lec 12 - pt.2 - rsystem

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© 2013 Pearson Education, Inc.

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Slides includes material (direct or modified) from © 2013 Pearson Education, Inc. Human Anatomy & Physiology, Ninth Edition and materialsupplied by Dr J Carnegie and other sources as referenced

The Respiratory System

Lecs 3 & 4

ANP 1105A&EAnthony Krantis, [email protected]

These slides contain material to be presented in lecture*.The information from the lecture should be used in combination with the

relevant chapters of the recommended Text book(s).Throughout this presentation, there are references to and use of figures

from the text book. In addition, specific animations/videosare also referenced and can be used by the student forstudy purposes, if they wish.*Slides marked with a STAR will not be covered in the lecture but are

provided as additional learning material

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Respiratory SystemRespiration

Respiration = the series of exchanges that leads to theuptake of oxygen by the cells, and the release of carbondioxide to the lungs

Step 1 = ventilation –

Inspiration & expiration

Step 2 = exchange between alveoli (lungs) and pulmonarycapillaries (blood)

–

Referred to as External Respiration

Step 3 = transport of gases in blood

Step 4 = exchange between blood and cells – Referred to as Internal Respiration

– Cellular respiration = use of oxygen in ATP synthesis

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Gas Exchanges Between Blood, Lungs, and Tissues

• External respiration –diffusion of gases in lungs

–

Thickness and surface area of respiratory membrane – Partial pressure gradients and gas solubilities

– Ventilation-perfusion coupling

•

Internal respiration –diffusion of gases at body

tissues

• Both involve

– Physical properties of gases

– Composition of alveolar gas

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External Respiration

Internal Respiration

Ventilation

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Basic Properties of Gases:

Dalton's Law of Partial Pressures

•

Total P exerted by mixture of gases

= sum of pressures exerted by each gas

•

Partial pressure (PP)

– Pressure exerted by each gas inmixture

– Directly proportional to its % inmixture

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Table 22.4 Comparison of Gas Partial Pressuresand Approximate Percentages in theAtmosphere and in the Alveoli

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Basic Properties of Gases:

Henry's Law

• Gas mixtures in contact with liquid

– Each gas dissolves in proportion to its PP

– At equilibrium, PP’s in two phases will be

equal – Amount of each gas that will dissolve

depends on

• Solubility: CO2 20x more soluble in

water than O2; little N2 dissolves inwater

• Temperature: as T0 rises, solubility

decreases

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Partial Pressure Gradients and Gas Solubilities

• Steep PP gradient for O2 in lungs

–

Venous blood Po2 = 40 mm Hg

– Alveolar Po2 = 104 mm Hg

•

Drives O2 flow to blood• Equilibrium reached across respiratory

membrane in ~0.25 seconds, about 1/3time a red blood cell is in pulmonary

capillary!

– Adequate oxygenation even if blood

flow increases 3X

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Figure 22.18 Oxygenation of blood in the pulmonary capillaries at rest.

100

5040

0 0 0.25 0.50 0.75

PO2 104 mm Hg

Time in thepulmonary capillary (sec)

End ofcapillary

Start ofcapillary

P O 2 ( m

m H g )

150

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Partial Pressure Gradients and Gas Solubilities

•

PP gradient for CO2 in lungs less steep – Venous blood Pco2 = 45 mm Hg

– Alveolar Pco2 = 40 mm Hg

• However CO2 diffuses in equal amounts with

oxygen

– CO2 is 20X more soluble in plasma than O2

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Ventilation-Perfusion Coupling

• Perfusion- blood flow reaching alveoli

• Ventilation- amount of gas reaching alveoli

• Ventilation and Perfusion matched

(coupled) for efficient gas exchange

– Never balanced for all alveoli due to

• Regional variations due to effect ofgravity on blood and air flow

• Some alveolar ducts plugged with

mucus

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Ventilation-Perfusion Coupling

Perfusion

–

Changes in gasses in alveoli cause changes in

diameters of arterioles

• Where alveolar O2 is high, arterioles - dilate

• Where alveolar O2 is low, arterioles - constrict

•

Directs most blood where alveolar oxygen high

• Where alveolar CO2 is high, bronchioles - dilate

•

Where alveolar CO2 is low, bronchioles - constrict• Allows elimination of CO2 more rapidly

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Figure 22.19 Ventilation-perfusion coupling

Ventilation less than perfusion Ventilation greater than perfusion

Mismatch of ventilation and perfusion ventilation and/or perfusion of alveoli

causes local P and PCO2 O2

Mismatch of ventilation and perfusion ventilation and/or perfusion of alveoli

causes local P and PCO2 O2

O2 autoregulatesarteriolar diameter

O2 autoregulatesarteriolar diameter

Pulmonary arteriolesserving these alveoli

constricts

Pulmonary arteriolesserving these alveoli

dilate

Match of ventilation

and perfusionventilation, perfusion

Match of ventilation

and perfusionventilation, perfusion

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Internal Respiration

Capillary gas exchange in body tissues

•

Partial pressures and diffusion gradients reversed

compared to external respiration

– Tissue Po2 always lower than in systemicarterial blood O2 from blood to tissues

–

CO2 from tissues to blood

– Venous blood Po2 40 mm Hg and Pco2 45 mm Hg

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Figure 22.17 Partialpressure gradients

promoting gas

movements in thebody.

Inspired air:

PO2

PCO2

160 mm Hg

0.3 mm Hg

Alveoli of lungs:

PO2

PCO2

104 mm Hg

40 mm Hg

Externalrespiration

Pulmonaryarteries

AlveoliPulmonary

veins (PO2

100 mm Hg)

Blood leaving

tissues andentering lungs:PO2

PCO2 40 mm Hg

45 mm Hg PO2

PCO2

Blood leaving

lungs andentering tissue

capillaries:

100 mm Hg

40 mm Hg

Systemicveins Systemicarteries

Internalrespiration

Tissues:PO2

less than 40 mm Hg

PCO2

greater than 45 mm Hg

Heart

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O2 Transport in Blood

Molecular O2 carried in blood

–

1.5% dissolved in plasma

– 98.5% loosely bound to each Fe of hemoglobin (Hb)in RBCs

• Maximum 4 O2 per Hb = Oxyhemoglobin (HbO

2)

Reduced Hb(has released it’s O2 )

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O2 and Hemoglobin

Rate of loading and unloading of O2 regulated to

ensure adequate oxygen delivery to cells

– Po2

– Temperature

– Blood pH

– Pco2

– Concentration of BPG–1,3-

bisphosphoglycerate, metabolite of glycolysis

in RBCs; levels rise when oxygen levels

chronically low promotes the release of the remainingoxygen molecules bound to the

hemoglobin, thus enhancing the ability ofRBCs to release oxygen near tissues that

need it most.

Figure 22 20 The amount of oxygen carried by hemoglobin depends on the P (the amount of oxygen) available

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Figure 22.20 The amount of oxygen carried by hemoglobin depends on the PO2 (the amount of oxygen) available

locally.

This axis tells you how much

O2 is bound to Hb. At 100%,

each Hb molecule has 4 bound

oxygen molecules.

In the lungs, where PO2 is

high (100 mm Hg), Hb isalmost fully saturated

(98%) with O2.

If more O2 is present,more O2 is bound.

However, because of

Hb’s properties (O2 binding strength

changes with

saturation), this is an

S-shaped curve, not astraight line.

Hemoglobin

Oxygen

100

80

60

40

20

0

0 20 40 60 80 100

P e r c e n t O 2 s a t u r a t i o n o f h e m o g l o b i n

P (mm Hg)

This axis tells you the relative

Amount (partial pressure) of

O2 disslolved in the fluid

Surrounding the Hb.

In the tissues of other organs,where PO2

is low (40 mm Hg), Hb

is less saturated (75%) with O2.

•

•

O2

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Influence of Po2 on Hemoglobin Saturation

•

Venous blood

–

Po2 = 40 mm Hg

–

Contains 15 vol % oxygen

–

Hb is 75% saturated

–

Venous reserve

•

Oxygen remaining in venous blood

•

Arterial blood

–

Po2 = 100 mm Hg

–

Contains 20 ml oxygen per 100 ml blood

(20 vol %)

–

Hb is 98% saturated

•

Further increases in Po2 (e.g., breathing deeply) produce minimalincreases in O2 binding

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In the lungs100

80

60

40

20

00 20 40 60 80

P e r c e n t O 2 s a

t u r a t i o n o f h e m o g l o b i n

100

PO2 (mm Hg)

At high PO2, large changes in PO2 cause only

small changes in Hb saturation. Notice that the

curve is relatively flat here. Hb’s properties

produce a safety margin that ensures that Hb is

almost fully saturated even with a substantial PO2

decrease. As a result, Hb remains saturated even

at high altitude or with lung disease.

At high altitude, there is less O2.

At a PO2 in the lungs of only 80

mm Hg, Hb is still 95% saturated.

At sea level, there is lots of O2.

At a PO2 in the lungs of 100 mm Hg,

Hb is 98% saturated.

98%

95%

Figure 22.20 The amount of oxygen carried by hemoglobin depends on the PO2 (amount of oxygen) available locally

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Figure 22.21 Effect oftemperature, PCO2

, and blood pHon the oxygen-hemoglobin

dissociation curve.

P e r c e n t O 2 s a t u r a

t i o n o f h e m o g l o b i n

P e r c e n t O 2 s a t u r a

t i o n o f h e m o g l o b i n

10ºC

20ºC38ºC

43ºC

0

20

40

60

80

100

0

20

40

60

80

100

Normal bodytemperature

Decreased carbon dioxide(PCO2

20 mm Hg) or H+ (pH 7.6)

Normal arterial

carbon dioxide

(PCO2 40 mm Hg)or H+ (pH 7.4)

Increased carbon dioxide

(PCO2 80 mm Hg)

or H+ (pH 7.2)

20 40 60 80 100

P

mm Hg)

O

2

a)

b)

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Factors that Increase Release of O2 by Hemoglobin

As cells metabolize glucose and use O2 – As Pco2 and H+ increase in capillary blood!

Bohr effect - Hb-O2 bond weakens! oxygenunloading where needed most

– As Heat production increases! directly andindirectly decreases Hb affinity for O2 !

increased oxygen unloading to active tissues

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Homeostatic Imbalance

Hypoxia

–

Inadequate O2 delivery to tissues! cyanosis

– Anemic hypoxia –too few RBCs; abnormal or toolittle Hb

– Ischemic hypoxia –impaired/blocked circulation

– Histotoxic hypoxia –cells unable to use O2, as inmetabolic poisons

– Hypoxemic hypoxia –abnormal ventilation;

pulmonary disease

– Carbon monoxide poisoning –especially from fire;

200X greater affinity for Hb than oxygen

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CO2 Transport in blood

CO2 transported in three forms

–

7 to 10% dissolved in plasma

– 20% bound to globin of hemoglobin(carbaminohemoglobin)

– 70% transported as bicarbonate ions (HCO3

– ) in

plasma

Occurs primarily in RBCs and is very fastIn plasma this reaction is slow

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Haldane Effect: Property of Hemoglobin(Hb)

De-oxygenation of blood increases its ability to carry CO2

• Reduced Hb (less O2 saturation) forms

carbaminohemoglobin and buffers H+ more easily!

– Lower Po2 and Hb saturation with O2; more CO2 carried in blood

• Encourages CO2 exchange in tissues and lungs

•

As more CO2 enters blood, more O2 dissociates fromhemoglobin (Bohr effect)

• As HbO2 releases O2, it more readily forms bonds withCO2 to form carbaminohemoglobin

Bohr Effect: hemoglobin's oxygen binding affinity is inversely related bothto acidity and to the concentration of carbon dioxide.

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Figure 22.22a Transport and exchange of CO2 and O2.

Tissue cell Interstitial fluid

(dissolved in plasma)

Binds to

plasma

proteins

Chlorideshift

(in) via

transport

protein

Blood plasma

(dissolved in plasma)

Slow

Carbonic

anhydrase

(Carbamino-

hemoglobin)

Red blood cell

Fast

Oxygen release and carbon dioxide pickup at the tissues

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Influence of CO2 on Blood pH

Carbonic acid–bicarbonate system – buffers blood pH

– If H+ concentration in blood rises, excess H+ isremoved by combining with HCO3

– ! H2CO3

– If H+ concentration begins to drop, H2CO3 dissociates, releasing H+

– HCO3 – is the alkaline reserve of carbonic acid-

bicarbonate buffer system

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Respiratory rate & depth affect blood pH

–

Slow, shallow breathing increased CO2 in

blood drop in pH

– Rapid, deep breathing decreased CO2 inblood rise in pH

• Changes in ventilation can adjust pH whendisturbed by metabolic factors

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Control of Respiration

Involves brain centers, chemoreceptors, and other reflexes

•

Brain control

–

Reticular formation of Medulla and Pons

– Pons neurons Influence and modify activity of VRG neurons

–

Smooth out transition between inspiration and expiration

–

Modify and fine-tune breathing rhythms during vocalization,sleep, exercise

–

Clustered neurons in medulla important

•

Ventral respiratory group

•

Dorsal respiratory group

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Medullary Respiratory Centers

• Ventral respiratory group (VRG) –

Rhythm-generating & integrative center

– Sets eupnea –normal breathing (12–15 breaths/min)

– Its inspiratory neurons excite inspiratory muscles via phrenic (diaphragm) and intercostal nerves (external intercostals)

–

Expiratory neurons inhibit inspiratory neurons

• Dorsal respiratory group (DRG) – Near root of cranial nerve IX

–

Integrates input from peripheral stretchand chemoreceptors; sends information! VRG

Figure 22 23 Locations of

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Pons

Medulla

Pontine respiratory centers

interact with medullaryrespiratory centers to smooththe respiratory pattern.

Ventral respiratory group (VRG) contains rhythm generatorswhose output drives respiration.

Pons

Dorsal respiratory group (DRG) integrates peripheral sensoryinput and modifies the rhythmsgenerated by the VRG.

To inspiratorymuscles

Externalintercostalmuscles

Diaphragm

Medulla

Figure 22.23 Locations ofrespiratory centers and theirpostulated connections.

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Factors influencing Breathing Rate and Depth

• Depth = how actively the respiratory center stimulates

respiratory muscles• Rate = duration of inspiratory center activity

• Both modified in response to changing body demands

– Most important are changing levels of CO2, O2, and H+

– Sensed by central and peripheral chemoreceptors

• Hyperventilation- depth & rate of breathing thatexceeds body's need to remove CO2

! decreases blood CO2 levels (hypocapnia)

! cerebral vasoconstriction and cerebralischemia ! dizziness, fainting

• Apnea – breathing cessation from abnormally lowPco2

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Chemical Factors

Rising CO2 levels most powerful respiratory stimulant

–

If blood Pco2 rises (hypercapnia), CO2

accumulates in brain!

– CO2 in brain hydrated to carbonic acid! dissociates, releasing H+ ! pH drops

–

H+ stimulates chemoreceptors of brain stem

– Chemoreceptors synapse with respiratoryregulatory centers! increased depth and rate

of breathing! lower blood Pco2 ! pH risesNormally blood Po2 affects breathing only indirectly by influencingperipheral chemoreceptor sensitivity to changes in Pco2

But when arterial Po2 <60 mm Hg, it becomes major stimulus forrespiration (via peripheral chemoreceptors)

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Chemical Factors

Influence of Po2

–

Peripheral chemoreceptors inaortic & carotid bodies – sense

arterial O2 level

– When stimulated, causerespiratory centers to increase

ventilation

–

Declining Po2 normally slighteffect on ventilation

• Huge O2 reservoir bound toHb

• Requires substantial drop in

arterial Po2 (to 60 mm Hg)to stimulate increased

ventilation

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Chemical Factors

Influence of arterial pH

–

Can modify respiratory rate & rhythm even if CO2 &

O2 levels normal

– Involves peripheral chemoreceptors

– Decreased pH may reflect

•

CO2 retention; accumulation of lactic acid; excessketone bodies

– Respiratory system controls attempt to raise pH by

increasing respiratory rate and depth

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Inflation Reflex

Hering-Breuer Reflex (inflation reflex)

•

Stretch receptors in pleurae and airways

stimulated by lung inflation

- Inhibitory signals to medullary respiratorycenters end inhalation and allow expiration

- Acts as protective response more than

normal regulatory mechanism

Figure 22.24 Neural and chemical influences on brain stem respiratory centers.

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Central

chemoreceptors

Other receptors (e.g., pain)and emotional stimuli actingthrough the hypothalamus

Peripheralchemoreceptors

Respiratory centers(medulla and pons)

Higher brain centers(cerebral cortex—voluntary

control over breathing)

-breath holding in anger

-gasping with pain-rise in body temperature

Stretch receptorsin lungs

Irritantreceptors

Receptors inmuscles and joints

+ –

+ –

+

–+

+

–

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Respiratory Adjustments: Exercise

Adjustments geared to intensity & duration of exercise

•

Hyperpnea – Increased ventilation (10 - 20 fold) in response to

metabolic needs

• Pco2, Po2, and pH remain surprisingly constant during

exercise•

Three neural factors increase ventilation as exercise begins

- Psychological stimuli — anticipation of exercise

- Simultaneous cortical motor activation of skeletal muscles

and respiratory centers

Excitatory impulses to respiratory centers from

proprioceptors in moving muscles, tendons, joints

R i t Adj t t E i

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Respiratory Adjustments: Exercise

•

Ventilation declines suddenly as exercise ends

because the three neural factors shut off

• Gradual decline to baseline because of declinein CO2 flow after exercise ends

• Exercise! anaerobic respiration! lactic acid

– Not from poor respiratory function; from

insufficient cardiac output or skeletal muscle

inability to increase oxygen uptake

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High Altitude

•

Quick move to > 2400m (8000 ft)! acute

mountain sickness (AMS) – Atmos P and Po2 levels lower

– Headaches, shortness of breath, nausea,dizziness

–

Possible, lethal cerebral & pulmonaryedema

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Acclimatization to High Altitude

• Respiratory & hematopoietic adjustments occur

•

Chemoreceptors more responsive to Pco2 when Po2 declines

• Lower Po2 directly stimulates peripheralchemoreceptors

• Ventilation increases to 2–3 L/min higher than sea

level• Always lower-than-normal Hb saturation levels

– Less O2 available

• Decline in blood O2 stimulates kidneys to accelerateproduction of EPO

•

RBC numbers increase slowly to provide long-termcompensation

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Chronic Obstructive Pulmonary Disease (COPD)

– Exemplified by chronic bronchitis & emphysema

–

Irreversible decrease in ability to force air out of lungs – Common features

• History of smoking in 80% of patients

• Dyspnea - labored breathing ("air hunger")

• Coughing & frequent pulmonary infections

•

Most develop respiratory failure (hypoventilation)accompanied by respiratory acidosis, hypoxemia

• Treated with bronchodilators, corticosteroids, oxygen,sometimes surgery

normal emphysema

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• Tobacco smoke• Air pollution

!-1 antitrypsindeficiency

Continual bronchialirritation and inflammation

Breakdown of elastin inconnective tissue of lungs

• Chronic productive cough• Loss of lung elasticity

• Frequent infections

• Respiratory acidosis

Chronic bronchitis

• Excess mucus production

Emphysema

• Destruction of alveolarwalls

• Airway obstructionor air trapping

• Dyspnea

• Hypoventilation• Hypoxemia

Figure 22.27 Thepathogenesis of COPD

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Asthma: Reversible COPD

– Characterized by coughing, dyspnea, wheezing, and

chest tightness

– Active inflammation of airways precedes bronchospasms

– Inflammation is immune response due to release ofinterleukins, production of IgE, and recruitment ofinflammatory cells

– Airways thickened with inflammatory exudate magnifyeffect of bronchospasms

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Tuberculosis (TB)

– Infectious disease caused by bacterium

Mycobacterium tuberculosis

– Symptoms-fever, night sweats, weight loss,racking cough, coughing up blood

– Treatment- 12-month course of antibiotics

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Cystic fibrosis

– Most common lethal genetic disease in North

America

– Abnormal, viscous mucus clogs passageways! bacterial infections

•

Affects lungs, pancreatic ducts, reproductive

ducts

– Cause–abnormal gene for Cl- membrane

channel

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