Respiratory Changes in Aortic Blood Velocity as an Indicator of Fluid Responsiveness in Ventilated Patients With Septic Shock

Feissel, M.; Michard, Frédèric; Mangin, I; Ruyer, O.; Faller, J; Teboul, Jean‐Louis

doi:10.1378/chest.119.3.867

Cited by 558 publications

(310 citation statements)

References 24 publications

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“…Volume expansion is not without adverse effects, including pulmonary edema, worsening gas exchange, and hyperchloremic acidosis (1). It has been shown that not all patients in circulatory collapse respond to volume with improved cardiac function (1)(2)(3)(4)(5)(6). Moreover, patients with capillary leak may have total body volume overload and yet still benefit from augmented intravascular volume.…”

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confidence: 99%

Advances in Critical Care for the Nephrologist

Davison

Junker

2008

Clinical Journal of the American Society of Nephrology

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The monitoring of physiologic variables is an integral part of the diagnosis and management of the critically ill patient. Restoration of tissue perfusion and oxygen delivery is the ultimate goal for any state of circulatory collapse. Insight into a patient's intravascular volume status and cardiac performance, particularly in the early stages of shock, can help guide management and potentially change outcome. In the past 30 years, various bedside monitoring techniques and indices have been developed in an effort to determine and optimize a patient's cardiac performance. This article reviews the physiologic parameters that best predict intravascular volume status and volume responsiveness. We examine the controversies surrounding the pulmonary arterial catheter and describe the less invasive methods of measuring cardiac performance.

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mentioning

confidence: 99%

Advances in Critical Care for the Nephrologist

Davison

Junker

2008

Clinical Journal of the American Society of Nephrology

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“…Relying on pulmonary capillary wedge pressure to reflect ventricular volume, Perel et al [ 12 ] and Szold et al [15] showed that pulmonary capillary wedge pressure was related to SPV with both volume loading and phlebotomy in mechanically ventilated dogs. However, filling pressure cannot be used to reflect preload during mechanical ventilation (as is clear in Figure 4) or predict volume responsiveness [31][32][33][34]. Indeed, Denault et al [35] found that changes in systolic arterial pressure reflected changes in airway and intrathoracic pressure better than changes in echocardiographic enddiastolic area measurements in cardiac surgery patients.…”

Section: Discussionmentioning

confidence: 99%

Left Ventricular Preload Determines Systolic Pressure Variation during Mechanical Ventilation in Acute Lung Injury

Mitchell¹,

Doig²,

Whitelaw³

2011

J Clinic Experiment Cardiol

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Although volume is commonly administered to patients with hemodynamic compromise during mechanical ventilation to improve cardiac output, excessive amounts may precipitate or aggravate pulmonary edema, especially in patients with predisposing pulmonary or cardiac conditions. The ability to predict the hemodynamic response to a volume challenge should facilitate patient management and might help to avoid harm in those who are unlikely to benefit from volume loading.Systolic arterial pressure variation (SPV) during mechanical ventilation is more pronounced in hypovolemic than in euvolemic patients [1][2][3]. Cyclical changes in left ventricular (LV) preload during mechanical ventilation and the resultant changes in stroke volume are related to complex cardiopulmonary interactions including changes in external constraint and LV afterload, as well as systemic and pulmonary venous return through series and direct ventricular interaction [4][5][6][7][8][9][10][11]. The magnitude of SPV has been shown to predict responsiveness to a volume challenge [1][2][3][12][13][14][15][16]. One might anticipate that as LV and right ventricular (RV) preload increase during volume loading, changes in intrathoracic pressure would affect ventricular filling (and output) less and thus, SPV would be less. Alternatively stated, at higher filling pressures, the ventricles are on a flatter part of the Starling curve (fiber length cannot be increased further by increasing the filling pressure further). Therefore, a given airway pressure is less likely to reduce fiber length at higher filling pressures than at lower pressures where the Starling curve is steeper.We therefore assessed the relations between LV preload, output and SPV in an oleic acid (OA) induced acute lung injury (ALI) model in which LV filling pressures and positive end-expiratory pressures (PEEP) were systematically varied. We also assessed the potential value of estimated transmural LV end-diastolic pressure [left atrial enddiastolic pressure (P LAED ) -RV end-diastolic pressure (P RVED )], which reflects LV preload, in predicting volume responsiveness in our model. MethodsThis study was approved by the institutional animal care committee whose criteria are consistent with those of the American Physiological Society. Animal preparationIn 8 mongrel dogs of either sex (20-30 kg, mean 24 kg), anesthesia was induced with thiopental sodium (25 mg/kg i.v.) and midazolam (5 mg/ml bolus) and was maintained with fentanyl citrate (0.04 mg/ml i.v., initially, followed by an infusion of 4 mg/h), which was adjusted AbstractBackground: Systolic pressure variation (SPV) predicts responsiveness to volume loading during mechanical ventilation and may be related to changes in LV preload and the resultant changes in stroke volume (SV). We, therefore, tested the relations between LV preload, output and SPV in an acute lung injury (ALI) model during mechanical ventilation.

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“…with a responder variation of 20% [38]. Figure 4 shows clearly the mechanical ventilation induced variations in the aortic Doppler signal.…”

Section: Mechanical Ventilator Induced Intra-thoracic Pressure Changementioning

confidence: 93%

Assessment of loading conditions with cardiac ultrasound. A comprehensive review

Poelaert¹

2015

Anaesthesiol Intensive Ther

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Optimization of the preloading conditions and concomitant determination of endpoints of fluid administration are the most frequent therapeutic actions in critically ill patients. Besides a clinical appraisal, reproducible data should be acquired at the bedside to estimate the adequacy of fluid resuscitation. The dynamic assessment and determination of fluid responsiveness plays a major role in this respect. Right-sided cardiac variables, such as inferior and superior caval vein diameter variation during mechanical ventilation, are easily obtained with cardiac ultrasound. Moreover, left sided variables, including aortic flow variation, with intermittent swings of intrathoracic pressure during mechanical ventilation, may be achieved non-invasively with Doppler-echocardiography. Both in terms of resuscitation, as well as correct interpretation of various two-dimensional and Doppler variables, it is essential to acquire a clear understanding of the filling status of a patient. Doppler-echocardiography plays herein a pivotal role.

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Respiratory Changes in Aortic Blood Velocity as an Indicator of Fluid Responsiveness in Ventilated Patients With Septic Shock

Cited by 558 publications

References 24 publications

Advances in Critical Care for the Nephrologist

Advances in Critical Care for the Nephrologist

Left Ventricular Preload Determines Systolic Pressure Variation during Mechanical Ventilation in Acute Lung Injury

Assessment of loading conditions with cardiac ultrasound. A comprehensive review

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