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مقاربة غازات الدم الشرياني (الماض الاستقلابي طبيعي الفجوة)

مقاربة غازات الدم الشرياني (الماض الاستقلابي طبيعي الفجوة)

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ABG3 Series Presentation Transcript

  • 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) Δ 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]
  • 6.
  • 7. Gap:gap ratio??
  • 8.
  • 9. HIGH AG M.AC
    Osmolal gap = measured serum osmolality - (2 NA + gluco18 + bun2,8)
    Corrected osmolal gap =
    measured serum osmolality - (2 NA + gluco18 + bun2,8 + ETOH4,6)
  • 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 = 201mgdl
    Urea =12.8 = 230 mgdl
    Creatinine= 0.188 =3,38mgdl.
    Anion gap was =11
    Mgdl = 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.
  • 17. CONTINUE
    • pre-oxygenation with 100% oxygen at 17:38 hrs
    (about 4.5 hours after onset of symptoms:
    • A lactate level collected at the same time as the blood gases was 8.3 mmol/l.
  • 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
  • 22.
  • 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:
  • 25.
  • 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.
  • 28.
  • 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
  • 35.
  • 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.
  • 39. Normal Renal Function
    Proximal Tubule
    Reabsorption:
    • HCO3- (90%) – carbonic anhydrase
    • 40. calcium
    • 41. glucose
    • 42. Amino acids
    • 43. NaCl, water
    Distal Tubule
    • Na+ reabsorbed
    • 44. H+ (NH4+ or phosphate salts) excreted
    • 45. molar competition between H+ and K+
    • 46. Aldosterone
  • Renal Tubular Acidosis
    Type 2 RTA
    Type 1 RTA
    Type 4 RTA
  • 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+
  • 50. Causes of Hypokalemic Distal RTA (Type I)
    • Primary
    • 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
    • 68. Renal transplant
  • Major Clinical Manifestations of Distal RTA
    • Nephrocalcinosis
    • 69. Hypercalcuria
    • 70. Hypocitraturia
    • 71. High urine pH -> calcium phosphate stones
    • 72. Hyperuricosuria
    • 73. Growth retardation
    • 74. Osteopenia
  • NEXT LECTURE
    Metabolic alkalosis
    MEXED DISORDERS
    (PH normal)