Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pulm > Acid-Base Regulation > Flashcards

Acid-Base Regulation Flashcards

1
Q

what is the main physiologic buffer and where is it produced?

A

bicarbonate (HCO3-), produced by the kidneys when there is acidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what happens when carbon dioxide reacts with water?

A

CO2 + H2O <> H2CO3 <> H+ + HCO3-

catalyzed by carbonic anhydrase, which is abundant in lung alveoli and renal peritubular epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the equation for the physiological bicarbonate buffer system? (this one is just straight memorization)

A

pH = 6.1 + log(HCO3-/0.03PCO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the fate of sulfur-containing amino acids, and why is this important when considering acid-base regulation?

A

sulfur-containing amino acids are oxidized into sulfuric acid (H2SO4)

H2SO4 is a significant contributor to the daily acid load

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is a key intracellular buffer within erythrocytes?

A

hemoglobin!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how does bone play a role in acid-base regulation?

A

skeletal system has massive reserve of base which can be released in response to acidemia, and bone can also uptake some H+

bone plays significant role in managing acute acid load, more so in metabolic acidosis than respiratory acidosis (sensitive to HCO3- levels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

explain how acidemia influences electroneutrality

A

when there is sufficient acidemia, H+ translocates into cells

electroneutrality must be maintained, so H+ moving into cells results in movement of other ions, for example: Cl- follows H+ (erythrocytes), or intracellular K+/Na+ is swapped out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the general time course of buffering in response to acidemia?

A
  1. plasma HCO3- increases immediately following introduction of acid load
  2. interstitial HCO3- increases ~15mins
  3. with decreased HCO3-, non-bicarbonate buffering systems (bone, intracellular buffering) become more important, ~2-4 hours as H+ translocates into cells
  4. changes in ventilation within hours
  5. several hours - days, kidneys mediate H+ excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

why does it make sense that venous blood is slightly more acidic than arterial blood?

A

higher CO2 content!

CO2 + H2O <> H2CO3 <> H+ + HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

in simplest form, how can you diagnose respiratory alkalosis/acidosis vs metabolic alkalosis/acidosis?

A

low pH + low HCO3- = metabolic acidosis

low pH + high PCO2 = respiratory acidosis

high pH + high HCO3- = metabolic alkalosis

high pH + low PCO2 = respiratory alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is going on (in a basic/general sense) if there is acidemia with a low HCO3- and an elevated PCO2?

A

metabolic acidosis + co-existing respiratory acidosis

no compensation because both systems are failing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the 5 basic steps of diagnosing what kind of acid-base disorder is going on?

A
  1. evaluate pH to determine acidosis/alkalosis
  2. compare HCO3- and PCO2 against pH to determine metabolic/respiratory
  3. evaluate whether compensation is occurring
  4. if compensation factor is not moving in the appropriate direction, there is at least 2 acid-base disorders co-existing
  5. use difference between plasma Na+ and sum of plasma Cl- and HCO3- to determine anion gap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the 3 ways by which metabolically generated CO2 carried in the blood?

A
  1. HCO3-
  2. carbaminohemoglobin
  3. protonated hemoglobin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what reaction does high O2 tension in the alveolar capillaries cause?

A

Haldane effect: erythrocytes trade CO2 (carbaminohemoglobin) and H+ bound to hemoglobin for inspired O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how do erythrocytes contribute to compensatory buffering following respiratory acidosis?

A

CO2 diffuses into erythrocytes, which then produce HCO3-

intracellular HCO3- is exchanged for extracellular Cl-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the predicted compensatory rise in HCO3- during acute vs chronic respiratory acidosis?

A

acute respiratory acidosis: 1 meq/L increase in HCO3- per 10mmHg increase in PCO2 (.1 to 1)

chronic respiratory acidosis: 4 meq/L increase in HCO3- per 10mmHg increase in PCO2 (.4 to 1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the predicted compensatory decrease in HCO3- during acute vs chronic respiratory alkalosis?

A

acute respiratory alkalosis: 2 meq/L decrease in HCO3- per 10mmHg decrease in PCO2 (.2 to 1)

chronic respiratory acidosis: 5 meq/L decrease in HCO3- per 10mmHg decrease in PCO2 (.5 to 1)

18
Q

what are 3 ways in which the kidneys regulate normal acid-base balance?

A
  1. HCO3- reabsorption
  2. generation of new HCO3-
  3. H+ excretion
19
Q

what are 3 ways by which metabolic acidosis can develop (generally speaking)?

A
  1. kidneys can’t handle dietary acid load
  2. increase in plasma [H+]
  3. decrease in plasma [HCO3-]
20
Q

what happens when low pH (during metabolic acidosis) triggers the chemoreceptors in the carotid bifurcations and aortic bodies?

A

cranial nerves IX (glossopharyngeal) and X (vagus) relay to medullary respiratory center, triggering increase in ventilation for the purpose of blowing off CO2, thereby lowering [H+]/raising pH

21
Q

chronic diarrhea is a very common cause of what type of acid-base disorder?

A

with diarrhea, a lot of HCO3- is lost in stool —> metabolic acidosis

22
Q

pattern of breathing associated with respiratory compensation for metabolic acidosis

A

Kussmaul breathing: deep, sighing breaths - increased tidal volume more than respiratory rate

23
Q

what is the predicted respiratory compensation for metabolic acidosis? How is this determined?

A

1.5mmHg drop in PCO2 per 1 meq/L decrease in HCO3-

Winter’s formula - used to determine whether appropriate respiratory compensation has occurred:
PCO2 = 1.5[HCO3-] + 8 +/- 2

if the calculated and measured PCO2 are equal, appropriate compensation has occurred, but if measured PCO2 is less than calculated there is respiratory alkalosis with no compensation

[remember that HCO3- and PCO2 should move in opposite directions]

24
Q

what is the predicted respiratory compensation for metabolic alkalosis? How is this determined?

A

Winter’s formula - used to determine whether appropriate respiratory compensation has occurred:
PCO2 = 0.7[HCO3-] + 20 +/- 5

if the calculated and measured PCO2 are equal, appropriate compensation has occurred, but if measured PCO2 is greater than calculated there is respiratory acidosis with no compensation

[remember that HCO3- and PCO2 should move in opposite directions]

25
Q

which acids do the kidneys primarily secrete as a compensatory mechanism for acidemia?

A

predominantly enhanced NH4+ elimination (as NH4Cl), some H+ elimination (urine acidification)

26
Q

how is anion gap calculated and what does it mean? what is the normal value range?

A

anion gap (AG) is the difference between the predominant plasma cation (Na+) and the sum of the most abundant plasma anions (HCO3- and Cl-)

AG = Na+ - (HCO3- + Cl-)
normal = 7-16 meq/L

the gap represents the difference between unmeasured cations minus unmeasured anions - increased gap results from decreased unmeasured cations or increase in unmeasured anions (most often)

for example, ketoacidosis or lactic acdiosis

27
Q

how would hypoalbuminemia affect the anion gap?

A

AG = Na+ - (HCO3- + Cl-)
normal = 7-16 meq/L

the gap represents the difference between unmeasured cations minus unmeasured anions

albumin is an unmeasured anion, so gap would be increased

28
Q

elevated anion gap strong suggests the presence of what?

A

AG = Na+ - (HCO3- + Cl-)
normal = 7-16 meq/L

the gap represents the difference between unmeasured cations minus unmeasured anions

elevated anion gap strongly suggests metabolic acidosis (ketoacidosis, lactic acidosis, etc)

29
Q

what would most likely cause the following anion gap metabolic acidosis?
a. lactic acidosis
b. ketoacidosis
c. salicylates acidosis
d. formic acidosis

A

a. lactic acidosis: common, several causes (hypoxia, extreme exercise, etc)
b. ketoacidosis: diabetes
c. salicylates acidosis: aspirin overdose
d. formic acidosis: methanol poisoning

30
Q

during metabolic acidosis, and in the absence of unmeasured anions, lost HCO3- is replaced by….

A

lost HCO3- is replaced by Cl- to maintain electroneutrality - normal anion gap metabolic acidosis (hyperchloremic metabolic acidosis)

hyperchloremia is common with normal anion gap metabolic acidosis

therefore, it is also common that plasma chloride is lowered with anion gap metabolic acidosis (due to unmeasured anions)

31
Q

how can the delta-delta difference be used to diagnose acid-base disorders?

A

delta-delta difference shows relationship between anionic acid accumulation and HCO3- loss

basal HCO3- = 24, normal anion gap is 12… so…
delta HCO3- = 24 - measured [HCO3-]
and
delta AG = AG - 12

if deltaHCO3- = deltaAG, then metabolic acidosis is the single acid-base disorder occurring

32
Q

from what is lactic acid derived and how is it metabolized?

A

derived from pyruvic acid, mostly from glycolysis or deamination of alanine

lactic acid buffered by HCO3- to yield lactate, which is metabolized into pyruvate

pyruvate is further metabolized into CO2 + H2O (preferred) or glucose, but either way new HCO3- is generated

33
Q

why does it makes sense that hypoxia or other reasons for hypoxemia cause lactic acid to build up?

A

catalysis of lactate requires entry into the mitochondria and oxidative metabolism, which requires sufficient O2

if O2 delivery is comprised, lactate (lactic acid) builds up

(cardiac arrest, shock, extreme exercise, alcoholism, etc)

34
Q

signs of hyperglycemia with ketones in the urine usually suggest what?

A

diabetic ketoacidosis

during starvation conditions or perceived starvation (lack of insulin/ insulin sensitivity), increased lipolysis results in abundance of free fatty acids which are delivered to the liver and metabolized into ketones

35
Q

what is the most common cause of normal anion gap metabolic acidosis?

A

diarrhea (GI loss of HCO3-)

36
Q

why would you likely see a lower urine [Cl-] in renal tubule acidoses (RTA)?

A

kidneys normally excrete H+ in response to acidosis, via distal acidification of urine (because it is excreted at distal portion of nephrons)

to maintain electroneutrality, Cl- is excreted with NH4+ as NH4Cl

however, if metabolic acidosis is due to renal dysfunction, there is an inability to excrete H+, and therefore Cl- would not follow

37
Q

how might diuretic usage cause metabolic alkalosis?

A

metabolic alkalosis = elevation in plasma [HCO3-] due to H+ loss

diuretic usage can cause hypovolemia —> contraction alkalosis around a set amount of HCO3-

38
Q

signs of hypokalemia and hypochloremia often accompany which type of acid-base disturbance?

A

metabolic alkalosis:

angiotensin II acts in kidneys to stimulate proximate Na+/H+ exchanger and Na+/HCO3- symporter - excess HCO3- impedes Cl- reabsorption (both negatively charged)

AII also stimulates aldosterone secretion, which causes K+ secretion as well

39
Q

explain the connection between metabolic alkalosis and hypokalemia

A

at cellular level, increased extracellular pH (low [H+]) creates favorable gradient for diffusion of H+ OUT of cells and K+ diffusion INTO cells (out of plasma —> hypokalemia)

hypokalemia can also CAUSE metabolic alkalosis, in which case low plasma K+ draws K+ out of cells, and H+ diffuses INTO cells (lower pH —> alkalosis)

all about maintaining electroneutrality in the plasma! K+ is moved because it is the most abundant intracellular cation

40
Q

what is the appropriate compensatory rules and shortcut for acute vs chronic respiratory acidosis?

A

acute:
1 meq/L rise in HCO3- per 10mmHg rise in PCO2 above 40
(up 1 for 10 or 0.1 for 1)

chronic:
4 meq/L rise in HCO3- per 10mmHg rise in PCO2 above 40
(up 4 for 10 or 0.4 for 1)

41
Q

what is the appropriate compensatory rules and shortcut for acute vs chronic respiratory alkalosis?

A

acute:
2 meq/L drop in HCO3- per 10mmHg drop in PCO2 below 40
(down 2 for 10 or 0.2 for 1)

chronic:
5 meq/L drop in HCO3- per 10mmHg drop in PCO2 below 40
(down 5 for 10 or 0.5 for 1)

42
Q

what is the appropriate compensatory rules and shortcut for metabolic acidosis vs alkalosis, respectively?

A

metabolic acidosis:
PCO2 = 1.5[HCO3-] + 8 +/- 2
(1.5 + 8)

metabolic alkalosis:
PCO2 = 0.7[HCO3-] + 20 +/- 5
(0.7 plus 20)

Pulm (30 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions