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Relation between global end-diastolic volume and left ventricular end-diastolic volume

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of spontaneously breathing patients. An important aspect of the suggested approach is its simplicity, requiring basic technical skills and making it suitable in any scenario where an ultrasound machine is available.

References

1. Dellinger RP, et al. Intensive Care Med. 2013;39:165-228. 2. Cook DJ. Am J Med Sci. 1990;299:175-8.

3. Donahue SP, et al. Am J Emerg Med. 2009;27:851-5. 4. Beigel R, et al. J Am Soc Echocardiogr. 2013;26:1033-42. 5. Rudski LG, et al. J Am Soc Echocardiogr. 2010;23:685-713. P172

Do intravascular hypovolaemia and hypervolaemia result in changes in pulmonary blood volume?

JJ Vos1, TW Scheeren1, SA Loer2, A Hoeft3, JK Wietasch1 1University of Groningen, University Medical Center Groningen, the

Netherlands; 2Institute for Cardiovascular Research, VU University Medical

Centre, Amsterdam, the Netherlands; 3University of Bonn, Germany

Critical Care 2015, 19(Suppl 1):P172 (doi: 10.1186/cc14252)

Introduction Hypovolaemia is generally believed to induce centrali sa-tion of blood volume. Therefore, we evaluated whether hypovolaemia and hypervolaemia result in a change in central blood volume (that is, pulmonary blood volume (PBV)) and we explored the eff ects on the distribution between PBV and circulating blood volume (Vd circ). Methods After local District Governmental Animal Investigation Committee approval, blood volume was altered in both directions randomly in steps of 150  ml (mild) to 450  ml (moderate) either by haemorrhage, retransfusion of blood, or infusion of colloids in six Foxhound dogs. The anaesthetised dogs were allowed to breathe spontaneously. Blood volumes were measured using the dye dilution technique: PBV was measured as the volume of blood between the pulmonary and aortic valve, and Vd circ by two-compartmental curve fi tting [1,2]. The PBV/Vd circ ratio was used as a measure of blood volume distribution. A linear mixed model was used for analysing the infl uence of blood volume alterations on the measured haemodynamic variables and blood volumes.

Results A total of 68 alterations in blood volume resulted in changes in Vd circ ranging from –33 to +31% (Figure 1). PBV decreased during mild and moderate haemorrhage, while during retransfusion PBV increased during moderate hypervolaemia only. The PBV/Vd circ ratio remained constant during all stages of hypovolaemia and hypervolaemia (Figure 1).

Conclusion Mild to moderate alterations of blood volume result in changes of PBV and Vd circ. However, against the traditional belief of centralisation we could show that the cardiovascular system preserves the distribution of blood between central and circulating blood volume in anaesthetised dogs.

References

1. Anesthesiology. 1994;81:76-86. 2. Intensive Care Med. 2001;27:767-74.

P174

Comparative study between fl uidless resuscitation with permissive hypotension using the impedance threshold device versus aggressive fl uid resuscitation with Ringer lactate in a swine model of hemorrhagic shock

C Pantazopoulos1, I Floros1, N Archontoulis1, D Xanthis1, D Barouxis2,

N Iacovidou2, T Xanthos2

1Laiko General Hospital of Athens, Greece; 2University of Athens, Medical

School, Athens, Greece

Critical Care 2015, 19(Suppl 1):P174 (doi: 10.1186/cc14254)

Introduction Permissive hypotension, which results in avoidance of intravascular overpressure and thereby avoidance of platelet plug dislodgement early in the clotting mechanism, improves the results after trauma and hemorrhage. The research hypothesis is that augmentation of negative intrathoracic pressure with the use of an impedance threshold device (ITD) will improve hemodynamic parameters, without aff ecting permissive hypotension or causing hemodilution. On the other hand, aggressive resuscitation with Ringer lactate will cause hemodilution and intravascular pressures that are very high for permissive hypotension, capable of platelet plug dislodgement.

Methods Twenty anesthetized Landrace/Large-White pigs (19 ± 2 kg, 10 to 15 weeks) were subjected to a fi xed hemorrhage (50% over 30 minutes). The pigs were randomly allocated into two groups (n = 10 per group). In group A, ITD was the only treatment for hypotension, while in group B, an intravenous administration of 1 l Ringer lactate was applied for treatment of hypotension. Hemodynamic parameters were continuously assessed for the fi rst 30 minutes after blood loss. Results Mean systolic arterial pressures (SAPs) 30  minutes after the intervention in each group were as follows: group A 80 ± 5 mmHg and group B 90 ± 4 mmHg. Maximum SAPs during the assessment period were: group A 89 ± 2 mmHg and group B 128 ± 5 mmHg. Mean pulse pressure was higher in the ITD group versus the fl uid resuscitation group (P  <0.05). After the assessment period, mean hematocrit in group A was 24 ± 2%, while in group B it was 18 ± 1% (P <0.001). Conclusion In our study, the ITD increased SAP and pulse pressure without overcompensation. On the other hand, aggressive fl uid resuscitation led to a signifi cant increase of SAP >100 mmHg capable of clot dislodgement and in addition led to hemodilution.

P175

Relation between global end-diastolic volume and left ventricular end-diastolic volume

A Pironet1, P Morimont1, S Kamoi2, N Janssen1, PC Dauby1, JG Chase2,

B Lambermont1, T Desaive1

1University of Liège, Belgium; 2University of Canterbury, Christchurch, New Zealand

Critical Care 2015, 19(Suppl 1):P175 (doi: 10.1186/cc14255)

Introduction Measurement of global end-diastolic volume (GEDV) is provided by cardiovascular monitoring devices using thermodilution procedures. The aim of this study was to assess the relation between this clinically available index and left ventricular end-diastolic volume (LVEDV), which is typically not available at the patient bedside. Methods Measurements were performed on six anaesthetised and mechanically ventilated pigs. Volume loading via successive infusions of saline solution was fi rst performed and was followed by dobutamine infusion. These two procedures provided a wide range of LVEDV values. During these experiments, GEDV was intermittently measured using the PiCCO monitor (Pulsion AG, Germany) during thermodilutions and LVEDV was continuously measured using an admittance catheter (Transonic, NY, USA) inserted in the left ventricle.

Results Table  1 presents the linear correlations obtained between LVEDV and GEDV. These correlations are good to excellent, with r2 values from 0.59 to 0.85. However, the coeffi cients of the linear

regressions present a large intersubject variability, which prevents the precise estimation of LVEDV using GEDV. Nevertheless, variations in LVEDV are well reproduced by the GEDV index. The variations in LVEDV actually equal 21 to 48% of those in GEDV. The coeffi cient b is always nonzero, indicating that some proportion of the GEDV index is actually not linked to LVEDV.

Figure 1 (abstract P172).

Critical Care 2015, Volume 19 Suppl 1 http://ccforum.com/supplements/19/S1

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Table 1 (abstract P175). Linear regressions between LVEDV and GEDV Subject a b (ml) r2 1 0.26 7.64 0.82 2 0.43 –47.10 0.66 3 0.21 –12.99 0.75 4 0.25 –11.42 0.59 5 0.41 –65.42 0.85 6 0.48 –65.75 0.68 LVEDV = a × GEDV + b.

Conclusion The results show that GEDV and LVEDV are generally well correlated, but the correlation coeffi cients are subject specifi c. A preliminary calibration step (for instance using echocardiography) is thus necessary to infer LVEDV from GEDV.

P176

Volume assessment in critically ill patients: echocardiography, bioreactance and pulse contour thermodilution

S Hutchings1, P Hopkins1, A Campanile2

1King’s College Hospital, London, UK; 2Papworth Hospital, Cambridge, UK

Critical Care 2015, 19(Suppl 1):P176 (doi: 10.1186/cc14256)

Introduction We performed an evaluation of three devices used for assessment of volume status in critically ill patients in our institution: transthoracic echocardiography (TTE) (CX50; Philips Ultrasound), bio reactance (NICOM; Cheetah Medical) and pulse contour-based thermodilution (PiCCO; Pulsion Medical).

Methods Ten mechanically ventilated critically ill patients with PiCCO monitoring in situ and a good quality of images on transthoracic view were included. All study measurements were made in triplicate. A single trained cardiologist, blinded to the results from the other monitors, performed the TTE study. Diff erences among the three methods were assessed for signifi cance using one-way ANOVA, Spearman’s coeffi cient and Bland–Altman analysis. All statistical analyses were performed using Graph-pad Prism 5 and P <0.05 was taken as signifi cant. Results Ninety measurements were obtained. NICOM and TTE-derived stroke volume appeared well matched but PICCO-derived values showed signifi cant variation (F = 2.4, P = 0.09). There was no correlation between TTE velocity time integer (VTI) and NICOM stroke volume variation (SVV) (r  = 0.24, P  =  0.20; Figure  1A) but a good correlation and small bias between TTE-VTI and PiCCO-SVV (r  = 0.76, P <0.0001; Figure  1B). Applying the following indications for volume expansion (PiCCO and NICOM SVV >15% and TTE VTI variability >15%) we found an agreement in 71% of cases between TTE and PiCCO and in 42% of cases between echocardiography and NICOM.

Conclusion Stroke volume produced by bioreactance appeared to be comparable with that measured by echocardiography but not with PiCCO. There was a good agreement between decision-making as

regards fl uid administration between PiCCO and echocardiography. NICOM appeared unreliable in this setting.

P177

Bioreactance-based passive leg raising test can predict fl uid responsiveness in patients with sepsis

C Hu1, H Tong1, G Cai1, J Teboul2, J Yan1, X Lv1, Q Xu1, J Chen1, Q Rao1,

M Yan1

1Zhejiang Hospital, Hangzhou, China; 2Bicetre Hospital – University

Paris-South, Paris, France

Critical Care 2015, 19(Suppl 1):P177 (doi: 10.1186/cc14257)

Introduction Fluid administration is always important and diffi cult during the therapy of patients with sepsis. Accurately predicting fl uid responsiveness and thus estimating whether the patient will benefi t from fl uid therapy seems particularly important. The present study intended to predict fl uid responsiveness in patients with sepsis using a bioreactance-based passive leg raising test, and to compare this approach with the commonly used central venous pressure (CVP) approach.

Methods This prospective, single-center study included 80 patients with sepsis from the Department of Critical Care Medicine of Zhejiang Hospital. Patients were randomly assigned to either Group A or Group B, with patients of in Group A fi rst taking the passive leg raising test and then taking the fl uid infusion test, while patients in Group B followed the opposite protocol. NICOM was used to continuously record hemodynamic parameters such as cardiac output (CO), heart rate (HR) and central venous pressure (CVP), at baseline1, PLR, baseline2, and volume expansion (VE). Fluid responsiveness was defi ned as the change in CO (ΔCO) ≥10% after VE.

Results CO increased during PLR (from 5.21  ±  2.34 to 6.03  ±  2.73 l/ minute, P <0.05); and after VE (from 5.09 ± 1.99 to 5.60 ± 2.11 l/minute, P <0.05). The PLR-induced change in CO (ΔCOPLR) and the VE-induced change in CO (ΔCOVE) were highly correlated (r = 0.80 (0.64 to 0.90)), while the CVP and ΔCOVE were uncorrelated (r = 0.12 (–0.16 to 0.32)). The areas under the ROC curves of ΔCOPLR and ΔCVP for predicting fl uid responsiveness were 0.868 and 0.514 respectively. ΔCOPLR ≥10% was found to predict fl uid responsiveness with a sensitivity of 86% and a specifi city of 79%.

Conclusion Bioreactance-based PLR could predict fl uid responsiveness in patients with sepsis, while CVP could not.

References

1. De Backer D. Can passive leg raising be used to guide fl uid administration? Crit Care. 2006;10:170.

2. Pinsky MR. Functional haemodynamic monitoring. Curr Opin Crit Care. 2014;20:288-93.

3. Teboul JL, Monnet X. Pulse pressure variation and ARDS. Minerva Anestesiol. 2013;79:398-407.

4. Monnet X, Teboul JL. Volume responsiveness. Curr Opin Crit Care. 2007;13:549-53.

Figure 1 (abstract P176).

Critical Care 2015, Volume 19 Suppl 1 http://ccforum.com/supplements/19/S1

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