Arterial blood gas sampling

Arterial blood gas sampling

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Arterial blood gas sampling is a medical technique used to check gas levels in the blood. It typically involves using a thin needle and syringe to puncture an artery, usually in the wrist, and withdraw a small amount of blood. This technique is useful for making sure that certain parts of the blood's chemistry are normal. This technique is commonly used on patients whose breathing is controlled by a mechanical respirator or who are having serious difficulties with breathing. When this procedure is performed on a small artery in the wrist, it is unlikely to cause serious complications, and the information gained may save the patient's life.

The purpose of arterial blood gas sampling is to assess patients' respiratory status as well as acid-base balance or for laboratory testing when venous blood is unavailable, and is frequently requested for seriously ill patients. An arterial blood gas (ABG) will help in the assessment of oxygenation, ventilation, and acid-base homeostasis. It can also aid in the determination of poisonings (carboxyhemaglobinemia or methemaoglobinemia) and in the measurement of lactate concentration.

It is sometimes called "arterial blood gas analysis" or "ABG" sampling."

Outcome Goal

Proper collection of arterial blood samples.

Arterial Blood Gas Test Definition

Blood is drawn anaerobically from a peripheral artery (Radial, Brachial, Ulnar, Femoral, Axillary, Posterior Tibial or Dorsalis pedis) via a single percutaneous needle puncture, or from an indwelling arterial cannula or catheter for multiple sample.

Each method provides a blood specimen for direct measurement of:

*partial pressures of carbon dioxide (PaCO2);

*oxygen (PaO2);

*hydrogen ion activity (pH);

*total hemoglobin (Hbtotal);

*oxyhemoglobin saturation (HbO2);

*dyshemoglobins carboxyhemoglobin (COHb);

*methemoglobin (MetHb).

Purpose and indications

The purpose of arterial blood gas sampling is to assess patients respiratory status as well as acid base balance or for laboratory testing when venous blood is unavailable, and is frequently requested for seriously ill patients. So, an arterial blood gas (ABG) will help in the assessment of oxygenation, ventilation, and acid-base homeostasis. It can also aid in the determination of poisonings (carboxyhemaglobinemia or methemaoglobinemia) and in the measurement of lactate concentration.

Pulse oximetry will give a reasonable estimate of the adequacy of oxygenation in many circumstances but does not assess acid-base status or ventilation and should not be used alone in cases where these measurements are important.

Basic conditions diagnosed by ABG's:

*Respiratory Acidosis

*Anything which prevents the body from getting rid of excess CO2, increases acid which decreases pH

*Respiratory Alkalosis

*Anything which makes the body lose CO2, decreases acid, which increases pH
*Metabolic Alkalosis

*Anything which increases HCO3 increases base which increases pH

*Metabolic Acidosis

*Anything which decreases HCO3 decreases base which decreases pH

Apart from helping to establish a diagnosis, blood gases may also help to as certain the severity of a particular condition (e.g. metabolic acidosis in sepsis). This information can help to establish diagnosis, monitor severity, progression, and prognosis as well as guide therapy of:

*respiratory failure,

*cardiac failure,

*renal failure,

*hepatic failure,

*diabetic ketoacidosis,



Table 1. Normal Values in an ABG report at sea level:

The pH of the blood is maintained within a normal range by a number of compensatory mechanisms, the most important being the body buffer mechanisms and the renal and respiratory systems. The degree of compensation varies between individuals and depends on the severity and duration of the primary problem and associated medical comorbidities. Respiratory compensation for metabolic problems is usually rapid and almost complete. The lungs respond quickly by increasing ventilation to blow off excessive carbon-dioxide (in metabolic acidosis) or decreasing ventilation to retain carbon-dioxide (in metabolic alkalosis). The latter compensation is less complete than the former for obvious reasons. The renal compensation for respiratory imbalances is slow and incomplete. The kidneys regulate extracellular fluid H+ ion concentration by secretion of H+ ions, reabsorption of filtered HCO3 ions, and the production of new HCO3 ions. Excess HCO3 is filtered into the renal tubules and eliminated in the urine. Depending on the need to excrete either an acid or a base load, the kidneys can excrete urine with a pH ranging from 4.5 to 8.0. A rough guide to the degree of compensation to primary changes in CO2 and HCO3 as a result of respiratory and metabolic imbalances respectively is shown in table 3.

Table 3. Metabolic Alkalosis:

Metabolic alkalosis can result from the loss of acid, addition of alkali or both in the kidneys or elsewhere. Extrarenal sites include stomach (loss of acid), redistribution of alkali from the intracellular stores to the ECF (as in potassium or chloride depletion), oral administration (antacids, ion-exchange resins, milk alkali syndrome, oral HCO3) and parenteral administration of alkali (citrate in blood transfusions, bicarbonate in severe metabolic acidosis). Renal causes of alkali excess include mineralocorticoid excess, response to long-standing hypercapnia (persists even after correction of respiratory acidosis), hypokalemia (promotes H+ secretion in the distal nephron) and ECF volume depletion (impaired HCO3 excretion). Certain conditions can cause metabolic alkalosis by a number of mechanisms (e.g. diuretic use causes both ECF depletion and hypokalemia).

Respiratory Alkalosis:

The principal cause of respiratory alkalosis (hypocapnia) is hypoxia and its causes (type I respiratory failure), further treatment of which has been detailed before. Other causes of acute respiratory alkalosis include anxiety, fever, pain, sepsis, hepatic failure, CNS disorders (stroke, infections), pulmonary disorders without hypoxia (infections and interstitial lung disease), delirium tremens and drugs (salicylate intoxication). Chronic causes include high altitude hypoxia, chronic hepatic failure, chronic pulmonary disease, CNS trauma, anaemia, hyperthyroidism, beriberi and pregnancy. Treatment should be directed towards the cause.

Contraindications/concerns for arterial puncture

Puncture sites

Approved puncture sites include radial, dorsalis pedis, and brachial arteries. The brachial artery will not be used on patients in Children’s Hospital. In the Emergency Department, femoral artery is an approved puncture site.Brachial and femoral arteries should be reserved as a last option. The radial artery on non dominant hand is the ideal site for an arterial puncture for the following reasons:
*It is small, but superficial and easily accessible, and stabilized.
*It is easily compressible with better control of bleeding
*There is no nerve near by to worry about.
*The collateral arch with ulnar artery minimizes the risk of occlusion.

The syringe has to be heparinized to prevent clotting. It is important to have the right amount of heparin in the syringe. “Too much” or “too little heparin can alter the results.”

Further reading



1. Armstrong PW, Parker JO: The complications of brachial arteriotomy. J Thorac Cardiovasc Surg 1971; 61:424

2. Browning JA, Kaiser DL, Durbin CG. The effect of guidelines on the appropriate use of arterial blood gas analysis in the intensive care unit. Respir Care 1989; 34:269-276.

3. Bruck E, Eichhorn JH, Ray-Meredith S. Shanahan JK, Slockbower JM. Percutaneous collection of arterial blood for laboratory analysis. National Committee for Clinical Laboratory Standards 1985;H11A;5(3):39-59.

4. Bucher, L. (2001). Arterial Puncture. In D.J. Lynn-McHale & K.K. Carlson (Eds.), AACN procedure manual for critical care (pp.496 – 502). Philadelphia, PA: W.B. Saunders Company.

5. Centers for Disease Control. Update: Universal Precautions for prevention of transmission of human immunodeficiency virus, hepatitis B virus, and other blood-borne pathogens in health care settings. MMWR 1988; 37:377-388.

6. Colley DP Vertebral arteriovenous fistula: an unusual complication of Swan-Ganz catheter insertion. Am J Neuroradiol 1985 Jan-Feb;6(1):103-4

7. Department of Labor, Occupational Safety and Health Administration. Occupational exposure to bloodborne pathogens. 29 CFRR Part 1910.1030. Federal Register, Friday December 06, 1991.

8. Depierraz B; Essinger A; Morin D; Goy JJ; Buchser E Isolated phrenic nerve injury after apparently atraumatic puncture of the internal jugular vein. Intensive Care Med, 15:132-4, 1989

9. DuBose Jr TD. Acidosis and alkalosis. Chapter 50. Section 7. Alteration in urinary function and electrolytes. In Fauci et al. Harrison's Principles of Internal Medicine 14th edition. 1998; 277-86.

10. Fleisher M, et al. Two whole-blood multi-analyte analyzers evaluated. Clin Chem 1989;35: 1532- 1535.

11. Frye M, DiBenedetto R. Lain D, Morgan K. Single arterial puncture vs arterial cannula for arterial gas analysis after exercise. Chest 1986;93:294-298.

12. Gardner RM, Clausen JL, Epler G. Hankinson JL, Permutt S. Plummer AL. Pulmonary function laboratory personnel qualifications. American Thoracic Society Position Paper, ATS News, November 1982.

13. Gluck SL. Acid-base. Electrolyte quintet. The Lancet 1998; 352: 474-9.

14. Hansen JE, Simmons DH. A systematic error in the determination of blood PCO2- Am Rev Respir Dis 1977; 115:1061-1063.

15. Harsten A, Berg B. Inerot S. Muth L. Importance of correct handling of samples for the results of blood gas analysis. Acta Anaesthesiol Scand 1988;32:365-368.

16. Hess D. Detection and monitoring of hypoxemia and oxygen therapy. Resp Care 2000;45:64-83.

17. Hess D, Good C, Didyoung R. Agarwal NN, Rexrode WO. The validity of assessing arterial blood gases 10 minutes after an Flo2 change in mechanically ventilated patients without chronic pulmonary disease. Respir Care 1985;30:1037-1041.

18. Luce EL, Futrell JW, Wilgis EFS, et al: Compression neuropathy following brachial artery puncture in anticoagulated patients. J Trauma 1976; 16:717-721

19. Macon WL, Futrell JW: Median-nerve neuropathy after percutaneous puncture of the brachial artery in patients receiving anticoagulants. N Engl J Med 1973: 288:139

20. McCready RA, Hyde GL, Bivins BA, Hagihara PF: Brachial arterial puncture: A definite risk to the hand. South Med J 1984; 77:6

21. [ Mitaishvili R] , ABG Sampling. [ RM Global Health]

22. [ Mitaishvili R] , Arterial Puncture. []

23. [ Mitaishvili R] , Radial artery Puncture. []

24. Moran RF, Van Kessel A. Blood gas quality assurance. NSCPT Analyzer 1981;11(I): 18-26.

25. National Committee for Clinical Laboratory Standards. Procedures for the collection of diagnostic blood specimens by skin puncture, 3rd ed. Villanova PA: NCCLS, 1992.

26. Neviaser RJ, Adams JP, May GI: Complications of arterial puncture in anticoagulant patients. J Bone Joint Surg 1976; 58A:218-220

27. Raffin TA. Indications for arterial blood gas analysis. Ann Intern Med 1986;105: 390-398.

28. Ries, AL, Fedullo PF, Clausen JL. Rapid changes in arterial blood gas levels after exercise in pulmonary patients. Chest 1983; 83: 454-456.

29. Shapiro BA, Harrison RA, Cane RD, Templin R. Clinical application of blood gases, 4th ed. St Louis: Year Book Medical Publishers Inc. 1989.

30. Sharzer LA, Baker WH: Nonthrombotic arterial occlusion. Arch Surg 1973; 106:344

31. Thorson SH, Marini JJ, Pierson DJ, Hudson LD. Variability of arterial blood gas values in stable patients in the ICU. Chest 1983;84(1): 14-18.

32. Weibley RE, Riggs CD. Evaluation of an improved sampling method for blood gas analysis from indwelling arterial catheters. Crit Care Med 1989; 17(8):803-805.

33. Williams AJ. ABC of oxygen. Assessing and interpreting arterial blood gases and acid-base balance. B M J 1998;317:1212-6.

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