ACID-BASE BALANCE

Dina Nilasari

Definition
Bronsted and Lowry's definition :
An acid is a substance that donates a proton in a
reaction, while a base is a substance that accepts a
proton in a reaction.
Arrhenius's definition :
An acid is a substance that increases the
concentration of hydrogen ion (H+) when dissolved
in water and a base is a substance that increases
the concentration of hydroxyl ion (OH-) when
dissolved in water.

Definition

Acidemia: PH < 7,36

Alkalemia: PH> 7,44

Acidosis: Proses yang menaikkan [H]+

Alkalosis: Proses yang menurunkan[H]+

Why a normal pH is
very important ?

Major Adverse consequences of

severe alkalemia
Cardiovascular
Arteriolar constriction
Reduction of coronary blood flow
Respiratory
Hypoventilation
Hypercarbia and hypoksemia
Metabolic
stimulation of anaerobic glycolysis
production of organic acid
hypokalemia
hypomagnesemia and hypophosphatemia
Cerebral
reduction of cerebral blood flow
tetany, seizure, stupor

Kondisi

[H+] nmol/L pH

Asidemi

> 100

< 7,0

Asidemi

50 80

7,1 7,3

Normal

40 2

7,4 0,02

Alkalemi

20 36

7,44 7,69

Alkalemi

< 20

> 7,70

Klinik
Letal
Perhatian
Normal
Perhatian
Letal

Dikutip dari kuliah dr.Parlindungan S, SpPD-KGH dalam kuliah mimbar FKUI tentang asam-basa

Henderson-Hasselbalch :

H2O + CO2

H+ + HCO3-

Law mass action k1.CO2 = k2.(H+xHCO3-)

k1/k2 = Ka = H+x HCO3-/CO2
[H+] = Ka x pCO2/HCO3pH = - log H+
pH = - log Ka + log (HCO3-/pCO2)
pH = 6,10 + log {[HCO3-] : [0,03 x pCO2]}
Atau
[H+] = 24 x pCO2 / [HCO3]

Normal Blood Gas Value

Measurement

Arterial blood

Mixed venous

Venous

7.40
(7.37-7.44)

7.36
(7.31-7.41)

7.36
(7.31-7.41)

pO2 (mmHg)
(decreases with age)

80-100

35-40

30-50

pCO2 (mmHg)

36-44

41-51

40-52

>95

60-80

60-85

22-26

22-26

22-28

-2 to +2

-2 to +2

-2 to +2

pH
(range)

O2 saturation
(decreases with age)
HCO3- (mEq/L)
[SI: mmol/L]
Base difference
(deficit/excess)

Clinicians pocket reference, 10th edition

Primary disorders
Primary disorder

Problem

Metabolic acidosis

Gain of H+ or loss of HCO3

Metabolic alkalosis

Gain of HCO3 or loss of H+

Respiratory acidosis

Hypoventilation

Respiratory alkalosis

Hyperventilation

pH

HCO3 pCO2

Pocket Medicine, 2nd edition

Kompensasi
Acidosis
Metabolic
acidosis

Respiratory
acidosis

Respiratory
compensation

VS

Alkalosis
Metabolic
alkalosis

Respiratory
alkalosis

Renal
compensation

Compensation

Kompensasi:

Respirasi: Hiper atau hipoventilasi

mempengaruhi CO2 untuk kompensasi proses
metabolik yang primer, terjadi dalam hitungan
menit
Renal: Retensi atau ekskresi H+ atau HCO3
oleh ginjal untuk kompensasi proses respirasi
primer, dalam hitungan jam sampai hari

Mekanisme kompensasi tidak pernah

mengkoreksi PH sampai normal Bila PH
normal mixed disorder

Acid-base nomogram

Harrisons Principles of Internal Medicine, 16th edition

Langkah penghitungan
Contoh:
PH 7,25 PCO2 48 HCO3 29
LANGKAH I
H+ = 24 x PCO2
HCO3
H+ =(7,8-pH) x 100 ~ 24x 48
29
= 55

~ 40

Ambil sample darah ulang

PH 7,25 PCO2 48 HCO3 29

LANGKAH II
Acidemia: pH < 7,36
Alkalemia: pH > 7,44
LANGKAH III
Kenali gangguan PRIMERNYA
Contoh: Cari yang arahnya sama
Asidemia (+) Kenaikan CO2 atau Penurunan HCO3
PCO2 =

48

HCO3 =

29= tidak cocok

Maka primernya asidosis respiratorik

Bila ke 2-2nya searah ??????

HCO3 = 6
pCO2 = 50
Primernya adalah yang paling besar
perbedaanya Asidosis metabolik

LANGKAH IV

Pergunakan tabel di bawah ini untuk menghitung

kompensasi

Bila berbeda mixed disorder

Prediction of compensatory responses on simple acid-base

disturbances

Harrisons Principles of Internal Medicine, 17th edition

PH 7,25 PCO2 48 HCO3 29

Asidosis respiratorik

kronik

HCO3 meningkat 4 tiap peningkatan PaCO2 10 mmHg

PaCO2 meningkat 8 8/10 x 4

HCO3 24 + 3,2 = 27,2

Simple asidosis respiratorik

Anion Gap
Anion gap = Na - (Cl + HCO3)

Normal value : 8-12 mEq/L

Refers to the relationship among the bodys cations

(Na), and anions (Cl and HCO3)

The gap represents the anions not routinely

measured (sulfates, phosphates, proteins, and
organic acids, such as lactic acid and ketone acids)

LANGKAH V

Hitung anion gap

Na- {Cl+ HCO3}

Normal : 8-12 mmol
Bila meningkat lanjutkan ke LANGKAH VI

AG= 29 HCO3 = 6
Langkah VI

Hitung delta AG dan EXPECTED HCO3

BANDINGKAN!!

Delta AG 29-10 = 19

HCO3 yang diharapkan = 24-19 = 5

metabolic acidosis

Contoh soal 2
Pasien 21 tahun dengan DM, nausea, vomiting, abdominal
pain.
Anion gap = 23
HCO3 = 18

Delta AG: 13
Expected HCO3 24-13 = 11
Berarti ada yang HCO3 nya asidosis metabolik mixed
alkalosis metabolik dari muntahnya.

ASIDOSIS METABOLIK
I.

PENINGKATAN PRODUKSI ASAM

II. KEHILANGAN BIKARBONAT

III. RETENSI ASAM (ion-H)

DIFERENSIASI ETIOLOGI
ASIDOSIS METABOLIK
I.

PENINGKATAN PRODUKSI ASAM

AG MENINGKAT (Asid.laktat, ketoasid.)

II.

KEHILANGAN BIKARBONAT
AG NORMAL (Diare, RTA, Inhibitor
Carbonic Anhidrase)

III. RETENSI ASAM (ion-H)

AG MENINGKAT (CKD Stage IV-V)
AG NORMAL (RTA1, RTA4)
Dikutip dari kuliah dr.Parlindungan S, SpPD-KGH dalam kuliah mimbar FKUI tentang asam-basa

Metabolic acidosis
Anion gap

normal
Gut

Renal

Exogenous

Endogenous

Diarrhea

RTA

Salicylates

Lactic acidosis

Fistule

Carbonic
anhydrase
inhibitor

Methanol

Ketoacidosis

Ileal loop

Paraldehyde

- diabetic
-starvation
Uremia

Differential diagnosis
Causes of high-anion-gap metabolic acidosis

Lactic acidosis
Ketoacidosis
Diabetic
Alcoholic
Starvation

Toxins

Ethylene glicol
Methanol
Salicylates
Renal failure
(acute and chronic)

Harrisons Principles of Internal Medicine, 16th edition

Differential diagnosis
Causes of non-anion-gap metabolic acidosis

Gastrointestinal bicarbonate loss

Diarrhea
External pancreatic or small-bowel drainage
Ureterosigmoidostomy, jejunal loop, ileal loop
Drugs

Calcium chloride (acidifying agent)

Magnesium sulfate (diarrhea)
Cholestyramine (bile acid diarrhea)

Renal acidosis

Hypokalemia

Proximal RTA (type 2)

Distal (classic) RTA (type 1)

Generalized distal nephron dysfunction (type

4 RTA)

Mineralocorticoid deficiency
Mineralocorticoid resistance
Na delivery to distal nephron
Tubulointerstitial disease
Ammonium excretion defect

Potassium-sparing diuretics (amiloride,

triamterene, spironolacton)
Trimethoprim
Pentamidine
Angiotensin-converting enzyme inhibitors and
AT-II receptor blockers
Nonsteroidal anti-inflammatory drugs
Cyclosporine

Other

Hiperkalemia

Drug-induced hyperkalemia (with renal

insufficiency)

Acid loads (ammonium chloride,

hyperalimentation)
Loss of potential bicarbonate: ketosis with
ketone excretion
Expansion acidosis (rapid saline
administration)
Hippurate
Cation exchange resins

Harrisons Principles of Internal Medicine, 16th edition

ANION-GAP URIN
AG darah, normal :
AG-urin = [(Na + K) Cl] urin
AG-urin menunjukkan hasil minus pada enteritis.
Ekskr. Amonia dan Cl tinggi dalam urin.
AG-urin menunjukkan hasil positip RTA-1,RTA-4,GGK
Tub.distal tak mampu
ekskr. Amonia, Cl dan
ion-H.

Management

Correct the underlying disorder

Treatment with bicarbonate should be

reserved for severe metabolic acidosis
(pH<7.20)

HCO3 needed = 0,4 x BW x HCO3

ALKALOSIS METABOLIK
I.

KADAR BIKARBONAT PLASMA MENINGKAT

1. PENGELUARAN ion-H MELALUI GINJAL DAN
SALURAN CERNA.
2. PERPINDAHAN ion-H KE DALAM SEL
3. BIKARBONAT BERLEBIHAN

II. REABSORBSI HCO3 DI TUBULUS MENINGKAT

1. VOLUME SIRKULASI EFEKTIP TURUN
2. DEPLESI ion-Cl
3. HIPOKALEMI

Dikutip dari kuliah dr.Parlindungan S, SpPD-KGH dalam kuliah mimbar FKUI tentang asam-basa

Aldosteron
di tub.distal

Volume sirkulasi
efektif turun
Renin Ang.II
dilepas meningkat

Aktif. Na3HCO3stimulasi
NaH-ATPase
& NaH-antiporter
dan ClHCO3exchanger

eks.ion-H
Reabsorbsi HCO3

Cl

pH

ion-K
keluar
dari sel
ion-H
masuk ke
dalam sel

KOMPENSASI RESPIRATORIK
PENINGKATAN pCO2
[HCO3] NAIK 1 meq/l pCO2 NAIK 0,75 mmHg

GEJALA KLINIK
1. SUSUNAN SARAF PUSAT
LEMAS, BINGUNG, TETANI, PARESTESIA,
KRAMP OTOT, KEJANG.
2. JANTUNG : ARITMI, HIPOKSEMI
3. ELEKTROLIT
HIPOKALEMI, HIPOFOSFATEMI.
Dikutip dari kuliah dr.Parlindungan S, SpPD-KGH dalam kuliah mimbar FKUI tentang asam-basa

Metabolic alkalosis
Urine chloride (UCl )
< 10 meq/l

10 meq/l

Chloride responsive

Chloride resistant
Excess
mineralocorticoid

Renal loss of
chloride

GI loss of H , Cl
-NG suction

- Diuretics

- Cushing syndrome

- Vomiting

- Cystic fibrosis

- Conns syndrome

- Villous adenoma

- Exogenous steroid

- Bartters syndrome

Differential
diagnosis
Harrisons Principles of
Internal Medicine, 17th edition

Management

Correct the underlying cause

Chloride-responsive

Replace volume with NaCl if depleted

Correct hypokalemia if present
NH4Cl and HCl should be reserved for extreme
cases

Chloride-resistant

Treat underlying problem

Respiratory Acidosis

Primary pCO2

pH , [HCO3-]

Alveolar hypoventilation

Differential Diagnosis

Central
Drugs (anesthetics,
morphine, sedative)
Stroke
Infection

Airway
Obstruction
Asthma

Parenchymal
Emphysema
Pneumoconiosis
Bronchitis
Adult respiratory
distress syndrome
Barotrauma

Neuromuscular
Poliomielitis
Kyphoscoliosis
Myasthenia
Muscular
dystrophies

Miscellaneous
Obesity
Hypoventilation
Permissive
hypercapnia

What happens in respiratory

acidosis?
H2O
Ventilatio
n

CO2

H2CO3

HCO3
H

Vasodilatation of
cerebral vessel
Excrete
Conserve
bicarbonate, hydrogen
ions
sodium ions
NaHCO3

Cerebral edema,
depress CNS

Respiratory
center

Respiratory
rate

Signs and symptoms

Headache

Altered LOC: restlessness coma

Fine flapping tremor, depresses reflexes

Nausea, vomiting

Tachycardia, ventricular arrhythmias

Cardiac arrest

Management

Intubation, mechanical ventilation

Increase ventilator rate, lowering pCO2

Treat underlying cause

Monitor vital signs, neurologic status, assess

cardiac rhythm

Respiratory Alkalosis

Primary pCO2

pH , [HCO3-]

Alveolar hyperventilation &

hypocapnia

Differential Diagnosis

Central stimulation
Anxiety,
hyperventilation
syndrome, pain,
psychosis
Head trauma or CVA
with central neurogenic
hyperventilation
Meningitis, encephalitis
Tumors
Fever, early sepsis
Drugs or hormones
Pregnancy,
progesterone
Catecholamines
Nicotine
Salicylates
Xanthines such as
aminophyline

Stimulation of chest
receptors
Flail chest
Cardiac failure
Pulmonary embolism

Hypoxemia or Tissue
hypoxia
High altitude
Pneumonia,
pulmonary edema
Aspiration
Severe anemia

Miscellaneous
Hepatic failure
Hyperthyroidism
Iatrogenic mechanical
overventilation

What happens in respiratory

alkalosis?
respiratory rate
or depth
CO2
elimination

PCO2

pH
ALKALO
SIS

Signs and symptoms

An increase in the rate and depth of respirations

Tachycardia

Anxious, restless, muscle weakness, difficulty

breathing

Confusion or syncope

Alternating periods of apnea and hyperventilation

Signs and symptoms

Hyperreflexia, carpopedal spasm, tetany,

arrhythmias, seizures, coma

ECG changes:
prolonged PR interval, a flattened T wave, a
prominent U wave, a depressed ST segment

Management

Monitor vital signs

Monitor intake and output

I.V. therapy

Monitor ABG and serum electrolyte levels

Oxygen therapy, breath into a paper bag,

mechanical ventilator if needed

Treat underlying cause

Thank You