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Predicting fluid responsiveness in theatre: response from the authors
- Benoit Tavernier, [Hélène Solus-Biguenet], [Maher Fleyfel], [Eric Kipnis], and [Benoit Vallet] (4 January 2007)
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Predicting fluid responsiveness in theatre
- Colin J Runcie (7 December 2006)
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Response from the authors
- Benoit Tavernier, [Hélène Solus-Biguenet], [Maher Fleyfel], [Eric Kipnis], [Benoit Vallet] (10 November 2006)
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Pulse oxymeter waveform to predict fluid responsiveness: how to acquire the good signal?
- Maxime Cannesson, [O Desebbe], [JJ, Lehot] (13 October 2006)
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Benoit Tavernier , [Hélène Solus-Biguenet], [Maher Fleyfel], [Eric Kipnis], and [Benoit Vallet]
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We thank Dr Runcie for his interest in our article [1] and for his additional comments. In his letter, Dr Runcie puts forward the value of the arterial systolic pressure variation (SPV) and its expiratory component (delta down) in assessing fluid responsiveness and regrets that these indices were not measured in our patients. In fact, the main aim of our study was to assess the value of various non-invasive variables for predicting fluid responsiveness in the operating theatre. This evaluation necessitated the selection of a "gold standard" measure and, from the currently available literature, the arterial pulse pressure variation (PPV) is likely the best candidate. The pulse pressure is directly proportional to stroke volume and inversely related to arterial compliance. Therefore, the respiratory variation in left ventricular stroke volume is the main determinant of PPV. In contrast, because the systolic pressure depends on both pulse and diastolic pressures, SPV also depends on changes in extramural aortic pressure, i.e., changes in pleural pressure [2]. Accordingly, several studies have found that (1) PPV predicted haemodynamic response to fluid expansion slightly but significantly better than SPV and delta down [3,4], and (2) PPV correlated more closely with the increase in stroke volume resulting of fluid infusion than both SPV and delta down [5]. A very recent study analyzed the correlation and agreement between PPV, SPV, and delta down (collected from the arterial pressure) and their corresponding photoplethysmographic indices (expressed in %) [6]. Cardiac output was not measured, and thus, fluid responsiveness was not directly assessed. The study however suggested that pulse variation was the only photoplethysmographic indice that may identify patients likely to respond to fluid administration (as assessed from arterial PPV and delta down values). We agree with Dr Runcie that, when using the "wedge pressure" menu of the monitor for quantification of respiratory changes in arterial pressure, as previously proposed by us [7] and others [8], SPV and delta down are obtained more easily and rapidly than PPV. The latter, however, can be measured and calculated in one-two minutes using this procedure, and this is now routinely done by many anaesthetists at our institution. Dr Runcie also claims that a benefit of SPV is that it does not depend on manufacturers' algorithm or their choice of measurement periods. Stroke volume variation (SVV) by pulse contour analysis was indeed shown less precise than PPV or SPV as a predictor of fluid responsiveness [4]. However, this result may depend only on a lack of accuracy for assessment of rapid changes (over a single breath) in stroke volume from the arterial pressure contour, and thus not concern automated calculation of PPV. Moreover, from a strictly evidence-based point of view, the value of PPV, SPV, and delta down as predictors of fluid responsiveness has been established from off-line measurements on computer recordings, not from the "frozen" arterial trace on the monitor screen. We believe that dynamic indices will be widely used by clinicians only when monitors allow automatic calculation and real monitoring (which cannot be done for delta down). These evolutions should be effective in most monitors in the near future. References 1.Solus-Biguenet H, Fleyfel M, Tavernier B, et al. Non-invasive prediction of fluid responsiveness during major hepatic surgery. Br J Anaesth 2006; 97: 808-16. 2.Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology 2005; 103: 419-28 3.Michard F, Boussat S, Chemla D, et al. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med 2000; 162: 134-8. 4.Preisman S, Kogan S, Berkenstadt H, Perel A. Predicting fluid responsiveness in patients undergoing cardiac surgery: functional haemodynamic parameters including the Respiratory Systolic Variation Test and static preload indicators. Br J Anaesth 2005; 95: 746-55. 5.Bendjelid K, Suter PM, Romand JA. The respiratory change in preejection period: A new method to predict fluid responsiveness. J Appl Physiol 2004; 96: 337-42. 6.Natalini G, Rosano A, Franceschetti ME, Facchetti P, Bernardini A. Variations in arterial blood pressure and photoplethysmography during mechanical ventilation. Anesth Analg 2006; 103: 1182-8. 7.Mallat J, Pironkov A, Destandau M, Tavernier B. Systolic pressure variation can guide fluid therapy during pheochromocytoma surgery. Can J Anesth 2003; 50: 998-1003. 8.Gouvea G, Gouvea FG. Measurement of systolic pressure variation on a Datex AS/3 monitor. Anesth Analg 2005; 100: 1864. Conflict of Interest:None declared |
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Colin J Runcie Glasgow, UK
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I read with interest the article by Solus-Biguenet and colleagues (1). They have demonstrated clearly the ability of dynamic tests of the circulation to predict fluid responsiveness intraoperatively and are the first group to do so with a non-invasive dynamic test, namely respiratory variations in non-invasive pulse pressure. They have not however discussed the value of systolic pressure variation (SPV) with respiration and I think this is a problematic omission. In 2003, Tavernier and colleagues found that the Δdown component of SPV could guide fluid therapy during phaechromocytoma surgery (2), illustrating its ability to clarify the mechanism of hypotension following tumour removal. This was the first study to show the value of dynamic tests during haemodynamic instability in theatre. When patients have reached the flat part of their Starling curve they no longer respond to fluids by increasing cardiac output and require other treatments if increased cardiac output is desired. This can be identified rapidly in mechanically ventilated patients by demonstrating minimal SPV and this was clear in Tavernier’s report. The ability of dynamic tests to identify the point at which resuscitation with fluids should stop and be followed by resuscitation with inotropes is a clinically invaluable feature not possessed by other measurement techniques. Other features make SPV the most valuable dynamic test of the circulation. It employs widely available equipment which can be calibrated easily by users using the fast-flush technique to ensure optimal damping (3). Repeated assessments of SPV can be made in theatre or at the bedside by labelling arterial pressure as pulmonary artery pressure and then using the wedge pressure function of the monitor. This has the effect of displaying two mechanical breaths on the screen accompanied by a simultaneous arterial pressure trace. SPV can be easily seen and quantified if desired using a cursor. This technique was described by Tavernier and amplified recently by Gouvea (4). An additional refinement is that pausing mechanical ventilation allows end-expiratory systolic pressure to be measured and Δdown calculated. It is not currently possible to measure pulse pressure variation in real time in theatre; perhaps software updates will change this. Another benefit of SPV is that it does not depend on manufacturers’ algorithms or their choice of measurement periods. The latter has rendered stroke volume variation by pulse contour analysis slightly less precise than pulse pressure or systolic pressure variation as a predictor of fluid responsiveness (5). Insertion of an arterial cannula under local anaesthesia (LA) before induction of general anaesthesia allows the circulatory changes of induction to be observed and treated. SPV subsequently serves as a good predictor of fluid responsiveness, even if there is haemodynamic instability, and can identify when patients with impaired ventricular function have reached the flat part of their Starling curve. The future may lie with observation of non-invasive pulse pressure variation but for the moment arterial cannulation under LA remains the core skill for anaesthetists managing the circulation of mechanically ventilated patients. References: 1. Solus-Biguenet H, Fleyfel M, Tavernier B, et al. Non- invasive prediction of fluid responsiveness during major hepatic surgery. Br J Anaesth 2006; 97: 808-16. 2. Mallat J, Pironkov A, Destandau M, Tavernier B. Systolic pressure variation (Δdown) can guide fluid therapy during pheochromocytoma surgery Can J Anesth 2003; 50: 998-1003. 3. Gardner RM. Direct blood pressure measurement: dynamic response requirements. Anesthesiology 1981; 54: 227-36. 4. Gouvea G, Gouvea FG. Measurement of systolic pressure variation on a Datex AS/3 monitor. Anesth Analg 2005; 100: 1864. 5. Preisman S, Kogan S, Berkenstadt H, Perel A. Predicting fluid responsiveness in patients undergoing cardiac surgery: functional haemodynamic parameters including the Respiratory Systolic Variation Test and static preload indicators. Br J Anaesth 2005; 95:746–55. Conflict of Interest:None declared |
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Benoit Tavernier , [Hélène Solus-Biguenet], [Maher Fleyfel], [Eric Kipnis], [Benoit Vallet]
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We appreciate Dr Cannesson's interest in our recent publication in the British Journal of Anaesthesia (1). While we found that the respiratory variation in the pulse oximeter waveform (quantified by the PPVsat) predicted fluid responsiveness less accurately than either the respiratory variation in radial artery pulse pressure (PPVart) or non- invasive PPV obtained using the Finapres™ device (PPVfina), Dr Cannesson suggests that technical problems in acquiring or processing the signal from the pulse oximeter waveform may be responsible for this lack of reliability. Dr Canesson first states that avoiding the potential influence of the signal processing on the displayed waveform by disengaging the automatic gain incorporated in the pulse oximeter may allow obtaining a stronger relation between PPVsat and PPVart, and postulates that we did not control this limiting factor. This, however, cannot be an explanation for our results, because we actually used a manual gain control in our study. Moreover, a change in gain between two sequences of measurements would not change the value of PPV because PPV is a relative indice (the difference between minimum and maximum pulse waveforms within a respiratory cycle divided by the mean of the two values). This can be easily verified by changing the gain between two successive waveform recordings. In addition, it should be mentioned that auto-centering algorithms, which are not deactivated when automatic gain is disengaged, rather than gain itself, are likely to alter the effects of ventilation on the waveform. Dr Cannesson then insists on the crucial importance of using only one site of measurement, because this has been shown to strongly influence the value of PPVsat (2). Dr Cannesson even states that PPVsat may be more than 10 times stronger in the region of the head when compared with the finger. This is an over-interpretation of the results of Shelley et al. (2) who quantified the amplitude of the power spectrum at the respiratory frequency following spectral analysis of the waveforms, not PPVsat itself, which quantifies only one component of the waveform variations induced by ventilation. Interestingly, the study by Shelley et al. strongly supports the notion that pulse oximetry cannot be recommended to accurately assess the respiratory variation in arterial pressure (2). Nevertheless, it is true that the whole waveform, including the respiratory change in its pulsatile component, and thus PPVsat, may vary in a given patient with the site of measurement. We have anecdotally observed in patients with septic shock, that the effect of ventilation on the pulse oximeter waveform could even be dramatically different between two fingers of the same hand (data not shown). In our study, measurements in a given patient were always performed at the same finger, and never at the ear or forehead location. Dr Cannesson also postulates that, because they are constant throughout a single respiratory cycle, humoral and neurogenic factors should not significantly impact the minimal and maximal waveform amplitudes, and thus PPVsat, during the same respiratory cycle. We agree that this hypothesis may be true, although, at this time, it remains to be demonstrated. In fact, the clinical evidence for this to be true comes from our results obtained not with PPVsat, but with PPVfina, since the Finapres™ device also measures arterial pressure at a distal site and predicted fluid responsiveness as accurately as PPVart. Finally, Dr Cannesson proposes that the pulse oximeter waveform should be used only when perfusion is good enough (as attested by the signal quality index of the monitor), the gain adequately controlled, the site of measurement unique, and the probe wrapped (to prevent outside light from interfering with the signal). In our study, poor signal or perfusion was explicitly recognized as a potential limitation of both PPVfina and PPVsat. Measurements were performed throughout major surgery, and reduced finger perfusion may in part account for the lack of agreement between PPVsat and PPVart. We feel that one of the most interesting results in our study was precisely that, in similar experimental conditions (of peripheral perfusion, temperature, light exposure…), PPVfina was a better predictor than PPVsat. These conditions are indeed different of those advocated by Dr Cannesson, but likely represent "real life", when anaesthetists wonder whether fluids should be given to their patient in the operative room. We agree with Dr Canesson that PPVsat, in these conditions, may be of some value and, accordingly, our study showed that PPVsat was a better predictor than the classical static pressure measurements. Nevertheless, in accordance with other reports (2,3), our results also suggest that PPVsat should be used with caution in this indication. From a theoretical point of view, it is conceivable that modifications in device algorithms may allow commercial pulse oximeters to provide results similar to those obtained with the Finapres™, but this evolution still belongs to the future. References: 1. Solus-Biguenet H, Fleyfel M, Tavernier B, Kipnis E, Onimus J, Robin E, et al. Non-invasive prediction of fluid responsiveness during major hepatic surgery. Br J Anaesth 2006. doi:10.1093/bja/ael250 2. Shelley KH, Jablonka DH, Awad AA, et al. What is the best site for measuring the effect of ventilation on the pulse oximeter waveform? Anesth Analg 2006;103:372-7. 3. Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology 2005;103:419-28. Conflict of Interest:None declared |
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Maxime Cannesson, Assistant Professor Hospices Civils de Lyon, Hôpital Louis Pradel, Anesthesiology Unit, [O Desebbe], [JJ, Lehot]
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We read with great interest the study by Solus-Biguenet et al.(1) regarding the evaluation of fluid responsiveness using non-invasive predictors during major hepatic surgery. The authors compared the value of several indices of fluid responsiveness and concluded that the respiratory variations in arterial pulse pressure obtained from the invasive (PPVart) and Finapress™ (PPVfina) arterial pressure curves were the most accurate predictors of response to volume expansion. Moreover, they concluded that respiratory variations in the pulse oximetry waveform (PPVsat) were greater in responders than in non-responders to volume expansion even if the predictive value of this parameter was weaker than PPVart and PPVfina. These results are extremely interesting since pulse oxymeters are non invasive, unexpensive, and are daily used in the operating room. Thus, the results from this study suggest that PPVsat may be a useful predictor of fluid responsiveness in the operating room. However, in our opinion, technical description regarding the way the pulse oximetry waveform was acquired in this study is not clear enough to sustain the hypothesis that PPVsat is a weaker predictor of fluid responsiveness than PPVart and PPVfina: 1) As Solus-Biguenet et al. claimed in their discussion: “proprietary software included in pulse oximeters are designed to provide a graphic display for pulse oximetry monitoring[…]. The software generates a signal that is substantially filtered, amplified and smoothed before display.” However, some data acquisition softwares allow disengaging the automatic gain incorporated in the pulse oxymeter in order to avoid the potential influence of the signal processing on the displayed waveform. Using this technique, PPVsat has been shown to be strongly related to PPVart with far lower limits of agreement than those described in the present study(2, 3). We can postulate that Solus-Biguenet et al. did not control this limiting factor since no mention is made concerning the gain and since agreement between PPVart and PPVsat was lower than those previously reported. 2) As some recently published studies are suggesting, PPVsat is strongly influenced by the site of measurements (ear, finger, forhead)(4). Consequently, it is of major importance to mention the site of measurement and to consistently use the same site between patients. PPVsat may be more than 10 times stronger in the region of the head when compared with the finger. Mixing the sites may induce an important bias. Solus-Biguenet et al. do not mention the site of measurements for each of the eight studied patients. 3) The authors postulate that the sensitivity of the plethysmographic signal to humoral and neurogenic factors may explain the poor predictive value of PPVsat. However, we can postulate that these potentially confounding factors are constant throughout a single respiratory cycle and that they do not impact the minimal and maximal pulse oxymeter waveform amplitudes during the same respiratory cycle. On the other hand, peripheral vasoconstriction may alter the pulse oxymeter signal quality. Most of the monitors display a signal quality index or a perfusion index providing informations regarding the quality of the curve. These data should have been controlled before pulse oxymeter waveform recording and analysis in order to avoid confounding factors related to poor signal quality. 4) Pulse oxymeter waveform is influenced by outside light absorption. Thus, the pulse oxymeter should be wrapped in order to prevent outside light from interfering with the signal. This is not mentioned in this study. In conclusion, pulse oximetry waveform has been shown to be strongly related to respiratory cycles in previously published studies(5). These variations have been shown to be related to PPVart(2, 3) and to loading conditions(3, 6). However, this waveform depends on signal processing, site of measurement, peripheral vasoconstriction, and outside light absorption. The study by Solus-Biguenet et al.(1) shows promising results regarding the ability of PPVsat to predict fluid responsiveness. We can postulate that further studies without automatic gain control, standardized site of measurements, and adequate signal quality index and recording will improve the predictive value of this new index. References 1. Solus-Biguenet H, Fleyfel M, Tavernier B, Kipnis E, Onimus J, Robin E, et al. Non-invasive prediction of fluid responsiveness during major hepatic surgery{dagger}. Br J Anaesth 2006. 2. Cannesson M, Besnard C, Durand PG, et al. Relation between respiratory variations in pulse oximetry plethysmographic waveform amplitude and arterial pulse pressure in ventilated patients. Crit Care 2005;9:R562-8. 3. Cannesson M, Desebbe O, Hachemi M, et al. Respiratory variations in pulse oxymeter waveform amplitude is influenced by venous return in mechanically ventilated patients under general anaesthesia. Eur J Anaesthesiol 2006 (In Press). 4. Shelley KH, Jablonka DH, Awad AA, et al. What is the best site for measuring the effect of ventilation on the pulse oximeter waveform? Anesth Analg 2006;103:372-7. 5. Shelley KH, Awad AA, Stout RG, Silverman DG. The use of joint time frequency analysis to quantify the effect of ventilation on the pulse oximeter waveform. J Clin Monit Comput 2006;20:81-7. 6. Shamir M, Eidelman LA, Floman Y, Kaplan L, Pizov R. Pulse oximetry plethysmographic waveform during changes in blood volume. Br J Anaesth 1999;82:178-81. Conflict of Interest:None declared |
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