Clinical Pathology

Med School, Padjadjaran

University

ACID BASE, ELECTROLYTES AND WATER

DISTURBANCES
I. GLOSSARY OF TERMS :
1.
2.
3.
4.
5.
6.

Acid
Base
Buffer
Buffer Base (BB)
Normal Buffer Base (NBB)
Base, Negative (-)

13.
14.
15.
16.
17.
18.

Hypocapnia
Hypoxemia
Hypoxia
Oxygen content (ct O2)
Oxygen saturation
pO2 (pressure-O2)

7. Base, Positive (+)

19. pO2 (0,5) or P50

8. Bicarbonate (HCO3-)

20. Total-CO2 (TC02)

9.
10.
11.
12.

Henderson-Hasselbalch Equation 21. pCO2

Dalton's law
22. pH
Henry's law
23. pKa
Hypercapnia

II. Normal values

1. pH
: 7.40 + 0.05
2. pCO2
: 40
+
5 mmHg
3. pO2
: 80
- 100 mmHg
4. (HCO3-)
: 24
+
2 mmol/L
5. TCO2
: 25,2 +
2 mmol/L
6. O2 - saturation: 95 - 98 %
7. Base, Negative (Base, deficient) : - 2,5
8. Base, positive (Base, Excess)
: + 2,5

III. Compensatory Mechanisms

1. Buffer System :
a. Carbonic acid
CO2 + H20

Bicarbonate Buffer System :

H2CO3
H+ + HCO3-

b. Non Bicarbonate Buffer System :

Hbuf
H+ + Buf -

2. Lungs :
Compensate by altering the acid or respiratory
component during :
a. Hypoventilation
b. Hyperventilation
3. Kidneys : Na+ - H+ Exchange
The kidneys tend to correct for primary
abnormalities in the basic or metabolic (HCO3-)
component.

Henderson-Hasselbalch Equation :
pH = 6.1 + Log [HCO3-] / [H2CO3]
6.1 + Log [HCO3-] / 0.03 x pCO2
6.1 + Log 24/1.2

24/1.2
24/1.2

= 6.1 + Log 20/1

= 6.1 + 1.3
= 7.40

The mechanism for bicarbonate synthesis reabsoption

( Na + - H+ exchange ) is illustrated in Fig.1,2,3

ECF

TUBULE
Na+ + HCO3-

Na+ Active Transport Na+

Na+
+
+ Active Transport
HCO
+H
H+
HCO3
3
H2CO3

H2CO3

Carbonic anhydrase

CO2

H2 O
+
CO2

HCO3-

CO2

H 2O

ECF

TUBULE
Na+ + Na+ + HPO4=

Na+ Active Transport Na+

Na+
+
+ Active Transport
HCO
+H
H+
HCO3
3

H2PO4-

H2CO3
Carbonic anhydrase

CO2

H2 O
+
CO2

Na+ H2PO4-

ECF

TUBULE
Na+

Cl-

Na+ Active Transport Na+

Na+
+
+ Active Transport
HCO
+H
H+
HCO3
3
H2CO3
Carbonic anhydrase

NH3 Diffusion NH3

CO2

H2 O
+
CO2 Glutamine

NH4+ + Cl-

IV. Types of Acid - Base Disturbances:

There are four types of Acid-Base disturbances:
1. Respiratory Acidosis
2. Respiratory Alkalosis
3. Metabolic Acidosis
4. Metabolic Alkalosis

pH = 6.1 + log [HCO3-] / 0.03 X pCO2

NaHCO3
H2CO3

Na+ + HCO3- ( I )
H+

+ HCO3- ( II)

1. Respiratory Acidosis
Henderson - Hasselbalch Equation :
pH = 6.1 + log [HCO3-] / 0.03 X pCO2
a. Primary Defect
CO2 excess

pH

HCO3-

20

20

H2CO3

< 7,35)

CO2 retention

H2CO3

(hypercapnea)
pH
( < 7,35)
Pa CO2 > 45 mmHg
PaO2 rendah
HCO3-

(< 30 mEq/L)

Etiology:
*Inhibition on resp center in OM
A Medicine : opiat, sedatives
B. O2 therapy
C. Cardiac arrest
D Apnea during asleep
*Resp muscle and thorax
A Muscle disease : myastenia gravis,
GuillainBarre syndrome
B Thoracal deformity : kiphoscoliosis
C Overt obesity
D Thoracal injury

2. Respiratory Alkalosis
Henderson - Hasselbalch Equation :
pH = 6.1 + log [HCO3-] / 0.03 X pCO2
a. Primary Defect
Alveolar hypervent
PaCO2
pH

CO2 excretion
(>45 mmHg)

B Hypoxia :
1. Pneumonia, bronchiale asthma,
pulmonary oedem
2. Congestive heart failure
3. Pulmonary fibrosis
4. Live in high place
C. Overt mechanical ventilation
D. Unexplained mechanism :
.Gram negative sepsis
.Hepatic cirrhosis
.Physical training

Compensation
a. Buffer :
HCO3- ( react II & I)
b. Renal :
No reabsorp HCO3No prod H+ & NH4+
No exchange Na+
base urine
pH Normal

3. Metabolic Acidosis
Henderson - Hasselbalch Equation :
pH = 6.1 + log [HCO3-] / 0.03 X pCO2
a. Primary Defect
* Noncarbonic acid accumulation
* HCO3- loss
HCO3

pH

 Renal failure : acid excretion

accumulation
DM: Insulin
Starvation
keton

Cardio pulm

O2

acid

ketosis
(H+)

unaerob metab

sepsis
lactate acidosis

lactate

Etiology:
Increased production of nonvolatile metabolic
acids
# Excess production of metab acids: Lactic
acidosis, diabetic ketoacidosis, fasting and
starvation, poisoning (salicylate,
methanol)
# Impaired elimination: failure or dysfunction
Excessive loss of bicarbonate
*Loss of intestinal secretions : diarrhea,
intestinal suction,
intestinal or biliary fistula
* Increased renal losses: RTA, th/ with
carbonic anhydrase inhibitor,
hyperaldosteronism

Compensation
a. Buffer :
H2CO3 ( X) (end prod)
HCO3b.Resp
CO2 expirate (Kussmaul)
H2CO3
c. Renal :
HCO3- reabsorp
H+ & NH4+ prod
replaced Na+

acid urine

4. Metabolic Alkalosis
Henderson - Hasselbalch Equation :
pH = 6.1 + log [HCO3-] / 0.03 X pCO2
a. Primary Defect
* noncarbonic acid loss
* HCO3- excess
pH

HCO3

pCO2

Etiology
Excess loss of hydrogens ions :
Vomiting, gastric suction
Potassium defisit (diuretic th/ ,
hyperaldosteronism)
Milk-alkali syndrome

Excess gain of bicarbonate or alkali :

Ingestion or administ of NaHCO3
Administ of citrate-containing blood
transfusions

H+ , Na+ , Cl- , K+ loss

NaHCO3

Na+ + HCO3- ( I )

H2CO3

H+

re II : HCO3-

+ HCO3- ( II)
, H2CO3

Compensation
a. Buffer:
H2CO3

HCO3b. Resp :
pH

carotid body

CO2 retention , H2CO3

hypoventil
hypoxia

Vol ECF
dehydration
renin-angiotensin-aldosteron
Na+ reabsorp
KHCO3 loss
K+ secretion

K+ def

H+ & NH4+ (tub secr)

HCO3-

acid urine

severe metab alkalosis

V. Collection of Blood for pH/Blood Gases

Determination
1. Unaerobic Collection : to avoid gas exchange
2. Blood gas determination should be performed
immediately (within 10 minutes)
If the determination is delayed, the specimen
should be placed in ice water or placed on
crushed ice, but should be assayed within 1
hour.
3. Whole blood samples (using Lithium heparin
as the anti-coagulant : 240 Unit / ml.

4. The blood may be obtained from arteries (it is

more uniform in composition): radialis, ulnaris,
brachialis, femoralis.
If the arterial blood cannot be obtained,
capillary blood may be used as a substitute as
long as moist heat is used before collection
(=Arterialized blood is obtained by warming a
limb to 450 C, 20 minutes.

 This method of collection is routinely used

when samples are obtained from infants.
Heparinized - capillary tubes are used for
collecting
arterialized
blood.
Before
sealing, a small piece of wire is inserted
into the capillary tube.
The wire may be moved with a magnet to
allow mixing of the blood prior to analysis.

 Delay without cooling > 10 mnt

pH
pCO2
pO2 (lactic ac)
Sampling aerobic (air contaminattion)
pH
pCO2
pO2
Condition: hyperventilation
pH
pCO2
pO2
Temp :
hyperthermia : pH
hypotermia

: pH

pCO2

pO2

pCO2

pO2

pH
pH

HCO3-/pCO2
/ N : metab alkalosis without compensation
/
part comp
N
/
complete comp

pH
N
pH

/N
/
/

: metab acidosis without compensation

part comp
complete comp

N /
/
/

: resp alkalosis without compensation

part comp
complete comp

N /
/
/

: resp acidosis without compensation

part comp
complete comp

pH

VI.

NORMOGRAM :
1. Siggaard - Andersen Alignment
2. pO2 - Oxygen Saturation

Inspired Air

Expired Air
pO2
pCO2
pH2O

pO2
pCO2
pH2O

= 115 mmHg
= 30 mmHg
= 47 mmHg

= 152
mmHg
= 0.25 mmHg
= variable

TRACHEAL OR BRONCHIAL AIR

pO2 = 149 mmHg
pCO2 = 0.25 mmHg
pH2O = 47 mmHg

ALVEOLAR AIR

Arterial Blood
pO2 = 100 mmHg
pCO2 = 40 mmHg
O2

pO2
pCO2
pH2O

= 102 mmHg
= 36 mmHg
= 47 mmHg

LUNG CAPILLARY
TISSUE CAPILLARY
CO2

pO2 = 20 mmHg
pCO2 = 60 mmHg
surface of tissue cell

pO & pCO in air, blood & tissue

CO2
Venous Blood
pO2 = 40 mmHg
pCO2 = 46 mmHg