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Human Pathophysiology: Final > Respiratory System I > Flashcards

Respiratory System I Flashcards

1
Q

What are the major and minor functions of the respiratory system?

A

major: supply oxygen, remove carbon dioxide
minor: humidify and filter air

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2
Q

What are the conducting zones and what are their functions/features?

A

Consists of: upper airways, trachea, bronchi, bronchioles
Function: get air to alveoli; filter and humidify air
Features: mucociliary ladder, mucous glands, ciliated cells, goblet cells, smooth muscle, cartilage

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3
Q

What is the translational zone?

A

respiratory bronchioles

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4
Q

What are the respiratory zones and what are their functions/features?

A

Consists of: alveolar ducts, alveoli
Functions: gass exchange, maintains mechanical stability via surfactant and connective tissue proteins
Features: Type I and Type II epithelial cells, macrophages, fibroblasts

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5
Q

What is the difference between Type I and Type II epithelial cells in the lungs?

A

Type I: make up 90-95% of alveolar surface; permeable and involved in gas exchange
Type II: secrete surfactant

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6
Q

What is VE?

A

minute ventilation - the amount of air one breaths per minute

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7
Q

What is VT?

A

tidal volume - size of the breath

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8
Q

What is VD?

A

anatomic dead space - the volume of all the airways that are not involved in gas exchange

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9
Q

What is VA?

A

alveolar ventilation - how much fresh air reaches the gas exchange region of the lung per minute

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10
Q

Definition: the volume of any air spaces that do not receive a blood supply plus the anatomic dead space

A

physiologic dead space

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11
Q

Definition: the volume of any equipment between the subject and the atmosphere

A

equipment dead space

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12
Q

What are the main muscle of inspiration? Or expiration?

A

Inspiration: diaphragm
Expiration: abdominal muscles

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13
Q

How does the respiratory muscle cause ventilation?

A

It lowers the pleural pressure

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14
Q

What is Ppl?

A

pressure in the pleural space

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15
Q

What is PA?

A

pressure in the airspaces

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16
Q

What is PL?

A

pressure difference across the lung; lung recoil pressure

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17
Q

What is Pao?

A

pressure at the airway opening

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18
Q

What is FRC?

A

functional residual capacity; the volume of the lung at the end of a breath

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19
Q

What happens during end expiration?

A

relaxed FRC; the Ppl (-4) balances with the PL (4), PA is zero

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20
Q

What happens during inspiration?

A

the diaphragm and the rib cage muscles contract; decreasing Ppl; PL increases to compensate; PA decreases and is now lower than atmospheric pressure (air moves in)

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21
Q

What happens during End inspiration?

A

the Ppl (now -7) balances with the PL (7) but lung volume is bigger; PA is zero

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22
Q

What happens during expiration?

A

muscles relax and Ppl increases; PL decreases to compensate; PA increases and is now higher than atmospheric pressure (air moves out)

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23
Q

What do the respiratory muscles have to work against?

A
  • lung recoil

- resistance of the airways

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24
Q

What is the difference between filling a lung with fluid vs. air? Why?

A

filling an air-filled lung requires a lot more pressure because the attractive forces between water molecules resists lung expansion

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25
Q

Definition: produced in the lungs to reduce surface tension by interposing itself between water molecules

A

surfactant

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26
Q

What happens during Respiratory Distress Syndrome in a baby?

A

Synthesis of surfactant begins at about 34 weeks of gestation. If a baby is born premature (

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27
Q

How is Respiratory Distress Syndrome treated?

A
  • tracheal installation of artificial surfactant
  • mechanical ventilation
  • if deliver can be delayed, treatment of mother with cortisol increases production of surfactant by fetus
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28
Q

What is VO2?

A

the flux, or movement, of gas

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29
Q

What is PAO2?

A

the partial pressure of oxygen in the alveoli

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30
Q

What is PcapO2?

A

the partial pressure of O2 in the capillary

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31
Q

What is VO2 (flux) proportional to? (equation)

A

area * (PAO2 - PcapO2) / thickness

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32
Q

What is the difference in diffusion rate of CO2 and O2?

A

CO2 diffuses much more quickly that O2 because it is more soluble in water/blood

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33
Q

What is the equation for PACO2?

A

PACO2 = VCO2 / VA * K

K = constant
VCO2 = rate of CO2 production by the body
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34
Q

How are PaCO2 and PACO2 related?

A

PaCO2 = PACO2

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35
Q

How are PaO2 and PAO2 related (in healthy lungs)?

A

PaO2 is almost but not quite equal to PAO2

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36
Q

What sensors monitor O2?

A

aortic and carotid chemoreceptors

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37
Q

What is special about the aortic and carotid chemoreceptors?

A

they have their own arterial blood supply and their blood flow is 20x higher than their metabolic needs

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38
Q

What is the flaw of aortic and carotid chemoreceptors?

A

the PO2 is the same as the arterial blood and what is sensed is PaO2 not the amount of O2 in the blood

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39
Q

How do the chemoreceptors in the medulla work?

A

CO2 diffuses across the blood brain barrier and combines with water to form carbonic acid. Carbonic acid dissociates to bicarbonate ion and H+. Increases in H+ in CSF stimulates medullary chemoreceptors.

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40
Q

How is H+ sensed in the carotid chemoreceptors?

A

CO2 and combines with water to form carbonic acid. Carbonic acid dissociates to bicarbonate ion and H+. H+ is sensed by carotid chemoreceptors.

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41
Q

Do changes in blood pH affect the medullary chemoreceptors?

A

No, H+ cannot cross the BBB.

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42
Q

Definition: respiratory center of the brain

A

integrating center in medulla

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43
Q

What else can stimulate (or inhibit) the respiratory center?

A
  • emotions
  • pain
  • voluntary motor centers
  • afferents from the lungs, chest wall, respiratory muscles, and skeletal muscle
  • temperature
  • hormones
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44
Q

How does anxiety affect the respiratory center?

A

anxiety –> increased ventilation –> decreased PaCO2 –> constriction of cerebral arteries –> restriction of blood flow to brain –> dizziness and maybe even impaired brain function

45
Q

How do you treat respiratory distress due to anxiety?

A

breath into a paper bag; rebreathing CO2 will prevent CO2 levels from dropping

46
Q

How does CCHS affect the respiratory center?

A

CCHS is congenital central hypoventilation syndrome, where the patient has no sensitivity to CO2 (malregulation of autonomic functions due to a genetic mutation; controls breaths consciously). Their body can’t sense when CO2 levels are too high and so they often need to be on a ventilator at night.

47
Q

How does the Hering Breuer reflex effect respiration?

A

Pulmonary stretch receptors present in the smooth muscle of the airways respond to excessive stretching of the lung during large inspirations to prevent overinflation.

48
Q

What effect does hyperventilation have? Why do dogs not suffer from this when they hyperventilate to cool off?

A

Hyperventilating cause CO2 levels to drop (pH to increase) causing respiratory alkalosis. Dogs pant with shallow breath that are high in frequency but low in volume (or gas exchange). Therefore, they are able to increase the amount of moisture evaporating with minimal gas exchange. (aka. high VE but no change in VA)

49
Q

How do hormones during pregnancy affect the respiratory center?

A

Progesterone increase the medulla oblongata’s sensitivity to CO2. This causes the patient to hyperventilate and decrease CO2 levels. A pregnant woman will usually have a PaCO2 of 36 vs. the normal 40.

50
Q

How does DVT affect dead space?

A

It adds to the physiologic dead space when a embolism breaks off from a thrombus in the leg and travels to the lung, eventually created a blood clot in the lungs somewhere. The areas that do not receive blood flow due to this blood clot now become dead space.

51
Q

What factors can increase the risk of DVT?

A
  • hip or leg fractures
  • standing or sitting for long periods of time
  • obesity
  • smoking
  • pregnancy, birth control pills, estrogen replacement therapy
52
Q

What are some things that can cause hypoventilation?

A
  • drugs that suppress the respiratory center (morphine)
  • myasthenia gravis
  • disease of the nerves
  • CCHS (Ondine’s curse)
53
Q

Definition: a neuromuscular autoimmune disease where antibodies block ACh receptors and cause muscle weakness and fatigue (voluntary muscles)

A

myasthenia gravis

54
Q

What can cause a decrease in ventilation despite normal effector function?

A
  • increased stiffness of lungs

- increased resistance to breathing

55
Q

How does altitude affect ventilation?

A

decreased atmospheric pressure –> decreased PO2 –> decreased PAO2 –> decreased PaO2 –> stimulation of peripheral chemoreceptors –> increased ventilation to increase PaO2 –> decreased PaCO2 –> decrease ventilation again (NET EFFECT: ventilation increases slightly)

56
Q

What are some of the acute affects of high altitude caused by the changes in PaO2 and PaCO2 levels?

A

PaO2 drops: fatigue, headache, irritability, dizziness, nausea, palpitation, loss of appetite, exertion dyspnea, abdominal cramps, impaired cerebration, insomnia
PaCO2: constriction of cerebral blood vessels (may contribute to some symptoms above)

57
Q

What are some of the acute affects of high altitude caused by the changes in PAO2?

A

decreased PAO2 can cause vasoconstriction of pulmonary arteries leading to increased pulmonary pressure –> can cause pulmonary edema

58
Q

What are the chronic effects of high altitude on the body?

A
  • decrease PaO2 stimulates kidney to increase production of erythropoietin –> acts on bone marrow to stimulate production of more red blood cells
  • HCO3- is pumped out of CSF, increasing H+ concentration and removes some of the inhibition to breathing provided by PaCO2 (increases ventilation)
  • vascularity and myoglobin content of muscle increases
  • 2,3-DPG levels of RBC increases causing rightward shift of the oxyhemoglobin dissociation curve
59
Q

What happens to VO2 (amount of O2 used) during exercise?

A

increases from 250 ml/min to as high as 3000 ml/min

60
Q

What happens to ventilation during increasing exercise?

A

It increases direct proportion to the magnitude of VO2 up until the anaerobic threshold. Then is increases exponentially.

61
Q

How does PaCO2, PaO2, and H+ levels change prior to and after the anaerobic threshold?

A

Prior: no changes, they stay constant
After: H+ rises (lactic acid), PaCO2 falls, and PaO2 increases

62
Q

What causes ventilation to increase prior to the anaerobic threshold?

A
  • afferents from receptors in the muscles and joints of exercising muscles
  • collateral discharge from brain centers that initiate muscle activity
  • increased temperature
  • adrenaline (stimulates breathing)
  • learned responses (seen even in patients with CCHS)
63
Q

What causes ventilation to increase after the anaerobic threshold?

A

all the things that contribute to ventilation prior to anaerobic threshold plus increased H+ ions due to lactic acid

64
Q

How is O2 carried in the blood?

A
  • 1-2% of it dissolves in the plasma

- rest is bound to hemoglobin?

65
Q

What are some characteristics of hemoglobin?

A
  • contains iron which oxygen binds to
  • 4 binding sites
  • oxyhemoglobin is reddish
  • deoxyhemoglobin is blueish
66
Q

The amount of O2 that blood can carry depends on what?

A
  • amount of hemoglobin in the blood

- PaO2

67
Q

A normal person has __g of hemoglobin per __mL of blood and __g of hemoglobin can carry __ ml of O2.

A

15
100
1
1.34

68
Q

A normal person has a solubility of ____ ml O2/ 100ml/mm Hg.

A

0.003

69
Q

What are the normal values for PaO2 and PaCO2?

A

PaO2: 100 mm Hg (set point: >80 mm Hg)
PaCO2: 40 mm Hg (set point: 40 mm Hg)

70
Q

What is the normal value for venous O2?

A

40 mm Hg

71
Q

Why is there still a lot of O2 in the blood?

A

It acts as a reserve

72
Q

What factors can shift the oxyhemoglobin associated curve to the right?

A

Right: increased temperature, increase PCO2, increased 2,3 DPG (improves O2 unloading)

73
Q

How does an exercising muscle get more oxygen?

A

When the muscle exercises, it uses up O2 and the PO2 of the tissue drops. According to the dissociation curve, this allows more O2 to come off the hemoglobin.

74
Q

How does exercise affect the oxyhemoglobin dissociation curve?

A

It increases CO2, H+ and heat, shifting the curve to the right causing there to be less affinity of the hemoglobin for O2.

75
Q

What is anemia and what is it caused by?

A

Its a decrease in the number of RBC resulting in a diminished capacity to carry O2. Usually results from a nutritional deficiency in iron.

76
Q

How does anemia affect the dissociation curve, PaO2, and ventilation?

A

It doesn’t change it, but the totally number of hemoglobin per ml of blood is lower so the O2 carrying capacity changes. However, PaO2 and ventilation remain unchanged.

77
Q

What is sickle cell anemia and why is it harmful?

A

It results from a genetic mutation that changes a single amino acid in the beta chain of Hb. The resulting hemoglobin is less soluble in water at low PO2 and comes out of solution and crystallizes. The RBCs are less flexible –> break during transit through capillaries –> anemia.

78
Q

How is sickle cell anemia treated?

A

Hydroxyurea - increases production of gamma instead of beta chains.

79
Q

Why are gamma chains of Hb important in a fetus?

A

They shift the dissociation curve to the left, which promotes O2 unloading from the mother’s hemoglobin to the baby. Gamma chains don’t bind 2,3 DPG.

80
Q

How does myoglobin differ from hemoglobin?

A
  • found in muscle
  • only has 1 molecule of iron per myoglobin (less O2 carrying capacity)
  • O2 dissociation curve is displaced to the left of the hemoglobin dissociation curve (so O2 unloads from hemoglobin to myoglobin)
  • serves as an O2 store in muscle
81
Q

What effect does CO have on the body?

A
  • competes with O2 for binding sites in Hb –> reduces amount of O2 bound
  • shifts dissociation curve to the left, making it more difficult to unload O2
  • does NOT change PaO2 so it does not activate chemoreceptors (aka. ventilation does not increase)
82
Q

In what 3 forms is CO2 carried in the blood?

A
  • physically dissolved (10%)
  • carried bound to hemoglobin (30%)
  • combined with water for form carbonic acid which dissociates into bicarbonate ion (60%)
83
Q

Definition: elevated PaCO2

A

hypercabnia

84
Q

Definition: elevated PaO2

A

hypoxemia

85
Q

What is the primary determinant of PaCO2?

A

PAO2

86
Q

What is the primary determinant of PAO2?

A

alveolar ventilation

87
Q

What is the equation for VE?

A

VT * f

88
Q

What is the equation for VA?

A

(VT - VD) * f

89
Q

Definition: any ventilation that decreases PaCO2 below 40 mmHg

A

hyperventilation

90
Q

Definition: any ventilation that increases PaCO2 above 40 mmHg

A

hypoventilation

91
Q

What is the primary determinant of hypercarbia?

A

hypoventilation

92
Q

What are some things that can increase the amount of dead space?

A
  • breathing through a tube (snorkel, mask, ventilator)
  • pulmonary embolus (blocks blood flow to parts of the lung)
  • any disease that alters the distribution of blood flow and ventilation to different parts of the lung
93
Q

What are the 4 primary causes of hypoxemia?

A
  • hypoventilation
  • diffusion impairment
  • shunt
  • V/Q abnormalities
94
Q

What is the equation for PAO2?

A

PAO2 = PIO2 - (K * VO2/VA)

PIO2 = partial pressure for O2 inhaled
VO2 = oxygen consumption
K = constant
95
Q

Why does hypoventilation cause hypoxemia?

A

When PAO2 is reduced, the PaO2 of the blood leaving those capillaries is also reduced because they come into equilibrium with the PAO2.

96
Q

What is a diffusion impairment and how does it cause hypoxemia?

A

When there is an increase in the time it takes for O2 to diffuse from the alveoli into red blood cells. Diffusion impairment alone actually is almost never the primary cause of hypoxemia, even in disease. (Exception: exercise with fibrosis)

97
Q

The rate of diffusion depends on what factors?

A
  • the surface area of the lung
  • the thickness of the pulmonary epithelial/capillary endothelial layer
  • the difference in PO2 between the alveolar gas and the capillary blood
98
Q

What are some diseases that can cause a diffusion impairment?

A
  • pulmonary fibrosis: scarring of lung tissue and thickening of the alveolar walls
  • emphysema: destruction of the alveolar walls results in a decrease in total surface area of the lung
99
Q

How can exercise in patient with severe fibrosis cause hypoxemia?

A

During exercise, the amount of time that RBCs spend in the pulmonary capillaries decreases, so not only does diffusion take more time by there is less time available.

100
Q

What is a shunt?

A

When blood passes from the right heart to the left without being oxygenated.

101
Q

What are two ways a shunt can occur? Give some examples.

A
  • blood goes from right heart to left heart without passing through lungs (Ex. bronchial arteries, patent ductus arteriosus in fetuses)
  • blood does go through the lung but never comes into contact with alveolar gas (Ex. foreign object in airway, pneumonia)
102
Q

How does pneumonia cause a shunt?

A

The alveolar airspaces become filled with pus and fluid instead of air, and the blood directed to those spaces never comes into contact with alveolar gas

103
Q

What will increasing ventilation do from someone with a shunt?

A

It will increase PAO2 in the good parts of the lungs but not the bad (since air isn’t reaching the blood anyway). Since the good parts have already fully saturated hemoglobin, increasing PAO2 won’t increase the O2 content and will have no effect on PaO2.

104
Q

What will increasing the O2 concentration of gas do from someone with a shunt?

A

The “bad” parts of the lungs will still never come in contact with the air and remain deoxygenated. The “good” parts will come into contact with the air but will already be fully saturated so there will be no effect on PaO2 (aside from a slightly higher amount of O2 dissolved in the blood).

105
Q

What is the most common cause of hypoxemia?

A

V/Q abnormalities

106
Q

What is the difference in blood flow between the upper and lower lungs and why?

A

The upper parts of the lungs receive less blood than the lower parts because of gravity.

107
Q

What is the difference in ventilation between the upper and lower lungs and why?

A

The upper parts of the lung receive less tidal volume because they are already more inflated and on a steeper part of the PV curve (less compliant).

108
Q

What are the differences between the upper and lower lungs in terms of ventilation and blood supply?

A

Upper: more ventilation, greater PAO2, lower PACO2
Lower: less ventilation, lower PAO2, great PACO2

109
Q

How do PAO2 an PaO2 compare in healthy patients? In a patient with lung disease?

A

PaO2 is slightly less than PAO2 (by maybe 3 mm Hg). In a patient with lung disease, not all parts of the lung are similarly affected and so ventilation and blood flow are unevenly distributed and it can cause big decreases in PaO2.

Human Pathophysiology: Final (6 decks)

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