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363
analysis depends on periodic recalibration through thermodilution (Agrò and
Vennari 2013b; Marik et al. 2011; Reuter et al. 2010). These systems require inva-
sive arterial lines and a central venous catheter, but they are less invasive than PAC.
The Picco system needs a modied arterial catheter with a temperature and pres-
sure sensor. It must be positioned in a central artery through femoral, brachial, axil-
lary, or radial access (Habicher et al. 2011). The Picco system lets a continuous
monitoring of SV, SVV, and CI, while it yields static parameters such as the GEDV/
GEDVI, ITBV/ITBVI, and EVLW through thermodilution methodology (Michard
et al. 2003). The Picco system uses a single-indicator thermodilution. It has been
shown as reliable in many studies on cardiac and noncardiac patients, although it
determines a slight overestimation of haemodynamic paramteters (Habicher et al.
2011). SVV evaluated by the Picco plus system (an evolution of Picco) adequately
indicates uid-responder patients in various clinical settings (Agrò and Vennari
2013b).
Another system based on pulse wave analysis is the FloTrac/Vigileo system. It
uses Langewouters’ algorithm to perform the wave analysis and does not require
thermodilution for calibration. Consequently, it can be used only with a normal
invasive arterial line connected to the FloTrac sensor (Agrò and Vennari 2013b).
A study on 40 patients undergoing cardiac surgery compared the SVV measured
with FloTrac/Vigileo and the PiCCO plus and found no signicant difference in the
prediction of uid responsiveness (Agrò and Vennari 2013b; Hofer et al. 2008). In
high-risk patients undergoing major abdominal surgery, Benes et al. found that
intraoperative uid optimization through the Vigileo/FloTrac system decreased the
incidence of postoperative complications, reducing hospitalization time (Agrò and
Vennari 2013b; Benes et al. 2010). The Vigileo/FloTrac system may be used with
the Presep catheter (Edwards Life Science, Irvine, CA). It is a central catheter that
allows S
C
VO
2
continuous monitoring. The limits of Vigileo involve the validity of
the wave pressure analysis and SVV values only in mechanically ventilated patients
(Agrò and Vennari 2013b).
A new, noninvasive monitor for the measurement of continuous CI is the Nexn
HD (Bmeye) monitor. It measures CI continuously completely noninvasively by an
inatable nger cuff. The Nexn HD using volume clamp technology continuously
measures nger blood pressure and converts the value into a blood pressure wave of
the brachial artery. The truly noninvasive nature of the Nexn HD allows the mea-
surement of CI and can be used in awake, not mechanically ventilated patients
(Agrò and Vennari 2013b).
13.15.2.4 Clinical Impact in Cardiac Surgery Patients
GDT has been demonstrated to reduce length of ICU stay, ameliorating outcomes
(Habicher et al. 2011). Since 1988, many studies on different monitoring systems
have demonstrated GDT benets in noncardiac major surgery patients, maintaining
a DO
2
≥ 600 mL/min/m
2
(Agrò and Vennari 2013b; Habicher et al. 2011; Shoemaker
et al. 1988; Pearse et al. 2005a, b; Giglio et al. 2009).
Considering a cardiac surgery population, only one study using PAC demon-
strated that an S
V
O
2
-oriented management may improve morbidity and hospital stay
length (Habicher et al. 2011; Polonen et al. 2000).
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In a more recent study on 30 cardiac surgery patients, monitored with oTrac in
order to optimize CI, SVV, and DO
2
, there was no signicant improvement on out-
come respect to standard management, probably due to the small sample (Habicher
et al. 2011; Kapoor et al. 2008).
The ICU use of esophageal Doppler owmetry (aimed at maintaining a stroke
index above 35 mL/m
2
) has been found to reduce the length of hospital stay in car-
diac surgery patients (Habicher et al. 2011; McKendry et al. 2004). Moreover, com-
paring 40 cardiac surgery patients treated with a GEDVI, ITBVI, CI, and
MAP-guided algorithm, with a historic sample treated with standard approach, the
GDT group presented a shorter duration of mechanical ventilation and a reduced
need for intensive therapies and catecholamines (Habicher et al. 2011; Goepfert
et al. 2007). In a similar study conducted in off-pump coronary artery bypass
patients, it was shown that GDT determined an increased use of dobutamine and
colloids, correlating with a reduction of the length ICU and hospital stay (Habicher
et al. 2011; Smetkin et al. 2009).
Although more studies are needed, the present evidences suggest GDT as a use-
ful clinical tool to improve cardiac surgery uid management during ICU stay,
favorable impacting on outcomes (Habicher et al. 2011).
13.16 Electrolyte Management
13.16.1 Sodium
In the cardiac surgery patient, sodium overload is the most common alteration due
to uid administration and to the surgical stress response (increased level of aldoste-
rone and cortisol). In this case, it is accompanied by hypervolemia and uid over-
load, with interstitial edema (Fanzca 2012). Hypernatremia may be also due to a
loss of hypotonic uids. Renal losses may be caused by furosemide use, osmotic
diuresis (severe hyperglycemia, uremia, mannitol overdose), preexisting renal dis-
eases, and the development of ATN (polyuric phase). In these cases, sodium losses
are associated to water losses, with a reduction of IVS uid and the presence of sign
and symptoms of hypovolemia (Agrò and Vennari 2013a). Less frequently, hyper-
natremia may be due to a loss of free body water (hypernatremia due to sodium
concentration). In this case, EVS volume is preserved. The most frequent cause of
normovolemic hypernatremia is the lack of an adequate restore of perspiratio insen-
sibilis, especially when it is increased (i.e., patients with fever) (Agrò and Vennari
2013a). A possible ow chart for hypernatremia diagnosis is presented below
(Fig. 13.21).
Thirst is one of the rst symptoms of hypernatremia, observable in awake
patients. Other symptoms are lethargy, reduction of consciousness up to coma and
convulsions, peripheral edema, myoclonus, ascites and/or pleural effusion, tremor
and/or rigidity, and increased reexes (Agrò and Vennari 2013a). If hypernatremia
develops slowly, it is well tolerated because the brain is able to regulate its own
volume in response to ECS uid and osmolarity changes. Acute and severe
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hypernatremia may lead to a shift of water from the ICS, causing brain shrinkage
and tearing of the meningeal vessels, with the risk of intracranial hemorrhage, espe-
cially when patients have started therapy with LMWH (Agrò and Vennari 2013a;
Miller 2009).
Hypernatremia management is based on normal osmolarity and volume restora-
tion. It includes the administration of hypotonic crystalloids or dextrose solutions.
The rate of correction depends on the symptoms and the development of hyperna-
tremia (acute, subacute, or chronic). Chronic hypernatremia needs more care in the
treatment. In fact the brain has yet developed compensation mechanism, and a too
rapid correction may lead to cerebral edema (Agrò and Vennari
2013a).
As a general rule, it is reasonable to have an initial sodium target of 145 mEq/L,
with a rate of correction of plasmatic [Na+], not greater than 1–0,5 mEq/h (Agrò
and Vennari 2013a).
A useful formula to establish the rate of infusion for an adequate corrected is
reported:
0,5mEq /h
infusedNameasured Na inmEq/L/total body water
1
,, 000 =mL/h
where
• 0,5 mEq/L is the recommendable rate of [Na+] correction
• Infused [Na] is the concentration of sodium in the solution chosen for the
correction
Hypernatremia (Na
+
>145 mEq/L)
Loss of pure water, no signs and symptoms of hypovolemia
Na
+
gain Hypotonic fluids loss (Na
+
+ H
2
O)
Hypertonic fluids infusions
Extrarenal loss
Renal loss
Extrarenal causes
Renal loss (urine osmolality <200 mOsm/kg)
Increased production of mineral-corticoids
Increased Decreased
Normal
Extra cellular volume
TPN
NaHCO
3
Adrenal tumors
Adrenal hyperplasia
Perspiratio insesibilis
Hypodipsia
Diabetes insipidus
Vomiting
Diarrhea
Burns
Excessive sweating
Renal diseases
Loop diuretics
Osmotic diuresis (glucose, urea, mannitol
)
ATN (polyuric phase)
Fig. 13.21 Flowchart for hypernatremia diagnosis
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• Measured [Na] is the sodium plasma concentration of the patient
• Body water is calculated as
Totalbodywater= correctionfactor body weight in Kg
+1×
()
Correction factor:
• 0,6 men and children
• 0,5 women
• 0,5 old men
• 0,45 old women
In the postoperative period, many cardiac surgery patients may present a
reduction of sodium plasma levels, due to a shift of water from ICS to IVS
rather than a reduction in total body sodium content. The shift is caused by
hyperglycemia (diluting hyponatremia) triggered by the surgical stress response,
the reduction in insulin production and insulin resistance, and by an overload in
the bypass pump prime (Fanzca 2012; Kutschen et al. 1985). A similar mecha-
nism may be triggered by mannitol overdose. In these cases, hyponatremia is
accompanied by hypertonicity (plasma osmolarity >300 mosm/L) (Agrò and
Vennari 2013a).
Other causes responsible for hyponatremia in the ICU cardiac surgery patient
are associated to a reduction of plasma osmolarity (true hyponatremia). In this
case, IVS volume may be normal, increased, or reduced (Agrò and Vennari
2013a).
Advanced heart failure, severe hypovolemia, and hepatic complications with
ascites alter ADH release and the kidneys’ capacity to dilute urines, leading to hypo-
natremia with IVS volume reduction and interstitial edema development.
The use of diuretics (especially if inappropriate), and the development of SIADH
due to cerebral complications or prolonged mechanical ventilation, may cause
normo-hypervolemic hyponatremia without edema.
Hyponatremia with hypovolemia may be due to cerebral salt wasting (cerebral
complications), hypokalemia, renal losses, and extrarenal losses. The most frequent
cause of renal losses in the cardiac surgery patient is diuretics use and the develop-
ment of ATN. Possible extrarenal losses are PONV, gastric suction, and diarrhea
(i.e., related to enteral nutrition in long-stay patient). In the critical patient, frequent
causes of hypovolemic hyponatremia are third-space syndromes.
Hyponatremia symptoms depend on the severity of the sodium decit. Clinical
features are weakness, nausea, vomiting, modication of consciousness (agitation,
confusion, coma, and seizures), visual alteration, cramps, and myoclonus. When the
sodium level falls below 123
mEq/L, cerebral edema occurs. At a sodium concen-
tration of 100 mEq/L, cardiac symptoms develop. In diluting hyponatremia, an
increase in IVS volume can lead to pulmonary edema, hypertension, and heart fail-
ure (Agrò and Vennari 2013a).
Sodium levels alteration are related to an increased risk of postoperative delir-
ium, especially in patients with preexisting hyponatremia (Fitzsimons and Agnihotri
2007).
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A possible ow chart for hyponatremia diagnosis is showed in the ow chart
below (Fig. 13.22).
The rst-line treatment of hyponatremia is the elimination of the underlying
cause. The second-line treatment is correction of the sodium decit, generally
through intravenous sodium administration (0,9 % saline solution or other hyper-
tonic saline solutions). The dose of sodium required to correct hyponatremia may be
calculated using the following formula (Agrò and Vennari 2013a):
SodiumdeficitmEq = 130mEqmeasuredserumNamEq Total body wa
()()
×− tter
The rate of infusion of the chosen uid may be calculated according to the same
formula explained for hypernatremia. A recommendable initial [Na] target is 125–
130 mEq/L. A slow rate (maximum rate = 0.5 mEq/L/h) of correction is always indi-
cated, because rapid correction can cause central pontine myelinolysis, especially in
the case of chronic hyponatremia. For this reason, it is suggested to use a velocity
rate correspondent to the half of the obtained value. In case of hypervolemia, it may
be preferred to utilize water restriction and a diuretic, such as furosemide (Agrò and
Vennari
2013a).
A possible ow chart for hyponatremia management is showed below
(Fig. 13.23).
13.16.2 Potassium
Maintaining adequate potassium levels is crucial for bypass pump separation and to
prevent postoperative dysrhythmias. In the perioperative setting, many factors may
Hypornatremia (Na
+
<136 mEq/L)
Plasm Osm <300 mEqu/L
Increase
dR
educed
Normal
Extra cellular volume
Urinary Na
+
Urinary Na
+
Urinary Na
+
>20mEq/L <20mEq/L
>20mEq/L <10mEq/L
>20mEq/L <10mEq/L
AK
I
Chronic renal failure
Nephrotic syndrome
Heart failure
Cirrhosis
Renal losses
Cerebral salt wasting
Adrenal insufficiency
Urine osmolality< 100 mosm/kg
with urine osmolality < 100 mosm/kg with urine osmolality < 100 mosm/kg
Urine osmolality < 100 mosm/k
g
Extrarenal losses
SI-ADH
Polydipsia
Fig. 13.22 Flow chart for hyponatremia diagnosis
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affect potassium plasma levels in different directions. Generally, factors determin-
ing a reduction of potassium levels are predominant; as a consequence, potassium
loss must be adequately prevented and managed (Fanzca 2012).
Hyperkalemia may be the consequence of an increase in total potassium body
stores or of a shift of potassium from the ICS to the ECS (Agrò and Vennari 2013a).
In the cardiac surgery patient, an increase in [K
+
] is commonly due to ICS shift
caused by academia, hypoinsulinemia, and hemolysis and to potassium IV load due
to cardioplegia (Fanzca 2012).
In the case of postoperative ATN, hyperkalemia often reects a reduced renal
excretion of potassium due to reduced tubular secretion, rather than a reduced glo-
merular ltration. Adrenal dysfunction (due to disease or drugs), with reduced aldo-
sterone production, can lead to potassium retention (Agrò and Vennari
2013a).
Muscular weakness, up to paralysis, is one of the main manifestations of hyperka-
lemia. Cardiac signs are increased automaticity and repolarization of the myocar-
dium, leading to ECG alterations and arrhythmias. Mild hyperkalemia may appear
with T waves and a prolonged PR interval; severe hyperkalemia may cause a wide
QRS complex, asystole, or ventricular brillation (Agrò and Vennari
2013a).
The management of hyperkalemia includes heart protection and facilitating in
ICS redistribution of potassium. Rapid-effect therapies are the administration of
calcium gluconate, insulin with glucose (considering patients’ glycemia), and cor-
rection of acidemia through bicarbonate administration or hyperventilation. In acute
and severe cases (often associated to AKI and development of postoperative com-
plication such as sepsis), CRRT may be indicated considering other electrolytes and
acid–base status. Additional therapies are resin exchange, diuretics, aldosterone
agonists, and β-adrenergic agonists. They act in a long term and their use is suitable
Extra cellular volume
Normal
Decreased
Increased
Symptoms
Symptoms
Symptoms
Yes
Yes
No
Furosemide
+
Isotonic
solutions
No
Furosemide
+
Isotonic solutions
Furosemide
+
Hypertonic solutions
Furosemide
+
Hypertonic
solutions
Yes No
Isotonic
solution
s
Hypertonic
solutions
Fig. 13.23 Flow chart for hyponatremia management
F.E. Agrò et al.
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in long-stay ICU patients who have developed a chronic condition responsible of
hyperkalemia (Agrò and Vennari 2013a).
Cardiac surgery patients often present hypokalemia, which may be caused by an
absolute deciency of total body potassium stores or by an abnormal shift of potas-
sium from the ECS to the ICS (despite normal total potassium) (Agrò and Vennari
2013a).
In the perioperative setting, a reduction in potassium level is due to augmented
catecholamine production with increased skeletal uptake; diuresis caused by hypo-
thermia, furosemide, and mannitol use during CPB; and increased cortisol and aldo-
sterone levels due to surgical stress. Other causes may be gastrointestinal loss or
renal losses due to diuretic or the development of acute renal damage. Hypokalemia
is always associated to metabolic alkalosis (see acid–base paragraph) (Fanzca 2012;
Agrò and Vennari 2013a).
Hypokalemia signs and symptoms depend on the potassium level. Arrhythmias
(frequently, atrial brillation and premature ventricular beat) and other electrocar-
diographic abnormalities (sagging of the ST segment, T-wave depression, and
U-wave elevation) appear at potassium concentrations <3 mEq/L (Agrò and Vennari
2013a).
The rate of potassium administration (generally potassium chloride) must be
adjusted considering the distribution within the ECS. The administration rate is lim-
ited to 0.5–1.0 mEq/kg/h (Agrò and Vennari 2013a).
13.16.3 Calcium
Hypocalcemia is frequent during the intraoperative period. Hypocalcemia refers to
free ionized calcium levels in the plasma. It develops when calcium concentrations
are low but plasma protein levels are normal. As a consequence, it is necessary to
know if the calcium values measured is the total plasma value (in this case, it should
be adjusted for albumin value) or the ionized fraction (Agrò and Vennari 2013a).
In cardiac surgery patients, hypocalcemia is generally limited, and it is caused by
citrate use, hemodilution, increase of albumin binding fraction, and hypomagnese-
mia. In these cases, hypocalcemia is treated in order to normalize calcium level and
to uptake its effects on myocardium (protection and inotropism) and vessels (vaso-
pressor) (Fanzca 2012). In the ICU setting, the most frequent cause of hypocalcemia
is hypoalbuminemia. Other causes are the development of postoperative renal dys-
functions, hyperventilation, blood transfusion (citrate chelation), and septic compli-
cations (the pathogenesis of the mechanisms correlating sepsis and hypocalcemia is
not fully understood) (Fanzca
2012).
The main clinical manifestations of hypocalcemia are due to the increased car-
diac and neuromuscular excitability and to the reduced contractile force of cardiac
and vascular smooth muscles. Tetanic syndrome, a result of increased neuromuscu-
lar excitability, is characterized by numbness (especially around the mouth, lips,
and tongue) and muscle spasms, particularly in the hands, feet, and face (character-
istic are Chvostek and Trousseau signs). Regarding the cardiovascular alterations,
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hypocalcemia causes prolongation of the PQ interval, which predisposes patients to
the onset of severe ventricular arrhythmias. Hypocalcemia may also lead to
hypotension.
Nervous symptoms are due to the impaired mental status (Agrò and Vennari
2013a).
The treatment of hypocalcemia should be causal but should also be aimed at
quickly increasing the serum calcium concentration. It may be corrected by admin-
istering 10 % calcium chloride (1.36 mEq/mL) or calcium gluconate (0.45 mEq/
mL) (Agrò and Vennari 2013a). The role of calcium administration has been dis-
cussed in literature. In particular, there is concern about the exacerbation of isch-
emia–reperfusion damage. In fact, in ischemic cells, there are high calcium levels
due to the impairment of ATP–calcium pump and to a reverse activity of Na
+
–Ca
2+
pump. Finally, calcium transport is impaired by the oxidative stress. Intracellular
hypercalcemia leads to mitochondrial dysfunction and cellular death. Calcium
administration may further increase calcium ux into cardiac cells, accelerating this
process (Fanzca 2012). In patients undergoing to CABG, (Fanzca 2012) found a
transient improvement (<10 min) in systolic function, associated to a diastolic dys-
function (reduced myocardial compliance), when calcium was administered early
after bypass separation. However, in a subsequent study the reduction of diastolic
function after CABG was not related to calcium administration (Fanzca 2012; Ekery
et al. 2003). Moreover, calcium has been shown to reduce adrenalin effect in the
postoperative period and in animal studies to increase the negative inotropic effect
of protamine (Fanzca 2012; Zaloga et al. 1990; David et al. 2001). Evidence sug-
gests that the use of calcium at the time or before the reperfusion has benet which
cannot be obtained using other agents, although implying potentially adverse effect
(Fanzca 2012).
Hypercalcemia is less frequent in the immediate postoperative period of cardiac
surgery. It is generally related to an overtreatment of hypocalcemia, while in the
long-stay ICU patient it may be due to the development of renal dysfunction or
increased bone reabsorption (immobilization) (Agrò and Vennari 2013a).
Main symptoms of hypercalcemia may be remembered using the rhyme: “groans
(constipation), moans (psychic moans, e.g., fatigue, lethargy, depression), bones
(bone pain, especially in hyperparathyroidism), stones (kidney stones), and psychi-
atric overtones (including depression and confusion).” Other symptoms are
anorexia, fatigue, vomiting, and nausea. ECG alterations, such as a short QT inter-
val or widened T wave, are suggestive of hypocalcemia. Symptoms are common at
high calcium concentration (>3
mEq/L). Severe hypocalcemia (>4 mEql/L) is a
medical emergency. It may lead to coma and cardiac arrest (Agrò and Vennari
2013a).
Hypercalcemia management involves increased diuresis and plasma dilution.
Accordingly, diuretics and saline solutions are used, because sodium reduces cal-
cium reabsorption by the kidneys. In patients with a chronic cause or status leading
to hypocalcemia, other possible treatments are calcitonin, bisphosphonate, and glu-
cocorticoids. In all patients, rapid mobilization and physiotherapy after the surgery
is fundamental to maintain bone balance (Agrò and Vennari 2013a).
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13.16.4 Magnesium
Hypomagnesemia is frequent in the postoperative period after cardiac surgery. It
may be triggered by hyperaldosteronism (heart failure, stress response), by calcium
alteration (hypercalcemia), and by the use of drugs such as diuretics or adrenergic
drugs (Agrò and Vennari 2013a). The effects of magnesium decits are neuromus-
cular excitability disorders (related to the concurrent development of hypercalce-
mia), such as involuntary contraction of the facial muscles, cramps, tetany, and
arrhythmias, or other symptoms mainly related to metabolism, such as morning
fatigue. Hypomagnesemia may lead to hypertension, coronary vasoconstriction,
and arrhythmias (Fanzca
2012; Kimura et al. 1989; Booth et al. 2003). It may also
be characterized by an alteration of consciousness, as demonstrated by confusion,
hallucinations, and epilepsy.
Magnesium supplementation has been demonstrated to reduce the reperfusion
injury, by blocking calcium ingress in myocardial cells and acting as a free radical
scavenger (Fanzca 2012; Garcia et al. 1998). In fact, in animal studies, magnesium
use has been related with a reduction of infarct size. The timing of administration
appears to be very important: no effects have been found when administration is
realized early after the reperfusion (Fanzca 2012; Ravn et al. 1999; Herzog et al.
1995). Literature also demonstrated that after CABG, magnesium supplementation
reduces the risk of postoperative arrhythmias, improves the short-term neurological
function, and may have a signicant opioid-sparing effect (Fanzca 2012; England
et al. 1992; Miller et al. 2005).
Magnesium inhibits platelet function with a prolongation of bleeding time at 24 h
after cardiac surgery. However, a correlation of this effect with an increase of postop-
erative blood losses is not clear (Fanzca 2012; Gries et al. 1999). On the other side,
a recent study demonstrated reduced postoperative bleeding and transfusional need
after CABG, in patient receiving magnesium (Fanzca 2012; Dabbagh et al. 2010).
Hypermagnesemia is less frequent in cardiac surgery patient. The most common
and probable cause is kidney failure. Hemolysis, hypocalcemia, adrenal insuf-
ciency, diabetic ketoacidosis, lithium intoxication, and hyperparathyroidism are
other predisposing conditions. Hypermagnesemia is characterized by weakness,
hypocalcemia, nausea and vomiting, hypotension, breathing symptoms, and arrhyth-
mias up to asystole (Agrò and Vennari
2013a).
In severe cases, the rst line in hypomagnesemia management is the administra-
tion of calcium gluconate, since calcium is the natural antagonist of magnesium.
Subsequently, according to renal function, diuretics or dialysis is needed (Agrò and
Vennari 2013a).
Conclusion
A perfect uid management for perioperative treatment of cardiac surgery patient
is still lacking. One of the rst goals is to contain the IVS losses to a minimum
using the cell savage technique and reducing the need for colloids (with their side
effect!) (Fanzca 2012).
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Preload assessment and DO
2
optimization by assessing uid responsiveness
represent the main goal in cardiac surgery patients. The best approach is using
GDT to measure preload and to restore it in patients with reduced circulating
volume (uid responders) while using a continuous infusion of uid to compen-
sate urinary loss and perspiration, being mindful of glycocalyx alterations caused
by cardiac surgery and that may generate tissue edema (Fanzca 2012; Becker
et al. 2010).
Colloids are needed when a fast hemodynamic improvement is necessary
(Agrò and Vennari
2013b). The volume effect of colloids depends on the IVS
volume and hydration state of the patient. Giving uids, not before but when
hypovolemia occurs, seems to be more rational because the volume effects of
colloids are more effective (Chappell et al. 2008; Roberts and Bratton 1998).
Treating relative hypovolemia with colloids in patients undergoing surgery or in
the critically ill who need sedation ignores the indirect vasodilator effect of anes-
thetic drugs. Thus, when vascular tone is restored, a relative hypervolemia can
occur, potentially causing postoperative pulmonary edema (Roberts and Bratton
1998).
Crystalloids are needed to compensate urinary and perspiration losses, avoid-
ing overload (Agrò and Vennari 2013b).
Possible future strategies could be aimed to protect and rapidly restore the
endothelial glycocalyx (Fanzca 2012).
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