Acid Base 1A Flashcards

1
Q

Physiologic acids originate from the metabolism of:

A
  • fats and carbohydrates (H2CO3)
  • protein (H2PO4; H2SO4)
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2
Q

Carbonic acid (H2CO3) is a product of:

A

metabolism of fats and carbohydrates

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3
Q

Steps in the formation of carbonic acid (H2CO3) from the products of fat and carbohydrate metaboilism:

(Equation)

A
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4
Q

What enzyme catalyzes the formation of H2CO3 from CO2 and H2O?

A

carbonic anhydrase (CA)

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5
Q

Products of protein metabolism/oxidation of sulfur-containing AAs:

A
  • H2PO4-
  • H2SO4-

ALSO BUFFERED BY BICARBONATE

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6
Q

Equation for determining physiologic plasma pH:

A

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

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7
Q

Plasma pH is derived from the ratio of what two molecules?

A
  • HCO3- : PCO2
  • pH = 6.1 + log([HCO3-]/0.03PCO2)
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8
Q

Plasma pH is dependent on what two molecules?

A
  • HCO3-
  • PCO2 (CO2)
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9
Q

Normal arterial blood pH range:

A

7.38 - 7.44

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10
Q

Abnormally elevated pH level and associated condition:

A

>7.44

alkalemia

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11
Q

Abnormally low pH level and associated condition:

A

<7.38
acidemia

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12
Q

The four primary acid-base perturbations:

A
  1. respiratory acidosis
  2. respiratory alkalosis
  3. metabolic acidosis
  4. metabolic alkalosis
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13
Q

Acid-base perturbations can exist singly or as combined pathologies. What is the only impossible combination?

A

respiratory alkalosis with respiratory acidosis

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14
Q

Metabolic and respiratory acid-base disorders result from:

A

Blood HCO3- and/or PCO2 imbalances

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15
Q

Normal compensation for a metabolic acid-base disorder (metabolic acidosis or metabolic alkalosis):

A

Lungs blow-off or retain CO2

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16
Q

Normal compensation for a respiratory acid-base disorder (respiratory acidosis or respiratory alkalosis):

A
  • Kidneys alter HCO3-, H+, K+ reabsorption or excretion
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17
Q

Derangements in plasma pH are usually caused by:

A
  • an underlying condition.
  • underlying condition needs to be corrected in order to resolve acid-base imbalance.
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18
Q

Morbidity and mortality of acid-base disorders depends on:

A
  • the risk associated with underlying disorder causing the acid-base imbalance.
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19
Q

Respiratory acidosis results from:

A
  • impaired ability to expire CO2.
  • CO2 equates with H+ load, pH decreases as plasma CO2 (i.e. PCO2) rises above normal.
20
Q

Hypercapnia is:

A
  • excessive carbon dioxide in the bloodstream.
  • typically caused by inadequate respiration.
21
Q

A nonvolatile acid (fixed acid) is:

A
  • an acid produced in the body from sources other than carbon dioxide.
  • not excreted by the lungs.
22
Q

The nonvolatile acids are excreted by:

A

the kidneys

23
Q

All acids produced in the body are nonvolatile except:

A
  • carbonic acid, which is the sole volatile acid.
  • excreted as CO2 by lungs.
24
Q

Charge of fixed (non-volatile) acids:

A
  • Net negative charge; anionic.
  • Buffered by renal HCO3- retention and H+ secretion.
25
Q

The endogenous buffering time line:

A
  • Seconds: plasma and interstitial bicarbonate buffers H+.
  • Minutes: bone & intracellular buffers buffer H+.
  • Hours: interstitium and plasma cells swap extracellular H+ for intracellular K+.
  • Several hours: changes in ventilation.
  • Days: kidneys mediate H+ excretion and increase bicarbonate secretion.
26
Q

Normal plasma bicarbonate (HCO3-) level:

A

24 meq/L.

27
Q

Normal plasma PCO2 level:

A

40 mm Hg.

28
Q

Acidemia can be caused by either:

A
  • increased PCO2 (respiratory)
  • decreased HCO3- (metabolic)
29
Q

Draw algorithm to determine whether respiratory or metabolic acidemia.

A
30
Q

Alkalemia can be caused by either:

A
  • decreased PCO2 (respiratory)
  • increased HCO3- (metabolic)
31
Q

Draw algorithm to determine whether respiratory or metabolic alkalemia.

A
32
Q

Two ways RBCs remove/carry CO2:

A
  1. CO2 diffuses through the plasma membrane of a RBC, and:
    • CO2 + H2O (CA catalyzed) → H2CO3 → H+ + HCO3-.
    • HCO3- swapped out of RBC for extracellular Cl-.
    • H+ build-up causes conformational change in Hb.
    • H+ binds to deoxyHb.
  2. CO2 diffuses through the plasma membrane of a RBC, and directly binds to deoxyHb to form carboxyhemoglobin.
33
Q

Steps in how RBCs release oxygen and HCO3- into plasma:

A
  1. CO2 diffuses through the plasma membrane of a RBC, and:
    • CO2 + H2O (CA catalyzed) → H2CO3 → H+ + HCO3-.
    • HCO3- swapped out of RBC for extracellular Cl-.
    • H+ build-up causes conformational change in Hb. Oxygen released into plasma.
    • H+ binds to deoxyHb.
34
Q

Normal respiratory rate (resting adult):

A

16/min

35
Q

Tachypnea:

A

elevated respiratory rate (>16/min)

36
Q

Bradypnea:

A

depressed respiratory rate (<16/min)

37
Q

Process of CO2 expiration at alveolus:

A
  • RBC gets to alveolus. Oxygen diffuses into RBC.
  • Increased oxygen tension in RBC causes hemoglobin conformation change from deoxyhemoglobin to oxyhemoglobin:
  1. HHb + O2 → O2Hb + H+ → H+ + HCO3- → H2CO3 → H2O + CO2 (expired)
  2. CO2Hb → O2Hb + CO2 (expired)
38
Q

The two rightward reactions in RBCs at the alveoli that lead to CO2 expiration:

A
  1. HHb + O2 → O2Hb + H+ → H+ + HCO3- → H2CO3 → H2O + CO2 (expired)
  2. CO2Hb → O2Hb + CO2 (expired)
39
Q

Steps in how decreased ventilations lead to respiratory acidosis:

A
  1. Less CO2 blown-off.
  2. Hypercapnia occurs.
  3. Increased CO2 impedes the rightward reaction in RBC at alveoli.
  4. Plasma [H+] increases.
  5. High plasma H+ leads to low pH.
  6. Respiratory acidosis.
40
Q

Draw algorithm for determining whether compensated or non-compensated respiratory acidosis:

A
  • respiratory acidosis
    • low pH + high PCO2 (> 40)
41
Q

Compensation rule one: acute respiratory acidosis:

A

HCO3- up 1 unit for every PCO2 up 10 units

42
Q

Compensation rule two: chronic respiratory acidosis:

A

HCO3- up 4 units for every PCO2 up 10 units

43
Q

Steps in how increased ventilations lead to respiratory acidosis:

A
  1. More CO2 blown-off.
  2. Reaction in RBCs at alveoli driven to the formation of CO2 + H2O.
  3. Plasma H+ lost as H2O.
  4. Low H+ leads to elevated pH.
  5. Respiratory alkalosis.
44
Q

Draw algorithm for determining whether compensated or non-compensated respiratory alkalosis:

A
  • respiratory alkalosis:
    • high pH + low PCO2
45
Q

Compensation rule three; acute respiratory alkalosis:

A

HCO3- down 2 for PCO2 down 10

46
Q

Compensation rule four; chronic respiratory alkalosis:

A

HCO3- down 5 for every PCO2 down 10

47
Q

The four respiratory compensation rules:

A
  • Acute respiratory acidosis: “Up 1 for 10”
  • Chronic respiratory acidosis: “Up 4 for 10”
  • Acute respiratory alkalosis: “Down 2 for 10”
  • Chronic respiratory alkalosis: “Down 5 for 10”