Acid Base Flashcards
the mechanisms for ___________ and __________ compensation occur rapidly, within minutes or hours
buffering; respiratory compensation
the mechanisms for ________ compensation are slower, requiring hours to days
renal
what are two forms of acid production?
volatile acid- CO2
non-volatile (or fixed) acid
____ is the end product of aerobic metabolism in the cells. Is this an acid?
CO2; NOT an acid, turns into a weak acid carbonic acid when combined with water
what is the rxn when CO2 reacts with H20?
CO2 + H20 —— H2CO3 ——— H+ + HCO3
H2CO3= carbonic acid (weak acid)
which enzyme catalyzes the rxn of CO2 and H20 to H2CO3?
carbonic anhydrase
what does H2CO3 dissociate into?
H+ and HCO3 (bicarb)
when carbonic acid dissociates into H and HCO3, what must happen with the H? where does this occur?
it MUST be buffered; occurs in the RBC
the CO2 produced by aerobic metabolism of cells goes where?
from the tissue to the capillary (more specifically the RBC)
Where is CO2 converted to H+ and HCO3?
in the RBC
what happens to H+ and HCO3 once formed in the RBC?
H+ is buffered and HCO3 diffuses out of the RBC into the plasma
where does HCO3 go once diffused into the plasma?
travels to the lungs to be converted back to CO2 (CO2 is then expired)
catabolism of what two things results in production of fixed acids?
proteins and phospholipids
what does being a volatile acid mean?
means that it will be expired in the lungs
which two acids are non volatile?
sulfuric acid (H2SO4) and phosphoric acid (H3PO4)
how do non volatile acids get excreted?
by the kidney
what must first happen to non volatile acids before getting excreted by the kidney?
they must be buffered in the body fluids
how are fixed acids buffered? what does this result in?
bicarb is pulled from the plasma/blood to buffer them in the body fluids (think of HCl and food when moving through the SI); results in loss of bicarb from the serum
what does a volatile acid and bicarb/base buffer form?
CO2 and H2O
how do the kidneys respond to loss of bicarb from buffering a fixed acid? what is the stable bicarb level the kidneys are aiming for?
they promote secretion of H and generate new bicarb; 24
primary disturbance of metabolic acidosis?
decrease in HCO3
normal range for bicarb?
24-31
normal range for anion gap?
8-12
normal range for PCO2?
35-45
normal range for Na?
135-145
normal range for Cl?
98-106
normal range for pH?
7.35-7.45
a decrease in bicarb and what affect on pH AND PCO2 will signal metabolic acidosis?
pH < 7.35 decreased PCO2 (more being ventilated out to bring out alkalosis)
what is the respiratory compensation for metabolic acidosis?
hyperventilation to get decreased PCO2 (<35)
what is the renal compensation of metabolic acidosis?
SLOWER response than resp
secretion of H+ and generation of new bicarb in the alpha intercalated cells
what are the two roles of the kidney on maintaining acid base balance? where do these processes occur?
1) . reabsorption of filtered HCO3 (ONLY occurs in the proximal tubule cells)
2) . excretion of H+ and generation of HCO3 (ONLY occurs in the distal tubule alpha intercalated cells)
why is excretion of H+ accompanied by new production of bicarb?
fixed H+ has to be buffered by bicarb and creation of new bicarb in the alpha intercalated cells occurs to replace those lost stores
we reabsorb filtered HCO3 to maintain a serum bicarb of __-___
24-26
what body problem can alter the balance of reabsorbing filtered bicarb?
volume depletion
alpha intercalated cell: what exchange happens on cell/lumen side?
H+ goes out of cell into the lumen while K+ goes into the cell from the lumen
alpha intercalated cell: what exchange happens on the cell/blood side with Na+ and K+?
Na+ goes into the blood from the cell and K+ goes into the cell from the blood
alpha intercalated cell: what exchange happens on the cell/blood side with HCO3 and Cl?
HCO3 goes into the blood from the cell and Cl goes into the cell from the blood
how is new bicarb made in the alpha intercalated cells?
aerobic metabolism causes formation of CO2…CO2 mixes with water and undergoes conversion to bicarb and H+
contraction alkalosis occurs during treatment of ________ and _________ diuretics; it is a complicating factor in the metabolic alkalosis caused by __________
loop and thiazides; vomiting
how do loop and thiazide diuretics cause contraction alkalosis?
diuretics remove fluid from the body and when they remove too much the body becomes volume contracted (depleted). then the RAAS system kicks in where angiotensin II acts on proximal tubule cells to increase Na/H exchange. H+ going out into lumen mixes with bicarb to form CO2 and H20…this goes into the cell to be converted back to H+ and bicarb, bicarb is then reabsorbed into the blood (with exchange of Cl)
what is the acid base disturbance with vomiting?
vomiting leads to loss of gastric HCl….loss of fixed H+ leads to metabolic alkalosis because HCO3 remains in the blood instead of the usual secretion to buffer H+
how is contraction alkalosis a complicating factor in the metabolic acidosis caused by vomiting?
so vomiting causes an ECF volume contraction…this activates RAAS, releasing angiotensin II and aldosterone…angiotensin II works in proximal tubule cells to promote H+ secretion and subsequently increase filtered bicarb reabsorption (causing metabolic alkalosis)….aldosterone acts on distal tubule alpha intercalated cells by promoting H secretion and bicarb reabsorption (leading to more alkalosis)
aldosterone also has an impact on what electrolyte during vomiting?
aldosterone increases K secretion in the principal cells so you can get hypokalemia
what affect does hyperkalemia have on aldosterone?
increased K in the blood increases aldosterone so that more K can be secreted
respiratory acidosis primary disturbance is?
increased PCO2 (pH is low)
acute respiratory acidosis: how is this corrected?
PCO2 enters RBCs for immediate buffering of high intracellular H+ (bicarb value HAS NOT changed)
chronic respiratory acidosis: how is this corrected?
there is a renal response to the acidosis with increase in H+ secretion and HCO3 regeneration (alpha intercalated cells)- there will be an INCREASE IN BICARB
Addison’s disease leads to what acid base disturbance?
leads to hypoaldosteronism….affects distal tubule cells…which can lead to hyperkalemia, metabolic acidosis due to decreased bicarb reabsorption, and volume contraction
an increase in serum CO2 content (bicarb) can represent what two acid base disorders? how do you distinguish between the two?
can be metabolic alkalosis or compensatory response to chronic respiratory acidosis (increase in pH with inc in bicarb represents metabolic alkalosis)
what is the primary disturbance for respiratory alkalosis?
decrease in PCO2 (increase in pH)
acute respiratory alkalosis: how is this corrected?
release of PCO2 from RBCs causing an intracellular alkalosis (NO CHANGE IN BICARB)
chronic respiratory alkalosis: how is this corrected?
renal compensation of decreased reabsorption of filtered bicarb in proximal tubule PLUS decreased distal tubule H secretion /HCO3 generation
proximal tubule cell: what exchange of ions occurs on the cell//lumen side?
Na goes into the cell from the lumen while H goes into the lumen
proximal tubule cell: what direction is the Na/K exchange on the cell/blood side ?
K moves into the cell and Na moves from the cell to the blood
proximal tubule cell: what direction is the HCO3/Cl exchange on the cell/blood side?
HCO3 moves into the blood and Cl goes from the blood into the cell
how is H+ and HCO3 inside the proximal tubule cell formed?
the proximal tubule cell only absorbs filtered bicarb….H/Na pump is increased so that H+ can combined with the filtered bicarb and create CO2 and H20. the CO2 and H20 enter the cell and convert back to bicarb and H+
what ion shares a pump with filtered bicarb in the proximal tubule cell (both things moving from the cell to the blood)?
Na
what are three effects of aldosterone on the late distal tubule and collecting ducts?
1) . Na reabsorption
2) . K secretion
3) . H secretion/HCO3 reabsorption
what three effects do you see in the distal tubule from hyperaldosteronism?
1) . volume expansion with hypertension
2) . hypokalemia
3) . metabolic alkalosis
what three effects do you see in the distal tubule from hypoaldosteronism?
1) . volume depletion with orthostatic hypotension
2) . hyperkalemia
3) . metabolic acidosis
what are two stimuli for aldosterone production?
1) . activation of RAAS secondary to decreased perfusion of kidney
2) . hyperkalemia
where is aldosterone produced?
in the adrenal cortex
how does chronic renal failure lead to metabolic acidosis?
decrease in GFR and reduced nephron numbers impair H secretion and generation of new bicarb
what is the anion gap of plasma?
when Na concentration is compared with the sum of HCO3 and Cl concentrations, the Na concentration is greater than HCO3 + Cl. The lack of anions must be filed with something else negative (in order to have electroneutrality) so there are unmeasured anions that make up this difference
what are 4 unmeasured anions of plasma?
plasma proteins, phosphate, citrate, sulfate
what is the equation to calculate anion gap?
Plasma anion gap = Na - (HCO3 + Cl)
the anion gap calculation is used most in diagnosing what acid base disorder?
metabolic acidosis (although can occur with metabolic alkalosis)
what anions can fill the anion gap?
one of the 4 unmeasured anions of plasma or Cl-
if lost HCO3 is filled by unmeasured anions, then the calculated anion gap is __________
increased
if lost HCO3 is filled by Cl-, then the calculated anion gap is ____________
normal
increased anion gap disorders (3)…why does this occur?
DKA, lactic acidosis, chronic renal failure: the decrease in bicarb is offset by the accumulation of organic anions created by these disorders
metabolic acidosis with normal anion gap disorders (2)
diarrhea and type 2 renal tubular acidosis (HCO3 depletion is offset by Cl accumulation)
DKA and lactic acidosis causes metabolic acidosis by what?
excessive production or ingestion of fixed H+
chronic renal failure causes metabolic acidosis by what?
inability to excrete fixed H+
diarrhea and type 2 renal tubular acidosis cause metabolic acidosis by what?
loss of HCO3
vomiting and hyperaldosteronism cause metabolic alkalosis by what?
loss of H+
loop or thiazide diuretics cause metabolic alkalosis by what?
volume contraction alkalosis
COPD causes respiratory acidosis by what?
disorder of gas exchange: decrease in CO2 exchange between pulmonary capillary blood and alveolar gas
hysterical hyperventilation cause respiratory alkalosis by what?
stimulation of medullary respiratory center
metabolic acidosis in DKA is caused by excessive production of what two fixed acids?
butyric acid and acetoacid acid
describe the ECF volume of DKA
volume contraction- loss of solute and water in urine due to an osmotic diuresis of glucose
____natremia is also seen in DKA
hypo
hyperkalemia in DKA is due to?
lack of insulin
what are the two things to give a pt for treatment of DKA?
insulin injection and IV saline
how is metabolic alkalosis due to vomiting treated?
IV saline and K+ (to correct the alkalosis, ECF volume must be restored even if the vomiting stops)
what happens to the ECF volume in vomiting?
volume contraction
what is the treatment for COPD causing respiratory acidosis?
ABX and lungs are mechanical ventilated
