Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3978_Библиотеки_им_академика_М_И_Перельмана
.pdf
313
A. Dabbagh et al. (eds.), Postoperative Critical Care for Cardiac Surgical Patients,
DOI 10.1007/978-3-642-40418-4_13, © Springer-Verlag Berlin Heidelberg 2014
F.E. Agrò, MD (*) • M. Vennari, MD • M. Benedetto, MD
Anesthesia, Department of Intensive Care and Pain Management,
Campus Bio-Medico of Rome, Via A. Del Portillo, 200 00128 Rome, Italy
e-mail: f.agro@unicampus.it; m.vennari@unicampus.it; m.benedetto@unicampus.it
13
Fluid Management and Electrolyte
Balance
Felice Eugenio Agrò, Marialuisa Vennari,
and Maria Benedetto
Contents
13.1 Introduction ................................................................................................................. 315
13.1.1 Physiology of Body Fluids ............................................................................ 315
13.1.2 Ionic Balance ................................................................................................. 317
13.1.3 Osmolar Balance ........................................................................................... 319
13.1.4
Fluid Movement Through Capillary Membranes .......................................... 321
13.2 Basis of Fluid and Electrolyte Pathophysiology in the Postoperative ICU
Setting of Cardiac Surgery .......................................................................................... 323
13.2.1 Water Distribution Modication ................................................................... 323
13.2.2 Electrolyte Modications .............................................................................. 325
13.3 Clinical Management of Fluid .................................................................................... 325
13.3.1 Which Kind of Fluid? .................................................................................... 325
13.3.2 Physical and Chemical Properties ................................................................. 326
13.4 Crystalloids ................................................................................................................. 327
13.4.1 Classication ................................................................................................. 328
13.4.2 Pharmacokinetics: Distribution and Duration of Action ............................... 329
13.4.3 Properties of the Main Crystalloids ............................................................... 329
13.4.4
Normal Saline Solution ................................................................................. 329
13.4.5 Ringer Lactate and Ringer Acetate ............................................................... 330
13.4.6 Latest-Generation Crystalloids ...................................................................... 330
13.4.7 Potential Risks and Side Effects .................................................................... 331
13.4.8 Hypertonic Crystalloids................................................................................. 332
13.5 Colloids ....................................................................................................................... 332
13.5.1
Classication ................................................................................................. 332
13.5.2 Physiological Properties of the Main Colloids .............................................. 333
13.5.3 Pharmacokinetics: Distribution and Duration of Action ............................... 333
https://t.me/med1917
314
Abstract
Cardiac surgery is responsible for profound modication in body water distribu-
tion, electrolyte plasma concentration, and acid–base balance. Maintaining uid,
electrolyte, and acid–base balance it must be taken into account the alterations
due to anaesthesia, the effects of cardiac surgery together with patient’s comor-
bidities and physiological response to the surgical stress. However the ideal
approach to perioperative uid management in cardiac surgery is still debated.
The debate involves the kind of uid to use (crystalloids vs colloids, colloid vs
colloid, balanced vs unbalance solutions) and the amount of uid to administer
(liberal vs restrictive). The goal-directed therapy seems to be the best choice to
guide the quantity of uid infused, potentially impacting on outcomes.
Electrolytes are always modied after cardiac surgery. With respect to the past,
the benet of their administration (in particular calcium) has been discussed in
literature. In this chapter, the basis of uid and electrolyte management in car-
diac surgery patient is explained, through understanding physiology and
pathophysiology.
13.6 Natural Colloids: Albumin (HA) ................................................................................ 334
13.6.1
Composition and Concentration .................................................................... 334
13.6.2
Pharmacokinetics: Distribution, Elimination, and Duration of Action ......... 334
13.6.3
Clinical Use ................................................................................................... 334
13.6.4
Potential Risks and Side Effects .................................................................... 336
13.7 Synthetic Colloids ....................................................................................................... 336
13.8 Dextrans ...................................................................................................................... 337
13.8.1
Pharmacokinetics: Distribution, Elimination, and Duration of Action ......... 337
13.8.2
Clinical Use ................................................................................................... 337
13.8.3
Potential Risks and Side Effects .................................................................... 338
13.9 Gelatins ....................................................................................................................... 338
13.9.1 Pharmacokinetics: Distribution, Elimination, and Duration of Effect .......... 339
13.9.2 Potential Risks and Side Effects .................................................................... 339
13.10 Hydroxyethyl Starches ................................................................................................ 339
13.10.1 Classication ............................................................................................... 340
13.10.2 Pharmacokinetics: Distribution, Elimination, and Duration of Action ....... 341
13.10.3 Clinical Use ................................................................................................. 343
13.10.4 Potential Risks and Side Effects .................................................................. 344
13.11 Hypertonic Colloid Solutions ..................................................................................... 347
13.12 Comparison Between Crystalloids and Colloids ........................................................ 348
13.13 Comparison Between HES and Other Colloids .......................................................... 350
Suggested References .............................................................................................................. 353
13.14 Comparison Between Balanced and Unbalanced Solutions ....................................... 353
13.15 How Much Fluid? ....................................................................................................... 353
13.15.1
Liberal vs. Restricted Approach .................................................................. 354
13.15.2 Goal-Directed Fluid Therapy ...................................................................... 356
13.16 Electrolyte Management ............................................................................................. 364
13.16.1 Sodium ........................................................................................................ 364
13.16.2 Potassium .................................................................................................... 367
13.16.3 Calcium ....................................................................................................... 369
13.16.4 Magnesium .................................................................................................. 371
Conclusion ............................................................................................................................... 371
References ................................................................................................................................ 372
F.E. Agrò et al.
https://t.me/med1917
315
13.1 Introduction
In 1865, Claude Bernard rstly referred to human body as a “milieu interieur,”
provided of its own homeostasis (Bernard 1865). The homeostasis is the prereq-
uisite of the performance of any physiological function, and it is founded on
three main systems, electrolyte system, acid–base system, and osmolar system,
that are strictly interconnected. Any change in one of them is responsible of
modication of both the remainders. In the “milieu interieur,” they are responsi-
ble for body water distribution and movements of uids and molecules.
Maintaining or restore the homeostasis of the “milieu interieur” acting on the
three systems is the nal goal of any clinical treatment, in particular, in the peri-
operative setting of cardiac surgery. In this case, the maintenance of uid, ionic,
osmolar, and acid–base balance is the sum of complex clinical evaluations and
actions, taking into account the kind of surgery, the alterations due to anesthesia,
the effects of cardiopulmonary bypass, patient’s comorbidities and his own
response to surgical stress (Fanzca
2012). In clinical practice, there is still much
uncertainty that should be in part overcome through an adequate knowledge of
human physiology.
13.1.1 Physiology of Body Fluids
The human body is divided into two main compartments: the intracellular space
(ICS) and the extracellular space (ECS). The ECS is divided into three addi-
tional compartments: the intravascular space (IVS, plasma), the interstitial
space (ISS), and the transcellular space (TCS). These compartments contain the
total amount of body water and are surrounded by a semipermeable membrane
through which uids pass from one space to another (Agrò and Vennari 2013a)
(Fig. 13.1).
Body water accounts for approximately 60 % of body weight; it is mainly dis-
tributed in the ECS and ICS. The ICS contains nearly 55 % of total body water and
the ECS approximately 45 % (about 15 L in a normal adult). Among the three
compartments, the IVS accounts for about 15 % of ECS water, the ISS for nearly
45 %, and the TCS for about 40 % (Agrò and Vennari 2013a) (Fig. 13.2).
The TCS is a functional compartment represented by the amount of uid and
electrolytes continually exchanged (in and out) by cells with the ISS and by the IVS
with the ISS (Agrò and Vennari 2013a). Other uids composing the ECS are secre-
tions, ocular uid, and cerebrospinal uid (Agrò and Vennari 2013a; Chappell et al.
2008).
Fluid and electrolyte balance is both an external balance between the body and
its environment and an internal balance between the ECS and ICS and between
the IVS and ISS. This balance is based on specic chemical and physical proper-
ties of body uids, such as ionic composition, pH, protein content, osmotic pres-
sure, osmolarity, and colloid osmotic pressure (Agrò and Vennari 2013a)
(Table 13.1).
13 Fluid Management and Electrolyte Balance
https://t.me/med1917
316
Extracellular space = 45 %
of body water
ICS: Intracellular space
55 % of body water
ISS:
Interstitial
space
I
n
t
r
a
v
a
s
c
u
l
a
r
s
p
a
c
e
Fig. 13.1 Body compartment representation (From Agrò and Vennari 2013a, pp. 1–26)
Extracellular
fluids = 45 %
of body fluids
Interstitial space
~
45 % of
extracellular fluids
Transcellular + other space
~
40 % of extracellular fluids
Intercellular fluids
~
55 %
Intravascular space
~
15 % of
extracellular fluids
ECS
Human body
60 %
water
Fig. 13.2 Body water distribution (From Agrò and Vennari 2013a, pp. 1–26)
F.E. Agrò et al.
https://t.me/med1917
317
13.1.2 Ionic Balance
Ionic balance is based on the principle of the “electric neutrality”: the sum of cat-
ions must be the same of the sum of anions. In other words, the net sum of the
electric charge in the body uids is zero. Ionic composition of ICS and ECS are
different and further differences exist in the ECS between the IVS and the ISS
(Table 13.1).
In clinical practice, the only value directly measurable is the plasma concentra-
tion of each ion is the only value directly measurable. Generally, this value is con-
sidered as a reference to evaluate the presence of electrolyte alterations.
The relationship between the ionic plasmatic composition and the neutrality prin-
ciple is expressed by the Gamble gram (Fig. 13.3). Examining the Gamble gram is
immediately evident that the sum of cations (Na
+
+ K
+
+ Ca
++
+ Mg
++
+ others) is
154 mEq/L and is the same of anions (Cl
−
+ bicarbonate + proteins + phosphates + sul-
fates + organic acids). Na
+
and K
+
represent 94 % of all IVS cations, while Cl
−
and
Table 13.1 Main properties of body uids
Properties
Plasma Interstitial uid
Intracellular uid
Colloid osmotic pressure (mmHg) 25 4 –
Osmolality (mOsmol/kg) 280 280 280
pH 7.4 7.4 7.2
Na
+
(mEqlL) 142 143 10
K
+
(mEqlL) 4 4 155
Cl
−
(mEqlL) 103 115 8
Ca
2+
(mEqlL) 2.5 1.3 <0.001
From Agrò and Vennari (2013a, pp. 1–26)
Na
+
Ca
++
Mg
++
K
+
Cl
–
HCO
3
–
Cations
+
Anions
–
140
105
Inorganic acids
Organic acids
Proteins
3
5
16
24
153
4
6
3
153
Fig. 13.3 Gamble gram.
Electric neutrality principle:
the sum of plasmatic cations
is equivalent to the sum of
plasmatic anions
13 Fluid Management and Electrolyte Balance
https://t.me/med1917
318
bicarbonate represent 84 % of all anions. Na
+
, K
+
, Ca
++
, and Mg
++
are generally
measured through laboratory exams, while bicarbonate is only calculated by using
the Henderson–Hasselbalch equation, when arterial blood sample is performed
(Gamble 1947) (see Chap. 15).
13.1.2.1 Sodium
Sodium is the most highly represented cation in the ECS, and it has a key hemody-
namic role: it is the main determinant of ECS volume, contributes to renin–angio-
tensin–aldosterone system activation, and regulates ADH secretion. Sodium
concentration determines body uid osmolarity. Changes in sodium plasma level
are responsible for modication in uid movement across the body space, determin-
ing ICS and ECS volume variation. The normal sodium concentration in plasma and
the ISS is about 142
mEq/L, and it is higher than the ICS concentration (10 mEq/L)
(Agrò and Vennari 2013a; Miller 2009).
13.1.2.2 Potassium
Potassium is the main cation of the ICS. It plays a central role in determining the
resting cell membrane potential, especially for excitable cells such as myocytes.
Therefore, it inuences the transmission of impulses along the cardiac pacemakers
(potentially predisposing to arrhythmias) and the contraction of myocardial cells.
It is also involved in a variety of metabolic processes, including energy production
and the synthesis of nucleic acids and proteins. The normal potassium concentra-
tion in plasma is about 4.5 mEq/L (Agrò and Vennari 2013a; Miller 2009).
13.1.2.3 Calcium
Several extra- and intracellular activities are regulated by calcium action. Calcium
is involved in endocrine, exocrine, and neurocrine secretion; coagulation activation;
muscle contraction (it has a great inotropic effect); potential membrane depolariza-
tion; cell growth; enzymatic regulation; and in the metabolism of other electrolytes
(especially potassium and magnesium). The normal calcium plasma concentration
is 2–2.6 mEq/L. Calcium may circulate in the plasma bound to albumin and free
from proteins. Free calcium may be ionized (physiologically active) or nonionized
(chelated with inorganic anions such as sulfate, citrate, and phosphate). The amounts
of the three forms are altered by many factors, such as pH, plasma protein levels
(hypoalbuminemia reduces total calcium, but not free fraction), and percentage of
anions associated with ionized calcium (blood products contain citrate) (Agrò and
Vennari
2013a; Miller 2009).
13.1.2.4 Magnesium
Magnesium is the physiological antagonist of calcium. It plays a crucial role in
neuromuscular stimulation and modulation of excitable cells activity (membrane
stabilizing activity); it also acts as a cofactor of several enzymes involved in the
metabolism of three major categories of nutrients: carbohydrates, lipids, and pro-
teins. The normal plasma concentration is about 0.85–1.25 mEq/L (Agrò and
Vennari 2013a; Miller 2009).
F.E. Agrò et al.
https://t.me/med1917
319
13.1.2.5 Chloride
Chloride is the most important anion of the ECS. Together with sodium, it deter-
mines the ECS volume. It is also responsible for the resting potential of the mem-
brane and action potential, acid–base balance, and plasma osmotic pressure. The
normal plasma chloride concentration is 97–107 mEq/L (Agrò and Vennari 2013a;
Miller 2009).
13.1.2.6 Bicarbonate
Bicarbonate is the main buffer system of the blood. It plays a crucial role in main-
taining acid–base balance. Two-thirds of the CO
2
in the human body is metabolized
as bicarbonate, through the action of carbonic anhydrase. The equilibrium between
CO
2
and bicarbonate leads to the elimination of volatile acid. The bicarbonate buffer
system is described by the following equilibrium reaction (Agrò and Vennari
2013a):
CO +H OHCO HCO+H
22 23 3
+
←→←→
−
When there is an increased concentration of H
+
, the system reacts by shifting the
reaction equilibrium to the left (towards the production of CO
2
), while when the
concentration of H
+
is reduced, the system moves to the right, resulting in the pro-
duction of H
+
. The bicarbonate buffer system works “in concert” with several organs
(see Chap. 15). Bicarbonate has a normal plasma concentration of about 24 mmol/L
(Agrò and Vennari 2013a).
13.1.3 Osmolar Balance
Chemical properties of ICS and ECS are very different (Table 13.1). According to
their Na
+
and glucose concentration, ICS is sweet, while ECS is salty. Despite such
difference, the principle of iso-osmolarity is crucial for body balance: ICS osmolar-
ity and ECS osmolarity must be the same. Osmotic pressure (μ) is the force exerted
by the sum of osmotically active particles (Na
+
and other electrolytes) that do not
freely pass through semipermeable membranes (Agrò and Vennari 2013a).
According to osmotic pressure difference among the compartments, water freely
passes form ICS to ECS, and vice versa, in order to achieve the equilibrium (Agrò
and Vennari 2013a) (Fig. 13.4). In particular, water shifts from the body compart-
ment with lower osmotic pressure to that with higher osmotic pressure. The osmotic
pressure gradient between the two compartments is described as tonicity (Agrò and
Vennari 2013a; Voet et al. 2001).
The osmotic pressure of the plasma osmotic pressure is 288 ± 5 mOsm/L, and it
can be calculated by measuring the plasma concentrations of Na, glucose, and urea.
Plasma osmoticpressure =2 Na mmol/L+urea /2,8 mg /dL
+gl
+
×
() ()
uucose/18 mg /dL
()
13 Fluid Management and Electrolyte Balance
https://t.me/med1917
320
The difference between measured osmolarity and calculated osmolarity is called
the osmolar gap. A high osmolar gap suggests either the presence of an exogenous
compound (e.g., ethanol) whose identity should be sought or the elevation of endog-
enous constituents that may not have been measured (e.g., proteins, ketoacids, lip-
ids) (Hendry 1961).
The main determinant of plasma osmolarity is Na
+
. Sodium salts are responsible
for the 95 % of the whole plasma osmotic pressure. Since osmotic pressure deter-
mines water tendency to move in or out of the cell, the Na
+
concentration is the main
determinant of the relative volumes and hydration of the ICS and ECS (Voet et al.
2001). When the ECS osmotic pressure increases (i.e., hypernatremia), water imme-
diately passes from ICS to ECS to restore osmotic equilibrium, leading to a reduc-
tion in ICS volume and an increase in ECS volume, while the opposite movement
develops when ECS osmotic pressure is reduced (i.e., hyponatremia), with an
increase in ICS volume and a reduction in ECS volume (Agrò and Vennari 2013a).
Sodium and water movements are further related by the mechanism of regulation of
osmolarity and volemia. They are hormonal systems such as ADH, renin–
angiotensin–aldosterone (RAA) system, ANP, BNP, and the thirst. Although with
different thresholds of sensibility (i.e., ADH is more sensible to osmolarity, while
RAA system to volemia), they are all enrolled both in case of osmolarity and vole-
mia alterations (Agrò and Vennari 2013a). Being the sole organ able to divide water
movement from Na
+
movement, the kidney is the main target of the regulatory sys-
tems. When an increase in plasmatic osmotic pressure develops, ADH and the thirst
promote water reabsorption and intake, while when plasmatic osmotic pressure
reduces, the reduction in water intake and its increased kidney excretion restore
normo- osmolarity (Agrò and Vennari 2013a) (Fig. 13.5).
Osmotic pressure
Permeable membrane
Fig. 13.4 Osmotic pressure. According to osmotic pressure, water diffusion will take place from
low to high electrolytic concentration (From Agrò and Vennari 2013a, pp. 1–26)
F.E. Agrò et al.
https://t.me/med1917
321
The RAA system is manly enrolled in sodium and water renal reabsorption,
when hypovolemia develops. In case of hypervolemia, the ANP and the RAA sys-
tem inhibition lead to excretion of sodium and water overload (Agrò and Vennari
2013a) (Fig. 13.6).
13.1.4 Fluid Movement Through Capillary Membranes
Fluid movements across capillary membrane are regulated by physical forces and
specic properties of the semipermeable membranes (Agrò and Vennari 2013a).
Accordingly, electrolyte and protein concentrations, as well as osmotic proper-
ties, play a crucial role, as expressed in the Starling equation:
Jv =K [P P)
fc
ic
i
−−
sd d
[]
()
Stimulates
Stimulates
Releases
Targets
Effects
Results in
↑
Na
+
concentration in plasma (
↑
osmolarity)
Osmo-receptors in hypothalamus
Posterior pituitary
Negative
feedback
inhibits
Antidiuretic hormone (ADH)
Collecting ducts of kindney
↑
Water reabsorption
Scant urine
↑
Plasma volume
↓
Osmolality
Fig. 13.5 Mechanism of ADH secretion: when uid volume decreases plasma sodium concentra-
tion and plasmatic osmolarity increases, leading to hypothalamic osmoreceptor stimulation. The
hypothalamus will then stimulate the posterior pituitary gland that releases antidiuretic hormone.
ADH will make renal distal tubules able to reabsorb water into the IVS in order to maintain
homeostasis of uid balance. ADH secretion is more sensible to plasmatic osmolarity than circu-
lating blood (From Agrò and Vennari
2013b, pp. 71–92)
13 Fluid Management and Electrolyte Balance
https://t.me/med1917
322
According to this equation, water ow depends on six variables:
1. Capillary hydrostatic pressure (P
c
)
2. Interstitial hydrostatic pressure (P
i
)
3. Capillary oncotic pressure (δ
c
)
4. Interstitial oncotic pressure (δ
i
)
5. Filtration coefcient (K
f
)
6. Diffusion coefcient (σ)
The equation states that the net ltration (Jv) is proportional to the net driv-
ing force ([P
c
− P
i
] − σ [δ
c
− δ
i
]). If this value is positive, water leaves the IVS
(ltration). If it is negative, water enters or remains in the IVS (absorption)
(Fig. 13.7). A modication of only one of the forces involved in the Starling
equation may alter uid movement across body compartment (Agrò and Vennari
2013a).
Pituitary gland:
posterior lobe: ADH
secretion
Collecting ducts:
H
2
O absorption
Arteriolar
vasocostriction
Increase in
blood pressure
Adrenal gland
cortex:
Aldosterone
secretion
Tubular Na
+
Cl
–
reabsorption and
K
+
excretion.
H
2
O retention
Sympathetic
activity
Water and salt retention. Effective
circulating volume increases.
Perfusion of juxtaglomerular
apparatus increases
Inhibitory signal
Stimulatory signal
Angiotensinogen
Renin
ACE
Angiotensin I
Angiotensin II
Fig. 13.6 Renin–angiotensin–aldosterone system: hypovolemia reduces perfusion of juxtaglo-
merular apparatus, with renin release. Circulating renin converts angiotensinogen to angiotensin I;
subsequently ACE (angiotensin-converting enzyme) acts on angiotensin I converting it to angio-
tensin II. This hormone increases NSS activity, increases reabsorption of Na and water by kidneys
directly and through aldosterone action, and determines vasoconstriction and ADH secretion
(From Agrò and Vennari
2013b, pp. 71–92)
F.E. Agrò et al.
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана