Flashcards in Acid Base Deck (105):
What is an acid?
substance that can donate H+
What is a base?
a substance that can accept H+
What are the 2 types of acids we produce?
carbonic = can be converted to CO2 = can be eliminated in the lungs
non-carbonic = cannot be converted to CO2 = must be excreted in kidney
Carbonic acids are made from the metabolism of ____
fats and carbohydrates
Non-carbonic acuds are made from the metabolism of _____
proteins and phospholipids
When we’re in a neutral balance, if we make 100 meq of acid, we’ll use 100 meq of _______ to stay stable.
Non-carbonic acids combine with _____ to be excreted by the kidney
buffers and anions
What is the clinical pH range?
7.8 and 6.8
What measures dissolved CO2 + bicarb conc in venous samples?
total CO2 conc
Why is pH outside of 7.8 to 6.8 incompatible with life?
bc every enzymes won't work outside this range
T or F: total CO2 conc always exceeds plasma bicarb conc.
(total CO2 is dissolved CO2 + bicrab)
What is the normal bicarb conc?
What is the difference between acidemia and acidosis?
acidemia is a condition and acidosis is a process
What is the equation for the bicarb buffer sys?
CO2 + H2O H+ + HCO3-
What is the key extracellular buffer?
Are humans an open or closed system? WHy is this important?
open (if we were closed out pH would be 6.1 = death)
*pH based on buffering ability of bicarb
What is the formula for determining pH?
(pH) H+ = 24 (CO2) / (HCO3)
What is the H+ when the pH = 7.4?
What is the trick to determine the H+ from the pH value?
80 - last 2 digits of pH to the right of the decimal pt
ex: pH 7.5 = H+ 30 nEq/L
What is the normal pH range?
7.35 to 7.45 (or 7.4)
What is the normla pCO2?
36-44 mmHg (40 mmHg)
Decreased bicarb is the primary dysfuction in ______
Increased bicarb is the primary dysfuction in ______
Metabolic disorders directly alter the conc of _______
Respiratory disorders directly alter ______
Increased CO2 is the primary dysfunction of _______
Decreased CO2 is the primary dysfunction of _______
T or F: The effects of bicarbonate as buffer is immediate in onset
What is the buffer effect in respirators disorders?
acidosis: bicarb increases
alkalosis: bicarb decreases
T or F: Buffers completely prevent pH changes.
F: they just attenuate, do not completely prevent the pH change
What is the isohydric principle?
all buffers change in the same direction
*if you know what one buffer system did (bicarb), you know what they all did
What is the buffer pair of the bicarb system? Where in the body does it act?
H+ donor: H2CO3
H+ acceptor: HCO3-
What is the buffer pair in the phosphate system? Where in the body does it act?
H+ donor: H2PO4
H+ acceptor: H2PO4 2-
What is the buffer pair in the ammonia system? Where in the body does it act?
H+ donor: NH4+
H+ acceptor: NH3
What is the buffer pair in the protein system? Where in the body does it act?
H+ donor: protein
H+ acceptor: protein
What do the buffer systems in the kidney do?
eliminate H+ in urine
What is the role of secondary (compensatory) mechanisms?
With a disturbance in pH, we need a whole body response above and beyond the buffer system to bring the pH back toward normal
*it is a second line of defense to maintain normal pH
T or F: compensatory mechanisms are invariable present in simple acid-base disorders.
What does the absence/dysfunction of a compensatory mechanism imply?
the pt has a mixed disorder
The respiratory system compensates for metabolic disrders by _____
altering CO2 (via lungs)
How is a respiratory disorder compensated?
alter bicarb levels
What is the difference in response time between respiratory compensation mechanisms and metabolic compensation mechanisms
the respiratory system can compensate very rapidly by inc CO2 levels when bicarb increases and vice versa
The metabolic compensation in the kidney takes longer
D. Intracellular buffers take longer to take effect, on the order of (mins, hours, days(
What is the fastest compensation mechanism?
bicarbonate in ECFV
What is the 2nd fastest compensation mechanism?
change of RR to change CO2 levels in lungs
how efficient is the respiratory compensatory mechanism
extremely efficient – even tiny changes in the pH, sensed by H+ sensors in the brainstem will result in ventilatory changes
Tell whether the following increase or decrease in metabolic acidosis:
HCO3-: decrease (primary)
pCO2: decrease (compensatory)
Tell whether the following increase or decrease in metabolic alkalosis:
HCO3-: increase (primary)
pCO2: increase (compensatory)
Tell whether the following increase or decrease in respiratory acidosis:
HCO3-: increase (compensatory)
pCO2: increase (primary)
Tell whether the following increase or decrease in respiratory alkalosis:
HCO3-: decrease (compensatory)
pCO2: decrease (primary)
What are the 3 golden rules of simple acid-base disorders:
1) PCO2 and HCO3 always change in the same direction.
2) The secondary physiologic compensatory mechanisms must be present. If not, it’s a mixed disorder
3) The compensatory mechanisms never fully correct pH, they bring toward normal. If they did overcorrect, then it’s a mixed disorder again
What is the process that reduces plasma bicarb conc?
What are the 6 causes of metabolic acidosis?
1. increased acid generation (lactic acid, ketoacid, ingestion of acids)
2. loss of bicarbonate (GI = diarrhea and intestinal fistulas; Renal = RTA type II)
3. decreased acid excretion (impaired NH4+ excretion)
4. renal failure/reduced GFR decreases NH4+ excretion
5. RTA type I (deficient ATPase and cannot excrete H+)
6. RTA type IV (hypoaldo)
What induces respiratory acidosis?
induced by hypercapnia (decreased alveolar ventilation/hypoventialtion) that causes and inc in CO2
In term of the buffering mechanisms, what happens during respiratory acidosis?
rapid rise in plasma HCO3-
kidney minimizes the change in extracellular pH by inc NH4+ excretion, generating new bicarb ions (slow response, takes 2-3 days)
What are some causes of acute respiratory acidosis?
What are some causes of chronic respiratory acidosis?
chronic muscular dystrophy
scoliosis that changes chest wall morphology
What process reduces CO3 due to increased alveolar ventilation?
Describe the buffering mechanism that goes on during respiratory alkalosis
rapid lowering of bicarb
then the kidney responds (1-2 days) by reducing net acid excretion (elim bicarb into the urine or decreases ammonium excretion)
What is a process that raises plasma bicarb substantially?
What is the etiology of metabolic alkalosis?
1. loss of H+ from GI tract (vomiting)
2. loss of H+ into urine (loop or thiazide diuretics)
3. excessive urinary net acid excretion (primary hyeraldosteronism)
WHat is the most common cause of chronic respiratory alkalosis?
What are causes of respiratory alkalosis?
acute CNS diseases (stroke, meningitis, or trauma)
acute respiratory alkalosis:
Acute respiratory acid base disorders always have a greater change in pH than chronic disorders because ....
A. Acute respiratory acid base disorders always have a greater change in pH than chronic disorders because the compensatory kidney mechanism is SLOW!!
How are respiratory acid base disorders differentiated as acute or chronic?
if bicarb conc has changed by...
1-2 mEq = acute
4-5 mEq = chronic
T or F: The Na levels (and therefore plasma osmolarity) is directly changed by respiratory acid-base disorders.
F: Na is NEVER changed DIRECTLY by acid-base disorders
T or F: Plasma Cl- is never directly changed by respiratory acid-base problems.
F: plasma Cl- changes inveselt with plasma HCO3 in respiratory acid base disorders
T or F: B. Excessive urinary net acid excretion (primary hyperaldosteronism or adrenal adenoma) makes blood progressively alkalemic. Explain.
T: bc because aldosterone also influences H+ secretion
Excessive urinary net acid excretion (primary hyperalsosteronism) makes blood progressively (acidemic or alkalemic) because aldosterone also influences H+ secretion.
How can metabolic alkalosis be assc with inc BP or volume explansion?
metabolic alkalosis caused by primary hyperaldosteronism bc aldo also regulates Na to inc its reabs. (it also makes blood more alkalemic bc it inc H+ excretion)
Whar are the only 2 disorders that cuase a blood sample to have bicarb > 30?
metabolic alkalosis and chronic respiratory acidosis (where they kidney is compensating)
If someone has metabolic alkalosis, and they have been vomiting/are volume contracted, what will thier urine chloride levels be?
low Urine Cl-
If someone has metabolic alkalosis, and they are hypervolemic, what do we think the cause of there alkalosis may be?
inappropriate secretion of acid into urine (urine Cl- >20 meq/L)
If a person has metabolis alkalosis due to primary hyperaldosteronism, will TB C- be low or high? Will giving them NaCl and water be helpful?
they would have excess total body Cl an giving them NaCl and water would not be helpful
What does urine Cl tell you?
if a person has metabolic alkalosis,
Cl- responsive (giving them saline will fix the problem) have urine Cl 20 meq/l
Describe how bicarb is reabsorbed
90% of FL of bicarb is reabs in the PCT:
*Na going in (via Na:H antiport) is the driving force
CO2 to diffuses into the cell or it enters via aquaporin 1 channels
CO2 combines with OH to form HCO2 via carbonic anahydrase which is then moved into ISF via Na-HCO3-CO3- cotransporter
Low pH drives bicarb reabs to (inc or decrease)
High pH drives bicarb reabs to (inc or decrease)
What drugs blocks carbonic anahydrase enzyme?
If a pt is taking acetazolamide, how could their pH be affected?
it blocks this Carbonic Anhydrase enzyme which will decrease the bicarb that is able to be reabs --> pH will decrease bc there will be less bicarb in the plasma to buffer it
acetazolamide will block the reabs of ...
Na and bicarb
T or F: we absorb all of the bicarb that the kidney makes
T or F: for every new molecule of bicarb that is made, a proton is excreted into the urine
What transporter secretes bicarb into the urine?
When do the H+:K+ ATPase perform more efficiently?
acidemia or excess also
What cells secrete bicarb (into urine)? What part of the nephron are they found?
beta-intercalated cell of the cortical collecting duct
What role the alpha intercalated cells play in renal acid-base balance?
they secrete H+ into the urine via H:K ATPase and make bicarb that is absorbed into the ISF thru bicarb:Cl- antiports
What type of cells do strict vegetarians have more of? Why?
Beta intercalated cells because their diet is more alkaline and therefore need to get rid of more HCO3- so that it doesn't bind up the H+ they have
Describe the movement of Na in the principal cell.
lumen --> epithelial cell --> ISF
Na channel ---> Na:K ATPase -->
What drugs and hormones work at the principal cells?
Amiloride and Triamterene inhibit the luminal Na channel here.
Aldosterone also works here.
Spironolactone and Epleronone (competitive antagonists of aldosterone) work on the blood side.
What are the 2 fates of the anions from strong acids (that fully dissociates at physiological pH)?
excretedf into the urine (creates normal plasma anion gap with inc plasma Cl-)
A- is reabs as an unmeasured anion (inc plasma anion gap, minimal change in plasma Cl-)
Why does Cl- stay they same when bicarb drops to buffer lactate when its present from poor perfusion?
because electroneutrality is maintained (the bicarb combined with equal amts of lactate to maintain neutrality in the body)
* but there wil be an inc AG to 20
Why does urine Cl- drop when bicarb is lost in the stool?
When bicarb is lost in the stool, electroneutrality is no longer balanced. Therefor`e, Cl- needs to be reabsorbed to maintain electro- homeostasis
(loss of bicarb = "there is no unmeasured anion so to keep elecroneutrality, so the kidney has to reabsorb more Cl-"
What do increases in the plasma anion gap from the normal value of10 -12 meq/l clinically reflect?
increased circulating unmeasured anions in the plasma.
What are the major causes of increased antion gap (with metabolic acidosis)?
1. renal failure
2. lactic acidosis
4. Ingestions of aspirin, ethylene glycol, methanol
What are the 3 major causes of normal gap metabolic acidosis?
3. some cases of chronic renal failure
Describe the assessment of low seum bicarb conc
1. check arterial blood gases to exclude chronic respiratory alkalosis
2. calculate serum AG
3. raised AG= lactic acidosis
4. normal AG --> calculate urine AG
5. positive UAG = RTA/problem with kidney acidification
6. negative UAG = GI bicarb losses (diarrhea)
How is phosphate homeostasis maintained?
urinary excretion of dietary phosphate
What is an effective urinary buffer?
How much H+ is excreted with phosphate daily?
10 - 40 meq
What is most frequently increased to handle an increased acid load/physiological needs?
NH4+ is ______ which is why it is trapped in the urine
Looking at two people, one with a low GFR and one with a normal GFR.
If you give them both an acid load, there’s only a slight drop in bicarb in the healthy person compared to a steep drop in plasma bicarb in the pt with the lower GFR. Why?
because the healthy person can drastically increase the NH4+ excretion they do not become acidotic. The person with the impaired GFR cannot secrete NH4+ as well
How is SIADH different than acid base disorders?
both Na and Cl would decreas (proportionally) in SIADH
it is acid base when Na is constant and Cl- is out of whack