2. Presented by: Samah Al Khawashki Medical Student December 20, 2008

3. An arterial blood gas (ABG) is a blood test that is performed specifically on arterial blood from the radial or femoral arteries. It is used to determine the concentrations of CO2, O2, HCO3 and the PH of the blood WHAT IS AN ABG ?

4. What do we look for in an ABG?? 1.PH: normal PH=7.4, OR the range between7.35-7.45 acidemic (pH < 7.35)or alkalemic (pH > 7.45)

5. 2.CO 2 : it tells us if there is a RESPIRATORY problem, Normal PCO2 is 35-45 mmHg A high PCO 2 (respiratory acidosis) indicates hypoventilation, a low PCO 2 (respiratory alkalosis) indicates hyperventilation.  PCO 2 levels can also become abnormal when the respiratory system is working to compensate for a metabolic issue so as to normalize the blood pH.

6. 3. HCO 3 - : tells us if there is a METABOLIC problem A normal HCO3 is 22-27 mmHg A low HCO 3 - indicates metabolic acidosis, a high HCO 3 - indicates metabolic alkalosis.  HCO 3 - levels can also become abnormal when the kidneys are working to compensate for a respiratory issue so as to normalize the blood pH.

7. 4. PO 2 : A low O 2 indicates that the patient is not respiring properly, and is hypoxemic. The normal PO 2 80-100 mmHg

8. 5. Match the PH with the CO 2 or HCO 3 -, what matches it is the primary imbalance. 6. Check the value opposite the PH this is the compensation So, ask yourself, if the PH is academic what is alkalemic? This is the compensated Then ask, is it complete compensation=does the PH go back to the normal range? Or is it partial=The PH is not in the normal range

9. THE PH: 7.40 acidosis alkalosis compensated compensated 7.35 7.45 Anything less is anything more is Uncompensated uncompensated OR partially compensated

10. So, when we look at an ABG WE HAVE TO CHECK IF: 1. it is compensated or not through PH 2. It is respiratory or metabolic through PH, CO 2 and HCO 3 - 3. It is acidosis or alkalosis through PH,CO 2 and HCO 3 -

11. The normal ranges: PH 7.35-7.45 CO 2 35-45 HCO 3 - 22-27 PO 2 80-100

12. CASE 1 Mr. abdulla is a 60 year-old with pneumonia. He is admitted with dyspnea, fever, and chills. His blood gas is below: pH 7.28 CO2 56 PO2 70 HCO3 25 SaO2 89% What is your interpretation?

13. Answer to case1 Mr. abdulla has an uncompensated respiratory acidosis with hypoxemia as a result of his pneumonia. This is due to inadequate ventilation and perfusion.

14. Respiratory acidosis It is due to Alveolar hypoventilation Hypercapnia and respiratory acidosis occur when impairment in ventilation occurs and the removal of CO 2 by the lungs is less than the production of CO 2 in the tissues.

15. Acute respiratory acidosis: an abrupt failure of ventilation occurs. Causes are: 1. depression of the central respiratory center by cerebral disease or drugs 2. inability to ventilate adequately due to neuromuscular disease (eg, myasthenia gravis) 3. airway obstruction related to asthma or COPD exacerbation.

16. Chronic respiratory acidosis: secondary to many disorders causes are: 1. COPD 2. obesity hypoventilation syndrome 3. severe restrictive ventilatory defects as observed in interstitial fibrosis and thoracic deformities.

17. How do we measure compensation? The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows: Acute respiratory acidosis: HCO 3 - increases 1 mmol for each 10-mm Hg rise in PCO 2. Chronic respiratory acidosis: HCO 3 - rises 3.5 mmol for each 10-mm Hg rise in PCO 2.

18. CASE 2 Ms. sara was admitted for a drug overdose. She is being mechanically ventilated and a blood gas is obtained to assess her for weaning. The results are as follows: pH 7.42 CO2 18 pO2 100 HCO3 11 SaO2 98% What is your interpretation?

19. Answer to case 2 Mrs. Sara is being overventilated which caused a compensated respiratory alkalosis. Treatment would consist of decreasing ventilatory support

20. Respiratory alkalosis results from hyperventilation leading to decreased PCO 2 concentration. the alkalosis may disrupt calcium ion balance, and cause the symptoms of hypocalcaemia, such as tetany and fainting with no fall in total serum calcium levels. Causes: 1. Hypoxemia: high altitudes 2. CNS stimulation: Anxiety and stress 3. Caffeine overdose, nicotine 4. Stimulation of chest receptors: pulmonary embolism

21. How do we measure compensation? The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows: acute respiratory alkalosis: HCO 3 decreases 2 mmol/L for each 10 mmHg decrease in PCO 2 Chronic respiratory alkalosis : HCO 3 decreases by 4 mmol/l for each 10 mmHg decrease in PCO 2

22. CASE 3 Ms. nada is a 24 year-old college student. She has a history of Crohn's disease and is complaining a of a four day history of bloody-watery diarrhea. A blood gas is obtained to assess her acid/base balance: pH 7.28 CO2 43 pO2 88 HCO3 20 SaO2 96% What is your interpretation?

23. Answer to case 3 Ms. nada has an uncompensated metabolic acidosis. This is due to excessive bicarbonate loss from her diarrhea. It is interesting to note that she has no compensation. Normally, the respiratory center compensates quickly for metabolic disorders

24. Metabolic acedosis increased production of H + by the body or the inability of the body to form HCO 3 - in the kidney. its consequences can be serious, including coma and death. The anion gap is important for the DDX of metabolic acidosis=( [Na + ] ) - ( [Cl - ]+[HCO 3 - ] )  As sodium is the main extracellular cation, and chloride and bicarbonate are the main anions, the result should reflect the remaining anions.

25. Normal anion gap metabolic acidosis: about 8-16 mmol/l (12±4) Causes: 1. Increased GI HCO 3 loss: diarrhea 2. Failure to absorb HCO 3 BY kidneys: proximal(type2)renal tubular acedosis(RTA) and acetazolamide ingestion 3. Decreased renal H Excretion: distal(type1) RTA and (type 4) RTA 4. Increased HCL production: ammonium chloride ingestion

26. Hypokalemic normal AG metabolic acedosis 1.Diarrhea 2.RTA -1 and RTA -2 3.Use of carbonic anhydrase inhibitors (acetazolamide) Hyperkalemic normal AG metabolic acedosis 1.RTA -TYPE 4 2.NH 4 Cl ingestion

27. High anion gap metabolic acedosis: > 16 mmol/l Causes: MUDPILES: M-Methanol U-Uremia D-Diabetic Ketoacidosis P-Paraldehyde I-Infection, Iron, Isoniazid L-Lactic acidosis E-Ethylene Glycol S-Salicylates AG > 25: ingestion of a poison (mostly an “_ol”)

28. How do we measure compensation? In metabolic acedosis PCO2 decreases 1.2 mmHg for every 1 mmol increases in HCO3

29. CASE 4 Ms. farah is a 17 year-old with intractable vomiting. She has some electrolyte abnormalities, so a blood gas is obtained to assess her acid/base balance. pH 7.49 CO2 40 pO2 92 HCO3 29 SaO2 97% What is your interpretation?

30. Answer to case 4 Ms. farah has an uncompensated metabolic alkalosis. This is due to vomiting that results in excessive loss of stomach acid. Treatment consists of fluids, anti-emetics, and management of her electrolyte disorders.

31. Metabolic alkalosis Either because of decreased hydrogen ion concentration, leading to increased bicarbonate, or direct increased bicarbonate concentrations.

32. Causes of metabolic alkalosis Loss of H ions in : Vomiting: loss of HCL Renal loss: with excess aldosterone secretion(Na retention, H secretion) Retention of bicarbonate As a compensatory mechanism for respiratory acidosis, this happens in prolonged respiratory acedosis Alkalotic agents : bicarbonate administrated in cases of peptic ulcer or hyperacidity or antacids Contraction alkalosis: Diuretics: water is lost while bicarbonate is retained Shift of hydrogen ions into intracellular space: Hypokalemia: potassium goes out of the cells and H goes in

33. How do we measure compensation? In metabolic alkalosis PCO2 inceases 0.75 mmHg for every 1 mmol increase in HCO3

34. IN SUMMARY The 6 steps to ABG interpretation are? CO2 primary changes tell us that the problem is respiratory HCO3 primary changes tell us that the problem is metabolic Respiratory compensation is faster that metabolic compensation