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Physiology I > W10 - Respiration II (3.3, 3.4., 3.6, 3.7) > Flashcards

W10 - Respiration II (3.3, 3.4., 3.6, 3.7) Flashcards

1
Q

How do pressure and resistance in the pulmonary circulation differ from that in the systemic circulation?

Values.

Consequence?

A

in supine position

  • driving P in the syst. circuit 90 - 3 = 87 mmHg
  • driving P in the pul. circuit 14 - 8 = 6 mm Hg

BUT: cardiac output can be pumped bc resistance is proportionately low to pressure (10% of systemic R)

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2
Q

What are the pressure values in

  • the pulmonary aa.
  • mean pressure in pulmonary aa.
  • pulmonary capillaries
  • pulmonary vv.
  • left aftrium

?

A
  • the pulmonary aa. = 24/9 mmHg
  • mean pressure in pulmonary aa. = 14 mmHg
  • pulmonary capillaries = 10 mmHg
  • pulmonary vv. = 9 mmHg
  • left aftrium = 8 mmHg
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3
Q

How does the blood flow in the lungs vary?

Why?

A

in supine position → gravitational effect on pulmonary blood flow = perfusion

  • lowest blood flow at apex
  • highest blood flow at base of lung

⇒ increases in craniocaudal direction
→ zoning: 1 - 3

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4
Q

Describe the pulmonary blood flow in zone 1.

When can such behavior be observed?

A

pathological condition, e.g. as a result of hemorrhage
Palv > Part > Pven

⇒ high alveolar P compresses capillaries → ↓Q

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5
Q

Describe the pulmonary blood flow in zone 2.

When can such behavior be observed?

A

anywhere moving down toward base of lung
Part > Palv > Pven

⇒ Q driven by ΔPart-alv

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6
Q

Describe the pulmonary blood flow in zone 3.

When can such behavior be observed?

A

base of lung
Part > Pven > Palv

⇒ Q driven by ΔPart<span>-</span>ven

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7
Q

How is pulmonary blood flow mainly regulated?

A

by hypoxic vasoconstriction

→ blood redirected from poorly ventilated, hypoxic regions toward well-ventilated regions

NOTE: in fetuses generalized hypoxic vasoconstriction, so only little blood flow through lung, reversed after first breath

(instead of vasodilation like in other organs)

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8
Q

What is the V/Q ratio?

Standard value?

A

ratio of alveolar ventilation V and pulmonary blood flow Q (perfusion)

→ important to achieve ideal exchange of O2 and CO2

usually ∽ 0.8

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9
Q

How does the perfusion, ventilation and V/Q ratio differ in different regions of the lung?

Graph.

A
  • perfusion = lowest at apex
  • ventilation = lowest at apex, but regional differences are lower than for perfusion

⇒ V/Q ratio is highest at apex, lowest at base of lung
BUT: at base of lung closer to optimal value

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10
Q

What is the reason for increased ventilation in the base of the lung?

Values.

A

gravity

  • pleural pressure at apex - 10 mmHg
  • pleural pressure at the base -2 mmHg

↓ transalveolar P → ↓ alveolar volume → ↑ compliance
⇒ capable of wider O2 exchanges with the external environment

at apex obviously vice versa, higher volume, lower compliance, lower ventilation

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11
Q

What is a shunt?

Consequence?

Reason?

A

vessel where V/Q ratio = 0, hence no gas exchange
bc ventilation does not occur

⇒ PO2 and PCO2 in pulm. capillary blood will approach values in mixed venous blood

e.g. in case of food being stuck in the trachea

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12
Q

What is dead space?

Consequence?

Reason?

A

lung tissue where V/Q = infinite, hence no gas exchange
bc perfusion is absent

⇒ PO2 and PCO2 of alveolar gas will approach values in inspired air

e.g. in case of pulmonary embolism

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13
Q

What are the 2 forms how O2 is transported in blood?

A
  • physically transported: dissolved in blood
  • chemically transported: bound to hemoglobin (increases O2-carrying capacity 70-fold)
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14
Q

What does Fick’s law of diffusion state?

Formula.

A

the diffusion of a gas across a sheet of tissue is

directly related to the

  • A = surface area of the tissue
  • D = diffusion constant of the specific gas
  • ΔP = partial pressure difference of the gas on each side of the tissue

inversely related to

  • T = tissue thickness

<u>NOTE:</u> CO2 diffuses more easily than O2 at same partial P

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15
Q

Fick’s law can be simplified.

How?

A

DL = lung diffusing capacity
equivalent of permeability of alveolar-pulmonary capillary barrier

  • directly proportional to D and A
  • inversely proportional to T
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16
Q

Which conditions change the value of the lung diffusion coefficient?

A

REMEMBER:

  • directly proportional to D and A
  • inversely proportional to T

hence:

  • ↑DL: during exercise bc more capillaries open → ↑A
  • ↓DL: during emphysema (↓A), in fibrosis/pulm. edema (↑T)
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17
Q

Which structures contribute to the alveolar-pulmonary capillary barrier?

A
  1. alveolar epithelium
  2. epithelial basement membrane
  3. interstitial space
  4. capillary basement membrane
  5. capillary endothelium
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18
Q

What are the PO2 and PCO2 values in

  • dry inspired air
  • humified tracheal air
  • alveolar air
  • systemic arterial blood
  • mixed venous blood

? Explain.

A
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19
Q

What is the driving pressure for diffusion of CO2 and O2 across the alveolar-pulmonary capillary barrier?

A
  • ΔPO2 = 100 - 40 = 60 mmHg
  • ΔPCO2 = 46 - 40 = 6 mmHg

​​BUT: [CO2] in capillary = 20* [O2]
due to incr. solubility of CO2

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20
Q

Differentiate btw types of limited gas exchange.
Examples.

Graph.

A

perfusion-limited exchange

  • N2O, CO2, O2 under normal conditions
  • gas equilibrates early along length of cap.
  • diffusion can be incr. if blood flow incr.

diffusion-limited exchange

  • CO, O2 during strenous exercise/disease states
  • gas does not equilibrate by the time it reaches end of capillary → ΔP maintained

BUT: diffusion can be limited in tissue if capillary length is not sufficient

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21
Q

How much dissolved O2 can be found in art. blood?

A

1 mmHg O2 = 0.03 ml O2/l blood

95 mmHg O2 = 95 * 0.03 = 3 ml O2/l blood

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22
Q

What is the average [Hb] in blood?

How much O2 can be transported this way?

A

2.3 mmol/l

→ 9.2 mmol/l O2 can be transported

in ml: 2.3 * 4 * 22.4 = 206 ml O2/l blood

= O2 binding capacity of blood

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23
Q

Describe the general structure of hemoglobin.

A

globular protein of 4 subunits, each subunit:

  • contains heme = iron containing porphyrin
    → Fe2+ binds O2
  • either α or β → normal adult hemoglobin has 2 each, hence called α2β2
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24
Q

What is hemoglobin S?

A

causes sickle cell disease

  • normal α subunits, but abnormal β subunits
    → α2Aβ2S
  • in deoxygenated form HbS forms sickle-shaped rods that deform RBCs
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25
Q

What is methemoglobin?

A

iron in Fe3+ state, hence cannot bind O2

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26
Q

xWhat is P50?

Values in art. and venous blood.

Why are they different?

A

PO2 when 50% of Hb is saturated

  • art. P50 = 26 mmHg
  • ven. P50 = 29 mmHg

​In the lung (arteries), the effect of the shift to the left caused by decreased [H+] enhances O2 uptake.

The rising [H+] caused by the entry of CO2 (veins) shifts the curve to the right, enhancing O2 dissociation

27
Q

Define O2 content of blood.

It depends on… ?

A

total amount of O2 carried in blood, including bound and dissolved O2

depends on:

  • [Hb]
  • P50<strong> </strong>(determines %O2 saturation)
  • PO2
28
Q

Explain the important points on the Hb-O2 dissociation curve.

Draw it.

A

percent saturation of Hb as a function of PO2

  • at PO2 = 100 mmHg, e.g. art. blood
    Hb is 100% saturated, all 4 heme groups bind O2
  • at PO2 = 40 mmHg, e.g. mixed venous blood
    Hb is 75% saturated, 3-4 heme groups bind O2
  • at PO2 = 26 mmHg
    Hb is 50% saturated → P50, 2 heme groups bind O2
29
Q

How would you describe the shape of the Hb-O2 dissociation curve?

Explain.

A

= sigmoidal, bc
change in affinity of Hb as successive O2 molecules bind = positive cooperativity
→ highest affinity for fourth O2

⇒ facilitates loading of O2 in lungs, unloading of O2 in peripheral tissues

30
Q

What happens with Hb in the lungs?

Explain w/r/t the Hb-O2 dissociation curve.

A

alveolar gas has PO2 = 100 mmHg

diffusion of O2 from alveoli into blood
→ “arterialized” PO2 of 100 mmHg

  • high affinity of Hb at 100 mmHg (flat portion of curve)
  • low free [O2] + PO2 → maintain pressure gradient that drives diffusion
31
Q

What is the physiological relevance of the almost flat portion of the Hb-O2 dissociation curve?

A

btw 60 and 100 mmHg

changes in atmospheric pressure (→ PO2) can be tolerated w/o compromising O2-carrying capacity of Hb

32
Q

What happens with Hb in peripheral tissue?

Explain w/r/t the Hb-O2 dissociation curve.

A

O2 diffuses from art. blood to cells

  • O2 gradient is maintained bc cells consume O2
  • lower affinity of Hb at low PO2 (steep portion of curve)
33
Q

Which parameters must be changed to cause a right shift of the Hb-O2 curve?

Consequence?

A

↓ affinity of Hb for O2
⇒ ↑ unloading in peripheral tissues

because:

  • ↑ PCO2 → ↓ pH (= Bohr effect)
  • ↑ T
  • ↑ [2,3-BPG]
34
Q

What does 2,3-BPG do?

Which situation would cause an increased synthesis of 2,3-BPG?

A

binds to β chains of deoxygenated Hb
→ ↓ affinity for O2 → ↑ unloading in tissue
(right shift of curve)

↑ synthesis in case of adaptation to chronic hypoxemia (e.g. living in high altitude) to facilitate unloading of O2 in tissues

35
Q

Which parameters must be changed to cause a left shift of the Hb-O2 dissociation curve?

Consequence?

A

↑ affinity of Hb for O2
⇒ ↓ unloading in peripheral tissues

because:

  • ↓ PCO2 → ↑ pH
  • ↓ T
  • ↓ [2,3-BPG], e.g. HbF
  • CO

= opposite of causes for right shift

36
Q

How is fetal hemoglobin different from that of adults?

A

fetal hemoglobin = HbF

  • β chains replaced by γ chains → α2γ2
  • higher O2 affinity than adult hemoglobin bc 2,3-BPG binds less strongly to γ chains
    → O2 movement from mother to fetus

higher O2 affinity implicates left shift on graph

37
Q

Explain the effects of CO w/r/t the Hb-O2 dissociation curve.

A
  • affinity of CO = 200* affinity of O2
    → occupies binding sites on Hb, ↓ O2 content
  • binding of CO incr. affinity for rem. sites for O2
    → left sheft of Hb-O2 dissociation curve

⇒ characteristic curve

38
Q

What is the A-a gradient?

Normal range?

A

difference btw alveolar PO2 and arterial PO2

  • under normal conditions: 0 - 10 mmHg
    → equilibration btw alveolar and arterial PO2
  • if > 10 mmHg
    → no equlibration, usually leads to hypoxemia
39
Q

What is hypoxemia?

Causes?

How is the A-a gradient affected?

A

↓ arterial PO2

(often a result of non-equilibration btw alveolar and arterial PO2)

40
Q

What is O2 delivery?

Formula + unit.

A

amount of O2 delivered to the capillaries per minute

O2 delivery = cardiac output * O2 content

41
Q

What is hypoxia?

Causes + mechanisms?

A

= reduced level of O2 in tissue

  • hypoxic hypoxia: inadequate saturation of blood O2 (due to a reduced supply of oxygen in the air, decr. lung ventilation or resp. disease)
  • anemic hypoxia: capacity of the blood to carry O2 is reduced (due to <span>anemia, CO poisoning)</span>
  • histotoxic hypoxia: cells fail to utilize it effectively because they cannot absorb O2 from blood (due to overuse of alcohol or drugs and is also seen in Cn poisoning)
  • stagnant hypoxia: decrease in blood flow preventing adequate blood supply to tissues (due to Heart attack, heart failure, or cardiac arrest)
42
Q

What is EPO?

Explain its effect.

A

growth factor synthesized in kidney in response to hypoxia

  1. ↓ O2 delivery to kidney
  2. ↑ production of hypoxia-inducible factor 1α
  3. ↑ synthesis of EPO

⇒ promotes development of mature RBCs

43
Q

What are the 3 forms how CO2 produced in tissues is transported to the lung?

A
  • dissolved CO2 (small amount)
  • carbaminohemoglobin (small amount) = bound to Hb
  • HCO3- from hydration of CO2 in RBCs = 90%
44
Q

Explain the process how CO2 is transported in form of HCO3- in the blood.

A
  1. CO2 generated in tissues, diffuses into venous plasma, then into RBCs
  2. carbonic anhydrase in RBCs:
    CO2 + H2O → H2CO3 → H+ + HCO3-
  3. chloride shift: HCO3- exported back into plasma, Cl- imported into RBC
  4. in the lungs: reverse reaction, then CO2 exhaled
45
Q

Explain how H+ is buffered inside the RBC.

A

deoxygenated Hb at venous end of capillaries binds H+ → no major changes in pH

46
Q

Which nerves are mainly responsible for the 2 phases of respiration?

Explain.

A

different activites during different phases

  • n. phrenicus: during inspiration, increasing activity btw 0.5 and 2s → smooth increase in lung V
  • nn. intercostales: during expiration
47
Q

Which structures contribute to the central control of breathing?

Where are they located?

A

controlled by brainstem, influenced by cerebral cortex

  • pneumotaxic center: upper pons
  • apneustic center: lower pons
  • medullary respiratory center:
    • ​dorsal respiratory group
    • ventral respiratory group
  • cerebral cortex​
48
Q

Which cranial nucleus froms the dorsal respiratory group?

What is its function?
Explain.

A

ncl. solitarius

integration of sens. information from resp. system + inspiration
mainly afferent role

  • input from:
    • n. IX: from per. chemoreceptors
    • n. X: from per. chemoreceptors + mechanoreceptors in lung
  • output mainly to inspiratory motor neurons in:
    • VRG
    • spinal cord
49
Q

What is the function of the ventral respiratory group?

Which important structure is part of the VRG?

A

expiration + inspiration
mainly efferent role

3 areas w/ different functions:

  • rostral VRG → expiration
  • intermediate VRG → assists inspiration, contains pre-Bötzinger complex
  • caudal VRG → expiration
50
Q

What is the function of the pre-Bötzinger complex?

A

generates rhythmic motor output to n. phrenicus and n. XII

⇒ possible explanation for pacemaker activity of respiration

51
Q

What is the function of the apneustic center?

Where is it located?

A

in lower pons

stimulates inspiration​
→ deep + prolonged inspiratory gasp (apneusis)

52
Q

What is the function of the pneumotaxic center?

Where is it located?

A

in upper pons

inhibits inspiration
→ regulates inspiratory volume + rate

BUT: not needed for eupnea

53
Q

How does the cerebral cortex control breathing?

A

under voluntary control
→ voluntary hyperventilation or hypoventilation

obv. time of hypoventilation limited by PO2 and PCO2, can be extended by previous hyperventilation

54
Q

What is described by the CO2-response curve?

Draw it.

A

ventilation as a function of inspired CO2
= test of CO2 sensitivity

  • ventilation increases as PCO2 increases
    ↑ 1 mmHg PCO2 → ↑ 3L/min. ventilation
  • sensitivity decr. during sleep (also: anesthesia, COPD)
  • sensitivity incr. during acidosis

curve for acidosis looks similar

55
Q

How does hypercapnia affect ventilation as the partial pressure of O2 is varied?

Graph.

A

increased sensitivity to PCO2 if the PO2 also decreased

→ left shift + steeper slope

56
Q

Where are central chemoreceptors located?

Explain the exact mechanism of their function.

A
  • *in ventrolateral medulla**
  • *sensitive to pH in CSF**
  1. ​CO2 diffuses from blood into CSF
    (H+ cannot due to blood brain barrier)
  2. hydrated → H2CO3 → H+ + HCO3-
  3. H+ acts directly on central chemoreceptor
  4. regulation to stabilize arterial PCO2
    • ↑PCO2, [H+] → hyperventilation
    • ↓PCO2, [H+] → hypoventilation
57
Q

As a review…

Where can peripheral chemoreceptors be found?

A
  • carotid bodies: in sinus caroticus
  • aortic bodies: above and below arcus aorticus
58
Q

How do peripheral chemoreceptors influence the rate of breathing?

A
  • decrease in art. PO2 (< 60 mmHg)
    most important factor that stimulates rec.
  • increase in art. PCO2
    less important
  • increase in art. [H+] = metabolic acidosis​
    direct stimulation of carotid bodies, ind. in changes of PCO2

⇒ hyperventilation

59
Q

Which other types of receptors are involved in the control of breathing?

A
  • lung stretch receptors
  • irritant receptors
  • J (juxtacapillary) receptors
  • joint + muscle receptors
60
Q

How do lung stretch receptors influence the rate of breathing?

Where are they located?

A

in the SMCs of the airway

stimulated by distension of the lung, produce Hering-Breuer reflex → ↓ rate of breathing

61
Q

Explain the function of irritant receptors.

Where are they located?

A

btw airway epithelial cells

stimulated by noxious substances like dust, pollen
→ induce coughing, might induce bronchoconstriction in patients w/ asthma

62
Q

Where are juxtacapillary receptors located?

When are they stimulated?
Example.

A

in the alveolar walls, close to capillaries

stimulated by engorgement of pulm. capillaries
→ rapid, shallow breathing

e.g. in case of left heart-failure

63
Q

What is the function of joint and muscle receptors?

How do they affect the rate of breathing?

A

activated during movement of limbs
→ early stimulation of breathing during exercise

64
Q

How does arterial PO2 and PCO2 change in response to decreasing atmospheric pressure?

Graph + values.

A
  • PCO2 = constant (bc still same amount produced by per. tissue)
  • PO2 = decreaes as altitude increases
    • = 60 mmHg at 480 mmHg (∽ 3000m)
    • = 40 mmHg at 420 mmHg (∽ 6000m)

Physiology I (10 decks)

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