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Cardiovascular and Pulmonary > Pulmonary Physiology I > Flashcards

Pulmonary Physiology I Flashcards

1
Q

What are the two vital purposes of the lungs?

A
  1. ) Gas exchange

2. ) Role of ventilation in controlling blood pH

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2
Q

The exchange of O2 for CO2 occurs within structures called

A

Alveoli

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3
Q

In order for air to reach the alveoli, which path does it have to travel?

A

Trachea, bronchi, bronchioles, terminal bronchioles, respiratory bronchioles, alveolar ducts, and finally alevoli

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4
Q

Resistance to flow is inversely proportional to

A

Cross-sectional area of the vessel

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5
Q

Airway resistance decreases as air approaches the

A

Alveoli

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6
Q

The ducts which compromise the bronchial tree are ringed with

A

Smooth muscle (under autonomic control)

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7
Q

We are negative pressure breathers. What this means is that under physiologic conditions, a negative pressure differential between the atmosphere and the alveoli allows for

A

Movement of air into the lungs

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8
Q

There are opposing elastic recoil forces inherent to the

A

Chest wall and alveoli

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9
Q

The chest wall wants to recoil

A

Outward (expand)

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10
Q

The alveoli want to recoil

A

Inward (Collapse)

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11
Q

Alveoli and the chest wall are separated by membranes which create an

A

Intrapleural space

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12
Q

At resting lung volumes, what is the

  1. ) Intra-alveolar pressure
  2. ) Intrapleural pressure
A
  1. ) 0 cm H2O

2. ) some negative value usually around -5 cm H2O

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13
Q

The difference between the intra-alveolar pressure and the intrapleural pressure creates the

A

Transpulmonary (transmural) pressure of 0 - (-5) = 5cm H2O

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14
Q

The transpulmonary pressure is sufficient to provide a slight outward tug on the alveoli and keep them from

A

Collapsing

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15
Q

Occurs as a result of chest wall expansion which causes the intrapleural pressure to become more negative, thereby increasing the transpulmonary pressure

A

Inspiration

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16
Q

This pulls on the alveoli essentially from all directions, increasing alveolar diameter and dropping

A

Intra-alveolar pressure below zero

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17
Q

Boyles law tells us that pressure is inversely proportional to

A

Volume

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18
Q

By convention, we assume that unless told otherwise that the atmospheric pressure equals

A

Zero

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19
Q

Thus a pressure gradient exists favoring the movement of air into the

A

Alveoli

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20
Q

Inspiration is an active process that requires contraction of the

A

Diaphragm

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21
Q

A normal non-stressed expiration is passive, owing to the relaxation of the

A

Diaphragm

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22
Q

Chest wall collapse causes the intrapleural pressure to become

A

Less negative (or even very positive with a forced expiration)

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23
Q

This alleviates the outward pull on the

A

Alveoli

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24
Q

Alveolar diameter then decreases, thus elevating

A

Intra-alveolar pressure

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25
Q

Once alveolar pressure supercedes that of atmospheric pressure, air moves

A

Outward (i.e. down the pressure gradient)

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26
Q

Keeps the lungs somewhat expanded during ventilation

A

Transpulmonary pressure

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27
Q

What happens if air is allowed to enter the intrapleural space?

A

Intrapleural pressure reaches or exceeds that of atmospheric pressure. Lung can collapse

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28
Q

Often caused by a chest wall trauma which creates open communication between the atmosphere and the intrapleural space

A

Simple pneumothorax

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29
Q

During a simple pneumothorax, as the chest wall expands during inhalation, the intrapleural pressure does not decrease in the affected

A

Hemithorax

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30
Q

Thus, the normal driving force for alveolar expansion (transpulmonary pressure) is not

A

Generated

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31
Q

Thus, as a result of the loss of the normal tug of war that exists between lung elastic recoil and chest wall expansion, we will eventually see

A

Lung collapse in the affected hemithorax

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32
Q

Results from some internal insult to the visceral or parietal pleura, or some region of the tracheobronchial tree

A

Tension pneumothorax

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33
Q

The nature of this damage is such that a one-way valve is created which enables

A

Air to enter but not exit the pleural space

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34
Q

Over time, intrapleural pressures rise which causes resistance to

A

Lung inflation

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35
Q

This will likely cause

A

collapse of lung ipsilateral to the region of injury

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36
Q

The pressure increase in the injured hemithorax can then cause deviation of the trachea toward the

A

Contralateral hemithorax

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37
Q

In addition to this deviation, we can also see compression of the

A

Heart, vena cava, and contralateral lung

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38
Q

If severe enough, venous return and cardiac output can be compromised so as to result in

A

Hypotension and hemodynamic instability

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39
Q

Defined as the change in lung volume (L) divided by the change in transpulmonary pressure (cm H2O)

A

Lung Compliance

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40
Q

An indicator of how efficiently the lung inflates and deflates (i.e. the work of breathing)

A

Lung compliance

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41
Q

When plotted using an X-Y graph, where the X-axis is transpulmonary pressure and the Y-axis represents lung volume, a very compliant lung is shown by a

A

Steep compliance curve (relative to normal)

42
Q

In other words, in a very compliant lung, a large change in volume occurs with a

A

Small change in pressure

43
Q

A steep compliance curve is clearly seen when dealing with

A

Emphysema

-a manifestation of COPD

44
Q

Why is too compliant of a lung a bad thing?

A

Harder to expel air

45
Q

Shows that a much greater change in pressure is required to move a given volume

A

Flat compliance curve

46
Q

A flat compliance curve is clearly observed in

A

Lung fibrosis (a form of restrictive lung disease)

47
Q

Abnormally high or abnormally low lung compliance both increase the work of

A

Breathing

48
Q

The sound that is heard due to vibrations of the ventricular and large vessel walls due to recoil of arterial and ventricular blood against the semilunar valve leaflets

A

S2

49
Q

Normal conditions where A2-P2 are fused on expiration but split during inspiration

A

Physiologic splitting

50
Q

Occurs due to the decreased intrathoracic pressure that is generated during inspiration

A

Physiologic splitting

51
Q

Decreased intrathoracic pressure allows for increased venous return to the right atrium, which in fact prolongs

A

Diastolic filling of RV

52
Q

This causes a lengthened systolic ejection from the RV and thus we see a delay in closure of th

A

Pulmonic valve

53
Q

Also low intrathoracic pressure increases capitance of the

A

Pulmonary arteries and veins

54
Q

Increased capitance of the pulmonary arteries and veins allows more blood to flow into the pulmonary system this also results in delayed closure of the

A

Pulmonic valve

55
Q

As mentioned, the decrease in intrathoracic pressure lowers pulmonary vein pressure and reduces left heart diastolic filling. With less diastolic volume, we see faster closing of the

A

Aortic semilunar valve

56
Q

Reduced left ventricular output during inspiration slightly lowers

A

Systolic BP

57
Q

During expiration, we see an increase in

A

Intrathoracic pressure

58
Q

The increase in intrathoracic pressure from expiration causes venous return to the right heart to be

A

Reduced

59
Q

When venous return to the right atrium is reduced, we get quicker RV output and thus an earlier

A

P2

60
Q

The so-called respiratory centers are housed within the

A

Medulla

61
Q

These respiratory centers consist of several regions that include the

A

Dorsal respiratory group (DRG) and Ventral respiratory group (VRG)

62
Q

Largely responsible for coordinating inspiratory function

A

DRG

63
Q

Assumes control over both inspiration and expiration

A

VRG

64
Q

The rythm of respiration is due to the highly coordinated activation/inactivation of respiratory neurons within the

A

Pre-Bötzinger complex of the VRG

65
Q

Axons from the DRG and VRG descend the spinal cord and activate neural tracts which ultimately innervate the

A

Muscles of respiraiton

66
Q

Which motor neurons mediate inspiration?

A

Phrenic and external intercoastal

67
Q

Contraction flattens and lowers the diaphragm, thus increasing the volume of the

A

Thoracic cavity

68
Q

This is complemented by contraction of so-called accessory muscles which include the

A

External intercostals and sternocleidomastoid

69
Q

Raise and enlarge the rib cage

A

External intercostals

70
Q

Elevates the sternum

A

Sternocliedomastoid

71
Q

Expiration is normally

A

Passive

72
Q

However, contraction of the internal intercostals, rectus abdominis, internal and external obliques, and transversus abdominis muscles support

A

Forceful expiration

73
Q

Bronchial smooth muscle is innervated by the

A

Vagus Nerve (X)

74
Q

Vagal innervation of bronchial smooth muscle enables PARASYMPATHETIC nervous system dependent

A

Constriction of bronchial smooth muscle

75
Q

Binds to the type 3 cholinergic-muscarinic receptors expressed in bronchial smooth muscle

A

Acetylcholine

76
Q

In addition to type 3 cholinergic-muscarinic receptors, bronchial smooth muscle also expresses

A

Type B2 adrenergic receptors

77
Q

Within bronchial smooth muscle, the activation of B2 adrenoreceptors induces

A

Dilation (opens airway)

78
Q

Albuterol and salmeterol are B2 agonists that are used in the treatment of

A

Asthma and COPD

79
Q

Since bronchial smooth muscle is not innervated by the SNS, SNS-dependent bronchiolar dilation relies upon

A

Circulating epinephrine

80
Q

Responsible for obtaining atmospheric O2 and eliminating CO2

A

Lungs

81
Q

This process is known as

A

Ventilation or respiration

82
Q

Gas exchange within the lungs occurs at the level of the

A

Alveolus

83
Q

A sac-like structure located within the respiratory zones of the lungs

-the terminal point reached by inspired air

A

Alveolus

84
Q

The alveoli are surrounded by

A

Capillaries

85
Q

Capillary blood flow ot alveoli is known as

A

Perfusion (Q)

86
Q

Air flwo to and from alveoli is known as

A

Ventilation (V)

87
Q

The amount of air traversing the nose and/or mouth with each breath

A

Minute ventilation

88
Q

Does the entire volume of air that is inspired with each breath reach the alveoli?

A

No

89
Q

Thus, alveolar ventilation is less than the

A

Minute volume

90
Q

For this reason, the conducting pathways (where gas exchange does not occur) are referred to as the

A

Anatomic dead space

91
Q

The other type of dead space is known as the

A

Alveolar dead space

92
Q

Any significant amount of alveolar dead space is pathologic. It develops when there are regions of

A

Ventilated but not perfused alveoli

93
Q

A person with impaired cardiac output may be likely to develop significant

A

Alveolar dead space

94
Q

Simply the sum of anatomic plus alveolar dead spaces

A

Physiologic dead space

95
Q

A healthy adult has approximately how much dead space per pound of body weight?

A

1mL per pound

96
Q

Transfer of gas across blood-gas barrier and blood-tissue barrier occur via diffusion as regulated by

A

Fick’s Law

97
Q

Fick’s law shows that the amount of gas transferred is proportional to what three things?

A
  1. ) Area of tissue layer
  2. ) Diffusion constant
  3. ) Difference in partial pressure (P1-P2)
98
Q

Fick’s law shows that the amount of gas transferred is inversely proportional to the

A

Tickness

99
Q

Proportional to the gas solubility but inversely proportional to the square root of it’s molecular weight

A

Diffusion constant

100
Q

About 20 times more soluble in liquids than H2O

A

CO2

Cardiovascular and Pulmonary (25 decks)

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