Week 5 Control of Breathing, Hypoxia, Respiratory Failure Flashcards

1
Q

what are normal pO2, pCO2, bicarbonate and pH?

A

pO2 = 4.2-6.0kPa
pCO2 = 9.8 -14.2kPa
bicarb= 21-29mmol.L
pH 7.38 - 7.46

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2
Q

what is hypercapnia and hypocapnia?

A

hypercapnia- rise in pCO2

hypocapnia- fall in pCO2

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3
Q

what is hyperventilation and hypoventilation and apply it to exercise?

A

hyperventilation is an increase in ventilation without changes in metabolism = in alveoli - increase in pO2, decrease in pCO2

hypoventilation is a decrease in ventilation without changes in metabolism = in alveoli - decrease in pO2, increase in pCO2

in exercise using O2 and producing more CO2 so pCO2
breathing faster (hyperventilation) will restore this by getting more O2 in and getting rid of more CO2
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4
Q

if pO2 changes without a change in pCO2 what will the correction of pO2 do to pCO2?

A

pCO2 will drop leading to hypocapnia

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5
Q

how does pCO2 effect plasma pH?

A

CO2 and H2O = (carbonic acid) H2CO3 which is in equilibrium with H and HCO3 (bicarbonate)
- increase in CO2= increase in H2CO3 and therefore increase in HCO3 and H
- if both change pH might not be affected
- if HCO3 remains the same and pCO2 increases pH falls
-if pCO2 decreases pH rises
small changes in pCO2 have large affects on pH

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6
Q

what effects does changes in pH have?

A

pH usually between 7.35 and 7.45
if falls bellow 7 = enzymes denatures
if rises above 7.6 = free Ca drops= tetany

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7
Q

how does hyper and hypoventilation affect plasma pH- respiratory acidosis/alkalosis?

A

hypoventilation = >pCO2 ….. hypercapnia = fall in plasma pH
= respiratory acidosis

hypeventilation =

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8
Q

describe the general effects of acute hypo and hyperventilation

A

d

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9
Q

generally what are respiratory and metabolic changes in pH compensated by?

A

respiratory compensated by kidney control over [HCO3]

metabolic compensated by breathing - altering pCO2

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10
Q

what is compensated respiratory acidosis and alkalosis?

A

as CO2 + H2O = H2CO3 which –> H + HCO3
plasma pH depends on a ration between [HCO3] and pCO2 not on their absolute values
- changes in pCO2 can be compensated by changes in [HCO3]
- the kidneys control [HCO3]

  • respiratory acidosis (hypoventilation= >pCO2) is compensated by the kidneys by increasing [HCO3]
  • respiratory alkalosis (hyperventilation =
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11
Q

what is metabolic acidosis, how does it arise and how can it be compensated for?

A

if the tissues produce acid (H) this reacts with HCO3 = H2CO3
if [HCO3] falls pH will fall as there will be more free H
= metabolic acidosis - this can be compensated for by changing ventilation- increased ventilation lowers pCO2 = restores pH
DECREASE [HCO3]- DECREASE PCO2 TO EVEN OUT PH

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12
Q

what is metabolic alkalosis, how does it arise and how can it be compensated for?

A

if plasma [HCO3] rises (eg after vomiting) will bind to free H and increase plasma pH = metabolic alkalosis
- this can be compensated to a degree by decreasing ventilation = >pCO2 balancing equilibrium

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13
Q

describe the acute effect on ventilation of;

  1. falling inspired pO2,
  2. increases in inspired pCO2,
  3. falls in arterial plasma pH
A

d

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14
Q

where are the peripheral chemoreceptors, what is there function and what role do they play in ventilation and other responses to hypoxia?

A

peripheral chemoreceptors are located in the carotid and aortic bodies

  • stimulated by large falls in pO2 (hypoxia)
  • increased breathing, changes in HR, changes in blood flow distribution- increased flow to brain and kidneys
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15
Q

what is the role and location of the central chemoreceptors?

A

central chemoreceptors in the medulla of the brain are much more sensitive to pCO2
they respond to changes in pH of CSF which is separated from the blood by the blood brain barrier

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16
Q

what role do the central chemoreceptors have in ventilation respiratory changes in arterial pCO2?

A
  • small rises in pCO2= increased ventilation (pCO2)

=NEGATIVE FEEDBACK CONTROL OF BREATHING

17
Q

what is the role of the blood brain barrier and how does this work with the central chemoreceptors?

A

blood brain barrier prevent H+ and HCO3- from crossing so that it cannot affect brain ECF or CSF
-CO2 can cross the blood brain barrier into the CSF where it combines with H20 to create H+ and HCO3- = the H then enters the ECF- fall in pH detected by the central chemoreceptors which drives increased ventilation to

18
Q

what is the role of choroid plexus in the ventilation respiratory to changes in arterial pCO2?

A

this plexus is involved in the longer term persistent changes in pH
CSF [HCO3-] is controlled by choroid plexus cells which let it into the CSF
CSF pCO2 is determined by arterial pCO2

19
Q

what is hypoxia?

A

fall in pO2

21
Q

describe type 1 and 2 respiratory failures

A

TYPE 1- not enough O2, CO2 normal

TYPE 2- not enough O2 in or CO2 leaving

22
Q

how does ventilation/perfusion mismatch and diffusion impairment result in type 1 respiratory failure and what are the important causes of each?

A

d

23
Q

how does hypoventilation result in type 2 respiratory failure and what are the important causes of this?

A

d

24
Q

interpret incomplicated blood gas abnormalities

A

d

25
Q

what is asthma and describe the natural air flow obstruction in asthma?

A

d

26
Q

what are the major precipitating factors for asthma attacks?

A

d

27
Q

what are the signs and symptoms of asthma?

A

d

28
Q

what are the tests used to assess a pt suspected on asthma and how are they interpreted?

A

d

29
Q

what are the principles of treatment of asthma?

A

d

30
Q

what is the overall pathophysiology of asthma?

A

d

31
Q

how is CSF pH maintained?

A

determined by a ratio of [HCO3-] to pCO2
HCO3 fixed in short term as BBB impermeable to HCO3
- falls in pCO2 = rise in CSF pH
- rises in pCO2 = fall in CSF pH
persisting changes in pH are corrected by choroid plexus cell which change the [HCO3-]