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اختلال اسيد - باز. Approach to the Arterial Blood Gas. عباس مدنی دكتر. کودک 3 ساله ای از نظراختلال رشد برسی شده ، دستگاههای آندوکرین ، گوارش ، قلب ، ریه وعصبی طبیعی اند. نکات مهم آزمایشات عبارتند از:. Important points for assessing tissue oxygenation.
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اختلال اسيد - باز Approach to the Arterial Blood Gas عباس مدنیدكتر
کودک 3 ساله ای از نظراختلال رشد برسی شده ، دستگاههای آندوکرین ، گوارش ، قلب ، ریه وعصبی طبیعیاند. نکات مهم آزمایشات عبارتند از:
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
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
9year 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
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
Lactic Acidosis INH Ketoacidosis DKA Alcoholic ketoacidosis Renal Failure Uremia Toxins Ethylene glycol Methanol Salicylates Paraldehyde Differential Diagnosis AG Metabolic Acidosis
Ethylene glycol poisoning Differential Diagnosis AG 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
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)