Background:
The anesthesiologists role in
predicting and assessing the hemodynamic responsiveness to volume expansion
(VE) during the intra-operative period is among the most challenging and
important part of the major surgeries. Intra-operative hypovolemia is common and may be a potential cause of
organ dysfunction, increased postoperative morbidity, and death in major surgeries. But in studies designed to measure changes
in cardiac index following fluid administration in hypotensive patients
receiving mechanical ventilation,28 to 60% of patients showed no significant
change(1).Fluids may not only be ineffective but harmful as well in
some cases, as suggested by the results of the ARDS Network Fluid and Catheter
Treatment Trial(2).
In the intra-operative period, fasting,
anaesthesia and surgery may affect the body’s physiological capacity in controlling its external fluid and
electrolyte balance and also the
internal balance between the various body fluid compartments(3).Majority
of anaesthetized patients undergoing surgery have functional intravascular
volume deficit even before surgery that may be due to fasting and bowel
preparations(4).Major surgeries cause significant tissue trauma and
are associated with systemic inflammatory response leading to vasodilatation
and capillary leakage . There could be major fluid shifts with third space
fluid loss associated with severe
haemorrhage that are difficult to estimate leading to inadequately corrected
hypovolemia and inappropriate use of vasopressors. In addition anaesthetic
drugs may cause variable degree of vasodilatory and myocardial depressing
effects leading to reduced effective intravascular circulating volume and
hypotension. All these factors cause patients undergoing surgery at risk of
hemodynamic instability, tissue hypoperfusion and adverse surgical outcome. Therefore
perioperative fluid therapy has a direct bearing on outcome and prescriptions
should be tailored to the needs of the patient. The practice of intra-operative
fluid therapy has changed from routine standard therapy measuring and replacing
estimated various losses to restrictive fluid strategy where third space losses
are not replaced. The goal of the fluid therapy in the elective setting is to
maintain the effective circulatory volume while avoiding interstitial fluid
overload whenever possible. Perioperative fluid approach and goal directed
therapy aiming to keep a neutral balance has shown to improve patient outcome (5,6).
With the revolutionary developments in
the area of hemodynamic monitoring the trend is moving more towards
non-invasive ways of assessing fluid responsiveness. Traditionally used static
hemodynamic parameters like central venous pressure (CVP), pulmonary capillary
wedge pressure (PCWP) are of limited value in predicting fluid responsiveness. Once
considered gold standard in hemodynamic monitoring, Pulmonary Artery Catheter
has fallen into disrepute as it is more invasive and because technological
advances have given minimally invasive alternatives(7).In past
years, many trials using different devices and goals have been published in the
literature demonstrating better outcomes in organ functions and morbidity, or even mortality Oesophageal
Doppler has been used by many for guiding fluid management with good results
but its use is partially limited by the need for deep sedation and experienced staff . Also, the reliability
in major vascular procedures requiring cross-clamping of descendent aorta could
be questioned(8).
With the introduction of arterial
pressure waveform analysis, the well-known interaction between stroke volume
variation (SVV) and lung inflation during mechanical ventilation has become
available for routine clinical use. Several studies documented the usefulness
of blood pressure variations and it surrogates (pulse pressure variation or
systolic pressure variation) in predicting position on the Frank-Starling curve
and hence fluid responsiveness. They have been shown to be superior to static
indices and accurately predict fluid responsiveness in both ICU and surgical
patients. (9)
Respirophasic radial artery pulse
pressure variation (PP) has been shown to predict volume responsiveness in
hemodynamically unstable patients receiving mechanical ventilation with a
positive predictive value (PPV) and a negative predictive value (NPV) of 94%
and 96%, respectively(10). But measurement of the PPV requires
invasive monitoring with a peripheral arterial catheter, which has been
associated with a risk of both infectious and embolic complications. In
addition, measurement of the Pulse Pressure variation requires a specialized
monitoring setup that is unavailable in many setup.
Ultrasound technology has been used to
address the specific limitations of indwelling arterial and Venous catheters. A
paradigm shift has occurred in the arena of hemodynamic monitoring which has
made Doppler evaluation of brachial artery velocity time integral and carotid
artery velocity time integral as a
method of assessing fluid responsiveness. Its advantage is that it is totally
non-invasive bedside approach (11, 12,13,14).
Thus, we would like to test whether a
brachial artery velocity time integral and carotid artery velocity time
integral could substitute as an accurate, noninvasive surrogate for Pulse
Pressure Variation in predicting fluid responsiveness in patients undergoing
major surgeries with controlled mechanical ventilation.
Aims and Objective
To determine whether brachial artery
velocity time integral and carotid artery velocity time integral could
substitute as an accurate, noninvasive surrogate for Pulse Pressure Variation in
predicting fluid responsiveness in patients
undergoing major surgeries with
controlled mechanical ventilation. Methods: After approval by the institutional
ethics committee and obtaining informed consent, the study will include 50
readings from the patients who fit to the inclusion criteria. Written informed
consent from the patients will be taken a day prior to surgery. A maximum of
three sets of readings before and after fluid bolus as decided by the treating
OT anesthesiologist will be allowed per patient in the study and the three sets
of readings will be at least two hours apart .All the study patients will be
sedated, paralysed and ventilated using volume-control settings with tidal
volume of 6-8 ml/kg of predicted body weight as adjusted by the OT
anesthesiologist and adjusted to a tidal volume of 8 mL/kg and PEEP of 5 cmsH2O
for the study period. The Pulse Pressure Variation (PPV)
will be recorded using the Philips Intel View Monitor (MP 70) and SVV, SV and
cardiac index (CI) will be recorded from cardiac output monitor (FlotracEV1000)
as/decided by the treating OT anesthesiologist one day prior to the surgery. The
arterial pressure transducer will be attached to the patient’s upper arm at the
level of the cardiac cavities. Demographic data of patients including age, sex,
height, weight, predicted body weight (PBW), primary diagnosis and details of
surgery will be recorded. Dose of vasopressors used if any, will be recorded. Supportive
therapies, ventilatory settings and vasopressor therapy will be kept unchanged
throughout the study time. Indications for the fluid challenge will be noted.
The respiratory and hemodynamic parameters will be recorded at various
intervals as per study design Study Design The hemodynamic and respiratory
variables readings will be recorded at baseline, before and after fluid bolus
given to the patient. We will take readings of following
hemodynamic parameters at baseline, prior to the fluid bolus and after fluid
bolus -.Readings taken will include
heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure
(DBP), mean arterial pressure (MAP), cardiac index (CI), Pulse Pressure
Variation, Stroke Volume Variation, Stroke Volume, Brachial artery velocity
time integral, Carotid artery velocity time integral (VTi) and respiratory
variables like tidal volume, Ppeak, Pplateau and the ratio of the heart rate and respiratory
rate (HR/RR) After a fluid bolus,we will record the
same parameters, i.e. heart rate (HR), systolic blood pressure (SBP), diastolic
blood pressure (DBP), mean arterial pressure (MAP), cardiac index (CI), PPV,
SVV, SV, Brachial artery velocity time integral, Carotid Velocity Time integral
and respiratory variables like tidal volume,
P peak, P plateau and the ratio of the heart rate and respiratory rate
(HR/RR) The decision for volume expansion will
be taken by the respective OT
anesthesiologist as per the
presence of one or more clinical signs of acute circulatory failure, defined as
a systolic blood pressure of less than 90mmHg (or a decrease of more than 50
mmHg in previously hypertensive patients) or the need for vasopressor drugs;
the presence of oliguria (urine output <0.5 ml/kg/min for at least two
hours); the presence of tachycardia; a delayed capillary refilling; or the
presence of skin mottling, lactate levels > 2 mmol/l.A fluid challenge of
5-10 ml/kg actual body weight of Ringer lactate will be given over 10 minutes
as decided by the OT anesthesiologist. Patients will be divided into two
groups Responders and Non-Responders based on increase in stroke volume (SV)
increased ≥ 15%after giving the fluid bolus(VE). A SonoSite Titan HCU (SonoSite;
Bothell, WA) device with a5-MHz broadband linear array transducer will be used
to obtain the measurements. A physician with previous formal training in
critical care ultrasound will be obtaining Doppler measurements of velocity
time integral from the brachial artery and carotid artery. Brachial Artery velocity time integral before and after fluid
bolus Arterial blood flow velocities will be
measured from the brachial artery just proximal to the antecubital fossa in the
arm contralateral to the arterial catheter over 30 secs. The velocity waveform
will be recorded from the midstream of the vessel lumen and the sample volume
will be adjusted to cover the center of the arterial vessel, in order to obtain
a clear Doppler blood velocity time integral. Clinicians obtaining ultrasound images
will be blinded to the results of the arterial pulse pressure variations that
will be collected independently by another clinician. All image angles will be
corrected up to 15° for the best signal and stored for immediate review
following each measurement. The brachial artery velocity time integral will be
calculated over a period of 30 seconds Carotid Artery velocity time integral before and after fluid bolus Carotid velocity time integral will be
measured after procuring a longitudinal view of the common carotid artery,
pulsed Doppler analysis at 2 cm from the bifurcation will be performed. The
sample volume will be positioned at the center of the vessel, with angulation
at no more than 60°. The carotid artery velocity time integral will be
calculated over 30 seconds. Arterial pulse pressure variation before and after fluid bolus Radial arterial pressure pulse
pressure variation will be recorded simultaneously with the ultrasound
measurement of the Brachial Artery and carotid artery velocity time integral
and by a clinician blinded to the ultrasound results. Cardiac output and stroke volume variation measurements A FloTrac sensor (Edwards Lifesciences
LLC, Irvine, CA, USA) will be connected
to the arterial line and attached to the Vigileo monitor, software version 1.10
(Edwards Lifesciences LLC, Irvine, CA, USA). The CO will be calculated from the
real-time analysis of the arterial waveform, using a proprietary algorithm
based on the relation between the arterial pulse pressure and stroke volume.
After zeroing the system against atmosphere, the arterialwaveform signal
fidelity will be checked using the square wavetest and hemodynamic measurements
will be initiated. CO, stroke volume and Δ Stroke Volume variation values will be
obtained over a period of 30 seconds. Statistics Non-parametric tests will be applied
for the data which is not normally distributed. Results will be expressed as
median and interquartile range (25th to 75th percentiles). Patients will be
classified according to stroke volume index (SVi) increase after VE in
responders (≥15%) and nonresponders (<15%), respectively. The effects of VE
on hemodynamic parameters will be assessed using the Wilcoxon rank sum test.
Differences between responder and nonresponder patients will be established by
the Mann-Whitney U test. The rate of vasopressor treatment will be
compared between responder and nonresponder patients using the chi-squared
test. The relations between variables will be analyzed using a linear
regression method. The area under the receiver operating characteristic (ROC)
curves for Carotid VTI and Brachial VTI, ΔPP radial, ΔSVVigileo and
according to fluid expansion response will be calculated and compared using the
Hanley-McNeil test. ROC curves will be presented as area ± standard error (95%
confidence interval (CI)). A P value less than 0.05 will be considered
statistically significant. Statistical analyses will be performed using SPSS 24
version Sample Size
Assuming
50% incidence of fluid responsiveness,it was determined that 50 readings would be required to detect differences of
0.15 between the areas under the receiver operating characteristic (AUROC)
curve of PPV (0.63) and DVpeak-CA (0.88) with an 80% power and type I error of
5%, and an estimated 20% attrition rate(14). |