Acid Base Physiology Flashcards

1
Q

Normal bicarb serum level?

A

24 mEq/L

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2
Q

How is bicarb measured in venous serum (normal blood lab draw)?

A

as total CO2, which is bicarb + dissolved CO2 (tiny portion)

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3
Q

Bicarbonate buffer equation?

A

CO2 + H2O HCO3- + H+

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4
Q

Normal pulmonary partial pressure of CO2?

A

40mmHg CO2

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5
Q

Normal serum pH?

A

7.4, which is 40nEq/L of H+, bicarb of 24 mEq/L, and CO2 of 40 mmHg

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6
Q

What is metabolic acidosis?

A

decreased bicarbonate

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7
Q

What is metabolic alkalosis?

A

increased bicarbonate

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8
Q

What is respiratory acidosis?

A

increased CO2

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9
Q

What is respiratory alkalosis?

A

decreased CO2

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10
Q

Effect of respiratory disorders on bicarbonate concentration?

A

minimal, slightly increased with respiratory acidosis and decreased with respiratory alkalosis (bicarb and CO2 always change in the same direction)

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11
Q

Buffers of the urinary tract?

A

phosphate and ammonia

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12
Q

What is the isohydric principle?

A

All buffers move in the same direction

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13
Q

Compensation if change in CO2 (respiratory) is the primary disturbance?

A

Change the CO2/bicarb ratio

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14
Q

Compensation if change in Bicarb (metabolic) is the primary disturbance?

A

Change the CO2 level

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15
Q

Timeline for lungs compensating for a metabolic disturbance?

A

Rapid, more difficult to correct metabolic alkalosis (have to try not to breathe to retain CO2)

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16
Q

Timeline for kidneys compensating for a respiratory disturbance?

A

Slower (hours-days), can tell the difference between an acute and chronic respiratory disturbance by the bicarb level

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17
Q

Relationship between changes in HCO3- and pCO2?

A

They always change in the same direction

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18
Q

2 causes of direct bicarbonate loss?

A

GI (diarrhea/intestinal fistulas), Type 2 RTA (impaired proximal tubule HCO3- reabsorption)

19
Q

Drug that can cause Type 2 RTA?

A

Acetazolamide, inhibits HCO3- reabsorption in the proximal tubule

20
Q

3 cause of increased acid generation?

A

Lactic acidosis (anaerobic respiration from shock), Ketoacidosis (DKA), or ingestion (ASA overdose, ethylene glycol, methanol)

21
Q

3 cause of decreased acid excretion?

A

Renal failure (reduced GFR)–> impaired NH4+ excretion, Type I RTA, and Type 4 RTA

22
Q

What is Type 1 RTA?

A

impairment of the distal H/ATPase; retain H+ ions when defective

23
Q

What is Type 4 RTA?

A

Hypoaldosteronism–> impaired H+ excretion and K+ secretion

24
Q

Causes of acute respiratory acidosis?

A

Anesthesia, sedative overdose, clogged airway

25
Q

Causes of chronic respiratory acidosis?

A

COPD, smoking

26
Q

Causes of H+ loss? (3)

A

1) GI loss (loss of gastric secretions- vomiting or NG suction),
2) urinary loss (loop/thiazide diuretics, hyperaldosteronism), and
3) movement into cells (hypokalemia)

27
Q

Most common cause of chronic respiratory alkalosis?

A

Pregnancy

28
Q

Acute causes of respiratory alkalosis?

A

Acute CNS diseases (CVA, meningitis, head trauma)

29
Q

Plasma AGAP change in respiratory disorders?

A

Doesn’t change

30
Q

Relationship between plasma Cl- and plasma HCO3- in respiratory acid base disorders?

A

Inverse relationship

31
Q

Plasma AGAP equation?

A

Na - (Cl +HCO3)

32
Q

Normal AGAP level?

A

8-12

33
Q

Why does acidosis cause hyperchloremia?

A

loss of HCO3- occurs due to buffering, Cl- ions are reabsorbed to maintain electroneutrality

34
Q

How do you make new bicarbonate?

A

IC carbonic anhydrase, every proton you pump into the urine comes from IC carbonic anhydrase (synonymous with sending bicarb to the blood)

35
Q

What happens to Cl- and AGAP when A- (strong acid anion) is excreted into the urine?

A

normal plasma AGAP; increased Cl- concentration (maintain electroneutrality)

36
Q

What happens to Cl- and AGAP when A- (strong acid anion) is retained in the plasma?

A

increased AGAP; normal Cl- concentration

37
Q

What does your body do with reabsorbed lactate?

A

metabolize it to consume a H+ and make bicarb

38
Q

What does increased plasma AGAP tell you?

A

Unmeasured anion is being conserved (normally lactic acid)

39
Q

Urinary AGAP equation?

A

(Na+K) - Cl

40
Q

Normal urinary AGAP?

A

+10

41
Q

What causes the urinary AGAP to become more negative?

A

loss of bicarb to diarrhea increases ammonium in the urine–> chloride follows it–> UAG gets more negative

42
Q

Na+ concentration remains constant, Cl- changes. What is it?

A

Acid Base disorder (100%)

43
Q

Why are patients with reduced GFR more susceptible to acidotic conditions?

A

Increased acid load in a pt with reduced GFR–> more sever acidosis because they can’t enhance NH4+ production

44
Q

How do loop/thiazide diuretics cause a metabolic alkalosis?

A

They cause more Cl- than Na+ wasting, therefore HCO3- is reabsorbed more to maintain electroneutrality