Fluid Responsiveness In Ventilated Patients Research Articles

Can carotid artery Doppler variations induced by the end-expiratory occlusion maneuver predict fluid responsiveness in septic shock patients?

BackgroundAn increase in cardiac index (CI) during an end-expiratory occlusion test (EEOt) predicts fluid responsiveness in ventilated patients. However, if CI monitoring is unavailable or the echocardiographic window is difficult, using the carotid Doppler (CD) could be a feasible alternative to track CI changes. This study investigates whether changes in CD peak velocity (CDPV) and corrected flow time (cFT) during an EEOt were correlated with CI changes and if CDPV and cFT changes predicted fluid responsiveness in patients with septic shock.MethodsProspective, single-center study in adults with hemodynamic instability. The CDPV and cFT on carotid artery Doppler and hemodynamic variables from the pulse contour analysis EV1000™ were recorded at baseline, during a 20-s EEOt, and after fluid challenge (500 mL). We defined responders as those who increased CI ≥ 15% after a fluid challenge.ResultsWe performed 44 measurements in 18 mechanically ventilated patients with septic shock and without arrhythmias. The fluid responsiveness rate was 43.2%. The changes in CDPV were significantly correlated with changes in CI during EEOt (r = 0.51 [0.26–0.71]). A significant, albeit lower correlation, was found for cFT (r = 0.35 [0.1–0.58]). An increase in CI ≥ 5.35% during EEOt predicted fluid responsiveness with 78.9% sensitivity and 91.7% specificity, with an area under the ROC curve (AUROC) of 0.85. An increase in CDPV ≥ 10.5% during an EEOt predicted fluid responsiveness with 96.2% specificity and 53.0% sensitivity with an AUROC of 0.74. Sixty-one percent of CDPV measurements (from − 13.5 to 9.5 cm/s) fell within the gray zone. The cFT changes during EEOt did not accurately predict fluid responsiveness.ConclusionsIn septic shock patients without arrhythmias, an increase in CDPV greater than 10.5% during a 20-s EEOt predicted fluid responsiveness with > 95% specificity. Carotid Doppler combined with EEOt may help optimize preload when invasive hemodynamic monitoring is unavailable. However, the 61% gray zone is a major limitation (retrospectively registered on Clinicaltrials.gov NCT04470856 on July 14, 2020).

Prediction of fluid responsiveness in ventilated patients.

Fluid administration is the first-line therapy in patients with acute circulatory failure. The main goal of fluid administration is to increase the cardiac output and ultimately the oxygen delivery. Nevertheless, the decision to administer fluids or not should be carefully considered, since half of critically ill patients are fluid unresponsive, and the deleterious effects of fluid overload clearly documented. Thus, except at the initial phase of hypovolemic or septic shock, where hypovolemia is constant and most of the patients responsive to the initial fluid resuscitation, it is of importance to test fluid responsiveness before administering fluids in critically ill patients. The static markers of cardiac preload cannot reliably predict fluid responsiveness, although they have been used for decades. To address this issue, some dynamic tests have been developed over the past years. All these tests consist in measuring the changes in cardiac output in response to the transient changes in cardiac preload that they induced. Most of these tests are based on the heart-lung interactions. The pulse pressure or stroke volume respiratory variations were first described, following by the respiratory variations of the vena cava diameter or of the internal jugular vein diameter. Nevertheless, all these tests are reliable only under strict conditions limiting their use in many clinical situations. Other tests such as passive leg raising or end-expiratory occlusion act as an internal volume challenge. To reliably predict fluid responsiveness, physicians must choose among these different dynamic tests, depending on their respective limitations and on the cardiac output monitoring technique which is used. In this review, we will summarize the most recent findings regarding the prediction of fluid responsiveness in ventilated patients.

Is internal jugular vein extensibility associated with indices of fluid responsiveness in ventilated patients?

Ultrasound of the inferior vena cava provides rapid and non-invasive assessment of fluid responsiveness. We hypothesized that the extensibility of the internal jugular vein (IJV) as well reflects intravascular volume state. We assessed IJV dimensions together with pulse pressure variation (PPV) as dynamic index for fluid responsiveness in mechanically ventilated patients. Of 50 patients after cardiac surgery were assessed. Ultrasound of IJV dimensions as well as collection of hemodynamic data were performed in 30° and horizontal (0°) position, and the ventilator- and position-induced IJV extensibilities (E-IJV) were calculated. Mean ventilator-induced E-IJV in 30° position was 56%, and mean PPV in 30° position was 13.7%. Changing the patient's position from 30° to 0° significantly reduced ventilator-induced E-IJV as well as PPV. Pearson's correlation test revealed significant association between ventilator-induced E-IJV and fluid responsiveness deduced from PPV in 0° position (r = 0.43, P < 0.005). An E-IJV threshold >5% identified patients with significantly elevated PPV values. Ultrasound of the IJV and PPV as a dynamic index for fluid responsiveness can be associated under certain defined conditions. Whether or not ultrasound of the IJV can be useful to predict patient intravascular volume state should be further studied using invasive cardiac output monitoring.

Inferior vena cava distensibility index predicting fluid responsiveness in ventilated patients

Echocardiography is a non-invasive procedure which enables full assesment of cardiac function. The inferior vena cava (IVC) is a compliant blood vessel, easily distended, especially in cases of hypovolemia. Assessment of the physiologic characteristics of the IVC provides a rapid distinction between low and high volume states and offers the clinician a rapid, noninvasive way to guide resuscitation in critically ill patients.

Plethysmographic variation index predicts fluid responsiveness in ventilated patients in the early phase of septic shock in the emergency department: A pilot study

PurposeFeasibility study examining whether plethysmographic variability index (PVI) can predict fluid responsiveness in mechanically ventilated patients in the early phase of septic shock in the emergency department. Materials and MethodsMonocentric, prospective, observational study that included 31 mechanically ventilated and sedated patients with septic shock in whom volume expansion was planned. The patients were equipped with a pulse oximeter that automatically calculated and displayed PVI. The intervention consisted in infusing 8 mL/kg of hydroxylethyl starch over a 20-minute period. Before and after intervention, we recorded PVI and measured the aortic velocity-time integral (VTIao) using transthoracic echocardiography. Responders were defined as patients who increased their VTIao by 15% or higher after fluid infusion. ResultsSixteen patients were classified as responders, and 15 as nonresponders. Mean PVI values before intervention were significantly higher in responders vs nonresponders (30% ± 9% vs 8% ± 5%, P < .001). Plethysmographic variability index values before intervention were correlated with percent changes in VTIao induced by intervention (R2 = 0.67; P < .001). A PVI threshold value of 19% discriminates responders from nonresponders with a sensitivity of 94% and a specificity of 87% (area under the curve, 0.97; P < .001). ConclusionOur study suggests that PVI is a feasible and interesting method to predict fluid responsiveness in early phase septic shock patients in the emergency department.

Respiratory pulse oximetry plethysmographic waveform amplitude correlates with arterial pulse pressure variations

Arterial pulse pressure (PP) respiratory variation is a good predictor of fluid responsiveness in ventilated patients. Recently, it has been shown that variation in PP may correlate with variation in pulse oximetry plethysmographic (POP) waveform amplitude, as they both depend on the stroke volume. We designed a prospective study to evaluate the correlation between respiratory arterial PP variation and POP waveform amplitude variations in ventilated patients and the influence of acute lung injury (ALI) in this relationship.

Pulse pressure and stroke volume variations during severe haemorrhage in ventilated dogs

Similarly to systolic pressure variation (SPV), pulse pressure variation (PPV) and stroke volume variation (SVV) derived from arterial pulse contour analysis have been shown to reflect fluid responsiveness in ventilated patients. However, unlike the SPV, both PPV and SVV have not been validated during extreme hypovolaemia. The aim of the present study was to examine whether these newly introduced variables respond to gradual hypovolaemia like the SPV by increasing gradually with each step of the haemorrhage even during extreme hypovolaemia. SPV, SVV and PPV were measured in 8 dogs following initial volume loading (10% of the estimated blood volume administered as colloid solution), 5 steps of graded haemorrhage, each consisting of 10% of the estimated blood volume, followed by retransfusion of the shed blood. The correlations of the SVV, SPV and PPV to the stroke volume (SV) throughout the study were -0.89, -0.91 and -0.91, respectively. Correlations of the CVP and the global end-diastolic volume (GEDV) of the heart chambers to the SV were 0.79 and 0.95, respectively. The SPV correlated significantly with both the PPV and the SVV (r=0.97 and 0.93 respectively). However, the PPV increased by more than 400% at 50% haemorrhage compared with increases of 200% and 120% for the SVV and %SPV, respectively. This study demonstrates that the present algorithm used for the calculation of the SVV and the formula used to calculate the PPV, perform well over a wide range of preload states including severe hypovolaemia. However, the PPV changes more than the SPV and SVV. This may be due to the changing relation of the SV to the pulse pressure when the filling of the aorta is greatly decreased.