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2. In case of vomitus, there is a loss of HCl. In order to respect electric neutrality,
chloride reduction is replaced by bicarbonate increase. The loss of hydogenions
and the reduction of bicarbonate increase will determine a metabolic alkalosis
(accompanied by hypochloremia). In case of prolonged vomitus, to restore uid
and chloride decit uid are administered. The restoration of chloride levels deter-
mines a reduction of bicarbonate and, consequently, a correction of alkalosis.
3. Bicarbonate is present in the plasma as sodium salt. As a consequence, any
variation in bicarbonate levels will modify sodium and osmolar balance and
vice versa. For example, when bicarbonate (NaHCO
3
) is administered to correct
a severe metabolic acidosis, osmolarity increases potentially developing hyper-
volemia. Moreover, sodium overload determines a reduction of other cations
(K
+
or Ca
2+
).
14.6 Basis of Pathophysiology of Acid–Base Balance
in the Postoperative ICU Setting of Cardiac Surgery
Maintaining acid–base balance during and after cardiac surgery is essential for the
success of the surgery, especially for procedures requiring prolonged bypass time.
As an example, cardiac surgery patients are at high risk for developing arrhythmias:
the presence of a neutral pH is necessary to obtain a response to pharmacological
and electric treatments. At the same time acid–base status is considered as an index
of adequate perfusion of tissue (i.e., lactate increase, adequate renal compensation)
and may modify blood ux distribution. Moreover pH and pCO
2
variation may
inuence Hb-curve dissociation reducing Hb saturation (acidosis, pCO
2
increases)
or reducing Hb capacity to transfer O
2
to tissue (alkalosis, pCO
2
decreases) (Agrò
et al. 2013). Literature demonstrated in experimental and clinical studies the inu-
ence of pH on vascular tone resulting in possible blood ux redistribution and blood
pressure alteration (Celotto et al. 2008). Both modication of ECS pH (pHe) and
ICS pH (pHi) may cause these alterations through many proposed mechanisms:
neurotransmitter release, prostanoids, purines, smooth cell hyperpolarization, NO,
and changes in intracellular calcium concentration (Franco-Cereceda et al. 1993;
Aalkjaer and Poston 1996; Ishizaka and Kuo 1996). Moreover, acid–base balance
alterations have been related to modication of endothelium activity, with different
effects according to the type of considered vessel (Celotto et al. 2008).
On the other hand, cardiac surgery is responsible for profound alteration in acid–
base system. The mechanism at the base of this modication is different, causing an
impact on acid–base balance in opposite directions (Dobell et al. 1960; Beecher and
Murphy 1950; Gibbon et al. 1950; Puyau et al. 1962). Some of these mechanisms
depend on the type of oxygenator and the type of blood ow during the CPB and
CPB duration, the kind and the duration of postoperative mechanical ventilation,
hypotension in the postoperative setting (need for inotropes and/or vasoactive drugs,
bleeding), kind of uid used for priming and for liquid management (balanced vs
unbalanced), temperature modications (hypothermia reduces buffer system disso-
ciation, determining a “natural alkaline shift,” while CO
2
becomes more soluble and
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pCO
2
is decreased), and hemolysis (Fanzca 2012; Ito et al. 1957; Cofn and
Ankeney 1960; Litwin et al. 1959; Kirklin et al. 1956).
The more frequent alteration of acid–base equilibrium in cardiac patients is met-
abolic acidosis (Fanzca 2012). It is thought to be due to preexisting respiratory
alkalosis, increased lactate levels, hypoxia, and hypoperfusion (Dobell et al. 1960;
Beecher and Murphy 1950; Gibbon et al. 1950; Puyau et al. 1962; Ito et al. 1957).
Acidosis induces systemic vasodilatation (included coronary) and pulmonary vaso-
constriction (Fanzca 2012). Although vasodilatation may have positive effect, such
as an increase in coronary blood ow, its consequence may be detrimental in patients
presenting a cardiac dysfunction after the surgery (Celotto et al. 2008; Clancy and
Gonzalez 1975; Ely et al. 1982). Moreover, acidosis reduces the responsiveness to
catecholamines, decreasing pharmacological effectiveness of the treatment of post-
operative hemodynamic instability and further precipitating patients’ conditions.
Pulmonary vasoconstriction may increase pulmonary resistance and decompensate
the hemodynamic and respiratory status of cardiac surgery patients (Celotto et al.
2008).
14.7 Fluid and Electrolyte Management Consequences
on Acid–Base Balance
The previous chapter evidenced the relation among uid administration and modi-
cation of acid–base status, according to uid properties. Moreover, Stewart’s
approach underlined the role of electrolyte in maintaining or modifying acid–base
balance. As a consequence, the debate on SID of infused solution has adjunct to
literature discussion.
14.7.1 Hyperchloremic Acidosis
When establishing uid therapy, both acid–base and electrolyte iatrogenic disorders
must be avoided. Generally, metabolic acidosis with hyperchloremia is the most
frequently induced alteration (Agro and Benedetto 2013). Many available solutions
do not contain Atot (anions), leading to a dilution of ECS Atot and, consequently, to
a metabolic alkalosis. However, this effect is commonly overwhelmed by the
increase of the SID with the infusion, contributing to acidosis development (Morgan
2005). Clinical studies have revealed that chloride excess causes a specic splanch-
nic and renal vasoconstriction, interferes with cellular exchanges, and reduces the
glomerular ltration rate (GFR), leading to sodium and water retention (Agro and
Benedetto 2013; Quilley et al. 1993; Wilcox 1983). Hyperchloremia is generally
associated with metabolic acidosis and may cause a further reduction in GFR (Agro
and Benedetto 2013; Wilcox 1983). It has been shown that balanced and plasma-
adapted solutions help to avoid hyperchloremic acidosis, while assuring the same
volume effect as unbalanced solutions and potentially reducing morbidity and mor-
tality (Agro and Benedetto 2013; Zander 2006).
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14.7.2 Dilution Acidosis
Currently available solutions used throughout the world do not contain the physi-
ological buffer base bicarbonate because it cannot be incorporated into polyelec-
trolyte solutions, since carbonate precipitation would occur (Agro and Benedetto
2013). For this reason, any uid infusion may cause “dilution” acidosis, i.e., a dilu-
tion of the HCO
3
-
concentration, while the CO
2
partial pressure (buffer acid) remains
constant (Agro and Benedetto 2013; Shires and Holman 1948; Asano et al. 1966). In
the recent literature, the classic view of dilution acidosis has been reviewed. In fact,
according to Stewart’s approach, bicarbonate is a dependent variable, while the SID
of the infused solution is the determinant of acid–base effects. When SID of used
uid is zero, such as saline solutions with [Cl
−
] = [Na
+
], dextrose, mannitol, or water,
the administration of large volume leads to a reduction (dilution) of SID, causing
metabolic acidosis, independently from plasma [Cl
−
] variations (Makoff et al. 1970;
Miller and Waters 1997; Storey 1999; Figge et al. 1998). Metabolic acidosis may
have catastrophic consequences, especially in patients with preexisting acidosis
(i.e., patient with reduced CI and hypoperfusion) (Agro and Benedetto 2013).
14.7.3 SID
In order to avoid iatrogenic alteration of acid–base balance, an infused solution
should reduce SID (acidifying power) in a minimal rate, necessary to counteract the
Atot dilution alkalosis. As a consequence, the concept of balanced solution should
be extended considering SID and, particularly, the need for a SID lower than plasma,
but higher than zero (Morgan 2005). The ideal SID value is 24 mEq/L. It means that
24 mEq/L of the strong anion Cl
−
should be replaced by other anions, such as metab-
olizable anions (Morgan 2005; Morgan et al. 2004).
14.7.4 Metabolizable Anions and Base Excess
To compensate the absence of bicarbonate, initially OH
−
, HCO
3
−
, and CO
3
2−
were
adjuncted in vitro as components of IV uids. It was immediately evident they rap-
idly equilibrate with CO
2
(Morgan 2005). To overcome this problem, metabolizable
anions were used. Metabolizable anions are organic anions that may be converted
to HCO
3
−
by tissues. The main metabolizable anions are gluconate, malate, lactate,
citrate, and acetate. In IV uid, the most frequently used metabolizable ions are
acetate, malate, and lactate (Agro and Benedetto 2013).
Acetate and malate are contained in plasma in very low concentrations. They
may be metabolizable in all tissues, especially in muscles, liver, and heart (Agro and
Benedetto 2013; Lundquist 1962). Acetate is an early-onset (within 15 min) alkalin-
izing anion, while malate has a slower action (Agro and Benedetto 2013; Mudge
et al. 1949; Knowles et al. 1974; Akanji et al. 1989).
The most commonly used metabolizable anion is lactate, which is normally
produced in the human body. In fact, lactate is the main product of anaerobic
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glycolysis. It is metabolizable only by the liver (Agro and Benedetto 2013).
However, the use of lactate has been the cause of debate in clinical practice and in
the literature, especially with respect to patients with preexisting lactic acidosis.
This condition is a manifestation of disproportionate tissue lactate formation, with
respect to hepatic lactate metabolism (Agro and Benedetto 2013; Johnson et al.
1969; Levraut et al. 1998). Lactate levels are major criteria in the routine evalua-
tion of critically ill patients; indeed, changes in lactate concentration can provide
an early and objective evaluation of patient responsiveness to therapy (Agro and
Benedetto 2013; Abramson et al. 1993; Bakker et al. 1996; Cowan et al. 1984;
Falk et al. 1985; Friedman et al. 1995; Henning et al. 1982; McNelis et al. 2001;
Vincent et al. 1983; Rivers et al. 2001). Furthermore, plasma lactate levels in the
rst 24–48 h have a high predictive power for mortality in patients with various
forms of shock, including cardiac, hemorrhagic, and septic shock (Agro and
Benedetto 2013). In these situations, the administration of lactate-containing u-
ids may exacerbate the already existing lactic acidosis and interfere with lactate
monitoring for diagnostic purpose (Agro and Benedetto 2013; Levraut et al. 1998;
Weil and A 1970). According to these evidences, common sense suggests that
in ICU patients any use of lactate- containing solutions should be avoided (Agro
and Benedetto 2013).
Another indicator of acidosis is base excess (BE). Since 1990, clinical trials have
demonstrated that evaluating BE at the time of admission of critically ill patients is
indeed the best prognostic indicator for mortality, complication rate, and transfusion
needs (Agro and Benedetto 2013). Persistent base excess disorders above or below
4 mmol/L differ with respect to mortality rates: 9 and 50 %, respectively (Agro and
Benedetto 2013; Kincaid et al. 1998).
Balanced, plasma-adapted solutions reduce the risk of acidosis and BE altera-
tions (Agro and Benedetto 2013).
14.7.5 Crystalloids and Acid–Base Status
The composition of widely used crystalloids is discussed in the 13th chapter (see
Table 13.3).
Normal saline solution is a solution with SID = 0, and literature has extensively
demonstrated that it causes metabolic acidosis, especially after large amount of infu-
sion during normovolemic hemodilution or for cardiopulmonary bypass (Morgan
2005; Morgan et al. 2004; Beers 2006; Scheingraber et al. 1999; McFarlane and
Lee 1994; Prough and Bidani 1999; Rehm et al. 2000; Hayhoe et al. 1999; Liskaser
et al. 2000; Himpe et al. 2003). In addition to renal effects (discussed in chapter
14th), metabolic acidosis inhibits cardiac contractility, adrenoceptor function, and
coagulation (Fanzca 2012).
Considering a stable and normal plasma lactate concentration of 2 mEq/L,
Ringer lactate and Ringer acetate SID is 27 mEq/L. As a consequence, they are
slightly alkalinizing solutions, reducing metabolic acidosis risk, typical of rst-
generation crystalloids (Morgan 2005; Reid et al. 2003; Traverso et al. 1986;
Waters et al. 2001).
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Both Ringer solutions are more plasma-adapted than normal saline but are none-
theless unbalanced.
Last generation crystalloids are isotonic, balanced, and plasma-adapted solutions
that reduce the risk of chloride excess and dilution acidosis, with a decreased inu-
ence on lactate monitoring, lactic acidosis, and base excess (BE). They have a SID
higher than zero but lower than plasma (SID ~ 29 mEq/L) and, like Ringers solu-
tions, have an alkalinizing power (Morgan 2005).
14.7.6 Colloids and Acid–Base Status
As for crystalloids, SID value of each colloid is an important feature to consider
before the administration. The possible effects of their SID is reduced by two
factors: the lower amount infused with respect to crystalloids and their possible
contribution to Atot (the colloidal molecules may be weak acid) (Finfer et al. 2004;
Liskaser and Story 1999). As a consequence, Atot dilution alkalosis is reduced, as
long as colloidal molecules persist in the extravascular space (Morgan 2005).
However, after the infusion, weak acid colloids with SID > 0, such as albumin (HA)
and gelatins, presented a tendency to induce metabolic acidosis similar to 0.9 %
saline solution and other colloids with SID = 0 (Morgan 2005).
Currently available HA solutions are prepared as NaCl solutions (SID =0), which
can lead to metabolic acidosis and hyperchloremia and interfere with sodium and
water excretion, thus impairing renal function, especially in hypovolemic shock
patients. In acute renal failure, HA may accumulate after its massive administration
(Morgan 2005).
Succinylated gelatins are dispersed in a 4 % polyelectrolyte solution generally
containing Na
+
154 mEq/L, K
+
0.4 mEq/L, Ca
2+
0.4 mEq/L, and Cl
−
120 mEq/L
(effective SID = 34). Their low chloride content reduces the risk of hyperchloremic
acidosis and may be helpful in patients with acid–base alterations.
Recent balanced HES presented SID closer to the ideal value (24 mmEq/L).
They have been demonstrated to reduce the risk of iatrogenic metabolic acidosis
and potentially improve gastric mucosal blood ow, with a possible impact on endo-
toxemia survival (Wilkes et al. 2001; Kellum 2002). In a prospective, randomized,
double-blind study of cardiac surgery patients, a balanced HES 130/0.4 preparation
was compared to an unbalanced HES 130/0.4: while the hemodynamic status did
not differ between the two groups, the base excess was signicantly less negative in
the balanced than in the unbalanced HES group (Base et al. 2011).
14.8 Maintaining Acid–Base Balance
14.8.1 Arterial Blood Gas Analysis Interpretation
The evaluation of seriated arterial blood gases analysis (ABG) appears as indispens-
able to guide the postoperative management of the cardiac surgery patients and to
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permit a precocious diagnosis of tissue hypoperfusion and DO
2
modication. In fact,
ABG gives direct information about the main determinant of DO
2
(pO
2
, SpO
2
, and Hb)
and indirect information about CI, tissue perfusion, and oxygenation (lactic acidosis,
hypoxic acidosis). Moreover it allows the identication of ionic, osmolar, and acid–
base alterations. Acid–base alteration are often cause of matter in clinical practice,
they should be unrecognized and have catastrophic impact on patients.
According to acid–base perspective, ABG interpretation may use one of the
approach previously presented (Henderson-Hasselbalch, BE, AG, or Stewart’s
approach) or more of one of them, in order to better understand the contemporary
ionic and osmolar alterations and the cause of acid–base disturbance.
Examining ABG it is important to take into account that pH, pCO
2
, and pO
2
are
measured while HCO
3
−
and BE values are calculated.
To evaluate the acid–base state of the patient, the rst value to consider is pH.
A pH <7.38 indicates acidemia; a pH >7.42 indicates alkalemia. According to
the presence of buffer and compensatory systems, pH may be normal, but the other
parameters may be changed indicating alkalosis or acidosis. This situation is the
more frequent in the clinical practice and requires a profound knowing of physiol-
ogy and of the meaning of the different parameters obtainable with ABG.
In clinical practice, it is useful to only consider pCO
2
and bicarbonates values.
This use should be disapproved in order to avoid disagreeable mistake. In fact an
increased pCO
2
(>40 mmHg) may suggest a respiratory acidosis or the compensa-
tion for a metabolic alkalosis, while a reduced pCO
2
(<40 mmHg) may indicate a
respiratory alkalosis or the compensation for a metabolic acidosis. At the same time
a reduced HCO
3
−
(<24 mEq/L) may suggest a metabolic acidosis or the compensa-
tion for a respiratory alkalosis, while an increased HCO
3
−
(>24 mEq/L) may indi-
cate a metabolic alkalosis or the compensation for respiratory acidosis (Fig. 14.4).
Acid–base disorders of different origin may be contemporarily present (i.e.,
a metabolic acidosis due to hypoperfusion with a respiratory alkalosis due to
hyperventilation). To better understand the number, the nature, and the grav-
ity of the acid–base disturbance, other factors may be considered. The time of
development of the observed alteration may be helpful. If an alteration appears
few hours ago, it is improbable that bicarbonate variation may represent a renal
compensation, but it is more probable that it represents an underlying metabolic
disturbance.
The evaluation of Boston rules, BE, AG, and SID may be more useful to solve
the “ABG enigma.”
An eight-step approach to ABG acid–base status interpretation:
1. pH (acidosis or alkalosis?)
2. pCO
2
(same or opposite direction with respect to pH?)
3. HCO
3
−
(same or opposite direction with respect to pH?)
4. Compensation (Boston rules)
5. AG
6. Delta gap (if AG increased)
7. SID–SBE
8. Electrolytes
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14.8.2 Boston Rules
Boston rules are mathematic relation between bicarbonate and pCO
2
values, based
on the observation of patients with note and compensate (normal pH) acid–base
alterations.
In case of metabolic acidosis, pCO
2
should reduce by 1,5 mmHg for each
1 mEq/L of HCO
3
−
reduction. If pCO
2
is lower with respect to the expected value,
there is a contemporary respiratory alkalosis; if it is higher there is a contemporary
respiratory acidosis (Beers 2006).
In case of metabolic alkalosis, pCO
2
should increase by 0,7 mmHg for each
1 mEq/L of HCO
3
−
increasing. If pCO
2
is lower with respect to the expected value,
there is a contemporary respiratory alkalosis; if it is higher there is a contemporary
respiratory acidosis (Beers 2006).
60
[HCO
3
−
]
PCO
2
56
52
48
44
40
36
32
28
24
20
16
12
8
4
0
7.0 7.1 7.2 7.3 7.4
pH
7.5 7.6 7.7 7.8
10
15
20
25
30
35
40
5060708090100120
Chronic
respiratory
acidosis
Normal
Metablic
alkalosis
Chronic
respiratory
alkalosis
Metabolic
acidosis
Acute
respiratory
acidosis
Acute
respiratory
alkalosis
Fig. 14.4 A Graphic tool to rapidly identify acid–base patient disorders knowing pH, [HCO
3
−
],
and pCO
2
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In case of acute respiratory acidosis, HCO
3
−
should increase by 1 mEq/L for each
10 mmHg of pCO
2
increasing; in case of chronic acidosis, the increase should be
4 mEq/L. If the bicarbonate is lower with respect to the expected value, there has
been no enough time for the development of compensation, or there is a contempo-
rary metabolic acidosis; while if it is higher there is an underlying metabolic alka-
losis (Beers 2006).
In case of acute respiratory alkalosis, bicarbonate should reduce by 1
mmEq/L
for each 10 mmHg of pCO
2
decreasing; while in case chronic respiratory alkalo-
sis, the reduction should be 5 mmEq/L. If bicarbonate is lower with respect to the
expected value, there is a contemporary metabolic acidosis; while if it is higher
there is a contemporary metabolic alkalosis or little time to develop compensation
(Beers 2006) (Table 14.3).
14.8.3 Base Excess and Standard Base Excess
A positive BE (>+2) suggests an alkalosis (metabolic), while a negative BE (<−2)
suggests an acidosis (metabolic).
SBE is a practical tool to replace SID at bedside (Morgan et al. 2000; Schlichtig
et al. 1998a; Schlichtig et al. 1998b). Normally it ranges in −3/+3 mEq/L and it
represents the change in SID value needed to restore acid–base balance. If SBE <−3
Table 14.3 Bicarbonate and pCO
2
variation according to Boston rules
pH
Disorder HCO
3
PCO
2
Compensation
evaluation
Comment
≤7.38
acidosis
Metabolic ≤24
mEq/L ↓ 1.5 mmHg
for each
1
mEq/L
of
HCO
3
↓
pCO
2
value
higher
Respiratory
acidosis
pCO
2
value
lower
Respiratory
alkalosis
Respiratory ↑ 1
mEq/L (acute),
↑ 4 mEq/L(chronic)
for each 10 mmHg
of pCO
2
↑
≥40
mmHg HCO
3
value
higher
Metabolic
alkalosis
HCO
3
value
lower
No time for
compensation
or
metabolic
acidosis
≥7.42
alkalosis
Metabolic ≥24
mEq/L ↑0.7 mmHg
for each
1 mEq/L of
HCO
3
↑
pCO
2
value
higher
Respiratory
acidosis
pCO
2
value
lower
Respiratory
alkalosis
Respiratory ↓ 1
mEq/L (acute),
↓ 4 mEq/L (chronic)
for each 10 mmHg
of pCO
2
↓
≤40
mmHg HCO
3
value
higher
No time for
compensation
or
metabolic
alkalosis
HCO
3
value
lower
Metabolic
acidosis
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there is a metabolic acidosis (SID increased); while if SBE >+3 there is a meta-
bolic alkalosis (Vulterini et al. 1992). In case of acidosis, SBE corresponds to the
theoretical NaHCO
3
dose (in mmol/L) per liter of ECS water, which is needed
to normalize acid–base balance; while in case of alkalosis it corresponds to the
theoretical dose of HCl (Fanzca 2012).
14.8.4 Anion Gap
An increased AG (>16 mEq/L) indicates a metabolic acidosis due to the presence of
nonmeasurable acids such as the organic lactate acid (ABG also reports lactate val-
ues) or other inorganic acids (i.e., phosphate retention in kidney dysfunctions)
(Beers 2006).
A normal AG may indicate a metabolic acidosis due to HCO
3
−
reduction (i.e.,
dilution acidosis, renal lost such as postoperative NTA) or to increased Cl
−
(uid
infused, hyperchloremia). According to the electro neutrality principle, the AG
remains stable because HCO
3
−
variations are compensated by Cl
−
, and vice versa:
metabolic acidosis with normal AG is always hyperchloremic.
In order to complete the evaluation of patient’s acid–base asset, it is important to
consider the rate between the difference of patient AG with respect to the normal
AG (AG gap) and the difference of normal bicarbonate with respect to the patient’s
bicarbonate (bicarbonate gap). This ratio is dened as delta gap and it may suggest
the presence of more than one acid–base disturbance (Beers 2006):
Deltagap Measured AG Normal AG Normal HCOMeasured HCO=− −
−−
()
()
/
33
==−−
=
−
−
()()
∆∆
Measured AG measured HCO
AG HCO
12 24
3
3
/
/.
If the only alteration is metabolic acidosis with AG, the delta gap value should
be 1, reecting the buffering of nonmeasurable acids. If the delta gap value is <1,
bicarbonate reduction is due to the presence of other acids rather than nonmea-
surable acids: there is another cause of metabolic acidosis with normal AG and
hyperchloremia should be present. When the delta gap value is >1, the reduction of
bicarbonate is contrasted by a factor leading to their increase: there is a contempo-
rary metabolic acidosis (Beers 2006).
Referring to AG, it is fundamental to establish the plasma levels of proteins
(especially albumin), nonmeasured cation (Ca
2+
and Mg
2+
) and measured cation
(especially Na
+
) levels, the presence of renal dysfunction with possible increased
uremia, and the lipidic asset.
In fact, AG may be increased by hyperalbuminemia (rare in ICU patients) and
uremia (increased anions) or by hypocalcemia and hypomagnesemia (reduced
cations); while it may be reduced by hypoalbuminemia (frequent in ICU post-
bypass patient) or by hypermagnesemia and hypercalcemia (increased cations).
Finally AG may result negative (artifact) in case of severe hypernatremia or
hyperlipidemia.
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14.8.5 Stewart’s Approach and SID
According to Stewart’s approach ([SID] + [H
+
] = [HCO
3
−
] + [A
−
] + [CO
3
2−
] + [OH
−
]),
acid–base alterations are due to modication of independent variables. As a conse-
quence, respiratory unbalance is caused by pCO
2
modication, while metabolic
alteration is imputable to SID and/or Atot modication.
SID decreases in metabolic acidosis and increases in metabolic alkalosis (Fanzca
2012; Kellum 2005a). In fact, a reduction of SID value (strong anions > strong cat-
ions; SID <38
mEq/L) leads to H
+
increase in order to maintain electric neutral-
ity. SID reductions may be due to an increase of organic acids such as lactate or
ketones, a loss of cations (i.e., diarrhea), an alteration of Cl
−
excretion by the kidney
(i.e., development of postoperative AKI), Cl
−
overload (unbalanced solution use), or
intoxication (i.e., salicylates). Another cause of SID reduction in postoperative ICU
patients may be phosphate retention (H
+
will increases to compensate) caused by
renal dysfunction, especially in patients with chronic renal diseases (Fanzca 2012;
Morgan 2005).
The reduction of SID (H
+
increase) will be compensated by homeostatic alkalin-
izing reactions:
• Kidney increases Cl
−
excretion (strong anions reduce, SID increases, and H
+
reduce).
• Association of weak acid such as phosphate and proteins with formation of HA
until 3–4 mEq/L (in severe cases).
• Hyperventilation: pCO
2
decreases by 1,2 mmHg for each 10 mEq/L of SID
reduction.
On the other hand, an increase of SID value (strong cations > strong anions; SID
>42 mEq/L) causes alkalosis leading to H
+
reduction in order to respect electric
neutrality. SID increases may be due to loss of anions (vomitus, diuretics) or cation
administration (i.e., transfusions, excess of unbalanced IV uids). Generally the
more frequent cause is hypochloremia. In cardiac surgery ICU patients, SID increase
may be due to hypoalbuminemia leading to reduction of Atot (Fanzca 2012; Morgan
2005).
The increase of SID (H
+
reduction) will be compensated by homeostatic acidify-
ing reactions:
• Kidney retains Cl
−
(strong anions increases, SID reduces, and H
+
increases).
• Na
+
shift into cell (strong cations reduce, SID reduces, and H
+
increases).
• Dissociation of weak acid with formation of A
−
and H
+
.
• Hypoventilation: pCO
2
increases by 0.7 mmHg for each 10 mEq/L of SID
increase.
The value of Atot depends primarily by plasmatic proteins and in minimal part
by other weak acids. An increase of its value is caused by an increase in plasma
proteins or phosphate levels. An increase of Atot has the same effect of a decrease in
SID: it causes metabolic acidosis. By contrast, hypoalbuminemia causes metabolic
alkalosis, as SID increases (Fanzca 2012; Morgan 2005).
In case of respiratory acidosis, the increase of H
+
is compensated by an increase
of SID (determining H
+
decrease) due to a reduction of Cl
−
. In acute cases the shift
14 Acid–Base Balance and Blood Gas Analysis
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