Acid Base Disorders

Introduction

• NOTE: For interpretation of arterial blood gasses, go to:
  • Respirology --> Arterial Blood Gasses

Anion Gap Metabolic Acidosis

Normal Anion Gap Metabolic Acidosis

• Acidosis without an unmeasured anion
• Causes:
• • Urine diversion (gastrointestinal conduit - i.e. ilial conduit)
  • Failure of kidneys to excrete acid load
  • GI loss of bicarb (diarrhea, laxative abuse)
• Workup:
  • HISTORY is the most important diagnostic test
  • Look at kidney causes (Renal Tubular Acidosis)
    • Renal Tubular Acidosis (If renal function normal)
    • CKD (if abnormal renal function)

Metabolic Alkalosis

• One of two mechanisms:
  • Loss of H+
  • Retention of HCO3-
• #1 --> Rule out Milk Alkali Syndrome & Hypercalcemia!!
• Kidneys recognize Cl and HCO3 as equal, if give patient Chloride, they will get rid of extra bicarb. (if problem outside kidneys, urine chloride is low) 
• Effects:
  • Reduces myocardial contractility
  • Promotes peripheral vasoconstriction (decreases calcium)
  • Shifts oxyhemoglobin dissociation curve to the left (Bohr effect) --> reduces tissue O2
  • Increased cellular O2 consumption (glycolytic activity increased)
• Approach:
  • Hypervolemia - Aldosterone is ON
    • (i.e. Liddle's Syndrome (ENaC active), renin-secreting tumor, malignant HTN, renovascular HTN, primary hyperadlosteronism, liquorish)
  • Hypovolemic (Low or Normal BP)
    • GI Losses of H+ (vomiting)  --> Urine Chloride very low
    • Urinary Losses of H+
      • Diuretics (i.e. Thiazides block NaCl transporter in DCT, increased distal delivery of Na + Cl.  Na taken up by principal cell ENaC channel, causing K+ to be lost.  The intercalated cell is in the vicinity, takes up K+, secretes H+, which prevents severe hypokalemia).
    • Bicarb reabsorption
      • Dehydration causes RAAS activation.  AngII stimulates proximal Na reabsorption, and HCO3- comes along, which perpetuates metabolic alkalosis. 
• Labs:
  • Check urinary chloride (down in vomiting)

    • Chloride-Responsive	Chloride-Resistant
      Urinary Chloride < 15 mEq/L (some say < 20)	Urinary Chloride > 25 mEq/L (some say > 20)
      EXTRA-RENAL LOSS	RENAL LOSS
      1.  Loss of gastric acid 2.  Diuretics 3.  Volume Depletion 4.  Post-hypercapnia	NORMOTENSIVE Bartter syndrome and Gitelman syndrome   (Loop                        Thiazide) Diuretics HypoK+ (kidney things K+ = acidosis) HypoMg++   HYPERTENSIVE RAAS Excess Mineralocorticoid excess
      Replace chloride	Correct cause

• Causes:
  • GI Losses of Acid (NG suction, vomiting)
    • Chloride depletion causes HCO3 reabsorption in kidneys
  • Diuretics (Thiazide, Loop)
    • Through the loss of chloride (HCO3 reabsorption to maintain electrical neutrality)
  • Volume Depletion
    • Two mechanisms:
      • Increased renal sodium reabsorption = increased HCO3 reabsorption
      • Renin release --> aldosterone production --> Promotes H+ secretion in distal tubules.
    • Interesting: volume replacement does not correct it, but CHLORIDE replacement does.  Most resuscitation fluids have chloride so not clinically relevant.
  • Hypokalemia
    • Trans-cellular shift of H+ into cells
    • Increased H+ secretion in distal tubules.
  • Chronic CO2 retention
  • Organic Anions (citrate in blood transfusions [but need >8u], lactate in lactated Ringers, etc..), small effect
  • Consider genetic disorders
    • Bartter syndrome (mnemonic: B-  BAD: a lot worse than Gitelman)
      • Behaves like chronically on a loop diuretic
      • If not recognized in childhood, hyperkalemia and metabolic alkalosis causes problems.
      • Diagnosed typically in childhood
    • Gitelman syndrome (mnemonic: G - GOOD: less severe than Bartter)
      • Acts as if chronically on a high-dose thiazide
      • Diagnosis often made in adulthood
• Treatments:
  • Mild metabolic alkalosis from diuretic use does not require treatment
  • Correct volume depletion with isotonic saline!! 
  • Fix Mg and K+ abnormalities!!!! (very common cause)
  • GI losses (i.e. NG suction chronically)
    • Use PPI
  • Chloride Responsive:
    • Replace chloride if chloride-responsive (usually dehydrated anyway)
      • CL deficit = 0.2 x wt (kg) x (normal - current plasma chloride)
      •  Volume of 0.9% NaCl (L) = CL deficit / 154
    • Use Potassium Chloride if hypokalemia concomitant
    • Hydrochloric Acid IV (not advisable - very sclerosing, tissue necrosis if extravasate) - prev used in ICU, but no longer needed due to PPIs.
  • Chloride Resistant
    • Fix underlying cause
    • Can use acetazolamide --> blocks HCO3 reabsorption in proximal tubule
      • Essentially creates renal-tubular acidosis - wastes bicarb.
      • 5-10 mg/kg IV (or PO) - max effect at 15 hours
      • Promotes volume + potassium depletion (fix these first before giving acetazolamide)