BASIC CONCEPT OF ACID - BASE

LILIK SUKESI
INTERNAL MEDICINE DEPARTMENT/PADJADJARAN UNIVERSITY
HASAN SADIKIN HOSPITAL - BANDUNG

DEFINITION :
acid
any molecule that dissociates in solution to release a
hydrogen ion (H+) or proton

base
any molecule capable of accepting a hydrogen ion
(H+) or proton

buffer
any substance that can reversibly bind hydrogen ion
(H+) or proton
Buffer + H+

HBuffer

ACID BASE HOMEOSTASIS :

Three (3) primary systems regulating H +
concentration in body fluids
1) chemical buffer systems of body fluids
2) respiratory center (regulating removal of
CO2)
3) kidneys (excreting acid and alkaline urine)

ACID BASE HOMEOSTASIS :

1) chemical buffer systems
a. bicarbonate buffer

HCO3- + H+

H2CO3

(20)

CO2 + H2O

(1)
H+ + HCO3- H2CO3 CO2 + H2O
excess CO2 will stimulate respiration
elimination of CO2

ACID BASE HOMEOSTASIS :

H+

= K x

CO2
HCO3-

amount of CO2 in blood is a linear function of PCO2

most clinical labs measure blood CO2 tension (PCO2)

CO2 = (0.03) x PCO2

H

(0.03 ) x PCO2
= K x
HCO3-

ACID BASE HOMEOSTASIS :

pH = - log H+
(0.03 )x PCO2
pH = pK - log
HCO3metabolic factor

HCO3pH = pK + log
(0.03 )x PCO2
respiratory factor

ACID BASE HOMEOSTASIS :

HCO3pH = pK + log
(0.03 )x PCO2
Nilai normal HCO3- : 20 - 26 mEq/L
Nilai normal PCO2 : 35 45 mmHg
increase in bicarbonate

pH

increase in Pco2

pH

ACID BASE HOMEOSTASIS :

1) chemical buffer systems
b. phosphate buffer

playing a major role in buffering renal tubular fluid

and intracellular fluids

HCl + Na2HPO4 NaH2PO4 + NaCl

NaCl + Na2H2PO4 Na2HPO4 + H2O

ACID BASE HOMEOSTASIS :

1) chemical buffer systems
c. proteins
- buffer systems within the cells help to prevent
changes in pH of extracellular fluids

- may take several hours to become maximally

effective

hemoglobin

H+ + Hb HHb

ACID BASE HOMEOSTASIS :

2) respiratory regulation of acid-base
balance
- increased hydrogen ion concetration (pH)
stimulates alveolar ventilation
[H+] alveolar ventilation
(-)

Pco2

- pulmonary expiration of CO2 balances

metabolic formation of CO2
increasing alveolar ventilation
decreases extracellular fluid H+ and pH

ACID BASE HOMEOSTASIS :

3) Renal regulation of pH

body normally consumes more acidproducing foods than base-producing foods

kidney tubules secrete (a) hydrogen, (b)
ammonium, and (c) phosphate ions into urine
when a hydrogen ion is secreted into tubular
urine, a sodium ion is simultaneously
reabsorbed

ACID BASE HOMEOSTASIS :

renal correction
acidosis
(1) increased excretion of H+
(2) addition of HCO3- to extracellular fluid

alkalosis
(1) decreased tubular secretion of H+
(2) increased excretion of HCO3-

RESPIRATORY /
EXCRETORY RESPONSE
CO2 + H2O

yperventilation removes
H+ ion concentrations

ypoventilation increases
H+ ion concentrations

H2CO3

H+ + H

Kidneys eliminate or retai

H+ or bicarbonate ions

Time course of buffering, respiratory

Compensation/renal excretion of an acid load
H+
Load
100

Distribution
and extraCellular
buffering

Cell
buffering
Respiratory
compensation

Renal H+
secretion

50

12
Hours

24

72

SIMPLE ACID-BASE
DISORDERS
Simple acid-base disorders have one
primary abnormality.
The four primary disorders are respiratory
acidosis, respiratory alkalosis, metabolic
acidosis and metabolic alkalosis.
Mixed acid-base disorders have more than
one abnormality

Acid-base changes in acidosis and alkalosis

pH

HCO3-

PCO2

Respiratory acidosis

Respiratory alkalosis

Acid-base Disturbance

Metabolic acidosis

Metabolic alkalosis

Thicker arrows indicate primary disorder

pH, PCO2 in
opposite
directions;
HCO3- will
follow PCO2
pH, HCO3in same
direction;
PCO2
will follow
HCO3-

Interpreting ABGs

1. Look at the pH

is the primary problem acidosis (low) or alkalosis (high)

2. Check the pCO2 (respiratory indicator)

is it less than 35 (alkalosis) or more than 45 (acidosis)

3. Check the HCO3 (metabolic indicator)

is it less than 22 (acidosis) or more than 26 (alkalosis)

4. Which is primary disorder (Resp. or

Metabolic)?
If the pH is low (acidosis), then look to see if pCO2 or HCO3 is
acidosis (which ever is acidosis will be primary).
If the pH is high (alkalosis), then look to see if CO2 or HCO3 is
alkalosis (which ever is alkalosis is the primary).
The one that matches the pH (acidosis or alkalosis), is the primary disorder.

Compensation

The Respiratory system and Renal systems

compensate for each other
attempt to return the pH to normal
ABGs show that compensation is present when
the pH returns to normal or near normal
If the nonprimary system is in the normal range
(pCO2 35 to 45) (HCO3 22-26), then that
system is not compensating for the primary.
For example:
In respiratory acidosis (pH<7.35, CO2>45), if the HCO3 is
>26, then the kidneys are compensating by retaining
bicarbonate.
If HCO3 is normal, then not compensating.

clinical causes of acid-base disorders

pH 7.34, PCO2 60mmHg, [HCO3- 31mEq/L]

1. respiratory acidosis
due to:
causes:

[pH, Pco2]

decreased CO2 removal from lungs

a. damage to respiratory centers
b. airway obstruction
c. pneumonia, chronic bronchitis
d. decreased pulmonary membrane
surface area
e. pulmonary edema

compensatory mechanism :
(1) body fluid buffers
(2) kidneys

clinical causes of acid-base disorders

pH 7.50, Pco2 29mmHg, [HCO3- 22mEq/L]

2. respiratory alkalosis
due to:
causes:

[pH, Pco2]

increased loss of CO2 from lungs

a. hyperventilation
(i) emotional disturbances
(ii) drug overdose
(iii) high altitude (low Po2)

compensatory mechanism:
(1) body fluid buffers
(2) kidneys

clinical causes of acid-base disorders

pH 7.20, [Pco2 21mmHg], HCO3- 8mEq/L

3. metabolic acidosis

[pH, HCO3-]

due to:

(1) failure of kidneys to excrete

metabolic acids
(2) metabolic production of acids
(3) addition of acids to body
(4) loss of bases

causes:

(1) renal tubular acidosis

(i) Addisons disease
(ii) Fanconis syndrome
(2) chronic renal failure
(3) diabetes mellitus

clinical causes of acid-base disorders

pH 7.20, [Pco2 21mmHg], HCO3- 8mEq/L

3. metabolic acidosis
causes:

[pH, HCO3-]

(4) acid ingestion

(i) aspirin
(ii) methanol
formic acid
(5) diarrhea
(6) vomiting from deeper GI tract
(7) malnutrition
(8) starvation

compensatory mechanism :
(1) lungs
(2) kidneys

clinical causes of acid-base disorders

pH 7.50, [Pco2 48mmHg], HCO3- 36mEq/L

4. metabolic alkalosis
due to: (1) excess loss of acid

[pH, HCO3-]

(2) uptake of alkaline substances

causes: (1) diuretics
H+ secretion
HCO3- reabsorption
(2) excess aldosterone
sodium reabsorption
H+ secretion
(3) vomiting of gastric contents
(4) ingestion of alkaline drugs (e.g. antacids)

compensatory mechanism:
(1) lungs
(2) kidneys

systemic effect of alkalosis

alkalosis
over-excitability of central and peripheral
nervous system
1) muscle tetany
2) convulsion
3) respiratory arrest death

systemic effect of acidosis

Principal effect of acidosis is depression of the CNS
through in synaptic transmission.
Generalized weakness
Deranged CNS function the greatest threat
Severe acidosis causes :
Disorientation
coma
death

Anion-Gap
total concentration of anions and cations in
plasma must be equal to maintain electrical
neutrality
but, only certain cation (Na+) and anions (Cl-,
HCO3-) are routinely measured in clinical
laboratory

Anion-Gap
anion gap : difference between unmeasured
anions and unmeasured cations

Na+
unmeasured
cations

Cl-

HCO3-

unmeasured
anions

Anion-Gap
Na+
unmeasured
cations

Cl-

HCO3-

unmeasured
anions

anion gap = [Na+] {[HCO3-] + [Cl-]}

= 144 - { 26
= 10 mEq/L

+ 108}

Anion-Gap
Na+
unmeasured
cations

Cl-

HCO3-

unmeasured
anions

if unmeasured anions relative amount of Cl- & HCO3albumin, phosphate, sulfate,

other organic anions

anion gap

calcium,
if unmeasured
relative amount of Na+
magnesium,cation
potassium

clinical use of anion-gap

In metabolic acidosis (low HCO3-)

if plasma Na+ is unchanged,

concentration of anions (Cl- or unmeasured anion)
must increase to maintain electro-neutrality
(1) if Cl- remains unchanged :
there must be increased unmeasured anion
(= anion gap)
a.
b.
c.
d.
e.
f.

diabetes mellitus (ketoacidosis)

lactic acidosis
chronic renal failure
aspirin (acetylsalicylic acid)
methanol
ethylene glycol

clinical use of anion-gap

(2) if Cl- increases in proportion to the fall of HCO3-:
(normal anion gap)
(hyperchloremic metabolic acidosis)
a. diarrhea
b. renal tubular acidosis

ASSESSMENT OF ACID-BASE DISTURBANCES

Arterial pH

Hx & Px

< 7.35 Acidemia

Check pH

Check pCO2
High pCO2
Low HCO3
and HCO3
Metabolic Acidosis Respiratory Acidosis
Expected
compensation
ACUTE
CHRONIC
Check
Anion Gap
Na-(Cl+HCO3)
Possible
Diagnoses

1 HCO3: 1 pCO2
1 HCO3: 1 pCO2
=12-16

>16

10 Pco2 :1 HCO3
10 Pco2 :3 HCO3

> 7.45 Alkalemia

High HCO3
Metabolic Alkalosis

Low pCO2
Respiratory Alkalosis

1 HCO3: 0.5 pCO2

1 HCO3: 0.5 pCO2

10 Pco2 :2 HCO3
10 Pco2 :5 HCO3

May be increased due

to increased negative
charge of proteins

COPD
Drugs-CNS/Resp
Depressants
Drugs
Normotensive
Hypertensive
Ketoacidosis
High Altitude
HCO3 Loss
Lactic
Acidosis
ASA
R.T.A.
Renal
Failure
Pregnancy
Diarrhea
Urine Cl
Intoxications
Sepsis
ASA
Methanol
> 10
Conns
Ethylene Glycol < 10
Diuretics
Cushings
Vomiting
Renal Artery Stenosis
Post-hypercapneia

ACIDIFICATION
OF URINE BY
EXCRETION OF
AMMONIA

THE ANION GAP

[Na] - (Cl + HCO3)
albumin
HCO3
Na
Cl

Anion gap

clinical measurements and analysis

of acid-base disorders
Step 1:

examine pH

Step 2:

check

acidosis (pH <7.4)

alkalosis (pH >7.4)
Pco2 (nl: 35-40 mmHg)
HCO3- (nl: 22-24 mEq/L)
pH

Pco2 HCO3-

respiratory acidosis

()

metabolic acidosis

()

respiratory alkalosis

()

metabolic alkalosis

()