Gangguan Keseimbangan Asam Basa

di bidang Penyakit Dalam

Dr A.Hadi Martakusumah SpPD-KGH

Sub Bagian Ginjal Hipertensi
Bagian I Penyakit Dalam
FK UNPAD/ RS Hasan Sadikin
Bandung

.. The reports of the demise of acid base

problem solving have been greatly
exaggerated !. As important as the non
invasive monitoring of oxygen saturation is
,the partial arterial oxygen tension is removed
from the context of acid base physiology, the
disease puzzle will not fit together
successfully. Fluctuation in pH and contingent
compensation by the kidneys and lungs are
the remaining pieces .
WL Whitter : Primer on clinical acid base problem solving
Disease-A-Month : 50: 1.2004

1.1.1 Approaches to Understanding Acid-Base

Physiology
Traditional Approach
The discussion of acid-base physiology outlined in most of
this book is the traditional empirical approach. The concepts
and explanations of this approach are still the most common
way that acid-base physiology is taught and understood by
many clinicians to some extent.
But this is not the only approach.
Physico-chemical Approach
An alternative approach derived from physico-chemical
principles was proposed by Stewart in 1981.

Kadar Anion dan Kation yang normal

Kation (mEq/L)

Anion (mEq/L)

Na+

140

Cl

103

K+

HCO 3

25

Ca + +

Protein

16

Mg + +

Organic

H+

0.000040
Other
(40 nmol/L) Inorganic

Protons have a very small radius of H+(10-9m) and a very

high charge density, resulting in very large electric field
gradients in their immediate environment
These gradients interfere with electrostatic interactions and
hydrogen-bonding among different chemical groups within a
macromolecule. This interference is likely to disrupt the all
important tertiary and quaternary protein structures.
The small radius also enables protons to reach and interact
with reactive sites in a protein molecule, altering its
conformation and function.
Stewart :

{H:(H2O)n}+

H + akan menimbulkan Asam

(Acid) dalam tubuh
Ada dua macam asam yang dibentuk
akibat H + ini :
1.Volatile Acid disebabkan CO2 akibat
pembakaran . Dalam keadaan istirahat
akan terbentuk 190 mmol/KgBB/hari.
Acid ini akan dikeluarkan oleh
paru
2.Fixed Acid terbentuk akibat metabolisme
terutama protein

H+ + HCO3CO2

PEMBENTUKAN H +
DAN PEMBUANGANNYA

Nutrient

Produk

H+ (mmol/hari)

REAKSI KIMIA MENIMBULKAN H+

Asam amino yang mengandung sulphur :
Cystein, Methionine

H+

70

H+

140

H+ +HPO42 -

30

Glutamat, aspartat

HCO3-

110

Anion organic misal sitrat

HCO3-

60

Asam Posfat organik

H2PO4-

30

Asam amino kationik :

Lysine, Arginin, Histidin
Posfat organik :

REAKSI KIMIA MENGIKAT H+

Asam amino anionik

NET TOTAL H+ YANG HARUS DIKELUARKAN SEBAGAI NH4+OLEH GINJAL

40

Protein
HCO3-

Glutamine

2NH4+ + 2- Oxoglutarate 2 ADP

CO2 + H2O

ATP

H+ (secreted)

URINE

LIVER

FILTERED
HPO42-

2 H2PO42(to urine)

UREA

2H+

2HCO 3 -

Blood

GFR 180 L/day

4500
mmol/day

Clinical Acid Base Problem Solving

Langkah Pertama :
Harus tahu harga normal parameter yang akan digunakan
untuk menganalisis kelainan asam basa :
a. pH 7.40 atau [H+ ] 40 nmol/L

Cara merubah pH kedalam [H+ ] :

Buang angka tujuh dan desimalnya jadi misal pH 7.26 didapat 26
Kurangi 40 dengan nilai tersebut jadi 40 26 = 14
Tambahkan 40 kedalam harga tersebut : 40 + 14 = 54 nmol/

b. pCO2 = 40 mm Hg
c. [HCO3 ] = 25 mmol/L
d. Anion gap plasma Na-Cl-[HCO3 ] = 12 mEq/L jika kadar
albumin normal yaitu 4 gr% . Setiap penurunan albumin 1
gram % dari harga normal maka kadar AG dikurangi 4

Clinical Acid Base Problem Solving

Langkah Kedua :
Apakah ada Lab Error ?
Cara mengetahuinya adalah masukkan harga PH ,
pCO2 dan [HCO3 ] kedalam persamaan
Henderson di bawah ini :
[H+ ] = pCO2 X 24/ [HCO3 ]
Jika penderita tidak demam dan harga [HCO3 ]
yang dihitung dan yang diukur berbeda lebih dari
10% maka ada lab error .
Kita harus mengulangi pemeriksaan. Kita tidak
ingin menganalisis hasil AGD berdasarkan hasil
laboratorium yang salah .

Clinical Acid Base Problem Solving

Langkah Ketiga :
Tetapkan hasil pH :
Acidemia jika kurang dari 7.36
Alkalemia jika lebih dari 7.44

Clinical Acid Base Problem Solving

Langkah Keempat :
Tentukan apakah kelainan primernya
respiratorik atau metabolik
Alkalemia :
Respiratory Alkalemia jika pCO2 kurang dari 38
Metabolic Alkalemia jika [HCO3 ] lebih dari 25

Acidemia :
Respiratory Acidemia jika pCO2 lebih dari 44
Metabolic Acidemia jika [HCO3 ] kurang 25

Clinical Acid Base Problem Solving

Langkah Kelima :
Hitung anion gap (AG) serum yaitu :
Kadar Na serum ( Cl + [HCO3 ]
serum
Other
Cation

Jika AG > 10 ada kemungkinan

metabolic acidemia
Jika AG > 20 dapat dipastikan Na+
ada metabolic acidemia

Jangan lupa factor albumin !

(140)

A-

Other
Anion

HCO3(25)

Cl(103)

Clinical Acid Base Problem Solving

Langkah Keenam :
Check derajat kompensasi tubuh :
Metabolic Acidemia :
Setiap penurunan pCO2 = 1.3 X penurunan [HCO3 ]

Metabolic Alkalemia :
Setiap kenaikan

pCO 2 = 0.6 X kenaikan [HCO3 ]

Respiratory Acidemia :
Akut :
Setiap pCO2 naik 10 mmHg = [HCO3 ] naik 1 mEq/L

Kronik :
Setiap pCO2 naik 10 mmHg = [HCO3 ] naik 4 mEq/L

Respiratory Alkalemia :
Akut :
Setiap pCO2 turun 10 mmHg = [HCO3 ] turun 2 mEq/L

Kronik :
Setiap pCO2 turun 10 mmHg = [HCO3 ] turun 5 mEq/L

Clinical Acid Base Problem Solving

Langkah Ketujuh :
Determine Delta ratio (Delta gap) =
(Increase in anion gap / Decrease in bicarbonate)

Guidelines for Use of the Delta Ratio in

Metabolic Acid-Base Disorders
Delta Ratio

Assessment Guideline

< 0.4

Hyperchloraemic normal anion gap acidosis

0.4 - 0.8

Consider combined high AG & normal AG

acidosis Ratio often <1 in acidosis assoc.
with renal failure

1 to 2

Usual for uncomplicated high-AG acidosis

Lactic acidosis: average value 1.6
DKA more likely to have a ratio closer to 1
due to urine ketone loss (esp if patient not
dehydrated)
Suggests pre-existing elevated HCO3 level:
consider a concurrent metabolic alkalosis
or a pre-existing compensated respiratory

>2

Other parameter to consider

The Urinary Anion Gap
The cations normally present in urine are Na+,
K+, NH4+, Ca++ and Mg++.
The anions normally present are Cl-, HCO3-,
sulphate, phosphate and some organic
anions.
Only Na+, K+ and Cl- are commonly measured
in urine so the other charged species are the
unmeasured anions (UA) and cations (UC).
Cl- + UA = Na+ + K+ + UC
Urinary Anion Gap =
( UA - UC ) = [Na+]+ [K+] - [Cl-]

Urinary Anion Gap

Clinical Use
Key Fact: The urinary anion gap can
help to differentiate between GIT and
renal causes of a hyperchloraemic
metabolic acidosis.
It has been found experimentally
that the Urinary Anion Gap (UAG)
provides a rough index of
urinary ammonium excretion.

Urinary Anion Gap

Clinical Use
In a patient with a hyperchloraemic
metabolic acidosis:
A negative UAG suggests GIT loss of
bicarbonate (eg diarrhoea)
A positive UAG suggests impaired renal
distal acidification (ie renal tubular
acidosis).
As a memory aid, remember neGUTive
- negative UAG in bowel causes

Osmolar Gap
Osmolar gap = (Measured osmolality) (Calculated osmolarity)
2 [Na+] + Glucose ( mmol/L) + Urea N (mmol/L)
0R
2 [Na+] + Glucose( mg% /18) + Urea N(mg% /2.8)
The osmolar gap can be very useful in assisting
diagnosis in metabolic acidosis due to toxic
alcohols & glycols (eg ethylene glycol, methanol).

[H+]

HIGH

NORMAL

LOW

Acidemia

Mixed Disorder if :
pCO2 & HCO3 both low
pCO2 &HCO3 both high
Plasma AG wide

Alkalemia

HCO3
LOW
METABOLIC
ACIDOSIS

pCO2
High

RESPIRATORY
ACIDOSIS

HCO3
HIGH

PCO2
LOW

METABOLIC
ALKALOSIS

RESPIRATORY
ALKALOSIS

Metabolic Acidosis
Definition
High [H+] / Low pH and Low [HCO3] in plasma. Metabolic
acidosis may also be detected by finding a wide plasma AG
(>15 meq/L) even without a pH or [HCO3] change
Expected physiological response :
Lung : Lower pCO2 to minimize fall in pH.Quantitatively the
fall in pCO2 from 40 mmHg should equal the fall in plasma
[HCO3] from 25 mmol/L
Kidney : Excrete NH4+ to make new [HCO3] .Normally the
kidney excrete 40 mmol NH4+ /day .During metabolic acidosis
should be at least 1 mmol/KgBW/day .Ideally as high as 300
mmol/day

Metabolic Acidosis
Clinical Classification :
Acid gain
Is recognized by finding anions that have
accumulated in plasma
Loss of [HCO3]
The plasma Anion |Gap normal

Other
Cation

Na+
(140)

Other
Anion

HCO3(25)

Cl-

Other
Cation

A-

Other
Anion

L-

(140)

(103)

Normal

A-

Added
Anion
HCO3-

Na+

Other
Cation

Cl

Other
Anion
HCO3-

Na+
(140)

Cl-

Metabolic Acidosis

Metabolic Acidosis

With increased

With normal

Anion Gap

Anion Gap

Acid Gain
Metabolic Acidosis With increased Anion Gap

Other
Cation

AL-

In Quantitative terms the rise in plasma AG

should equal the fall in plasma [HCO3]

The major Acids are :

1.L Lactic acid (tissue hypoxia)
2.Ketoacids ( insulin deficiency)
3.D Lactic acid (Low GI motility or altered GI
flora eg blind loop syndrome
4.Intoxicants which are or become acids :
Methanol to formic acid
Ethyle glycol to glyoxalic acid
Paraldehyde to acetic acid
Toluene to hippuric acid
Acetosalicylic acid ( never that high)

Na+
(140)

Other
Anion
Added
Anion
HCO3-

Cl-

Metabolic Acidosis due to

Acid Gain
Osmolal gap in plasma is very
helpful to recognize the intoxicant
,methanol,ethylene glycol and
also ethanol
Excess anions in the urine are
recognized by finding positive
urinary anion gap

Other
Cation

AL-

Na+
(140)

Other
Anion
Added
Anion
HCO3-

Cl-

Metabolic Acidosis due to

of [HCO3]

Loss

The plasma anion gap is normal

1.Loss of [HCO3] via GI tract
(diarrhoea,ileus,fistula). In this case,the
urinary anion gap is negative
2.Loss of [HCO3] in the urine. The most
convenient way to detect this loss is to find
urine pH >6. Causes include proximal RTA
or acetazolamide
3.Failure of the kidney to make new [HCO3

] like in distal RTA.In this case Urinary

anion gap positive
3.Exception to AG rule is renal failure.

Other
Cation

A-

Other
Anion
HCO3-

Na+
(140)

Cl

Metabolic Acidosis in Renal Failure .Increased anion gap but

an acid load is not the major problem

Low GFR (reduced

excretion af anion such as
phosphate or sulfate
caused Increased AG

The Acidosis is due to a Low

excretion of NH4+

HCO3
=
pCO2
NO

YES
Plasma AG
=
HCO3

Respiratory
Acidosis
or Alkalosis
YES

No Rise AG
Loss Na HCO3
GI
GU
Indirect

AG >

Met Alkalosis
Chr Resp
Acidosis

Plasma
Keton
4 + undiluted
YES

NO

Ketoacidosis

Hypoxia
NO

YES

GFR < 20% normal

YES
Renal
Failure

HCO3

Lactic Acidosis

NO
Plasma Osmolal Gap
> 20 mOsm
YES

Methanol
Ethanol
Ethylene Glycol

NO
Type B Lactic Acidosis
D Lactic Acidosis
Other acids

Treatment of Metabolic Acidosis

The therapeutic decisions about patients
with metabolic acidosis revolve around
the following issues :
What emergency measures are required ?
How can the threats to life be avoided ?
What are the options for treating the acidosis
per se ?

EMERGENCY MEASURES
Before the biochemical results are
available , measure to ensure a proper
airway , adequate circulation and O2
delivery must be pursued vigorously.

Avoiding Threats to Life

There are three critical reasons for making a
specific diagnosis :
It is important to determine the rate of H+
production
The cause of the metabolic acidosis may pose a
serious but independent threat to the patient e.g.
methanol overdose.Ethanol administration is the
most important measure
In certain type of metabolic acidosis that are
associated with hypokalemia (low distal tubular H+
secretion,Diarrhea) ,K replacement may be
necessary before or along with NaHCO3 in order
to avoid cardiac arrythmia or respiratory failure

Treatment of The H load

+

To Assess the need for NaHCO3 therapy, use the

plasma [HCO3] instead of pH
The use of NaHCO3 in L Lactic acidosis is a
controversial area.
Treatment of patients with a normal plasma AG and
defect in NH4+excretion .Assume volume distribution
of 50%
Treatment of patients with severe degree metabolic
acidosis. It should raise the [HCO3] to close to 5
mmol/L ifpCO2 less than 20 mm Hg
Halperin ML and Goldstein MB : Fluid,Electrolyte and Acid Base
Physiology.2nd edition.WB Saunders Company.1994

Treatment of Ketoacidosis
In ketoacidosis the rate of H+ production is slow
NaHCO3 may provoke severe hypokalemia
NaHCO3 should be avoided in most cases except :
When hyperkalemia is severe despite insulin theraphy
In very severe acidemia [HCO3] < 5 mmol/L to raise the
plasma [HCO3] close to twofold
When acidemia worsens despite insulin theraphy
( perhaps insulin resistance )

Halperin ML and Goldstein MB : Fluid,Electrolyte and Acid Base

Physiology.2nd edition.WB Saunders Company.1994

Treatment of Metabolic acidosis

The treatment of metabolic acidosis consists of
the treatment of primary pathophysiologic
process and if pH is severely decreased ,
administration of NaHCO3 . If [HCO3] is infused
arterial blood gases should be measured again
after approximately 5 minute
Prough DS :Physiologic Acid Base and Electrolyte Changes in Acute and Chronic Renal
Failure Patients. Anesthesiology Clinics of North America 4:1-15.2000

Give Na HCO3
What are the benefits and
What are the risks ?
Benefits

Risks

What are the effects

of removing H+

Metabolic
benefit
Glycolysis is faster
so more ATP is
made in vital
organ

HYPOKALEMIA

CAN CAUSE
RESPIRATORY FAILURE

Can the Na+ load

be tolerated

RETURN THE NET

Charge on proteins
to normal

Heart pumps better

direct effect
indirect effect via
adrenergic receptors

NO

ACUTE
PULMONA
RY EDEMA

YES

What risks might

be present ?

RAPID
PRODUCTION
OF CO2

PRECIPITATE
CaCO3

NOT TRUE BECAUSE CELLS HAVE

TO BE LESS ACIDIC TO MAKE H+
VIA BACKTITRATING PROTEIN
MORE ATP IS MADE WITH L
LACTIC ACID FORMATION

ACUTE HYPOCALCEMIA