Biais, Matthieu M.D.*; Ouattara, Alexandre M.D., Ph.D.; Janvier, Gérard M.D., Ph.D.; Sztark, FranÇois M.D., Ph.D.
The authors sincerely thank Dr. Roth for his letter regarding their recent article1
and are happy to respond to his comments and anecdotes.
The problematic of chest wall compliance is of interest and is not new. In 1989, Pizov et al
demonstrated in a canine model that reducing chest wall compliance by external chest compression induced an increase in the deltadown component of the systolic pressure variation, suggesting a decrease in the venous return. More recently, Mesquida et al
found an increase in pulse pressure variations and stroke volume variations after reduction in chest wall compliance induced by chest and abdominal binders in an experimental study. As suggested by Dr. Roth, decrease in chest wall compliance may be due to truncal rigidity. This situation may be related to a lack of sedation (which contraindicates the use of dynamic indices) or may be provoked by high doses of opioids (an uncommon practice actually even in cardiac surgery). In contrast, a decrease in chest wall compliance secondary to abdominal hypertension is a common situation in an operating room (laparoscopy) or an intensive care unit. As highlighted in the article, abdominal hypertension may lead to an increase in pulse pressure variations in this setting.1
To our knowledge, the ability of dynamic index to predict fluid responsiveness in the specific obese population has not yet been tested. The possible impact of obesity should be more complex than stated by Dr. Roth. Indeed, a direct effect of the fat distribution in obese patients is a reduction in the respiratory system compliance due to the reduction in lung and chest wall compliance.4
As mentioned previously, decrease in chest wall compliance will induce an increase in pulse pressure variations. In contrast, during decreased lung compliance, airway pressure transmission is reduced such that the cyclic changes in intrathoracic pressure could be attenuated even in case of marked changes in alveolar pressure.6
Thus, Monnet et al
recently demonstrated that the predictive value of pulse pressure variations is related to lung compliance. The clinical impact of these hypothetic mechanisms, which is probably low, except for morbid obese patients, remains to be demonstrated.
We do not agree with Dr. Roth when he claims that administering neuromuscular blockade may result in a lower volume infusion. This affirmation is not supported by any publication. The impact of neuromuscular blockade administered in anesthetized patients without pathological decrease in chest wall compliance on dynamic index has never been demonstrated. Furthermore, most of the patients included in validation studies of dynamic index in intensive care unit were not paralyzed.8
On the contrary, we totally agree with Dr. Roth that stroke volume variations and its surrogates should not be the endpoint of therapy. As clearly mentioned in the article, the dynamic index must be considered as useful tools to predict an increase in stroke volume after volume expansion. But they clearly cannot help to answer the following question: Does my patient need an increase in stroke volume?
Matthieu Biais, M.D., * Alexandre Ouattara, M.D., Ph.D., Gérard Janvier, M.D., Ph.D., FranÇois Sztark, M.D., Ph.D.
, *Hospital Pellegrin, CHU de Bordeaux, and Université Bordeaux, Adaptation cardiovasculaire à l’ischémie, Bordeaux, France. matthieu.biais@chu-bordeaux
1. Biais M, Ouattara A, Janvier G, Sztark F. Case scenario: Respiratory variations in arterial pressure for guiding fluid management in mechanically ventilated patients. ANESTHESIOLOGY. 2012;116:1354–61
2. Pizov R, Ya’ari Y, Perel A. The arterial pressure waveform during acute ventricular failure and synchronized external chest compression. Anesth Analg. 1989;68:150–6
3. Mesquida J, Kim HK, Pinsky MR. Effect of tidal volume, intrathoracic pressure, and cardiac contractility on variations in pulse pressure, stroke volume, and intrathoracic blood volume. Intensive Care Med. 2011;37:1672–9
4. Eriksen J, Andersen J, Rasmussen JP, Sørensen B. Effects of ventilation with large tidal volumes or positive end-expiratory pressure on cardiorespiratory function in anesthetized obese patients. Acta Anaesthesiol Scand. 1978;22:241–8
5. Zerah F, Harf A, Perlemuter L, Lorino H, Lorino AM, Atlan G. Effects of obesity on respiratory resistance. Chest. 1993;103:1470–6
6. Teboul JL, Pinsky MR, Mercat A, Anguel N, Bernardin G, Achard JM, Boulain T, Richard C. Estimating cardiac filling pressure in mechanically ventilated patients with hyperinflation. Crit Care Med. 2000;28:3631–6
7. Monnet X, Bleibtreu A, Ferré A, Dres M, Gharbi R, Richard C, Teboul JL. Passive leg-raising and end-expiratory occlusion tests perform better than pulse pressure variation in patients with low respiratory system compliance. Crit Care Med. 2012;40:152–7
8. Marik PE, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: A systematic review of the literature. Crit Care Med. 2009;37:2642–7
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