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)