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

Abstract

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.

Full text

1
Stewart’s 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
E-mail: ttwyl123@yahoo.com
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
Introduction
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
[HCO3
-] 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
2
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
words,
Kw = [H+] × [OH-],
Where Kw is the dissociation constant for
water(9,10).
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.
Examples
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)

3
Stewart’s 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
+ +
HCO3
-. Here, R-NH2 is THAM and R-NH3
+
is the
protonated form of THAM. Both treatments can
donate bicarbonate, cause an increase in plasma
[HCO3
-] 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
4
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
pH
[H+] (nmol/l)
7.35
[44.67]
7.31
[48.98]
7.22
[60.2]
7.36
[43.65]
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
ions.
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

5
Stewart’s 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
6
compensation leads to changes in pCO2 t o
compensate for primary metabolic disorders. Since
HCO3
- 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 =
{[(Na++K+)-(Cl-+HCO3
-)] + 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] +
[H2PO4
-] + [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
pH
[H+] (nmol/l)
7.32
[47.9]
7.40
[39.8]
pCO2 (mmHg) 25 35
HCO3
-
(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)]

7
Stewart’s 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).
Conclusion
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.
References
1. H a ss e lb a lc h KA. D i e be r ec h nu n g d er
wasserstoffzahl des blutes auf der freien und
gebundenen kohlensaure desselben, und die
sauerstoffbindung des blutes als funktion der
wasserstoffzahl. Biochem Z 1916;78:112-44.
2. Siggaard-Andersen O. The van Slyke equation.
Scand J Clin Lab Invest (Suppl) 1977;37:15-20.
3. Stewart PA. Independent and dependent variables
of acid-base control. Respir Physiol 1978;33:9-26.
4. St e w art PA. H o w to unde r stand acid base
balance, in A Quantitative Acid-Base Primer
for Biology and Medicine, edited by Stewart
PA, New York: Elsevier, 1981.
5. S t ew a rt PA. M o d er n q ua n ti t a t iv e a ci d -
ba s e chemistry. Can J Physiol Pharmacol
1983;61:1444-61.
6. Corey HE. Stewart and beyond: new models of
acid-base balance. Kidney Int 2003;64:777-87.
7. Schlichtig R, G r o g o n o AW, Severinghaus
JW. Human PaCO2 and standard base excess
compensation for acid-base imbalance. Crit
Care Med 1998;26:1173-9.
Table 3 The correlation between changes in SBE and pCO2 in acid-base disturbances
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
(Modied from reference 16)

J Emerg Crit Care Med. Vol. 21, No. 1, 2010
8
8. Morgan TJ, Clark C. Endre ZH. Accuracy of
base excess: an in vitro evaluation of the Van
Slyke equation. Crit Care Med 2003;28:2932-6.
9. Geissler PL, Dellago C, Chandler D, Hutter J,
Parrinello M. Autoionization in liquid water.
Science 2001;291:2121-4.
10. Rini M, Magnes BZ, Pines E, Nibbering ETJ.
Real-time o bs e r va t io n o f b i m o d a l p r o t o n
transfer in acid-base pairs in water. Science
2003;301:349-52.
11. H ub b le S MA. A ci d -b a se a nd b lo o d g as
analysis. Anaesthesia & Intensive Care Med
2007;8:471-3.
12. Tuhay G, Pein MC, Masevicius FD, Kutscherauer
DO, Dubin A. Sev ere h ype rla cta tem ia wi th
normal base excess: a quantitative analysis using
conventional and Stewart approaches. Crit Care
2008;12:R66.
13. Emmett M, Narins RG. Clinical use of the
anion gap. Medicine 1977;56:38-54.
14. Figge J, Jabor A, Kazda A, Fencl V. Anion gap
and hypoalbuminemia. Crit Care Med 1998;
26:1807-10.
15. Moviat M, van Haren F, van der Hoeven H.
Conventional or physicochemical app roa ch
in intensive care unit patients with metabolic
acidosis. Criti Care 2003;7:R41-5.
16. Kellum JA. Determinants of blood pH in health
and disease. Criti Care 2000;4:6-14.
17. Story DA, Poustie S, Bellomo R. Quantitative
phy s i cal c h emis t r y ana l y sis o f a cid b a se
disorders in critically ill patients. Anaesthesia
2001;56:530-3.
18. Fencl V, Jabor A, Kazda A, Figge J. Diagnosis
of m e ta b ol i c a ci d -b a s e d i st u rb an c es i n
critically ill patients. Am J Respir Criti Care
Med 2000;162:2246-51.
19. Gilfix BM, Bique M, Magder S. A physical
chemical approach to the analysis of acid-base
balance in the clinical setting. Crit Care Med
1993;8:187-97.
20. Dub in A, Menis es MM, Maseviciu s F D, et
al. Comparison of three different methods of
evaluation of metabolic acid-base disorders.
Crit Care Med 2007;35:1254-70.
21. Boniatti MM, Cardoso PR, Castilho RK, Vieira
SR. Acid-base disorders evaluation in critically
ill patients. Inten Care Med 2009;35:1377-82.

9
以斯圖爾特方式處置酸鹼問題
收件：98年6月5日 接受刊載：98年8月27日
輔仁大學醫學院，耕莘醫院1內科部腎臟科 2急診部
通訊及抽印本索取：楊忠謀醫師 231台北縣新店市中正路362號 輔仁大學醫學院，耕莘醫院急診部
電話：(02)22193391轉65343 傳真：(02)29107920
E-mail: ttwyl123@yahoo.com
以斯圖爾特方式著手處置臨床酸鹼問題
鄭彩梅1 盧國城1 鄭景泉1 楊忠謀2
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
估與處置以及了解其潛在之病生理極其重要。傳統著手處理酸鹼平衡異常，多依循亨德森-黑索巴克公式
(Henderson-Hasselbalch equation)原理處置，其主要著眼於血中重碳酸(HCO3
-)濃度的改變、二氧化碳的分
壓(pCO2)以及二氧化碳(CO2)的溶解度這三方面。然而斯圖爾特處置(Stewart’s approach)是基於分析血液
內複雜的各種陰陽離子(強離子)及各種弱酸性蛋白質、磷酸、乳酸等對水釋放氫離子的影響，以期了解
更精確及完整的酸鹼失衡機制及原理。在這篇回顧裡，我們經由兩個酸鹼失衡病例的介紹，讓讀者了解
由傳統著手處理與由斯圖爾特方式處置的差異。
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