Acid-Base (pH)

Imbalance
Prepared by: SYAFIQAH HANI BT ZABLE

Arterial Blood Gases

Arterial blood gas analysis provides
information on the following:
1] Oxygenation of blood through gas exchange in the
lungs.
2] Carbon dioxide (CO2) elimination through
respiration.
3] Acid-base balance or imbalance in extra-cellular
fluid (ECF).

Arterial blood gas (ABG) and acid-base values (normal ranges)

H+

35-45 nmol/L

pH 7.35-7.45

PO2 (breathing room air)

10.6 13.3 kPa

(80 100 mmHg)

PCO2

4.8 6.1 kPa

(36 46 mmHg)

Base deficit

2.5

Plasma HCO3-

22 26 mmol/L

O2 saturation

95 100%

 Deviations from normal acid-base status are divided

into 4 general categories, depending on the source and
direction of the abnormal change in hydrogen
concentration, [H+].
Causes of acid-base disturbance:
- Abnormal CO2 removal in lungs (respiratory acidosis or
alkalosis)
- Abnormalities in the regulation of bicarbonate and other
buffers in blood (metabolic acidosis or alkalosis)
both may, and usually co-exist.

 Acidosis occurs in the fall in the ratio of [HCO3-]:

[H2C03] of blood below 20:1, alarming lower blood pH
Alkalosis is caused by the increase in the ratio of
[HCO3-]: [H2CO3] of blood above 20:1, results in rise in
blood pH

1- Respiratory acidosis
Hypercapnic acidosis
Caused by excess retention of C02 arising from hypoventilation
As less-than-normal amount of C02 are lost through the lungs
increase in CO2 generated more H+ from this source.
PaCO2 and [H+] rise
A chronically raised PaCO2 is compensated by renal retention of
bicarbonate, and the [H+] returns toward normal.
CAUSES: include ventilatory failure, COPD (type II respiratory failure),
other lung diseases, depression of respiratory center by drugs or
disease, nerve or muscle disorders that reduce respiratory muscle
ability or (transiently) even the simple act of holding ones breath.

1- Respiratory acidosis
In uncompensated state, [CO2] is elevated, whereas
[HCO3-] is normal. So the normal ratio [HCO3-]: [H2C03]
(20:1) and pH is reduced.
Compensation for Respiratory acidosis.
The chemical buffers (immediately take up
additional H+)
Respiratory mechanism- usually cannot
respond
with
compensatory
increased
ventilation, because impaired respiration is the
problem in the first place
The
kidneys
are
most
important
in
compensating
for
respiratory
acidosis.
Conserved all filtered HC03- and add new

2- Respiratory alkalosis
The primary defect in respiratory alkalosis is excessive
loss of C02 from the body, as a result of
hyperventilation.
Pulmonary ventilation increased out of proportion to the
rate of C02 production, too much C02 is blown off.
Consequently, less [H+] is formed this source.
CAUSES: fever, anxiety, aspirin poisoning (all
excessively stimulate ventilation without regard to
status of oxygen, C02 or H+ in body fluids. Also a result
of physiologic mechanism at high altitude)

2- Respiratory alkalosis
In uncompensated respiratory alkalosis, the increase pH
reflects a reduction in [CO2], whereas [HC03-] remains
normal.
Compensatory mechanism.
The chemical buffers systems (liberate H+ to
diminish severity of alkalosis)
Respiratory mechanism- plasma [CO2] AND [H+]
fall below normal, these 2 are normally potent stimuli
for driving ventilation put brakes on the extent to
which some non-respiratory factors (fever, anxiety)
can
overdrive
ventilation.
Therefore,
hyperventilation does not continue completely
unabated.
if the situation continues for a few days, the kidneys

3- Metabolic acidosis
Also known as non-respiratory acidosis encompasses all
type of acidosis besides that caused by excess C02 in
body fluid.
In uncompensated state, metabolic acidosis is always
characterized by reduction in plasma [HCO3-] whereas
[C02] remains normal. The problem may arise from
excessive loss of HCO3- -rich fluids from the body
of from an accumulation of noncarbonic acid (where
plasma HCO3- is used up in buffering additional H+).

3- Metabolic acidosis- causes

Severe diarrhoea- HCO3-rich digestive juice is lost from the body
rather than reabsorbed. Less HC03- is available to buffer H+, leading to
more H+ in body fluids.
Diabetes mellitus- abnormal fat metabolism resulting from inability of
cells to preferentially use glucose because of inadequate insulin action
which leads to formation of excess keto acids, increase plasma [H+]
Strenuous exercise- when muscle resort to anaerobic glycolysis
during strenuous exercise, excess lactic acid is produced, raising plasma
[H+]
Uremic acidosis- In severe renal failure (uraemia), the kidneys
cannot rid the body of even normal H+ generated from noncarbonic
acid formed by ongoing metabolic processes, so H+ starts to
accumulate in body fluids. Also, the kidneys cannot conserve an
adequate amount of HCO3- for buffering normal acid load.

3- Metabolic acidosis
Compensation for metabolic acidosis.
The buffers take up extra H+
The lungs blow off additional H+ -generating CO2
The kidneys excrete more H+ and conserve more
These
compensatory measures restore the ratio to normal by
HC03reducing [C02] to 75% of normal and by raising [HCO3-] halfway
back toward normal (up from 50% to 75% of normal value)
When kidney disease is the cause, complete compensation is
not possible because renal mechanism is not available for pH
regulation.

4- Metabolic alkalosis
A reduction in plasma [H+] caused by relative
deficiency of noncarbonic acids.
This acid-base disturbance is associated with an
increase in [HC03-], which in uncompensated state, is
not accompanied by a change in [C02].
CAUSES: Vomiting, Ingestion if alkaline drugs

4- Metabolic alkalosis
In metabolic alkalosis, chemical buffer systems
immediately liberate H+
Ventilation is reduced so that extra H+generating C02 is
retained in body fluids.
If condition persists for several days, the kidneys
conserve H+ and excrete excess HC03- in urine