RESPIRATORY PHYSIOLOGY Flashcards

1
Q

what does the binding of O2 cause in Hb subunits

A

change from tense to relaxed state

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2
Q

What causes the Bohr effect

A

chloride shift increasing salt bridge formation

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3
Q

what effect does BPG have on the 02 dissociation curve

A

reduces affinity as resists salt bridge formation

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4
Q

how does BPG differ in foetal Hb

A

BPG level are decreased therefore Hb has higher affinity

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5
Q

How much O2 is associated with Hb and how much is dissolved

A

5% dissolved

95% HB

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6
Q

how long does it take for blood to be saturated with 02 in the alveoli

A

0.25 seconds

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7
Q

At rest blood spends 0.75 seconds in the alveoli, how does this change with exercise

A

time reduced to 0.25 seconds

progressive lung diseases will affect people during exercise first

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8
Q

methods of automatic neural control of breathing

A

PRE BOTZINGER COMPLEX in medulla –> rhythmical breathing

STRETCH RECEPTORS in lungs inhibit inspiration to protect lungs

PROPRIOCEPTORS in muscles, tendons and joints –> increase ventilation

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9
Q

Chemical control of ventilation

A

CENTRAL chemoreceptors (sensitive to PCO2 via H+ ions)

PERIPHERAL chemoreceptors
sensitive to love PO2 [and ph]

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10
Q

what is resting O2 consumption

A

250ml/min

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11
Q

How does the global part of Hb modify the properties of haem

A

Makes reaction reversible

O2 can bind co-operatively

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12
Q

What is Henry’s law

A

content of dissolved gas X in liquid Y= solubility of XinY. pp of X

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13
Q

3 mechanisms of CO2 transport in the blood

A
  1. dissolved in blood
  2. carbaminos
  3. as carbonic acid in RBCs
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14
Q

What is the Haldane effect

A

deoxy blood can carry more CO2 as Hb mops up H+ ions forming carbamino groups

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15
Q

what is the normal PO2 in arterial blood

A

100mmHg (roughly same as mean alveolar)

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16
Q

what is the Bohr effect

A

reduced affinity for O2 owing to:

  1. fall in pH
  2. rise in PO2
  3. Rise in temp
  4. 2,3-BPG
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17
Q

what is the PO2 in capillary beds

A

40mmHg

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18
Q

What is Ficks law?

A

measures rate of diffusion.
Directly proportional to area, diffusion constant, partial pressure gradient
Inversely proportional to thickness

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19
Q

The alveolar gas equation

A

PAO2= PIO2 -(PACO2/0.8)

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20
Q

what is starling’s equation

A

measures the flow of blood

F=Kfc[^P-reflection coef .^colloid]

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21
Q

what is the total blood volume in the pulmonary circulation

A

500ml

10% of total

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22
Q

what cause active and passive changes in perfusion

A
Passive:
- recruitment
- distension
Active:
- hypoxic pulmonary vasoconstriction
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23
Q

what is the normal VQ ratio

A

0.8

24
Q

what is the V/Q at the base of the lung

A

<1

25
Q

what is the V/Q at the apex

A

> 1 (~3)

26
Q

how much of the CO is shunted via the bronchial and mediastinal veins into the pulmonary veins

A

2-3%

27
Q

how does venous pooling occur in the standing position

A
  1. veins expand –> greater capacity unto 600ml
  2. hydrostatic forces force fluid out

can mimic effect of haemorrhage

28
Q

how music water is in the average adult male

A

64% (42L)

53% in females

29
Q

explain the 20:40:60 rule

A

20 ECF
40 ICF
60% of body weight is water

30
Q

what is the osmolarity of blood

A

300-310 mOsm/L

31
Q

what is the osmolarity of 0.9% NaCl

A

308 mOsm/L

32
Q

what is the osmolarity of intracellular fluid

A

290 mOsm/L

33
Q

what percentage of a unit of 5% dextrose would stay in the plasma after equilibration

A

7%

34
Q

what is the osmolarity of 5% dextrose

A

252mOsm/L

35
Q

which 2 systems regulate body fluid compartments

A

osmoregulation

volume regulation

36
Q

how does osmoregulation work

A

osmoreceptors in the hypothalamus (OVLT, SO) communicate with the posterior pituitary to secrete ADH when osmolarity falls

37
Q

how does volume regulation help maintain body fluid compartments

A

sensed by ECV, carotid sinus, afferent arterioles and atria

acts on: RAAS, SNS, SNP, ADH, pressure natriuresis

38
Q

what is oedema

A

osmotic expansion leading to increased ECW vol

39
Q

what might cause hyPERosmotic expansion

A

Oral rehydration therapy

40
Q

what might cause hypOsmotic expansion

A

water retention

41
Q

what might cause osmotic contraction

A

cholera

osm stays the same

42
Q

what might cause hyPERosmotic contraction

A

loss of water

43
Q

what might cause hypOsmotic contraction

A

loss of solute e.g. in adrenal disease

44
Q

what is starling’s law of the heart

A

decreased blood volume leads to decreased cardiac output

45
Q

how long is the normal PR interval

A

120-200ms

3-5 small squares

46
Q

how long is the normal QRS

A

120ms

3 small squares

47
Q

how long should the QT interval be

A

350ms

proportional to HR

48
Q

what is the duration of a ventricular action potential

A

400ms (4 in muscle)

49
Q

how would you calculate HR from an ECG

A

300/RR or 1500/RR for small squares

50
Q

what are the difference between atrial/nodal APs and ventricular APs

A

atrial has shorter plateau phase, slower upstroke and uses a different Na channel in depolarisation

51
Q

in a normal axis what would you expect to see on an ECG

A

Positive:
I, II, aVL, AVF

Negative:
III, aVR

52
Q

what are the short term, intermediate and long term controls of blood pressure

A

SHORT: baroreceptor

INT: transcapillary shift
vascular stress relaxation (10-60min)
RAAS (after 20mins)

LONG : kidney –> aldosterone, ADH

53
Q

Which cells mostly fire during expiration

A

The VRG

54
Q

Which cells most fire during inspiration

A

The DRG also inhibits VRG

55
Q

What is the role of the pontine respiratory group

A

To fine tune breathing

Transaction at this level leads to abnormal gasping pattern

56
Q

Which cells in the cerebral cortex are involved in the conscious modification of breathing

A

The pyramidal tracts

57
Q

Which 4 reflexes are present in the lung and modify breathing

A

Irritants in nose and upper airways –> vagus –> coughing, aspiration reflex, diving reflex

Pulmonary stretch detectors –> vagus –> decr resp via herring breuher

Irritant receptors: noxious gases –> bronchoconstriction

J receptors detect fluid in lungs –> dyspnoea in left sided heart failure