2.4 Gas Exchange Flashcards

1
Q

Gas exchange during respiration

A

*occurs between lungs and blood as well as blood and tissues

External respiration: diffusion of gases by the wayn blood and lungs

Internal respiration: diffusion of gases between tissues

*toal pressure exerted by mixture of gases = sum of pressures exerted by each gas (daltons law)

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2
Q

gas partial pressure

A

Pressure exerted by each gas in mixture
• Directly proportional to its percentage in mixture

daltons law: Total pressure exerted by mixture of gases is equal to sum of pressures exerted by each gas

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3
Q

partial pressure of oxygen and nitrogen

A

Oxygen makes up 20.9% of air

PO2 : 0.209 x 760 mm Hg =159 mm Hg

Nitrogen makes up ~78.6% of air

PN2 : 0.786 x 760 mm Hg = 597 mm Hg

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4
Q

What is Henry’s law

A

* for gas mxitures in cotneact w/ liquid

  • each gas disolves in liquid proportion to its partial pressure
  • at equilibrium, partial pressure of two phases are equal
  • amount of each gas that will dssiolve depends on:
  • > Solubility: CO2 is 20􏰁 more soluble in water than O2, and little N2 will dissolve
  • > Temp: temperature of liquid rises, solubility decreases
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5
Q

what is external respiration?

what influences it?

A

External respiration (pulmonary gas exchange) involves the exchange of O2 and CO2 across respiratory membranes

influened by:

  • > Partial pressure gradients and gas solubility
  • > thickness and surface area of respiratory membrane
  • > ventilation-perfusion coupling: mathcing of alveolar ventilation w/ pulmonary blood perfusion
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6
Q

describe exchange of CO2 and O2 during external respiration

A
  • inspired air (O2:160, C02: 03) –mixes w/-> aleoli of lungs (O2 ↓ 104, CO2 ↑ 40)

– > pulmonary veins –> blood leaving lungs & entering tissue cap ( O2 ↓ 100, CO2 40)

*slight decrease here because lung tissue iteself is using a bit)

—> systemic arteries —> blood delivered to tissues (O2 ↓ 40, CO2 ↑ 45) —> Systemic veins

–> blood leaving tissues and entering lungs (O2 40, CO2 45) —–> pulmoanry arteries

–> inspired air and back to (O2:160, C02: 03)

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7
Q

describe the pressure gradient of O2 vs CO2

A
  • O2
    • steep gradient: venous blood is 40 mm Hg, aleolar is 104mmHg
    • equilibrium is reached across resp memrbane in ~0.25 s, takes RBC ~0.75s to travel from start -> end fo capillary
    • ensures adequate oxygenation even if bloodf lwo inc 3x
  • CO2
    • less steep gradient: venous blood 45 mmHg, alveolar 40 mmHg
    • even tho not steep, CO2 still diffuses in equal amoutns w/ O2 bc CO2 is 20x mroe soluble
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8
Q

thickness of respiratory memrbane

A

– Respiratory membranes are very thin 0.5 to 1 um thick

– Large total surface area of the alveoli is 40X the surface area of the skin

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9
Q

what can cause effective thickness of respiratory memrbane

A
  • if lungs become waterlogged and edematous
    ex: pneumonia or left heart failure
  • the 0.75s RBC require to travel thru pulmonary capillaries may not be sufficient for adequate gas exchange resulting in oxygen deprivation
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10
Q

what is ventilation perfusion coupling

what does O2 control? what does CO2 control?

A

– Perfusion: blood flow reaching alveoli

– Ventilation: amount of gas reaching alveoli

  • ventilation and eprfusion rates much be matched for optimal efficient gas exchange
  • both are controlled b local autoregulatory mechanisms

*PO2 controls perfusion by changing arteriolar diameter

*PCO2 controls ventilation by changing bronchiolar diameter

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11
Q

What is the influence of local PO2 on perfusion

A

*Changes in PO2 in alveoli cause changes in diameters of arterioles

  • > where alveolar O2 is high, arterioles dilate (INC perfusion aka blood flow)
  • > where alveolar O2 is low, arterioles constrict

*diects blood to go to alveoli where oxygen is high so blood can pick up more O2

*OPP MECH SEEM IN SYSTEMIC ARTEROLES THAT DILATE WHEN OXYGEN IS LOW AND CONSTRICT WHEN HIGH

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12
Q

What is the influence of local PCO2 on ventilation

A

• Changes in PCO2 in alveoli cause changes in diameters of bronchioles

Where alveolar CO2 is high, bronchioles dilate

Where alveolar CO2 is low, bronchioles constrict

*Allows elimination of CO2 more rapidly

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13
Q

how is perfusion and ventilation balanced?

A
  • Changing diameters of local arterioles and bronchioles synchronizes ventilation-perfusion
  • If ventilation < Perfusion
    • will get ↑ PCO2 and ↓ PO2
      • O2 regualres arteriolar diameter
    • Pulmonary arterioles serves alveoli constrict
    • get a match of ventilation and perfusion (corrects the ratio)
  • If ventilation > Perfusion
    • ↓ PCO2 and ↑ PO2
    • bc of INC O2, arterolies serving alveoli DILATE
    • get inc in both ventilation and perfusion
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14
Q

why is ventilation and perfusion never balanced for all alveoli

A
  • > Regional variations may be present, due to effect of gravity on blood and air flow
  • > Occasionally, alveolar ducts plugged with mucus cause unventilated areas
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15
Q

describe gas exchange in internal respiration

A

in alveoli of lungs: (O2: 104, CO2: 40) —-> pulmonary veins (O2 100)

—> Blood leaving lungs and entering tissue capillaries (O2 100, CO2 40)

—> Systemic arteries —> tissues (O2 40, CO2 45) —> systemic veins

—> Blood leaving tissues and enting lungs (40 mmHg 45 mmHg)

—> pulmonary arteries —> Inspired air (O2 160, CO2 0.3)

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16
Q

what is internal respiration

describe the partial pressues of O2 and CO2

A

Internal respiration involves capillary gas exchange in body tissues

  • Partial pressures and diffusion gradients are reversed compared to external respiration
  • Tissue PO2 always lower than in arteriol blood PO2 (40 vs 100 mmHg)
    • oxygen moves from blood to tissue
    • Tissue PCO2: always higher than arterial blood PCO2 (45 vs 40 mmHg)
      • CO2 moves from tissues into blood
      • Venous blood returning to heart has PO2 of 40 mmHg and PCO2 of 45
17
Q

how is oxygen carried in blood

A

2 ways

  • 1.5% if dissolved in plasma
  • 98.5% is bound to each iron of hemoglobin (Hb) in RBCs
18
Q

structure of hemoglobin

A

Hb molecule is composed of four polypeptide chains, each with a iron-containing heme group

  • each Hb can transport four oygen molecules
  • Oxyhemoglobin (HbO2): hemoglobin-O2 combination
  • Reduced hemoglobin (deoxyhemoglobin (HHb): hemoglobin that has released O2

*Rate of loading and unloading of O2 is regulated to ensure adequate oxygen delivery to cells

19
Q

What happens to hemoglobin as oxygen binds and is released

A
  • O2 binds: Hb changes shape, increasing its affinity for O2

As O2 is released, Hb shape change causes a decrease in affinity for O2

*when all 4 heme groups have O2 bound it is fuly saturated

*partially saturated when onle 1-3 hemes carry O2

20
Q
A
21
Q

what factors that influence hemoglobin saturation:

A
  • PO2
    • Other factors: Temperature, Blood pH, PCO2, Concentration of bisphosphoglycerate (BPG, from glycolysis)
22
Q

how does PO2 influence hemoglobin saturation

A
  • PO2 influences binding and release of O2 with hemoglobin
  • % Hb saturation can be plotted against PO2 concentrations

* Resulting graph is not linear, but an S-shaped curve called the oxygen-hemoglobin dissociation curve

23
Q

Saturation of Hb in arterial vs venous blood

A
  • Arterial blood
    • PO2 is 100 mmHg and contains 20mL of O2/100mL blood
    • Hb is 98% saturated and durther increases in PO2 (depp breath) produce minimal increases in O2 for binding
  • Venous blood
    • PO2 is 40 mmHg
    • Hb is still 75% saturated
    • venous reserve: oxygen remaining in venous blood that can still be used
24
Q

Describe the Oxygen Hemoglobin dissocaition curve

A
  • A: In metabolically active tissues (e.g. exercising muscle)
    • the PO2 is even lower
    • At a PO2 of 20mmHg, Hb is only 40% Saturated.
  • B: in tissues PO2 is low (40 mmHg)
    • Hb is less saturated (75%) with O2
  • C: At high altitude, ther eis less O2
    • at a Po2 in lugs of only 80 mmHg, Hb still 9% saturated
  • D: if more O2 present, more O2 is bound
    • bc of Hb’s properies O2 binding strength changes with saturation
  • E: in lungs where PO2 is high (100 mmHg) Hb is almost fully saturated (98%) with O2
25
Q

what factors other than PO2 can influence Hb saturation

A

Increases in temperature, H+, PCO2, and bisphosphoglycerate (BPG) can modify structure of hemoglobin and decrease for Hb’s affinity for O2

  • > enhance O2 unloading causing a shift in O2 hemoglobin dissociation curve to the right
  • when O2 is chronically low BPG is produced by RBCs during glycolysis
26
Q

what is the Bohr effect on Oxygen trasnport

A

As cells metabolize glucose, they use O2 causing

  • > INC in PCO2 (bc using O2 nd nutrients)
  • > INC H+ in capillary blood causing Hb-P2 bond to weaken, resulting in O2 unloading
  • Heat production in active tissue directly and indirectly decreases Hb affinity for O2
27
Q

what is hypoxia?

what are the 5 different types?

A

Hypoxia = inadequate O2 delivery to tissues; can result in cyanosis

  • Anemic hypoxia: few RBCs, abnormal or too little Hb
  • Ischemic hypoxia: impaired or blocked circulation
  • Histotoxic hypoxia: cells unable to use O2 (e.g. metabolic poisons)
  • Hypoxemic hypoxia: abnormal ventilation; pulmonary disease
  • Carbon monoxide poisoning: especially from fire
    • Hb has a 200x greater affinity for carbon monoxide than oxygen