Respiratory Flashcards

1
Q

Why is there less resistance in the pulmonary circulation as compared to systemic?

A

to ensure that the rate of flow is equal to systemic because the pressure in the systemic circulation is greater so the decreased resistance in the pulmonary circulation makes up for that. Qdot=pressure difference/resistance

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2
Q

What two physiologic mechanisms can occur to keep resistance low during exercise, etc when pressure increases?

A

-recruitment of more vessels
-distension, so increased radius of vessels

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3
Q

Describe vascular resistance in the alveoli and how complete occlusion in limited

A

initially with an inspiration, resistance increases because alveolar vessels are compressed, but then extralveolar vessels can be expanded by the manual pull on CT to pull them open

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4
Q

Where can you measure blood pressure directly via a catheter with a transducer placed into venous circulation?

A

-right atrium
-right ventricle
-pulmonary arteries

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5
Q

How would you measure blood pressure in the pulmonary vein and left atria?

A

indirectly estimate by pulmonary wedge pressure

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6
Q

Describe pulmonary wedge pressure

A

catheter is fed into right heart then into pulmonary circulation where a balloon at the end of the catheter is opened.this occludes the arteriole, and as long as the capillary/venule is continuous, the indirect pressure flowing back from other venules is equivalent to the left atrial pressure

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7
Q

Describe hypoxic pulmonary vasoconstriction

A

occurs in times of hypoxia and is adaptive to reduce blood flow to regions of the lungs that are poorly ventilated. this response locally matches ventilation/profusion to normal

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8
Q

How is hypoxic pulmonary vasoconstriction modulated?

A

pulmonary endothelial cells release vasodilating (PGI2,ANF, NO) or vasoconstricting agents (thromboxane or endothelin-1)

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9
Q

what can result from damage to pulmonary endothelial cells?

A

can result in decrease to vascular tone molecules as well as increase pro-inflammatory and procoagulant factors due to the necrosis of cells. this all favors vasoconstriction and coagulation

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10
Q

True/False: fetal lungs participate in gas exhange

A

false

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11
Q

fetal pulmonary circulation is characterized as what three things?

A

-high pressure
-high resistance
-low flow

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12
Q

Why is blood flow favored through the foramen ovale and the ductus arteriosis in fetal circulation

A

because Po2 is low, this results in prolonged vasoconstriction, this causes higher resistance in the pulmonary circulation as compared to the systemic circulation

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13
Q

At birth what causes the diversion of blood into pulmonary circulation?

A

the pressure in the pulmonary circulation falls rapidly and less to systemic as the ductus closes and active pulmonary vasodilation occurs. this increase in left atrial pressure which closes the foramen ovale

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14
Q

Pulmonary vasodilation at birth is a response to what?

A

mechanical effects of ventilation mediated by histamine and PGD2 from mast cells and rising PO2

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15
Q

Pulmonary vasodilation at birth is a response to what?

A

mechanical effects of ventilation mediated by histamine and PGD2 from mast cells and rising PO2

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16
Q

Fluid flex out of pulmonary capillaries is determined by what two things?

A

relative hydrostatic pressure and oncotic pressure

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17
Q

What is the reserve to help prevent alveolar edema?

A

lymphatics

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18
Q

Briefly describe two situations that would lead to pulmonary edema

A

-increased pressure in the left atria causing back flow and increased hydrostatic pressure
-increased capillary permeability

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19
Q

True/False: conducting airways (i.e bronchus and bronchioles) are involved in gas exchange

A

false

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20
Q

What respiratory structures are responsible for gas exhange?

A

the lung parenchyma (alveolar septa and alveoli)

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21
Q

What is total lung capacity

A

the volume of gas that can be contained within the maximally inflated lungs

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22
Q

Define tidal volume

A

the volume of a single expired breath

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23
Q

Define vital capacity

A

the maximal volume that can be expelled from the lungs after maximal inspiration

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24
Q

Define residual volume

A

the volume of gas that remains in the lungs after maximal expiration

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25
Q

Define functional residual volume

A

the volume remaining in the lungs at the end of a normal tidal expiration

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26
Q

How would you measure all the standard lung volumes in a conscious cooperative patient?

A

spirometry

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27
Q

What is the total pressure of ambient air?

A

760mmHg

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28
Q

What is the partial pressure of H2O?

A

47mmHg

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29
Q

What is the normal PIO2?

A

150mmHg

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30
Q

Define respiratory dead space

A

lung compartment with ventilation but no blood flow (so no gas exchange)

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31
Q

What does minute ventilation measure?

A

total gas flow in and out of the lungs per minute, this includes dead space + alveolar ventilation

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32
Q

What value is an accurate estimate for PACO2?

A

PaCO2

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33
Q

What information do you need to be able to calcualte PAO2?

A

PIO2 and lab measured PaCO2

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34
Q

What is the basic foundation of how air enters the lungs?

A

The alveolar pressure has to be less than atmospheric

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35
Q

Why is there a loss of velocity of air in periphery airways?

A

the same vol of inspired air is distributed among many airways as total cross sectional area increases rapidly in terminal airways

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36
Q

What are the 2 ways lungs can be inflated? when would each be used?

A

-Negative pressure which is normal circumstances
-Positive pressure which would be manual inflation under sedation etc

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37
Q

___ within alveolar walls contributes to the passive delflation of the lungs

A

elastin

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38
Q

____ within the pulmonary interstitium resists further expansion at high lung volumes

A

collagen

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39
Q

Define lung compliance

A

the change in volume as expanding pressure is applied

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40
Q

True/False: compliance of lung parenchyma is the same for negative pressure and positive pressure inflation

A

True

41
Q

what would increase compliance?

A

loss of elastic tissue

42
Q

what would decrease compliance?

A

CT proliferation or interstitial fluid

43
Q

What is the force that acts to reduce alveolar surface area and volume which contributes to the passive recoil of lungs?

A

surface tension

44
Q

True/False: a saline filled lung will have less compliance than an air filled lung. Why?

A

False because the saline filled lung obliterates the air-liquid interface making it have a lower tendency to recoil as compared to the air filled lung

45
Q

small alveoli have a tendency to collapse into larger ones with surface tensions which then require large distending pressures to reopen them. What substance reduces surface tension then reducing pressure needed to reopen alveoli?

A

surfactant

46
Q

What is surfactant

A

a phospholipid synthesized by type II cells

47
Q

if an alveoli begins to collapse what manual mechanism helps to keep them open

A

the tension on the walls exerted through collagen fibers by neighboring alveoli

48
Q

The chest wall tends to recoil in which direction?

A

outward

49
Q

define relaxation volume (Vrx)

A

the equilibrium point where inward recoil of the lungs is balanced by the outward recoil of the chest

50
Q

How can airway resistance be assessed in conscious compliant patients (humans)

A

determined by the volume that can be forcefully expired in 1 second (FEV1)

51
Q

What circumstances can slow diffusion of gas across the air-blood barrier?

A

-decreased PO2
-thickening if the alveolar membrane

52
Q

What molecule is used to measure diffusion?

A

carbon monoxide

53
Q

What is the normal concentration of Hb in blood?

A

15g Hb/100mL blood

54
Q

Why is the relationship between PO2 and Hb saturation non linear?

A

due to the changes in oxygen affinity for Hb as oxygen molecules progressively bind

55
Q

What is the major mechanism of transport of CO2?

A

bicarbonate

56
Q

hypoxemia is defined as below what value?

A

PaO2<85mmgHg

57
Q

What is the most common cause of hypoxemia?

A

ventilation profusion mismatch

58
Q

What is the most common cause of hypercapnia

A

hypoventilation

59
Q

What is the major stimulus for increasing ventilation?

A

increased PaCO2

60
Q

When is the V/Q ratio 0?

A

When there is no ventilation. so when there is a complete collapse or obstruction of an airway (aka a shunt)

61
Q

When is there dead space/ V/Q ratio is infinity

A

when there is no perfusion so no gas exchange occurs (ie completely occluded capillary supply)

62
Q

True/False: the A-a gradient is a sensitive indicator of V/Q mismatch

A

true

63
Q

a low V/Q ratio indicate ___

A

impaired ventilation

64
Q

a high V/Q ratio indicates ___

A

impaired circualtion

65
Q

increased V/Q ratio leads to ____ PCO2

A

reduced

66
Q

True/False: increasing inspired oxygen (FIO2) will not improve hypoxia due to V/Q inequity

A

False, it will improve hypoxia UNLESS there is a great inequity which will yield less response to FIO2

67
Q

What condition of V/Q mismatch is resistant to correction by increasing FIO2? why?

A

shunts because there is no ventilation, so higher inspired oxygen will not raise the alveolar O2

68
Q

What is the normal range of the A-a gradient?

A

4-6mmHg

69
Q

True/False: there is no discrete respiratory center

A

true

70
Q

What receptors are important for minute to minute control of ventilation?

A

chemoreceptors

71
Q

What mechanoreceptor is responsible for the reflex that helps to prevent overinflation of the lung?

A

stretch receptor

72
Q

What receptor augment inspiratory activity and constricts airways to promote rapid shallow breathing that limits penetration of noxious agents?

A

irritant receptors

73
Q

Define eupnea

A

normal, quiet breathing

74
Q

Define Tachypnea

A

increased respiratory rate

75
Q

Define Hyperpnea

A

increased rate and depth of respiration

76
Q

Define Dyspnea

A

refers to the subjective sensation of breathlessness

77
Q

Define orthopnea

A

dyspnea while recumbent

78
Q

Define apnea

A

cessation of breathing

79
Q

Define cheyne-stokes respiration

A

abnormal pattern of waxing and waning tidal volume and periodic apnea

80
Q

Define Kussmaul breathing

A

regular, rapid rate with large tidal volume

81
Q

What cells synthesize surfactant?

A

epithelial type II cells

82
Q

Deposition of gasses and vapors in airways depends on ____

A

solubility

83
Q

Deposition of particles in airways depends on ___

A

particle size and breathing patterns

84
Q

Where does mucociliary transport occur?

A

in airways down to terminal bronchioles

85
Q

What is responsible for clearance of particles in alveoli?

A

alveolar macrophages

86
Q

What is the predominant immunoglobulin in secretions from the nasal mucosa and upper airways?

A

IgA

87
Q

there is ___ flow of blood vs. water at the gas exchange surface in gills

A

countercurrent

88
Q

Since most amphibian larvae have ineffective lungs they use ____ to move water

A

buccal pumping

89
Q

Why do amphibian lungs have limited surface area for diffusion?

A

their lungs, while internal, have rudimentary septation and few if any developed alveoli

90
Q

True/false: birds have a diaphragm

A

false, they have a common thoraco-abdominal cavity

91
Q

What have birds evolved anatomically to allow gas exchange to occur at both inspiration and respiration?

A

separation of ventilation and gas exchange

92
Q

In avian parabronchi, sequential capillary loops have a ____ blood flow pattern vs air

A

cross current

93
Q

True/False: avian parabronchi are rigid

A

true

94
Q

True/False: there is gas exchange in avian air sacs

A

false

95
Q

Why must avian keels be able to move freely

A

to allow body cavity and air sac volume to change since the lungs (parabronchi) are rigid

96
Q

what is the sequential order of most to least efficient gas change between mammals, fish, and avian

A

fish, avian, mammals

97
Q

Why is the avian blood gas barrier so extremely thin?

A

because the parabronchi do not expand and contract with each breath so less structural support is needed than in alveolar lungs

98
Q

Why would collateral ventilation across interlobular septae be beneficial and detrimental

A

beneficial because it determines consequences of airway obstruction, detrimental because it allows for the lateral flow of pathogens