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pulmonology > Respiratory phys part 2 and 3 > Flashcards

Respiratory phys part 2 and 3 Flashcards

1
Q

What are the 4 lung volumes?

A
  • tidal volume (amt of air inhaled or exhaled with each breath at rest)
  • inspiratory reserve volume (inspiration above normal tidal volume)
  • expiratory reserve volume (exhale beyond normal tidal volume, active expiration)
  • residual volume (can’t measure with PFT, what is left over, necessary to keep lung inflated)
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2
Q

What are the 4 lung capacities?

A

(sum of 2 or more lung volumes)

  • inspiratory capacity
  • functional residual capacity
  • vital capacity
  • total lung capacity
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3
Q

What is the inspiratory capacity?

A
  • TV+ IRV

- how much total can you inhale

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4
Q

What is functional residual capacity? (FRC)

A
  • expiratory reserve volume + residual volume
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5
Q

What is the vital capacity (VC)?

A
  • TV+ IRV+ ERV (total amt except RV)
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6
Q

What is TLC?

A

total lung capacity, sum of all lung volumes

TV+IRV+ERV+RV

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7
Q

What is a spirometer? Why is spirometry important?

A
  • spirometer is an instrument used to measure respiratory volumes and capacities
  • spirometry can distinguish between obstructive pulmonary disease - increased airway resistance (bronchitis)
    and restrictive disorders - rduction in TLC due to structural or functional lung changes (fibrosis or TB)
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8
Q

What values can you obtain from spirometry?

A
  • FVC: gas forcibly expelled after taking a deep breath
  • FEV: amt of gas expelled during specific time intervals of FVC (FEV1= amt expelled in 1 second)
  • peak expiratory flow rate
  • flow volume loop
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9
Q

When would you see an increase in TLC, FRC, and RV?

A
  • as a result of obstructive disease (can’t breathe out as easily)
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10
Q

When would you see a reduction in VC, TLC, FRC, and RV?

A
  • result from restrictive disease

- smaller volumes, problems opening up airway

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11
Q

Why are PFTs ordered?

A
  • to distinguish b/t obstructive and restrictive pulmonary disease
  • useful for following course of disease
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12
Q

What is dead space?

alveolar dead space?

A

inspired air that never contributes to gas exchange
anatomical dead space: volume of the conducting zone conduits (150 ml)
- alveolar dead space: alveoli that cease to act in gas exchange due to collapse or obstruction
- total dead space: sum of above nonuseful volumes

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13
Q

What is alveolar ventilation rate? (AVR)

A

flow of gases into and out of alveoli during a particular time
AVR= breaths/minx (TV-dead space)
- this is the amount of air that will get into alveoli in one minute
- dead space is normally constant
- rapid, shallow breathing decreases AVR

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14
Q

What is MVR? AVR?

A

MVR= RRx TV

AVR= RR (TV-ds)

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15
Q

What is external and internal respiration?

A

external: lungs
internal: body tissues

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16
Q

What is Dalton’s law of partial pressures?

A
  • total pressure exerted by a mix of gases is the sum of the pressures exerted by each gas
  • the partial pressure of each gas is directly proportional to its percentage in the mix
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17
Q

What is Henry’s law?

A

gas will dissolve in a liquid in proportion to its partial pressure

  • the amount of gas that will dissolve in a liquid also depends on it’s solubility and temp of liquid
  • CO2 is 20x more soluble in water than O2
  • very little N2 dissolves in water
  • direction and movement of a gas are determined by its partial pressure: when pCO2 is higher in pulmonary capillaries than lungs CO2 will move into the lungs
  • bigger the pressure gradient the faster the rate of exchange is
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18
Q

Why do alveoli contain more CO2 and water vapor than the atm?

A

due to:

  • gas exchange in the lungs
  • humidification of air
  • mixing of alveolar gas that occurs with each breath
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19
Q

What is the partial pressure gradient for O2 in the lungs?

A
  • it is steep, venous blood PO2 = 40 mm Hg
  • alveolar PO2 = 104 mm Hg
  • O2 partial pressures reach equil. of 104 in 0.25 seconds, about 1/3 the time of RBC is in a pulmonary capillary
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20
Q

What is partial pressure gradient for CO2 in the lungs?

A
  • less steep
  • venous blood PCO2 = 45 mm Hg
    alveolar PCO2 = 40 mm Hg
  • CO2 is 20x more soluble in plasma than oxygen
  • CO2 diffuses in equal amounts with oxygen
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21
Q

What is ventilation?

A
  • amount of gas reaching alveoli
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22
Q

What is perfusion?

A
  • blood flow reaching alveoli
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23
Q

What is ventilation-perfusion coupling?

A
  • ventilation and perfusion must be matched (coupled, working together) for efficient gas exchange
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24
Q

What effect do changes in the PO2 in the alveoli have on diameters of the arterioles?

A
  • where alveolar O2 is low, arterioles constrict in an attempt to redirect blood to areas where PO2 is higher
  • where alveolar O2 is high, arterioles dilate to increase blood flow into the area to pick up the O2
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25
Q

What effect do changes in the PCO2 in the alveoli have on the diameters of the bronchioles?

A
  • where alveolar CO2 is high, bronchioles dilate, this allows CO2 to be eliminated
  • where alveolar CO2 is low, the bronchioles constrict
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26
Q

How thick are the respiratory membranes?

A
  • 0.5 to 1 micrometer thick
  • have large surface area (40x that of one’s skin)
  • thicken if lungs become waterlogged and edematous and gas exchange becomes inadequate (pulmonary edema)
  • reduction in surface area with emphysema, when walls of adjacent alveoli break down
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27
Q

What happens during internal respiration?

A
  • capillary gas exchange in the body tissues
  • partial pressures and diffusion gradients are reversed compared to external respiration
  • PO2 in tissue is always lower than in systemic arterial blood
  • PO2 of venous blood is 40 mm Hg and PCO2 is 45 mm Hg
28
Q

2 ways that O2 is transported in the blood?

A
  • 1.5% dissolved in plasma

- 98.5% loosely bound to each Fe of Hb in RBCs (4 O2/Hb)

29
Q

What is oxyhemoglobin?

A
  • O2 is attached

- reduced hemoglobin is Hb that has released O2

30
Q

How is loading and unloading of O2 facilitated?

A
  • by change in shape of Hb
  • As O2 binds, Hb affinity for O2 increases
  • in reverse, as O2 is released Hb affinity for O2 decreases
  • Fully 100% saturated if all 4 heme groups carry O2
  • partially saturated when 1 to 3 hemes carry O2
31
Q

How is the rate of loading and unloading of O2 regulated?

A
  • PO2
  • temp
  • blood pH
  • PCO2
  • concentration of BPG (rises when O2 uptake in lungs is compromised - altitude and obstructive lung disease)
32
Q

Where is the highest % of saturated hemoglobin?

A
  • in the arterial blood
  • PO2 = 100 mm Hg
  • Hb is 98% saturated
33
Q

Why is Hb saturation lower in the venous blood?

A
  • because of O2 uptake by the tissues
  • PO2= 40 mm Hg
  • Hb is 75% saturated
34
Q

at what PO2 is hemoglobin almost completely saturated?

- when is O2 loading and delivery to tissues most adequate?

A
  • at a PO2 of 70 mm Hg
  • further increases in PO2 produce only small increases in O2 binding
  • O2 loading and delivery to tissues is adequate when PO2 is below normal levels (offload more efficient - exercising tissues)
35
Q

What % of bound O2 is unloaded during one systemic circulation?

A
  • only 20-25% of bound O2 is unloaded
  • if O2 levels in tissues drop: more O2 dissociates from Hb and is used by cells
  • respiratory rate or cardiac output need not increase
36
Q

What other factors other than PO2 influence Hb saturation?

A
  • increases in temp, H+ (decreased pH), PCO2, and BPG
  • modify the structure of Hb and decrease its affinity for O2
  • occur in systemic capillaries
  • enhance O2 unloading
  • shift the O2 hb dissociation curve to the right (fever, metabolic rate increases- need increased O2)
  • decreases in these factors shift the curve to the left (hypothermia)
37
Q

What is BPG?

A
  • 2,3-biphosphoglycerate
  • produced by RBCs as they break down glucose through glyocolysis
  • binds reversibly to Hb
  • increases when O2 levels are critically low: decreases affinity of O2 for Hb allowing the O2 to be released (unbound) so that it can go to tissues where needed - ex: at high altitudes
38
Q

How does the affinity for oxygen to Hb change as cells metabolize glucose?

A
  • cellular respiration: cells metabolize glucose, use O2 and release CO2 so PCO2 and H+ increase in concentration in capillary blood - leads to decrease in pH
    declining pH weakens the Hb-O2 bond (bohr effect) so that O2 is unloaded here (in tissues where it is most needed)
  • Heat production increases (by prod of metabolism): increasing temp directly and indirectly decreases Hb affinity for O2
39
Q

What occurs during Hypoxia?

A
  • inadequate O2 delivery to tissues
    due to variety of causes:
  • too few RBCs (anemia) - abnormal or not enough Hb
  • blocked circulation (pump failure or emboli)
  • metabolic poisons (cyanide): changes binding of O2 to hemoglobin so O2 can still bind but can’t dissociate
  • pulm disease (abnormal ventilation)
  • CO (takes up O2 binding sites on Hb)
40
Q

What are the 3 ways that CO2 is transported in the blood?

A
  • dissolved in plasma (7-10%)
  • bound to Hb (20%): binds to diff site than O2
  • transported as bicarb ions in plasma (70%)
41
Q

What does CO2 form when combined with water?

where does this occur most of the time?

A
  • forms carbonic acid which quickly dissociates

- most of this occurs in RBCs

42
Q

How does the transport of CO2 occur in systemic capillaries?

A
  • HCO3 (bicarb) quickly diffuses from RBCs into the plasma

- then the chloride shift occurs: outrush of HCO3 from RBCs is balanced as Cl- moves in from the plasma

43
Q

How does the transport and exchange of CO2 occur in the pulmonary capillaries?

A
  • HCO3 moves into RBCs and binds with H+ to form H2CO3 (carbonic acid)
  • H2CO3 is split by carbonic anhydrase into CO2 and water and CO2 then diffuses into the alveoli
44
Q

What is the Haldane effect?

A
  • the amount of CO2 transported is affected by the PO2
  • the lower the PO2 and Hb saturation with O2, the more CO2 can be carried in the blood
  • at the tissues, as more CO2 enters the blood: the more O2 dissociates from Hb (Bohr) and as Hb)2 releases O2, it more readily forms bonds with CO2 to form carbaminohemoglobin
45
Q

What influence does CO2 have on blood pH?

A
  • HCO3 in plasma is alkaline reserve of carbonic acid-bicarb buffer system
  • if H+ concentration in blood rises, excess H+ is removed by combining with HCO3
  • if H+ begins to drop, H2CO3 dissociates releasing H+
  • changes in resp. rate can also alter blood pH - slow shallow breathing allows Co2 to accum. in blood causing the pH to drop
  • changes in ventilation can be used to adjust pH when it is disturbed by metabolic factors
46
Q

How do H+ ions and bicarb work to regulate blood pH?

A
  • if H+ concentration in blood rises, then excess H+ is removed by combining with HCO3 to form carbonic acid and blood pH lowers (more acidic)
  • if H+ concentration goes too low then carbonic acid dissociates and becomes HCO3 and pH increases (more alkalotic) ??
47
Q

What parts of the brain is involved in neural control of respiration?

A
  • involves neurons in the reticular formation of the medulla and the pons
  • medulla: ventral respiratory group (VRG)
    dorsal respiratory group
  • pons: pontine respiratory group
48
Q

What factors influence respiration?

A
  • neural mechanisms: medullary respiratory centers
    pontine respiratory centers
  • chemical factors: arterial pH, PO2, and PCO2
  • lung reflexes
  • emotions (anxiety and pain)
49
Q

Function of the DRG? Where is it located?

A
  • near root of CN IX

- integrates input from peripheral stretch and chemoreceptors

50
Q

Function of the VRG?

A
  • rhythm generating and integrative center
  • sets eupnea (12-15 breaths/min)
  • inspiratory neurons excite the inspiratory muscles via the phrenic and intercostal nerves
  • expiratory neurons inhibit the inspiratory neurons
51
Q

Function of the pontine respiratory centers?

A
  • influence and modify activity of VRG

- smooth out transition b/t inspiration and expiration and vice versa

52
Q

Hypothesis of genesis of respiratory rhythm?

A
  • not well understood
  • most widely accepted that: reciprocal inhibition of 2 sets of interconnected neuronal networks in medulla sets the rhythm
53
Q

How are depth and rate of breathing determined?

A
  • depth is determined by how actively the respiratory center stimulates the respiratory muscles
  • rate is determined by how long the inspiratory center is active
  • both are modified in response to changing body demands
54
Q

Chemical factors influence of PO2?

A
  • peripheral chemoreceptors in the aortic and carotid bodies are O2 sensors: when excited they cause respiratory centers to increase ventilation
  • substantial drops in arterial PO2 (to 60 mm Hg) must occur in order to stimulate increased ventilation
55
Q

Chemical influence of arterial pH?

A
  • can modify RR and rhythm even if CO2 and O2 levels are normal
  • decreased pH may reflect:
    CO2 retention, accum. of lactic acid, or excess ketone bodies in patients with DM
  • resp. system controls will attempt to raise the pH by increasing RR and depth
56
Q

When does arterial PO2 become a major stimulus for respiration and via what?

A
  • when it falls below 60 mm Hg, via the peripheral chemoreceptors
57
Q

How do changes in arterial pH resulting from CO2 retention or metabolic factors act on respiration?

A
  • indirectly through the peripheral chemoreceptors
58
Q

What is the most powerful respiratory stimulant?

A
  • rising CO2 levels
  • normally blood PO2 affects breathing only indirectly by influencing peripheral chemoreceptor sensitivity to changes in PCO2
59
Q

What is the influence of higher brain centers on respiration?

A
  • hypothalamic controls act through the limbic system to modify rate and depth of respiration (emotional response)
  • a rise in body temp increases RR
  • cortical controls are direct signals from the cerebral motor cortex that bypass medullary controls: voluntary breath holding
60
Q

What are the pulmonary irritant reflexes?

A
  • receptors in the bronchioles respond to irritants
  • promote reflexive constriction of air passages
  • receptors in the larger airways mediate the cough and sneeze reflexes
61
Q

What is the inflation reflex?

A
  • Hering-Breuer Reflex: stretch receptors in the pleurae and airways are stimulated by lung inflation, inhibitory signals to the medullary respiratory centers end inhalation and allow expiration to occur
  • acts more as a protective response than a normal regulatory mechanism
62
Q

How do respirations adjust during exercise?

A
  • adjustments are geared to both the intensity and duration of exercise
  • hyperpnea: increase in ventilation (10-20 fold) in response to metabolic needs
  • PCO2, PO2, and pH remain suprisingly constant during exercise
63
Q

What 3 neural factors cause an increase in ventilation as exercise begins?

A
  • phsycological stimuli: anticipation of exercise
  • simultaneous cortical motor activation of skeletal muscles and respiratory centers
  • excitatory impulses reaching respiratory centers from proprioceptors in moving muscles, tendons and joints
64
Q

Why does ventilation decline suddenly when exercise ends?

A
  • because the three neural factors shut off
65
Q

What happens when you travel to altitudes above 8000 feet in a short time?

A
  • may produce sxs of acute mountain sickness (AMS)
  • HA, SOB,nausea, and dizziness
  • in sever cases, lethal cerebral and pulmonary edema
66
Q

What acclimatization respiratory adjustments are made when there is an increase in altitude?

A
  • chemoceptors become more responsive to PCO2 when PO2 declines
  • substantial decline in PO2 directly stimulates peripheral chemoreceptors
  • the result is minute ventilation increases and stabilizes in a few days to 2-3 L/min higher than at sea level
67
Q

What hematopoietic adjustments are made for the acclimatization to high altitude?

A
  • decline in blood O2 stimulates the kidneys to accelerate production of EPO
  • RBC numbers increase slowly to provide long-term compensation
  • increased BPG

pulmonology (20 decks)

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