Causes Anion Gap Metabolic acidosis (MUDPILES) Non-Gap Metabolic Acidosis Methanol (wood alcohol) blindness Renal tubular acidosis (RTA)renal bicarb loss Uremia Diarrhea & other bowel loss GI losses Diabetic ketoacidosis Carbonic anhyrdrase inhibitors* Paraldehyde (sedative hypnotic) Infection, INH, iron tablets Lactic acid Ethylene glycol (antifreeze) renal failure Salicylate *Although carbonic anhydrase inhibitors can cause non-gap acidosis, other diuretics (ie-thiazide and loop diuretics) cause metabolic alkalosis

Electrolytes: [Na+] [K+] [HCO3-] [Cl-]

140mEq/L 5.0 mEq/L 16 mEq/L 85 mEq/L

Arterial blood gas: pO2 95 mmHg pH 7.35 (-7.45) pCO2 30 mmHg 4 Steps in Assessment of AB Disorders 1. Examine pH: acidosis or alkalosis 2. What is a min or primary diagnosis: metabolic or respiratory 3. Calculate anion gap 4. Determine if there’s compensation Step 1: Determine acid or alkaline. pH = 7.35 acidosis Step 2: Determine type of acidosis. Low [HCO3-] (normal ~26mEq/L) metabolic acidosis Step 3: Determine cause of metabolic acidosis via anion gap  Anion gap = [Na+]-([Cl-] + [HCO3-]) or [Na+]- [Cl-] - [HCO3-]= 140-(85 +16) =39  Normal anion gap = 10± 2 mEq/L  Dx: metabolic acidosis with an anion gap increase

diuretic therapy (↑ bicarb conc) o Causes  Vomiting or GI suction (which liberates HCO3.reabsorption  Metabolic alkalosis (CP. Fall in ECF bicarbonate concentration b.151) o High pH.to plasma) + +  ECF decreasesstimulates aldosterone and ↑ distal exchange of Na and H ion ↑pH  Net result ↑*HCO3-+ and ↓ *H++  Diuretics or “Contraction alkalosis”  Proximally-acting or loop diuretics ↓ ECF and stimulation of aldosterone + distal tubule H secretion  ECF “contracts” (loses volume) around fixed amount of bicarb AKA contraction alkalosis  pH rises  Net result ↑*HCO3-+ and ↓ *H++ . Describe common metabolic acid base disorders. ↑ in pCO2 Alkalosis induced by either c. Elevation in ECF bicarbonate conc d.from +  Gut = diarrhea  loss of bicarb w/ attendant/resultant secretion of [H ] into plasma  Kidney = renal tubular acidosis o Characterisitics:  Chronic metabolic acidosis  Normal plasma anion gap  Absence of renal failure o Types  Distal: H+ secretion impaired  Proximal: faulty HCO3. ↓ in pCO2 Pathologic change in HCO3 Metabolic Acidosis o ↑*H++ and/or ↓*HCO3-]  Endogenous or exogenous acid addition. high bicarb o [HCO3-] added and/or [H+] loss  Vomiting.1. recognize them Acidosis induced by either a. renal leakage of HCO 3 o Causes  Impaired renal excretion  Renal failure  Tubular disorders impairing bicarb reabsorption  Increased acid production – diarrhea or endogenously – lactic acid or ketoacids  MUDPILES (CP. aldosteronism (↑ bicarb production). 148)  addition of H+  Loss of HCO3.

brain tumor o Pulmonary  COPD. acute obstruction. o Metabolic – myxedema (hypothyroidism) Respiratory Alkalosis (hyperventilation)  High pH. severe pulmonary edema or pneumonia. salicylates. pregnancy (proges stimulates resp drive).4 o HCO3 = 15 mEq/L  lowered (n. EXTRA Respiratory Acidosis (hypoventilation)  Low pH.26-28) o pCO2 = 15 mm . respiration arrest. primary alveolar hypoventilation. gram neg sepsis. hi metab COMPENSATION  Immediate buffering  Rapid compensation o Respiratory compensation  hours o Metabolic compensation  days o Compensation can be complete or partial  Ultimate correction (ideally) Concept  Every acid base disorder has PRIMARY change and COMPENSATORY change  Compensatory change is in system (resp or renal) that is OPPOSITE to primary change  Primary metabolic problem  resp compensation  Primary resp problem  metabolic compensation  Degree of compensation predictable -> bring pH back to normal is goal Renal Compensation for Chronic Respiratory Acidosis (COPD)  pCO2 rise = primary insult (normal 40-60)  Kidney – retains more HCO3  pH normalizes  Reflection of this in blood o pH 7.4 o HCO3 = 35 mEq/L  elevated (n.26-28) o pCO2 = 50 mm Renal Compensation for Respiratory Alkalosis -/  pCO2 drop = primary insult /kidney – excretes more HCO3 pH normalizes  Reflection in blood o pH 7. restrictive lung ds. low pCO2  pCO2 ↓ (hyperventilation due to anxiety. high pCO2  pCO2 ↑ (hypoventilation secondary to lung ds. brainstem lesions) causing rise in pH o Metabolic  Fever. drugs slowing RR) cause fall in pH  Causes  Sedative overdose.

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