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Clinician's Pocket Reference > Chapter 8. Blood Gases and AcidBase Disorders >

Blood Gas Basics

Blood gases provide information concerning the oxygenation, ventilatory, and acid-base
status of the patient. Blood gas results are usually given as pH, PO2, PCO2, [HCO3], base
excess or deficit (base difference), and O2 saturation. This test gives information on acid
base homeostasis (pH, PCO2, [HCO3], and base difference) and on blood oxygenation
(PO2, O2 saturation). Arterial blood gases (ABG) are most commonly measured; venous,
mixed venous, and capillary blood gases are measured less frequently. Indications for
blood gas determinations are as follows (Respir Care 2001;46:498505):

To determine a patient's ventilatory (PaCO2), acidbase (pH and PaCO2), and

oxygenation and O2-carrying capacity (PaO2 and O2Hb)

To quantitate the response to therapeutic intervention (eg, supplemental O2

administration, mechanical ventilation) or diagnostic evaluation (eg, exercise
desaturation)

Monitoring the severity and progression of documented disease processes (eg,

COPD)

Normal Blood Gas Values

Normal values for blood gas analysis are given in Table 81, and capillary blood gases are
discussed in a following section. Mixed venous blood gases are reviewed in Chapter 20.
The bicarbonate concentration ([HCO3]) from the blood gas is a calculated value
and should not be used in interpretation of blood gases; the [HCO3] from a
concurrent chemistry panel should be used. Note: The HCO3 values on the chemistry
panel and those calculated from the blood gases should be about the same. A major
discrepancy (> 10% difference) means one or more of the three values is in error (pH,
PCO2, or [HCO3]). The most common cause of discrepancies is drawing the blood gas and
chemistry panel samples at different times. ABGs and chemistry panels [HCO3] should be
obtained at the same time for the most accurate interpretation.

Table 81 Normal Blood Gas Values

Measurement

Arterial Blood Mixed Venous

Blooda

Venous Blood

pH (range)

7.40 (7.37
7.44)

7.36 (7.317.41)

7.36 (7.31
7.41)

PO2 (mm Hg) (decreases with age) 80100

3540

3050

PCO2 (mm Hg)

3644

4151

4052

O2 saturation (%) [decreases with

age]

>95

6080

6085

HCO3 (mEq/L)

2226

2226

2228

Base difference (deficit/excess)

2 to +2

2 to +2

2 to +2

Obtained from the right atrium, usually through a pulmonary artery catheter.

Venous Blood Gases

There is little difference between arterial and venous pH and [HCO3] (except in severe
CHF and shock). Venous blood gas levels may occasionally be used to assess acidbase
status, but venous O2 levels are significantly less than arterial values (see Table 81).
Capillary Blood Gases
A CBG is obtained from a highly vascularized capillary bed. CBG is often used for
pediatric patients because obtaining the sample is easier (through the heel) and less
traumatic (no risk of arterial thrombosis, hemorrhage) than obtaining an ABG sample.
(See Chapter 13, Heelstick Technique.)
When interpreting a CBG, apply the following rules:

pH: Same as arterial or slightly lower (Normal = 7.357.40)

PCO2: Same as arterial or slightly higher (Normal = 4045 mm Hg)

PO2: Lower than arterial (Normal = 4560 mm Hg)

O2 saturation: > 70% is acceptable. Saturation is probably more useful than PO2
itself in interpretation of a CBG.

General Principles of Blood Gas Determinations

Interpretation of O2 values is discussed in Hypoxia
1. The blood gas analyzers in most labs measure pH and PCO2 as well as PO2.
[HCO3] and base difference are calculated with the HendersonHasselbalch
equation:

or the Henderson equation:

2. For a rough estimate of [H+], [H+] = (7.80 pH) x 100, or add 1 mEq/L to 40
mEq for every 0.01 below 7.40 and subtract 1 mEq/L from 40 mEq for every 0.01
above 7.40 (accurate for pH 7.257.48); 40 mEq/L = [H+] at the normal pH of
7.40. pH is a log scale; for every change of 0.3 in pH from 7.40 the [H+] doubles or
halves. For pH 7.10, [H+] = 2 x 40, or 80 nmol/L, and for pH 7.70, [H+] = 1/2 40,
or 20 nmol/L.
3. The calculated [HCO3] should be within 2 mEq/L of the [HCO3] of a venous
measurement drawn at the same time. If not, an error has been made in collection
or in determination of the values, and both samples should be recollected.
4. Two additional relationships derived from the HendersonHasselbalch equation
should be committed to memory. These two rules are helpful in interpreting blood
gas results, particularly in defining a simple versus a mixed blood gas disorder:
Rule I:
A change in PCO2 up or down 10 mm Hg is associated with an increase or decrease in pH
of 0.08 units. As PCO2 decreases, pH increases; as the PCO2 increases, pH decreases.
Rule II:
A pH change of 0.15 is equivalent to a base change of 10 mEq/L. A decrease in base (ie,
[HCO3]) is termed a base deficit, and an increase in base is termed a base excess.
AcidBase Disorders: Definition
1. Acidbase disorders are common clinical problems. Acidemia is a pH < 7.37,
and alkalemia is a pH > 7.44. Acidosis and alkalosis are used to describe the
process by which pH changes. The primary causes of acidbase disturbances are
abnormalities in the respiratory, metabolic, and renal systems. As the Henderson
Hasselbalch equation shows, a respiratory disturbance leading to an abnormal
PCO2 alters the pH, and similarly a metabolic disturbance altering [HCO3] changes

the pH.
2. Any primary disturbance in acidbase homeostasis invokes a normal
compensatory response. A primary metabolic disorder leads to respiratory
compensation, and a primary respiratory disorder leads to an acute metabolic
response due to the buffering capacity of body fluids and chronic compensation
(12 d) due to alterations in renal function.
3. The degree of compensation can be expressed in terms of the degree of primary
acidbase disturbance. Table 82 lists the major categories of primary acidbase
disorders, the primary abnormality, the secondary compensatory response, and the
expected compensation based on the primary abnormality. These changes are
defined graphically in Figure 81.
Table 82 Simple AcidBase Disturbances

AcidBase
Disorder

Primary
Abnormality

Expected
Compensation

Metabolic acidosis

[HCO3]

PCO2

Metabolic alkalosis

[HCO3]

PCO2

Acute respiratory
acidosis

PCO2

Chronic respiratory
acidosis

PCO2

Acute respiratory
alkalosis

PCO2

Chronic respiratory
alkalosis

PCO2

[HCO3]
[HCO3]

[HCO3]

[HCO3]

Expected Degree of
Compensation
PCO2 = (1.5 x [HCO3])+8
in PCO2 = [HCO3] x 0.6
in [HCO3] = PCO2/10
in [HCO3] = 4 x
PCO2/10
in [HCO3] = 2 x
PCO2/10
in [HCO3] = 5 x
PCO2/10

Mixed AcidBase Disorders

1. Most acidbase disorders result from a single primary disturbance of the normal
physiologic compensatory response (called simple acidbase disorders). In some
cases (eg, serious illness), two or more primary disorders may occur
simultaneously, resulting in a mixed acidbase disorder. The net effect of mixed
disorders can be additive (eg, metabolic acidosis and respiratory acidosis) and
result in extreme alteration of pH. Or, the effects can be opposite (eg, metabolic
acidosis and respiratory alkalosis) and nullify somewhat the effect of the other on
pH.
2. To determine the presence of a mixed acidbase disorder with a blood gas value,
follow the six steps in the Interpretation of Blood Gases. Alterations in either

[HCO3] or PCO2 that differ from expected compensation levels indicate a second
process. Two of the examples given in the following section illustrate the strategies
used in identifying a mixed acidbase disorder.
Interpretation of Blood Gases
Use a consistent, stepwise approach to interpretation of blood gases. (See Figure 81.)

Figure 81.

Nomogram for acid-base disorders. (Reprinted, with permission, from: Cogan MG: Fluid
and Electrolytes, Originally published by Appleton & Lange, Copyright 1991 by the
McGraw-Hill Companies, Inc.)

Step 1:
Determine whether the numbers fit.

The right side of the equation should be within about 10% of the left side. If the numbers
do not fit, obtain another ABG and chemistry panel for [HCO3].
Example. pH 7.25, PCO2 48 mm Hg, [HCO3] 29 mEq/L.

This blood gas cannot be interpreted, and samples for ABG and [HCO3] must be
recollected. The most common reason for the numbers not fitting is that the ABG and the
chemistry panel [HCO3] were obtained at different times.
Step 2:
Next, determine whether acidemia (pH < 7.37) or alkalemia (pH > 7.44) is present.
Step 3:
Identify the primary disturbance as metabolic or respiratory. For example, if acidemia is
present, is the PCO2 > 44 mm Hg (respiratory acidosis), or is the [HCO3] < 22 mEq/L
(metabolic acidosis)? In other words, identify which component, respiratory or metabolic,
is altered in the same direction as the pH abnormality. If both components act in the same
directioneg, both respiratory (PCO2 > 44 mm Hg) and metabolic [HCO3] < 22 mEq/L)
acidosis are presentthen this is a mixed acidbase problem (see Step 4). The primary
disturbance is the one that varies the most from normal. That is, with a [HCO3] of 6
mEq/L and PCO2 of 50 mm Hg, the primary disturbance would be metabolic acidosis; the
[HCO3] is only 25% of normal, whereas the increase in PCO2 is only 25% above normal.
Step 4:
After identifying the primary disturbance, use the equations in Table 82 to calculate the
expected compensatory response. If the difference between the actual value and the
calculated value is great, a mixed acidbase disturbance is present.
Step 5:
Calculate the anion gap:

A normal anion gap is 812 mEq/L. If the anion gap is increased, proceed to Step 6.
Step 6:

If the anion gap is elevated, compare the changes from normal between the anion gap and
[HCO3]. If the change in anion gap is similar to the change in [HCO3] from normal, gap
acidosis is present and there is no metabolic alkalosis or nongap metabolic acidosis. If the
change in anion gap is greater than the change in [HCO3] from normal, metabolic
alkalosis is present in addition to gap metabolic acidosis. If the change in the anion gap is
less than the change in [HCO3] from normal, nongap metabolic acidosis is present in
addition to gap metabolic acidosis. (See Examples 5, 6, and 7.)
Finally, be sure the interpretation of the blood gas is consistent with the clinical setting.
Metabolic Acidosis: Diagnosis and Treatment
Metabolic acidosis represents an increase in acid in body fluids reflected by a decrease in
[HCO3] and a compensatory decrease in PCO2.
Differential Diagnosis
The diagnosis of metabolic acidosis (Figure 82) can be classified as anion gap or non
anion gap acidosis. The anion gap (Normal range, 812 mEq/L) is calculated as:

Figure 82.

Differential diagnosis of metabolic acidosis.

Anion Gap Acidosis:

Anion gap > 12 mEq/L; caused by a decrease in [HCO3] balanced by an increase in an

unmeasured acid ion from either endogenous production or exogenous ingestion

(normochloremic acidosis).
NonAnion Gap Acidosis:
Anion gap = 812 mEq/L; caused by a decrease in [HCO3] balanced by an increase in
chloride (hyperchloremic acidosis). Renal tubular acidosis is a type of nongap acidosis
that can be associated with a variety of pathologic conditions (Table 83). The anion gap
is helpful in identifying metabolic gap acidosis, nongap acidosis, and mixed metabolic gap
and nongap acidosis. If an elevated anion gap is present, a closer look at the anion gap and
[HCO3] helps differentiate (a) pure metabolic gap acidosis, (b) metabolic nongap
acidosis, (c) mixed metabolic gap and nongap acidosis, and (d) metabolic gap acidosis and
metabolic alkalosis.

Table 83 Renal Tubular Acidosis: Diagnosis and Management

Clinical Renal
Conditio Defect
n

GF Serum
R [HCO3
]
(mmol/
L)

Serum
[K+]
(mmol/
L)

Minim Associated
al
Disease States
Urine
pH

Treatment

Normal

2428

3.55

4.85.2 None

N/A

Proximal Proximal
RTA (type H+
II RTA) secretion

1518

<5.5

Drugs, Fanconi
syndrome,
various genetic
disorders,
dysproteinemic
states, secondary
hyperparathyroidi
sm, toxins (heavy
metals),
tubulointerstitial
diseases,
nephrotic
syndrome,
paroxysmal
nocturnal
hemoglobinuria

NaHCO3 or
KHCO3 (10
15
mmol/kg/d),
thiazide
diuretics

Classic
Distal H+
distal
secretion
RTA (type
I RTA)

2030

>5.5

Various genetic NaHCO3 (1

disorders,
3
autoimmune
mmol/kg/d)
diseases,
nephrocalcinosis,

None

Clinical Renal
Conditio Defect
n

GF Serum
R [HCO3
]
(mmol/
L)

Serum
[K+]
(mmol/
L)

Minim Associated
al
Disease States
Urine
pH

Treatment

drugs, toxins,
tubulointerstitial
diseases, hepatic
cirrhosis, empty
sella syndrome
Buffer
Distal NH3
deficiency delivery
(type III
RTA)

1518

Distal Na+
reabsorpti
on, K+
secretion,
and H+
secretion

2428

Generaliz
ed distal
RTA (type
IV RTA)

<5.5

Chronic renal
NaHCO3 (1
insufficiency,
3
renal
mmol/kg/d)
osteodystrophy,
severe
hypophosphatemi
a

<5.5

Primary
mineralocorticoid
deficiency (eg,
Addison disease),
hyporeninemic
hypoaldosteronis
m, diabetes
mellitus,
tubulointerstitial
diseases,
nephrosclerosis,
drugs), saltwasting
mineralocorticoid
-resistant
hyperkalemia

Fludrocortiso
ne (0.10.5
mg/d) dietary
K+
restriction,
NaHCO3 (1
3
mmol/kg/d)
furosemide
(40160
mg/d)

Treatment of Metabolic Acidosis

1. Correct the underlying disorder (eg, control diarrhea).
2. Bicarbonate therapy is reserved for severe metabolic gap acidosis. If the pH <
7.20, correct to above 7.20 with sodium bicarbonate. The total replacement dose of
HCO3 can be calculated as follows:

3. Replace with one-half the total amount of bicarbonate over 812 h and
reevaluate. Be aware of sodium and volume overload during replacement. A

normal or isotonic bicarbonate drip is made with 3 amp NaHCO3 (50 mEq
NaHCO3/amp) in 1 L D5W.
Metabolic Alkalosis: Diagnosis and Treatment
Metabolic alkalosis represents an increase in [HCO3] with a compensatory rise in PCO2.
Differential Diagnosis
In two basic categories of diseases the kidneys retain HCO3 (Figure 83). They can be
differentiated in terms of response to treatment with sodium chloride and also by the
urinary [Cl] as determined by ordering a "spot," or "random" urine for chloride (UCl).

Figure 83.

Differential diagnosis of metabolic alkalosis.

Chloride-Sensitive (Responsive) Metabolic Alkalosis:

The initial problem is a sustained loss of chloride out of proportion to the loss of sodium
(either by renal or GI losses). This chloride depletion results in renal sodium conservation
leading to a corresponding reabsorption of HCO3 by the kidney. In this category of
metabolic alkalosis, the urinary [Cl] is < 10 mEq/L, and the disorders respond to
treatment with intravenous NaCl.
Chloride-Insensitive (Resistant) Metabolic Alkalosis:
The pathogenesis in this category is direct stimulation of the kidneys to retain HCO3
irrespective of electrolyte intake and losses. The urinary [Cl] > 10 mEq/L, and these

disorders do not respond to NaCl administration.

Treatment of Metabolic Alkalosis
Correct the underlying disorder.
1. Chloride-responsive
a. Replace volume with NaCl if depleted.
b. Correct hypokalemia if present.
c. NH4Cl and HCl should be reserved for extreme cases.
2.Chloride-resistant
a. Correct the underlying problem, such as stopping exogenous steroids.
Respiratory Acidosis: Diagnosis and Treatment
Respiratory acidosis is a primary rise in PCO2 with a compensatory rise in plasma
[HCO3]. Increased PCO2 occurs in clinical situations in which decreased alveolar
ventilation occurs.
Differential Diagnosis
Neuromuscular Abnormalities with Ventilatory Failure:
Muscular dystrophy, myasthenia gravis, GuillainBarr syndrome, hypophosphatemia
Central Nervous System:
Drugs (sedatives, analgesics, tranquilizers, ethanol), CVA, central sleep apnea, spinal cord
injury (cervical)
Airway Obstruction:
Chronic (COPD), acute (asthma), upper airway obstruction, obstructive sleep apnea
ThoracicPulmonary Disorders:
Bony thoracic cage (flail chest, kyphoscoliosis), parenchymal lesions (pneumothorax,
severe pulmonary edema, severe pneumonia), large pleural effusions, scleroderma,

marked obesity (pickwickian syndrome)

Treatment of Respiratory Acidosis
Improve Ventilation:
Intubate patient and initiate mechanical ventilation, increase ventilator rate, reverse
narcotic sedation with naloxone (Narcan), etc.
Respiratory Alkalosis: Diagnosis and Treatment
Respiratory alkalosis is a primary fall in PCO2 with a compensatory decrease in plasma
[HCO3]. Respiratory alkalosis occurs with increased alveolar ventilation.
Differential Diagnosis
Central Stimulation:
Anxiety, hyperventilation syndrome, pain, head trauma or CVA with central neurogenic
hyperventilation, tumors, salicylate overdose (often mixed metabolic gap acidosis and
respiratory alkalosis), fever, early sepsis
Peripheral Stimulation:
PE, CHF (mild), interstitial lung disease, pneumonia, altitude, hypoxemia of any cause
(see Hypoxia)
Miscellaneous:
Hepatic insufficiency, PRG, progesterone, hyperthyroidism, iatrogenic mechanical
overventilation
Treatment of Respiratory Alkalosis
Correct the underlying disorder.
Hyperventilation Syndrome:
Best controlled by having the patient rebreathe into a paper bag to increase PCO2, decrease
ventilator rate, increase amount of dead space with ventilator, or manage underlying
cause.
Hypoxia
The second type of information gained from a blood gas level, in addition to acidbase
results, is oxygenation. Results usually are given as PO2 and O2 saturation (see Table 81

for normal values). These two parameters are related to each other.
Oxygen saturation at any given PO2 is influenced by temperature, pH, and the level of 2,3diphosphoglycerate (2,3-DPG) as shown in Figure 84.

Figure 84.

Oxyhemoglobin dissociation curve.

Oxygenation can also be determined noninvasively with pulse oximetry. Pulse oximetry
is used to measure pulse rate and SaO2 and can reduce the need for ABG measurements.
The transcutaneous technique (detector placed on the finger, toe, top of the ear, earlobe of
adults and the foot, palm, great toe, or thumb of children) is sensitive in the detection of
arterial desaturation only. The technology is based on the different red and infrared light
absorption characteristics of oxygenated and deoxygenated hemoglobin. The technique
may be less accurate in cases of poor perfusion, motion, sensor exposure to ambient light,
skin pigmentation (usually at saturations < 80% only), use of IV contrast agents, and the
presence of abnormal hemoglobins (carboxy hemoglobin, methemoglobin). Normal pulse
oximetry readings should be 9599% in a healthy person on room air and can vary slightly
according to age, state of fitness, and altitude. Anemia, elevated bilirubin, and sickle cell
disease do not affect readings.
Hypoxia Differential Diagnosis
/ Abnormalities:

COPD (emphysema, chronic bronchitis, asthma), atelectasis, pneumonia, PE, ARDS,

pneumothorax, pneumoconiosis, CF, obstructed airway
Alveolar Hypoventilation:
Skeletal abnormalities, neuromuscular disorders, pickwickian syndrome, sleep apnea
Decreased Pulmonary Diffusing Capacity:
Pneumoconiosis, pulmonary edema, drug-induced pulmonary fibrosis (bleomycin),
collagenvascular diseases
Right-to-Left Shunt:
Congenital heart disease (eg, tetralogy of Fallot, transposition of the great arteries)
Sample AcidBase Problems
In each of these examples, use the technique in Step 1 of Interpretation of Blood Gases to
identify the acidbase disorder.
Example 1
A patient with COPD has a blood gas of pH 7.34, PCO2 55 mm Hg, and [HCO3] 29
mEq/L.
Step 1:

The numbers fit because the difference between the calculated and observed values is <
10%.
Step 2:
pH < 7.37, acidemia.
Step 3:
PCO2 > 44 mm Hg, and [HCO3] is not < 22 mEq/L, respiratory acidosis.
Step 4:
Normal compensation for chronic (COPD) respiratory acidosis (from Table 82).

Expected [HCO3] is 24 mEq/L + 6 = 30, which is close to the measured [HCO3] of 29

mEq/L, simple respiratory acidosis. This patient has chronic respiratory acidosis due to
hypoventilation (simple acidbase disorder).
Example 2
Immediately after cardiac arrest a patient has pH 7.25, PCO2 28 mm Hg, and [HCO3] 12
mEq/L.
Step 1:

The numbers fit.

Step 2:
pH < 7.37, acidemia.
Step 3:
[HCO3] is < 22 mEq/L and PCO2 is not > 44 mm Hg, metabolic acidosis.
Step 4:
(See Table 82)

The expected PCO2 of 26 mm Hg is very similar to the measured value of 28 mm Hg, so

this condition is simple metabolic acidosis. The patient has lactic acidosis following
cardiopulmonary arrest (simple acidbase disorder).
Example 3
A young man with a fever of 103.2F and a fruity odor on his breath has a blood gas of pH
7.36, PCO2 9 mm Hg, and [HCO3] 5 mEq/L.
Step 1:

The numbers fit.

Step 2:
pH < 7.37 indicates acidemia.
Step 3:
[HCO3] < 22 mEq/L and PCO2 is not > 44 mm Hg, thus metabolic acidosis is present.
Step 4:
The expected compensation in PCO2 can be calculated as follows (see Table 82):

The expected PCO2 is 17.5 mm Hg, but the reading is 9 mm Hg, indicating a second
process, respiratory alkalosis. This patient has metabolic acidosis due to DKA and
concomitant respiratory alkalosis possibly due to early sepsis and fever (mixed acidbase
disorder).
Example 4
A 30-year-old woman who is 30 wk PRG presents with nausea and vomiting. Blood gas
analysis reveals pH 7.55, PCO2 25 mm Hg, and [HCO3] 22 mEq/L.
Step 1:

The numbers fit.

Step 2:
pH < 7.44 indicates alkalemia.
Step 3:
PCO2 < 36 mm Hg, and [HCO3] is not > 26 mEq/L, thus respiratory alkalosis is present.
Step 4:
The expected compensation for chronic respiratory alkalosis (ie, pregnancy) is calculated
from Table 82:

The calculated [HCO3] is 24 7.5, or 1617 mEq, but the actual [HCO3] is 22 mEq/L,
indicating relative secondary metabolic alkalosis ([HCO3] is higher than expected). This
patient has respiratory alkalosis due to pregnancy and relative secondary metabolic
alkalosis due to vomiting.
Example 5
A 19-year-old patient with diabetes has an anion gap of 29 mEq/L and a [HCO3] of 6
mEq/L.
Step 1:

Step 2:

Actual [HCO3] is 6 mEq/L, close to the expected [HCO3] of 5 mEq/L. Thus pure
metabolic gap acidosis is present, most likely from DKA.
Example 6
A 21-year-old patient with diabetes presents with nausea, vomiting, and abdominal pain.
The anion gap is 23 mEq/L, and the [HCO3] is 18 mEq/L.
Step 1:

Step 2:

The [HCO3] is 18 mEq/L and not the 11 mEq/L expected from pure metabolic gap
acidosis. Because the actual [HCO3] is higher than expected, this condition is mixed
metabolic gap acidosis and metabolic alkalosis. The patient has metabolic gap acidosis
from DKA and metabolic alkalosis from vomiting.
Example 7
A 55-year-old patient who drinks a fifth of whiskey per day has a 2-wk history of diarrhea.
The anion gap is 17 mEq/L, and the [HCO3] is 10 mEq/L.
Step 1:

Step 2:

Actual [HCO3] is 10 mEq/L and not the expected 17 mEq/L of pure metabolic gap
acidosis. Because the actual [HCO3] is lower than expected, mixed metabolic gap
acidosis and metabolic nongap acidosis must be present. The patient has metabolic nongap
acidosis from diarrhea and metabolic gap acidosis from alcoholic ketoacidosis.