Key Benefits of the Randox CO2 Total Reagent
Exceptional correlation with standard methods
The Randox methodology was compared against other commercially available methods and the Randox CO2 Total assay showed a correlation coefficient of r=0.94
Wide measuring range
The healthy range for CO2 Total is 18 – 28 mmol/l. The Randox CO2 Total assay can comfortably detect levels outside of this healthy range measuring between 0.004 – 50 mmol/l
Suitable for use on a range of automated analysers
The Randox CO2 Total reagent is suitable for use on a number of third party automated analysers. To enquire about an Instrument Specific Application (ISA), please click the Contact Us button below.
Other features of the Randox CO2 Total Reagent
- Enzymatic method
- Available as liquid and lyophilised reagents
- Stable until expiry date when stored at +2 to +8°C
- Open vial stability of 14 days at +10°C
- Measuring range 0.004 – 50 mmol/l
Instrument Specific Applications (ISA’s) are available for a wide range of biochemistry analysers. Contact us to enquire about your specific analyser.
What is the CO2 Total assay used for?
What is CO2?
Carbon dioxide (CO2) is a metabolic waste product of cellular respiration. It is transported in the bloodstream to the lungs and expelled from the body. CO2 exists in the body in two forms: 90% exists as bicarbonate (HCO3) and the remaining exists as carbonic acid (H2CO3) or dissolved CO2. The kidneys and lungs are responsible for the regulation on CO2, H2CO3 and HCO3 in the blood.
What is the CO2 Total assay used for?
The Randox CO2 Total assay is used for the quantitative in vitro determination of CO2 in serum and plasma. It aids in diagnosing diseases associated with high and low levels of CO2 in the bloodstream.
Slightly elevated levels of CO2 do not have any serious consequences on the body, but overexposure to CO2 due to decreased alveolar ventilation or the inhalation of CO2 enriched air can cause serious implications in the body including: deterioration of respiratory functions due to respiratory acidosis and asphyxiation, cardiovascular effects due to low blood pressure and cardiac arrhythmia and nerve damage due to hypercapnia and acidemia.
For more information on the contrasting effects of hypoxia and hypercapnia, please click here [external link].
High CO2 levels usually indicates that the lungs are not functioning properly and are unable to expel the required amount of CO2. During an acute illness, the levels of CO2 can increase suddenly, however, over time, some people are able to establish a new ‘baseline’ for CO2. An example of this is a person with stable chronic obstructive pulmonary disease (COPD) This means that the body is able to function with higher than normal levels of CO2.
There are some medical conditions and drugs that can cause low CO2 levels including: kidney disease as the kidneys are unable to carry out their functions, diabetic ketoacidosis due to the production of ketones resulting in reduced CO2 levels, hyperchloremic acidosis due to diarrhea, Addison’s disease, and metabolic acidosis due to chemical toxicity.
- McNeill, A.J. Thrombolytic therapy within one hour of the onset of acute myocardial infarction. Q. J. Med. 1991, 79: 487-494
- Huang, Z-Q., et al. Effects of N-n-butyl haloperidol iodide on rat myocardial ischemia and reperfusion injury and L-type calcium current. Acta Pharmacol. Sin 2003, 24(8): 757-763
- Mohiti, J., et al. The significance of troponin T and CK-MB release in coronary artery bypass surgery. Indian J. Clin. Biochem.2004, 19(1): 113-117
- Lu, H-K., et al. Preventive effects of Spirulina platensis on skeletal muscle damage under exercise-induced oxidative stress.Eur. J. Appl. Physiol. 2006, 98: 220-226
- Randazzo-Moura, P., et al. A Study of the Myotoxicity of Bothropstoxin-I Using Manganese in Mouse Phrenic Nerve-Diaphragm and Extensor digitorium longus Preparations. Braz. J. Morphol. Sci. 2006, 23 (2): 237-246
- Akpanabiatu, M.I., et al. Effects of interaction of vitamin A and Rauwolfia vomitoria root bark extract on marker enzymes of cardiac diseases. Indian Journal of Clinical Biochemistry. 2009, 24(3): 241-244