Regulation of Acid Base Flashcards
Volatile acids eliminated by
lungs
CO2
hyperventilation- low pCO2
Hypoventilation- high Pco2
Nonvolatile acids eliminated by
kidneys
phosphoric and organic acids, HCO3
Normal pH of blood
7.4
Normal [HCO3]
24
Normal Pco2
40 mmHg
Normal ratio of [HCO3] and [H2co3]
20- most important to keep pH normal
What is the most principle form of transport of CO2 in blood
Bicarbonate
CO2 + H20 H2CO3 HCO3 + H
Mechanisms involved in pH regulation at kidney level
1) bicarbonate reabsorption- H+ secretion
2) urine acidification- H+ titration using bicarb or phosphate
3) ammonium production
carbonic anhydrase
dissociates H2CO3–> H20 + CO2 and CO2 is expired from lungs in order to prevent blood from becoming too acidic
Respiratory regulation of acidosis
decrease pH–> increase respiration rate–> dec CO2 and dec H2CO3–> increase pH
Respiratory regulation of alkalosis
inc pH–> dec respiration–> inc CO2 and H2CO3–> dec pH
Proximal tubule proton secretion and bicarb reabsorption
Apical membrane there is Na+/H+ antiporter, expelling H+ into tubular fluid and bringing Na into cell
CO2 from the blood enters the cell and is turned into H2CO3 via carbonic anhydrase. The H2CO3 is dissociated into HCO3 and H+. The H+ is secreted into the lumen, while the HCO3 is reabsorbed into the blood by the HCO3 and Na symporter
The Na/K/ATPase allows the gradient for the Na/HCo3 symporter
1:1 ratio of H+ secretion to bicarb absorption
80% of bicarb reabsorbed here
Distal and collecting tubule (alpha intercalated) proton secretion and bicarb reabsorption
Protons secreted via H ATPase and H/K ATPase
H+ formed via CO2 and carbonic anhydrase like in proximal tubule
1:1 ratio of H and bicarb
Distal and collecting tubule (beta intercalated) proton secretion and bicarb reabsorption
Inverted from the alpha intercalated cells
Secretes bicarb when there is excess HCO3 in blood and absorbs protons
Apical membrane has HCO3/Cl exchanger
Basolateral membrane has H+ ATPase
H+ titration in renal tubules use what buffer
Phosphate
H+ + HPO4 H2PO4
Allows acidification of urine
Bicarbonate can also be used to buffer H+ because of presence of carbonic anhydrase
Ammonium production in renal tubules
Enables kidney to excrete additional acid
Ammonium produced in tubular cells by deamidation of glutamine via glutaminase
NH3 combines with the H that dissociates from H2CO3 forming NH4 and is secreted into luminal fluid by the NH4/Na antiporter (also functions as Na/H exchanger) (bicarb is reabsorbed via Na/HCO3 symport)
Net Acid Secretion=
NAE= titratable acidity + [NH4] - [HCO3-]
estimation of total renal contribution to regulation of body fluids [H]
Urine anion gap=
UAG= ([Na+] + [K+])- [Cl-]
Normally, excretion of protons involves titration with NH3 to form NH4, so the anion gap in a normal individual is negative.
Anion gap for individuals who are unable to secrete protons or produce ammonium
amt of NH4 is reduced, so UAG is zero or positive
Plasma anion gap
PAG= [Na+] - ([Cl-] + [HCO3])
Normal conditions- PAG ranges from 8-16 mEq/L
PAG does what in metabolic acidosis
Increases bc HCO3 concentration in blood lowers
Davenport diagram
graphical representation of henderson hasselbach equation
plasma HCO3 plotted as function of pH
Acute causes of respiratory acidosis
depression of respiration– CNS alterations, neuromuscular disease (miasthenia gravis, guillan barre, muscular dystrophy), airway obstruction
Chronic causes of respiratory acidosis
COPD, neuromuscular disease, obesity hypoventilation syndrome
Respiratory acidosis
Increase in CO2 due to hypoventilation will result in an increase in pH (because of formation of carbonic acid).
Long term, the kidneys will start to secrete protons with ammonium, bicarb will increase, and pH will also rise back towards normal.
Respiratory alkalosis acute and chronic causes
hyperventilation, salicilate intoxication, fever
- acute- PaCO2 is below normal, serum pH is high
- chronic- PaCO2 is below normal, pH level is near normal
Respiratory alkalosis
CO2 eliminated by lungs, equilibrium of CO2 + H20–> Hc203 is now shifted towards left
H+ released by nonbicarbonate buffers combines with HCO3 and forms H2CO3 which forms CO2 and H20
- increasing CO2 eliminated, pCO2 decreases, plasma HCo3 decreases and pH increases
- with compensation, kidneys will start secrete more alkaline urine by secreting HCO3 and raising pH
Metabolic acidosis with normal PAG due to
due to bicarbonate loss (diarrhea, or proximal renal tubular acidosis) or decreased acid secretion/bicarb consumption (distal renal tubular acidosis or aldosterone deficiency)
Metabolic acidosis with high PAG due to
high acid input (ketoacidosis, lactic acidosis or intoxication with salicylate, methanol, ethylene glycol) or low acid output (renal failure)
Noncompensated metabolic acidosis
Additional H+ will buffer with HCO3 with non-bicarb buffers. That which is buffered by HCO3 will be transformed to CO2 and exhaled (chemoreceptors will activate ventilation).
Decrease in HCO3, and pH decrease, pCO2 will remain
Respiratory Compensated metabolic acidosis
Overtime, Increase in ventilation leads to decrease in PCO2
The equilibrium of H2CO3CO2 + H20 shifts towards right because of low CO2. This slows down the reaction of H + A–> HA (non bicarb buffers), making more H+ available for combination of HCO3 and generation of CO2 to be eliminated by lungs
Metabolic acidosis with resp and renal compensation
In addition to generation of more CO2, there is an increased reabsorption of HCO3 from beta intercalated cells in collecting tubule, increase in H+ excretion, increase in NH4 generation.
Causes of metabolic alkalosis
Loss of H+ due to vomiting or diuretic therapy (thiazides)
or Gain of HCO3 due to ingestion if anti acids, or renal HCO3 retention
Causes of renal HCO3 retention
Causes metabolic alkalosis
Due to ECF volume depletion (vomiting, diuretics, diarrhea) which is saline responsive, mineralocorticoid excess syndromes, gitelman’s syndrome, barter’s syndrome, renal failure
Metabolic alkalosis
Either when base is added or acid is removed (seen less frequently)
Decrease in H+ increases dissociation of HA and H2CO3. pH and plasma HCO3 increase at constant pCO2
Metabolic alkalosis w/ respiratory compensation
Respiratory compensation of increased base or decreased acid, but decreasing respiration and CO2 retention
Metabolic alkalosis w/ respiratory and renal compensation
Increased CO2 retention by lungs, and renal compensation by increasing HCO3 excretion and reducing rate of excretion of acid and ammonium generation
Treatment of acid base disturbance
treat underlying cause whether it’s systemic, respiratory, or renal
