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Respiratory Physiology > Acid-Base Homeostasis > Flashcards

Acid-Base Homeostasis Flashcards

(43 cards)

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1
Q

pH

A

-log[H] (no units)

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2
Q

[CO2]

A

(0.0301 mM/ mm Hg) x PCO2

units of mM OR mmol/L

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3
Q

strong acid

A

completely dissociated at physiologic pH

HCl -> H+ + Cl-

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4
Q

strong cations

A

completely dissociated

ex: Na+, K+, Mg2+ and Ca2+

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5
Q

strong anions

A

completely dissociated

ex: Cl-, SO4(2-)

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6
Q

weak acid

A

exists in both dissociated and undissociated forms

-> act as buffers

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7
Q

buffer

A

molecule or molecular system that resists changes in [H+]

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8
Q

acid dissociation constant

A

Ka = [products]/[reactants]

*[H20] concentration can be ignored because it’s concentration in the body is generally constant

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9
Q

equilibrium expression for bicarbonate buffer

A

Ka’ = [H+][HCO3-]/[CO2] = 800 x 10^-9M

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10
Q

equilibrium constant for bicarbonate buffer

A

800 x 10^-9M

800 nM

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11
Q

normal values in arterial blood for H+, HCO3- and CO2 concentrations

A 
[H+] = 40 nM (40 x 10^-9M)
[HCO3-] = 24 mM (24 x 10^-3M)
[CO2] = 1.2 mM (1.2 x 10^-3M)

*carbonic acid occurs 1:320 to CO2 -> 4 uM

So,
[H+] < [H2CO3] < [CO2] < [HCO3-]

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12
Q

hyperchloremia

A

bicarbonate anion is replaced by the chloride anion

HCl + HCO3- = CO2 + H2O + Cl-

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13
Q

closed system

A

retains CO2

large change in pH with each addition of acid

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14
Q

open system

A

elimination of CO2

small change in pH with each addition of acid

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15
Q

PCO2 isobar

A

In an open system, dissolved [CO2] remains constant. So the pH-bicarbonate diagram illustrates the relationship that forms a line called the PCO2 isobar

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16
Q

Henderson-Hasselbalch equation

A

mathematical rearrangement of the equilibrium expression for CO2-bicarbonate
-> generates family of PCO2 isobars by choosing various [HCO3-] for given

pH = 6.1 + log ([HCO3-]/(.0301 x PCO2))

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17
Q

CO2-bicarbonate system

A

effectively buffers hydrogen ions from non-carbonic acids

-cannot buffer itself

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18
Q

isohydric principle

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A

pH can be known if [CO2] (or PCO2) AND [HCO3-] are both known

19
Q

CO2-bicarbonate rxn

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A

CO2 + H20 H+ + HCO3-

futile cycle of buffering bc the CO2 that is added is regenerated

THUS the body requires other buffers to remove free H+ without regenerating CO2

*not good for respiratory (carbonic acid) challenge

20
Q

buffer line

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A

formed by pH-bicarbonate values

flat is undesirable, ex: increasing PCO2 -> no change in bicarbonate and pH drops

steep is desirable- large amounts of bicarbonate formed with little change in pH

21
Q

metabolic acidosis

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A

increase in non-carbonic acid

22
Q

respiratory acidosis

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A

increase in PCO2 (hypoventilation)

23
Q

advantages of other buffers

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A

1) buffer H+ produced by CO2

2) transport added CO2 as HCO3- not as dissolved CO2

24
Q

other buffers

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A

1) plasm and interstitial phosphate
2) plasma and interstitial protein
3) red cell
4) intracellular buffering
5) bone

25
plasm and interstitial phosphate
H+ + HPO4(2-) H2PO4-
26
plasma and interstitial protein
H+ + (protein) (protein-H+)
27
red cell buffer
a) dissolve CO2 crosses cell membrane b) some remains dissolved, some becomes carbamino compound on hemoglobin c) rest catalyzed by carbonic anhydrase -> H+ and HCO3- d) H+ is buffered by hemoglobin, cannot rapidly diffuse across membrane e) HCO3- diffuses out of cell and is exchanged for Cl- (chloride shift) *not metabolic acid challenge
28
intracellular buffering
H+ enters cell and then either: a) Cl- follows b) Na+ or K+ leaves (could lead to hyperkalemia)
29
bone buffering
may lose calcium carbonate -> lose bone density
30
Renal System
compensation and correction of acid-base homeostasis
31
time course of buffering
ECF: millisec- plasma and hemoglobin in rbc 10-30min- interstitial fluid compartment ICF: 2-4hrs- intracellular buffering several days- renal system minutes-years- bone
32
buffer value
= d(HCO3-)/d(pH) units = slykes (sl) or mmol/L per pH ability of all boady buffer systems other than CO2-bicarbonate to buffer a change in [H+] caused by changes of PCO2 ie how effective can they turn CO2 into HCO3- high value is preferred -> can indicate relationships on pH-bicarb diagram plasma (4sl) < ECF (11sl) < blood (25sl) individual variation of buffer values
33
base excess
amount of strong acid to return blood to pH of 7.4 represent increase in bicarbonate cause by: 1) intracellular/bone buffering and renal compensation for chronic respiratory acidosis 2) metabolic alkalosis 3) administration of sodium bicarbonate
34
base defecit
amount of strong base to return blood to pH of 7.41) represent decrease in bicarbonate cause by: 1)intracellular/bone buffering and renal compensation for chronic respiratory alkalosis 2) metabolic acidosis
35
metabolic acidosis
caused by a) bicarbonate loss due to renal or diarrheal disease b) bicarbonate loss due to buffering of metabolic acids (lactic acid and ketoacids increase H+ load) c) gain of non-carbonic acid ("metabolic" or "non-volitle") d) inability to excrete H+ thus bicarbonate is consumed- renal disease dx: < 22mM compensation: hyperventilation PCO2, 35 mmHg correction: increasing plasma HCO3- a) administer NaHCO3 (dangerous) b) kidney restores bicarbonate by excreting H+
36
ABG
arterial blood gases pH 7.35-7.45 Pa(CO2) 35-45 mmHg HCO3- 22-26mM
37
acid-base disorder
- respiratory and/or renal abnormality | - acid-base load exceeds capacity of these systems to handle it (ex: diarrhea)
38
respiratory acidosis
- abnormal PCO2 from hypoventilation compensation: renal creation and retention of bicarbonate correction: treating respiratory problem if possible dx: PCO > 45 mm Hg, pH < 7.35, normal or above HCO3- causes: a) depressed ventilation (drug overdose) b) obstructive lung disease (COPD and pulmonary fibrosis) c) chest wall/ muscle disorders d) pulmonary fibrosis
39
respiratory alkalosis
- abnormal PCO2 from hyperventilation compensation: renal secretion of bicarbonate correction: treating respiratory problem dx: PCO2 < 35mm Hg, pH > 7.45, normal or below HCO3- causes: 1) hypoxia -> hypoxic drive 2) pain/ anxiety -> psychogenic hyperventilation 3) dyspnea 4) mechanical overventilation
40
metabolic alkalosis
- loss of non-carbonic acid - gain of bicarbonate dx: >7.45pH and HCO3- > 26mM compensation: hypoventilation (PCO2 > 45 mmHg) causes: a) GI loss of H+ due to vomiting bc pancreas secretes bicarbonate b) hypokalemia (K+ leaves cell, H+ enters so ECF becomes alkaline) c) contraction alkalosis (from diuretics -> loss of NaCl->H2O follows salt-> ECF volume decreases -> [HCO3-] increases stages: 1) initiation 2) maintenance
41
compensation
physiologic adjustment when acid-base homeostasis is disturbed to restore pH ->PCO2 or bicarbonate will become abnormal bc pH is priority
42
correction
resolution or cure when acid-base homeostasis is disturbed to restore pH
43
plasma anion gap
= [Na+] - ([HCO3-] + [Cl-]) | normal range is 8-16mM

Respiratory Physiology (4 decks)

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