Ch. 4 Respiratory Physiology Flashcards

1
Q

Tidal volume

A

volume inspired and expired with each normal breath

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2
Q

Inspiratory reserve volume

A

volume that can be inspired over and above the tidal volume
used during exercise

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3
Q

Expiratory reserve volume

A

volume that can be expired after the expiration of a tidal volume

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4
Q

Residual volume

A

the volume that remains in the lungs after maximal expiratory
**cannot be measured by spirometry

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5
Q

Anatomic dead space

A

volume of the conducting airways
**approximately 150 mls

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6
Q

Physiologic dead space

A

volume of the lungs that does not participate in gas exchange
**approx equal to the anatomic dead space in normal lungs
**is a functional measurement with equation( VD= VT X ((PACO2- PECO2)/PACO2))

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7
Q

Inspiratory capacity

A

sum of tidal volume and IRV

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8
Q

Functional residual capacity (FRC)

A

sum of ERV (exp reserve vol) and RV (residual vol)
**volume remaining in the lungs after a tidal volume is expired
**cannot be measured by spirometry

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9
Q

Vital capacity or forced vital capacity

A

sum of tidal volume, IRV & ERV
**volume that can be forcibly expired after a maximal inspiration

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10
Q

Total lung capacity

A

sum of all four lung volumes
-volume of lungs after a maximal inspiration
**cannot be measured by spirometry

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11
Q

Forced expiratory volume

A

volume of air that can be expired in teh first second of a forced maximal expiration
**normal 80% of the forced vital capacity

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12
Q

Which respiratory muscles are not used during normal quiet breathing, but during exercise and in respiratory distress?

A

external intercostal and accessory muscles

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13
Q

Expiration is normally an active or passive process?

A

Normally passive
**used during exercise or when airway resistance is increased b/c of disease

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14
Q

Which law describes surface tension of the alveoli?

A

Laplace law:
P= 2T/r
p=collapsing pressure on alveolus (or pressure required to keep alveolus open)
T= surface tension
r=radius of the alveolus

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15
Q

Which alveoli have high/low collapsing pressures and are difficult/easy to keep open?

A

large alveoli– low collapsing pressure & easy to keep open

Small alveoli– high collapsing pressure & hard to keep open

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16
Q

In the absence of what susbstance, the small alveoli have a tendency to collapse?

A

surfactant

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17
Q

What is the mechanism of surfactant?

A

-lines alveoli
-reduces surface tension– by disrupting the intermolecular forces between liquid molecules= INC compliance

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18
Q

What cells of the lungs produce surfactant?

A

type II alveolar cells

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19
Q

What is surfactant primarily made up of?

A

phospholipid– dipalmitoylphhatidylcholine (DPPC)

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20
Q

In babies, neonatal respiratory distress syndrome, what occurs due to lack of surfactant?

A

atelectasis
–decreased V/Q and right to left shunt, hypoxemia

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21
Q

Airflow in the lungs is driven by what?

A

the pressure difference between the mouth and the alveoli
**proportional to pressure difference & inversely proportional to airway resistance
Q= Change P/R
Q=airflow
Change P= pressure gradient
R= airway resistance

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22
Q

How is resistance to the airway described?

A

Poiseuille Law

R= (8nL)/ pieR^4)
R= resistance
n= viscosity of the inspired gas
l=length of the airway
r= radius of teh airway

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23
Q

What is the major site of airway resistance?

A

medium sized bronchi

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24
Q

Which response (parasympathetic vs sympathetic) causes constriction of the airways, decrease the radius and increase the resistance to airflow?

A

Parasympathetic stimulation
**ie asthma

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25
Q

Which response (parasympathetic vs sympathetic) causes dilation of the airways, increase in the radius and decrease in the resistance to air flow?

A

sympathetic stimulation
**through beta 2 receptors

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26
Q

Describe pressures and airflow: at rest (before inspiration begins)

A

-alveolar pressure equals atmospheric pressure
-intrapleural pressure is negative
-lung volume is the FRC

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27
Q

Describe pressures and airflow: during inspiration

A

-inspiratory muscles contract and cause the volume of the thorax to increase (pressure gradient allows air to flow into the lungs)
-intrapleural pressure becomes more negative
-lung volume increases by one VT

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28
Q

Describe pressures and airflow:
during expiratoin

A

-alveolar pressure becomes greater than atmospheric pressure (air flows out of lungs)
-intrapleural pressure returns to its resting value during a normal (passive) expiration
-lung volume returns to FRC

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29
Q

What percentage of systemic cardiac output bypasses pulmonary circulation?
**admixture of venous oxygenated and arterial blood making the PO2 of arterial blood slightly lower than alveolar air

A

2% of systemic cardiac output
physiologic shunt

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30
Q

Which form of iron binds O2?

A

ferrous state (Fe2+)

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31
Q

Each subunit of hemoglobin contains an iron-containing porphyrin?

A

a heme moiety

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32
Q

How is the movement of O2 from mother to fetus facilitated?

A

B/c fetal hemoglobin (alpha2gamma2) has a higher affinity for O2 than adult hemoglobin= left shift

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33
Q

Which form of iron is in methemoglobin, thus no binding of O2 occurs?

A

Fe 3+ state

34
Q

What causes shifts in the hemoglobin-O2 dissociation curve: TO THE RIGHT?
**meaning affinity of hemoglobin for O2 is decreased (dec O2 content of blood)

A
  1. INC in PCO2 or decreases in pH
  2. INC temperature
  3. INC 2,3-DPG
35
Q

What is the adaptation to chronic hypoxemia (such as living at a high altitude)?

A

increases synthesis of 2,3 DPG, which binds to hemoglobin and facilitates unloading of O2 in the tissues

36
Q

What causes shifts in the hemoglobin-O2 dissociation curve: TO THE LEFT?
**meaning affinity of hemoglobin for O2 is increased

A
  1. decreased PCO2, or INC pH
  2. DEC temperature
  3. decreased 2,3 DPG
37
Q

Carbon monoxide poisoning causes what shift in the hemoglobin-O2 dissociation curve?

A

shift of the curve to the left
–> CO competes for O2 binding sites on hemoglobin, decreasing O2 content of blood

38
Q

What are causes of hypoxemia

A

decreased PAO2
Diffusion defect
V/Q defects
right to left shunts

39
Q

define hypoxemia

A

decrease in arterial PO2

40
Q

define hypoxia

A

decreased O2 delivery to the tissues

41
Q

How does cyanide poisoning cause hypoxia?

A

decrease O2 utilization by tissues

42
Q

What growth factor is synthesized in the kidneys in response to hypoxia?

A

erythropoietin (EPO)
**promotes development of mature RBCs

43
Q

What are the 3 forms of CO2 in blood?

A
  1. Dissolved CO2
  2. Carbaminohemoglobin (CO2 bound to hemoglobin)
  3. HCO3-
44
Q

What is the major form of CO2 in blood?

A

HCO3-
**90%

45
Q

The reaction of CO2 combining with H20 to form HxCO3 is catalyxed by what enzyme?

A

carbonic anhydrase

46
Q

What dose H2CO3 dissociate into on RBCs

A

H and HCO3

47
Q

Explain the chloride shift that occurs on RBCs

A

HCO3- leaves RBCS in echange for CL
– then trasnported to teh lungs in the plasma

48
Q

What is the major form in which CO2 is transported to the lungs?

A

HCO3-

49
Q

What buffers H inside RBCs?

A

deoxyhemoglobin

50
Q

IN the lungs, how is CO2 transported from RBCs?

A

HCO3 enters the RBCS in exchange for Cl-
–HCO3 recombines with H to form H2CO3– decomposes into CO2 and H20
—Then CO2 expired

51
Q

in which zone of the lungs is pulmonary blood flow its lowest?

A

Zone 1 (apex)

alveolar pressure > arterial pressure> venous pressure

52
Q

in which zone of the lungs is blood flow the highest?

A

Zone 3 (base)

arterial pressure> venous pressure> alveolar pressure

53
Q

What is the result of alveolar hypoxia on pulmonary blood flow?

A

Causes vasoconstriction
**opposite of other organs where hypoxia causes vasodilation
–vasoconstriction redirects blood flow away from poorly ventilated, hypoxic regions of the lung and toward well-ventilated parts of lung

54
Q

What is an example of a right to left shunt?

A

tetraology of fallot
– decrease ina rterial PO2 because of admixture of venous blood with arterial blood

55
Q

What is an example of a left to right shunt?

A

**patent ductus arteriosus

**do not result in a dec in arterial PO2

56
Q

What does V/Q ratio stand for?

A

V= alveolar ventilation
to
Q= pulmonary blood flow

57
Q

If breathing rate, tidal volume and cardiac output are normal, what is the normal V/Q ratio?

A

0.8
–arterial PO2 100 mmHg
–arterial PCO2 of 40 mmHg

58
Q

In what areas of the lung is ventilation at its lowest and highest?

A

lowest– apex
highest– base

59
Q

Where is the V/Q ratio highest?

A

at the apex of the lung (gas exchange is most efficient)
**lowest at the base of the lung

60
Q

In what part of the lung is gas exchange most efficient?

A

at the apex
** b/c PO2 is at its highest and PCO2 is at its lowest

61
Q

If the airways are completely blocked and ventilation is zero, what is the V/Q?

A

zero

**right to left shunt, see an increase in A-a gradient

62
Q

What is the V/Q , in the case of a pulmonary embolism?

A

V/Q= infinite
– called dead space

63
Q

What occurs to PO2 and PCO2 when the airways are blocked and ventilation is zero?

A

PO2 and PCO2 of pulmonary capillary blood (therefore of systemic arterial blood) will approach their values in mixed venous blood

64
Q

What occurs to PO2 and PCO2 when there is a pulmonary embolism?

A

no gas exchange in the lung tha tis ventilation but not perfused
PO2 and PCO2 of alveolar gas will approach their values in inspired air

65
Q

Sensory information is coordinated in what part of the CNS?

A

brainstem

66
Q

Output from the dorsal respiratory group travel sin what nerve?

A

phrenic nerve
– travels ot the diaphgram

67
Q

Input to the dorsal respiratory group comes from what nerves?

A

vagus: info from peripheral chemoreceptors and mechanoreceptors in the lung

glossopharyngeal nerve: relays info from peripheral chemoreceptors

68
Q

The apneustic center located in the lower pons, is responsible for?

A

stimulates inspiration– produces deep and prolonged inspiratory gas (apneusis)

69
Q

The pneumotaxic center located in the upper pons, is responsible for?

A

inhibits inspiration– regulates inspiratory volume and respiratory rate

70
Q

What part of the brain is responsible for voluntary control of breathing?

A

cerebral cortex

71
Q

What is the effect of increases in PCO2 and H on central chemoreceptors in the medulla?

A

stimulate breathing
**hyperventilation

72
Q

What is the effect of decreases in PCO2 and H on central chemoreceptors in the medulla?

A

inhibit breathing
**hypoventilation

73
Q

Central chemoreceptors in the medulla are sensitive to

A

pH of the CSF

74
Q

What form of CO2 acts directly on central chemoreceptors in the medulla to effect breathing?

A

H
**In CSF, CO2 combines with H2O to produce H and HCO3-

75
Q

Where are peripheral chemoreceptors located for CO2, H and O2 located?

A

Carotid and aortic bodies

76
Q

At what level of PO2, are the peripheral chemoreceptors stimulated to effect respiration?

A

PO2 <60 mmHg

77
Q

Where are J (juxtacapillary) receptors responsible for and their location?

A

location: alveolar walls, close to the capillaries

engorgement of pulmonary capillaries, such that may occur with LCHF, stimulates J receptors, causing rapid, shallow breathing

78
Q

list substances that are biologically activated by the lung?

A

angiotensin I is converted to the vasocconstrictor, angiotensin II via ACE

79
Q

List substances that are biologically inactivated by the lung

A

bradykinin
serotonin
PGE1, E2, and F2alpha
norepinephrine (partially)

80
Q

What are substances that are metabolized and released by the lungs?

A

arachidonic acid metabolites– the luekotrienes and prostaglandins

81
Q

What are substances that are secreted by the lungs?

A

immunoglobulins– particularly IgA, in bronchial mucus