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Respiratory > Physiology > Flashcards

Physiology Flashcards

1
Q

Boyle’s Law

A

At any constant temperature the pressure exerted by a gas varies inversely with the volume of the gas

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2
Q

what 2 forces holds lungs to thoracic wall

A

1) intrapleural fluid cohesiveness (water in pleural gap)
2) negative intrapleural pressure (lungs and environment have same pressure, intrapleual fluid has lower pressure so both squeeze together to crush intrapleural fluid) - called transmural pressure gradient

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3
Q

what is a pneumothorax

A

air in intrapleural space- increases pressure in intrapleural space= lung collapse

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4
Q

what 2 things causes lung recoil for expiration

A

1) elastic connective tissue

2) alveolar surface tension

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5
Q

what does surfactant do

A

lowers alveolar surface tension- prevents alveolar collapse

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6
Q

what causes Respiratory Distress Syndrome (RDS) in new borns

A

premature babies may not have enough surfactant- hard inspiration

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7
Q

what 3 things keep alveoli open

A

1) transmural pressure gradient
2) pulmonary surfactant
3) alveolar interdependece

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8
Q

passive inspiration muscles

A

diaphragm + external intercostal

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9
Q

forceful inspiration muscles

A

Sternocleidomastoid, scalenus + pectoral

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10
Q

active expiration muscles

A

Abdominal muscles and internal intercostal

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11
Q

Tidal volume

A

volume entering/leaving in 1 breathe

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12
Q

Insp/ Exp reserve volume

A

extra volume of air that forceful breathing will give

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13
Q

Vital capacity

A

max volume of air for exp after a max insp

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14
Q

Total Lung Capacity

A

Vital capacity + residual volume

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15
Q

Residual volume

A

Vol left after a max exp.

Can’t be measured by spirometry

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16
Q

FVC (forced vital capacity)

A

max vol expirable after max insp

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17
Q

FEV1/FVC normal

A

> 70%

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18
Q

Obstructive vs Restrictive spirometry

A

Obst- FEV1/FVC = low

Restr- FEV1/FVC = normal

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19
Q

Parasymp vs symp effects on airways

A

Para- bronchoconstriction

Symp- bronchodilation

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20
Q

What is dynamic airway compression

A

During active expiration pleural pressure rises= > pressure on alveoli + airways. No problems in normal people. With obstructive disease can cause airway compression/ collapse.

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21
Q

What can cause decreased elastic recoil?

A

Emphysema or obstructed airway

= harder to expire

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22
Q

Describe obstructive airway

A

Not a physical obstruction- constricted airway. Restrictive is more like physical problem stopping air getting in/out of lungs- pulmonary fibrosis

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23
Q

Why and how to use peak flow

A

Best of 3 blows. For obstructive diseases.

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24
Q

what is compliance

A

effort needed to stretch lungs.

Less compliant= harder

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25
Q

what can increase compliance

A

emphysema- hyper inflation

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26
Q

pulmonary vs alveolar ventilation

A

pulmonary= air breathed in/ min= tidal volume x rr.
alveolar= air available for transfer w blood.
alveolar is < pulmonary because of dead space

27
Q

ventilation perfusion matching

A

not equal. more blood flow at bottom of lungs =

28
Q

four factors which influence gas transfer across the alveolar membrane

A

1) partial pressure gradient of O2 and CO2
2) Diffusion Coefficient for O2 and CO2 (solubility of gas in membranes)
3) Surface Area of Alveolar Membrane
4) Thickness of Alveolar Membrane

29
Q

dead space

A

ventilated but not perfused alveoli

30
Q

more ventilation=

more perfusion=

A

more o2 in alveoli= more blood flow

more co2 in blood = wider airways

31
Q

effect of partial pressure on gas solubility

A

henrys law- more partial pressure = more volume of gas dissolved in liquid

32
Q

o2 carriage in blood

A

on Hb. Po2 mainly determines o2 saturation.

33
Q

describe oxygen-haemoglobin dissociation curve

flat upper and steep lowe

A

sigmoid
co-operativity
flat upper portions - means that moderate fall in alveolar PO2 will not much affect oxygen loading (o2 sats at high end at pulmonary caps because go higher Po2).
steep lower portions- the peripheral tissues get a lot of oxygen for a small drop in capillary PO2.

34
Q

Bohr effect on o2 disassociation curve

A

Po2 vs Hb saturation curve shifts to right in lower pH= more 02 given up by hb at given Po2.

35
Q

foetal hb (HbF) vs adult

A

Hbf- 2 alpha and 2 gamma

- higher o2 affinity (curve shifted to left)= get o2 from mother even if mother po2 low

36
Q

myoglobin (Mb)

A 
1 heam per molecule 
no cooperativity 
hyperbolic 
releases o2 at low Po2s
= temp o2 storage in muscles  for anaerobic conditions
37
Q

what is difference in obstructive vs restrictive diseases effects

A

obstructive- airways

restrictive- lungs

38
Q

forms CO2 is carried in blood

A

solution,
BICARBONATE (HCO3),
CARBAMINO compounds (HbCO3)

39
Q

how are CO2 transport forms made?

A

some co2 dissolves from cells straight to blood.

most co2 picked up in RBCs from cells. IN RBC:
1) co2 binds to Hb. = carbamino
2) co2 + h2o -> h3co3-> H+ + HCO3. 
H+ -> HbH
HC03 leaves RBC to blood. = bicarbonate
40
Q

Haldane effect

A

Removing O2 from Hb increases its ability to pick-up CO2 and H+ (from Bohr effect)

41
Q

Haldane and Bohr work in synchrony for

A

for hb to release o2 at tissue and pick up CO2. And opposite at alveoli.

42
Q

what makes inspiration happen

A

pre botzinger complex in medulla, excited dorsal group = inspiration.

43
Q

what 2 centres modify respiration and how?

A

Pneumotaxic Centre- terminates inspiration. Stimulated when dorsal fires, without inspiration is prolonged. (APNEUSIS- long insp gasps, short exp)
Apneustic Centre- prolong inspiration

44
Q

homeostasis for arterial o2 and co2

A

hypercapnia- central chemoreceptors

hypoxia- peripheral chemoreceptors

45
Q

how does resp system regulate blood h+ conc

A

acidosis- peripheral chemoreceptors

46
Q

reflexes that modify breathing

A

1) Pulmonary stretch receptors/ Hering Breuer reflex. Stops insp
2) Joint receptors
3) Cough reflex

47
Q

What are 2 types of chemoreceptors

A

peripheral and central

48
Q

what and where are peripheral chemoreceptors

A

sense o2, co2 and H+ pressure in blood.

in carotid and aortic bodies

49
Q

what and where are central chemoreceptors

A

near medulla

50
Q

what and where are central chemoreceptors

A

near medulla
respond to H+ conc in CSF
aka respond to CO2 in blood as only H+ from CO2 is permeable

51
Q

where are central chemoreceptors and what do they respond to

A

near medulla
respond to H+ conc in CSF
aka respond to CO2 in blood as only H+ not permeable to the blood brain barrier (to get into CSF) but CO2 is. when in CSF, Co2 -> H+.

52
Q

what is hypoxic drive

A

PERIPHERAL chemoreceptors detect low arterial Po2 = hyperventilation and > cardiac output.
CENTRAL only pick up severe hypoxia.

53
Q

what can cause hypoxia

A

High altitude and maybe patients with co2 retention like COPD

54
Q

H+ drive of respiration

A

peripheral chemoreceptors sense H+ in blood. They correct for acidosis.

55
Q

Acidosis causes

A

Excess non-carbonic h+ in blood (maybe this H+ doesn’t get buffered as Hb doesn’t pick it up) by lactic acid or diabetic ketoacidosis.

56
Q

tests for airway function

A

spirometry,
peak flow,
bronchial challenge testing (exercise or allergens or drugs),
Nitrogen washout for functional residual volume,
DLCO- diffusion capacity.

57
Q

main equation for buffering H+

A

H+ + HCO3-> H2CO3 ->

CO2 + H2O

58
Q

what causes metabolic acidosis + how compensated

A

too little HCO3-
= too much H+
= LESS co2 in blood and more blown off
it is compensated by respiratory alkalosis.

59
Q

what causes respiratory acidosis + how compensated

A

too much CO2 in blood, kidneys get rid of H+.

60
Q

what changes in metabolic acidosis/ alkalosis

A

HCO3-

61
Q

what changes in metabolic acidosis/ alkalosis

A

CO2

62
Q

what do changes in h+ show

A

Only if its acidosis or alkalosis (not if its resp or metabolic)

63
Q

partial vs full compensation

A

full is where H+ is normal?

Respiratory (8 decks)

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