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Chapter 16Respiration

• Functions of the respiratory system–––––––

Respiration• The term respiration includes 3 separate

functions:• Ventilation:

– Breathing.• Gas exchange:

– Occurs between air and blood in the lungs.– Occurs between blood and tissues.

• 02 utilization:– Cellular respiration.

Steps inRespiration

Fig notin book

Type I cell

Type II cell

Fig. 16.1

Organization of therespiratory system.

Fig. 16.4

The conducting zone• Low -resistance

pathway forairflow

• Defends againstyucky stuff

• Warms andmoistens air

• When you havekids it enablesyou to yell atthem.

ϖ No gas exchangeFig. 16.5

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Respiratory Zone

• Region of gasexchange betweenair and blood.

• Includes respiratorybronchioles.

• Must containalveoli.

• Gas exchangeoccurs by diffusion.

Fig. 16.4Figure not in book

Fig. 16.8

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Ventilation and Lung MechanicsStep 1: Getting air into and out of lungs

• Remember: F = ΔP/R– F = flow– ΔP = pressure difference (mmHg)– R = resistance to flow.

Ventilation and Lung MechanicsStep 1: Getting air into and out of lungs

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Really, Really Important Point!

• During inspiration and expiration volume oflungs is made to change.

¬By Boyle’s law, these changes causechanges in alveolar pressure which drivesair into or out of lungs.

Volume of lungs depends on:

• Transpulmonary pressure - difference inpressure between outside and inside oflungs.

• Elasticity (stretchability) of lungs.

Surface Tension

• Law of Laplace:• Pressure in alveoli is

directly proportionalto surface tensionand inverselyproportional toradius of alveoli.

Fig. 16.11

Creating the Intrapleural Pressure

• Pull of lungs inward and chestwall outwardon intrapleural fluid causes a negativepressure within this space.

Fig. 16.15

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Fig not in bookFig not in book

Lung Compliance

• CL = magnitude of change in lung volume(ΔVL) produced by a given change intranspulmonary pressure.

• CL = ΔVL/Δ (Palv - Pip)• Greater the lung compliance the _______ it

is to expand the lungs at any giventranspulmonary pressure.

Fig not in book

Determinants of LungCompliance

• Stretchability• Surface tension at air-water interfaces

within alveoli.– Assets of surfactant.

Surfactant• Phospholipid

produced byalveolar type IIcells.

• Lowers surfacetension.

• Reduces attractiveforces of hydrogenbonding bybecominginterspersedbetween H20molecules.

• As alveoli radiusdecreases,surfactant’s abilityto lower surfacetension increases. Fig. 16.12

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Fig. 16.14 See also table 16.2

Pulmonary Function Tests

• Assessed by spirometry.• Subject breathes into a closed system in

which air is trapped within a bell floating inH20.

• The bell moves up when the subject exhalesand down when the subject inhales.

Schematic of aspirometer (left)and the spirometeryou will be using in lab (above).

Spirogram

• Tidal volume:Amount of air expired with each breath.• Vital capacity:The maximum amount of air that can be forcefully exhaled

after maximum inhalation.

Fig. 16.16

Table 16.3 Terms Used to Describe Lung Volumes andCapacities

Term DefinitionLung Volumes The four nonoverlapping components of the total lung

capacity

Tidal volume The volume of gas inspired or expired in an unforcedrespiratory cycle

Inspiratory reserve volume The maximum volume of gas that can be inspired duringforced breathing in addition to tidal volume

Expiratory reserve volume The maximum volume of gas that can be expired duringforced breathing in addition to tidal volume

Residual volume The volume of gas remaining in the lungs after a maximumexpiration

Lung Capacities Measurements that are the sum of two or more lungvolumes

Total lung capacity The total amount of gas in the lungs after a maximuminspiration

Vital capacity The maximum amount of gas that can be expired after amaximum inspiration

Inspiratory capacity The maximum amount of gas that can be inspired after anormal tidal expiration

Functional residual capacity The amount of gas remaining in the lungs after a normaltidal expiration

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Anatomical Dead Space

• Not all of the inspired air reaches the alveoli.• As fresh air is inhaled it is mixed with anatomical

dead space.• Conducting zone and alveoli where 02

concentration is lower than normal and C02concentration is higher than normal.

• Alveolar ventilation: F x (TV- DS)– F = frequency (breaths/min.).– TV = tidal volume.– DS = dead space.

Airway resistance andrestrictive vs. obstructive disorders

• Recall:• F = (Patm - Palv) / R• Resistance depends on:

–––

Airway Radii and Resistance

• Airway radii affected by– Physical factors

• “going down the wrong pipe”• Asthma caused by chemical factors (see below).

– Neural factors• Epinephrine

– Chemical factors• CIGARETTE SMOKE, pollutants, viruses allergens,

bronchoconstrictor chemicals

Restrictive and ObstructiveDisorders

• Restrictivedisorder:– Vital capacity is

reduced.– FVC is normal.

• Obstructivedisorder:– VC is normal.– FEV1 is reduced.

Fig. 16.17

Gas Exchange• Dalton’s Law:• Total pressure of a gas mixture is = to the

sum of the pressures that each gas in themixture would exert independently.

• PATM = PN2 + P02 + PCo2 = 760 mm Hg– 02 humidified.

• H20 contributes to partial pressure(~ 47 mm Hg)

– P02 (sea level) = 150 mm Hg.

Fig. 16.20

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Significance of Blood P02 and PC02Measurements

• At normal P02arterial blood isabout 100 mmHg.

• P02 systemicveins =

~ 40 mm Hg.• PC02 systemic

veins = ~ 46 mm Hg

Fig. 16.23Figure not in book - Applying numbers to previous figure.

Gas Exchange

• Dalton’s Law:• Total pressure of a gas mixture is = to

the sum of the pressures that each gasin the mixture would exertindependently.

• PATM = PN2 + P0 + PCo2 = 760 mm Hg

Fig. 16.32

Measuring efficacy of lung function.

NOTE these numbers

Fig. 16.23

Defining Ventilation• Minute ventilation - total ventilation per

minute

• Alveolar Ventilation - total volume of fresh airenter the alveoli per minute = efficacy ofbreath

• Physiologic dead space - sum of anatomic andalveolar dead space.

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Restrictive and ObstructiveDisorders

• Restrictivedisorder:– Vital capacity is

reduced.– FVC is normal.

• Obstructivedisorder:– VC is normal.– FEV1 is reduced.

Fig. 16.17

FEV1Forced Expiratory Volume/sec.

• Fraction of total “forced” vital capacityexpired in 1 sec.

• The FEV1 of a person with obstructive lungdisease would be ________ 80% of vitalcapacity.

• The FEV1 of a person with restrictive lungdisease would ________ 80% of vitalcapacity.

Alveolar Gas Pressure

• Alveolar PO2 and PCO2 determine the systemicarterial PO2 and PCO2.

• Alveolar PO2 values determined by– PO2 of atmospheric air– Rate of alveolar ventilation– Rate of total body oxygen consumption

• Alveolar PCO2 values determined by– Rate of alveolar ventilation– Rate of total body carbon dioxide production

Relevance of Partial Pressures

• High altitude => _______ in PO2 of inspiredair and _________ in alveolar PO2.

• Decreased alveolar ventilation => ______ inPO2 of inspired air and ________ inalveolar PO2.

• Increased cellular metabolism => ________in alveolar PO2.

Getting O2 into and CO2 out ofbody: the bottom line(s)

• In alveoli– PO2 and PCO2 on two sides of alveolar-capillary

membrane result in net diffusion, CO2 out andO2 in.

– More capillaries involved, more total O2/CO2exchange.

– Need for fewer or greater numbers of alveoli ingas exchange (impairment of gas exchange:O2).

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Getting O2 into and CO2 out ofbody: the bottom line(s)

• In alveoli– Ventilation-perfusion inequality = mismatching

of air supply and blood supply on an individualalveoli.

– Lowers PO2 of systemic arterial blood.– Caused by

• Ventilated blood in alveoli with no blood supply• No blood flowing to some alveoli.

– Compensation by vasoconstriction

Getting O2 into and CO2 out ofbody: the bottom line(s)

• In tissues– Low PO2 and high PCO2 in tissues results in net

movement of O2 into tissues and net CO2movement out of tissues.

• We will revisit this momentarily.

Breathing Lesson(control of breathing)

• Medulla oblongata (medullary inspiratoryneurons).

• Pons• Pulmonary stretch receptors• Peripheral chemoreceptors -• Central chemoreceptors

Regulation of Breathing• Neurons in the

medulla oblongataforms the rhythmicitycenter:– Controls automatic

breathing.• Brain stem

respiratory centers:– Medulla.– Pons.

Fig. 16.25

Rhythmicity Center• Dorsal respiratory group (DRG).

– Regulate activity of phrenic nerve.– Project to and stimulate spinal interneurons that

innervate respiratory muscles.– Considered the “I” neurons.

• Ventral respiratory group (VRG).– Passive process.– Controls motor neurons to the internal intercostal

muscles.– Considered the “E” neurons.

• Activity of expiratory neurons inhibit inspiratoryneurons.

• Apneustic center:– Promote inspiration by stimulating the

inspiratory neurons in the medulla.– Provide constant stimulus for inspiration.

• Pneumotaxic center:– Antagonize the apneustic center.– Inhibits inspiration.

Pons Respiratory Centers:Influence medullary rhythmicity

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Fig. 16.28

Adequacy of ventilation

• Hypoventilation– increase in ratio of carbon dioxide production

to alveolar ventilation.– hypercapnia

• Hyperventilation– decrease in ratio of carbon dioxide production

to alveolar ventilation.– hypocapnia

Chemoreceptor Control• Chemoreceptor input modifies the rate and depth

of breathing.– Oxygen content of blood decreases more slowly

because of the large “reservoir” of oxygen attached tohemoglobin.

– Chemoreceptors are more sensitive to changes in PC02.• H20 + C02• Rate and depth of ventilation adjusted to maintain

arterial PC02 of 40 mm Hg.

H+ + HC03-H2C03

Chemoreceptors• 2 groups of chemoreceptors

that monitor changes inblood PC02, P02, and pH.

• Central:– Medulla.

• Peripheral:– Carotid and aortic

bodies.– Control breathing

indirectly via sensorynerve fibers to themedulla.

Fig. 16.27

Fig. 16.29 Fig. 16.31

Can say that chemoreceptor sensitivity toPCO2 is augmented by low PO2.

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Moving Oxygen in Blood

• Amount of oxygen dissolved in blooddirectly proportional to PO2 of blood.

• But oxygen NOT very soluble in water(blood).

• Hemoglobin to the rescue!!!!

HemoglobinStructure

Fig. 16.33

Hemoglobin• Hemoglobin production controlled by

erythropoietin.• Production stimulated by P02 delivery to kidneys.• Loading/unloading depends:

– P02 of environment.– Affinity between hemoglobin and 02.

• Oxyhemoglobin vs. Deoxyhemoglobin.

Fig. 16.34

• So what doespH do to O2affinity ofhemoglobin?

• Temperature?

• 2,3 DPG =

Fig. 16.35

More on 2,3-DPG

• Anemia and– Increased production of 2,3-DPG with low

hemoglobin concentration.– Causes increased unloading of oxygen in

tissues.• Fetal hemoglobin and

– Gamma chains in lieu of beta chains.– Do not bind 2,3-DPG– Becomes oxygen “pig”

I want my OXYGEN!

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Inherited defects in hemoglobin• Sickle-cell anemia

– Valine substitued for glutamic acid at position #6.– Low PO2 causes cross-linking and formation of

paracrystalline gel - “sickling” of cells.• Thalassemia

– Decreased synthesis of alpha or beta chain ofhemoglobin.

– Get increases in gamma chain synthesis.

Muscle Myoglobin• Slow-twitch skeletal fibers

and cardiac muscle cells arerich in myoglobin.– Higher affinity for 02 than

hemoglobin.• Acts as a “go-between” in

the transfer of 02 fromblood to the mitochondriawithin muscle cells.

• May also have an 02 storagefunction in cardiac muscles.

Fig. 16.37

Carbon dioxide in blood

• Dissolved CO2: 1/10• Carbaminohemoglobin: 1/5• Bicarbonate: 7/10

Fig. 16.38

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Fig. 16.39

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Adequacy of ventilation

• Hypoventilation– increase in ratio of carbon dioxide production

to alveolar ventilation.– hypercapnia

• Hyperventilation– decrease in ratio of carbon dioxide production

to alveolar ventilation.– hypocapnia

Respiratory acidosis vs.respiratory alkalosis

• Respiratory acidosis - increased arterial H+ concentrationdue to CO2 retention.

• Metabolic acidosis - increased production of “nonvolatile”acids or loss of blood bicarbonate, resulting in a fall ofblood pH.

• Respiratory alkalosis - lowering of arterial PCO2 and H+

concentration.• Metabolic alkalosis - rise in blood pH produced by loss of

nonvolatile acids or by excessive accumulation ofbicarbonate base.

Compensating acidosis or alkalosis.

• Metabolic acidosis or alkalosis -

• Respiratory acidosis or alkalosis -

Chemoreceptors• 2 groups of chemoreceptors

that monitor changes inblood PC02, P02, and pH.

• Central:– Medulla.

• Peripheral:– Carotid and aortic

bodies.– Control breathing

indirectly via sensorynerve fibers to themedulla.

Fig. 16.27

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Response to exercise

• Neurogenic– Sensory nerve activity from exercising limbs

stimulate respiratory muscles.– Input from cerebral cortex stimulates brain stem

respiratory centers.• Humoral

– Changes in blood concentrations of gases andsignaling molecules.

Fig. not in book

• Hypoxic ventilatoryresponse to highaltitude (low PO2)– produces

hyperventilation– Increase in tidal

volume.– Lowers arterial PCO2– Produces respiratory

alkalosis whicheventually “blunts”hyperventilatoryresponse.

Figure not in book

Other respiratory changes due tohigh altitudes

• Increased productionof 2,3-DPG.

• Increased productionof RBCs andhemoglobin.

• “Barrel-chest”

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