• affect reaction rate (product/reactant in many reactions)
• affect protein function (affect charge)
• affect free plasma conc. of other cations (ex: calcium)
• can exchange with other cations (Na/H) (K/H)

• acidemia- below 7.37
• alkalemia- above 7.42

volatile

fixed

• catabolism of proteins and phospholipids (produce 50 mmol/day of fixed acid)
• pathophysiological states
  • ketoacids
  • lactic acids
  • ingestion of salicylic acid
  • formic acid
  • glycolic and oxalic acid

sulfuric acid

phosphoric acid

• mix of weak acid and its conjugate or weak base and its conjugate acid
• resists change in pH when H is added or removed from buffered solution

• chemical buffer (form bicarb)
• respiration (blow of CO2)
• kidney

• EC fluid
  • bicarb
  • inorganic phosphate
  • plasma proteins
• IC fluid
  • cell proteins (Hb)
  • organic phosphates
  • bicarb/CO2
• bone
  • mineral phosphate
  • mineral carbonates

• concentration of buffer system components
• nearness of buffers pKa to pH of solution

• we can blow off CO2
• the kidney can make HCO3

• abundant (350 mEq of HCO3)
• bicarb system is open
  • conc. of HCO3 and CO2 are readily adjusted by respiration and kidney function

• increases in CO2 and decreases in HCO3
• removal of extra carbon dioxide via lungs to bring CO2 back to normal
• CO2 goes below normal due to hyperventilation
• kidneys add new HCO3 to blood and excrete hydrogen
• plasma pH is back to normal

organic phosphates

proteins

• in CO2 form
• accompany with organic anion
• exchange for potassium

In alkalemia, H leaves the cells

In acidemia, H enters cells

• present in high conc.
• oxyHb has lower pKa (6.9)
• deoxyHb has higher PKa (7.9)
• pH in venous blood is 7.37, so deoxyHb can serve as great buffer for H

• reabsorb filtered HCO3
• excrete fixed H
  • titratable acid buffered by phosphate
  • as NH4
• synthesis and reabsorption of new HCO3 accompanies both excretion of H as titratable acid and NH4

1. HCO3 filtered into nephron
2. H moved into PCT cell via Na/H antiport
3. HCO3 reabsorbed wtih no net secretion of H and little change in tubular pH
4. create H2CO3
5. via carbonic anhydrase, form CO2 and H2O

• ECF volume expansion and contraction (change starling forces at peritubular capillaries)
• increases in Ang II increase Na/H exchange in PCT, lead to increase in HCO3 reabsorption (contraction alkalosis)
• loop diuretics, thiazide diuretics, vomitting lead to contraction alkalosis as well)

• stimuates Na/H antiporter in PCT with decreased E.C volume
• increase secretion of H into lumen leads to increased HCO3 reabsoption
  • this leads to alkalosis

• leads to decrease reabsoption
  • decreased capillary oncotic pressure
  • increase hydrostatic capillary pressure

• in acidosis, we increase secreted hydrogen, leading to increase in HCO3 reabsorption
• in alkalosis, we decrease secretede H, leadin to decrease reabsorption of bicarb.

• mainly at alpha intercalated cells in CD via H/ATPase and K/H ATPase
• depends on amount of urinary buffer available in urine (20 mEq/day)
• for each H secreted, one HCO3 is synthesized and reabsorbed

Remember, minimum urine pH is 4.4 (at this point, H/ATPase wont pump H's into lumen because gradient against the pump is too strong)

PCT

thick ascending limb

alpha intercalated cells of CD

Remember, we only can get 20 mEq/day excreted as titratable acid, so the other 30 needs to go via NH4.

• NH3 diffuses or NH4 secreted through Na/H antiporter into lumen
• HCO3 reabsorbed

1. diffuse into lumen in CD
2. secreted H traps it there
3. NH4 is excreted

Remember, for every H secreted, HCO3 regenerated.

Lower pH, the higher NH3 diffusion into lumen

• cause
  • increased production of ingestion of fixed acid
  • decreased excretion of fixed acid
• associated symptoms/signs
  • H/K exchange in ICF affected
  • decreased plasma pH, decrease HCO3, decrease PCO2 
  • increased anion gap
• compensation mech.
  • hypervent. (decrease PCO2)
  • kidney excrete H and synthesize HCO3

• increase pH, increase bicarb., increase PCO2
• cause
  • loss of fixed acid
  • increase HCO3, so pH increase
• associated symptoms
  • H leave ICF in exchange for K, so hypokalemia
• compensation
  • hypoventilation (increase PCO2)
  • if vomitting, excess HCO3 not excreted in kidney due to contraction alkalosi

• cause
  • hypovent. cause increase PCO2 and decrease pH
  • ICF buffers CO2 in RBC's
• clinical signs
  • increase PCO2, decrease pH, increase HCO3
• compensation
  • increase titratable acid and NH4 excretion
  • HCO3 synthesis and reabsorption increase
  • lungs cant compensate since they are the cause of disorder

• cause
  • hyperventilation leading to decrease PCO2, which increase pH
  • ICF buffers when CO2 leave RBC
• clinical sign
  • increase pH, decrease HCO3, decrease PCO2
• compensation
  • decrease titratable acid excretion
  • decrease NH4 excretion
  • decrease HCO3 synthesis and reabsorption
  • lungs cant compensate because they cause the problem