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PPV
100
18 Perioperative Fluid Management andVolume Assessment
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Dynamic Parameters
Classically in mechanically ventilated patients, during inspiration positive intrathoracic pressure decreases venous return to the heart, leading to a reduction in
right ventricular SV, resulting in reduced left ventricular preload and SV.During
expiration, the opposite is observed where both right ventricular and left ventricular SV increase. These cyclic changes may be accentuated in patients who
are hypovolemic, and contribute to evaluate volume responsiveness [28]. More
modern investigations focus on pulse pressure variation (PPV), systolic pressure
variability (SPV), stroke volume variation (SVV), and pulse oximetry plethysmography variability index (PVI), and their ability to predict uid responsiveness [29].
Pulse Pressure Variation
PPV is calculated using the following equation:
()
PPV along with SVV have been documented in several small series, and their
value for detecting uid responsiveness is promising [30]. PPV can be less reliable
during spontaneous ventilation, low tidal volumes in mechanically ventilated
patients, high-frequency ventilation such as jet ventilation, presence of pulmonary
hypertension, limited lung compliance, altered chest compliance such as open chest
conditions, aberrant cardiac rhythms, and elevated intraabdominal pressure [9].
PPmax PPmin
PPmax PPmin
%
=
−
+
2
×
Systolic Pressure Variability
SPV is the difference between the maximal and minimal systolic blood pressure
(SBP) following a positive pressure breath and can be calculated using measurements from an arterial waveform. In patients receiving positive pressure ventilation,
systolic pressure variability has utility in assessing volume responsiveness. SPV can
be calculated using this equation:
290
S
S
−
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SBPmax SBPmin
PV mmHg
()
In intravascularly depleted patients, a signicant SPV can be expected, and an
SPV >10mmHg is consistent with uid responsiveness [31, 32].
=
SBPmax SBPmin
−
+
2
R. Bangalore et al.
Stroke Volume Variation
SVV is given by the following equation:
VV
SV can be estimated using invasive or non-invasive hemodynamic monitoring
devices including echocardiography. Some devices that provide direct or indirect
SVV measurements during the perioperative period include, LiDCO LXi™, Masimo
Corporation, Irvine, CA, USA), FloTrac/Vigileo® and ClearSight™ (Edwards
Lifesciences, Irvine, CA, USA), PiCCO (Pulse Index Contour Cardiac Output,
Getinge, Wayne, NJ, USA), Argos® (Retia Medical, White Plains, NY, USA).
These devices tend to provide a much less invasive method compared to pulmonary artery (PAC) or Swan Ganz catheter derived measurements of CO, and have
been shown to measure similar mean CO values, albeit with inconsistencies in measuring the dynamic trends among various techniques [33].
The FLoTrac® needs a specic transducer whereas the Argos® monitor does not
require a special transducer as it analyzes information from the regular arterial
transducer and incorporates its proprietary Multi-Beat Analysis (MBA
late the cardiac output and other hemodynamic variables. The ClearSight™
depends on a noninvasive nger cuff. As with some other measurements, complex
computation is essential to calculate SVV, potentially introducing errors in the
estimate [34].
Like PPV, an SVV > 13% can predict volume responsiveness [29, 31]. Although,
in mechanically ventilated patients with tidal volume <6mL/kg, SVV may have
limited ability in recognizing a uid responder [36]. By increasing the tidal volume
from 6 to 8mL/kg and causing a greater impact to preload, volume responsiveness
can be identied using the absolute change in SVV. The threshold for ΔSVV is
2.5% with a sensitivity of 81% and specicity of 80% [35, 36]. The presence of
normal sinus rhythm, absence of valvular heart disease, relatively normal lung and
chest compliance, and normal intraabdominal pressure are generally required for
SVV to accurately predict uid responsiveness.
Plethysmographic Variability Index (PVI) and Perfusion Index (PI).
()
SVmaxSVmin
=
%
SVmean
×
™
) to calcu-
PV
−
100
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Perfusion index (PI) is the ratio of pulsatile blood ow to the non-pulsatile blood
in peripheral tissues, and most pulse oximetry devices can display PI continuously.
With PI values, PVI can be obtained using this equation:
291
%
=
PImaxPImin
PImax
×
I
PVI is a dynamic index between 0 and 100 with higher values indicating
increased variability, signaling a higher likelihood that a patient may be uid
responsive [37–39].
Nevertheless PPV and SVV are more widely employed. One meta-analysis
focusing these two indexes indicated reduced mortality (odds ratio 0.55, 95% CI
0.30–1.03) and ICU-related costs (−1619, 95% CI −2174 to −1063 USD) for criti-
cally ill patients [40, 41].
()
Clinical Tests forFluid Responsiveness
Passive Leg Raising
The passive leg raising (PLR) test allows a clinician to directly observe the response
to augmented cardiac output with an increase in preload. To accurately test for uid
responsiveness, the patient is positioned in a semi-recumbent position with the head
of the bed at a 45° angle as shown in Fig.18.2 with legs extended, and a baseline
CO is obtained. The bed is then positioned to elevate the legs, and CO is measured
again within a minute. This positional shift mobilizes approximately 300cc of uid
from the legs to the central venous system, thereby increasing the preload to the
right heart, which would increasing the CO by 10% in volume-responsive patients
[9]. CO measurement is superior to arterial blood pressure in predicting hemodynamics that will improve with volume expansion [40, 41].
Fig. 18.2 Passive leg raising test. The patient is positioned with head of the bed raised to 45°
elevating the torso while the legs remain at. The position is shifted to elevate the legs 45° above
the heart to augment preload. The cardiac output is measured at baseline (on the left) which is
compared to the cardiac output with change in position (on the right)
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End-Expiratory Occlusion Test
In situations where PLR cannot be performed, the end-expiratory occlusion (EEO)
test is an alternative for volume assessment during passive ventilation. At the end of
expiration, ventilation is paused for 15–30s while evaluating for any changes in
cardiac output. With a ventilatory pause, there is a physiologic increase in venous
return to the right side leading to increased preload and, in turn, an augmented
CO.If the measured CO is greater than 5% from baseline, it is indicative of uid
responsiveness [42, 43]. EEO may be able to detect volume responsiveness during
the intraoperative and postoperative periods independent of ventilatory settings and
the duration of the expiratory hold [43]. Nevertheless it is not a standard procedure
in most services yet.
R. Bangalore et al.
Echocardiography
Both transesophageal (TEE) and transthoracic (TTE) echocardiography have been
around for decades, yet they are not recommended by guidelines nor are they routinely employed in the perioperative period, except for specic interventions notably concerning cardiac surgery. Both suffer from quality limitations, compared to
CT and magnetic resonance imaging, and TEE utilization can be followed by upper
gastrointestinal injuries. Imaging shortcomings have been substantially improved
by more modern three-dimensional echocardiography (3D-TEE).
Echocardiographic measurement of left ventricular end-diastolic volume can be
used as a surrogate for preload, and the subaortic velocity time integral (VTI) measured at the left ventricular outow tract (LVOT) can reect SV and thus help assess
volume responsiveness. Additionally, ultrasonographic examination of the IVC can
also help evaluate uid status and gauge uid responsiveness.
LVOT andVTI
In the parasternal long-axis view, the LVOT diameter can be measured at 0.5cm
into the ventricle from the aortic cusp insertion (Fig. 18.3). In the apical vechamber view, a doppler signal placed across the LVOT and tracing along the ejection signal is calculated to be the VTI representing the blood ow during the cardiac
cycle (Fig.18.4). Similar to SV, variation in VTI is observed during the cardiac
cycle and is calculated using the following equation.
TI variation
%
()
VTImax VTImin
=
VTImax VTImin
−
+
2
×
Cardiac Output Stroke VolumeHeart Rate=×
S
TI=×
LV
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Fig. 18.3 Parasternal long-axis view. The diameter of the left ventricular outow tract is measured
as shown in red
293
VTImax represents the highest value while VTImin represents the lowest value
measured during 10 cardiac cycles.
In septic mechanically ventilated patients, a VTI variation of 15.9% can detect
volume responsiveness with a sensitivity of 87.5% and specicity of 95% [44].
LVOT VTI can also be used with the PLR test, and an increase in VTI >12% is
indicative of volume responsiveness [45]. Additionally, a series of calculations
using the LVOT diameter and VTI can be used to estimate the CO (Fig.18.4).
troke VolumeLVOT areaLVOTV
OT area
LVOT diameter
=
π
2
IVC Diameter
From the subxiphoid view, the IVC diameter can be visualized (Fig.18.5). It is a
static parameter that approximates the CVP or right atrial pressure. An IVC diameter of <2.1cm is consistent with right atrial pressures between 0 and 5mmHg and
a diameter >2.1cm is indicative of pressure between 10 and 20mmHg. However,
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Right
Ventricle
Right
Atrium
R. Bangalore et al.
Left
Ventricle
Left
Atrium
Time
Velocity
Fig. 18.4 Apical ve-chamber view with doppler across left ventricular outow tract (Top).
Doppler placed as shown in red to obtain velocity time integral by tracing around the curve
(Bottom)
like CVP and PAOP, the diameter of IVC, when used alone, is a poor marker for
volume responsiveness [21]. On the contrary, the variance of the inferior vena cava
throughout the respiratory cycle, as a dynamic marker, can be used to evaluate volume responsiveness [46]. The collapsibility of the IVC can be calculated using the
equation:
Velocity Time
Integral
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Fig. 18.5 Inferior Vena Cava in the subcostal view with doppler. (Top) M-Mode view of inferior
vena cava with maximum and minimal diameter. (Bottom) Dmax Maximum diameter, Dmin
Minimum diameter
where Dmax is the maximal diameter and Dmin is the minimal diameter of the
IVC during the respiratory cycle.
IVCCollapsibility =
−
DD
maxmin
+
DD
maxmin
2
×
1000
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R. Bangalore et al.
IVC diameter and collapsibility have been shown to accurately estimate CVP
and right atrial pressure, particularly in spontaneously breathing patients [47]. The
diagnostic accuracy is less consistent in mechanically ventilated patients, making
this assessment less useful for patients under general anesthesia. The collapsibility
index of >12% is indicative of volume responsiveness in a spontaneously breathing patient. In mechanically ventilated patients, the distensibility of the IVC can
be measured and volume responsiveness is likely if the distensibility index
>18% [21].
DD
maxmin
IVCDistensiblity =
−
D
min
()
×
100
Perioperative Fluid Management
The commonly used 0.9% normal saline (NS) is an unbalanced isotonic crystalloid
as it has a non-physiologic chloride concentration [48, 49]. More balanced alternatives are shown in Table18.1.
In spite of controversial reports, the SMART (Isotonic Solutions and Major
Adverse Renal Events) protocol demonstrated less renal complications and less
mortality with balanced preparations [50–55].
Table 18.1 Composition of commonly used crystalloid solutions
3%
Saline
Sodium (mmol/L) 513 154 140 130 77 77
Chloride (mmol/L) 513 154 98 109 77 77
Potassium (mmol/L) 0 0 5 4 0 0
Magnesium (mmol/L) 0 0 3 0 0 0
Calcium (mmol/L) 0 0 0 3 0 0
Acetate (mmol/L) 0 0 27 0 0 0
Gluconate (mmol/L) 0 0 23 0 0 0
Lactate (mmol/L) 0 0 0 28 0 0
Dextrose (mEq/L) 0 0 0 0 25 0
Osmolarity
(mOsm/L)
pH 5 5 7.4 6.5 4.5 5.6
D5 5% Dextrose, NS Normal saline, D5 ½ NS 5% Dextrose combined with diluted normal saline,
½ NS Normal saline diluted in water 1:1
1026 308 294 273 280 154
0.9%
Saline
Plasmalyte
Lactated
ringers
D5 ½ NS½
NS
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Colloids
They have been widely prescribed in the past, as a means of minimizing capillary leakage, replacing expensive and not always available blood transfusions
[56]. However, morbidity and mortality increased and their use has been
discontinued.
At this moment only human serum albumin (5% and 25% formulations) is an
option, for selected cases of decompensated cirrhosis, ascites as well as other rare
conditions, not for routine administration. Synthetic colloids still exist in the market; however, most countries discourage their use [57].
Crystalloids Versus Colloids
After traumatic brain injury (TBI), mortality rate was higher and neurologic outcomes poorer when albumin was administered [58, 59]. In contrast, a post-hoc anal-
ysis showed a decreased risk of mortality in patients with septic shock when
receiving albumin to correct hypoalbuminemia [60]. The Surviving Sepsis
Guidelines recommend considering albumin in patients who have received largevolume crystalloid resuscitation [61–63].
Liberal Versus Restrictive Fluid Management
In a 2003 study, patients in the liberal group gained 4kg compared to 1kg in the
restrictive group by the rst postoperative day [64]. There has been much variability
in the practice of perioperative uid administration over the past two decades, as
outcomes research has prompted changes in practice [64–67]. Current existing evidence comparing liberal and restrictive uid replacement strategies is rather inconclusive. In earlier studies, liberal uid management strategy was associated with
increased perioperative morbidity, hospital costs, and length of stay [68]. After
colorectal surgery, uid overload is still incriminated for postoperative ileus [66],
and surgical complications such as pneumonia and anastomotic leakage, seem more
frequent in the same circumstances of excessive uid utilization after esophagectomy [67].
In a large randomized controlled trial focusing major abdominal surgery, no
difference in overall 1-year survival was observed; however, patients in the
restrictive group had a higher incidence of acute kidney injury [69]. A subsequent meta- analysis found no difference in early or late postoperative mortality [70].
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R. Bangalore et al.
Enhanced Recovery After Surgery (ERAS)
Despite not uncommon criticisms, the increasingly popular ERAS programs advocate for a “zero-balance” uid goal [17, 71]. For high-risk surgical patients, ERAS
guidelines endorse goal-directed uid therapy techniques, which are discussed
below [16, 19].
Goal-Directed Therapy
Goal-directed therapy (GDT) is a strategy that aims to provide clear objectives for
uid administration during the perioperative period. This approach involves realtime assessments of hemodynamic and cardiac output parameters to guide uid
therapy. A predened algorithm, as illustrated in Fig.18.6, is selected depending on
the operation, setting, and experience of the team, to determine when a uid bolus
is necessary. For example, if SVV remains above 13% for 5–10min, and the patient
is also hypotensive, this may indicate that the patient could benet from additional
uid administration.
The evidence supporting GDT is not entirely conclusive, much like the uid
strategies described earlier [72–75].
A large meta-analysis found moderate evidence of benet only concerning infectious postoperative complications and anastomotic leakage [76]. One should
Fig. 18.6 Sample algorithm for goal directed uid therapy with uid administration guided by
stroke volume variation. SVV Stroke volume variation, MAP Mean arterial pressure
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