ABG3 Series


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مقاربة غازات الدم الشرياني (الماض الاستقلابي طبيعي الفجوة)

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ABG3 Series

  1. 1. ABG series<br />ANAS SAHLE , MD<br />DAMASCUSE HOSPITAL<br />
  2. 2. Acid-Base Disorders and the ABG 3<br />
  3. 3. BREIF PREVIEW<br />
  4. 4. Summary of the Approach to ABGs<br />Check the pH<br />Check the pCO2<br />Select the appropriate compensation formula<br />Determine if compensation is appropriate<br />Check the anion gap <br />AG=NA – (HCO3 + CL):12±4<br />If the anion gap is elevated, check the delta-delta<br />G:G Ratio =Δ AG (12-AG) Δ HCO3 (24-HCO3)<br />If a metabolic acidosis is present, check urine pH<br />Generate a differential diagnosis<br />
  5. 5. EXPECTED CHANGES IN <br />ACID-BASE DISORDERS <br />From: THE ICU BOOK - 2nd Ed. (1998) [Corrected]<br />
  6. 6.
  7. 7. Gap:gap ratio??<br />
  8. 8.
  9. 9. HIGH AG M.AC<br />Osmolal gap = measured serum osmolality - (2 NA + gluco18 + bun2,8)<br />Corrected osmolal gap = <br /> measured serum osmolality - (2 NA + gluco18 + bun2,8 + ETOH4,6)<br />
  10. 10. HIGH AG M.AC<br />High <br /> normal <br />
  11. 11. Expected PCO2 : Measured PCO2<br />
  12. 12. YES<br />NO<br />YES<br />NO<br />YES<br />NO<br />YES<br />NO<br />
  13. 13. <5,5<br />>5,5<br />Urine AG = (UNA +UK) - UCL<br />
  14. 14. CASE:1An old man with abdominal pain & shock <br />An 85 year old man was admitted with severe abdominal pain and shock. <br />The abdominal pain started about 15:00hrs and quickly became quite severe. <br />There was no radiation to the back. <br />The patient was known to have an abdominal aortic aneurysm (AAA). <br />On arrival at hospital, the patient was shocked with peripheral circulatory failure and hypotension (BP 70-80 systolic). <br />The abdomen was guarded and quite tender. <br />He was distressed but able to talk and could understand instructions. <br />Past history was of hypertension (on metoprolol and prazosin) and angina (on Isordil).<br /> Prior to this event, the patient was mobile and independent.<br />
  15. 15. Biochemistry<br />at 15:20hrs was:(All results in mmol/l)<br /> Na+ =138,<br /> K+= 4.9,<br />Cl- =107,<br />Glucose= 11.2 = 201mgdl<br />Urea =12.8 = 230 mgdl <br />Creatinine= 0.188 =3,38mgdl. <br />Anion gap was =11<br />Mgdl = mmol /L * 18<br />
  16. 16. CONTINUE<br />A ruptured AAA was diagnosed clinically and he was transferred to theatre for emergency laparotomy. <br />On arrival in theatre BP was 120 systolic. <br />The patient was talking but distressed by pain with rapid respirations at a rate of 30/min.<br /> It was noted that neck veins were very distended. <br />An external jugular triple lumen central line and a brachial arterial line were placed before the surgical team had arrived in theatre. <br />CVP was +40 mmHg.<br />
  17. 17. CONTINUE<br /><ul><li>pre-oxygenation with 100% oxygen at 17:38 hrs </li></ul>(about 4.5 hours after onset of symptoms:<br /><ul><li>A lactate level collected at the same time as the blood gases was 8.3 mmol/l.</li></li></ul><li>
  18. 18. CONTINUE<br />Intra-operative findings were of almost total infarction of the small bowel and part of the stomach due to acute mesenteric vascular obstruction. <br />The AAA was un-ruptured. <br />The patient arrested and died on the table at 18:05hrs<br />
  19. 19. discussion<br />The anion gap is 11 & the chloride is slightly elevated.<br /> The urea & creatinine are elevated but are not high enough to support the idea of an acute renal failure causing an acidosis. <br />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. <br />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. <br />The bicarbonate on the initial biochemistry was 20but had decreased to 13.8 by the time of the gas collection. <br />This indicates the progressive development of the disorder.<br />
  20. 20. An Intoxicated Baby <br />An 8 month old female baby was admitted with a one day history of lethargy. <br />She had vomited several times. <br />Her mother said she appeared "intoxicated".<br />Examination confirmed :<br />the obtunded mental state but she was easily rousable and muscle tone was normal. <br />Resp rate was 60/min. <br />Pupils were normal. <br />There was no evidence of dehydration.<br />Abdomen was soft and non-tender. <br />BP was 112/62.<br />Peripheral perfusion was clinically assessed as normal. <br />Heart and chest examination was normal. <br />Plantar response was normal<br />
  21. 21. Investigations<br />Urine: pH 5.0, negative for glucose and ketones. Numerous calcium oxalate crystals were seen on urine microscopy<br />
  22. 22.
  23. 23.  A young man who ingested barium carbonate<br />A 22 year old man was admitted to hospital 1.5 hours after ingestion of about 10G of barium carbonate dissolved in hydrochloric acid.<br /> Symptoms included abdominal pain, generalisedareflexic muscle paralysis, increased salivation and diarrhoea.<br /> BP 180/110. <br />Pulse 92/min<br />
  24. 24. Initial biochemistry (in mmol/l) was:<br />
  25. 25.
  26. 26. Clinical Diagnosis<br />Acute self-inflicted poisoning with barium carbonate resulting in muscle paralysis (due to hypokalaemia) and acute lactic acidosis.<br />The hypokalaemia on presentation was due to the barium.<br /> 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). <br />The immediate cause of the lactic acidosis is not clear as their is not evidence of circulatory failure.<br />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.<br />
  27. 27. A man with diarrhoea and dehydration<br />A 44 year old moderately dehydrated man was admitted with a two day history of acute severe diarrhea. <br />
  28. 28.
  29. 29. YES<br />NO<br />
  30. 30. Comments<br />Pertinent points were the <br />acidaemia,<br /> elevated chloride, <br />normal anion gap<br />elevation of urea and creatinine. <br />Some pre-renal renal failure is present but there is no evidence of a high anion gap acidosis due to renal failure. <br />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). <br />Similarly tissue perfusion is still adequate enough to prevent development of a lactic acidosis. <br />Hypovolaemia results in secondary hyperaldosteronism which increases sodium reabsorptionbut increases excretion of K+ resulting in hypokalaemia.<br />
  31. 31. CASE<br />23-year-old Caucasian female referred for further evaluation of hypokalemic acidosis. <br />She was in her usual state of excellent health with normal growth and development until her second month of pregnancy. <br />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. <br />She was treated with oral potassium and bicarbonate supplements and then weaned these off after 4 months of therapy. <br />Six weeks later, she developed myalgias and collapsed due to profound weakness. <br />She was found to have a serum bicarbonate level of 14 mEq/L with a serum potassium of 1.9 mEq/L.<br />
  32. 32. P.E<br />Normal stature<br />BP 120/80 <br />No rash <br />Normal heart and lungs<br />No edema<br />No synovitis<br />
  33. 33. :LAB<br />
  34. 34. Which of the following is the correct diagnosis?<br />Type IV RTA<br />Diarrhea<br />Type I RTA<br />Renal tubular alkalosis<br />Proximal RTA<br />
  35. 35.
  36. 36. >5,5<br /><5,5<br />Urine AG = (UNA +UK) - UCL<br />
  37. 37. Which of the following is the correct diagnosis?<br />Type IV RTA<br />Diarrhea<br />Type I RTA<br />Renal tubular alkalosis<br />Proximal RTA<br />
  38. 38. Points to Remember<br />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.<br />Without proper treatment, chronic acidity of the blood leads to<br /> growth retardation, <br />kidney stones, <br />bone disease, <br />chronic kidney disease, <br />and possibly total kidney failure.<br />If RTA is suspected, additional information about the:<br /> sodium, <br />potassium, <br />and chloride levels in the urine <br />and the potassium level in the blood will help identify which type of RTA a person has.<br />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.<br />
  39. 39. Normal Renal Function<br />Proximal Tubule<br />Reabsorption: <br /><ul><li> HCO3- (90%) – carbonic anhydrase
  40. 40. calcium
  41. 41. glucose
  42. 42. Amino acids
  43. 43. NaCl, water</li></ul>Distal Tubule<br /><ul><li> Na+ reabsorbed
  44. 44. H+ (NH4+ or phosphate salts) excreted
  45. 45. molar competition between H+ and K+
  46. 46. Aldosterone</li></li></ul><li>Renal Tubular Acidosis<br />Type 2 RTA<br />Type 1 RTA<br />Type 4 RTA<br />
  47. 47. Type I Classic Distal RTA-Mechanism 1<br />Tubular lumen<br />Na+<br />Peritubular<br />Capillary<br />Na+<br />3Na+<br />ATPase<br />(-)<br />2K+<br />(-)<br />H+<br />Retention<br />K+<br />R-Aldo<br />K+ Wasting<br />Urine pH > 5.5<br />Ca-P stones<br />Cl-<br />ATPase<br />3Na+<br />H+<br />ATPase<br />H2O<br />2K+<br />(-)<br />T<br />HCO3-<br />OH- + CO2<br />K+<br />Cl-<br />ATPase<br />(-)<br />H+<br />
  48. 48. Type I Classic Distal RTA-Mechanism 2<br />Tubular lumen<br />Na+<br />Peritubular<br />Capillary<br />Na+<br />3Na+<br />ATPase<br />(-)<br />2K+<br />(-)<br />H+<br />Retention<br />K+<br />R-Aldo<br />K+ Wasting<br />Urine pH > 5.5<br />Ca-P stones<br />Cl-<br />ATPase<br />3Na+<br />H+<br />ATPase<br />H2O<br />2K+<br />(-)<br />T<br />HCO3-<br />OH- + CO2<br />K+<br />Cl-<br />ATPase<br />(-)<br />H+<br />
  49. 49. Type I Distal RTA-Mechanism 3<br />Tubular lumen<br />Na+<br />Peritubular<br />Capillary<br />Na+<br />3Na+<br />ATPase<br />(-)<br />2K+<br />(-)<br />K+<br />R-Aldo<br />K+ Wasting<br />Urine pH > 5.5<br />Ca-P stones<br />Cl-<br />Backleak of H+<br />ATPase<br />3Na+<br />H+<br />H+<br />ATPase<br />H2O<br />H+<br />Retention<br />2K+<br />(-)<br />T<br />HCO3-<br />OH- + CO2<br />K+<br />Cl-<br />ATPase<br />(-)<br />H+<br />
  50. 50. Causes of Hypokalemic Distal RTA (Type I)<br /><ul><li>Primary
  51. 51. Idiopathic
  52. 52. Sporadic
  53. 53. Familial
  54. 54. Autosomal dominant
  55. 55. Autosomal recessive
  56. 56. CA anhydraseII
  57. 57. Deficiency (mixed I and II)
  58. 58. Secondary
  59. 59. Sjögren’s syndrome
  60. 60. Hypercalcuria
  61. 61. Rheumatoid arthritis
  62. 62. SLE
  63. 63. Hyperglobulinemia
  64. 64. Ifosfamide
  65. 65. Primary biliary cirrhosis
  66. 66. Lithium
  67. 67. Amphotericin B
  68. 68. Renal transplant</li></li></ul><li>Major Clinical Manifestations of Distal RTA<br /><ul><li>Nephrocalcinosis
  69. 69. Hypercalcuria
  70. 70. Hypocitraturia
  71. 71. High urine pH -> calcium phosphate stones
  72. 72. Hyperuricosuria
  73. 73. Growth retardation
  74. 74. Osteopenia</li></li></ul><li>NEXT LECTURE<br />Metabolic alkalosis<br />MEXED DISORDERS<br /> (PH normal)<br />