Post on 30-Dec-2015
description
Approach to the Arterial Blood Gas
مدنی دكتر عباس
اسيد - اختالل باز
، 3کودک شده برسی رشد نظراختالل از ای سالهوعصبی ریه ، قلب ، گوارش ، آندوکرین دستگاههای
از. طبیعی عبارتند آزمایشات مهم نکات اند :
Important points for assessing tissue oxygenation
• This is the O2 that’s really available at the tissue level.
• Is the THb normal?– Low THb means the ability of the blood to
carry the O2 to the tissues is decreased
• Is perfusion normal?– Low perfusion means the blood isn’t even
getting to the tissues
Let’s Practice
12 year old diabetic presents with Kussmaul breathing
• pH : 7.05
• pCO2: 12 mmHg
• pO2: 108 mmHg
• HCO3: 5 mEq/L
• BE: -30 mEq/L– Severe partly compensated metabolic
acidosis without hypoxemia due to ketoacidosis
17 year old w/severe kyphoscoliosis, admitted for pneumonia
• pH: 7.37
• pCO2: 25 mmHg
• pO2: 60 mmHg
• HCO3: 14 mEq/L
• BE : -7 mEq/L– Compensated respiratory alkalosis due to
chronic hyperventilation secondary to hypoxia
9 year old w/hx of asthma, audibly wheezing x 1 week, has not slept in 2 nights; presents sitting up and using accessory
muscles to breath w/audible wheezes
• pH: 7.51
• pCO2: 25 mmHg
• pO2 35 mmHg
• HCO3: 22 mEq/L
• BE: -2 mEq/L– Uncompensated respiratory alkalosis with
severe hypoxia due to asthma exacerbation
7 year old post op presenting with chills, fever and hypotension
• pH: 7.25
• pCO2: 32 mmHg
• pO2: 55 mmHg
• HCO3: 10 mEq/L
• BE: -15 mEq/L– Uncompensated metabolic acidosis due to
low perfusion state and hypoxia causing increased lactic acid
Objectives
• Review causes of Non-anion gap Metabolic Acidosis
• Distinguish RTA Types 1, 2 and 4
• Treatment of RTA
Metabolic acidosis
Anion-Gap:• Acids associated with an
unmeasured anion are produced or exogenously gained
Metabolic Acidosis
Differential Diagnosis AG Metabolic Acidosis
“MUDPILES”• Methanol • Uremia• DKA• Paraldehyde• INH• Lactic acidosis• Ethylene glycol• Salicylates
Differential Diagnosis AG Metabolic Acidosis
Lactic Acidosis• INH
Ketoacidosis• DKA• Alcoholic ketoacidosis
Renal Failure• Uremia
Toxins• Ethylene glycol• Methanol• Salicylates• Paraldehyde
Differential Diagnosis AG Metabolic Acidosis
• Ethylene glycol poisoning
Metabolic acidosis
Anion-Gap:• Acids associated with an
unmeasured anion are produced or exogenously gained
• Treatment: – Correct underlying cause– (Bicarbonate: severe
acidemia)
Non-anion gap: Bicarbonate, chloride• “Hyperchloremic” acidosis• Renal vs. GI loss of HCO3-
• Treatment:– Bicarbonate therapy
Metabolic Acidosis
Figure obtained from MKSAP Edition 14
Non-anion gap Metabolic Acidosis
• “USED CAR”• U Uretero-Sigmoid Diversions
– Accum of urine in colon reab chloride & water by intestine secretion of bicarb into intestine
• S Saline administration• E Ethanol or Endocrinopathies
– Addisons, Spirinolactone, Triamterene, Amiloride, Primary Hyperparathyroidism
• D Diarrhea
• C Carbonic Anhydrase Inhibitors• A hyper-Alimentation• R Renal Tubular Acidosis
Metabolic Acidosis
Figure obtained from MKSAP Edition 14
Urine anion gap (UAG)
Urine anion gap = [Na+] + [K+] – [Cl-]
• Normal: zero or positive
• Metabolic acidosis: NH4+ excretion increases (which is excreted with Cl-) if renal acidification is intact
• GI causes: “neGUTive” UAG
• Impaired renal acid excretion (RTA): positive or zero
• Often not necessary b/c clinically obvious (diarrhea)
Metabolic Acidosis
“USED CAR”“MUDPILES”
Figure obtained from MKSAP Edition 14
Renal Tubular Acidosis
Normal Renal FunctionProximal Tubule
Reabsorption:
• HCO3- (90%) – carbonic anhydrase
• calcium
• glucose
• Amino acids
• NaCl, water
Distal Tubule
• Na+ reabsorbed
• H+ (NH4+ or phosphate salts) excreted
• molar competition between H+ and K+
• Aldosterone
Renal Tubular AcidosisType 2 RTA Type 1 RTA
Type 4 RTA
Type 1 RTA
• First described, classical form
• Distal defect decreased H+ secretion
• H+ builds up in blood (acidotic)
• K+ secreted instead of H+ (hypokalemia)
• Urine pH > 5.5
• Hypercalciuria
• Renal stones
Type 1 RTA
Causes:• Primary
– Idiopathic, sporadic– Familial – AD, AR
• Secondary –– Autoimmune (SLE, Sjogren’s, RA)– Hereditary hypercalciuria, hyperparathyroidism, Vit D
intoxication– Hypergammaglobulinemia– Drugs (Amphotericin B, Ifosfamide, Lithium)– Chronic hepatitis– Obstructive uropathy– Sickle cell anemia– Renal transplantation
Type 1 RTA
Treatment:
• Alkali replacement:– 1-3mmol/kg/day bicarbonate– Sodium citrate tolerated better than sodium
bicarb– Potassium citrate if hypokalemia
Serrano A and Batlle D. N Engl J Med 2008;359:e1
A 37-year-old man was referred for evaluation of distal renal tubular acidosis
Type 2 RTA
• Proximal defect
• Decreased reabsorption of HCO3-
• HCO3- wasting, net H+ excess
• Urine pH < 5.5, although high initially
• K+: low to normal
Type 2 RTA
Causes:• Primary
– Idiopathic, sporadic– Familial: Cystinosis,
Tyrosinemia, Hereditary Fructose intolerance, Galactosemia, Glycogen storage disease (type 1), Wilson’s disease, Lowe’s syndrome
• Fanconi’s Syndrome– Generalized proximal tubule
dysfunction– Proximal loss of phos, uric
acid, glucose, AA
• Acquired– Multiple Myeloma– Carbonic anhydrase inhibitors
(Acetazolamide)– Other drugs (Ampho B, 6-
mercaptopurine)– Heavy Metal Poisonings (Lead,
Copper, Mercury, Calcium)– Amyloidosis– Disorders of protein, Carb, AA
metabolism
– Hypophosphatemia, hypouricosuria, renal glycosuria with normal serum glucose
Type 2 RTA
Treatment:
• Alkali therapy:– 5-15mmol/kg/day bicarbonate
• Supplemental potassium
• Vit D
Type 4 RTA
• Aldosterone deficiency or distal tubule resistance to Aldosterone
• Impaired function of Na+/K+-H+ (cation) exhange mechanism
• Decreased H+ and K+ secretion plasma buildup of H+ and K+ (hyperkalemia)
• Urine pH < 5.5
Renal Tubular AcidosisType 2 RTA Type 1 RTA
LOW serum K+
Type 4 RTA
HIGH serum K+
Type 4 RTA
Acquired Causes Renin:
– Diabetic nephropathy– NSAIDS– Interstitial Nephritis
• Normal renin, Aldo:– ACEs, ARBs– Heparin– Primary adrenal response
response to Aldo:– Medications: K+ sparing
drugs (Sprinolactone), TMP-SMX, pentamidine, tacrolimus
– Tubulointerstitial ds: sickle cell, SLE, amyloid, diabetes
Type 4 RTA
Treatment:
• Dietary restriction of sodium
• Furosemide
What happened to Type 3 RTA?
• Very rare
• Used to designate mixed dRTA and pRTA of uncertain etiology
• Now describes genetic defect in Type 2 carbonic anhydrase (CA2), found in both proximal, distal tubular cells and bone
Renal Tubular Acidosis
Primary defect Serum K+
Urine pH
Other Causes
Type 1distal
H+ secretion decreased
Low-nl > 5.5 Renal stones
Autoimmune (SLE, Sjogrens)HypercalciuriaDrugs (Ampho B, Ifosfamide, lithium)Hypergammaglobulinemia
Type 2proximal
HCO3- reab decreased
Low-nl < 5.5, although high initially
Multiple MyelomaAcetazolamideHeavy Metal Poisonings (Lead, Copper, Mercury, Calcium)AmyloidosisDisorders of protein, Carb, AA metabolism
Type 4 Aldosterone deficiency, cation exchange decreased
High < 5.5 Aldosterone deficiencyDiabetic nephropathy SpirinolactoneInterstitial nephritisObstructive uropathyRenal transplant
Take Home Points
• Review causes of Non-anion gap Metabolic Acidosis– Renal vs. GI losses– “USED CAR”
• Distinguish RTA Types 1, 2 and 4– See Table + Some clues:– Type 1: renal stones, hypercalciuria, high urine pH despite
metabolic acidosis– Type 2: think acetazolamide and bicarbonate wasting; Fanconi
syndrome– Type 4: aldosterone deficiency and hyperkalemia
• Mainstay of treatment of RTA– Bicarbonate therapy
Anion Gap
Unmeasured Cations:
• total 11 mEq/L– Potassium 4– Calcium 5– Magnesium
2
Unmeasured Anions:• total 23 mEq/L
– Sulfates 1– Phosphates 2– Albumin 16– Lactic acid 1– Org. acids 3Na + UC = Cl + HCO3 + UA
140 + 11 = 104 + 24 + 23151 = 151
UA - UC = Na - (Cl + HCO3); Anion Gap = Na - (Cl + HCO3)