Acid-Base Balance &

Blood Gases
Analyte
Physiology Methodology
and
Instrumentation
Disease /
abnormality
interference Normal
values
pCO
2

Physiology of
CO2

SEVERINGHAUS
electrode


Respiratory Acidosis
pCO2
Respiratory alkalosis
pCO2
Interferfence of
PCO
2

Arterial :
35 - 45
mmhg
4.7 5.3 kPa
(SI)
Venous :
40-45 mmhg
HCO
3
-


Physiology of
HCO
3
-


Computed by using
HENDERSON -
HASSELBACH
equation
Metabolic alkalosis
HCO
3
-

Metabolic acidosis
HCO
3
-



The same as the
interferences for
pCO2 and pO2
24 27
mmol/ L
pO
2

Physiology of
O2
CLARKE
electrode

TRANSCUTANEOUS
electrode


Oxyen toxicity
pO2
Hypoxia
pO2

Interference of
clarke electrode

Interference of
TC electrode
Arterial :
95 100
mmgh
12.7 13.3
kPa (SI)
CO
2

- End product of most aerobic metabolic processes

BACK
HCO
3
-


Bicarbonate-carbonic Acid Buffer System
carbonic Acid (H
2
CO
3
) is a weak acid with
bicarbonate (HCO
3
-
) serving as its conjugate
base
when acid is added to this system, H ion react
with bicarbonate to form more carbonic acid
and thus minimizing changes in pH.

BACK
O
2

Necessary for ATP production
Carried in the blood in the physically
dissolved state and bound to transport
proteins, primarily hemoglobin

BACK
Proceed to gas exchange
Gas Exchange
(lungs and tissues)
The diffusion of oxygen
and carbon dioxide
across the alveolar
membranes and tissues
is governed by gradients
in the partial pressures
of the gases.
BACK
Measurement of O
2

amperometric amount of current flow is an indication of the
oxygen present

1) CLARKE electrode PO
2
electrode; measure the amount
flow in a circuit which is related to the amount of O
2
being
reduced at the cathode.
Principle: A gas-permeable membrane covering the tip of the electrode
selectively allows the O
2
to diffuse into an electrolyte and contact the
cathode. Electrons are drawn from the anode surface to the cathode
surface to reduce the O
2
. A small, constant polarizing potential (-0.65 V) is
applied between the anode and cathode.

MICROAMMETER measures the movement of electrons (current)
BACK
Measurement of O
2

2. TRANSCUTANEOUS (TC) electrode
- placed directly on the skin
- most commonly used on NEONATES and INFANTS
- heating the electrode placed on the skin enhance diffusion of
O
2
to the electrode

Principle: depends on oxygen diffusing from the capillary bed
through the tissue to the electrode.

BACK
Measurement of CO
2

SEVERINGHAUS electrode
- modified pH electrode

Principle: an outer semipermeable membrane allows CO
2
to
diffuse into a layer of electrolyte, usually a HCO
3
-
buffer, covers
the glass pH electrode. The CO
2
that diffuses across the
membrane reacts with the buffer, forming carbonic acid, which
then dissociates into HCO
3
-
plus H
+
.
Change in activity of the H
+
is measured by pH electrode and
related to PCO
2
.

BACK
CO
2
Measurement Interference
1. Build up of protein material on the membrane
2. Erroneous calibration caused by incorrect or
contaminated calibration material

NOTE: PCO
2
electrodes are the slowest to
respond because of the chemical reaction that
must be completed
Interference in Clarke electrode
measurement of O2
Buildup of protein material on the surface of the membrance
= retards diffusion, slows electrode response
bacterial contamination within measuring chamber
= consume O
2
and cause low and drifting values
system malfunction (incorrect calibration)
room air
= DO NOT EXPOSE SPECIMEN TO ROOM AIR
high WBC counts
= leukocytes continue to metabolize O
2


Interference in trancutaneous
electrode measurement of O2
Interferences: skin thickness and tissue
perfusion with arterial blood
Disadvantage: caused burns (unless
electrodes are moved regularly)

CALCULATED PARAMETERS
(from measured pH and PCO
2
values)
HCO
3
-

- Henderson Hasselbalch equation
- basic assumption: pK of HCO
3
-
buffer system in plasma at 37
o
C is 6.1

H
2
CO
3

- calculated using the solubility coefficient od CO
2
in plasma at 37
o
C.
- the solubility constant to convert PCO
2
to mmol/L of H
2
CO
3
is 0.0307

ctCO
2
(total carbon dioxide content)
= cHCO
3
-
+ (0.0307 x PCO
2
)

NEXT
Base Excess
- asses the nonrespiratory (metabolic) component of a patient acid-base
disorder
- calculated from an algorithm that uses patient pH, PCO
2
. Hemoglobin.

Interpretation:
POSITIVE value (base excess) - excess of HCO
3
-
or relative deficit of
non-carbonic acid = NONRESPIRATORY ALKALOSIS
NEGATIVE value (base deficit) deficit of HCO
3
-
or relative excess of
NONRESPIRATORY ACIDOSIS

NOTE: 37
o
C temp. measurement required

BACK
ACID BASE METABOLISM
BUFFER
- System that can resist change in pH
- Composed of a weak or a weak base and its
corresponding salt

FOUR MAJOR BUFFER
SYSTEMS
1. Bicarbonate carbonic acid buffer system
2. Protein buffer system
3. Phosphate buffer system
4. Hemoglobin buffer system
DIFFERENCE
BUFFER SYSTEM SUBSTANCE TO USE
Bicarbonate carbonic acid HCO
3

and H
2
CO
3

Protein Plasma proteins
Phosphate HPO
4
2
and H
2
PO
4


Hemoglobin Hemoglobin in RBC
DEFINITION OF TERMS
RESPIRATION process to supply cells with
oxygen for metabolic processes and remove
the carbon dioxide produced during
metabolism.

PARTIAL PRESSURE In a mixture of
gases, partial pressure is the amount of
pressure contributed by each gas to the total
pressure exerted by the mixture.
ACIDEMIA
occurs when arterial blood pH <7.35
ALKALEMIA
occurs when arterial blood pH >7.45


HYPERCAPNIA increased blood PCO
2

HYPOCAPNIA decreased blood PCO
2

PARTIAL PRESSURE OF CO
2
(PCO
2
)
- Measured in blood as mmHg

CONCENTRATION OF DISSOLVED CO
2
(cdCO
2
)
- Includes undissociated carbonic acid (H
2
CO
3
) and
carbon dioxide dissolved in blood (represented by
PCO
2
)

CONCENTRATION OF TOTAL CO
2
(ctCO
2
)
- Includes bicarbonate (primary component),
carbamino bound CO
2,
carbonic acid, and
dissolved CO
2

REFERENCE RANGES
(arterial blood gas analysis)
pH: 7.35 7.45
ctCO
2
: 22 26 mmol/L
PCO
2
: 35 45 mmHg
ACID BASE DISORDERS
CLASSIFICATIONS
Metabolic acid base disorders involve
bicarbonate concentration
1. Metabolic acidosis
2. Metabolic alkalosis

Respiratory acid base disorders involve
dissolved CO
2
concentration
1. Respiratory acidosis
2. Respiratory alkalosis

METABOLIC ACIDOSIS
Definition: Primary bicarbonate deficit

Occurrence: the bicarbonate concentration
decreases, causing in the 20:1 ratio between
cHCO
3
- and cdCO
2,
which results in a decrease
in the blood pH.

Laboratory findings:
1. ctCO
2
decreased
2. PCO
2
normal
3. pH decreased
Caused by:
1. Diabetic ketoacidosis due to production of
acetoacetic acid and hydroxybutyric acid
2. Lactic acidosis due to the production of
lactic acid
3. Poisonings such as salicylate, ethylene
glycol, and methyl alcohol
4. Reduced acid excretion due to renal failure
or tubular acidosis
5. Loss of bicarbonate due to diarrhea or
excessive renal excretion
Respiratory compensatory mechanism: a
decreased pH triggers hyperventilation that
lowers PCO
2
ande results in an increase in pH.
This increases the ratio between cHCO
3
- and
cdCO
2
to 20:1, which increases the blood pH.

Laboratory findings in compensation:
1. ctCO
2
decreased
2. PCO
2
decreased
3. pH normal

METABOLIC ALKALOSIS
Definition: primary bicarbonate excess

Occurrence: the bicarbonate concentration increases, causing
an increase in the 20:1 ratio between cHCO
3
- and cdCO
2

which results in an increase in the blood pH.

Laboratory findings:
1. ctCO
2
increased
2. PCO
2
normal
3. pH increased


Caused by:
1. Ingestion of excess alkali (antacids)
2. intravenous administration of bicarbonate
3. renal bicarbonate retention
4. prolonged diuretic use
5. loss of HCL from the stomach after
vomiting, intestinal obstruction, or gastric
suctioooon
6. glucocorticoid excess as in cushing
syndrome
7. mioneralocorticoid excess as in
hyperaldosteronism

Respiratory compensation mechanism:
the ph increase slows breathing
(hypoventilation), thus increasing the
amount of CO2 retained by the lungs. This
increased CO2 retention causes an increase
in H2CO#, which results in more dissol;ved
CO2 in the blood. The carbonic acid lowers
the pH. This decreases the ration between
cHCO3 and cdCO2 to 20:1, which decreases
the blood pH.
Laboratory findings in compensation:
1) ctCO2 increased
2) pCO2 increased
3) pH normal
Respiratory acidosis
Respiratory acidosis : primary cdCO2
excess expressed as increase in pCO2
(hypercapnia)
Inability of the person to exhale CO2
through the lungs (hypoventilation) causes
an increase of PCO2. the increased PCO2
causes an increase in the concentration of
dissolved CO@, which forms carbonic acid
in the blood. This decreases the 20:1 ration
between cHCO3 and cdCO2, which
decrases the blood pH.
Respiratory acidosis may be caused by
chronic obstructive pulmonary disease, such
as chronic bronchitis and emphysema,
ingestion of narcotics and barbiturates, and
severe infections of the central nervous
system such as meningitis.
Laboratory findings:
1) ctCO2 normal
2) pCO2 increased
3) pH decreased
Renal compensatory mechanism:
the kidneys increase sodium-hydrogen
exchange, ammonia formaation, and
bicarbonate retention. The increased
bicarbonate concentration aids the return of
the 20:1 ratio, which raises the blood pH.
Laboratory findings in compensation
1) ctCO2 increased
2) pCO2 increased
3) pH normal
RESPIRATORY ALKALOSIS
Definition: primary cdCO
2
deficit as decrease in
bicarbonate excess PCO
2
(hypocapnia)

Occurrence:
Decreases PCO
2
results from an accelerated rate or depth of
respiration.
Excessive exhalation of carbon dioxide (hyperventilation)
reduces the PCO
2,
causing a decrease in the concentration of
dissolved carbon dioxide, which forms less carbonic acid in
the blood. This increase the 20:1 ratio between cHCO
3
- and
cdCO
2,
which increases the blood pH.
Laboratory findings:
1. ctCO
2
normal
2. PCO
2
decreased
3. pH increased

Caused by:
1. Hypoxia
2. Anxiety
3. Nervousness
4. Excessice crying
5. Pulmonary embolism
6. Pneumonia
7. Congestive heart failure
8. Salicylate overdose
Respiratory compensatory mechanism: by excreting
bicarbonate.

Laboratory findings in compensation:
1. ctCO
2
decreased
2. PCO
2
decreased
3. pH normal