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Acid Base Disorders

- - - - Normal AG: Adding HCl lowers HCO3 and raises Cl-
        
        Normokalemic
        
        K+ sparing diuretics: Spironolactone
        
        Type 4 RTA
        
        Adrenal Failure
        
        Isotonic NaCl administration: Cl- replaces HCO3 in ECF. HCO3 deficiency causes NAGMA
        
        Hypokalemic
        
        Enteric HCO3 loss: Diarrhea, Fistulas
        
        Renal HCO3 loss: Type 2 RTA
        
        Decreased urinary acidification: Type 1 RTA
      - High AG
        
        Lactic Acidosis: Hospitalized patients, serum lactate > 4 mol/L, AG frequently > 25 mEq/L. Can be due to hypoxemic causes or Non-hypoxemic (main ones = Metformin toxicity, Zidovudine toxicity)
        
        Uremia: Increased H2SO4 and H2PO4 in plasma. GFR < 20 mL/min. AG rarely > 20 mEq/L. Serum HCO3 usually > 15 mEq/L
        
        Ketoacidosis: DM, EtOH abuse, prolonged starvation. Excess H+ consumes ECF HCO3- . B-hydroxybutyrate + acetoacetate replace ECF HCO3- and raise AG. AG > 25 mEq/L
        
        Toxins: ASA, Ethylene Glycol, Methanol, Acetominophen in the critically ill
        
        ASA: tinnitus, vertigo, nausea. Mixed acid base disorder in adults. 1st respiratory alkalosis (ASA directly stimulates CNS respiratory centers), then AG metabolic acidosis (ASA uncouples oxidative phosphorylation, AG usually 20-25 mEq/L)
        
        Ethylene glycol: Sx of acute inebriation (w/o EtOH odor). Increased serum osmolality, urine and vomitus may fluoresce (Wood's light). Onset of AGMA after 12-18 hours. It is metabolized to glycol and oxalic acids . The oxalate anions precipitate with **Ca2+ -> calcium oxalate crystals**. Oliguria after 2-3 days. Oxalate precipitates with Ca2+ in renal tubules.
        
        Methanol toxicity: Sx of acute inebriation (w/o odor of EtOH). Increases serum osmolality. Onset of AGMA after 8-18 hours. Formic acid raises AG > 25 mEq/L. Formaldehyde -> bilateral retinal injury (12-36 hrs). Cystoid macular edema (snow storm vision) -> optic neuritis -> optic atrophy. Osmolal gap = measured Sosm - calculated Sosm
        
        Pyroglutamic acidosis (PGA): Critically ill patients treated with acetaminophen.-> pyroglutamic acidosis (due to glutathione depletion) -> AG > 25 mEq/L
      - Delta Gap: Used clinically to ID a mixed acid-base disorder when there is an AG metabolic acidosis. It is the (amount of increase in AG) - (amount decrease in HCO3). If > + 6 or < -6 then 2nd acid-base process.
  - - - Chronic:
        -Serum HCO3 increases 3.5 mEq/L for each 10 mmHg increase in PaCO2
        -Increased renal NH4+ secretion -> new HCO3 production
      - Acute:
        -Serum HCO3 increases 1 mEq/L for every 10 mmHg increase in PaCO2
- - - - NaCl responsive (UCl < 20): metabolic alkalosis resolves when you administer isotonic NaCl solution
        
        NaCl loss
        
        CF: increased NaCl loss in sweat. Urine Cl- concentration is < 20 mEq/L.
        
        Fecal NaCl loss: Cl- losing diarrheas (congenital chloridorrhea, villous adenoma)
        
        Renal H+ loss
        
        Previous loop or thiazide diuretic use
        
        Gastric H+ loss
        
        Vomiting: generates 1 mEq of plasma HCO3 for each H+ lost from the stomach
        
        NG suctioning
      - NaCl resistant (UCl > 20): metabolic alkalosis does not improve with administration of isotonic NaCl solution. If you give these patients isotonic NaCl, it will actually make their metabolic alkalosis worse
        
        Low or Normal BP
        
        Current loop or thiazide diuretic use
        
        Maintain:
        Decreased ECF volume -> increased RAAS -> increased proximal NH4+ secretion and increased distal H+ secretion -> maintains metabolic alkalosis.
        Decreased ECF Cl- -> decreased HCO3 secretion by type B intercalated cells -> maintains metabolic alkalosis
        Note: ENaCs are not mentioned. They cause NAGMA, not metabolic alkalosis.
        
        Initiate: Increased NaCl delivery to CCDs -> increased flow rate and increased luminal (-) charge in the CCD -> increased renal H+ and K+ loss -> initiates metabolic alkalosis
        
        Tubulopathies (Bartter syndrome, Gitelman syndrome)
        
        Elevated BP
        
        Liddle Syndrome
        
        Cushing Syndrome
        
        Hyperaldosteronism
        
        SAME
        
        Renal Artery Stenosis
  - - - Acute: Serum HCO3 decreases 2 mEq/L for each 10 mmHg decrease in PaCO2
      - Chronic: Serum HCO3 decreases 4 mEq/L for each 10 mmHg decrease in PaCO2