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Stewart's approach to acid-base disorders Evaluation of Acid-Base Disorders in Two Patients Using Stewart's Approach

  • Taipei Medical University,Shuang Ho Hospital, Ministry of Health and W


Disturbances of acid-base balance can result from serious cellular and general consequences. Monitoring of blood pH is clinically important to evaluate and understand the physiological condition of a critically ill patient. The traditional approach to acid-base equilibrium based on the Henderson –Hasselbalch equation focuses on changes in the concentration of bicarbonate (HCO 3 -), the partial pressure of carbon dioxide (pCO 2), the dissociation constant and the solubility of CO 2 . The Stewart's approach, however, based on the analysis of the complex components of physiologic fluid, such as sodium (Na +), potassium (K +), calcium (Ca 2+), magnesium (Mg 2+), chloride (Cl -), pCO 2 , lactate, phosphorus, and protein, provides better information and a more accurate conceptual view of acid-base mechanism. In this review, we evaluate two cases of acid-base disturbance, one after major surgery, and the other after liver transplantation, using the Stewart's approach, and compare it with the traditional approach.
Stewarts approach to acid-base disorders
Received: June 5, 2009 Accepted for publication: August 27, 2009
From the 1Division of Nephrology, Department of Medicine, 2Department of Emergency
Cardinal Tien Hospital, Fu-Jen Catholic University School of Medicine
Address reprint requests and correspondence: Dr. Jung-Mou Yang
Department of Emergency, Cardinal Tien Hospital
362 Chungcheng Road, Hsintien City, Taipei County 23137, Taiwan (R.O.C.)
Tel: (02)22193391 ext 65340 Fax: (02)29107920
Evaluation of Acid-Base Disorders in
Two Patients Using Stewart’s Approach
Cai-Mei Zheng1, Kuo-Cheng Lu1, Jing-Quan Zheng1, Jung-Mou Yang2
Disturbances of acid-base balance can result from serious cellular and general consequences.
Monitoring of blood pH is clinically important to evaluate and understand the physiological condition
of a critically ill patient. The traditional approach to acid-base equilibrium based on the Henderson
–Hasselbalch equation focuses on changes in the concentration of bicarbonate (HCO3
-), the partial
pressure of carbon dioxide (pCO2), the dissociation constant and the solubility of CO2. The Stewart’s
approach, however, based on the analysis of the complex components of physiologic uid, such as sodium
(Na+), potassium (K+), calcium (Ca2+), magnesium (Mg2+), chloride (Cl-), pCO2, lactate, phosphorus, and
protein, provides better information and a more accurate conceptual view of acid-base mechanism. In this
review, we evaluate two cases of acid-base disturbance, one after major surgery, and the other after liver
transplantation, using the Stewart’s approach, and compare it with the traditional approach.
Key words: acid-base balance, strong ion, Henderson–Hasselbalch, Stewart’s approach, anion gap,
metabolic acidosis, respiratory alkalosis
Acid-base disturbances remain sophisticated
problems in clinical practice. The pH is tightly
controlled in acid-base physiology by changes in
the plasma hydrogen ion concentration [H+]. The
traditional approach to acid–base control is based
on the Henderson–Hasselbalch equation(1,2). An
alternative clinical approach to acid-base balance
was cited by Peter A. Stewart, Ph.D in 1981(3-5).
In Stewart’s approach, the strong ion difference
(SID) of dissociated ions, partial pressure of carbon
dioxide (pCO2), and the sum of acids present in
the plasma become the major determinant of [H+]
in the plasma(5,6). This revolutionalized concept is
accepted and widely applied in many European
hospitals, especially in critical care units, trauma
centers and anesthetic centers, since this approach
can identify more major acid-base disturbances than
the traditional approach.
The Traditional Approach to
Altering pH
In traditional acid-base evaluation, the
Henderson and Hasselbalch equation is used: pH
= pKa + log ([HCO3
-] / [0.03 pCO2 mmHg]) where
the pKa value at 37°C is 6.1(1,2). With this equation,
metabolic disorders are not clearly quantied since
-] depends on the partial pressure of (pCO2)
in vivo. So, the standard base excess (SBE) and
standard bicarbonate theories were introduced
J Emerg Crit Care Med. Vol. 21, No. 1, 2010
to reveal underlying metabolic disorders(7,8). The
calculated bicarbonate value is adjusted under a
pCO2 of 40 mmHg (5.3 kPa) to achieve the standard
bicarbonate value. The SBE represents the amount
of base that needs to be added to the blood to get
a normal pH at a pCO2 of 40 mmHg. The more
negative the SBE, the more acidic the blood results.
Stewart’s Physicochemical Approach
to Altering pH
With the Stewart concept, autoionization
of water results in H+ and OH -, a nd the water
dissociation can be written as:
H2O H+ + OH-
Water dissociation remains constant, in other
Kw = [H+] × [OH-],
Where Kw is the dissociation constant for
If [H+] increases, [OH-] decreases by the
same amount. Three variables that determine water
dissociation, i.e. the pCO2, SID, and total weak
acid concent ration ( ATOT), bec ome importa nt in
determining the pH (Fig. 1)(11).
Our goal in this report is to compare the
traditional approach to acid-base equilibrium based on
the CO2 and HCO3
- buffering system with the Stewart’s
approach based on the so-called SID and ATOT.
Case 1
A 72 years old woman had a motor vehicle
accident and sustained severe injuries to the right
anterior chest and lower abdomen. She had a
history of type 2 diabetes mellitus and hypertension
for 5 years, chronic obstructive lung disease for
3 years, and a cholecystectomy for gallstones 2
years previously. Her regular medications include
Fig. 1 The three independent factors that determine water dissociation, [H+] and plasma pH,
are: (1) pCO2; (2) SID; and (3) ATOT. The degree of water dissociation with the release
of H+ is the determinant of body pH. The pCO2 reects respiratory disturbances in the
pH; SID and ATOT reects metabolic disturbances in pH. (Abbreviations: ATOT, total
weak acid concentration; A, dissociated weak acids; AH, associated weak acids; SID,
strong ion difference) (Modied from reference 11)
Stewarts approach to acid-base disorders
glidiab, nifedipine, and atrovent inhalers prescribed
by an endocrinologist in the out-patient department.
In the Emergency Room, she was in critical
condition with fractures of multiple ribs, pulmonary
contusion, and intestinal perforation. Emergency
exploratory laparotomy was done and a massive
amount of blood was found intraperitoneally. During
surgery, large amounts of lactated Ringer’s solution and
packed red blood cells were given intravenously. Arterial
blood gases obtained in the operating room revealed
the pH, PaCO2, and SBE were 7.10, 30 mmHg,
and -19 mEq/l, respectively. The plasma lactate
concentration was 11.5 mEq/l after additional blood
products and 120 mmol of NaHCO3 were given for
resuscitation. Here, the patient had lactic acidosis
secondary to blood loss and tissue destruction (SBE
of -19 mEq/l, increased lactic acid) with acute
respiratory acidosis (calculated pCO2 of 21 mmHg,
less than the actual PaCO2 of 30 mmHg) from poor
ventilation because of rib fractures and pain.
After transfer to the intensive care unit (ICU),
ventilation was supported with a mechanical
ventilator. Her blood gas analysis revealed pH
was 7.35, pCO2 35 mmHg, and SBE -5 mEq/l,
and the serum lactate was 8.0 mEq/l. Because her
hematocrit was low at 29%, she received 4 units
of packed red blood cells intravenously. Six hours
later, blood gas analysis showed that her blood
pH and SBE had increased to 7.58 and +11 mEq/l,
respectively, and pCO2 and [lactate] had decreased
to 34mmHg and 2.1 mEq/l, respectively. Here,
the patient had primary metabolic alkalosis due
to increased SBE and mild respiratory alkalosis
with a pCO2 of 34 mmHg. The components of the
metabolic alkalosis were a combination of lactate
clearance, massive blood transfusion (citrate), and
NaHCO3 administration. The ventilator settings
af t e r adju s t ment t o comp e n s ate f o r meta b o lic
acidosis contributed to the respiratory alkalosis. So,
the minute ventilation was reduced to allow mild
hypercapnea to normalize the pH to 7.40.
On postoperative day 3 (POD3), the patient
had fever and hypotension. An arterial blood gas
analysis revealed a pH of 7.31, SBE of -9 mEq/l
and arterial lactate of 5.9 mEq/l. The calculated
anion gap (AG) was 17 mEq/l, and concentrations
of plasma phosphate and albumin were in the
normal range. Owing to low central venous pressure
and hypotension, she received 8 liters of normal
saline and a norepinephrine infusion over the next
24 hrs. Her urine output was only 200 cc despite
resuscitation. On post-operative day 4 (POD 4), her
arterial blood gas analysis showed a pH of 7.22,
pCO2 of 30 mm Hg, [HCO3
-] of 12 mEq/l, and SBE
of -13 mEq/l, and the arterial lactate was 4.2 mEq/l.
There was metabolic acidosis despite the reduction
in plasma lactate levels. This was because of the
large volume of normal saline infused on POD3,
indicating the classic situation of hyperchloremic
metabolic acidosis from resuscitation uids.
On POD5, the patient received 3.5 liters of
fluid supplemention with lactated Ringers (Na+:
130 mEq/l, lactate: 28 mEq/l). The urine output
increased and her acid-base status improved with
decreased [Cl-] in the plasma. The patient’s blood gas
and biochemistry data are summarized in Table 1.
Traditional approach
In this case, the traditional approach indicated
that hyperchloremic acidosis should be treated
with sodium bicarbonate solution: NaHCO3
Na+ + HCO3
- or Tris-hydroxymethyl aminomethane
(THAM): R-NH2 + H 2O + C O 2 R-NH3
+ +
-. Here, R-NH2 is THAM and R-NH3
is the
protonated form of THAM. Both treatments can
donate bicarbonate, cause an increase in plasma
-] and restore the pH to normal.
Application of Stewart’s strong ion concept
The traditional approach does not explain how
and why the hyperchloremic metabolic acidosis
occurs from large amounts of infused normal saline.
J Emerg Crit Care Med. Vol. 21, No. 1, 2010
Table 1 Case 1 patient’s blood gas and biochemistry data
Blood chemistries On Arrival ICU 7am POD3 8am POD4 6am POD5
Na (mEq/l) 140 139 142 139
K (mEq/l) 3.9 3.2 3.5 3.9
Mg (mEq/l) 1.65 - 1.64 -
Cl (mEq/l) 102 103 114 108
HCO3 (mEq/l) 18.8 22.1 12 22
[H+] (nmol/l)
pCO2 (mmHg) 35 45.1 30.1 40.0
SBE (mEq/l) -5 -9 -13 -5
Lactate (mEq/l) 85.9 4.2 2.1
Albumin (g/dl) 4.1 - 4.0 -
Phosphate (mg/dl) 3.8 - 3.9 -
Anion Gap (mEq/l) 23.1 17.1 19.5 12.9
SID (mEq/l) 40.6 40.0 34.0 39.5
- SID= { [Na+] + [K+] + [Ca2+] + [Mg2+] } - { [Cl-] + [lactate] }
- Conversion of lactate in mg/dl to mEq/l (mmol/l) involves multiplying by 0.111
Stewart’s approach explains the mechanism of
hyperchloremic acidosis and its rational treatment.
This is important since normal saline is widely used
nowadays as a rst line resuscitative uid in most
hospitals and may deteriorate underlying acidosis if
it is unnoticed.
The Stewart concept starts with strong ions,
completely dissociated ions which exist only
as charged forms at physiologic pH in biologic
solutions. In plasma, strong ions may be inorganic,
e.g. Na+, Cl-, K+ or organic, e.g. lactate, where Na+
and Cl- are the major and most abundant strong
Strong ion difference
SID = (the sum of all measurable strong cation
concentrations in the plasma) minus (the sum of
all measurable strong anion concentrations in the
plasma)(11). SID= { [Na+] + [K+] + [Ca2+] + [Mg2+ ] }
- { [Cl-] + [lactate] }
The normal plasma SID is 40 to 42 mmol/l of
a net positive charge. Plasma SID changes have a
signicant inuence on water dissociation via the
laws of electrical neutrality and mass conservation.
A net increase in the strong cation concentration
in the plasma will increase the SID. The increase
in the SID level decreases H+ release from water,
and thus reduces plasma [H+] and elevates pH(1,2).
Similarly, a decreased serum SID from strong anion
elevation may increase water dissociation with a
resultant increase in [H+] and lower pH.
Normal human plasma is on the alkaline
side of neutral with a positive SID. Plasma [Na+]
and [Cl-] are in the ranges of 135-155 mEq/l and
95-105 mEq/l, respectively. Normal saline solution
with no other strong ions present has a SID of
0 mEq/l ([Na+]=[Cl-]=154 mEq/l). When normal
saline is infused intravenously, a net increase in
Cl- anion compared with Na+ cation results in a
decreased SID that causes dissociation of H+ from
H2O. An increase in plasma [H+] and a fall in pH
could be expected with normal saline infusion.
Here, hyperchloremia was the cause of metabolic
acidosis. The more negative ions of Cl- infused, the
more acidic the plasma becomes. The rate and dose
of normal saline infusion is the main determinant of
hyperchloremic acidosis.
The specific treatment for hyperchloremic
Stewarts approach to acid-base disorders
acidosis is to increase the SID by adding strong
cation to compensate for water dissociation and
hydrogen ion release. A solution with a strong
cation concentration exceeding the strong anion
concentration by 40-42 mEq/l can be given for this
purpose since the normal plasma SID is 40-42 mEq/l.
Both 130 mmol of sodium bicarbonate (e.g. 7.5%
sodium bicarbonate; Na+ without Cl-, effective SID
of 130 mEq) and 128 mmol of THAM have a high
effective SID and can correct this type of acidosis.
Therefore, the strong ion approach explains how
and why sodium bicarbonate and THAM are
us e d t o tre at h yperch loremi c ac i dosis. On the
contrary, if critically ill patients present with severe
hyperlacta tem ia ass oci ated with hypochloremic
alkalosis, the laboratory data may show normal
values for the pH, [HCO3
-] and SBE(12 ).
Case 2
A 58 years old man had liver transplantation.
Because of allograft function impairment, the lactate
concentration increased to 16 mEq/l 5 hours after
transplantation. At tha t ti me, arterial blo od gas
analysis revealed a pH of 7.18, pCO2 of 30 mmHg,
and SBE o f - 1 7 m E q /l , i n d i c a t i n g metabolic
acidosis secondary to lactic acid accumulation with
respiratory acidosis due to inadequate postoperative
respi r a t i o n. M e as ur em en ts o f t h e p u lm on ar y
capillary wedge pressure, right v entri cular end-
diastolic volume, and serum albumin were
12 mmH g , 118 ml, and 2.2 g/dl, respectively.
Here, the increase in plasma lactate and decrease
in SBE were found simultaneously and primary
lactic acidosis was easily dened. We adjusted the
mechanical ventilator in an effort to maintain the
PaCO2 at a level of 26-28 mmHg. Additional uid
supplements were given to reduce the anaerobic
metabolism. A total of 50 gm albumin (200 ml of
25% albu min ) was admi nistere d i ntr avenous ly.
Normal saline resuscitation was not done since it
might have increased the metabolic acidosis.
Six hours later, the patient’s urine output was
reduced and the serum [Na+] and [Cl-] were 132
and 104 mEq/l, respectively. Arterial blood gas
data showed a pH of 7.32, pCO2 of 25 mmHg, and
SBE of -12 mEq/l. The lactate was still 16 mEq/l.
Therefore, an infusion of 100 mEq of 7.5% NaHCO3
was given. Twelve hours later, the patient awoke.
The liver function resumed with bile production,
and the urine output increased. Arterial blood gas
analysis revealed a pH of 7.40, pCO2 of 35 mmHg
and SBE of -1 mEq/ l. The blood lactate decreased
by 6 mEq/l to 10 mEq/l. The serum [Na+] and [Cl-]
were 134 and 101 mEq/l, respectively, showing an
increase of [Na+] by 2 mM and a decrease of [Cl-]
by 3 mM. Although these changes were small, they
resulted in a signicant increase in the SID from
21 mEq/l to 32 mEq/l. The reduction of serum
[Cl-] occurred because of preserved renal excretion
and/or other inter-compartmental shifts. The serum
[Na+] was increased by exogenous Na+ administra-
tion from the NaHCO3 and 25% albumin infusion.
An overview of the patient’s data, showed
that the SID was low at 32 mEq/l which might be
attributed to a low level of ATOT (albumin is 2.7 g/dl,
phosphate is 2.9 mg/dl). When the [lactate] then
decreased, the SID increased to nearly 40 mEq/l and
with pending metabolic alkalosis. Thus the minute
ventilation needed to be reduced. The kidneys
retained Cl- over the next few hours and restored
the SID to the baseline. When the transplanted
liver started to produce albumin, the ATOT increased
gradually and reached a new steady SID. The
patient’s blood gas and biochemistry data 6 hrs and
12 hrs after albumin infusion are summarized in
Table 2.
Traditional approach
According to t h e Henderson-Hasselbalch
equation: pH = pKa × log[HCO3
-/(0.03 × (pCO2)](1,2).
Changes in plasma HCO3
- lead to metabolic or
non-respiratory acid-base anomalies. Respiratory
J Emerg Crit Care Med. Vol. 21, No. 1, 2010
compensation leads to changes in pCO2 t o
compensate for primary metabolic disorders. Since
- and pCO2 are interdependent, this formula
can’t be used to explain the complex metabolic
acid-base disturbances noted on clinical grounds,
especially in critically ill patients. So, an alternate
approach to quantify the metabolic component was
suggested by Siggard-Anderson and colleagues. The
SBE was calculated by the Van Slyke equation(7,8).
The correlation between changes in the SBE and
pCO2 during metabolic acid-base disturbances is
shown in Table 3.
The major drawback of the SBE approach is
that weak acids, such as plasma proteins and other
unmeasured anions, are not included. Most patients
in critical units have reduced proteins and increased
metabolic anions. Emit and Narins developed the
anion gap (AG) approach to determine metabolic
disorders(13). The law of electro-neutrality is applied
in this approach.
The sum of cations = The sum of anions
(electrical neutrality)
Na+ + K+ + unmeasured cations = Cl + HCO3
+ unmeasured anions
Anion gap = (Na+ + K+) – (Cl + HCO3
-) =
10–12 mmol/litre.
In most critically ill patients, hypoalbuminemia
is encountered frequently. For hypoalbuminemic
and hypophosphatemic patients, the corrected anion
gap = [(Na++K+)−(Cl-+HCO3
-)] − [(0.2 × albumin
g/l + 1.5 × phosphate mmol/l)]( 14). In patients with
severe hyperlactatemia, the corrected anion gap =
-)] + 0.25 × (40–[albumin
(g/l)])–lactate}(15). The drawback of this approach is
that this equation involves [HCO3
-]. The SBE and
AG approach is inadequate since [HCO3
-] can be
changed accordingly with respiratory disturbances,
e.g. in hyperventilation.
Application of Stewart’s weak acid (ATOT) concept
Stewart’s approach includes the non-volatile
weak acids (ATOT ) as a major component in acid-
base disturbances. Plasma ATOT includes inorganic
phosphate, albumin and other plasma proteins.
1. Proteins ([PrTot] = [Pr-] + [HPr])
2. Phosphate s ( [P i To t] = [PO4
-3] + [H P O4
-2] +
-] + [H3PO4])
Albumin acts as a weak acid in plasma
Table 2 Case 2 patient’s blood gas and biochemistry data
Blood chemistries 6 hrs later 12 hrs later (6 hrs after HCO3
- infusion)
Na (mEq/l) 132 134
K(mEq/l) 3.8 3.6
Cl (mEq/l) 104 101
Lactate (mEq/l) 16 10
Phosphate (mg/dl) 3.8 2.9
Albumin (g/dl) 2.6 2.7
[H+] (nmol/l)
pCO2 (mmHg) 25 35
(mEq/l) 12.5 21
SBE (mEq/l) -12 -1
Anion gap (mEq/l) 19.3 15.6
Corrected anion gap (mEq/l) 17.0 13.7
SID (mEq/l) 21.45 32.25
Phosphate in mg/dL is converted to mmol/L by multiplying by 0.323
Anion gap = (Na++K+)-(Cl-+HCO3
Corrected anion gap = [(Na++K+)(Cl-+HCO3
-)][(0.2 × albumin g/l + 1.5 × phosphate mmol/l)]
Stewarts approach to acid-base disorders
proteins which greatly determines the pH and
it’s increase might cause acidosis. Thus, in
hypoalbuminemic patients, a normal plasma pH
and anion gap might be seen despite underlying
severe acidosis. In other words, hypoalbuminemia
may mask severe metabolic acidosis. This concept
is clinically very important since most critically ill
patients presenting with metabolic acidosis are in
a hypoalbuminemic condition. If this condition is
not taken into account, the underlying metabolic
acidosis will be missed and uncorrected(17-19).
Normally serum phosphate levels are so low that a
change does not affect acid-base disorders much.
However, in renal failure patients, hyperphosphate-
mia could result in acidemia.
Previous studies found that after adjusting for
hypoalbuminemia (e.g. corrected anion gap), both
the traditional and Stewart approach are similarly
reliable in determining acid-base disorders(18,20). A
prospective study in 2007 by Boniatti and colle-
agues found that Stewart’s approach can identify
more major acid-base disturbances than the
traditional approach(21).
Acid-base disorders are still a great problem
in clinical practice, especially in emergency and
intensive care units. Many proposed theories for
those disturbances have arisen over the years. The
Stewart approach may be more accurate than other
concepts in determining acid-base disturbances.
This “new approach” helps us understand the
underlying mechanisms of hyperchloremic acidosis,
hyperalbuminemic acidosis, dilution acidosis,
contraction alkalosis, and renal tubular acidosis,
leading to appropriate treatment.
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Acid-base disturbance pCO2 (mmHg) SBE (mEq/L)
Acute respiratory acidosis >45 = 0
Acute respiratory alkalosis <35 = 0
Chronic respiratory acidosis >45 =0.4 × (pCO2-40)
Chronic respiratory alkalosis <35 =0.4 × (pCO2-40)
Metabolic acidosis = (1.5×HCO3
-)+8, or = 40+SBE < -5
Metabolic alkalosis = (0.7×HCO3
-)+21, or = 40+(0.6×SBE) > +5
(Modied from reference 16)
J Emerg Crit Care Med. Vol. 21, No. 1, 2010
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酸鹼平衡的異常可能起因於嚴重細胞或全身性代謝問題引起。監控血液pH值對 臨床重症病患的評
(Henderson-Hasselbalch equation)原理處置,其主要著眼於血中重碳酸(HCO3
(pCO2)以及二氧化碳(CO2)的溶解度這三方面。然而斯圖爾特處置(Stewarts approach)基於分析血液
關鍵詞: 酸鹼平衡,強離子,亨德森-黑索巴克,斯圖爾特,陰離子差,代謝性酸中毒,呼吸性鹼毒症
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Full-text available
Acid–base disorders are common in critically ill patients, and they are generally associated with greater morbidity and mortality. The objectives of this study are to find out whether the diagnostic evaluation of acid–base disorders in a population of critically ill patients can be improved using Stewart's method compared with the traditional model, and whether acid–base variables are associated with hospital mortality.
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Renal and respiratory acid-base regulation systems interact with each other, one compensating (partially) for a primary defect of the other. Most investigators striving to typify compensations for abnormal acid-base balance have reported their findings in terms of arterial pH, PaCO2, and/or HCO3-. However, pH and HCO3- are both altered by both respiratory and metabolic changes. We sought to simplify these relations by expressing them in terms of standard base excess (SBE in mM), which quantifies the metabolic balance and is independent of PaCO2. Meta-analysis. Historical synthesis developed via the Internet. Arterial pH, PaCO2, and/or HCO3- data sets were obtained from 21 published reports of patients considered to have purely acute or chronic metabolic or respiratory acid-base problems. We used the same data to compute the typical compensatory responses to imbalances of SBE and PaCO2. Relations were expressed as difference (delta) from normal values for PaCO2 (40 torr [5.3 kPa]) and SBE (0 mM). The data of patient compensatory changes conformed to the following equations, as well as to the traditional PaCO2 vs. HCO3- or H+ vs. PaCO2 equations: Metabolic change responding to change in PaCO2: Acute deltaSBE = 0 x deltaPaCO2, hence: SBE = 0, Chronic deltaSBE = 0.4 x deltaPaCO2. Respiratory change responding to change in SBE: Acidosis deltaPaCO2 = 1.0 x deltaSBE, Alkalosis deltaPaCO2 = 0.6 x deltaSBE. Data reported by many investigators over the past 35 yrs on typical, expected, or "normal" human compensation for acid-base imbalance may be expressed in terms of the independent variables: PaCO2 (respiratory) and SBE (metabolic).
The Henderson-Hasselbalch equation has always occupied a central place in the description of the acid-base status of the blood. An equation of similar importance is the equation for the CO2 equilibration curve of blood in vitro. It is proposed to name this the Van Slyke equation: a - 24.4 = - (2.3 X b + 7.7) X (c - 7.40) + d/(1 - 0.023 X b), where a = bicarbonate concentration in plasma/(mmol/l), b = hemoglobin concentration in blood/(mmol/l), c = pH of plasma at 37 degrees C, d = base excess concentration in blood/(mmol/l). These two equations provide an arithmetic algorithm for calculation of the various acid-base variables of the blood after measuring the pH, the pCO2, and the hemoglobin concentration.
Basic physical principles and concepts plus computer-implemented numberical techniques now make possible a thorough quantitative analysis of acid-base systems. Some important conclusions from that analysis are presented: 1. Acid-base balance for physiological solutions hould be defined as the value of [OH-]/[H+]. 2. pH is a dangerously misleading indirect representation of [H+]. 3. Strong electrolytes affect [H+] and other deendent acid-base variables primarily through their resultant, the strong ion difference. 4 Hydrogen ion concentration in biological solutions is determined by the strong ion difference, the carbon dioxide partial pressure, and the total weak acid present. Changes in hydrogen ion concentration can be broght about only by changing one or more of these three independent variables. The same statements apply to all the other dependent variables, notably bicarbonate ion concentration. None of the dependent variables determines any other dependent variable, although their quantitative behaviors are necessarily correlected. 5. Solutions separated by membranes can interact in acid-base terms only by processes which alter the values of their independent variables. Interaction of intra- and extracellular acid-base balance can only occur by the cell membrane altering these independent variables in the extracellular fluid and in the cytosol.
The concepts underlying the clinical use of the anion gap (AG) and those disorders associated with its alteration are reviewed. A substantial increase in the AG usually indicates the presence of a metabolic acidosis, unless large doses of certain antibiotics or sodium salts of organic acids are being used. The etiology, pathogenesis and diagnosis of high AG metabolic acidoses are discussed. Stress is placed upon the utility of the AG in defining the cause of the acidosis, and as a guide to therapy in certain organic acidoses. A decrease in the normal AG occurs in dilutional states, hypoalbuminemia, hypercalcemia, hypermagnesemia, hypernatremia, diseases associated with hyperviscosity, bromide intoxication, and in certain paraproteinemias. The important clue provided by a low or negative AG in the diagnosis of certain of these life-threatening disorders is emphasized.
We evaluated the clinical application of a model of acid-base balance, which is based on quantitative physical chemical principles (Stewart model). This model postulates that acid-base balance is normally determined by the difference in concentration between strong cations and anions (strong ion difference [SID]), PCO2, and weak acids (primarily proteins). We measured electrolytes and blood gases in arterial blood samples from 21 patients in a medical or surgical intensive care unit or emergency room of a tertiary care hospital. The measured SID frequently differed from SID calculated from the measured blood components, which indicates that unmeasured cations or anions are present; these could not be accounted for by lactate, ketones, or other readily identifiable ions. We used an approach to acid-base analysis that is based on changes in base excess or deficit due to changes in: (1) free water as assessed by [Na+]; (2) in [Cl-]; (3) protein concentration; and (4) "other species" (ie, anion and cations other than [Na+], [K+], and [Cl-]). The contribution of "other species" was obtained from the difference between the SID measured and that predicted from Stewart's equation. It could also be calculated from the difference between the standard Siggaard-Anderson calculation of base excess and base excess attributable to free water, [Cl-], and proteins (ie, base-excess gap). Our results indicate that the SID gap, base excess gap, and anion gap reflect the presence of unmeasured ions, and both the anion-gap and base-excess gap provide readily available estimates of the SID gap. This provides a simple bedside approach for using the Stewart model to analyze the nonrespiratory component of clinical acid-base disorders and indicates that, in addition to unmeasured anions, unmeasured cations can be present.
To show how hypoalbuminemia lowers the anion gap, which can mask a significant gap acidosis; and to derive a correction factor for it. Observational study. Intensive care unit in a university-affiliated hospital. Nine normal subjects and 152 critically ill patients (265 measurements). None. Arterial blood samples analyzed for pH, PCO2, and concentrations of plasma electrolytes and proteins. Marked hypoalbuminemia was common among the critically ill patients: 49% of them had serum albumin concentration of <20 g/L. Each g/L decrease in serum albumin caused the observed anion gap to underestimate the total concentration of gap anions by 0.25 mEq/L (r2 = .94). The observed anion gap can be adjusted for the effect of abnormal serum albumin concentrations as follows: adjusted anion gap = observed anion gap + 0.25 x ([normal albumin] [observed albumin]), where albumin concentrations are in g/L; if given in g/dL, the factor is 2.5. This adjustment returns the anion gap to the familiar scale of values that apply when albumin concentration is normal.
To evaluate the precision, bias and CO2 invariance of base excess as determined by the Van Slyke equation over a wide P(CO2) range at normal and low hemoglobin concentrations. Prospective in vitro study. University research laboratory. Normal human blood, both undiluted and diluted with plasma. Two experiments were conducted. In the first, blood unmodified or after adding HCl or sodium bicarbonate was rendered hypercarbic (P(CO2) >70 torr) by gas equilibration. Rapid Pco2 reduction in > or =10 steps to a final P(CO2) < or =20 torr was then performed. In the second experiment, blood unmodified or diluted to a hemoglobin concentration of approximately 4 G% was mixed anaerobically (9:1, vol:vol) with varying concentrations of lactic acid in saline (0-250 mmol/L). In the first experiment, blood gas analysis at each step during the progressive P(CO2) reduction revealed that base excess remained nearly constant (SD all specimens < or =0.6 mmol/L) whereas P(CO2) changed by >80 torr. In the second experiment, simultaneous blood gas and plasma lactate analyses showed that changes in base excess correlated closely with changes in both plasma and whole blood lactate concentrations (r2 > or = 0.91) despite concurrent P(CO2) elevations as great as 200 torr. Quantification by base excess of change in whole blood lactate concentration was precise with slight negative bias (mean negative bias, 1.1+/-1.9 mmol/L) in both diluted and undiluted blood. There was significant underestimation of change in plasma lactate concentration in undiluted blood, presumably because base excess is a whole blood variable. Base excess calculated using the Van Slyke equation accurately quantifies metabolic (nonrespiratory) acid-base status in blood in vitro. This accuracy is little affected by large simultaneous alterations in P(CO2), or by very low hemoglobin concentrations similar to that used to calculate standard base excess.
An advanced understanding of acid-base physiology is as central to the practice of critical care medicine, as are an understanding of cardiac and pulmonary physiology. Intensivists spend much of their time managing problems related to fluids, electrolytes, and blood pH. Recent advances in the understanding of acid-base physiology have occurred as the result of the application of basic physical-chemical principles of aqueous solutions to blood plasma. This analysis has revealed three independent variables that regulate pH in blood plasma. These variables are carbon dioxide, relative electrolyte concentrations, and total weak acid concentrations. All changes in blood pH, in health and in disease, occur through changes in these three variables. Clinical implications for these findings are also discussed.