Respiratory Physiology Flashcards

1
Q

Blood-gas interface

A

gas moves from high pressure to low pressure (diffusion)
oxygen moves from air to blood (PO2 in air 150 mmHg and PO2 in blood 40 mmHg)
CO2 moves from blood into air (PCO2 in air is negligible and PCO2 in blood is 46 mmHg)

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2
Q

Gas movement across barrier

A

Cross-sectional area
Inversely proportional to thickness of barrier
Capillary permeability

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3
Q

Conducting airways order

A

Trachea –> L and R bronchi –> lobar bronchi –> segmental bronchi –> terminal bronchioles

  • anatomic dead space - 30% of inspiration
  • not involved in gas exchange
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4
Q

Respiratory Zone

A

terminal bronchioles divide into respiratory bronchioles lined with alveoli

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5
Q

Airflow

A

initiated by expansion of thoracic cavity (diaphragm contracts and intercostals raise ribs)
- dust and particles will settle in terminal bronchioles

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6
Q

Compliance of lungs

A

lungs are VERY compliant = 500 ml/3 cm of water
LOW RESISTANCE
fibrosis of lungs impinges on expansion

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7
Q

Surface tension issue

A

alveoli should want to collapse into each other because of how small they are
SURFACTANT reduces the surface tension and prevents alveolar collapse

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8
Q

Inhaled particles

A

Nose filters
Mucous-ciliary elevator
Macrophages

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9
Q

Ventilation

A

how gas gets to alveoli

reduction in ventilation –> hypoxia (can be caused by drugs, brain damage, breathholding)

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10
Q

Tidal Volume

A

amount of air inspired and expired in routine breathing

500 mL

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11
Q

Total Lung Capacity

A

volume capacity of entire lung

7000 mL

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12
Q

Vital Capacity

A

Maximum volume of air that can be exhaled after max inspiration
6000 mL

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13
Q

Residual Volume

A

amount remaining in lungs after maximal expiration

~1500 mL

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14
Q

Functional Residual Capacity

A

amount remaining after typical exhalation

~2500 mL (measured by gas dilution technique)

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15
Q

Total Ventilation

A

amount of air entering and leaving lung each minute

about 30% is “filling” anatomic dead space

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16
Q

Alveolar Ventilation

A

actual gas amount that is exchanging in alveoli (70% of inhaled air)
Va = Vco2 / Pco2 x K

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17
Q

Measuring dead space volume

A

Breathe in 100% O2 –> expired gas plotted vs. N2 –> [N2] increases with expiration until reaching peak
- midpoint on graph is the volume of anatomic dead space

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18
Q

Physiologic Dead Space

A

Vd/Vt = (PAco2 - PEco2)/PAco2

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19
Q

Regional differences in ventilation

A

lower portions of lung are ventilated better than apex

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20
Q

Diffusion across blood-gas barrier

A

Pressure difference (driving force)
Surface area of barrier
Inversely related to thickness of barrier
Inversely related to molecular weight of molecule
Solubility of gas barrier

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21
Q

Diffusion capacity

A

volume of CO transferred/partial pressure difference

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22
Q

Barrier Resistance

A

partial pressure difference/volume of gas transferred

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23
Q

Diffusion limited process

A

CO reaction with blood (not dependent on flow, will diffuse no matter what)
RBC affinity is so great, there is little rise in blood partial pressure
Oxygen transfer can be diffusion limited in pulmonary diseases (thickening)

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24
Q

Perfusion limited process

A

Reaction of N2O with blood (doesn’t react with RBCs)
Partial pressure of N2O builds as blood goes through capillaries –> saturated 10% of way through capillary
Oxygen - perfusion limited, reaches equilibrium 1/3 of way through capillary (limited by blood flow)

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25
Oxygen uptake in pulmonary capillaries
Blood enters with pO2 of 40 mmHg | Alveolar pO2 is 100 mmHg --> O2 moves from alveoli to capillary (saturated in .25 sec)
26
Measurement of diffusing capacity
use CO because its not perfusion limited | Diffusion capacity = Vco/(P1-P2)
27
RBC reaction rate
Takes 0.2 sec for O2 to combine with RBC | R = (P1-P2)/V
28
Pulmonary Circulation
pressures are relatively low (25/8 mmHg) low resistance pulmonary capillaries surrounded by alveoli (pressure on capillaries from alveoli)
29
Pulmonary artery resistance decreases with an increase in pulmonary artery pressure.....why?
Recruitment of additional capillaries Distention of capillaries conducting blood Expansion of lung also reduces resistance NE, 5-HT, histamine --> increase resistance ACh, Iso, prostacyclin --> reduce resistance
30
Fick Principle
O2 consumption = CO x (CAo2 - CVo2) | CO = VO2 / (CAo2 - CVo2)
31
Zone 1 of pulmonary blood flow
PA > Pa > Pv doesn't occur naturally --> but during hemorrhage or PPB *alveoli "crushes" arteriole Apex of lung
32
Zone 2 of pulmonary blood flow
Pa > PA > Pv blood flow is determined by pressure differential between arteries and alveoli (venous doesn't influence) Apical regions of lungs
33
Zone 3 of pulmonary blood flow
Pa > Pv > PA flow is dependent on arterial/venous pressure difference (normal situation) occurs in midregion/base of lungs
34
Hypoxic pulmonary vasoconstriction
Alveolar hypoxia --> constriction of blood vessels perfusing that hypoxic region of lung Independent of nerves Involves inhibiting VG K+ channels --> depolarize membrane potential Causes increase in [Ca] leading to vasoconstriction
35
Fluid movement out of vasculature
(Pcap – P int) – ∂ (πcap – πint) | - too much fluid movement out --> alveolar edema --> shortness of breath
36
Other functions of pulmonary circulation
Reservoir for blood | Filter blood -> clots (PE)
37
Metabolic functions of lung
Ang I --> Ang II by ACE ACE inactivates bradykinin (side effect of ACE inhibitors in increased bradykinin and cough) Synthesizes PGE and leukotrienes
38
Causes of hypoxia
hypoventilation diffusion limitation R --> L shunt ventilation-perfusion mismatch
39
Hypoventilation
If O2 is not replenished fast enough, alveolar PO2 declines
40
Alveolar Gas Equation
PAo2 = PIo2 - [PAco2/R]
41
Hypoventilation by diffusion limitation
reducing area available for gas exchange or increasing the distance can cause hypoxia
42
Shunt
Occurs when not fully oxygenated blood mixes with fully oxygenated blood --> if you give 100% oxygen, it won't correct the shunt because you will still have mixing
43
Ventilation-perfusion mismatch
Major cause of hypoxia in lung disease PE = Tons of ventilation and no perfusion (V/Q = infinity) --> will equilibrate to room air Airway obstruction = tons of perfusion but no ventilation (V/Q = 0) --> will equilibrate to blood gas
44
Areas of V/Q in lung
``` Apex = high V/Q Base = low V/Q ```
45
Oxygen in the blood
2 forms 1. dissolved in blood (0.3 ml/dL at Po2 of 100 mmHg) 2. Hemoglobin (20 ml/dL at Po2 of 100 mmHg)
46
O2 dissociation curve shifted to right by?
``` EXERCISE 1. Decreased pH 2. Increased O2 3. Increased temp 4. Increased 2,3-BPG O2 is released easier at the tissues ```
47
CO2 in blood
3 Forms 1. Dissolved in blood (much more soluble than O2) 2. Bicarbonate (involves CA) Major form 3. Carbamino compounds (hemoglobin)
48
CO2 dissociation curve
much more linear than O2 curve, O2 curve affects CO2 curve
49
Inhalation
diaphragm contracts down and intercostals contract bringing ribs and sternum out --> increases intrathoracic volume
50
Expiration
``` typically passive (elastic recoil of lungs) active expiration --> abdominals and intercostals pull ribs downward ```
51
Elastic properties of lungs
inflation of lung occurs when pressure around lung becomes subatmospheric Pressure differential is greater to inflate lung than to deflate it = hysteresis Lung volume is never 0
52
Compliance of lung
Lungs are very compliant Fibrotic disease --> reduced compliance Emphysema --> increased compliance
53
Surface Tension of lungs
surfactant greatly reduces surface tension of lungs | - without it, smaller alveoli would empty into larger one and collapse
54
Regional Differences in Ventilation
intrapleural pressure is less at base than apex (less negative) --> weight of lung is pressing against the chest wall
55
Airway closure
Increased pressure associated with exhalation can result in collapse of airways --> occurs at low lung volumes Airway disease patients --> purse lips to create back pressure to keep airways open so they don't trap air
56
Lung-chest equilibrium
at functional residual capacity
57
Airway resistance
Smallest at large lung volumes, greatest at small lung volumes determined by radius of airways --> resistance decreases in smaller airways because total cross-sectional area is greater than large airways Medium-sized bronchi are main source of resistance
58
ACh effect on airway resistance
increases because ACh binds muscarinic receptors causing contraction
59
Epi effect on airway resistance
decreases because Epi binds beta-2 receptors causing dilation
60
Dynamic compression of airways
Rate of flow during expiration is rapid initially then falls Drop in flow caused by compression of airway when thoracic volume is decreased to expel air Flow determined by alveolar pressure - pleural pressure
61
Major feedback mechanism for control of ventilation?
``` central controller (pons and medulla) peripheral sensors (chemoreceptors) efferent mechanisms (nerves and muscles) ```
62
Central controller of ventilation
pons and medulla (cortex can override to increase/decrease breathing) - respond to pH --> H+ stimulates respiration, alkalosis suppresses respiration - H+ cannot cross BBB, so CO2 diffuses across and is converted by ca to H and HCO3
63
Peripheral Chemoreceptors
carotid bodies and aortic arch sense hypoxia (increased firing rate as Po2 decreases) carotids respond to decrease in pH both carotid and aortic respond to hypercapnia (but not as much as central)
64
Most relevant controller of minute-minute ventilation?
CO2 --> each 1 mmHg increase in Pco2 causes 2-3 L increase in ventilation if O2 held constant
65
Response to hypoxia?
If CO2 is held constant, most individuals don't respond to hypoxia until Po2 drops below 50 mmHg EXCEPTIONS --> high altitude, COPD
66
Response to acidosis
low pH stimulates ventilation when Pco2 and Po2 are constant (sensed by carotid bodies)
67
Response to exercise
typically observe fall in Pco2 and rise in Po2 --> pH is stable during exercise until very intense levels