Acid-Base Balance Flashcards
two types of acid in the body
volatile and non-volatile
volatile acid
CO2
non-voltatile acids (fixed acids)
Sulfuric acid
Phosphoric acid
Fixed acids overproduced in dz or ingested
ketoacids, lactic acid, salicylic acid
major extracellular buffer
HCO3-
minor extracellular buffer (most important as a urinary buffer)
H2PO4-
excretion of H+ as H2PO4-
titratable acid
major intracellular buffer
hemoglobin
deoxyhemoglobin vs oxyhemoglobin - which is the better buffer?
deoxyhemoglobin
pH = pKa + log[A-]/[HA]
Henderson-Hasselbalch
pH = pKa + log ([HCO3-] / 0.03 x PaCO2)
pH arterial blood
PCO2 = 1.5[HCO3-] + 8 ± 2
Winter’s formula
used to measure the appropriateness of the compensatory response and to evaluate for a mixed acid/base disorder.
winter’s formula
If measured PCO2 is higher than expected →
additional primary respiratory acidosis
If measured PCO2 is lower than expected –>
additional primary respiratory alkalosis
Serum anion gap =
[Na+] – ([HCO3-] + [Cl-])
Sodium - (bicarb + chloride)
mnemonic for ↑ Serum anion gap metabolic acidosis (aka “gap acidosis”)
MUDPILERS
M in mudpilers
Methanol (formate), Metformin
U in mudpilers
Uremia—advanced (chronic) renal failure—vs. early renal failure, which may cause normal anion gap metabolic acidosis
D in mudpilers
Diabetic ketoacidosis (β-hydroxybutyrate, acetoacetate)
P in mudpilers
Paraldehyde, Phenformin
I in mudpilers
Iron, Isoniazid
L in mudpilers
Lactic acidosis—shock, hypoxia, poor tissue perfusion; carbon monoxide, cyanide
E in mudpilers
Ethanol ketoacidosis (β-hydroxybutyrate, acetoacetate), Ethylene glycol (glycolate, oxalate)
R in mudpilers
Rhabdomyolysis
S in mudpilers
Salicylates—with concomitant respiratory alkalosis; prolonged Starvation ketoacidosis (β-hydroxybutyrate, acetoacetate)
Mneumonic for Normal anion gap metabolic acidosis (aka, hyperchloremic metabolic acidosis, “non-gap acidosis”)
“FUSED CARS”:
F in fused cars
Fistula (small bowel, pancreatic) → loss of HCO3-
U in fused cars
Ureterogastric conduits (eg, urine-diverting colostomy) → loss of HCO3-
S in fused cars
Saline administration (ie, saline worsens metabolic acidosis!) → gain of Cl-
E in fused cars
Endocrine—eg, hyperparathyroidism (a cause of type 2 renal tubular acidosis), Addison’s disease (aldosterone deficiency)
D in fused cars
Diarrhea → loss of HCO3-
C in fused cars
Carbonic anhydrase inhibitors (eg, acetazolamide)(most common cause of type 2 renal tubular acidosis in adults) → loss of HCO3-
A in fused cars
Acid infusion (eg, NH4Cl; hyperalimentation with TPN (total parenteral nutrition) if arginine HCl or lysine HCl are used as amino acids) → gain of Cl-
R in fused cars
- type 1 (↓ distal tubule H+ secretion): hypokalemia, urine pH>5.5
- type 2 (↓ proximal tubule HCO3- reabsorption): hypokalemia, urine pH<5.5.
S in fused cars
Spironolactone - blocks aldosterone receptors
Normal anion gap metabolic acidosis is caused by
loss of HCO3- or gain of Cl-, both of which usually result in hyperchloremic metabolic acidosis:
gain of Cl- is usually compensated by
loss of HCO3- → hyperchloremic metabolic acidosis
- loss of HCO3- is usually compensated by
Cl- retention → hyperchloremic metabolic acidosis