Acid Base Balance Flashcards
Buffers
- Prevent change in pH when H+ added or removed from solution
- Most effective w/in 1 pH unit of pK of the buffer
Extracellular Buffers
- Major buffer is HCO3-
- Produced from CO2 and H2O
- pK of CO2/HCO3- buffer pair is 6.1
- Minor buffer: Phosphate
- pK of H2PO4-/HPO42- buffer pair is 6.8
- important as a urinary buffer
Intracellular Buffers
- Organic phophates
- Proteins
- Imidazole & alpha-aminos have pKs in physiologic pH range
- Hemoglobin is major intracellular buffer
- deoxyHb better buffer than oxyHb @ physiologic pH
Henderson Hasselbalch Equation
pH=pK+ log([A-]/[HA]
A- is base form of buffer (proton acceptor)
HA is acid form of buffer (proton donor)
-When concentrations of A- and HA are equal the pH of the solution is equal to the pK of the buffer
Reabsorption of Filtered HCO3-
- Occurs mainly in proximal tubule
- H+ & HCO3- produced in proximal tubule cells
- From CO2 and H2O
- CO2 and H2O combine to form H2CO3
- Catalyzed by carbonic anhydrase
- H2CO3 dissociates into H+ and HCO3-
- H+ secreted into the lumen
- via Na+/H+ exchanger
- HCO3- reabsorbed
- In the lumen, H+ combines w/ filtered HCO3- to form H2CO3
- Dissociates into CO2 and H2O
- Catalyzed by brush border carbonic anhydrase
- Results in net reabsorption of filtered HCO3-
- Does NOT result in net secretion of H+
Regulation of Reabsorption of Filtered HCO3-
- Filtered load:
- Increases result in increased rate of HCO3- reabsorption
- If plasma HCO3- high, filtered load exceed reabsorptive capacity- Metabolic Alkalosis
- HCO3- will be excreted in the urine
- pCO2
- Increases result in increased rates of HCO3- reabsorption- b/c supply of intracellular H+ for secretion increased
- Basis for renal compensation in respiratory acidosis
- Decreases result in decreased rates of HCO3- reabsorption - b/c supply of intracellular H+ for secretion is decreased
- Basis for renal compensation for respiratory alkalosis
- ECF Volume - Expansion results in decreased HCO3- reabsorption
- Contraction results in increased HCO3- reabsorption
- Angiotensin II - Stimulates Na/H exchange, increases HCO3- reabsorption
- Contributes to contraction alkalosis
Excretion of H+ as H2PO4-
- Amt of H+ excreted as H2PO4- depends on amt of urinary buffer
- H+ & HCO3- produced from CO2 & H2O
- H+ secreted into lumen by H+ ATPase
- HCO3- reabsorbed (“new” HCO3-)
- In urine, secreted H+ combines w/ filtered HPO42-
- Forms H2PO4- which is excreted
- H+ ATPase increased by aldosterone
- Process results in net secretion of H+ & reabsorption of HCO3-
- H+ secretion decreases urinary pH (minimum of 4.4)
- Amt of H+ as H2PO4- determined by urinary buffer and pK
Excretion of H+ as NH4+
-Depends on amount of NH3 synthesized and urine pH
-NH3 produced in renal cells from glutamine
-Diffuses down concentration gradient
-H+ & HCO3- produced from CO2 & H2O
-H+ secreted into lumen and combo w/ NH3 forming NH4+
-Diffusion trapping: NH4+ trapped in urine and excreted
-HCO3- reabsorbed
-The lower the pH in TF, the greater the excretion of H+ as NH4+
At low urine pH, NH4+>NH3
-In acidosis, adaptive increase in NH3 synthesis occurs
-Aids in excretion of excess H+
-Hyperkalemia inhibits NH3 synthesis
-Decreases H+ excretion as NH4+
-TYpe 4 renal tubular acidosis
Metabolic Acidosis
-Overproduction or ingestion of acid or loss of base
-Produces increase in arterial [H+]
-HCO3- buffers extra fixed acid
-Arterial [HCO3-] decreases
-Causes hyperventilation: respiratory compensation for metabolic acidosis
-Correction: increased excretion of fixed H+ as NH4+
-Increased reabsorption of HCO3-
-Chronic: Adaptive increase in NH3 synthesis
-
Serum Anion Gap
[Na+]-([Cl-] + [HCO3-])
- Represents unmeasured anions in serum
- Phosphate, citrate, sulfate, and protein
- Normal value: 12 mEq/L (range 8-16)
- In metabolic acidosis, [HCO3-] decreases as it buffers acid
- Anion gap increases if concentration of unmeasured anion increases to replace HCO3-
- Anion gap normal if [Cl-] increased to replace HCO3-
- Hyperchloremic metabolic acidosis
Metabolic Alkalosis
- Loss of fixed H+ or gain of base
- Decrease in arterial [H+]
- Arterial [HCO3-] increases
- Vomiting: H+ lost from stomach
- HCO3- remain s in blood and [HCO3-] increases
- Causes hypoventilation: respiratory compensation
- Correction: increased HCO3- excretion
- If accompanied by ECF contraction, HCO3- reabsorption increases secondary to activation of RAAS (worsens alkalosis)
Respiratory Acidosis
- Caused by decrease in respiratory rate and retention of CO2
- Increased arterial pCO2 causes increase in [H+] & [HCO3-]
- No respiratory compensation
- Renal Compensation: increased H+ excretion (titratable & NH4+)
- Increased reabsorption of HCO3-
- Acute: no renal compensation
- Chronic: Increased HCO3- reabsorption: pH increased
Respiratory Alkalosis
- Caused by increase in respiratory rate and loss of CO2
- Decreased arterial pCO2 causes decrease in [H+] & [HCO3-]
- No respiratory compensation
- Renal Compensation
- Decreased H+ excretion
- decreased reabsorption of HCO3-
- Hypocalcemia may occur b/c H+ and Ca2+ compete for binding sites on plasma proteins
- Decreased [H+] causes increased protein binding of Ca2+
