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
383
pressure preload parameters derived from a pulmonary artery catheter. J Cardiothorac Vasc
Anesth 15:584–588
Wiesenack C, Prasser C, Rodig G et
al (2003) Stroke volume variation as an indicator of uid
responsiveness using pulse contour analysis in mechanically ventilated patients. Anesth Analg
96:1254–1257
Wiesenack C, Fiegl C, Keyser A et
al (2005) Continuously assessed right ventricular end diastolic
volume as a marker of cardiac preload and uid responsiveness in mechanically ventilated
cardiac surgical patients. Crit Care 9:R226–R233
Wilkes NJ, Woolf R, Mutch M et
al (2001) The effect of balanced versus saline-based hetastarch
and crystalloid solutions on acid-base and electrolyte status and gastric mucosal perfusion in
elderly surgical patients. Anesth Analg 93:811–816
Williams EL, Hildebrand KL, McCormick SA et al (1999) The effect of intravenous lactated
Ringer’s solution versus 0.9 % sodium chloride solution on serum osmolality in human volun-
teers. Anesth Analg 88:999–1003
Wittkowski U, Spies C, Sander M et al (2009) Haemodynamic monitoring in the perioperative
phase. Available systems, practical application and clinical data. Anaesthesist
58:764–778–780–766
Zaloga G, Strikland R, Butterworth J et
al (1990) Calcium attenuates epinephrine’s betaadrenergic
effects in postoperative surgery patients. Circulation 81:196–200
Zander R (2009) Fluid management. Bibliomed, Medizinische Verlagsgesellschaft mbH,
Melsungen
13 Fluid Management and Electrolyte Balance
https://t.me/med1917
385
A. Dabbagh et al. (eds.), Postoperative Critical Care for Cardiac Surgical Patients,
DOI 10.1007/978-3-642-40418-4_14, © 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
14
Acid–Base Balance and Blood
Gas Analysis
Felice Eugenio Agrò, Marialuisa Vennari,
and Maria Benedetto
Contents
14.1 Introduction ................................................................................................................. 386
14.2 The Descriptive Approach ........................................................................................... 387
14.3 The Semiquantitative Approach .................................................................................. 388
14.4 The Quantitative Approach ......................................................................................... 389
14.5 Relation Among Fluid, Electrolyte, and Acid–Base Balance ..................................... 392
14.6 Basis of Pathophysiology of Acid–Base Balance in the Postoperative
ICU Setting of Cardiac Surgery .................................................................................. 394
14.7 Fluid and Electrolyte Management Consequences on Acid–Base Balance ................ 395
14.7.1 Hyperchloremic Acidosis .............................................................................. 395
14.7.2 Dilution Acidosis .......................................................................................... 396
14.7.3 SID ................................................................................................................ 396
14.7.4 Metabolizable Anions and Base Excess ........................................................ 396
14.7.5 Crystalloids and Acid–Base Status ............................................................... 397
14.7.6
Colloids and Acid–Base Status ..................................................................... 398
14.8 Maintaining Acid–Base Balance ................................................................................. 398
14.8.1 Arterial Blood Gas Analysis Interpretation................................................... 398
14.8.2 Boston Rules ................................................................................................. 400
14.8.3 Base Excess and Standard Base Excess ........................................................ 401
14.8.4 Anion Gap ..................................................................................................... 402
14.8.5 Stewart’s Approach and Strong Ions Difference ........................................... 403
14.9 Metabolic Acidosis ...................................................................................................... 404
14.10 Metabolic Alkalosis..................................................................................................... 407
14.11 Respiratory Acidosis ................................................................................................... 409
14.12
Respiratory Alkalosis .................................................................................................. 411
Conclusion ............................................................................................................................... 412
References ................................................................................................................................ 412
https://t.me/med1917
386
Abstract
Cardiac surgery patients may present many alterations of acid–base balance due
to cardiac pathology, comorbidities, type and duration of surgery, and CPB.
Acid–base status evaluation through Arterious Blood Gas (ABG) is the base for
an adequate perioperative treatment. ABG interpretation needs more useful tools
than those proposed by the Henderson–Hasselbach approach, such as anion gap,
standard base excess, and strong ions difference, in order to identify the underly-
ing acid–base disorders. In this chapter the physiology and pathophysiology of
acid–base balance in cardiac patients and their consequence on perioperative
management are described; an overview on ABG interpretation and its relation
with diagnostic hypothesis and therapeutic management are presented.
14.1 Introduction
“The most signicant and the most conspicuous property of blood is the extraordi-
nary ability to neutralize large amounts of acids or bases without losing its neutral
reaction” (Henderson 1908).
Acid–base balance represents a complex system through which the body main-
tains a neutral pH (7.38–7.42) in order to prevent protein degradation and alteration
of all biochemical reactions leading to death. In the human body there are many
acids produced by proteic, glicidic, and lipidic metabolisms. Every day the ener-
getic systems generate 15,000–20,000 mEq of CO
2
. Moreover a normal diet deter-
mines the formation of 50–100 mEq of H
+
. As a consequence our body has to ght
against acidity. Although a conspicuous production of acids, normally free H
+
plasma concentration is very low (0.00004 mEq/L) and pH homeostasis is guaran-
teed. The body has three systems opposing acid and base concentration blood varia-
tion: blood buffer systems, lungs, and kidneys, with different time of action (Agro
and Vennari 2013; Kellum and Weber 2009) (Table 14.1).
Blood buffer systems have an immediate action time. They are present in a total
amount lower than produced acids (2,400 mEq/L). This difference entails the need
for a continuous renovation of buffer systems.
The most important blood buffer is the HCO
3
−
/H
2
CO
3
system (see Chap. 13). Its
main role is imputable to three factors: it represents the 65 % of whole buffer power
of our body, it has an ubiquitarious distribution (interstitial space (ISS), intracellular
space (ICS), plasma, red cells, bones), and it has a pathway of elimination and a
pathway of renovation (Rose 1995).
Other buffer systems are hemoglobin, plasma proteins, and phosphate systems.
Hemoglobin lies the H
+
(carbaminohemoglobin) formed by the diffusion of CO
2
from plasma into erythrocytes (formation and dissociation of H
2
CO
3
for combina-
tion with H
2
O), while bicarbonate returns in the plasma (Rose 1995).
Table 14.1 Body
compensatory system and
time of action
Homeostatic system Action time
Blood buffer systems Immediate (fraction of second)
Lung (ventilation regulation) 1–15 min
Kidney (alkaline or acid
urine elimination)
Hours–days
F.E. Agrò et al.
https://t.me/med1917
387
Other plasma proteins present as anion may buffer H
+
excess, exchanging Ca
2+
with H
+
: the aminic group NH
2
−
lies H
+
, becoming NH
3
and releasing Ca
2+.
(acidosis
increases free Ca
2+
) (Rose 1995). Phosphate ions act as a buffer system in a similar
way as bicarbonate, but they are present in very low concentration in the extracel-
lular space (ECS) with respect to bicarbonate, while are very important in maintain-
ing ICS pH (Rose 1995):
HPOHHPONHPO
24 4
2
24
−+ −
↔+ ↔ .
The kidneys and lungs eliminate acids or bases in excess, permitting a regen-
eration of blood buffer systems. When the primitive cause of an acid–base altera-
tion is respiratory, a metabolic compensation develops (see Chap. 14): the kidney
eliminates excess H
+
and nonvolatile acids, regenerating bicarbonate through their
production (from amino acid metabolism) and their increased reabsorption from
proximal tubules (acid urine excretion) or increasing bicarbonate elimination and
H
+
reabsorption (alkaline urine excretion). When the primitive alteration is meta-
bolic, a respiratory compensation develops hyperventilation leads to CO
2
elimina-
tion when metabolic acidosis occurs, while hypoventilation generates CO
2
retention
when metabolic alkalosis develops. The lung acts in some minutes, while the kidney
in some hours (8–12 h) (Agro and Vennari 2013; Rose 1995).
There are three approaches to interpreting acid–base balance physiology. They
use distinct variables derived from a set of master equations that can be trans-
ferred from one approach to the other two (Agro and Vennari 2013; Kellum 2000)
(Fig. 14.1).
14.2 The Descriptive Approach
The traditional descriptive approach is based on arterial pH, pCO
2
, and bicarbon-
ate measurements. This approach originated at the end of the nineteenth century,
when Henderson revisited the Law of Mass Action from an acid–base equilibrium
perspective (Agro and Vennari 2013; Kellum 2005a). The result was
[] []
[]
HKaH
AA
+−
= •
/.
HCO
3
−
Hederson-Hasselbach Base excess Physical chemical
SBE
SIG
pCO
2
“Fixed acids”
H
+
pCO
2
Buffer base
pCO
2
SID
A
To t
Fig. 14.1 The three possible approaches to acid–base balance system description. Some factors
(i.e., pCO
2
) are considered by all the approach (Modied from Agro and Vennari (2013, pp. 1–26))
14 Acid–Base Balance and Blood Gas Analysis
https://t.me/med1917
388
where [H
+
] is the hydrogen ion concentration in solution, HA is a weak acid, A
−
a
strong base, and Ka is the dissociation constant of the acid. Henderson’s equation
revealed that when [HA] = [A
−
], [H
+
] does not change as a result of small variations
in the amount of acid or base in the solution (Agro and Vennari 2013).
For the H
2
CO
3
/HCO
3
−
system, the relation is
[] •[ ]HKaHCO HCO
+−
=
23 3
/.
Considering that H
2
CO
3
is CO
2
dissolved in water, the relation may be
rewritten:
[] []
•HKapCO HCO
+−
=
23
/.
In 1917, K.A. Hasselbalch applied Henderson’s equation to the main physiologi-
cal buffer system (CO
2
/HCO
3
−
) using logarithms, giving rise to the Henderson–
Hasselbalch equation (Agro and Vennari 2013; Kellum 2005b):
pH pKaHCO pCO
=+
−
lo
g/([ [])]
32
The pCO
2
value describes the respiratory contribution (CO
2
elimination/reten-
tion) to acid–base imbalances, while the metabolic contribution (acid overproduc-
tion, accumulation, reduced metabolism) is described by the bicarbonate
concentration in the blood. When pCO
2
is increased, H
+
production increases and a
respiratory acidosis develops, while when pCO
2
is reduced H
+
production reduces,
leading to a respiratory alkalosis. When bicarbonate is reduced, free H
+
increases
and a metabolic acidosis develops, while when bicarbonate increases, free H
+
is
reduced, causing metabolic alkalosis (see Chap. 13).
Since the 1940s, researchers have recognized the limitations of this approach to
acid–base physiology: blood bicarbonate concentration is useful in determining the
type of acid–base abnormality, but it is not able to quantify the amount of acid or
base excess–decit in the plasma, unless pCO
2
is held constant. This observation
promoted more researches, in order to quantify the metabolic component (Agro and
Vennari 2013; Kellum 2005a).
14.3 The Semiquantitative Approach
In 1957, K.E. Jörgensen and P. Astrup developed a tool to calculate bicarbonate concen-
tration, in which fully oxygenated whole blood was equilibrated with a pCO
2
of 40 mmHg
at 37 °C. This measurement was called standard bicarbonate. However, subsequent stud-
ies determined the role of the other plasma buffer systems (albumin, hemoglobin, and
phosphates), which were not considered using either the bicarbonate concentration or the
standard bicarbonate method (Agro and Vennari 2013; Astrup et al. 1960).
In 1948, Singer and Hastings dened the sum of the nonvolatile weak acid as the
“buffers” and bicarbonates as the “buffer base” (Agro and Vennari 2013; Siggaard-
Andersen 1962). This led to several revisions of the method to calculate changes
F.E. Agrò et al.
https://t.me/med1917
389
in the buffer base, including the base excess (BE) methodology (Agro and Vennari
2013; Kellum 2005a, b; Astrup et al. 1960; Siggaard-Andersen 1962; Grogono et al.
1976; Severinghaus 1976).
BE is the quantity of metabolic acidosis or alkalosis, dened as how much base
or acid should be added to an in vitro whole blood sample to reach a pH of 7.40,
while the pCO
2
is maintained at 40 mmHg. The most widely used formula for cal-
culating BE is the equation of Van Slyke (Agro and Vennari 2013; Kellum 2005a;
Siggaard-Andersen 1977; Wooten 1999; Brackett et al. 1965):
BE HCOHbp
HH
b
=−+×+×−×−×
()
−
([][ ])
3
24 423777410 023.. ...
where HCO
3
and hemoglobin (Hb) are expressed in mmol/L.
Subsequently the standard base excess (SBE) was developed (Siggaard-Andersen
and Fogh-Andersen 1995). SBE is the BE corrected for the buffer effect of hemo-
globin (assuming a mean extracellular hemoglobin concentration of 50 g/L), and it
better quanties the acid–base status in vivo with respect to BE (Agro and Vennari
2013; Brackett et al. 1965; Prys-Roberts et al. 1966):
SBEHCO pH=× +×−−
−
093148474244
3
..
..
{[
()
}.]
14.4 The Quantitative Approach
Another approach to acid–base pathophysiology is the calculation of the anion gap
(AG), which is the difference in the main measured plasma anion and cation con-
centrations (Fanzca 2012; Astrup et al. 1960):
[( ())]Na Cl HC
Om
Eq
++ −−
+−+=−
KL
3
81
6/
.
The AG corresponds to the difference between nonmeasured anions and cations:
[( )( )].Ca Mg PO SO organicanions proteins
22
4
3
4
2++ −−
+−++ +
Generally, AG values indicate a variation in the concentration of organic acids
(lactic acidosis, ketoacidosis). In fact, when their levels increase, the produced H
+
consumes bicarbonate, increasing AG values, while the organic anions maintain
electric neutrality of the plasma (Agro and Vennari 2013). A possible limit of the
AG is the wide variability in both plasma albumin concentrations and renal function
with respect to phosphate storage, especially in critically ill patients (Agro and
Vennari 2013; Kellum 2005a).
In the 1980s, P. Stewart introduced a new approach nalized to identify dependent
and independent variables enrolled in H
+
concentration determination (pH) (Agro and
Vennari 2013). This approach was based on (Agro and Vennari 2013; Kellum 2005a):
• The Law of Mass Conservation
• The electric neutrality
• Water dissociation constant
14 Acid–Base Balance and Blood Gas Analysis
https://t.me/med1917
390
Stewart’s approach considers three independent variables (Agro and Vennari
2013; Kellum 2005a):
• The strong ion difference (SID)
• Total weak acid concentration (Atot)
• pCO
2
The relationship between SID, pCO
2
, and Atot is the only determinant of pH, as
well as of [HCO
3
−
], which are dependent variables (Morgan 2005).
SID is the difference in the total amount of strong (totally dissociated) anions and
cations:
SID = ([Na
+
] + [K
+
] + [Ca
2 +
] + [Mg
2 +
])–([Cl
−
] + [A
−
] + [SO
4
2
–
]) (Fig. 14.2).
Considering water electric neutrality and water constant dissociation, it is pos-
sible to demonstrate two fundamental principles (Mercieri and Mercieri 2006):
1. SID is the independent variable inuencing H
+
and OH
−
concentrations.
2. SID may vary only adding or reducing strong ions.
As a consequence, H
+
or OH
−
variations are index of a primary SID modication,
and the primum movens of acid–base alteration is the variation of strong ions con-
centration. If strong anions increase with respect to strong cations, SID will be
negative and H
+
are increased with respect to OH
−
: H
+
concentration is the same of
the opposite of SID value (electro neutrality principle); while OH
−
are inversely
related to the opposite of SID value (Mercieri and Mercieri 2006):
[] []HS
ID
+
=−
[] []
OH SID
−′
=−
Kw
/.
On the other hand, if strong cations prevail on strong anions, SID is positive. In
this case OH
−
are higher than H
+
and OH
−
are the same of SID value (electro neutral-
ity principle), while H
+
are inversely related to SID (Mercieri and Mercieri 2006):
[][]
OH SID
−
=
160
80
0
mEq/L
[Na+] = 142
[K+] = 4.1
[Ca++] = 4.6
[Mg++] = 1.6
[CI
−
] = 106
[XA
−
] = 8
SID
Normal
= 38−42
SID = 152.3 −114
114
152.3
Fig. 14.2 SID representation. SID strong ion difference, XA
−
dissociated organic acids (Modied
from Agro and Vennari (2013, pp. 1–26))
F.E. Agrò et al.
https://t.me/med1917
391
[]
[]
OH SID
−′
=−Kw
/.
SID is physiologically positive (38–42 mEq/L). To preserve electric neutrality it
must be balanced by a corresponding excess of negative charges, represented by a
dissociated weak acid such as HCO
3
−
, proteins (especially albumin), phosphate, and
minimal concentrations of CO
3
2−
and OH
−
. Generally, proteins, phosphate, and
other nonvolatile acids are indicated as A
−
(Kellum 2005a; Mercieri and Mercieri
2006; Kellum et al. 1995).
As a consequence (Mercieri and Mercieri 2006):
SIDbicarbonate
=+
−
A.
The SID value obtained with this formula is called effective SID (eSID) vs the
apparent SID (aSID), obtained by the calculus of the sum of strong anions and
strong cations. When there is a difference between aSID and eSID, a strong, non-
measured anion is present (i.e., lactate, ketoacids), and it is causing a consumption
of buffer systems (bicarbonate and A
−
), with a reduction of eSID (Mercieri and
Mercieri 2006).
The balance between aSID and eSID is dened as SID gap (SIG) and is an index
for strong anions that are not measurable (XA
−
) (Fencl et al. 2000):
SIGXAaSIDeSI
Dm
Eq==−=−
−
61
0/
.L
In body uid compartments there are varying concentrations of nonvolatile weak
acids. In plasma they are represented by inorganic phosphate and albumin. The
same applies to ISS, although total concentrations here are very small. In red cells
the predominant source is hemoglobin (Morgan 2005).
The undissociated form of weak acids (HA) is neutral; the dissociated form (A
−
)
is negative. Their concentrations reect the Law of Mass Conservation
([ ][ ][ ])Atot HA=+
−
A
and the dissociation equilibrium
([ []
[]
)]HA
+−
=
**
.Ka HA
As a consequence A
−
, HA, and H
+
may vary with pH, but Atot remains the same
and is the independent variable inuencing other parameters (Mercieri and Mercieri
2006).
When CO
2
is present in water solution, it originates four kinds of molecules: dis-
solved CO
2
, H
2
CO
3
, HCO
3
−
, and CO
3
2−
. These species are involved in a chemical
reaction in our body resulting in effects on acid–base balance (Mercieri and Mercieri
2006).
Adding CO
2
to solutions (body uids) containing strong ions and weak acids,
Stewart needed six equations to describe acid–base balance modication (Table 14.2).
Knowing the independent variables (pCO
2
, SID, Atot), the system may be solved
for the remaining unknown variables ([A
−
], [HCO
3
−
], [OH
−
], [CO
3
2−
], [HA], and
[H+]) (Morgan 2005).
14 Acid–Base Balance and Blood Gas Analysis
https://t.me/med1917
392
Resolving the system for pH (−log [H
+
]), a resultant is a simplied equation that
may be written as (Mercieri and Mercieri 2006)
pH pK SIDATO
Tp
CO
Ka pH
=+ +− +
−
11
10
2
log/
/.
{()]}[ p
When SID = HCO
3
−
and Atot = 0, the equation becomes the same of Henderson–
Hasselbalch (Mercieri and Mercieri 2006):
pH pK HCOpCO=+
−
1
32
lo
g/
.[]
14.5 Relation Among Fluid, Electrolyte,
and Acid–Base Balance
In the 13th chapter and in the previous paragraphs, it has been evidenced that body
homeostasis is mainly based on three principles (Fig. 14.3):
– The electric neutrality principle (ionic)
– The iso-osmolarity principle (osmolar)
– The neutrality principle (acid–base)
These three principles are strictly interconnected as is immediately evident from
Stewart’s approach to acid–base balance.
Hydro-electrolytic and acid–base balances are related by bicarbonate: it is pres-
ent in the Gamble gram and in the Henderson–Hasselbalch equation. Variation of
bicarbonate plasma levels may affect the electric neutrality and the neutrality prin-
ciples. Hydrogen ions are also present in Gamble ionogram and in the Henderson–
Hasselbalch equation.
Osmolar and hydro-electrolytic balances are mainly connected by sodium,
present in Gamble gram and osmolarity equation, where sodium concentration
is multiplied for two. As a consequence, little sodium variation may have great
influences on osmolarity. Generally sodium is contained in the plasma as
salts such as NaHCO
3
or NaCl.
If bicarbonates are reduced other anions have to increases in order to maintain
electric neutrality. Chloride and bicarbonates are strictly related and their sum must
be constant in any moment: if one of them increases, the other reduces and vice
Table 14.2 The six equations of Stewart’s approach
Physical and chemical law Equation
Water constant dissociation [H
+
] × [OH
−
] = K ′w
Weak acid constant dissociation [H
+
] × [A
−
] = Ka × HA
Mass conservation law [HA]
+ [A
−
] = A
tot
Acid carbonic constant dissociation [H
+
] × [HCO
3
−
] = Kc × pCO
2
Bicarbonate constant dissociation [H
+
] × [CO
3
2
−
] = Kc × [HCO
3
−
]
Electric neutrality SID
+ [H
+
]–[H
+
] − [HCO
3
−
] − [CO
3
2
−
] − [A
−
] − [OH
−
] = 0
F.E. Agrò et al.
https://t.me/med1917
393
versa, in a rate of 1:1. In order to maintain electric neutrality, when both chloride
and bicarbonates are reduced, other anions concentration should be increased
(see Gamble gram and AG) (Sgambato and Prozzo 2003; Vulterini et al. 1992).
Finally, all acid–base interventions, including uid administration, act through
SID (electrolyte, osmolarity) or Atot or in combination (Morgan 2005; Sgambato
and Prozzo 2003).
The clinical consequences of the relations between the three systems are pre-
sented in some examples:
1. In case of diarrhea, bicarbonate will be reduced. To respect electric neutrality
principle, a hypobicarbonatemia causes hyperchloremia. It is also responsible of
a variation in Henderson–Hasselbalch equation with an increase of hydrogen ion
concentration and the development of metabolic acidosis.
Cations 153
Anions 153
K
+
4
[H
+
] = K
Posm = 2 [Na
+
]+
18
[Glucose] [N-ureic]
+
2.8
[HCO
3
−
]
P CO
2
HCO
3
−
24 Proteins 16
The electric neutrality
principle (ionic)
The neutrality
pr
inciple (acid-base)
The iso-osomolarity
principle (osmolar)
Orgnaic and
inorganic ac. 8
Ca
++
6Mg
++
3
Na
+
140
CI
−
105
Fig. 14.3 Relation among the ionic, acid–base, and osmolar balances
14 Acid–Base Balance and Blood Gas Analysis
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана