under the ROC curves for Pra and Ppao indicated that measuring these parameters to assess fluid responsiveness was no better than chance. These findings are in agreement with other reports (14, 22, 23) demonstrating that Pra and Ppao are of little value in predicting the hemodynamic effects of VE in septic patients.
In contrast, our results demonstrate that Pp is an accurate
indicator of fluid responsiveness in mechanically ventilated patients with acute circulatory failure related to sepsis. Indeed, a patient with a baseline Pp value of more than 13%
was very likely to respond to VE by increasing CI by 15%
(positive predictive value of 94%). In contrast, if Pp was < 13%, the patient was unlikely to respond to a fluid challenge (negative predictive value of 96%). Moreover, Pp before VE closely correlated with the VE-induced increase in
CI. Interestingly, the percent increase in CI induced by the infusion of 500 ml 6% hydroxyethylstarch was approximately
equal to Pp before VE (Figure 3). These findings suggest
that analysis of Pp could be particularly helpful in the decision-making process concerning VE in such patients.
VE induced a significant decrease in Pp in our patients.
This decrease could be explained as follows. First, VE is assumed to increase RV preload such that the operating point of
the right ventricle moves rightward, i.e., toward the flatter
portion of the Frank-Starling curve (9, 10). Each inspiratory
decrease in RV preload would therefore have a less marked
effect on RV stroke volume after VE than before (9, 10). Second, by increasing pulmonary capillary pressure, VE may induce recruitment of pulmonary capillaries, leading to a decrease in West's zone 2 (16, 24) and hence a potential decrease
in RV afterload during insufflation. Thus, through these two
mechanisms, VE should attenuate the inspiratory decrease in
RV stroke volume and hence the subsequent expiratory decrease in LV preload. This latter phenomenon, in combination with a VE-induced rightward shift of the LV operating point,
should result in attenuated changes in LV stroke volume and
Pp over the respiratory cycle. However, because our study was
not designed to elucidate why Pp decreased with VE, we
cannot determine which mechanism was predominant. It is interesting to note that the decrease in Pp induced by VE correlated with the contemporaneous increase in CI (Figure 4).
This finding suggests that analysis of changes in Pp could be
useful in assessing the effects of VE on .
Ps results not only from changes in aortic transmural
pressure (mainly related to changes in LV stroke volume) but
also from changes in extramural pressure (i.e., from changes in
pleural pressure) (7). Accordingly, in all of our patients, the
difference between Psmax and Psmin was greater than the difference between Ppmax and Ppmin (8 ± 6 versus 5 ± 4 mm Hg).
This finding suggests that Ps was a less specific indicator of
changes in LV stroke volume than Pp and probably explains
why (1) the area under the ROC curve was significantly higher
for Pp than for Ps, and (2) there was a closer correlation
between Pp and VE-induced changes in CI than between
Ps and changes in CI. Consequently, it may be preferable to
use Pp rather than Ps for monitoring fluid responsiveness.
It must be underlined that arrhythmias and spontaneous
breathing activity lead to misinterpretation of respiratory
changes in arterial pressure. Patients with arrhythmias were
therefore excluded from the present study and those with spontaneous breathing activity were temporarily paralyzed during the protocol. As mentioned previously, the Pp depends
not only on stroke volume but also on arterial compliance.
Therefore, for a given change in LV stroke volume, Pp may
vary from one patient to another according to the arterial compliance. To this extent, large changes in Pp could be theoretically observed despite small changes in LV stroke volume if arterial compliance is low (elderly patients with peripheral vascular disease). Similarly, small changes in Pp could be observed despite large changes in LV stroke volume if arterial
compliance is high (young patients without any vascular disease). In fact, our results observed in patients with a large
range of age and comorbidities suggest that arterial compliance
poorly affected the relationship between respiratory changes in
LV stroke volume and Pp. Given that we studied patients with
acute circulatory failure related to sepsis, our results cannot be
extrapolated to other clinical situations. Finally, although analysis of Pp may be an attractive alternative approach to pulmonary artery catheterization in these patients, it does not allow measurement of and pulmonary pressures.
To summarize, our findings suggest that in mechanically
ventilated patients with acute circulatory failure related to
sepsis, (1) Pp accurately predicts the hemodynamic effects of
VE, (2) changes in Pp could be used to assess changes in CI
induced by VE, and (3) Pp is a more reliable indicator of
fluid responsiveness than Ps. The analysis of Pp is easy to
perform in patients who have an indwelling arterial catheter
for continuous monitoring of blood pressure. Therefore, calculation of Pp could facilitate the hemodynamic management of ventilated patients with acute circulatory failure related to sepsis.
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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, Hôpital de Bicêtre, 78 rue du Général Leclerc, 94275, Le Kremlin-Bicêtre Cedex, France. E-mail: jlTeboul.bicetre{at}invivo.edu
(Received in original form March 4, 1999 and in revised form December 29, 1999).
Part of this study has been presented at the American Thoracic Society international conference, 1999, San Diego, California.Acknowledgments: The authors thank the physicians and nursing staff of the ICU for their valuable cooperation and Dr. Pierre Ducq for statistical advice.
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References |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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M. R. Pinsky Hemodynamic Evaluation and Monitoring in the ICU Chest, December 1, 2007; 132(6): 2020 - 2029. [Abstract] [Full Text] [PDF]
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J-H. Lee, J-T. Kim, S. Z. Yoon, Y-J. Lim, Y. Jeon, J-H. Bahk, and C. S. Kim Evaluation of corrected flow time in oesophageal Doppler as a predictor of fluid responsiveness Br. J. Anaesth., September 1, 2007; 99(3): 343 - 348. [Abstract] [Full Text] [PDF]
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G. Natalini Variations in Photoplethysmographic Waveform During Mechanical Ventilation Anesth. Analg., June 1, 2007; 104(6): 1599 - 1600. [Full Text] [PDF]
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J. M. Brennan, J. E. A. Blair, C. Hampole, S. Goonewardena, S. Vasaiwala, D. Shah, K. T. Spencer, and G. A. Schmidt Radial Artery Pulse Pressure Variation Correlates With Brachial Artery Peak Velocity Variation in Ventilated Subjects When Measured by Internal Medicine Residents Using Hand-Carried Ultrasound Devices Chest, May 1, 2007; 131(5): 1301 - 1307. [Abstract] [Full Text] [PDF]
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C. Runcie, B. Tavernier, H. Solus-Biguenet, M. Fleyfel, and B. Vallet Predicting fluid responsiveness in theatre Br. J. Anaesth., April 1, 2007; 98(4): 545 - 547. [Full Text] [PDF]
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S. Magder and F. Bafaqeeh The Clinical Role of Central Venous Pressure Measurements J Intensive Care Med, January 1, 2007; 22(1): 44 - 51. [Abstract] [PDF]
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A. Mekontso-Dessap, L. Tual, M. Kirsch, G. D'Honneur, D. Loisance, L. Brochard, and J.-L. Teboul B-type natriuretic peptide to assess haemodynamic status after cardiac surgery Br. J. Anaesth., December 1, 2006; 97(6): 777 - 782. [Abstract] [Full Text] [PDF]
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G. Natalini, A. Rosano, M. Taranto, B. Faggian, E. Vittorielli, and A. Bernardini Arterial Versus Plethysmographic Dynamic Indices to Test Responsiveness for Testing Fluid Administration in Hypotensive Patients: A Clinical Trial Anesth. Analg., December 1, 2006; 103(6): 1478 - 1484. [Abstract] [Full Text] [PDF]
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G. Natalini, A. Rosano, M. E. Franceschetti, P. Facchetti, and A. Bernardini Variations in Arterial Blood Pressure and Photoplethysmography During Mechanical Ventilation Anesth. Analg., November 1, 2006; 103(5): 1182 - 1188. [Abstract] [Full Text] [PDF]
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C. Charron, C. Fessenmeyer, C. Cosson, J.-X. Mazoit, J.-L. Hebert, D. Benhamou, and A. R. Edouard The Influence of Tidal Volume on the Dynamic Variables of Fluid Responsiveness in Critically Ill Patients. Anesth. Analg., May 1, 2006; 102(5): 1511 - 1517. [Abstract] [Full Text] [PDF]
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S. Preisman, S. Kogan, H. Berkenstadt, and A. Perel Predicting fluid responsiveness in patients undergoing cardiac surgery: functional haemodynamic parameters including the Respiratory Systolic Variation Test and static preload indicators Br. J. Anaesth., December 1, 2005; 95(6): 746 - 755. [Abstract] [Full Text] [PDF]
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R. J. Wright Make No Bones About It: Increasing Epidemiologic Evidence Links Vitamin D to Pulmonary Function and COPD Chest, December 1, 2005; 128(6): 3781 - 3783. [Full Text] [PDF]
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F. Michard Volume Management Using Dynamic Parameters Chest, October 1, 2005; 128(4): 1902 - 1903. [Full Text] [PDF]
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C. K. Hofer, S. M. Muller, L. Furrer, R. Klaghofer, M. Genoni, and A. Zollinger Stroke Volume and Pulse Pressure Variation for Prediction of Fluid Responsiveness in Patients Undergoing Off-Pump Coronary Artery Bypass Grafting Chest, August 1, 2005; 128(2): 848 - 854. [Abstract] [Full Text] [PDF]
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