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Panic value < 7.2 or > 7.6 < 7.2 or > 7.6

PCO2 38–50 mm Hg 5.0–6.7 kPa

PO2 20–49 mm Hg 2.6–6.5 kPa

HCO3 22–26 mEq/L 22–26 mmol/L

Panic value < 10 mEq/L < 10 mmol/L

> 40 mEq/L > 40 mEq/L

O2 saturation 60–80% 0.60–0.80

Partial Pressure of Carbon Dioxide (PCO2)

Normal Values

PaCO2 (arterial blood) 35–45 torr

PvCO2 (venous blood) 38–50 torr.

Carried in blood in two ways: 10% carried in plasma,

90% carried in RBCs.

Explanation of Test

This test is a measurement of the pressure or tension

exerted by dissolved CO2 in the blood and is proportional

to the partial pressure of CO2 in the alveolar air. The test

is commonly used to detect a respiratory abnormality

Blood gases interpretation

Blood Gases and Electrolytes 551

and to determine the alkalinity or acidity of the blood. In

order to maintain CO2 within normal limits, the rate and

depth of respiration vary automatically with changes in

metabolism. It is an index of alveolar ventilation and is

the most physiologically reflective blood gas measurement. When taken as an arterial sample, it directly

reflects how well air is exchanging with blood in the

lungs.

CO2 tension in the blood and cerebrospinal fluid (CSF)

is the major chemical factor regulating alveolar ventilation.

When the CO2 of arterial blood rises from 40 to 45 torr, it

causes a three-fold increase in alveolar ventilation. A CO2

of 63 torr in arterial blood increases alveolar ventilation

tenfold. When the CO2 concentration of breathed air

exceeds 5%, the lungs can no longer be ventilated fast

enough to present a dangerous rise of CO2 concentration in

tissue fluids. Any further increase in CO2 begins to depress

the respiratory center, causing a progressive decline in

respiratory activity rather than an increase.

Procedure

1. Obtain an arterial blood sample.

2. Do not expose sample to air.

3. A small amount of blood is then introduced into a

blood gas analyzer and the CO2 tension is measured

with a silver-silver chloride electrode (Severinghaus

electrode).

Clinical Implications

1. A rise in PCO2 is usually associated with hypoventilation, a decrease, with hyperventilation. Reduction

in PCO2 through its effect on plasma bicarbonate

concentration decreases renal bicarbonate reabsorption. For each mEq/L fall in HCO3, the PCO2 falls

by 1 to 1.3 mm of Hg. Because HCO3 and PCO2 bear this

close mathematical relationship, and this ratio in turn

defends the hydrogen ion concentration, the outcome

is that the steady state PCO2 in simple metabolic

acidosis is equal to the last two digits of the pH. Also,

addition of 15 to the bicarbonate level also equals the

last two digits of the pH. Failure of the PCO2 to achieve

predicted levels defines the presence of superimposed

respiratory acidosis on alkalosis.

2. The causes of decreased PCO2 include:

Hypoxia

Nervousness

Anxiety

Pulmonary emboli

Pregnancy

Other cause of hyperventilation.

3. The causes of increased PCO2 are:

a. Obstructive lung disease

Chronic bronchitis

Emphysema.

b. Reduced function of respiratory center

Over-reaction

Head trauma

Anesthesia.

c. Other more rare causes of hypoventilation, such as

Pickwickian syndrome.

Clinical Alert

Increased PCO2 may occur even with normal lungs if the

respiratory center is depressed. Always check laboratory

reports for abnormal values. In interpreting laboratory

reports remember that PCO2 is a gas and is regulated by

the lungs, not the kidneys.

Oxygen Saturation (SO2)

Normal Values

Arterial blood saturation SaO2 = 95% or higher mixed

venous blood saturation SvO2 = 75%.

Explanation of Test

This measurement is a ratio of the actual oxygen (O2)

content of the hemoglobin compared to the potential

maximum O2 carrying capacity of the hemoglobin.

The percentage of SO2 saturation is a measure of the

relationship between O2 and hemoglobin. The percentage

of saturation does not indicate the O2 content of arterial

blood. The maximum amount of O2 that can be combined

with hemoglobin is called the O2 capacity. The combined

measurements of O2 saturation, partial pressure of O2, and

of hemoglobin will indicate the amount of O2 available to

the tissue (tissue oxygenation).

Procedure

Obtain an arterial blood sample. Two methods for

determining oxygen saturation are used.

1. The blood sample is introduced into the oximeter,

which is a photoelectric device for determining the

oxygen saturation of the blood. The value is measured

directly with an oximeter (i.e. spectrometry).

2. Oxygen saturation is calculated from the oxygen

content and oxygen capacity determinations.

100 × O2 content volume%

 Percentage saturation = O2 capacity volume%

552 Concise Book of Medical Laboratory Technology: Methods and Interpretations i.e., Percentage saturation =

100 × volume of O2 actually combined with Hb

volume of O2 with which Hb is capable of combination

The O2 content of blood sample is measured before and

after exposure to atmosphere.

Oxygen (O2) Content

Normal Values

Aterial blood : 15–22 volume%

Venous blood : 11–16 volume%

(Volume% = volume percentage = mL/100 mL of blood).

Explanation of Test

The actual amount of oxygen (O2) in the blood is termed the

oxygen content. Blood can contain less O2 than it is capable

of carrying. About 98% of all O2 delivered to the tissues is

transported in chemical combination with hemoglobin.

One gram of hemoglobin can carry or is capable of

combining with 1.34 mL of O2, whereas 100 mL of blood

plasma can carry upto 0.3 mL of O2. This measurement is

determined mathematically by multiplying the number of

grams of hemoglobin in 100 mL of blood by 1.34 times the

partial pressure of oxygen in the blood.

Procedure

1. An arterial or venous blood sample is obtained

2. Mathematical formula

 O2 content = SaO2 × Hb × 1.34 + PaO2 × 0.003.

Clinical Implications

Decreased arterial blood O2 associated with increased

arterial blood CO2 can be due to:

1. Chronic obstructive lung disease

2. Patients with respiratory complications postoperatively

3. Flail chest

4. Kyphoscoliosis

5. Neuromuscular impairment

6. Obesity hypoventilation.

Partial Pressure of Oxygen (PO2)

Normal Values

PaO2 80 torr or greater: arterial sample

PvO2 30–40 torr: venous or peripheral blood sample.

Background

Oxygen (O2) is carried in the blood in two forms dissolved

and in combination with hemoglobin. Most of the O2 in the

blood is carried by hemoglobin. It is the partial pressure

of a gas that determines the force it exerts in attempting

to diffuse through the pulmonary membrane. The partial

pressure reflects the amount of O2 passing from the

pulmonary alveoli into the blood and is directly influenced

by the amount of O2 being inhaled.

Explanation of Test

This is a measure of the pressure exerted by the amount

of O2 dissolved in the plasma. It is a test that measures

the effectiveness of the lungs to oxygenate the blood. The

severity of impairment of the ability of the lungs to diffuse

O2 across the alveolar membrane into the circulating blood

is indicated by the level of partial pressure of oxygen (PO2).

Procedure

1. An arterial blood sample is obtained.

2. A small amount of blood is then introduced into a blood

gas analyzing machine and the O2 tension is measured

with a polarographic electrode (Clark electrode).

Clinical Implications

1. Increased levels are associated with:

a. Polycythemia

b. Hyperventilation in an arterial blood sample.

2. Decreased levels are associated with:

a. Anemias

b. Cardiac decompensation

c. Insufficient atmospheric O2

d. Intracardiac shunts

e. Chronic obstructive disease

f. Restrictive pulmonary disease

g. Hypoventilation due to neuromuscular disease.

3. Decreased arterial PO2 with normal or decreased

arterial blood PCO2 tension is associated with:

a. Diffuse interstitial pulmonary infiltration

b. Pulmonary edema

c. Pulmonary embolism

d. Postoperative extracorporeal circulation.

Carbon Dioxide (CO2) Content or Total

Carbon Dioxide (TCO2)

Normal Values

24–30 mEq/L.

Background

In normal blood plasma, more than 95% of the total CO2

content is contributed by bicarbonate (HCO3), which

is regulated by the kidneys. The other 5% of the CO2 is

contributed by the dissolved CO2 gas and carbonic acid

(H2CO3). Dissolved CO2 gas, which is regulated by the

Blood Gases and Electrolytes 553

lungs, therefore, contributes little to the total CO2 content.

Total CO2 content gives little information about the lungs.

HCO3

 in the extracellular spaces exists first as CO2 then

as H2CO3, and thereafter, much of it is changed to sodium

bicarbonate (NaHCO2) by the buffers of the plasma and

red cells.

Explanation of Test

This test is a general measure of the alkalinity or acidity of

the venous, arterial or capillary blood. This test measures

CO2 from:

1. Dissolved CO2

2. Total H2CO3

3. HCO3¯

4. Carbamino carbon dioxide

 Total CO2 = HCO3¯ + 0.03 × PCO2

Procedure

1. A venous or arterial blood sample of 6 mL is collected

in a heparinized syringe.

2. If the collected blood sample cannot be studied

immediately, the syringe should be placed in an iced

container.

Clinical Implications

1. Elevated CO2 content levels occur in:

a. Severe vomiting

b. Emphysema

c. Aldosteronism

d. Use of mercurial diuretics.

2. Decreased CO2 content levels occur in:

a. Severe diarrhea

b. Starvation

c. Acute renal failure

d. Salicylate toxicity

e. Diabetic acidosis

f. Use of chlorothiazide diuretics.

(Note: In diabetic acidosis the supply of ketoacids exceeds

the demands of the cell. Blood plasma acids rise. Blood

plasma HCO3 decreases because, it is used in neutralizing

these acids).

Clinical Alert

A double use of the CO2 is one of the main reasons why

understanding acid-base problems may be difficult. Use

the terms CO2 content and CO2 gas to avoid confusion.

Remember the following:

1. CO2 content is mainly bicarbonate and a base. It is a

solution and is regulated by kidneys.

2. CO2 gas is mainly acid. It is regulated by the lungs.

Interfering Factors

1. Drugs that may cause increased or decreased levels

include:

 a. Nitrofurantoin

 b. Salicylates.

2. Drugs that may cause decreased levels include:

 a. Dimercaprol (BAL)

 b. Lipomul oil injection

 c. Methicillin.

Blood pH

Normal Values

Arterial blood : 7.35–7.45

Venous blood : 7.32–7.43.

Background

The pH is the negative logarithm of the hydrogen ion

concentration in the blood. The sources of hydrogen ions

are: (i) volatile acids, which can vary between a liquid and

a gaseous state, and (ii) non-volatile acids that cannot be

volatilized and are fixed (e.g. dietary acids, lactic acids and

ketoacids).

Explanation of Test

This is a measurement of the chemical balance in the

body and is a ratio of acids to bases. A determination of

the blood pH is one of the best ways to tell if the body is

too acid or too alkaline. Low pH numbers (< 7.35) indicate

an acid stage, and higher pH numbers (> 7.45) indicate an

alkaline state. This balance is extremely intricate and must

be kept within the very slight margin of 7.35 to 7.45 pH

(alkaline) in the extracellular fluid. pH limits compatible

with life are 6.9 to 7.8.

The respiratory response to changes in blood pH is

almost instantaneous. Acidosis (CO2 retained; pH falls)

stimulates ventilation; alkalosis (CO2 blown off; pH

rises) depresses ventilation. The respiratory center in the

medulla appears to respond to a pH intermediate between

those of the blood and CSF (7.35–7.40).

Procedure

1. An arterial blood sample is obtained.

2. Two methods of determining the pH are used, the

direct method and the indirect method:

a. Direct method: A small amount of blood is introduced into a blood gas machine and the pH is

measured.

b. Indirect method: The Henderson-Hasselbalch

equation is solved.

554 Concise Book of Medical Laboratory Technology: Methods and Interpretations Form Cause Occurrence Compensatory mechanism

1. Respiratory

 acidemia

Primary increase in

PCO2 and decreased

pH

Depression of respiratory centers

(a) Drug overdose

(b) Barbiturate toxicity

(c) Use of anesthetics

Interference with mechanical function of

thoracic cage

(a) Deformity of thoracic cage

(b) Kyphoscoliosis

Airway obstruction

(a) Extrathoracic tumors

(b) Asthma

(c) Bronchitis

(d) Emphysema

Circulatory disorders

(a) Congestive heart failure

(b) Shock

Renal reabsorption of the

bicarbonate ion. Examples:

(a) Uncompensated respiratory

 acidemia (acute ventilatory failure)

 Values pH = 7.26 ↓

 PCO2 = 56 ↑

 Bicarbonate = 4 normal

(b) Compensated respiratory

 acidemia (chronic respiratory failure)

 Values: pH = 7.36

 PCO2 = 63

 Bicarbonate = 34

2. Respiratory

 alkalemia

Primary decrease in

PCO2 and in

increased pH

Hyperventilation —Hysteria

Lack of oxygen.

Toxic stimulation of

the respiratory centers

(a) High fever

(b) Cerebral hemorrhage

(c)  Excessive artificial respiration

(d) Salicylates

Glomerular filtration of the

bicarbonate on. Examples

(a) Uncompensated respiratory alkalemia

(acute alveolar hyperventilation)

 Values: pH = 7.52 ↑

 PCO2=28 ↓

Bicarbonate = 22 normal

(b) Compensated respiratory alkalemia

(Chronic alveolar hyperventilation)

 pH = 7.43

 PCO2 = 24

 Bicarbonate = 15

3. Nonrespiratory

acidemia

metabolic

acidemia

Increase in hydrogen

ions with a secondary

decrease in

bicarbonate

Acid addition

(a) Renal failure

(b) Diabetic ketoacidosis

(c) Lactic acidosis

(d) Anaerobic metabolism

Hypoxia

Base subtraction

(a) Diarrhea

(b) Renal tubular acidosis

Hyperventilation through stimulation of

central chemoreceptors

Examples

(a) Uncompensated nonrespiratory

acidemia (acute)

 Values: pH = 7.20 ↓

 PCO2 = 38 ↓

 Bicarbonate = 15 ↓

(b) Compensated respiratory acidemia

(chronic)

 Values: pH = 7.35

 PCO2 = 25

 Bicarbonate = 15

4. Nonrespiratory

 alkalemia or

 metabolic

 alkalemia

Increase in

bicarbonate

secondary to a

decrease

in hydrogen ions

Acid subtraction

(a) Loss of gastric juice

(b) Vomiting

Potassium or chloride depletaion base

addition

(a) Excessive bicarbonate or

 lactate administration

Hypoventilation. Examples

(a) Uncompensated nonrespiratory alkalemia

(acute)

Values: pH = 7.56

PCO2 = 44 ↑

 Bicarbonate = 38 ↑

(b) Compensated respiratory alkalemia

(chronic)

 Values: pH = 7.44

 PCO2 = 55

 Bicarbonate = 38

Note

1. Although these four basic imbalances occur individually, more frequently a combination of two or more is observed. These disturbances may have an

antagonistic or a synergistic effect upon each ones.

2.  Compensation is most efficient is respiratory and nonrespiratory acidemia.

3. The degree of hypoventilation is precisely related to the degree of hypobicarbonatemia. For each mEq/L fall in bicarbonate, PCO2 falls by 1–1.3 torr. A

close mathematical relationship prevails between bicarbonate and PCO2. Their ratio (HCO3 and PCO2) defines the prevailing hydrogen ion concentration.

For this reason, the steady state PCO2 in simple metabolic acidosis is equal to the last two digits of the pH. Failure of the PCO2 to reach predicted levels

defines the presence of superimposed respiratory acidosis or alkalosis.

TABLE 21.1: Four basic forms of acid-base imbalance and their compensatory mechanism

Blood Gases and Electrolytes 555

major blood base pH = pk + log major blood acid

Clinical Implications

1. Generally speaking, the pH is decreased in acidemia

because of increased formation of acids. pH is increased in alkalemia because of a loss of acids.

2. When attempting to interpret an acid-base abnormality,

one must:

a. Check the pH to see if there is an alkalemia or an

acidemia.

b. Check PCO2 to see if there is a respiratory abnormality.

c. Check HCO3

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