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Renal > Physiology acid base balance > Flashcards

Physiology acid base balance Flashcards

1
Q

what is the normal plamsa pH

A

7.4 (7.35-7.45)

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2
Q

what can hydrogen ions combine with to reduce plasma pH

A

bicarb

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3
Q

what regulates plasma conc of bicarb

A

kidneys

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4
Q

what are the types of acid base disturbances

A

resp acidosis and alkanosis

metabolic acidosis and alkanosis

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5
Q

what provides the immediate buffering for a pH change

A

immediate dilution of the acid/ base in ECF

blood buffers (Hb, HCO3-)
buffers in the ECF (particularly HCO3-)
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6
Q

do immediate buffers have prolonged effect

A

no- get depleted quickly and have to be replaced by the kidney

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7
Q

how does Hb work as a buffer

A

deoxygenated blood has a greater affinity for H+ so helps reduce acid in the blood

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8
Q

what does an resp acidosis do to blood HCO3- levels

A

increases as more free H+ and acting as a buffer, being formed in response to the acid

(rise in H+ more tho)

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9
Q

what diagram shows pH blood gas

A

davenport diagram

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10
Q

what causes respiratory acidosis

A 
= retention of CO2 as a result of: 
chronic bronchitis 
chronic emphysema 
airway restriction (bronchial asthma, tumour)
chest injuries 
resp distress (morphine/ GA)
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11
Q

what does CO2 retention cause

A

the formation of carbonic acid which dissociates into free H+= acidosis

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12
Q

what are bicarb levels like in a resp acisosis

A

high

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13
Q

what is the compensation method for resp acidosis

A

no ECF buffering for this
(as resp system cause renal must compensate)
blood PCO2 drives H+ secretion by the kidney= CO2 stimulates H+ secretion into the filtrate (creates titratable acid and NH4+ in the urine)
reabsorbtion of all secreted bicarb ions

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14
Q

what rises in resp acidosis compensation

A

HCO3-

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15
Q

what is required for resp acidosis correction

A

restoration of normal ventilation

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16
Q

what is compensation

A

restoring normal pH irrespective of HCO3- and PCO2 concentrations

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17
Q

what is correction

A

restoration of pH and concentrations of HCO3- and PCO2 to within normal ranges

18
Q

what causes a respiratory alkalosis

A

= excessive removal of CO2 by the body:

low inspired Po2 @ altitude (hypoxia stimulates hyperventilation)
hyperventilation (fever, brainstem damage)
hysterical breathing

19
Q

what does excessive CO2 loss in resp alkanosis cause

A

both H+ and HCO3- fall

fall in H+ is what makes it an alkanosis- pH only measures free pH

20
Q

what is pH a measure of

A

free H+ ONLY

21
Q

what is HCO3- like in resp alkanosis

A

low (both H+ and HCO3- fall in resp to low CO2)

22
Q

what is the compensation for a resp alkanosis

A

(resp causes so renal compensates)
blood PCO2 drives H+ secretion- excessive removal of CO2 reduces H+ secretion into the tubule
HCO3- is excreted and urine is alkaline
no titrabable acid or NH4+ are formed so ‘new’ HCO3- is generated

23
Q

what does correction of resp alkanosis require

A

restoration of normal ventilation

24
Q

what causes a metabolic acidosis

A

= excess H+ from any source other than CO2:
-ingestion of acids or acid producing foodstuffs
-excessive metabolic production of H+ (lactic acid or ketoacidosis)
excessive loss of base from the body (diarrhoea- loss of HCO3-)

25
Q

what happens to HCO3- in metabolic acidosis

A

depleted as a result of buffering or lost from the body (diarrhoea)

26
Q

what is HCO3- like in a metabolic acidosis

A

LOW

27
Q

what is the compensation for metabolic acidosis

A

(resp not cause so can help compensation)
decrease in plasma pH stimulates peripheral chemoreceptors- ventilation is quickly increased blowing off more CO2 (lowering H+ AND HCO3-)

renal:
H+ is lowered via secretion- titratable acid and NH4+
filitered HCO3- is reabsorbed

HCO3- IS LOWERED

28
Q

why is resp compensation of metabolic acidosis essential

A

as acid load cannot be excreted immediately so need help from resp quickly

29
Q

what happens to HCO3- conc in compensation of metabolic acidosis

A

IS LOWERED

30
Q

what causes metabolic alkanosis

A

excessive loss of H+ from the body:

  • loss of HCL from the stomach (vomiting)
  • ingestion of alkali or alkali producing foods)
  • aldosterone hypersecretion (stimulates Na+/H+ exchange at the tubule = acid secretion)
31
Q

what happens to HCO3- in metabolic alkanosis

A

as a result of loss of H+ or addition of base HCO3 rises

32
Q

what is HCO3- like in metabolic alkanosis

A

high

33
Q

what is the compensation for metabolic alkanosis

A

increased pH slows ventilation (perpheral chemoreceptors)
CO2 retained, PCO2 rises
H+ rises lowering pH
HCO3- also rises further

34
Q

what happens to HCO3- in resp compensation of metabolic alkanosis

A

rises

35
Q

what is the correction for metabolic alkanosis

A

filtered HCO3- load is so large compared to normal so not all can be reabsorbed
no TA or NH4- produced
HCO3- is excreted
HCO3- falls back towards normal

36
Q

how long does renal excretion of H+ in resp acidosis take

A

hours to days- why you need restoration of normal ventilation

37
Q

what type of acidosis can undergo immediate ECF bufferning by HCO3-

A

non CO2 (metabolic)

38
Q

how long do the compensation mechanisms take for metabolic acidosis

A

resp comp- minutes
intracellular buffering 2-4 hours
renal excretion of H+ (days- weeks)

39
Q

What is ROME

A

resp opposite metabolic equal

resp opposite:

  • acidosis= low pH= low CO2 (high HCO3)
  • alkalosis= high pH= high CO2 (low HCO3)

metabolic equal:

  • acidosis= low pH= low HCO3
  • alkalosis= high pH= high HCO3
40
Q

is potassium low in alkalosis or acidosis

A

alkaLOsis

Renal (27 decks)

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