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ANP 1105 > Chapter 22 - respiratory system pt2 > Flashcards

Chapter 22 - respiratory system pt2 Flashcards

1
Q

What are the 2 phases in pulmonary ventilation?

A
  • inspiration (air in)
  • expiration (air out)
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2
Q

What is atmospheric pressure (Patm)?

A
  • pressure exerted by air (gases) surrounding the body
  • at sea level, Patm=760 mmHg or 1 atmosphere
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3
Q

what is the difference between positive, negative and neutral respiratory pressure?

A

(+) - respiratory pressure greater than Patm
(-) - respiratory pressure less than Patm (ex. -4mmHg=756 mmHg)
(+/-) - respiratory pressure is equal to Patm

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4
Q

What is intrapulmonary pressure (Ppul)/ intra-alveolar?

A

pressure in the alveoli
- fluctuates during breathing, but equalizes with Patm to end each phases of breathing - inspiration and expiration

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5
Q

What is the intrapleural pressure (Pip) and why is it always negative?

A

the pressure in pleural cavity
- fluctuates with breating, but always negative (<Patm) - 4mmHg less than Ppul
- opposing force try to pull visceral and parietal pleurae apart

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6
Q

What is the importance of the surface tension of the alveolar fluid?

A

attraction between water draws alveolar walls inwards, acting to shrink alveoli to smallest size possible

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7
Q

What way does the chest walls pull the thoracic wall (parietal pleura)?

A

outward

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8
Q

Intrapelural pressure - What is the function of surface tension of pleural fluid and how is it removed?

A

helps secure layers of pleura together
- fluid level must be kept at a minimum, excess removed by lymphatic system
- if fluid builds, Pip pressure is positive

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9
Q

What is transpulmonary pressure?

A

the difference between intrapulmonary and intrapleural pressure (Ppul-Pip)
- this pressure keeps lungs from collapsing
- size of lung is determined by transpulmonary pressure

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10
Q

What will happen if the transpulmonary pressure equalizes and why is it important to keep the Pip negative?

A
  • the lung will collapse
  • to keep he lungs inflated
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11
Q

What does the volume change in the lungs affect?

A

leads to pressure change, and pressure changes lead to the flow of gases to equalize the pressure

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12
Q

What is Boyle’s law, how does it affect air flow in the lungs, and what is the equation?

A

relationship between pressure and volume of a gas
- high pressure = air moves out
- low pressure = air moves in
- P1V1=P2V2

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13
Q

How does normal quiet inspiration affect lung volume and air flow?

A

thoracic volume increases by 500ml
1. Ppul decreases to -1mmHg (Ppul<Patm)
2. Until Ppul = Patm
3. Pip falls to -6mmHg

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14
Q

What are the 5 steps to inhalation?

A
  1. inspiratory muscles contract
  2. the thoracic cavity volume increases
  3. the lugs stretch, increasing the intrapulmonary volume
  4. intrapulmonary pressure drops
  5. air flows into lungs, down the pressure gradient
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15
Q

what is expiration during quiet expiration (a passive process)?

A

inspiratory muscles relax and thoracic cavity volume decreases (-500ml) as the lungs recoil
- air flows out until Ppul=Patm

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16
Q

What is forced expiration (active process)?

A

abdominal wall muscles to increase intra-abdominal pressure (diaphragm up) and pulls the ribs in (depression)
- internal intercoastal muscles to assist in depression

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17
Q

What is nonpreparatory air movement?

A

other processes move air into or out of lungs, altering respiratory rhythm
- voluntary or reflexive (like sneezing/ hiccup)

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18
Q

What are the 5 steps of breathing out?

A
  1. inspiratory muscles relax
  2. the thoracic cavity volume decreases
  3. the elastic lungs recoil passively, decreasing the intrapulmonary volume
  4. intrapulmonary pressure rises
  5. air flows out
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19
Q

What muscles are involved in the inspiration process?

A

diaphragm and external intercostals.

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20
Q

How does the diaphragm contribute to inspiration?

A

increases the height of the thoracic cavity, thus increasing its volume. It moves inferiorly and flattens out as it contracts.

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21
Q

What role do the intercostal muscles play during inspiration?

A

increase the diameter of the thorax, thus increasing its volume.

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22
Q

How do the intercostal muscles affect the ribs during inspiration?

A

pull the ribs up and out, similar to raising a bucket handle.

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23
Q

What causes airway resistance and what is the equation of flow (F)?

A
  • friction
  • flow (F) is proportional to the difference in pressures (Ppul-Patm) or pressure gradient (delta P)
  • F= delta P/ R (resistance)
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24
Q

What is delta P during normal quiet breathing?

A

1-2 mmHg

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25
Q

What are the 2 reasons resistance in respiratory tree insignificant?

A
  1. conducting zone airways have huge diameters (relative to low air viscosity)
  2. all the bronchioles running in parallel
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26
Q

Where is the greatest resistance in the lungs?

A

medium-sized bronchi

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27
Q

What is the pressure difference between inhalation and expiration?

A

I - (-) in order to pull air in
E - (+) in order to push air out

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28
Q

What is the purpose of measuring pulmonary volumes?

A

to assess respiratory status.
- these volumes are combined to measure pulmonary capacities.

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29
Q

Why are pulmonary volumes often abnormal in people with pulmonary disorders?

A

these conditions can affect lung function and air exchange

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30
Q

What is a spirometer, and how is it used?

A

a clinical tool originally used to measure pulmonary volumes

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31
Q

What are pulmonary (lung) capacities and how many are there?

A
  • are combinations of two or more lung volumes
  • four main ones
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32
Q

What is Inspiratory Capacity (IC)?

A

the amount of air that can be inspired after a normal tidal expiration
- the sum of tidal volume (TV) and inspiratory reserve volume (IRV)
- IC=TV+IRV

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33
Q

What is Functional Residual Capacity (FRC)?

A

the amount of air remaining in the lungs after a normal tidal expiration
- the sum of residual volume (RV) and expiratory reserve volume (ERV)
- FRC = RV+ERV

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34
Q

What is Vital Capacity (VC)?

A
  • total amount of exchangeable air
  • VC= TV+IRV+ERV
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35
Q

What is Total Lung Capacity (TLC)?

A

sum of all lung volumes
- TLC = TV+IRV+ERV+RV

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36
Q

What are the 3 factors affecting pulmonary gas exchange?

A
  • partial pressure gradient and gas solubilities
  • thickness and SA of the respiratory membrane
  • ventilation-perfusion coupling: matching alveolar ventilation with pulmonary blood perfusion
37
Q

What is the partial pressure gradient?

A

the difference in concentration of a gas between two areas, causing the gas to move from the higher concentration to the lower concentration
- responsibility for gas coming into the body

38
Q

What is the partial pressure gradients of venous blood and the alveolar?

A
  • Po2 = 40 mmHg
  • Po2 = 104 mmHg
39
Q

What does it mean to have a large deltaPo2 (64mmHg), when is equilibrium across respiratory membrane reached and when have the RBC travelled across the entire pulmonary capillary?

A
  • drives diffusion of O2 into blood
  • reached at 0.25 sec
  • reached at 0.75 sec (ensures all oxygenation even if blood flow increases)
40
Q

What is the partial pressure gradient and gas solubility of CO2 in venous blood and the alveolar?

A

much smaller (5 mmHg)
- Pco2 = 45 mmHg
- Pco2 = 40 mmHg

41
Q

describe the thickness and surface area of the respiratory membrane?

A
  • very thin
  • alveoli provide most of the surface area
42
Q

What is the relationship between ventilation-perfusion coupling?

A

ventilation (amount of gas reaching alveoli) and perfusion (amount of blood flowing through pulmonary capillaries) must be coupled for optimal, efficient gas exchange

43
Q

What local autoregulatory mechanisms is the ventilation-perfusion coupling controlled by?

A
  • alveolar Po2 controls perfusion by changing arteriolar diameter
  • alveolar Pco2 controls ventilation by changing bronchiolar diameter
44
Q

What influences the local Po2 on perfusion?

A

changes in local alveolar Po2 causes change in diameters of local arterioles
- high Po2 (good ventilation), arterioles dilate to increase perfusion
- low Po2 (poor ventilation), arterioles constrict to decrease perfusion

45
Q

How does local Po2 levels control blood flow?

A
  • directs blood to go to well ventilated (high in O2, low in CO2), so blood can pick up more oxygen (and remove more CO2)
  • opposite mechanisms are seen in systemic arterioles that dilate when O2 is low and constriction is high
46
Q

How does the local Pco2 influence perfusion?

A

causes changes in diameter of local bronchioles
- when Pco2 is high, bronchioles dilate to increase alveolar ventilation (allows elimination of O2 faster)
- when Pco2 is low, bronchioles constrict

47
Q

what happens when there is poor alveolar ventilation?

A

low alveolar Po2 (high Pco2) causes pulmonary arterioles serving these alveoli to constrict (bronchioles dilate)

48
Q

Why is ventilation-perfusion never balanced?

A
  1. regional variations, due to effect of gravity on blood and air flow
  2. occasional (mucus) plugged alveolar ducts cause unventilated areas
49
Q

What is tissue gas exchange?

A

involves capillary gas exchange in body tissues, where partial pressures and diffusion gradients are reversed compared to pulmonary gas exchange

50
Q

Is tissue Po2 lower than arterial blood Po2?

A

yes
- o2 diffuses from blood to tissues until equilibrium is reached

51
Q

Is tissue Pco2 higher than arterial blood Pco2?

A

yes
- CO2 diffuses from tissues into blood until equilibrium is reached

52
Q

What does venous blood have in reactions to partial pressure?

A
  • Po2 of 40 mmHg
  • Pco2 of 45 mmHg
53
Q

How do molecules carry O2 in the blood?

A
  • 1.5% dissolved in plasma
  • 98.5% bound to hemoglobin in RBC
54
Q

What does O2 binding to hemoglobin change?

A
  • O2 binds, Hb changes shape, increasing its affinity for O2
  • O2 released, Hb changes shape, decreasing its affinity for O2
55
Q

What is the difference between fully and partially saturated Hb?

A

F - 4 Hb
P - 1-3 Hb

56
Q

What are the factors that influence the rate of loading and unloading of O2?

A
  • Po2
  • temp
  • blood pH
  • Pco2
  • conc. of BPG
57
Q

What are the 4 influences of Po2 on hemoglobin saturation?

A
  • local Po2 controls loading and unloading of Hb
  • % Hb sat can be plotted against Po2, producing S-shaped curve called oxygen-hemoglobin dissociation curve
  • arterial blood contain 20 ml of O2/ 100 ml blood; Po2 = 100 mmHg and Hb is 98% sat.
  • venous blood contains 15 of O2/ 100 ml blood; Po2= 40 mmHg and Hb is still 75% sat.
58
Q

What happens when you increase the factors of that influence the rate of loading and unloading of O2?

A

reduces affinity of Hb for O2
- occurs in systemic capillaries (tissues)
- enhances O2 unloading, shifting the O2-Hb dissociation curve to the right (lower the sat - higher the dissociation at any Po2

59
Q

What happens when you decrease the factors of that influence the rate of loading and unloading of O2?

A

increases the affinity of Hb for O2
- occurs in pulmonary capillaries (lungs)
- enhances O2 loading, shifting the O2-Hb dissociation curve to the left (higher sat at any Po2)

60
Q

How does RBC producing BPG during glycolysis affect hemoglobin saturation?

A

levels rise as temperature rises (and O2 levels fall)

61
Q

What is the Bohr effect?

A

reduced affinity of Hb for O2 resulting from falling blood pH and rising Pco2

62
Q

How does the glucose and O2 cells consume to make ATP affect CO2 levels and Hb affinity?

A
  • the more heat and CO2 they release, increasing Pco2 and H+ in local capillary blood
  • increasing temperature directly and indirectly decreases Hb affinity for O2
63
Q

What are the 3 ways CO2 is transported in blood?

A
  1. dissolved in plasma (small % - responsible for Pco2)
  2. chemically bound to hemoglobin (20%)
    - forms carbaminohemoglobin
  3. as bicarbonate ions in plasma (70%)
    - forms HCO3- , then breaks into H+ and HCO3-
    - primarily in RBC where enzyme (carbonic anhydrase) catalyze reaction
64
Q

How is CO2 transported in capillaries?

A

diffuse from RBC into plasma
- outrush of HCO3- from RBC is balanced as Cl- moves into RBC from plasma
- referred to as chloride shift

65
Q

How is CO2 transported in the pulmonary capillaries?

A
  • HCO3- moves into RBC while Cl- moves out
  • HCO3- binds with H+ to fomr H2CO3
  • H2CO3 splits by carbonic anhydrase into CO2 and water
  • Co2 diffuses into alveoli
66
Q

What is the Haldane effect?

A

the lower the Po2 and Hb sat., the more Co2 can be carried in by blood

67
Q

What does the haldane effect do?

A

reduced Hb buffer H+ and forms carbaminohemoglobin more easily
- process encourages CO2 exchange

68
Q

What is the Dorsal Respiratory Group (DRG)?

A

a network of neurons located near the root of the cranial nerve

69
Q

What does the Dorsal Respiratory Group (DRG) do?

A

it integrates input from peripheral stretch and chemoreceptors, then sends information to the Ventral Respiratory Group (VRG) neurons.

70
Q

Are all the details of how the Dorsal Respiratory Group (DRG) operates known?

A

no, researchers are still working out the remaining details.

71
Q

What does the Pontine Respiratory Centers influence?

A

centers in the pons that influence and modify the activity of the Ventral Respiratory Group (VRG).

72
Q

How do Pontine Respiratory Centers affect breathing?

A

they appear to smooth out transitions between inspiration and expiration. Damage can cause prolonged inspirations, known as apneustic breathing.

73
Q

What role do the Pontine Respiratory Centers play during activities like vocalization, sleep, and exercise?

A

they communicate with the Ventral Respiratory Group (VRG) to fine-tune breathing rhythms.

74
Q

Do Pontine Respiratory Centers receive inputs from other areas of the brain?

A

yes, like the Dorsal Respiratory Group (DRG), they receive inputs from higher brain centers and peripheral receptors.

75
Q

What is the origin of the breathing rhythm?

A

Not yet fully understood

76
Q

What is one hypothesis regarding the generation of the respiratory rhythm?

A

one hypothesis suggests that pacemaker neurons in the VRG (ventral respiratory group) control intrinsic rhythmicity.

77
Q

What happens when pacemaker-like activity in the VRG is suppressed?

A

suppressing pacemaker-like activity in the VRG doesn’t stop breathing.

78
Q

What is the most widely accepted hypothesis for the generation of the respiratory rhythm?

A

the most widely accepted hypothesis is reciprocal inhibition of interconnected neuronal networks in the medulla.

79
Q

How do pacemaker cells contribute to the respiratory rhythm?

A

two (possibly three) sets of pacemaker cells inhibit each other and cycle their activity to generate the rhythm.

80
Q

How is breathing rate and depth fluctuations detected by chemoreceptors?

A
  • central chemoreceptor located throughout brain stem, including medulla
  • peripheral chemoreceptors found in aortic arch and carotid arteries
81
Q

What is the influence of Pco2 on breathing rate?

A

strongest influence on ventilation
- if arterial Pco2 rises (hypercapnia), CO2 accumulation in CSF of brain and joins with water to become carbonic acid which releases H+ (triggers chemoreceptors)

82
Q

What determines the depth of breathing?

A

depth is determined by how actively the VRG (ventral respiratory group) stimulates respiratory muscles. Greater stimulation activates more motor units, increasing the depth (tidal volume) of inspiration.

83
Q

What happens if arterial Pco2 fall abnormally low?

A

respiration becomes slow and shallow
- periods of apnea occurs until arterial Pco2 rises again
- swimmers can control hyperventilation to hold their breath longer

83
Q

How is the rate of breathing determined?

A

the rate of breathing is determined by how long inspiratory neurons are active or how quickly they are switched off.

84
Q

What factors determine both the depth and rate of breathing?

A

both depth and rate of breathing are determined by the changing demands of the body.

84
Q

What are the respiratory centers affected by?

A
  • Chemical factors
  • Influence of higher brain centers
  • Pulmonary irritant reflexes
  • The inflation reflex
85
Q

What happens if arterial Po2 drops substantially?

A

becomes major stimulant for ventilation

85
Q

What influence does arterial pH have on breathing rate and depth?

A
  • influence ventilation (peripheral chemoreceptors)
  • decrease pH may reflect Co2 retention, accumulation of lactic acid or ketones
  • respiratory centers attempts to raise pH by increasing ventilation, which increases CO2 removal from body (lowers pH)

ANP 1105 (12 decks)

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