Abbott i-STAT 1

PCO2 - 2 Art: 714182-00R Rev. Date: 02-Aug-11
medical gas standards. i-STAT System controls and calibration verification materials are validated for use
only with the i-STAT System and assigned values may not be commutable with other methods. Further
information regarding metrological traceability is available from Abbott Point of Care Inc..
Expected Values
Reportable Reference
Test/Abbreviation Units* Range Range
(arterial) (venous)
Partial Pressure
Carbon Dioxide/PCO
2
mmHg 5 – 130 35 – 45
3
41 – 51
kPa 0.67 – 17.33 4.67 – 6.00 5.47 – 6.80
Bicarbonate/HCO
3
mmol/L 1.0 – 85.0 22 – 26** 23 – 28**
Base Excess/BE mmol/L (-30) – (+30) (-2) – (+3)
3
(-2) – (+3)
3
Anion Gap/AnGap mmol/L (-10) – (+99) 10 – 20
3
10 – 20
3
*The i-STAT System can be configured with the preferred units.
**Calculated from Siggaard-Andersen nomogram.
4
To convert PCO
2
results from mmHg to kPa, multiply the mmHg value by 0.133.
The reference ranges programmed into the analyzer and shown above are intended to be used as guides
for the interpretation of results. Since reference ranges may vary with demographic factors such as
age, gender and heritage, it is recommended that reference ranges be determined for the population
being tested.
Clinical Significance
PCO
2
along with pH is used to assess acid-base balance. PCO
2
(partial pressure of carbon dioxide), the
respiratory component of acid-base balance, is a measure of the tension or pressure of carbon dioxide
dissolved in the blood. PCO
2
represents the balance between cellular production of CO
2
and ventilatory
removal of CO
2
and a change in PCO
2
indicates an alteration in this balance. Causes of primary respiratory
acidosis (increase in PCO
2
) are airway obstruction, sedatives and anesthetics, respiratory distress syndrome,
and chronic obstructive pulmonary disease. Causes of primary respiratory alkalosis (decreased PCO
2
) are
hypoxia (resulting in hyperventilation) due to chronic heart failure, edema and neurologic disorders, and
mechanical hyperventilation.
HCO
3
(bicarbonate), the most abundant buffer in the blood plasma, is an indicator of the buffering capacity
of blood. Regulated primarily by the kidneys, HCO
3
is the metabolic component of acid-base balance.
Causes of primary metabolic acidosis (decrease in HCO
3
) are ketoacidosis, lactate acidosis (hypoxia), and
diarrhea. Causes of primary metabolic alkalosis (increase in HCO
3
) are vomiting and antacid treatment.
Base excess of the extracellular fluid or standard base excess is defined as the concentra tion of titratable
base minus the concentration of titratable acid when titrating the average intracellular fluid (plasma plus
interstitial fluid) to an arterial plasma pH of 7.40 at PCO
2
of 40 mmHg at 37°C. Excess concentration of
base in the average ECF remains virtually constant during acute changes in the PCO
2
and reflects only
nonrespiratory component of pH-disturbances.
Anion gap is reported as the difference between the commonly measured cations sodium and potassium
and the commonly measured anions chloride and bicarbonate. The size of the gap reflects unmeasured
cations and anions and is therefore an analytical gap. Physiologically, a deficit of anions cannot exist. While
relatively nonspecific, anion gap is useful for the detection of organic acidosis due to an increase in anions
that are difficult to measure. Anion gap can be used to classify metabolic acidosis into high and normal
anion gap types. Anion gap may be only slightly increased in diarrhea and renal failure, but elevated (often
>25) due to an increase in organic anions in lactic acidosis, ketoaci dosis (alcoholic, diabetic, starvation) and
uremia, an increase in inorganic anions in uremia, and an increase in anions from drugs such a salicylate
and carbenicillin or toxins such as methanol and ethanol.