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Pulm > Physiology > Flashcards

Physiology Flashcards

1
Q

tidal volume (VT)

A

volume of normal breathing

0.5 L

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2
Q

inspiratory reserve volume (IRV)

A

additional amount of air that can enter during forced inspiration

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3
Q

expiratory reserve volume (ERV)

A

difference between tidal end volume and forceful expiration end volume

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4
Q

residual volume (RV)

A

amount of air remaining in the lung at max expiration

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5
Q

inspiratory capacity (IC)

A

VT + IRV

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6
Q

functional residual capacity (FRC)

A

ERV + RV

volume of air in the lungs after normal expiration

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7
Q

vital capacity (VC)

A

IC +ERV

volume that can be expired after max inspiration

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8
Q

total lung capacity (TLC)

A

VC + RV
includes all lung volumes
6-7 L
most sensitive test for restrictive lung disease

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9
Q

forced vital capacity (FVC)

A

TV + IRV + ERV

amount of air exhaled during a forceful expiration

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10
Q

forced expiratory volume in 1 second (FEV1)

A

max inspiration then forced expiration

normal is 80% of FVC

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11
Q

obstructive lung disease

A

FEV1: FVC ratio reduced: less than 70%
increased: TLC, RV, FRC
reduced: FVC, FEV1
difficult expiration: increased compliance, decreased Patm and Palv pressure: collapses airways on forced exhalation
ex: asthma, emphysema, chronic bronchitis, bronchiectasis

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12
Q

restrictive lung disease

A

reduced FVC, FEV1, TLC, RV, FRC
normal or increased FEV1: FVC ratio
difficult inspiration: decreased compliance, increased resistance
ex: obesity, weak inspiratory mescles, neuromuscular disorder, interstitial lung disease (fibrosis), ARDS, sarcoidosis, pneumonitis

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13
Q

atelectasis

A

unstable alveoli that collapse on expiration

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14
Q

Normal arterial PO2 and PCO2.
Normal venous PO2 and PCO2.
Normal alveolar PO2 and PCO2.

A 
systemic arterial/ pulmonary venous:
PO2: 100
PCO2: 40
systemic venous/ pulmonary arteries: 
PO2: 40
PCO2: 46
alveolar:
PO2: 105
PCO2: 40
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15
Q

hypoventilation

A

increase in PACO2

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16
Q

hyperventilation

A

decrease PACO2

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17
Q

V/Q ratio for base and apex of lung

A

apex: high V/Q ratio (wasted ventilation)
base: low V/Q ratio (wasted perfusion)

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18
Q

What part of the lung is most perfused and has the most alveolar ventilation? least?

A

most perfused and alveolar ventilation: base

least perfused and alveolar ventilation: apex

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19
Q

A-a gradient for different causes of hypoxemia:

  1. hypoventilation
  2. decreased PIO2
  3. diffusion limitation
  4. R to L shunts
  5. V/Q mismatch

Which cannot be corrected by 100% O2?

A
  1. normal
  2. normal
  3. increased
  4. increased, NOT corrected with 100% O2
  5. increased
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20
Q

Decreased PIO2

  1. Example?
  2. A-a gradient increase? Intrinsic lung disease?
  3. Corrected with 100% O2?
A
  1. increased altitude
  2. A-a does NOT increase; no
  3. corrected with 100% O2
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21
Q

Hypoventilation

  1. Example?
  2. A-a gradient increase? Intrinsic lung disease?
  3. Corrected with 100% O2?
A
  1. drug overdose
  2. A-a does NOT increase; no
  3. corrected with 100% O2
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22
Q

Diffusion limitation

  1. Example?
  2. A-a gradient increase? Intrinsic lung disease?
  3. Corrected with 100% O2?
A
  1. pulmonary fibrosis, hard exercise, emphysema
  2. increased; yes
  3. yes
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23
Q

R to L Shunt

  1. Example?
  2. A-a gradient increase? Intrinsic lung disease?
  3. Corrected with 100% O2?
A
  1. ASD/VSD after pulmonary HTN reverses original L to R shunt; ARDS (alveolar flooding and collapse causes shunt)
  2. increased; yes
  3. NO
    IMPORTANT: 100% oxygen should have a very large increase in PaO2: do the equation for A-a gradient to see if it is corrected
    ex: PAO2= (760-47) x 1 - PaCO2/1
    FiO2=1 at 100% O2
    R= 1 at 100% O2
    PaO2 should be in 600s; if not: shunt
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24
Q

V/Q mismatch

  1. example
  2. A-a gradient increase? Intrinsic lung disease?
  3. Corrected with 100% O2?
A 
MOST COMMON cause of hypoxemia
1. emphysema, obstructive
2. increased; yes
3. yes
normal whole lung V/Q: 0.8
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25
Q

Low V/Q diseases

A

V/Q less than 1: low ventilation

  1. obstructive disease (asthma, COPD)
  2. pulmonary edema
  3. SHUNT (most extreme of low V/Q)
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26
Q

High V/Q diseases

A

V/Q more than 1: low perfusion

  1. pulmonary embolism
  2. DEAD SPACE like no blood flow (most extreme high V/Q)
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27
Q

DLCO

A

High: early asthma, pulmonary alveolar hemorrhage, exercise, early CHF, obesity
Low: COPD, fibrosis, emphysema, interstitial lung disease, PAH/PE, anemia

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28
Q

pulmonary shunt

A

V/Q= 0

unventilated alveoli with preserved perfusion or A-V malformations

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29
Q

How can you use DLCO to differentiate between obstructive diseases (asthma and COPD)?

A

high: asthma
low: emphysema

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30
Q

How can you use DLCO to differentiate between restrictive diseases (chest wall vs. interstitial lung disease)?

A

high: chest wall
low: interstitial lung disease

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31
Q

isolated low DLCO indicates what type of disease

A

pulmonary vascular disease

pulmonary HTN/ pulmonary embolism

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32
Q

ventilation

A

exchange of gas between atmosphere and alveoli

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33
Q

diffusion

A

exchange of O2 and CO2 between alveolar air and lung capillaries
DOWN pressure gradient

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34
Q

inspiratory muscles

A

diaphragm (phrenic nerve)

accessory: scalene, sternocleidomastoid, external intercostal muscles

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35
Q

expiratory muscles

A

passive at rest

exercise/force: rectus abdominus, internal and external oblique, transverse abdominus, internal intercostal muscles

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36
Q

interdependence

A

if one alveolus has a tendency to collapse, it will be counteracted by expanding forces of surrounding alveoli

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37
Q

how does surfactant work

A

phospholipid (dipalmitoyl phosphatidylcholine, lecithin, sphingomyelin) that breaks polar attraction of water molecules and reduces surface tension: prevents atelectasis
deep breath stretches type II cells and stimulates surfactant production

38
Q

surface tension

A

attractive forces between liquid molecules pulls surface molecules together at air-liquid interface

39
Q

Which has more airway resistance: mouth or nose?

A

nose

40
Q

How does lateral traction affect airway resistance?

A

elastic connective tissue fibers attach to airway exterior and pull outward: holding airways open

41
Q

How does lung volume affect airway resistance?

A

increase in lung volume increases airway diameter and resistance decreases

42
Q

How does relaxation/contraction of bronchial smooth muscle affect airway resistance?

A

relaxation: decreases resistance
contraction: increases reaction

43
Q

What is the driving stimulus for respiration?

A

PaCO2

hyperventilation attenuates stimulation of respiration because PaCO2 is decreased

44
Q

hypoxemia

A

lower than normal arterial PO2

normal = 100 mmHg

45
Q

hypoxia

A

decreased O2 delivery to tissues

due to: decreased blood flow or decreased O2 content

46
Q

hypercapnia

A

high arterial PCO2
normal= 40 mmHg
most often due to hypoventilation

47
Q

where is most of gas exchange completed (even in exercise)?

A

initial region of pulmonary capillary

PERFUSION limited: all blood leaving capillary has reached equilibrium with alveolar gas

48
Q

diffusion limited gas exchange diseases

A

gas does not equilibrate between capillaries and alveolar gas

  1. CO poisoning
  2. fibrosis (thick barrier)
  3. emphysema (decrease SA)
  4. high altitude
  5. INTENSE exercise
49
Q

What determines pulmonary blood flow?

A

PAO2

50
Q

How is edema fluid cleared?

A

repair epithelium
Na from interstitium comes into cell (ENaC) and is then pumped to basolateral side (Na-K ATPase) and water follows (aquaporin)

51
Q

partial pressure (PO2)

A

dissolved O2 in plasma

52
Q

methhemoglobin

A

Fe3+: O2 can’t bind

caused by nitrites and sulfonamides

53
Q

HbF

A

alpha2gamma2

high affinity O2

54
Q

adult Hb

A

alpha2beta2

Fe2+

55
Q

HbS

A

sickle cell

56
Q

cyanosis

A

unsaturated hemoglobin is purple

low Hb saturation causes blue color

57
Q

CO poisoning

A
  1. decreases O2 carrying capacity because it binds more strongly to Hb (decreases O2 content)
  2. also increases affinity of O2 for Hb and makes unloading in tissues more difficult
58
Q

Hamburger’s phenomenon

A

diffusion of HCO3- into plasma causes a decrease in net neg. charge in cell
Cl- moves into cell to compensate dragging water into cell causing it to swell

59
Q

band three protein

A

drives Cl- shift into cells HCO3- leaves cell

60
Q

How are H+ ions buffered in RBC after HCO3- leaves?

A

buffered by deoxyhemoglobin to prevent acidification

61
Q

Bohr effect

A

when CO2 is produced by tissues, HCO3 and H+ are produced in blood.
due to H+ production, pH becomes lower.
higher H+ concentration increases H+ binding to Hb and decrease in O2 affinity: O2 unloads in tissues (right shift)

62
Q

Haldane effect

A

oxygenation of Hb displaces CO2 from carboxyhemoglobin to form oxyhemoglobin
shifts equilibrium toward CO2 formation: CO2 is released from RBC’s into plasma
increases PCO2

63
Q

respiratory acidosis

A 
low pH
PCO2 greater than 40
cause: hypoventilation
ex: obstruction, acute or chronic lung disease, sedatives/opioids, weak respiratory muscles
compensation: increase HCO3 (slow)
64
Q

respiratory alkalosis

A 
high pH
PCO2 less than 40
cause: hyperventilation
ex: hysteria, hypoxemia, high altitude, salicylate, tumor, PE
compensation: decrease HCO3 (slow)
65
Q

metabolic acidosis

A

low pH
PCO2 less than 40
low HCO3
compensate: hyperventilation (immediate)

66
Q

metabolic alkalosis

A

high pH
PCO2 greater than 40
high HCO3
compensate: hypoventilation (immediate)

67
Q

central chemoreceptors

A

MOST IMPORTANT
respond to change in brain extracellular fluid
MEDULLA
stimulus: decrease in pH (increased PCO2)
MINUTE to MINUTE breathing

68
Q

peripheral chemoreceptors

A 
respond to changes in arterial blood  
1. PO2 less than 60 mmHg: increase ventilation 
2. changes in pH
increase (exercise): hyperventilation
decrease (vomit): hypoventilation 
1. carotid bodies
2. aortic bodies
anemia does not stimulate
69
Q

carotid bodies

A

stimulus: decreased PO2 greater than PCO2 greater than decreased pH
RAPID: PO2 less than 60 mmHg
high blood flow is key: EXERCISE

70
Q

aortic bodies

A

RAPID

stimulus: decreased P02 greater than PCO2

71
Q

lung receptors

A
  1. pulmonary stretch receptors
  2. irritant receptors
  3. J receptors
72
Q

pulmonary stretch receptors

A

stimulated by lung distention

Bering-Breuer reflex: slows down frequency

73
Q

irritant receptors

A

stimulated by noxious gas, smoke, dust, cold air, low PCO2
causes hyperpnea and bronchoconstriction
hypersensitive: asthma

74
Q

juxtapulmonary capillary receptors (J receptors)

A

stimulated by increase in pulmonary interstitial fluid

causes shallow, rapid breathing, apnea, hypotension

75
Q

nose and upper airway receptors

A

role in sneezing, coughing, bronchoconstriction

76
Q

joint and limb muscle receptors

A

role in early adjustment to exercise

77
Q

muscle spindles within respiratory muscles

A

sense muscle elongation

78
Q

arterial baroreceptors

A

increase BP can cause reflexive hypoventilation

79
Q

pain and temperature receptors

A

trigger period of apnea followed by hyperventilation

80
Q

What happens when a patient has a chronic elevation of PCO2?

A

adaptation of central chemoreceptors: brain extracellular pH reset by increased HCO3 transport (normal brain fluid pH at high arterial PCO2)
ex: COPD
oxygen becomes chief stimulus of ventilation through peripheral chemoreceptors
IMPORTANT: raising PO2 by placing patient on O2 may remove any stimulus to breathe and cause sudden death (MONITOR)

81
Q

response to exercise

A
  1. arterial PO2 constant: ventilation and O2 consumption increase in proportion
  2. moderate: alveolar ventilation increases in proportion to CO2 production; venous PCO2 increases but arterial PCO2 remains constant
  3. strenuous: lactic acid is released increasing arterial pH; arterial PCO2 decreases due to hyperventilation
82
Q

response to high altitude

A

decreased inspired PO2

  1. immediate: hyperventilation: respiratory alkalosis
  2. several days: renal HCO3 excretion increases, HCO3 leaves CSF, pH of CSF decreases to normal; hyperventilation resumes
  3. hypoxia stimulates EPO synthesis
  4. increased 2,3- DPG causes right shift (decreased affinity)
  5. increase pulmonary resistance: hypertrophy of right ventricle
83
Q

causes for worsening hypercapnia with supplemental O2

A
  1. Haldane effect

2. increased O2 abolishes hypoxic induced vasoconstriction: increased blood flow to low ventilation (low V/Q) areas

84
Q

spirometry

A

expiration for at least 6 sec
measures vital
predictors: age, sex, Ht

85
Q

What can a plethysmograph measure that a spirometer cannot?

A

residual volume

86
Q

What part of the flow volume loop is effort independent?

A

end of expiration

87
Q

Scoop on flow volume loop

A

COPD

88
Q

hamburger on flow volume loop

A

upper airway obstruction (inspiratory stridor): vocal cord paralysis, tracheal stenosis, goiter

89
Q

How is DLCO measured?

A 
single breath 
need inhaled VC greater than 1 L
hold breath for 10s
CO due to high affinity for Hb
normal 81-140%
90
Q

What decreases FRC?

A

obesity, pregnancy, ascites

restrictive disease

91
Q

Is peak flow effort dependent or effort independent?

A

dependent

Pulm (11 decks)

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