This document provides an overview of acid-base disorders and the approach to interpreting arterial blood gases (ABGs). It begins with a brief preview of the topic and then provides more detailed information about: 1. The expected changes in different acid-base disorders 2. Formulas and ratios used to evaluate ABGs such as the anion gap and G:G ratio 3. Case studies of patients with various acid-base imbalances like a ruptured abdominal aortic aneurysm causing lactic acidosis It also includes sections on renal tubular acidosis which summarize the mechanisms, causes and clinical manifestations of different types of RTA. Overall, the document serves as a guide for clinicians to systematically evaluate ABGs

1. ABG series ANAS SAHLE , MD DAMASCUSE HOSPITAL

2. Acid-Base Disorders and the ABG 3

3. BREIF PREVIEW

4. Summary of the Approach to ABGs Check the pH Check the pCO2 Select the appropriate compensation formula Determine if compensation is appropriate Check the anion gap AG=NA – (HCO3 + CL):12±4 If the anion gap is elevated, check the delta-delta G:G Ratio =Δ AG (12-AG) HCO3 (24-HCO3) If a metabolic acidosis is present, check urine pH Generate a differential diagnosis

5. EXPECTED CHANGES IN ACID-BASE DISORDERS From: THE ICU BOOK - 2nd Ed. (1998) [Corrected]

7. Gap:gap ratio??

9. HIGH AG M.AC Osmolal gap = measured serum osmolality - (2 NA + gluco8 + bun,8) Corrected osmolal gap = measured serum osmolality - (2 NA + gluco8 + bun,8 + ETOH,6)

10. HIGH AG M.AC High normal

11. Expected PCO2 : Measured PCO2

12. YES NO YES NO YES NO YES NO

13. <5,5 >5,5 Urine AG = (UNA +UK) - UCL

14. CASE:1An old man with abdominal pain & shock An 85 year old man was admitted with severe abdominal pain and shock. The abdominal pain started about 15:00hrs and quickly became quite severe. There was no radiation to the back. The patient was known to have an abdominal aortic aneurysm (AAA). On arrival at hospital, the patient was shocked with peripheral circulatory failure and hypotension (BP 70-80 systolic). The abdomen was guarded and quite tender. He was distressed but able to talk and could understand instructions. Past history was of hypertension (on metoprolol and prazosin) and angina (on Isordil). Prior to this event, the patient was mobile and independent.

15. Biochemistry at 15:20hrs was:(All results in mmol/l) Na+ =138, K+= 4.9, Cl- =107, Glucose= 11.2 = 201mgl Urea =12.8 = 230 mgl Creatinine= 0.188 =3,38mgl. Anion gap was =11 Mgl = mmol /L * 18

16. CONTINUE A ruptured AAA was diagnosed clinically and he was transferred to theatre for emergency laparotomy. On arrival in theatre BP was 120 systolic. The patient was talking but distressed by pain with rapid respirations at a rate of 30/min. It was noted that neck veins were very distended. An external jugular triple lumen central line and a brachial arterial line were placed before the surgical team had arrived in theatre. CVP was +40 mmHg.

18. CONTINUE Intra-operative findings were of almost total infarction of the small bowel and part of the stomach due to acute mesenteric vascular obstruction. The AAA was un-ruptured. The patient arrested and died on the table at 18:05hrs

19. discussion The anion gap is 11 & the chloride is slightly elevated. The urea & creatinine are elevated but are not high enough to support the idea of an acute renal failure causing an acidosis. The glucose is elevated but there is no urine test results given so we don't know whether ketonuria is present but ketoacidosis as the cause is not supported by the history. The lactate level was quite elevated (at 17:38hrs) and this was collected about 2 hours after the biochemistry which showed a normal anion gap. The bicarbonate on the initial biochemistry was 20but had decreased to 13.8 by the time of the gas collection. This indicates the progressive development of the disorder.

20. An Intoxicated Baby An 8 month old female baby was admitted with a one day history of lethargy. She had vomited several times. Her mother said she appeared "intoxicated". Examination confirmed : the obtunded mental state but she was easily rousable and muscle tone was normal. Resp rate was 60/min. Pupils were normal. There was no evidence of dehydration. Abdomen was soft and non-tender. BP was 112/62. Peripheral perfusion was clinically assessed as normal. Heart and chest examination was normal. Plantar response was normal

21. Investigations Urine: pH 5.0, negative for glucose and ketones. Numerous calcium oxalate crystals were seen on urine microscopy

23. A young man who ingested barium carbonate A 22 year old man was admitted to hospital 1.5 hours after ingestion of about 10G of barium carbonate dissolved in hydrochloric acid. Symptoms included abdominal pain, generalisedareflexic muscle paralysis, increased salivation and diarrhoea. BP 180/110. Pulse 92/min

24. Initial biochemistry (in mmol/l) was:

26. Clinical Diagnosis Acute self-inflicted poisoning with barium carbonate resulting in muscle paralysis (due to hypokalaemia) and acute lactic acidosis. The hypokalaemia on presentation was due to the barium. Barium causes a large transfer of K+ from the ECF to the ICF in muscle cells due to a marked reduction in passive permeability of the membrane to K+(minimising K+ loss from the cell) without initially affecting the Na+-K+ATPase (allowing continued uptake of K+ by the cell). The immediate cause of the lactic acidosis is not clear as their is not evidence of circulatory failure. A respiratory acidosis due to ventilatory failure associated with the muscle weakness was considered a clinical possibility but there was no blood-gas evidence of this.

27. A man with diarrhoea and dehydration A 44 year old moderately dehydrated man was admitted with a two day history of acute severe diarrhea.

29. YES NO

30. Comments Pertinent points were the acidaemia, elevated chloride, normal anion gap elevation of urea and creatinine. Some pre-renal renal failure is present but there is no evidence of a high anion gap acidosis due to renal failure. As a general guideline, acidosis usually does not occur in renal failure until GFR is less than 20 mls/min (or a creatinine level of about 0.30-0.35 mmol/l). Similarly tissue perfusion is still adequate enough to prevent development of a lactic acidosis. Hypovolaemia results in secondary hyperaldosteronism which increases sodium reabsorptionbut increases excretion of K+ resulting in hypokalaemia.

31. CASE 23-year-old Caucasian female referred for further evaluation of hypokalemic acidosis. She was in her usual state of excellent health with normal growth and development until her second month of pregnancy. She had a spontaneous miscarriage, and was found to have a serum potassium of 3.2 mEq/L and a bicarbonate level of 19 mEq/L during a hospitalization. She was treated with oral potassium and bicarbonate supplements and then weaned these off after 4 months of therapy. Six weeks later, she developed myalgias and collapsed due to profound weakness. She was found to have a serum bicarbonate level of 14 mEq/L with a serum potassium of 1.9 mEq/L.

32. P.E Normal stature BP 120/80 No rash Normal heart and lungs No edema No synovitis

33. :LAB

34. Which of the following is the correct diagnosis? Type IV RTA Diarrhea Type I RTA Renal tubular alkalosis Proximal RTA

36. >5,5 <5,5 Urine AG = (UNA +UK) - UCL

37. Which of the following is the correct diagnosis? Type IV RTA Diarrhea Type I RTA Renal tubular alkalosis Proximal RTA

38. Points to Remember Renal tubular acidosis (RTA) is a disease that occurs when the kidneys fail to excrete acids into the urine, which causes a person's blood to remain too acidic. Without proper treatment, chronic acidity of the blood leads to growth retardation, kidney stones, bone disease, chronic kidney disease, and possibly total kidney failure. If RTA is suspected, additional information about the: sodium, potassium, and chloride levels in the urine and the potassium level in the blood will help identify which type of RTA a person has. In all cases, the first goal of therapy is to neutralize acid in the blood, but different treatments may be needed to address the different underlying causes of acidosis.

40. calcium

41. glucose

42. Amino acids

44. H+ (NH4+ or phosphate salts) excreted

45. molar competition between H+ and K+

47. Type I Classic Distal RTA-Mechanism 1 Tubular lumen Na+ Peritubular Capillary Na+ 3Na+ ATPase (-) 2K+ (-) H+ Retention K+ R-Aldo K+ Wasting Urine pH > 5.5 Ca-P stones Cl- ATPase 3Na+ H+ ATPase H2O 2K+ (-) T HCO3- OH- + CO2 K+ Cl- ATPase (-) H+

48. Type I Classic Distal RTA-Mechanism 2 Tubular lumen Na+ Peritubular Capillary Na+ 3Na+ ATPase (-) 2K+ (-) H+ Retention K+ R-Aldo K+ Wasting Urine pH > 5.5 Ca-P stones Cl- ATPase 3Na+ H+ ATPase H2O 2K+ (-) T HCO3- OH- + CO2 K+ Cl- ATPase (-) H+

49. Type I Distal RTA-Mechanism 3 Tubular lumen Na+ Peritubular Capillary Na+ 3Na+ ATPase (-) 2K+ (-) K+ R-Aldo K+ Wasting Urine pH > 5.5 Ca-P stones Cl- Backleak of H+ ATPase 3Na+ H+ H+ ATPase H2O H+ Retention 2K+ (-) T HCO3- OH- + CO2 K+ Cl- ATPase (-) H+

51. Idiopathic

52. Sporadic

53. Familial

54. Autosomal dominant

55. Autosomal recessive

56. CA anhydraseII

57. Deficiency (mixed I and II)

58. Secondary

59. Sjögren’s syndrome

60. Hypercalcuria

61. Rheumatoid arthritis

62. SLE

63. Hyperglobulinemia

64. Ifosfamide

65. Primary biliary cirrhosis

66. Lithium

67. Amphotericin B

69. Hypercalcuria

70. Hypocitraturia

71. High urine pH -> calcium phosphate stones

72. Hyperuricosuria

73. Growth retardation