NP15 Nephrology

Acid-Base Disorders

Essential Med Notes 2015

2. Evaluate compensation. If compensation is not appropriate, a second acid-base disorder is

likely present
compensation occurs in the same direction as the primary disturbance
metabolic acidosis: for every 1 mEq/L decrease in HCO3-, pCO2 should decrease by
1 mmHg
metabolic alkalosis: for every 10 mEq/L increase in HCO3-, pCO2 should increase by
5-7 mmHg
respiratory acidosis: for every 10 mmHg increase in pCO2, HCO3- should increase by
1 (acute) or 3 (chronic) mEq/L
respiratory alkalosis: for every 10 mmHg decrease in pCO2, HCO3- should decrease by
2 (acute) or 5 (chronic) mEq/L
3. Calculate Plasma AG
AG = [Na+] ([HCO3-] + [Cl-])
baseline = 12, range 10-14 mEq/L
AG can be altered by plasma albumin level: for each 10 g/L fall in albumin, lower baseline
AG by 3 mEq/L (e.g. if plasma [albumin]= 20 g/L, expect AG = 6 mEq/L)
4. If AG elevated, compare increase in AG with decrease in HCO3 if increase in AG < decrease in HCO3-, there is a coexisting non-AG metabolic acidosis
if increase in AG > decrease HCO3-, there is a coexisting metabolic alkalosis
5. Calculate Osmolar Gap
osmolar gap = measured osmolality calculated osmolality
calculated osmolality = (2 x [Na+]) + [urea] + [glucose] (all units are in mEq/L)
normal osmolar gap <10
if AG >10, consider: methanol poisoning, ethylene glycol poisoning, or another cause of
acidosis plus ethanol ingestion

Metabolic Acidosis
Etiology and Pathophysiology
1. Increased AG Metabolic Acidosis (4 types)
a. Lactic acidosis (2 types)
L-lactic acid
Type A: due to tissue hypoperfusion (any cause of shock), ischemic bowel, profound
hypoxemia
Type B: non-hypoxic multiple causes; the most common is failure to metabolize
normally produced lactic acid in the liver due to severe liver disease; other causes
include: excessive alcohol intake, thiamine deficiency, metformin accumulation
(metformin interferes with electron transport chain), certain antiretrovirals, large
tumours, mitochondrial myopathies
D-lactic acid: rare syndrome characterized by episodes of encephalopathy and metabolic
acidosis
occurs in the setting of carbohydrate malabsorption (e.g. short bowel syndrome),
colonic bacteria metabolize carbohydrate load into D-lactic acid, diminished colonic
motility and impaired D-lactate metabolism
b. Ketoacidosis
diabetic
starvation
alcoholic (decreased carbohydrate intake and vomiting)
c. Toxins
methanol (toxic to brain and retina, can cause blindness and brain death): metabolized to
formic acid
ethylene glycol (toxic to brain and kidneys): metabolized to oxalic acid (envelope shaped
crystals in urine) and multiple other acids
salicylate (e.g. ASA) overdose: causes acidosis due to salicylic acid, and also accumulation
of lactic acid (salicylate at toxic levels impairs electron transport chain) and ketoacid
(salicylate activates fat breakdown)
d. Advanced renal failure (e.g. serum Cr increased at least 5x above baseline a very low GFR
causes anion retention, and renal disease leads to impaired bicarbonate production)
2. Normal AG Metabolic Acidosis (Hyperchloremic Acidosis)
diarrhea (HCO3- loss from GI tract)
RTA
type I RTA (distal): inability to secrete H+ in collecting duct, leading to impaired
excretion of ammonium into urine
type II RTA (proximal): impaired HCO3- reabsorption
type IV RTA: defective ammoniagenesis due to decreased aldosterone, hyporesponsiveness
or hyperkalemia

Useful Equations
AG = [Na+] - [Cl] - [HCO3] (normal
range = 10-14 mEq/L)
Calculated serum osmolality =
2Na + BUN/2.8 + glucose/18

Causes of Osmolar Gap

Methanol
Ethylene glycol
Ethanol
Polyethelene glycol
Mannitol
Sorbitol

Causes of Increased AG Metabolic

Acidosis
MUDPILES CAT
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde
Isopropyl alcohol/Iron/Ibuprofen/
Indomethacin
Lactic acidosis
Ethylene glycol
Salicylates
Cyanide and Carbon monoxide
Alcoholic ketoacidosis
Toluene
or
KARMEL
Ketoacidosis
ASA
Renal failure
Methanol
Ethylene glycol
Lactic acidosis