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
