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Physiology > BIOL 0800 Reading- Chapter 13 > Flashcards

BIOL 0800 Reading- Chapter 13 Flashcards

1
Q

Every minute, approximately how much air and blood flows through the lungs/pulmonary capillaries?

A

4L air, 5L blood

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2
Q

What is the structure of the pulmonary system after the larynx?

A

Trachea, into two bronchi, into two bronchioles, into terminal bronchioles, into respiratory bronchioles, into alveolar ducts, into alveolar sacs: alveoli show up in respiratory bronchioles and increase in alveolar ducts and alveolar sacs

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3
Q

What is the conducting zone?

A

From the top of the trachea to the beginning of the respiratory bronchioles; contains to alveoli and no gas exchange

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4
Q

What is the respiratory zone?

A

From the respiratory bronchioles downwards; contains alveoli and gas exchange

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5
Q

What are type I alveolar cells?

A

One-cell thick, flat layer of epithelial cells lining the air-facing surfaces of alveolar walls

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6
Q

What are type II alveolar cells?

A

Interspersed between type I cells; thicker, specialized: produce surfactant

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7
Q

What is inside the alveolar wall?

A

Capillaries and a very small interstitial space: interstitial fluid and loose mesh of connective tissue

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8
Q

What are intercostal muscles?

A

Muscles that run between ribs

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9
Q

What is the pleural sac?

A

Completely closed sac that encloses each lung, made of thin sheet of cells called pleura

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10
Q

What is the difference between visceral and parietal pleura?

A

Internal surface touching the lung, and external surface touching the thoracic cavity interior

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11
Q

What is intrapleural fluid?

A

Fluid between the visceral and parietal pleura

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12
Q

What is the equation for bulk flow?

A

F = deltaP/R

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13
Q

In the equation for bulk flow, what is delta P?

A

Alveolar pressure (Palv) minus atmospheric pressure (Patm)

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14
Q

What happens when Palv is less than Patm?

A

Negative flow, or inspiration

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15
Q

What happens when Palv is greater than Patm?

A

Positive flow, or expiration

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16
Q

What is Boyle’s law?

A

PV = PV

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17
Q

Lung volume depends on what two factors?

A

Transpulmonary pressure and lung stretchability

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18
Q

What is transpulmonary pressure?

A

The difference in pressure between the inside and outside of the lung; Palv minus Pip (intrapleural)

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19
Q

What are the formulas for transmural pressure on the lungs and on the chest cavity?

A

On the lungs is Palv - Pip, and on the chest cavity is Pip - Patm

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20
Q

How does transmural pressure affect inspiration/expiration?

A

Transmural pressure increases for inspiration (decreases Pip relative to Palv), and uses elastic recoil to drive passive expiration

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21
Q

When there is no airflow, why is Pip negative?

A

Because there is always a positive transmural pressure, so Palv > Pip, but Palv = 0

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22
Q

What forces cause intrapleural pressure to be zero when there is no airflow?

A

Elastic recoil of the lungs and the chest cavity causes the lungs to shrink and thoracic cavity to expand: pulls the pleural walls apart and decreases pressure

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23
Q

What is the crucial factor in keeping the lungs partially expanded between breaths?

A

The negative (subatmospheric) intrapleural pressure

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24
Q

What causes the diaphragm to contract?

A

Activation of the phrenic nerves

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25
Q

How does inspiration occur?

A

Thorax expands, Pip becomes subatmospheric, transpulmonary pressure increases, lungs expand, Palv becomes subatmospheric, air flows into alveoli

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26
Q

How does expiration occur?

A

Diaphragm and chest wall recoil inward; Pip returns to normal value, transpulmonary pressure decreases, elastic recoil overcomes transpulmonary pressure, and lungs passively recoil

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27
Q

What is lung compliance?

A

The magnitude of the change in lung volume produced by a given change in transpulmonary pressure

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28
Q

What is the formula for lung compliance?

A

Delta V/delta Ptp

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29
Q

What are two major determinants of lung compliance?

A

Stretchability of lung tissues, and surface tension on alveoli

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30
Q

What is surfactant for?

A

Reduces cohesive forces between water molecules on the alveolar surface: lowers the surface tension and increases lung compliance

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31
Q

What is the law of Laplace?

A

P = 2T/r

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32
Q

Why do alveoli of different sizes exist?

A

Because of Laplace’s law: if the radius is smaller, then the surfactant is denser and surface tension is less, which allows for a higher pressure to prevent the small alveolus from condensing into larger ones

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33
Q

How does transpulmonary pressure affect resistance?

A

Increase in transpulmonary pressure increases airway radius, and airway resistance is decreased (inspiration)

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34
Q

What is lateral traction?

A

When the elastic connective-tissue fibers around the alveolar tissue help pull the airways open when the lungs pull on them.

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35
Q

How does epinephrine affect airway resistance?

A

Relaxes airway smooth muscle through beta-adrenergic receptors

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36
Q

What substance contracts airways to increase airway resistance?

A

Leukotriene, an eicosanoid

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37
Q

What is the tidal volume?

A

The volume of air taken in during a single expiration; usually the same volume as is expired

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38
Q

What is the inspiratory reserve volume (IRV)?

A

The maximal amount of air that can be increased above TV

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39
Q

What is functional reserve capacity (FRC)?

A

The amount of air left in the lungs after a normal tidal expiration: ERV + RV

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40
Q

What is expiratory reserve volume (ERV)?

A

The maximal amount of air that can be expired below TV

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41
Q

What is residual volume?

A

The amount of air remaining in the lungs after maximum expiration

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42
Q

What is the function of residual volume?

A

Keeps alveoli inflates between breaths, mixes with fresh air on next inspiration

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43
Q

What is the vital capacity (VC)?

A

The maximum amount of air you can exhale after a maximum inspiration; ERV + TV + IRV

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44
Q

What is inspiratory capacity (IC)?

A

Maximum amount of air that can be inhaled after a normal tidal expiration; RV + ERV

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45
Q

What is minute ventilation?

A

Total ventilation per minute: TB x RR (respiratory rate)

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46
Q

What is the approximate minute ventilation of a normal person?

A

6 L: (0.5 TV)(12 breaths each minute)

47
Q

What is anatomical dead space?

A

The space within the airways that doesn’t permit gas exchange

48
Q

How do you calculate how much fresh air enters the lungs?

A

TV - deadspace = fresh air volume

49
Q

What is alveolar ventilation?

A

The total volume of fresh air entering the alveoli per minute: = (TV - deadspace)(respiratory rate)

50
Q

Why is breathing depth more important than breathing frequency to increase alveolar ventilation?

A

Because you still need to overcome dead space

51
Q

What is alveolar dead space?

A

The volume of air that isn’t used for gas exchange because alveoli have little or no blood supply; small in normal lungs

52
Q

What is physiological dead space?

A

The sum of anatomical and alveolar dead space

53
Q

What is the respiratory quotient?

A

The ratio of CO2 produced to O2 consumed; approximately 0.8

54
Q

What is Dalton’s law?

A

The sum of all the partial pressures of gases is the total pressure, since the pressures of different gases don’t depend on each other

55
Q

What is Henry’s law?

A

The amount of gas dissolved in a liquid will be directly proportional to the partial pressure of the gas with which the liquid is in equilibrium; partial pressures at equilibrium of a gas in liquid and gas phases is identical

56
Q

What are normal alveolar gas pressures?

A

105 for oxygen, 40 of CO2

57
Q

Why are air pressures of O2 and CO2 different from alveolar pressures?

A

Because of diffusion in the pulmonary capillaries

58
Q

What are three factors that determine the precise value of alveolar PO2?

A

PO2 of atmospheric air (decreased causes decrease); rate of alveolar ventilation (decreased causes decrease); rate of oxygen consumption (increased causes decrease) assuming only one factor changes at a time

59
Q

What is hypoventilation?

A

When alveolar ventilation can’t keep up with CO2 production: increase in PCO2

60
Q

What is hyperventilation?

A

When alveolar ventilation is too great for CO2 production; decrease in PCO2

61
Q

What is the major disease-induced cause of inadequate oxygen movement between alveoli and pulmonary capillary beds?

A

Ventilation-perfusion inequality

62
Q

What is the major effect of ventilation-perfusion inequality?

A

To lower the PO2 of systemic arterial blood

63
Q

Why is the PO2 of blood in circulation normally about 5 mmHg less than that of average alveolar air?

A

Because gravity causes a different blood flow distribution in the lung, which contributes to ventilation-perfusion inequality, which reduces PO2

64
Q

What is shunt?

A

Blood flow to an area without ventilation

65
Q

What is the main homeostatic mechanism to avoid ventilation-perfusion inequality for low ventilation and low perfusion?

A

When there is low alveolar PO2 (due to decrease in ventilation), the vessel vasoconstricts and directs blood elsewhere to properly ventilated areas; of when there is low alveolar PCO2, the bronchioles constrict and direct airflow elsewhere

66
Q

What is hemoglobin?

A

Four subunits made of one polypeptide and one heme each (a globin and four heme groups); heme groups contain iron for cooperative binding to oxygen

67
Q

What is percent hemoglobin saturation?

A

(O2 bound to Hb) / (maximal capacity of Hb to bind to O2) x 100

68
Q

What factors determine the % Hb saturation?

A

Blood PO2

69
Q

What is the oxyhemoglobin dissociation curve?

A

The experimentally determined quantitative relationship between blood PO2 and the combination of oxygen with hemoglobin; sigmoid because of cooperative binding

70
Q

What is the approximate shape/range of the oxyhemo dissoc curve?

A

Steep slope from 10-60 mmHg, plateaus at 70-100 mmHg PO2; **at a PO2 of 60 mmHg, 90% hemoglobin saturation

71
Q

What is the biological significance of the plateau in the oxyhemo dissoc curve?

A

Safety net! Even if atmospheric PO2 decreased from 100 to 60 mmHg, total hemoglobin saturation would only decrease by 10% or so

72
Q

What is the biological significance of the steep slope of the oxyhemo dissoc curve?

A

Allows for easy unloading of oxygen: small PO2 changes can lead to a big decrease in hemoglobin saturation

73
Q

How does temperature affect the OHD curve?

A

Increased temperature shifts the curve right: makes it more difficult to unload oxygen

74
Q

How does acidity affect the OHD curve?

A

Increased acidity (lower pH) shifts the curve right: makes it more difficult to unload oxygen

75
Q

How does DPG concentration affect the OHD curve?

A

Increased DPG concentration shifts curve right: makes it more difficult to unload oxygen

76
Q

How does PCO2 affect the OHD curve?

A

Increased PCO2 increases H+ concentration, which increases acidity: shifts curve right: lowers affinity of Hb for O2

77
Q

How do CO2 and H+ affect hemoglobin’s affinity for oxygen?

A

Allosterically modulate the globin

78
Q

How does DPG affect Hb’s affinity for oxygen?

A

DPG = released during glycolysis (only respiration for RBCs, so lots of DPG in RBCs); allosterically modulates Hb

79
Q

Which is more soluble in water, CO2 or O2? Why is this important?

A

CO2: blood carries more dissolved CO2 than dissolved O2

80
Q

How is CO2 transported in the blood?

A

Some by dissolving, some by binding with Hb to form carbaminohemoglobin, and most converted to bicarbonate and hydrogen ions by carbonic anhydrase

81
Q

What is carbaminohemoglobin?

A

When CO2 binds to Hb (deoxyhemoglobin, which has a higher affinity for CO2 than for O2, than does HbO2)

82
Q

Why is it important that the chloride-bicarbonate exchange removes HCO3- from the RBC?

A

So that the reaction still favors dissociation of bicarbonate

83
Q

Why is venous blood slightly more acidic than arterial blood?

A

Because dissociation of bicarbonate produces H+, which binds to deoxyhemoglobin, but there’s still some left: decreases the pH (more acidic)

84
Q

What is associated with hypo/hyperventilation, respiratory acidosis or alkalosis?

A

Acidosis associated with hypoventilation, alkalosis associated with hyperventilation

85
Q

What initiates nerves impulses to the respiratory skeletal muscles?

A

Medulla oblongata activity: in medullary respiratory center

86
Q

What are the two components of the medullary respiratory center?

A

The dorsal and ventral respiratory groups (DRG and VRG)

87
Q

What is the DRG?

A

Primarily fire during inspiration; input to spinal motor neurons that activate inspiratory muscles: diaphragm and inspiratory intercostal muscles

88
Q

What is the nerve that innervates the diaphragm?

A

Phrenic nerve

89
Q

What is the VRG?

A

Rhythm generator: pacemaker cells and complex neural network that sets basal respiratory rate; respiratory rhythm generator located in the pre-Botzinger complex in the upper VRG; nerves in lower half that fire for inspiration AND expiration

90
Q

What is the upper half of the VRG?

A

Rhythm generator in the pre-Botzinger complex; pacemaker cells; inspiratory neurons (input from DRG inspiratory neurons, from respiratory rhythm generator; output to inspiratory motor neurons)

91
Q

What is the lower half of the VRG?

A

Expiratory neurons: important for large increases in ventilation like in exercise: active expiration through contraction

92
Q

How is medullary inspiratory nerve activity modulated?

A

By the pons: apneustic center in lower pons, pneumotaxic center in uppon pons

93
Q

What is the apneustic center?

A

In the lower pons: modulates medullary inspiratory activity, inhibitory to end inspiration

94
Q

What is the pneumotaxic center?

A

In the upper pons: modulates apneustic center; smooths transition between inspiration/expiration

95
Q

What are pulmonary stretch receptors for?

A

Cutting off inspiration: activated by large lung inflation: afferent nerve fibers send action potentials to inhibit medullary inspiratory neuron activity

96
Q

What is the Hering-Breuer reflex?

A

When afferent nerve fibers from stretch receptors send action potentials to the brain to inhibit medullary inspiratory behavior and end inspiration; BUT only under conditions of large TV like during exercise

97
Q

What are peripheral chemoreceptors for respiration?

A

Located in neck by common carotid arteries and in thorax on aortic arch: carotid bodies and aortic bodies (distinct from carotid and aortic baroreceptors); stimulated by decrease in arterial PO2 or increase in H+; provide excitatory input to medullary respiratory systems

98
Q

What are the central chemoreceptors for respiration?

A

Located in medulla oblongata; provide excitatory input to medullary respiratory systems; stimulated by increase in H+

99
Q

Why do changes in PCO2 trigger ventilation control reflex?

A

Mostly through increases or decreases in H+ concentration, which is detected by the central chemoreceptors and dealt with accordingly

100
Q

Which chemoreceptors respond to H+ concentration changes, peripheral or central?

A

Peripheral for metabolic acidosis/alkalosis (not caused by CO2 changes), and central for respiratory acidosis/alkalosis (caused by CO2 changes)

101
Q

How does H+ concentration affect chemoreceptor activity?

A

Increase in H+ increases chemoreceptor activation of medullary respiratory neurons, which increases respiration

102
Q

What is associated with hyper/hypoventilation, metabolic alkalosis or acidosis?

A

Metabolic acidosis triggers hyperventilation (reduces arterial PCO2, so H+ back to normal); metabolic alkalosis triggers hypoventilation (increases arterial PCO2, so H+ back to normal)

103
Q

Why doesn’t arterial PCO2 increase during exercise?

A

Because arterial PCO2 depends on alveolar PCO2, and alveolar PCO2 depends on ratio of CO2 production to alveolar ventilation: ventilation increase proportionally with CO2 production during exercise, so no increase in alveolar PCO2

104
Q

What is the limiting factor in strenuous exercise, ventilation or cardiac output?

A

CO: ventilation can increase enough to maintain PO2

105
Q

Why is lactic acid partially responsible for hyperventilation during exercise?

A

Because it increases blood H+ concentration, which triggers the peripheral chemoreceptors to innervate the medullary inspiratory neurons to increase ventilation

106
Q

How do J receptors act as a protective respiratory reflex?

A

In capillary walls/interstitium: stimulated by increase in lung interstitial pressure cased by fluid collection: rapid breathing, dry cough

107
Q

What are the four kinds of hypoxia?

A

Hypoxic hypoxia (hypoxemia); anemic hypoxia (CO hypoxia); ischemic hypoxia; histotoxic hypoxia

108
Q

What is hypoxic hypoxia?

A

Hypoxemia: arterial PO2 reduced

109
Q

What is anemic hypoxia?

A

CO hypoxia; arterial PO2 normal but total oxygen content of blood is reduced because of inadequate numbers of RBCs, deficient Hb, or CO poisoning

110
Q

What is ischemic hypoxia?

A

Blood flow to tissues is too low

111
Q

What is histotoxic hypoxia?

A

Normal quantity of oxygen to tissues, but cell can’t use it properly because of toxic agent interference

112
Q

What is hypercapnea?

A

Increased retention of CO2 that leads to increased arterial PCO2

113
Q

Why does ventilation-perfusion inequality affect O2 more than CO2?

A

Because of the oxyhemo dissoc curve: increasing ventilation doesn’t really increase PO2 because of the curve, so PO2 remains low (hypoxia); but CO2 is linear: poor ventilation does increase PCO2, but then increased ventilation brings it right back down again

Physiology (13 decks)

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