AcidBasePathoFall2012

Is it normal or elevated na 149 cl 103 k 42 hco3 13 1

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Is it normal or elevated? Na: 149 Cl: 103 K 4.2 HCO3- 13 1. 33, elevated 2. 33, normal 3. 37, elevated 4. 37, normal
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Which acid-base disorder is present? Metabolic acidosis, compensated, with elevated anion gap
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Types of Acid-Base Disorders 1. Metabolic acidosis 2. Metabolic alkalosis 3. Respiratory alkalosis 4. Respiratory acidosis 5. Mixed acid-base disorders
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MG is a 56 y/o female with the following labs: ABG: pH 7.11, PaCO2 = 22, HCO3- = 10 Lytes (venous blood): Na = 140, Cl = 107, HCO3- = 10 What is her acid-base disturbance? 1. Metabolic acidosis 2. Metabolic alkalosis 3. Respiratory alkalosis 4. Respiratory acidosis
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MG is a 56 y/o female with the following labs: ABG: pH 7.11, PaCO2 = 22, HCO3- = 10 Lytes (venous blood): Na = 140, Cl = 107, HCO3- = 10 Is there compensation? 1. Yes 2. No
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Was the compensation appropriate? PaCO2 should decrease by 1.3 times the fall in plasma HCO3- 24 mEq/L – 10 mEq/L = 14 mEq/L 14 mEq/L x 1.3 = 18.2 So, you would expect the PaCO2 to fall by ~18 mmHg from the normal PaCO2 PaCO2 = 40 mmHg – 18 mmHg = 22 mmHg Hers is 22 mmHg! The compensation was appropriate.
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MG is a 56 y/o female with the following labs: ABG: pH 7.11, PaCO2 = 22, HCO3- = 10 Lytes (venous blood): Na = 140, Cl = 107, HCO3- = 10 What is her anion gap? What does it mean? 1. 23-No anion gap 2. 23-Elevated anion gap 3. 43-No anion gap 4. 43-Elevated anion gap
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Metabolic Acidosis ↓ pH due to ↓ serum HCO3- Determining the presence of an anion gap Helps determine etiology Guides treatment decisions
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Metabolic Acidosis Causes of elevated anion gap metabolic acidosis M ethanol U remia* D iabetic ketoacidosis (DKA)* P oisoning I ntoxication/Infection L actic acid* E thylene glycol S alicylates/Sepsis/Starvation
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Metabolic Acidosis Renal failure Accumulation of phosphate, sulfate, organic anions DKA Insulin deficiency  acute severe hyperglycemia  free fatty acid release and degradation  accumulation of β–hydroxybutyrate and acetoacetate (unmeasured anions)  HCO3- buffering of β–hydroxybutyrate and acetoacetate
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Metabolic Acidosis Lactic acid End product of anaerobic glucose metabolism Lactic acidosis Serum lactate > 4 mmol/L
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Metabolic Acidosis Shock Most common cause of lactic acidosis Poor tissue perfusion  tissue hypoxia anaerobic metabolism Medications Nucleoside-analog reverse transcriptase inhibitors (NRTIs) Metformin Propylene glycol (solvent for some IV medications) Propofol
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Metabolic Acidosis Normal anion gap/hyperchloremic states GI bicarbonate loss Diarrhea Drugs Cholestyramine  diarrhea Magnesium oxide  diarrhea Acid ingestion Rapid infusion of NaCl
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Metabolic Acidosis Normal anion gap/hyperchloremic states Renal tubular acidosis (RTA) Inability of kidneys to appropriately regulate acid-base homeostasis: 3 types Distal (Type I) Proximal (Type II) Distal (Type IV)
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Metabolic Acidosis Normal anion gap/hyperchloremic states Distal (Type I) RTA Impaired H+ secretion from distal tubule
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