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* From the Service de Réanimation et de Maladies Infectieuses (Drs. Feissel, Mangin, Ruyer, and Faller), Centre Hospitalier, Belfort, France; and the Service de Réanimation Médicale (Drs. Michard and Teboul), CHU de Bicêtre, AP-HP, Université Paris XI, Le Kremlin Bicêtre, France.
Correspondence to: Frédéric Michard, MD, Service de Réanimation Médicale, CHU de Bicêtre, 78 Rue du Général Leclerc, 94275 Le Kremlin-Bicêtre Cedex, France; e-mail: f.michard{at}wanadoo.fr
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Abstract |
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Design: Prospective clinical study.
Setting: Medical ICUs of a university hospital (20 beds) and of a nonuniversity hospital (15 beds).
Patients: Nineteen sedated septic shock patients who were receiving mechanical ventilation and who had preserved left ventricular (LV) systolic function.
Intervention: Volume expansion.
Measurements and results: Analysis of aortic blood flow by
transesophageal echocardiography allowed beat-to-beat measurement of
Vpeak before and after volume expansion. Maximum values of Vpeak
(Vpeakmax) and minimum values of Vpeak (Vpeakmin) were determined over
one respiratory cycle. The respiratory changes in Vpeak (
Vpeak) were
calculated as the difference between Vpeakmax and Vpeakmin divided by
the mean of the two values and were expressed as a percentage. The
indexed LV end-diastolic area (EDAI) and cardiac index were obtained at
the end of the expiratory period. The volume expansion-induced increase
in cardiac index was 
15% in 10 patients (responders) and < 15%
in 9 patients (nonresponders). Before volume expansion, Vpeak was
higher in responders than in nonresponders (20 ± 6% vs 10 ± 3%;
p < 0.01), while EDAI was not significantly different between the
two groups (9.7 ± 3.7 vs 9.7 ± 2.4
cm2/m2). Before volume expansion, a Vpeak
threshold value of 12% allowed discrimination between responders and
nonresponders with a sensitivity of 100% and a specificity of 89%.
Volume expansion-induced changes in cardiac index closely correlated
with the Vpeak before volume expansion
(r2 = 0.83; p < 0.001).
Conclusion: Analysis of respiratory changes in aortic blood velocity is an accurate method for predicting the hemodynamic effects of volume expansion in septic shock patients receiving mechanical ventilation who have preserved LV systolic function.
Key Words: aortic blood velocity • cardiac output • fluid responsiveness • left ventricular end-diastolic area • mechanical ventilation • septic shock • transesophageal echocardiography • volume expansion
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Introduction |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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By increasing pleural pressure and transpulmonary pressure (ie, alveolar pressure minus pleural pressure), mechanical insufflation may decrease RV filling6 and impair RV ejection.7 8 Therefore, RV stroke volume may decrease during the inspiratory period, leading to a reduction in LV preload during the expiratory period because of the long pulmonary transit time of blood.9 These respiratory changes in LV preload may induce cyclic changes in LV stroke volume.9 10 Interestingly, the cyclic changes in RV preload induced by mechanical ventilation should result in greater cyclic changes in RV stroke volume when the RV operates on the steep rather than on the flat portion of the Frank-Starling curve.11 12 The cyclic changes in RV stroke volume, and hence in LV preload, also should result in greater cyclic changes in LV stroke volume when the LV operates on the ascending portion of the Frank-Starling curve.11 12 Thus, the magnitude of the respiratory changes in LV stroke volume should be an indicator of biventricular preload dependence, and hence of fluid responsiveness. To this extent, several clinical studies5 13 14 have demonstrated that the respiratory changes in arterial pressure (mainly related to the respiratory changes in LV stroke volume) accurately predict the hemodynamic effects of volume expansion in patients receiving mechanical ventilation. Transesophageal echocardiography allows a beat-to-beat measurement of aortic blood velocity. Because aortic blood flow is directly proportional to LV stroke volume, we postulated that an analysis of the respiratory changes in aortic blood velocity might provide an accurate estimation of the respiratory changes in LV stroke volume and, thus, might be used to assess biventricular preload dependence and, hence, fluid responsiveness.
Therefore, in septic shock patients receiving mechanical ventilation, we investigated whether EDAI and respiratory changes in aortic blood velocity could predict the hemodynamic effects of volume expansion.
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Materials and Methods |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Patients
We studied 19 patients receiving mechanical ventilation in whom
septic shock had been diagnosed. This group comprised 11 men and 8
women who had an age range between 25 and 87 years (mean [± SD]
age, 58 ± 16 years). Inclusion criteria were as follows: (1) septic
shock defined by the criteria of the American College of Chest
Physicians/Society of Critical Care Medicine Consensus
Conference15
; and (2) hemodynamic stability, defined by a
variation in heart rate and BP of < 10% over the 15-min period
before starting the protocol. Patients were excluded if they had
arrhythmias, severe hypoxemia
(PaO2/fraction of inspired oxygen
ratio of < 100 mm Hg), any contraindication to transesophageal
echocardiography, aortic valvulopathy, or LV systolic dysfunction
(fractional area of contraction < 30%), and if Doppler LV output
recordings using the transgastric view could not be obtained.
LV End-Diastolic Measurements
A transesophageal multiplane probe was positioned to obtain a
transgastric, short-axis, cross-sectional view of the LV at the
mid-papillary muscle level. Echocardiographic images were recorded
together with the ECG. End-diastole was defined as the frame
corresponding to the largest LV cross-sectional area immediately after
the R-wave peak on the ECG. The LV short-axis, end-diastolic,
cross-sectional area was measured by manual planimetry of the area
circumscribed by the leading edge of the LV endocardial border. The
anterolateral and posteromedial papillary muscles were included within
the ventricular area. LV areas were divided by the surface body area of
the patient to obtain EDAI. The mean of five measurements performed at
the end of the expiratory period was used for statistical analysis.
Cardiac Output Measurements
By rotating the imaging array to approximately 120°, the LV
outflow tract and ascending aorta were imaged when parallel to the
ultrasound beam. Aortic blood flow then was measured by a pulsed-wave
Doppler beam at the level of the aortic valve so that the click of the
aortic closure was obtained. The aortic valve area was calculated from
the diameter of the aortic orifice, measured at the insertion of the
aortic cusp, as aortic valve area =
x (aortic
diameter/2).2
The stroke volume was calculated as stroke
volume = aortic valve area x the velocity time integral of aortic
blood flow. The cardiac output was calculated as cardiac
output = stroke volume x heart rate. Stroke volume and cardiac
output were divided by the surface body area to obtain the stroke
volume index and cardiac index. The mean of five measurements performed
at the end of the expiratory period were used for statistical analysis.
Respiratory Changes in Aortic Blood Velocity
A simultaneous recording of the airway pressure curve and aortic
blood flow allowed beat-to-beat measurement of peak velocity (Vpeak)
and determination of maximum Vpeak values (Vpeakmax) and minimum Vpeak
values (Vpeakmin) over a single respiratory cycle. The respiratory
changes in Vpeak (Vpeak) were calculated using a formula similar to
that recently proposed to assess the respiratory changes in pulse
pressure in mechanically ventilated patients with acute lung
injury13
or acute circulatory failure related to
sepsis14
:
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Vpeak was evaluated over each of five consecutive respiratory
cycles. The mean value of the five determinations was used for
statistical analysis.
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Statistical Analysis
Results were expressed as mean ± SD. The effects of volume
expansion on hemodynamic parameters were assessed using a nonparametric
Wilcoxon rank sum test. Patients were divided into two groups according
to the percent increase in cardiac index in response to volume
expansion. Assuming that a 15% change in cardiac index was needed for
clinical significance, patients with a volume expansion-induced
increase in cardiac index of 15% and < 15% were classified as
responders and nonresponders, respectively. The comparison of
hemodynamic parameters prior to volume expansion in responder and
nonresponder patients was performed using a nonparametric Mann-Whitney
test. Linear correlations were tested using the Spearman rank method. A
p value < 0.05 was considered to be statistically significant.
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Results |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Hemodynamic parameters before and after volume expansion are given in
Table 1
. Ten patients were responders (cardiac index increase, 15%) and 9
patients were nonresponders
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Vpeak was higher in responder patients
than in nonresponder patients (20 ± 6% vs 10 ± 3%;
p < 0.001), while EDAI was not significantly different between the
two groups (9.7 ± 3.7 vs 9.7 ± 2.4
cm2/m2). Before volume
expansion, all responders had a Vpeak > 12%, while eight of the
nine nonresponders had a Vpeak 
12% (Fig 2 ). Therefore, the threshold Vpeak value of 12% allowed for
discrimination between responder and nonresponder patients with a
sensitivity of 100% and a specificity of 89%.
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Vpeak
before volume expansion and volume expansion-induced changes in cardiac
index (r2 = 0.83; p < 0.001) such
that the higher the Vpeak before volume expansion, the greater the
increase in cardiac index in response to fluid infusion (Fig 3
). In contrast, baseline EDAI did not correlate significantly with the
volume expansion-induced changes in cardiac index
(r2 = 0.11; p = 0.17) [Fig 3
].
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Vpeak and a
significant increase in EDAI (Table 1)
. The decrease in Vpeak was
significantly correlated with the volume expansion-induced increase in
cardiac index (r2 = 0.45;
p < 0.01), such that the greater the decrease in Vpeak, the
higher the increase in cardiac index. The increase in EDAI was also
significantly correlated with the percent increase in cardiac index
(r2 = 0.49; p < 0.01), such that
the greater the increase in EDAI, the higher the increase in cardiac
index in response to volume expansion. |
Discussion |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Vpeak and the effects of volume expansion on cardiac output. They
strongly suggest that Vpeak before volume expansion is an accurate
indicator of fluid responsiveness while EDAI is of little value in
predicting the effects of volume expansion on cardiac output. Volume expansion is proposed as a first-line therapy for septic shock in order to improve hemodynamics.16 Both the increase in microvascular permeability and venous pooling reduce cardiac preload to such an extent that a large amount of fluid is usually needed during the early phase of resuscitation.16 However, as previously demonstrated5 14 17 and confirmed by the present study, volume expansion does not improve hemodynamics in all patients and, in some patients, may lead to interstitial fluid accumulation, which may worsen gas exchange, decrease myocardial compliance, and limit oxygen diffusion to the tissues.18 Therefore, in patients with septic shock, reliable predictors of a positive response to fluid administration are needed at the bedside. Unfortunately, the prediction of fluid response remains particularly difficult in clinical practice. Indeed, in patients with septic shock who require ventilation, invasive measurements of cardiac filling pressures poorly reflect cardiac preload19 and have been shown to be of little value in predicting volume expansion efficacy.5 14 Transesophageal echocardiography allows a measurement of EDAI, which has been shown to reflect more accurately LV preload when compared with pulmonary artery occlusion pressure.3 In nine anesthetized mongrel dogs, Swenson et al20 reported a significant relationship between baseline EDAI and changes in cardiac index induced by IV fluid therapy, suggesting that EDAI may be an indicator of fluid responsiveness. However, a 1998 study5 performed in 15 patients with sepsis-induced hypotension demonstrated that EDAI was of little value in predicting volume expansion efficacy. Our results are quite consistent with this study since (1) baseline EDAI was not significantly different between responder and nonresponder patients and (2) baseline EDAI was not significantly correlated with the volume expansion-induced increase in cardiac index. These findings could be explained as follows. If the RV operates on the flat portion of the Frank-Starling curve, a beneficial hemodynamic effect of volume expansion cannot be expected, even in the case of low LV preload.21 22 This phenomenon is more likely to occur in patients with septic shock17 23 24 and/or in patients whose lungs are being mechanically ventilated.8 In three patients, we observed a significant RV dilation. These three patients were nonresponders, and in two of them EDAI slightly decreased in response to volume expansion. These findings suggest that RV dysfunction may have limited the effect of volume expansion on cardiac index and emphasize the fact that LV preload measurement is not a useful tool to assess fluid responsiveness in this setting. In patients undergoing repair of abdominal aortic aneurysms, a close relationship was reported between EDAI and LV end-diastolic volume.25 In contrast, in patients following coronary artery bypass grafting, Urbanowicz et al26 found a significant but weak relationship between EDAI and LV end-diastolic volume, demonstrating that EDAI does not provide a reasonable estimate of LV end-diastolic volume in all clinical situations. To our knowledge, the relationship between EDAI and LV end-diastolic volume has not been investigated in patients with septic shock. Since LV end-diastolic volumes were not measured in our patients, the relationship between EDAI and LV end-diastolic volume was not analyzed. Therefore, we cannot definitely exclude that EDAI was a poor indicator of LV end-diastolic volume and, hence, of LV preload in our patients, which may also explain why EDAI was found to be a poor indicator of fluid response in the present study.
In contrast, our results demonstrate that Vpeak accurately predicts
fluid response in patients with septic shock who are receiving
mechanical ventilation. Indeed, a patient with a Vpeak value of
> 12% was very likely to respond to volume expansion by increasing
cardiac index by 15% (positive predictive value, 91%).
Conversely, if Vpeak was 12%, the patient was unlikely to
respond to a fluid challenge (negative predictive value, 100%).
Moreover, the Vpeak before volume expansion closely correlated with
the volume expansion-induced increase in cardiac index, such that the
higher the Vpeak before fluid infusion, the greater the increase in
cardiac index in response to volume expansion (Fig 3) . These findings
are in excellent agreement with recent clinical studies demonstrating
that the respiratory changes in arterial pressure (mainly related to
the respiratory changes in LV stroke volume) accurately predict the
hemodynamic effects of volume expansion in patients receiving
ventilation who have acute lung injury13
or acute
circulatory failure related to sepsis.5
14
They suggest
that an analysis of the Vpeak could be of particular help in the
decision-making process concerning volume expansion in such patients.
Volume expansion induced a significant decrease in the Vpeak in our
patients. This decrease could be explained as follows. First, volume
expansion is assumed to increase RV preload such that the operating
point of the RV moves rightward (ie, toward the flatter
portion of the Frank-Starling curve).11
12
Each
inspiratory decrease in RV preload would, therefore, have a less marked
effect on RV stroke volume after volume expansion than
before.11
12
Second, volume expansion may induce a
recruitment of pulmonary capillaries, leading to a decrease in
West’s zone 227
28
and, hence, to a potential
decrease in RV afterload during insufflation. Through these two
mechanisms, volume expansion 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 volume
expansion-induced rightward shift of the LV operating point, should
result in attenuated changes in LV stroke volume and aortic blood flow
over the respiratory cycle. However, because our study was not designed
to elucidate why the Vpeak decreased with volume expansion, we
cannot determine which mechanism was the most important. Interestingly,
the volume expansion-induced decrease in Vpeak was significantly
correlated with the volume expansion-induced increase in cardiac index.
This finding emphasizes the fact that the Vpeak is strongly related
to cardiac preload.
It must be emphasized that arrhythmias lead to misinterpretation of
respiratory changes in aortic blood flow. Patients with arrhythmias,
therefore, were excluded from the present study. For standardization of
the protocol and to ensure the best conditions for measurements, only
sedated patients were studied by transesophageal echocardiography.
Therefore, further studies are required in which a transthoracic
approach is used and in which nonsedated patients are included in order
to extend the clinical utility of the Vpeak as an indicator of fluid
responsiveness. Moreover, since we studied patients with a fractional
area of contraction of > 30%, our results cannot be extrapolated to
patients with an LV systolic dysfunction. Finally, cardiac output was
not measured by the reference thermodilution technique. However,
transesophageal echocardiographic measurement of ascending aortic flow
velocity has been improved by the use of a multiplane
probe,29
and cardiac output was measured using a
methodology previously validated against the thermodilution technique
in critically ill patients.30
To summarize, our findings suggest that, in contrast with EDAI,
Vpeak is an accurate indicator of fluid responsiveness in sedated
septic shock patients who are receiving mechanical ventilation and who
have preserved LV systolic function. Therefore, an analysis of the
Vpeak could facilitate the hemodynamic management of such patients.
Whether the Vpeak could predict the hemodynamic effects of volume
expansion in other clinical situations remains to be determined.
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Acknowledgements |
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Footnotes |
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Vpeak = respiratory changes in peak velocity; Vpeakmax = maximum
peak velocity; Vpeakmin = minimum peak velocity Received for publication February 24, 2000. Accepted for publication August 2, 2000.
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References |
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