ACID BASE DISORDER

in clinical practice

Erwin Kresnoadi
INTRODUCTION OF
QUANTITATIVE METHOD OF
ACID BASE BALANCE
STEWART APPROACH
Warning.!
Most Physician has determined that....
This lecture may be harmful to your mental health.
The disadvantage of men not
knowing the past is that they do not
know the present.
G. K. Chesterton
Keseimbangan asam basa
Saya punya hasil
astrup, artinya
apa nich..?
Who cares
about
acidbase
balance?
ASAM BASA..
pH
[H
+
]
Analytic tools used in acid
base chemistry
CO
2
-bicarbonate (Boston) approach
Schwartz, Brackett et al
H-H equation
The Base deficit/excess (Copenhagen) approach
1948 Singer-Hasting, Buffer Base (BB)
1958 Siggaard-Andersen Base Deficit/Excess
(BDE)
1960, Hb into calculation, modified Standard Base
Deficit/Excess (SBE)
1977 Van Slyke equation to computed SBE
Has been validated by Schlitic and Morgan
Analytic tools used in acid
base chemistry
1977, Anion Gap approach
Emmet and Narins
To address the limitation of Boston and Copenhagen
1978, Stewart introduced the physical-chemical
approach
3 independent variable;
PCO2, SID and weak acid
1993, Stewart-Fencl approach
1998, Anion Gap Corrected
Fencl and Figge
2004, simplified Stewart-Fencl approach
Story DA, Morimatsu et al
GENERAL PRINCIPLES
Three widely accepted methods are used to analyze and
classify acid-base disorders, yielding mutually compatible
results. The approaches differ only in assessment of the
metabolic component (i.e., all three treat PCO
2
as an
independent variable):
(1) HCO
3
-
concentration ([HCO
-
]);
(2) standard base-excess;
(3) strong ion difference (Stewart Approach)
For the most part, the differences among these three
approaches are conceptual; in other words, they differ in
how they approach the understanding of mechanism
Boston Style
1. HCO
3
-
Brief historical perspective
ACID BASE WORKSHOP PERDICI
2006
[H
+
] x [HCO
3
-
] = K x [CO
2
]x[H
2
O]
Henderson LJ. Das Gleichgewicht zwischen Sauren und Basen im tierischen Organsimus. Ergebnisse der
Physioogie Biologischen Chemie und Experimentellen Pharmakologie 1909;8: 254325
Henderson, 1908
Discovered buffering power of CO
2
and
applied law of mass action:
K = [H
+
][HCO
3
-
]/[dCO
2
]
(where dCO
2
= dissolved CO
2
)
Acid Base
Notasi pH diciptakan oleh seorang ahli kimia dari Denmark yaitu
Soren Peter Sorensen, yang berarti log negatif dari konsentrasi ion
hidrogen. Dalam bahasa Jerman
disebutWasserstoffionenexponent (eksponen ion hidrogen) dan
diberi simbol pH yang berarti: potenz (power) of Hydrogen.
1909
+
defined by Sorensen
[H
+
] pH
1 x 10
-6
6.0
1 x 10
-7
7.0
8 x 10
-8
7.1
4 x 10
-8
7.4
2 x 10
-8
7.7
1 x 10
-8
8.0
pH = 6.1 + log
[ HCO
3
-
] = KIDNEY
0.03 x
PCO
2
= LUNG
Hasselbalch KA. Die Berechnung der Wasserstoffzahl des Blutes aus der freien und
gebundenen Kohlensaure desselben und die Sauerstoffbindung des Blutes als Funktion der
Wasserstoffzahl. Biochemische Zeitschrift 1916; 78: 11244.
1916
Hasselbach:
Used Sorensen's terminology for Henderson's equation
in logarithmic form:
Hendersen-Hasselbach equation (H-H)
Regulasi asam basa diatur melalui proses di:
1. Ginjal dengan cara mempertahankan [HCO
3
-
] sebesar
24 mM dan
2. Mekanisme respirasi dengan cara mempertahankan
tekanan parsial CO
2
arteri (PaCO
2
) sebesar 40mmHg.
Hendersen-Hasselbalch
pH = 6.1 + log
[ HCO
3
-
]
0.03 x
1. Change in
Metabolic disturbance
2. Change after
Renal compensation for
Respiratory disturbance
1. Change in
Respiratory disturbance
2. Change after
Respiratory compensation for
Renal disturbance
pCO2
pH = 6.1 + log
[HCO
3
-
]
pCO
2
GINJAL
PARU
BASA
ASAM CO
2
HCO
3
HCO
3
CO
2
Kompensasi
Normal
Normal
Diagram Davenport
[

H
C
O
3
-

]

PCO
2
= 80 40
20
pH
7.0 7.2 7.4 7.6 7.8
10
20
30
40
50
pH = 6.1 + Ginjal
Paru
B
A
C
7.4 / 40 / 24
7.2 / 80 / 30
7.6 / 20 / 18
Normal
pH
Alkalosis Metabolik
pH
Alkalosis Respiratori
pH
Asidosis Respiratori
pH
Asidosis Metabolik
Gangguan asam-basa primer
Diagnosis menggunakan nilai asam basa serum:
Davenport Diagram
[

H
C
O
3
-

]

PCO
2
= 80 40
20
pH
7.0 7.2 7.4 7.6 7.8
10
20
30
40
50
Henderson- Hasselbalch:

pH = pK + log [HCO
3
-
]

s PCO
2
Asidosis
Respiratori
Alkalosis
Metabolik
Alkalosis
Respiratori
Asidosis
Metabolik
pH = 6.1 + Ginjal
Paru
atau,
Normal
RESPON KOMPENSASI
Alkalosis Respiratori
[

H
C
O
3
-

]

PCO
2
= 80 40
20
pH
7.0 7.2 7.4 7.6 7.8
10
20
30
40
50
Alkalosis
Respiratori
terkompensasi
Penyebab:
1) Nyeri
2) Histerik
3) Hipoksia
Alkalosis
Respiratori
Normal
kompensasi = [HCO
3
-
]
Asidosis Respiratori
[
H
C
O
3
-
]

PCO
2
= 80 40
20
pH
7.0 7.2 7.4 7.6 7.8
10
20
30
40
50
Asidosis
Respiratori
kompensasi = [HCO
3
-
]

Penyebab:
1) PPOK, Gagal jantung
kronik, bbrp pnykt
paru
2) Obat anestesi
Asidosis
Respiratori
terkompensasi
Metabolic Alkalosis
[

H
C
O
3
-

]

PCO
2
= 80 40
20
pH
7.0 7.2 7.4 7.6 7.8
10
20
30
40
50
Alkalosis
Metabolik
kompensasi = PCO
2
Penyebab:
1) Intake basa >>
2) Kehilangan asam
(Muntah,
penyedotan lambung)
Alkalosis
Metabolik
terkompensasi
Metabolic Asidosis
[

H
C
O
3
-

]

PCO
2
= 80 40
20
pH
7.0 7.2 7.4 7.6 7.8
10
20
30
40
50
Asidosis
Metabolik
kompensasi = PCO
2
Penyebab:
1) Kehilangan basa
(eg. diare)
2) Akumulasi asam
(diabetes, gagal ginjal)
3) Asidosis Tubular Ginjal


Asidosis
Metabolik
terkompensasi
Kompensasi ginjal terhadap asidosis resp. kronik
Kompensasi ginjal & paru terhadap asidosis non ginjal
PPOK
Keto/Laktat asidosis
DISORDER pH PRIMER RESPON
KOMPENSASI
ASIDOSIS
METABOLIK
HCO
3
- pCO
2

ALKALOSIS
METABOLIK
HCO
3
- pCO
2

ASIDOSIS
RESPIRATORI
pCO
2
HCO
3
-
ALKALOSIS
RESPIRATORI
pCO
2
HCO
3
-
RANGKUMAN GANGGUAN
KESEIMBANGAN ASAM BASA
TRADISIONAL
2. BDE (Base Deficit Excess)
&
SBE (Standard Base Excess)
Copenhagen style
Singer and Hastings, 1948,
Whole blood buffer base (BB), defined as the sum of
bicarbonate [HCO
3
-
] & nonvolatile buffer anions (A
-
)
The change in BB from "normal" was called delta BB
(BB). This change in BB was an expression of the
metabolic component of an acid-base disturbance
BE (Base Excess)
Singer RB, Hastings AB: An improved clinical method for the estimation of disturbances of the
acid-base balance of human blood. Medicine (Baltimore) 1948; 27:223-242
Introduced the concept of buffer base [BB]
[BB] = [HCO
3
-
] + [A
-
]
Modified Base Excess
ECF includes plasma, red cells, and the
surrounding interstitial fluid. Its where the action
takes place in the body regarding acid-base
movement.
Blood-gas machines calculate SBE as:

Standard Base Excess
SBE = (1 - 0.014Hgb) (HCO
3
24 + (1.43Hgb + 7.7) (pH - 7.4)`
[
H
C
O
3
-
]

pCO
2
= 80 40
20
pH
7.0 7.2 7.4 7.6 7.8
10
20
30
40
50
Asidosis
Metabolik
Base deficit;
Kekurangan Basa;
Jumlah Basa (HCO
3
) yg
harus ditambahkan agar
pH normal
Alkalosis
Metabolik
Base excess;
Kelebihan Basa; Jumlah
Basa (HCO
3
) yang harus
dikurangi agar pH
normal
Base Excess/
Base Deficit
Normal
Base Defisit
Base Excess
Unmeassured anion
Limitasi dari H-H tidak dapat
mengukur metabolic acidosis yang
disebabkan unmeassured anion
seperti laktat dan keton
Emmet dan Narins Anion Gap
AG= Na
+
- (Cl
-
+ HCO
3
-
)
Normal Gap 10-15
How to determine the
cause of Metabolic
acidosis?
Anion Gap
Improve Anion Gap
Strong Ion Gap
Anion Gap
Anion gap (AG) was introduced by Emmet and
Narins and is derived from the electroneutrality
principle.
It determines the gap between measured and
unmeasured ions, in this instance, in plasma. It is
computed as:
Narins RG, Emmett M: Simple and mixed acid-base disorders: A
practical approach. Medicine 59:161-187, 1980
[AG] = [Na
+
] + [K
+
] - [Cl
-
] - [HCO
3
-
]
Increased anion gap acidosis Normal anion gap acidosis
Na

K


Cl
AG
HCO
-
3
AG = 10-15
25
105
145
Normal

Na

K


Cl
HCO
-
3
AG
15
115
145
= 15 (normal)
Na

K


Cl
HCO
-
3
AG/
Other
anion
= 25
15
105
(normal)
145
HCO
3
-
decreases and replaced by Cl
-
so
there is a Cl
-
shift :Eg. Diarrhea or
simple gain of H+
HCO
3
-
decreases and replaced by anions
other than Cl
-
so no Cl
-
shift: Eg.renal
failure and diabetic keto-acidosis
Metabolic acidosis
HCO
3
-

Perbedaan dgn AG pd SIG, nilai albumin ikut dalam kalkulasi


Na
+
K
+
4
Ca
++
Mg
++
Cl
-
HCO
3
-
KATION ANION
SID
a
STRONG ION GAP
= [Na
+
] + [K
+
] + [Mg
++
] + [Ca
++
] - [Cl
-
] [Lactate
-
]
Lactate
A-


= 12.2pCO
2
/(10-pH )+10[alb](0.123pH0.631) +[PO
4

](0.309pH0.469)
SID
e
SIG = SID
a
SID
e
Normal value = zero
Jika SIG > terdapat
SIG
UA
Kellum JA, Kramer DJ, Pinsky MR: Strong ion gap: A methodology for
exploring unexplained anions. J Crit Care 1995,10:51--55.
Figge J, Jabor A, Kazda A, Fencl V: Anion gap and hypoalbuminemia. Crit Care Med 1998,
26:1807-1810.
Improved Anion Gap ?
Anion Gap corrected
AG = pH ((1.16 * alb) + (0.42 * phos)) (5.83 * alb) (1.28 * phos)
1. AG per se is helpful only for discriminating the cause of a
metabolic acidosis, diabetic ketoacidosis, lactic acidosis,
salicylate, and the like.
2. It is of no value in discriminating the cause of a metabolic
alkalosis because the ions responsible (usually decreased Cl- )
are all measured
Schlichtig R, Grogono AW, Severinghaus JW. CURRENT STATUS OF ACID-BASE
QUANTITATION IN PHYSIOLOGY AND MEDICINE; Anesthesiology Clinics of North
America. B. Saunders Co. Vol 16, No 1, March 1998
3. STEWART AND
TRADITIONAL APPROACH
(Stewart-Fencl approach)
Now for something new
Na
+
140
K
+
4
Ca
++
Mg
++
Cl
-
102

HCO
3


A
-
Buffer Base = SID = HCO
3
-
+ A
-
SID & BASE EXCESS
(expected if pH = 7.4 and pCO
2
= 40)
Any deviation in [Na
+
], [Cl
-
] or [Alb
-
] from normal values will
produce a base excess or deficit
Cl
-
102
A
-


HCO
3
-

BE
Cl
(-)
Buffer
Base
a
Siggaard-Andersen, Base excess or buffer base (strong ion difference) as a measure of a
non-respiratory acid-base disturbance. Acta Anaesthesiol Scand, 1995
Buffer Base
a
-
Expected Buffer Base
BE
Cl
=
SID = Buffer Base
0
20
40
60
80
100
120
140
160
Cations Anions
Na
+
Cl
-
K
+
, Mg
++
, Ca
++
m
E
q
/
L

Lactate,
Other
anions
Cl
-
A
-
HCO
3
-
SID
BB
SID = Buffer Base
0
20
40
60
80
100
120
140
160
Cations Anions
Na
+
Cl
-
K
+
, Mg
++
, Ca
++
m
E
q
/
L

Cl
-
A
-
HCO
3
-
SID BB
Base
Deficit
SID = Buffer Base
The standard base
excess corresponds to
the change in SID
required to restore the
plasma (in vivo) to pH
7.40 with pCO
2
of 40
mm Hg

R
2
=0.9527
-10
-8
-6
-4
-2
0
2
4
6
-8 -6 -4 -2 0 2 4
A/V SIDe
A
/
V

S
B
E

Kellum et al. J Crit Care 1997; 12: 7-12
SBE = SIDex
[SIDex] mEq/L
[
S
B
E
]

m
E
q
/
L

-30
-20
-10
0
10
20
-30 -20 -10 0 10 20
Schlichtig R. Adv Exper Med Bio. 1997;411:91-95
The Fencl-Stewart
Formula
Efek SID
Blood Gas Analysis
Step 1; Base-excess effect of the Na & Cl
[(efek Na + efek Cl) + efek Alb] BE
UA
= BE
Step 2; Base-excess of the albumin
BE
UA
effect is the residual difference
If there were no abnormalities in
Na,Cl,Alb, or UA anions, then BE would be
equivalent to BE
UA
.
Fencl V, Leith DE: Stewarts quantitative acid-base chemistry:
Applications in biology and medicine. Resp Physiol 1993, 91:1--16.

BE from the Blood Gas Machine
SID effect, mEq/l = A + B
A. Free Water effect on Na
+
= 0.3 x ([Na
+
] 140)
B. Corrected Cl
-
effect
= 102 ([Cl
-
] x 140/[Na
+
])
Total weak acids effect, mEq/l
= 0.123 x pH - 0.6310 x (42 - [Albumin])
UA effect = BE ef SID ef A
Tot
ef
BASE EXCESS DAN STEWART
Stewart-Fencl, 2000
BDE adjustment for serum albumin
Strong Ion Difference in
Gastrointestinal Tract


1. Magder S. Pathophysiology of metabolic acid-base disturbances in patients with critical illness. In:Critical
Care Nephrology. Kluwer Academic Publishers, Dordrecht, The Netherlands, 1998. pp 279-296.Ronco C,
Bellomo R (eds).
2. Sirker AA et al.Acid base physiology: the traditional and the modern approaches. Anaesthesia,
2002, 57; 348-356


WORKSHOP ACIDBASE
STEWART PERDICI 2006
Sekresi
gaster
Na
Cl
H
+
Cl-
Cl-
Cl-
SID cairan lambung < / () ; asam
Antasida: MgOH, CaOH SID

Pancreas
Na+

Empedu
Na+
Na+
SID plasma
Alkalosis
SID plasma -
Asidosis
SID plasma
normal
SID cairan
intestinal normal
Na+
Na+
Na+
Diare: Na loss
Plasma site
Cl
Na
Cl
Na
H
+
Cl
Na
Muntah, penyedotan
Lambung, sekresi EF >>
Cl loss
Cl-
Na+
Absorbsi
Jejunum
Na+
Na
Cl
SID plasma
normal
Cl-
Na+
Erwin, 2014
Cl-
Na+
Na+
Cl-
Cl-
Na+
Volume dan komposisi elektrolit cairan gastrointestinal
24 h vol.
(mL)
Na
+

(mEq/L)
K
+
(mEq/L) Cl
-
(mEq/L) HCO
3
-
SID
Saliva 500-2000 6 25 13 18
Stomach 1000-2000 80 15 115 -20
Pancreas 300-800 140 7.5 80 67.5
Bile 300-600 140 7.5 110 37.5
Jejunum 2000-4000 130 7.5 115 22.5
Ileum 1000-2000 115 5 92.5 27.5
Colon - 60 30 40 -
Miller, 5th ed,2000.
WORKSHOP ACIDBASE
STEWART PERDICI 2006
24 h vol.
(mL)
Na
+

(mEq/
L)
K
+

(mEq/
L)
Cl
-

(mEq/
L)
HCO
3
-
SID
Saliva 500-2000 6 25 13 18
Stomach 1000-2000 80 15 115 -20
Pancreas 300-800 140 7.5 80 67.5
Bile 300-600 140 7.5 110 37.5
Jejunum 2000-4000 130 7.5 115 22.5
Ileum 1000-2000 115 5 92.5 27.5
Colon - 60 30 40 -
From Miller, Anesthesia, 5th ed,2000.
Boron & Boulpaep, Medical Physiology,ch 27,
2003.
pH of Body fluids
Volume dan komposisi elektrolit
cairan gastrointestinal
CO
2

pH
H
2
O OH
-
+H
+
Cl
-
Na
135 Cl
90
HCO
3
30
Na
140
Cl
100
HCO
3
Normal
Renal Compensation for
Chronic Respiratory Acidosis
COPD
Na
140
Cl
100
HCO
3

H
+
H
+
SID



CO
2
+ OH HCO
3
CO
3
-2
+ H
+

SID n
CO
2
CO
2
+ OH HCO
3


HCO
3
Cl
-
Chloride shift
Carbonic anhidrase
Na
140
Cl
100
HCO
3

Brain
Stem
pH
Hours


Days
NH3 Sintesis
(Ammoniagenesis)
TA
Na
140
Cl
100
HCO
3
22
Non Renal
Met Acidosis
Renal & Respiratory Compensation
for non Renal Metabolic Acidosis
H
+
Na
140
Cl
90
HCO
3
22
NH
4
Cl

Removal
CO
2

Hypochloraemia
H
+
A simplified Fencl
Stewart approach
Strong ions, weak acids and base excess:
a simplified FenclStewart approach to
clinical acidbase disorders
Story, Morimatsu, Bellomo (2004), British Journal of Anaesthesia. Vol. 92,
SBE = from a blood gas machine =
NaCl effect = [Na
+
][Cl

]38 =...
Albumin effect = 0.25 x [42Alb(g/l)] =
UA = SBE (NaCl)effect Albumin effect =
Interpretation of blood gas
results using combination
the base-excess (BE) with
the Stewart approach (SID)
SBE = -10
NaCl effect = [Na
+
][Cl

]38 = 14011238 = -10

Albumin effect = 0.25 x [4240(g/l)] = 0.5
UA = -10 (-10) 0.5 = -0.5
Kasus 1:

7.25 / 30 / -10 / 14
Na 140; Cl 112; Alb 4.0
SBE = from a blood gas machine =
NaCl effect = [Na
+
][Cl

]38 =...
Albumin effect = 0.25 x [42Alb(g/l)] =
UA = SBE (NaCl)effect Albumin effect =
Alb
BASE EXCESS DAN STEWART
140
150
102
112
BE akibat pe Cl
-
-10
HCO
3
-
Na
+
Cl
-
Alb
7.25 / 30 / -10 / 14
WD/: Asidosis metabolik karena hiperkloremia
Causal: - Pemberian Lar NaCl berlebihan
- Gagal ginjal akut
Th/: Batasi NaCl
HD/CRRT
SBE = from a blood gas machine =
NaCl effect = [Na
+
][Cl

]38 =...
Albumin effect = 0.25 x [42Alb(g/l)] =
UA = SBE (NaCl)effect Albumin effect =
Kasus 2:

7.48 / 50 / + 9 / 34
Na 140; Cl 93; Alb 4.2
SBE = +9
NaCl effect = [Na
+
][Cl

]38 = 1409338 = 9
Albumin effect = 0.25 x [4242(g/l)] = 0
UA = 9 9 0 = 0
Alb
BASE EXCESS DAN STEWART
140
Na
+
Cl
-
HCO
3
-
BE akibat Cl- +9
Alb
7.48 / 45 / + 9 / 34
WD/: Alkalosis metabolik karena hipokloremia
Causal:
- Diuretik Lasik
- Muntah, Enterokutan Fistula
Th: NaCl 0.9%, kurangi furosemide, cairan fistel
dimasukkan lagi
SBE = from a blood gas machine =
NaCl effect = [Na
+
][Cl

]38 =...
Albumin effect = 0.25 x [42Alb(g/l)] =
UA = SBE (NaCl)effect Albumin effect =
Kasus 3:

7.30 / 27 / -7 / 18
Na 128; Cl 100; Alb 3.0
SBE = -7
NaCl effect = [Na
+
][Cl

]38 = 12810038 = -10

Albumin effect = 0.25 x [4230(g/l)] = 3
UA = -7 + 10 3 = 0
Alb
BASE EXCESS DAN STEWART
140
Na
+
Cl
-
BE akibat Na -7
7.30 / 27 / -7 / 18
WD/: Acidosis metabolik karena hiponatremia
Causal:
- hemodilusi
- Overload cairan, fase awal shock oligouri
Th: perbaiki shock, inotropik, HD/CRRT
128
Kasus 4 :

7.42 / 35 / 100 / -2 / 21 ;
Na 140; Cl 102; Alb 1.8
Menurut H-H normal
SBE = from a blood gas machine =
NaCl effect = [Na
+
][Cl

]38 =...
Albumin effect = 0.25 x [42Alb(g/l)] =
UA = SBE (NaCl)effect Albumin effect =
SBE = -2
NaCl effect = [Na
+
][Cl

]38 = 14010238 = 0
Albumin effect = 0.25 x [4218(g/l)] = 6
UA = -2 0 6 = -8
BASE EXCESS DAN STEWART
140
102
HCO
3
-
24

Alb
Na
+
Cl
-
hipoalbumin

HCO
3
-
30.7

SID normal
BE
astrup
= - 8 + 6 = - 2
HCO3-
22

BE akibat lact - 8 UA = - 8
BE akibat hipoalb + 6
7.42 / 35 / 100 / -2 / 21
Lactic Asidosis metabolik masking oleh hipoalbumin
New calculator of
stewart acidbase
How to interpret acid base disorder
with quantitative approach
The three
independent
variable
The UA
Alkalinizing
process
Acidifying
process



The interpretation of
the results
Acidosis Alkalosis
URB-21112
Soal
Pria 50 th, riwayat DM dgn th/ OAD,
Ditemukan tidak sadar di tempat tidur.
Empat hari sebelumnya os menderita infeksi paru disertai mual
muntah.
Di UGD somnolen, S; 330C, dyspnea, RR 30-35x/mnt,
Leukosit; 20.000, GD; 400.
AGD pertama; 6.8 / 12 / 1.8 / -33.1, Na 140, Cl 103, Alb 4.2,
keton darah 32 mmol/L
24 jam setelah th/ insulin, dan pemberian NaCl 0.9 3 L/hari,
pasien mulai sadar dan respon, hasil AGD ke 2; 7.23 / 28 / 11.7 /
-13.4. Na 155, Cl 130. Alb 40, KETON 1 mmol

6.8 / 12 / 1.8 / -33.1, Na 140, Cl 103, Alb 4.2, keton darah 32
24 jam setelah th/ insulin, dan pemberian NaCl 0.9 3
L/hari, pasien mulai sadar dan respon, hasil AGD ke 2;
7.23 / 28 / 11.7 / -13.4. Na 155, Cl 130. Alb 40, KETON 1
mmol
Kesimpulan
Dalam keadaan metabolic acidosis, tubuh mempunyai
kemampuan homeostasis alkalinizing response:
Rapid response (within minutes):
Ventilasi paru (pCO
2
), hyperventilation
Late response (within hours and days):
Chloride adjustment with hypochloremic
Albumin adjustment with hypoalbuminemia
Dalam keadaan metabolic alkalosis, tubuh mempunyai
kemampuan homeostasis acidifying response:
Rapid response:
Ventilasi paru pCO
2
, hypoventilation
SID
PCO
2
Weak acid
pH
Renal Failure
Lactic acidosis
Keto-acidosis
Vomiting
Diare
Heart Failure
Lung disease
Hyperventilation
Hypoventilation
Nephrotic Syndrome
Dehydration
Malnutrition
Charge Balance
Dissociation of:
Water
Protein
Carbonic acid
CONCLUSION
KESIMPULAN