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Systems Phys 2022 > Respiratory II > Flashcards

Respiratory II Flashcards

1
Q

Pulmonary System is a ___ flow, ___ resistance, ___ pressure system

A

high flow, low resistance, low pressure system

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2
Q

Ventilation

A

how gas gets from the atmosphere to the alveoli

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3
Q

What does Boyle’s Law mean and how does it apply to us?

A

a gas in a closed container has a given pressure → ⇡ volume, ⇣ pressure

when the diaphragm contacts the volume of the thoracic cavity ⇡ and intrapleural pressure ⇣

⇣ in Pip causes lungs to expand

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4
Q

Henry’s Law

A
  • the amount of gas that dissolves into a fluid is related to:
    • the solubility of the gas into the fluid → CO2 is more soluble than O2
    • the temperature of the fluid → the higher the temp the lower the solubility
    • the partial pressure of the gas → the greater the pp gradient the better we can get a gas into a fluid
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5
Q

Dalton’s Law

A

the total pressure of a gas mixture is equal to the sum of the pressures that each gas exerts independently

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6
Q

What does Dalton’s Law mean for respiratory physio?

A
  • air is composed of multiple gases → mostly N2 and O2
  • each gas has a pressure (partial pressure) that is independent of other gasses
  • add up partial pressures of all gases for total pressure

total partial pressure: PB = PO2 + PN2…

to calculate PP

PO2 = PB x FO2 (fraction of gas that is oxygen)

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7
Q

What happens to PO2 as you go up in altitude?

A

it decreases

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8
Q

Why does the function of inspired air stay the same but atmospheric pressure drop as you go up?

A

because gravity decreases as you go up

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9
Q

Inspiration begins

A
  • ambient air brought into airways warmed and humidified
    • by larynx, saturated with water vapor (water vapor = a gas (PH2O = 47 mmHg)
    • PP of other gases diluted
    • PO2 in a humidified mixture → PO2trachea = 150 mmHg

water vapor does not change the % of O2, it decreases PP

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10
Q

Total ventilation (VE)

A

VE (ml/min) = tidal volume (VT) (ml/breath) x respiratory rate (f)(breaths/min)

rest: 6,000 mL = 500 mL/breath X 12 breaths/min

Max: 150L (2X rest) = ⇡⇡ X ⇡ → both VT and f ⇡ but depth of breathing increases more because of anatomical dead space

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11
Q

Dead Space

A
  • Not all inspired air gets to site of gas exchange
  • part remains in conducting pathway
    • useless for gas exchange
    • anatomical dead space (= 150 mL)
    • Pronounced effect on efficiency of VE
    • 500 mL air moved in and out/breath → only 350 mL exchanged between atmosphere and alveoli

must be considered to determine alveolar ventilation

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12
Q

2 types of dead space

A
  • anatomical dead space (=150mL)
    • in conducting airways → everyone has it
  • Alveolar dead space (later)
    • in alveoli with poor circulation
    • insignificant in healthy lung; lethal in diseased lung

physiological dead space (anatomical + alveolar dead space) is the same as anatomical in healthy people

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13
Q

What is more important: Tidal Volume or Total Ventilation?

A

Tidal volume

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14
Q

Alveolar Ventilation (VA)

A

Alveolar Ventilation (VA) = (tidal volume (VT) - anatomic dead space (VD)) x respiratory rate (f)

4200 mL = (500 ml/breath - 150 ml) x 12 breaths/min

  • at the end of expiration → old air from previous breath is in dead space
  • next inspiration → old air is pushed into alveoli
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15
Q

Alveolar ventilation is best increased by….

A

increasing tidal volume

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16
Q

Wasted ventilation

A

drawing air in and out of dead space and not inspiring fresh air

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17
Q

PCO2 Equation

A

PaCO2 = (VECO2 x 0.863)/VA

PCO2 in arterial blood is inversely related to alveolar ventilation (VA)

  • if you hyperventilate (high level of ventilation), PaCO2 goes down
  • if you hypoventilate (under ventilate), PaCO2 goes up
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18
Q

How do you regulate PaCO2 and pH?

A

changing VA

  • if PaCO2 is high, VA is not adequate for level of CO2
    • not enough ventilation (CNS depression or respiratory muscle weakness)
    • too much ventilation ending up as dead space ventilation (COPD or rapid, shallow breathing
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19
Q

Eucapnia

A

PaCO2 = 35-45 mmHg

alveolar ventilation = normal

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20
Q

Hypercapnia

A

PaCO2 = >45 mmHg

alveolar ventilaiton = hypoventilation

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21
Q

Hypocapnia

A

PaCO2 = < 35 mmHg

alveolar ventilation = Hyperventilation

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22
Q

How do we measure the amount of O2 reaching the alveoli?

A

The alveolar gas equation → PAO2 = PIO2 - (PACO2/R)

R = respiratory exchange ratio → ratio of how much CO2 is produced and how much O2 is taken in

PAO2 = 102

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23
Q

Respiratory Quotient

A

Ratio of CO2 produced (VCO2) to O2 taken up (VO2)

depends on the rate of metabolism and substrate burned (0.7-1); assumed to be 0.8

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24
Q

Alveolar Gas Composition

A

PP of gases and H2O from atmosphere to blood

  • in healthy individuals, PAO2 is very close to PaO2
    • difference is the A-a gradient
    • 50% due to regional differences in VA/Q (⇡ at top of lung)
    • 50% due to anatomic shunt (blood bypasses alveoli); bronchial veins drain into pulmonary veins
  • due to high diffusibility, PACO2 = PaCO2
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25
Q

Systemic circulation

A

Left ventricle → aorta → rest of body → returns to right atria

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26
Q

Pulmonary circulation

A

right ventricle → the main pulmonary artery → lungs → pulmonary veins → left atria

the lungs receive the entire right ventricle cardiac output

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27
Q

Dual circulation in the lungs: Pulmonary Circulation

A

blood comes from heart → oxygenated by lungs → returns to heart

  • job: perfuse alveoli for gas exchange
  • arises from RV
  • receives 100% of RV output
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28
Q

Dual circulation in the lungs: bronchial circulation

A

bring nutrients and O2 to areas not involving gas exchange

  • Job: meet the needs of the lung; similar to coronaries for the heart
    • nourishes conducting airways and parenchyma up to terminal bronchioles
  • arises rom aorta
  • part of systemic circulation
  • receives 2% of LV output

blood from bronchial circulation (deoxygenated) mixes with O2 enriched blood in the pulmonary vein → contributed to the small A-a O2 difference

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29
Q

Pulmonary Blood Flow

A

blood coming from RV going to lungs

  • High flow → 5 L/min
    • flow rate = flow rate thru systemic circulation
  • Low pressure → weak pump, doesn’t pump as hard or long
    • only need to pump to top of lungs
    • not redirect blood flow like systemic circulation
      • minimal smooth muscle in arteries
      • less resistance
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30
Q

What contributes to the low resistance of the Pulmonary Circulation System?

A
  • Pulmonary arteries are shorter, and in a dilated state (large diameter)
  • Pulmonary arterioles are thin walled, have less smooth muscle and lower resting tone
  • more distensible (7X more compliant)
    • highly compliant state required less work (lower pressures)
  • enormous number of capillaries, in a unique arrangement (like a sheet → parallel) to create sheets of blood flowing past alveoli

all these factors contribute to a very compliant, low resistance circulatory system which relied on a weak pump (RV)

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31
Q

3 factors that alter pulmonary vascular resistance

A
  • changes in blood flow (perfusion)
    • ⇡ pulmonary artery pressure → ⇣ pulmonary vascular resistance (PVR) due to recruitment and distention
  • changes in lung volume
    • pulmonary resistance follows a U shape curve with resistance lowest a FRC
  • changes in local O2 concentration
    • hypoxia has the opposite effect on pulmonary vascular smooth muscle that it does in systemic smooth muscle

pulmonary vasculature is not significantly regulated by the ANS

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32
Q

Pulmonary Vascular Resistance and Perfusion

A

⇡ CO (exercise) → ⇡ pulmonary blood flow → ⇣ resistance (R)

⇣ CO (heart failure) → ⇣ pulmonary blood flow → ⇡ R

⇡ SA (for diffusion) and no high capillary pressure → pulmonary edema

  • why?
    • capillary recruitment
    • capillary distention

they keep pressure low

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33
Q

Capillary recruitment

A

all available vessels not open at rest (esp. apex) because low perfusion pressure

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34
Q

Capillary distension

A

⇡ diameter with minimal pressure

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35
Q

Pulmonary Vessels: Extra-alveolar

A

arteries and veins

by virtue of their location, not influenced directly by PA

subject to Pip

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36
Q

Pulmonary Vessels: Alveolar

A

arterioles, caps, venules

capillaries within interalveolar septa

subject to PA

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37
Q

At high lung volumes (inspiration)…

A

Pip more negative → ⇡ transmural pressure → distended extra-alveolar vessels → ⇣R

alveolar diameter increases, crushing alveolar vessels (⇡R)

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38
Q

At low lung volumes (expiration)…

A

Pip more positive → compresses extra alveolar vessels (⇡R)

alveolar diameter decreases (⇣R)

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39
Q

When is PVR lowest?

A

at FRC and increases at lower and higher lung volumes

resistance additive because vessels in series

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40
Q

Hypoxia and Hypoxemia

A

low O2 in alveoli or in blood

trigger vasoconstriction

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41
Q

Why would we want to deliver blood to a region of lung that has low O2?

A

NO synthase needs O2 to produce NO

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42
Q

Types of alveolar hypoxia: Regional

A

vasoconstriction localized to specific region of lungs

often caused by bronchial obstruction

little effect on pulmonary arterial pressure

when hypoxia gone, vessels dilate, BF returns

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43
Q

Types of alveolar hypoxia: Generalized

A

vasoconstriction throughout both lungs

leads to significant increases in R and pulmonary arterial pressure

causes by high altitudes and chronic hypoxia (asthma, emphysema)

can leas to pulmonary hypertension

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44
Q

What happens to blood flow in the lungs in an upright person?

A

BF is highest near the base and lowest near the apex

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45
Q

What happens to hydrostatic pressure as blood travels towards the apex of the lungs?

A

every 1 cm above the heart, hydrostatic pressure ⇣ 0.74 mmHg

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46
Q

What happens to arterial pressure as blood travels through the pulmonary system?

A

10 cm above the heart, arterial pressure = 6.6 → capillaries at apex, reduced blood flow

10 cm below the heart, arterial pressure = 21.4 → capillaries at base, distended and flow increased

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47
Q

regional distribution of blood flow is due to..

A

effects of gravity on hydrostatic pressure

influence of alveolar pressure on alveolar vessels

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48
Q

Pressures affecting pulmonary blood flow: Zone 1

A

occurs when PA > Pa

pulmonary capillaries collapse; no flow

usually small/nonexistent in healthy people

increases alveolar dead space: ventilated, not perfused

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49
Q

When is zone 1 created?

A

when alveolar pressure is increased (positive pressure ventilation) or arterial pressure is decreased (hemorrhage)

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50
Q

Pressures affecting pulmonary blood flow: Zone 2

A

middle ⅓ of lung

Pa (from ⇡ hydrostatic pressure) > PA

flow driven by this difference

B/c PA > Pv, PA partially collapses downstream caps

primary area of distention, recruitment of vessels during exercise

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51
Q

Pressures affecting pulmonary blood flow: Zone 3

A

Pa > Pv > PA

optimal gas exchange; V/Q = 0.8 - 1.0

gravities effects and alveolar pressure influence how much blood flow perfuse different regions of the lungs in an upright person

52
Q

Gas Movements in the Lungs: Bulk Flow

A

how gas moves in airways from trachea to alveoli

due to mass movement → like water out of a faucet

occurs when there are differences in total pressure

53
Q

Gas Movements in the Lungs: Diffusion

A

how has moves in us from air → liquid; liquid → air

gases moving due to their individual pressure gradients

54
Q

Gas diffusion determined by 2 factors:

A
  • Diffusion properties of membrane (Fick’s Law)
    • Vgas α (A*D*(P1-P2))/T
  • Pulmonary Capillary Blood Flow
55
Q

Fick’s Law of Diffusion: Partial pressure gradients (ΔP)

A

rate of diffusion ⇡s as partial pressure ⇡s

56
Q

Fick’s Law of Diffusion: Surface area of membrane (A)

A

rate of diffusion ⇡s as surface area ⇡s

constant at rest

increases with exercise

57
Q

Fick’s Law of Diffusion: Thickness of the membrane (T)

A

rate of diffusion ⇣s as thickness ⇡s

thickness ⇡s with edema, pneumonia, fibrosis

58
Q

Fick’s Law of Diffusion: Diffusion constant (D)

A

rate of diffusion ⇡s as D ⇡s

D for CO2 20x > than O2; changes in diffusion seen in O2 first

59
Q

Major determinant of rate of diffusion is…

A

Partial Pressure gradient

60
Q

Transport of Gases in the Blood: O2 has 2 forms

A
  • Physically dissolved
    • O2 is poorly soluble in body fluids
    • amount dissolves is directly proportional to PO2
    • 1.5% of O2 is free
  • Bound to Hemoglobin (Hb) → storage
    • O2 bound to Hb does not contribute to PO2 in blood
    • 98.5% of O2 is chemically bound to Hb
61
Q

Total O2 content

A

20 mL O2/100 mL blood → 19.7 mL O2 bound to Hb, 0.3 mL free

62
Q

Binding of O2 to hemoglobin is readily…..

A

reversible

critical in the delivery of O2 to tissues

63
Q

Oxyhemoglobin (HbO2)

A

Hb attached to O2

when attached to four oxygen → saturated

saturated Hb is relatively unstable and easily releases O2 in regions where the PO2 is low

blood is bright red color

64
Q

Deoxyhemoglobin

A

Non-O2 bound Hb

blood is deep maroon color

65
Q

The amount of HbO2 depends on…

A

the amount of PO2 in the blood

When blood PO2 is high (pulmonary capillaries) → form HbO2 → ⇡ % saturation

When blood PO2 is low (systemic capillaries) → O2 released from Hb → ⇣ % saturation

66
Q

___ is the primary factor in determining the % of Hb saturation

A

PO2

PO2 is determined by where you are in the body

67
Q

Binding of O2 to each heme group….

A

increases affinity of the Hb to bind additional O2

68
Q

% of saturation of Hb with O2

A

SO2 = (HbO2 content/ HbO2 capacity) x 100

content = O2 actually bound to Hb

capacity = O2 potentially bound to Hb

69
Q

Oxyhemoglobin Dissociation Curve

A

How plasma PO2 affects O2 loading and unloading from Hb

S shaped

when PO2 is high → hemoglobin is very saturated

small drops in PO2 → able to dump off a lot of O2

70
Q

Oxyhemoglobin Dissociation Curve: Plateau

A
  • enables O2 to saturate Hb in lungs (high PO2)
  • At a PO2 of 60, Hb is 90% saturated
  • increases above 60, have minor effect on Hb saturation

*is PO2 drops from 100 → 60, Hb saturation is still 90%

71
Q

Oxyhemoglobin Dissociation Curve: Steep

A

Gives up large amounts of O2 in tissues (small change in PO2)

72
Q

P50

A

the PO2 when hemoglobin is 50% saturated

~ 27 under normal conditions

73
Q

Hb results in a Large net transfer of O2 by…

A

keeping PO2 Low

HB acts as a storage depot for oxygen

once bound to Hb oxygen molecules no longer exert any pressure

Hb soaks up O2 (keeping PO2 low) → more O2 can enter blood

74
Q

Factors that shift the oxyhemoglobin dissociation curve RIGHT

A
  • ⇣ in Hb’s affinity for O2
    • decrease in Hb binding at a given PO2
    • increase in P50
    • Aids in release/unloading of O2
75
Q

Factors that shift the oxyhemoglobin dissociation curve LEFT

A
  • ⇡ in Hb’s affinity for O2
    • ⇡ Hb binding at a given PO2
    • lower P50
    • Aids in uptake/binding of O2
76
Q

Shifting the oxyhemoglobin dissociation curve has the greatest effect on which phase?

A

the steep phase

77
Q

Factors that shift the oxyhemoglobin dissociation curve RIGHT: Hb Unloading of O2

A

Even though primary factor determining % Hb saturation is PO2 in blood, other factors ⇡ O2 unloading from Hb

  • CADET face right
    • CO2
    • Acidity
    • 2,3 diphosphoglycerate
    • Exercise
    • Temperature
  • shift curve to right
78
Q

Effects of carbon monoxide on the oxyhemoglobin curve

A

CO prevents O2 loading (via competition) and unloading (shifting)

CO and O2 compete for Hb binding sites

CO has higher affinity for Hb

HbCO shifts curve left

inhibits unloading/delivery of O2 to tissues

PO2 > 0.5, all Hb binding sites occupied by CO

Healthy: 1-2% HbCO at Hb binding sites

Smokers/urban residents: 10%

79
Q

How is CO2 Transported in the blood

A

As bicarbonate ions (60%)

Physically dissolved (10%)

Chemically bound to Hb (30%)

total CO2 content in arterial blood is 59 mL CO2/100 mL blood

80
Q

What tells us how much O2 is in the blood?

A

CaO2

content of O2

need to know how much O2 is also bound to Hb → given by SaO2a and Hb content

81
Q

What does PaO2 tell us? (partial pressure)

A
  • O2 molecules dissolved in plasma
  • adequacy of gas exchange within the lungs when it is subtracted from the calculated PAO2
82
Q

What does SaO2 tell us? (saturation)

A

Heme sites (on Hb) occupied by O2 molecules → saturated

the % of all the available heme binding sites saturated with oxygen

SaO2 is determined mainly by PaO2

83
Q

What does CaO2 tell us?

A

directly reflects the total number of O2 molecules in arterial blood (both bound and unbound)

84
Q

PaO2 is determined by…

A

PAO2 and the state of alveolar capillary membrane

85
Q

PaO2 determines….

A

the O2 saturation of Hb (along with other factors that affect the position O2 disassociation curve

86
Q

__ determines the total amount of O2 in blood or CaO2

A

The SaO2, the [] of hemoglobin (~15 gm/dl) and PaO2

87
Q

CaO2 is…

A

20 ml O2/ d;

88
Q

Effects of gravity on Upright Lung: Apex

A

⇣⇣ blood flow

⇣ ventilation (overventilated)

⇡ V/Q ratio

⇡ PaO2

⇣ PaCO2

89
Q

Effects of Gravity on Upright Lung: Base

A

⇡⇡ blood flow (over perfused)

⇡ ventilation

⇣ V/Q ratio

⇣⇣ PaO2 (bl not fully oxygenated)

⇡ PaCO2

90
Q

What is the functional importance of V/Q ratios?

A

matching Regional ventilation to blood flow (not total V and total Q)

91
Q

Alveolar - arterial O2 difference

A

measure of gas exchange efficiency across alveolar-cap membrane

PAO2 = calculated (alveolar gas equation)

PaO2 = measured (sampling arterial blood)

Helps to determine cause of hypoxemia

92
Q

What is the normal P(A-a)O2?

A

≤ 20 mm Hg

Normal V/Q mismatch (50% responsible)

return of bronchial and coronary blood (deoxygenated) through the Thesbesian veins to the left side of the heart (50%)

Predict normal: age/4+4; ⇡ with age

93
Q

Five causes of hypoxemia

A
  • hypoventilation → can’t ventilate sufficiently
  • low inspired O2 → due to altitude or ventilator (under ventilating)
  • Right-to-left shunt → blood from right side of heart goes to left side of the heart (Pulmonary AV malformation)
  • V/Q mismatch → not doing a good job matching ventilation and perfusion
  • diffusion impairment → i.e. ⇡ thickness, ⇣ diffusion

Divided into:

those with an ⇡ P(A-a)O2 vs. those with a normal P(A - a)O2

94
Q

Hypoventilation

A

PaO2 →⇣

A-aO2 difference → normal

FIO2 = 1.0 → ⇡

95
Q

Low PIO2

A

PaO2 →⇣

A-aO2 difference → normal

FIO2 = 1.0 → ⇡

96
Q

Right to left shunt

A

PaO2 →⇣

A-aO2 difference → ⇡

FIO2 = 1.0 → No mostly

97
Q

V/Q mismatch

A

PaO2 →⇣

A-aO2 difference → ⇡

FIO2 = 1.0 → ⇡

98
Q

Diffusion Limitation

A

PaO2 →⇣

A-aO2 difference → ⇡

FIO2 = 1.0 → ⇡

99
Q

Respiration demonstrates both:

A

Automaticity → begins at birth

Self-modulation (voluntary) allows us to → voluntarily hyperventilation, hold our breath, change breathing patterns for speech and singing

100
Q

What makes up the ventilatory control system?

A

Sensors → chemoreceptors and mechanoreceptors = feedback

central controller → respiratory control center = the driver

Effectors → respiratory muscles = carries out

101
Q

Neural Control of Breathing: Voluntary

A

Cerebral Cortex

102
Q

Neural Control of Breathing: Autonomic

A

Medullary Centers → dorsal Respiratory Group, Ventral Respiratory Group

Pontine Centers → Pneumotaxic Center, Apneustic Center

103
Q

Respiratory Control Centers: Medullary Centers

A
  • Dorsal respiratory group (DRG) → comprised mainly of inspiratory neurons
    • pre-botzinger complex → the anatomic location of the respiratory pattern generator; these neurons display pacemaker activity
  • Ventral respiratory group (VRG) → responsible for both expiration and inspiration, but inactive during quiet breathing; active in exercise
104
Q

Respiratory Control Center: Pontine Centers

A

Rhythm generated in the medulla can be modified by neurons in the pons

medulla is the major rhythm generator

105
Q

What happens if you cut the spinal cord between the medulla and pons?

A

fairly normal ventilation but erratic

106
Q

What happens if you cut below the medulla?

A

ventilation ceases

107
Q

What controls the transition from inspiration and expiration?

A

Pneumotaxic Center and Apneustic center in the pons

108
Q

Pneumotaxic Center

A

dominants

Terminates Inspiration

this has a secondary effect of ⇡ing the rate of breathing, because limiting inspiration also shortens expiration

109
Q

Apneustic center

A

prevent inspiratory neurons from being shut off; prolongs inspiration

110
Q

Mechanoreceptors

A

detect distention and irritation → airways and lung parenchyma

111
Q

Chemoreceptors

A

chemical content of blood or CSF

PO2

PCO2

H+

112
Q

Central Chemoreceptors

A
  • lose sensitivity to CO2
  • located on surface of medulla; separate from respiratory center
  • sensitive to pH
  • BBB impermeable to H+,but CO2 readily diffuses
  • When PaCO2 increases, CO2 crosses the BBB, not H+
  • Lass of mass action ⇡s H+
  • Synaptic connection to respiratory control center ⇡s ventilation
  • Excess CO2 blown off; decreased PaCO2 slows ventilation rate
113
Q

Most important mechanism controlling ventilation at rest:

A

CO2-induced H+ in CSF

114
Q

What happens to chemoreceptors during prolonged hypoventilation (chronic lung disease)?

A
  • some lose sensitivity to elevated PaCO2
    • the increased H+ gets buffered by HCO3- (actively transported across BBB)
    • central chemoreceptors no longer “aware” of elevated PCO2
    • Hypoxic drive becomes primary respiratory stimulus

should you administer O2? No

115
Q

How do central chemoreceptors respond to hypoxia?

A

They adapt

116
Q

Peripheral Chemoreceptors

A

glomus cells in the carotid* and aortic bodies → increase ventilation during hypoxia

not sensitive to modest reductions in PaO2

117
Q

Peripheral Chemoreceptors: Hypoxia

A

when PaO2 < 60 mmHg

important emergency mechanism

respond to PaO2 not oxygen content → anemia and CO = normal PO2; no response

inhibit K+ channel; depolarizes cell

118
Q

Peripheral Chemoreceptors: Hypercapnia

A

central receptors more sensitive

CO2 diffuses into glomus; H+ inhibits K+ channel

119
Q

Peripheral Chemoreceptors: Acidosis

A

Arterial H+ inhibits K+ channel

120
Q

The effect of dangerously low PaO2 on peripheral chemoreceptors

A

The activity of all other nervous tissue becomes reduced with O2 deprivation

If not for stimulatory effect on peripheral chemoreceptors, ventilation would cease

121
Q

Arterial PCO2

A

The most important regulator of ventilation

Response primarily arises from central chemoreceptors with added input from peripheral chemoreceptors

122
Q

Arterial PO2

A

when PO2 ⇣⇣⇣ low, ventilation increases

response from peripheral chemorects (central do not directly sense PO2)

123
Q

Arterial pH

A

As h+ increase, ventilation increases, but H+ cannot diffuse into CSF as well as CO2

124
Q

Pulmonary Stretch Receptors

A

Mechanoreceptors in smooth muscle of conducting airways

keep from over expanding lungs

respond to lung distention → excites inspiratory off switch, shortens inspiration when VT large

125
Q

Joint and Muscle Receptors

A

Mechanoreceptors in joints and muscles signal DRG to increase breathing frequency

activated during movement when O2 demand is or will be high

possibly part of a feed forward mechanism with exercise to prepare

126
Q

Irritant Receptors

A

Mechanoreceptors in airway epithelium of larger conducting airways

respond to irritation of the airways by touch, dust, smoke

protects by inducing a cough and hypernea

127
Q

Juxtapulmonary Capillary Receptors (J receptors)

A
  • Stimulated by distortion
    • pulmonary C-fibers
      • next to alveoli
      • accessible to pulmonary circulation
      • sensitive to mechanical events (edema and embolism)
  • high yield info in boxes and handouts

Systems Phys 2022 (25 decks)

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