Introduction
Perioperative fluid management influences patients’ outcomes. It is a controversial and challenging issue in the anaesthesia setting. Both overhydration and conservative fluid therapy can lead to perioperative complications. The problem facing anaesthesiologists is that we do not know the volume needed by the patient. Goal-directed therapy sheds light on this debate, demonstrating that its use reduces postoperative complications and hospital stay.1–3
In the immediate postoperative period, signs of low cardiac output (CO) such as oliguria, tachycardia or arterial hypotension are frequent. However, these signs could be secondary to other factors. There could also be patients with real hypovolaemia but their ventricles operate at the non-responder point of the Frank–Starling curve. Is it possible to know if our patient will respond to fluids without administration, avoiding the negative consequences of excessive volume? A simple, non-invasive manoeuvre to predict response to volume in postoperative patients is passive leg raising (PLR). Raising the patient from a semi-recumbent position to a position with the head at 0° and the legs raised to a 45° angle, it is possible to increase venous return, mobilising blood from the lower limbs and splanchnic territory to the central compartment.
PLR has been demonstrated to produce changes in pre-load, increasing stroke volume (SV) significantly in patients who meet at the responder part of the ventricular function curve of Frank–Starling. Likewise, this is considered a reversible filling volume test as its effect on SV disappears after the patient returns to the supine position.4
Studies validating PLR have been carried out mostly on critical, non-surgical patients and less frequently in a postoperative population.5,6 7,8
Methods
Ethical approval for this study (Ethical Committee no. NAC 140155) was provided by the Ethical Committee NAC of Hospital Universitario de Gran Canaria Dr Negrín, Las Palmas de Gran Canaria, Spain (Chairperson Prof P. Lara) on 1 August 2014. We carried out a prospective observational study in an 18-bed post-anaesthesia care unit (PACU) between January and July 2015. After obtaining their informed consent, patients in whom low CO was suspected in the immediate postoperative period (general, vascular or orthopaedic surgery) were included. The following clinical signs were selected: arterial hypotension, systolic arterial pressure below 90 mmHg, mean arterial pressure (MAP) less than 70 mmHg or blood pressure (BP) decreased by more than 40 mmHg compared with usual BP; oliguria, urine output less than 0.5 ml kg−1 h−1 for more than 2 consecutive hours; tachycardia, heart rate (HR) higher than 100 bpm; delayed capillary refill, longer than 3 s.
Patients with aortic valvulopathy (known or discovered during the study) and mitral valvulopathy (mitral insufficiency greater than grade II or mitral stenosis) were not included, as well as patients who had undergone intracranial surgery, patients with any contra-indication to PLR manoeuvres (hip replacement or deep venous thrombosis), clinical signs of haemorrhage and patients with severe pain [visual analogue scale (VAS) > 3)]. We excluded patients with unsatisfactory cardiac echogenicity, such as poor echocardiographic window or misalignment between the Doppler and the outflow tract of the left ventricle (LV).
Data collected at the beginning were age, sex , American Society of Anesthesiologists’ physical status, weight and height, to calculate BSA. The presence of arterial hypertension, diabetes mellitus, coronary arterial disease, chronic obstructive pulmonary disease and atrial fibrillation were recorded, as were the types of anaesthesia and surgery, postoperative analgesia, Ramsay sedation scale and VAS. The presence or absence of motor block in the lower limbs was also registered.
During the study, the following variables were collected: haemodynamic parameters, HR and MAP; echocardiographic parameters, LV outflow tract diameter (LVOTd), maximum velocity originated in the LV outflow tract ( LVOTv) and velocity-time integral of the outflow tract (VTiOT). These measurements were made at four different times (Fig. 1 ).
Fig. 1: Graphic description of the study protocol and positions in which measurements were performed: (1) Baseline measurement in the supine position with chest raised to 45°. (2) The bed was then raised to elevate the patient's legs to 45°. After 90 s, the second measurement was taken. (3) The patient was then returned to the basal position for 90 s, when measurements were recorded. (4) Finally, 500 ml of lactated Ringer's solution (B. Braun Medical SA, Barcelona, Spain) was administered quickly, and the final measurements were done. LR, lactated Ringer's solution.
We considered ‘Responders’ to be patients in whom SV increased by 15% or more after volume expansion with 500 ml of lactated Ringer's solution (B. Braun Medical SA, Barcelona, Spain).
The echocardiographic examination was performed by the same trained operator using a transthoracic ultrasound device, MyLab Five (Esaote, Maastricht, Netherlands).
LVOTd was measured using the parasternal long axis view 1 cm below the insertion of the aortic annulus. Assuming that the LV outflow tract area (LVOTa) was spherical, the LVOTa was calculated as follows: LVOTa = 0.78 × LVOTd2 . As the diameter was assumed to remain constant during the study, it was measured only once at the baseline position.
LVOTv was measured using the apical five-chamber view, with the pulsed-wave Doppler aligned to the LV outflow tract, and the sample volume fixed 1 cm below the aortic annulus, and the VTiOT was calculated. SV was measured as follows: SV = LVOTa × VTiOT. Then, CO was determined as follows: CO = SV × HR. These values were averaged over four measurements at the end-expiratory period. In patients suffering from atrial fibrillation, these values were averaged over more than eight measurements when no significant changes in the ventricular rate were noticed.
Statistical analysis
Statistical analysis was performed using R Core Team 2014 version (R Foundation for Statistical Computing, Vienna, Austria) and MedCalc version 9.2.1.0 software (MedCalc Software, Mariakerke, Belgium).
Results of qualitative variables are expressed as frequency and percentage. Quantitative variables are expressed as mean ± SD. Normality was tested by using the Shapiro–Wilk test. Variables were compared using a Student t test for continuous variables and a χ2 test for frequencies. Variables were compared between responders and non-responders before PLR and after volume expansion using the non-parametric Mann–Whitney U test. Quantitative variables with more than two categories were compared using the Kruskal–Wallis test. Receiver-operating characteristic curves were constructed to evaluate the ability of the changes of each variable during PLR to predict the fluid responsiveness after volume expansion. The area under the curve (AUC) was calculated for all parameters and expressed as AUC ± SD. Sensitivity, specificity, negative and positive predictive values, negative and positive likelihood ratio and rate of correct classification were calculated to choose the cut-off values. Probability (P ) values of less than 0.05 were considered statistically significant.
Results
Fifty-one patients were considered for the study. Six patients were excluded because of a poor echocardiographic window, and four due to misalignment between the Doppler and the outflow tract of the LV. Consequently, 41 patients were included in the study. Table 1 summarises the characteristics of the patients as well as their distribution between responders and non-responders.
Table 1: Characteristics of the study population
The reason for inclusion was oliguria in half of the patients (51.2%) followed by arterial hypotension (26.8%), hypotension and tachycardia (9.8%), tachycardia (4.9%) and oliguria and tachycardia (2.4%). Only two patients (4.9%) required vasoactive support with norepinephrine, but no modification of its dose was required during the study. Twenty patients (48.8%) had been submitted to general surgery, 16 (39.0%) to orthopaedic surgery and only five (12.2%) to vascular surgery. The Ramsay score was II in all patients except one. VAS scores reported by patients were 1 in 34.2%, 2 in 48.8% and 3 in 17%.
Twenty-two patients (54%) were considered to be fluid responders, with an increase of SV at least 15% after 500 ml of lactated Ringer's solution. The remaining 46% were considered ‘Non-Responders’. No statistical significant differences were found in clinical characteristics between these groups (Table 1 ).
When analysing baseline data (haemodynamic and echocardiographic measurements), no statistically significant differences were found between ‘Responders’ and ‘Non-Responders’ except in MAP, which was higher in the ‘Responders’ (Table 2 ). Registered data during the different times of the study are shown in Table 3 .
Table 2: Baseline data in responders and non-responders
Table 3: Evolution of haemodynamic parameters during the study (baseline, 90 s after passive leg raising and after fluid infusion)
An increase in CO greater than 11% during the PLR test distinguished responders from non-responders with a sensitivity of 68.2% and a specificity of 100% (Table 4 , Fig. 2 ). Similarly, an increase in VTiOT higher than 11% during PLR was able to predict an increase in SV at least 15% after volume administration, with a sensitivity of 81.8% and a specificity of 89.5%.
Table 4: Accuracy of velocity–time integral of the outflow tract and cardiac output changes after passive leg raising to predict fluid responsiveness
Fig. 2: Cardiac output variation in responders and nonresponders. CO, cardiac output.
The highest AUC was found for an increase in CO [0.91 ± 0.05; 95% confidence interval (CI) 0.78 to 0.97] and an increase in VTiOT (0.89 ± 0.05; 95% CI 0.75 to 0.96) (Fig. 3 ). No haemodynamic or echocardiographic data measured in the basal position were able to predict a positive response to volume infusion (Fig. 4 ).
Fig. 3: Receiver-operating characteristic curves showing the ability of passive leg raising-induced increases in cardiac output and velocity-time integral of the outflow tract to discriminate between responders and non-responders.
Fig. 4: Receiver operating characteristic curves showing the lack of ability of measurements in the basal position to discriminate responders from non-responders. HR, heart rate; LVOTv, maximum velocity originated in left ventricular outflow tract; MAP, mean arterial pressure; VTiOT, velocity–time integral of the outflow tract.
Discussion
The current study shows that CO measured by transthoracic echocardiography along with a reversible and well-tolerated PLR manoeuvre can predict a positive response to volume infusion with high sensitivity and specificity in spontaneously breathing post-surgical patients with suspected central hypovolaemia.
Traditionally, volaemic status has been evaluated using MAP, HR, capillary refill and diuresis.9 10
Other invasive static measurements have been used to evaluate volaemia, such as central venous pressure or pulmonary capillary wedge pressure. It has been demonstrated that these parameters are bad indicators of volaemia and are not useful as predictors of an adequate response to fluid therapy.11,12 7,8 13
As an alternative to situations in which parameters that depend on the lung–heart interaction cannot be used, CO variation after PLR has been studied as a predictor of fluid response.4,14 8 7 15 5,6 16 17 et al. ,6 et al. 5 5 18
Moreover, the response to PLR may be affected by frequent situations that arise in the postoperative period. Adrenergic vasoconstriction due to postoperative pain may reduce the total volume of blood stored in the lower limbs, underestimating the amount of blood displaced during the manoeuvre. For that reason, patients with a VAS higher than 3 were excluded. In contrast, the presence of sympathetic block due to regional analgesia techniques may mask the effect of the PLR test on a patient's volume status.19
The CO measurement has already been validated as effective compared with other invasive techniques that use thermodilution.20
The main limitation of our investigation is the sample size. Ten patients were excluded because of misalignment of the Doppler axis and the LV outflow tract or because of poor echogenicity. Placing patients in the left lateral decubitus position could have resulted in excluding fewer patients due to a bad echocardiographic window. However, we could not place patients in this position because they had just undergone surgery. It is also difficult to place a patient in left lateral decubitus position at the same time as a PLR manoeuvre is performed. Another limitation is that measurements were performed by a single observer, which made it impossible to take inter-individual variability into account. In relation to the assessment of PLR in patients with sympathetic block, we only recorded whether the patient had motor block at the time of the test, ignoring the persistence of sympathetic block.
Despite these limitations, our results show that the prediction of response to volume with echocardiography and PLR is useful in the postoperative period after low-risk surgery. Our study is the first to confirm that in a low-risk surgical population, an increase in CO higher than 11% measured by echocardiography after a PLR manoeuvre predicts that the patient will respond to fluid infusion with high sensitivity and specificity. No haemodynamic or echocardiographic data (HR, MAP, LVOTv and VTiOT) measured in the basal position were able to predict a positive response to volume infusion. The potential benefits of our results on clinical outcomes remain to be clarified.
Acknowledgements relating to this article
Assistance with the study: none.
Financial support and sponsorship: none.
Conflicts of interest: none.
Presentation: none.
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