ABG INTERPRETATION By Dr Ashraf Al Tayar MD

ABG INTERPRETATION By: Dr. Ashraf Al Tayar, MD, MRCP(I), Assistant Consultant Critical Care, KKNGH.

ABG Interpretation: Comprises 4 steps. • • Determine the process Determine the primary disorder Sharpen the diagnosis Determine compensation

I. Step 1: Use p. H to determine Acidosis - < 7. 35 Alkalosis - > 7. 45

II. Determine metabolic vs. Respiratory Metabolic disorders: - p. H changes in same direction as PCO 2 and HCO 3 - Metabolic acidosis p. H PCO 2 HCO 3 - Metabolic alkalosis p. H PCO 2 HCO 3

Respiratory disorders: - p. H change in opposite direction of HCO 3 and PCO 2 - Respiratory acidosis p. H PCO 2 HCO 3 - Respiratory alkalosis p. H PCO 2 HCO 3

Sharpen the Diagnosis - Calculate the AG - Calculate Osm. Gap - Calculate Urinary AG

AG: Na – ( CL + HCO 3) normal 10 (+/-) 2

• AG: - Paraproteinaemia - Hyperchloraemia - Hypoalbumenaemia ( AG 2. 5 / 1 gm /d. L in albumin) - Hypermagnesaemia - Hyponatraemia

AG : Metabolic acidosis (DD) (MUDPILERS) Methanol Uremia DKA Paraldehyde Isopropyl alcohol – Isoniazide Lactic acid Ethylene glycol Rhabdomyolosis Salycylate

Normal AG Metabolic acidosis (Hyperchloremia) A. Hypokalemia - Diarrhea - Urethral diversion - RTA - Mineralocorticoid deficiency - CAI: Acetazolamide B. Hyperkalemia - Renal failure (Early) - Renal disease: SLE Amylodosis Sickle cell - Sulphur toxicity

Urine AG - < - 10 extra renal causes - > + 10 Renal causes

Osmolal Gap - measured serum osm. – calc. osm. normal (10 – 15) OG DD: ( MEDIE ) Methanol Ethylene glycol Diuretic : Mannitol Isoprophyl alcohol Ethanol

Determine Compensation Metabolic acidosis PCO 2 = 40 + BE Metabolic alkalosis PCO 2 = 40 + 0. 6 X BE

Respiratory acidosis Acute : HCO 3 = PCO 2 – 40 / 10 + 24 Chronic : HCO 3 = PCO 2 – 40 / 3 + 24 Respiratory alkalosis: Acute : 40 – PCO 2 / 5 + 24 Chronic: 40 – PCO 2 / 2 + 24

Example 1: p. H: 7. 07 PCO 2: 28 HCO 3: 8 SBE: - 20

Example 2: p. H : 7. 33 PCO 2 : 20 HCO 3 : 12 BE : 12

Example 3 p. H : 7. 48 PCO 2 : 28 HCO 3: 22 BE : 2

Effects of Acid base change Acidosis CVS Inotropy Conduction- defect Arterial VD Venous VD Oxygen Delivery O 2 Hb binding 2, 3 DPG Neuromuscular Resp. dep Sensorium alkalosis Inotropy Altered coronary flow Digoxin toxicity Affinity 2, 3 DPG NM excitability Encephalopathy Seizures Resp. dep Electrolytes Hyper K+ Hyper Ca+ Hyperuricaemia Hypo K+ Hypo Ca+ Hypophosphatemia

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