Arterial Blood Gases.

F. Normal values
p
pCO2
p O2
HCO3
BE
SaO2

7.35 -7.45
35 -45mm g
more than 100 mm Hg
22 - 26 mmol/L
-5 to 5 mmol/L
more than 95%

 Definitions :
1. p
defined as negative logarithm of hydrogen activity

plasma concentration H ion

p
H mmol/L
6.8
160
7.1
80
7.4
40
7.6
20

2. Acidemia
defined as a condition where the arterial pH is less than 7.35

3. Alkalaemia
defined as a condition where the arterial pH is higher than 7.45

4. Acidosis
defined as an abnormal condition that lowers the arterial pH if

no secondary changes occur in response to primary disease

process.

5. Alkalosis
defined as an abnormal condition which tends to raise the

arterial pH if there is no secondary changes in response to the

primary disease process.

6. Mixed Disorder
two or more primary acid-base disorder occurs.

7. Compensation
refers to normal body processes tending to return arterial pH

to normal (respiratory or renal)

 Interpretation of acid-base status from analysis of blood gases

requires a systematic approach. A recommended approach follows
1) Look at arterial pH : Is acidemia or alkalemia present ?
pH
Decreased

Increased

PaCO2

PaCO2

Decreased

Increased

Decreased

Increased

Metabolic
acidosis

Respiratory
acidosis

Respiratory
alkalosis

Metabolic
alkalosis

Figure 30-6. Diagnosis of simple acid-base disorders

2) Look a PaCO2 : Is the change in PaCO2 consistent with a

respiratory component ?
3) If the change PaCO2 does not explain the change in arterial pH,
does the change in (HCO3) indicate a metabolic component ?
4) Make a tentative diagnosis (Table 30-1)
5) Compare the change in (HCO3) with the change in PaCO2. Does a
compensatory response exist (Table 30-7) ? Because arterial is
related to the ratio of PaCO2 to (HCO3) , both pulmonary and renal
compensatory mechanisms are always such that PaCO2 and
(HCO3) , change in the same direction. A change in opposite
directions implies a mixed acid-base disorder.
6) If the compensatory response is more or less than expected, by
definition a mixed acid-base disorder exists.

Acid Base Disorder

Resp. Acd
Resp. Alk
Met. Acd
Met. Alk

PaCO2 up
PaCO2 dn
HCO3 dn
HCO3 up

HCO3 up
HCO3 dn
PaCO2 dn
PaCO2 up

A. Respiratory Acidosis
1. Central Nervous System Depression
Drugs
Cerebral Trauma
2. Neuro-muscular Disorders
Neuropathies
Myopathies
3. Airway Obstruction
Tumour
Foreign Body
4. Increased CO2 Production
Malignant Hyperthermia
Burns

B. Metabolic Acidosis
1. Increased production of acids
Renal Failure
Diabetic Ketoacidosis
Starvation
2. Ingestion of Toxins
Salicylates
Methanol
3. Rhabdomyolysis
4. Increased GIT loss
Diarrhoea
Fistula (pancreatic, small bowel)

C. Respiratory Alkalosis
1. Central Nervous System
pain
anxiety
2. Drugs
Salicylates
doxapram
3. Ventilator Induced
4. Peripheral Stimulation
hypoxia
high altitude

D. Metabolic Alkalosis
1. Drugs
diuretics
antacids
2. GIT causes
vomiting
3. Alkaline administration
4. Severe Hypokalemia

E. Measurement of Blood Gas parameters :

1. p

Silver/silver chloride electrode and a mercury/mercurous

chloride (calomel) electrode are used.

2. pCO2

Modification of the p electrode or also known as the

Severinghaus electrode is used.

3. pO2

Clark electrode utilizing platinum and silver/silver chloride

electrodes are used.

Oxygen saturation, bicarbonate and base excess are

calculated once the above parameters have been measured.

G. Compensatory Mechanisms
Physiological responses to change in Hydrogen ion
concentration are characterized by three phases : 1.
2.
3.

Immediate chemical buffering

Respiratory compensation
Slower but more effective renal compensatory
response that may nearly normalize arterial pH.

1. Bicarbonate (H2CO3/HCO3)
2. Hemoglobin (HbH/b)
3. Intra-cellular proteins (HPr/Pr)
4. Phosphates (H2PO4/HPO4)
5. Ammonia (NH3/NH4)

 Treat the underlying disorder giving

rise to the acid-base disorder.
1. Metabolic Acidosis.
Sodium Bicarbonate = B.E. 30% body weight.
Half the calculated dose is given and an ABG is
repeated

2. Metabolic Alkalosis.
acetazolamide
vitamin C
ammonium chloride

3. Respiratory Alkalosis
intra-venous ammonium chloride
intra-venous hydrochloric acid (0.1 mol/L)

4. Respiratory Acidosis
increasing alveolar ventilation (bronchodilation,
respiratory stimulant-doxapram, reversal of
narcosis-naloxone, improving lung compliancediuretics)

Mediated b chemoreceptors in the brain-stem

Minute ventilation increases 1-4 L/min for
every 1 mm Hg increase in Pa CO2

Ability to control amount of HCO3 reabsorbed

in renal tubules, able to form new HCO3, and
eliminate H in the form of titrable acids and
ammonium ions.