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Marieb EN. Human Anatomy andPhysiology 6th ed.

The Respiratory System.Pearson Inc. Cummings: 2004

Presented by: Afadiyanti, A. UNDIP

Slide PPT by:Austin, V. University of Kentucky


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Respiratory System

Consists of the respiratory and conducting zones

Respiratory zone

Site of gas exchange

Consists of bronchioles, alveolar ducts, and alveoli


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Respiratory System

Conducting zone

Provides rigid conduits for air to reach the sites of

gas exchange Includes all other respiratory structures (e.g., nose,

nasal cavity, pharynx, trachea)

Respiratory musclesdiaphragm and other musclesthat promote ventilation


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Respiratory System

Figure 22.1


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Airway to Alveoli


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Alveoli to Red Blood Cell


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Major Functions of the Respiratory System

To supply the body with oxygen and dispose of

carbon dioxide

Respirationfour distinct processes must happen

Pulmonary ventilationmoving air into and out of

the lungs

External respirationgas exchange between the

lungs and the blood


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Major Functions of the Respiratory System

Transporttransport of oxygen and carbon dioxide

between the lungs and tissues

Internal respirationgas exchange between

systemic blood vessels and tissues


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Breathing

Breathing, or pulmonary ventilation, consists of two

phases

Inspirationair flows into the lungs

Expirationgases exit the lungs


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Pressure Relationships in the Thoracic Cavity

Respiratory pressure is always described relative to

atmospheric pressure

Atmospheric pressure (Patm)

Pressure exerted by the air surrounding the body

Negative respiratory pressure is less than Patm Positive respiratory pressure is greater than Patm


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Pressure Relationships in the Thoracic Cavity

Intrapulmonary pressure (Ppul)pressure within the

alveoli

Intrapleural pressure (Pip)pressure within the

pleural cavity


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Pressure Relationships

Intrapulmonary pressure and intrapleural pressure

fluctuate with the phases of breathing

Intrapulmonary pressure always eventually

equalizes itself with atmospheric pressure

Intrapleural pressure is always less thanintrapulmonary pressure and atmospheric pressure


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Two forces act to pull the lungs away from thethoracic wall, promoting lung collapse

Elasticity of lungs causes them to assume smallest

possible size

Surface tension of alveolar fluid draws alveoli to

their smallest possible size

Opposing forceelasticity of the chest wall pulls

the thorax outward to enlarge the lungs


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Figure 22.12

P h


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Pressure changes


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Lung Collapse

Caused by equalization of the intrapleural pressure

with the intrapulmonary pressure

Transpulmonary pressure keeps the airways open

Transpulmonary pressuredifference between the

intrapulmonary and intrapleural pressures(PpulPip)


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Pulmonary Ventilation

A mechanical process that depends on volume

changes in the thoracic cavity

Volume changes lead to pressure changes, which

lead to the flow of gases to equalize pressure


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Intercostals


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Intercostals


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Inspiration

The diaphragm and external intercostal muscles(inspiratory muscles) contract and the rib cage rises

The lungs are stretched and intrapulmonary volume

increases

Intrapulmonary pressure drops below atmospheric

pressure (1 mm Hg)

Air flows into the lungs, down its pressure gradient,

until intrapleural pressure = atmospheric pressure


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Inspiration

Figure 22.13.1


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Expiration

Inspiratory muscles relax and the rib cage descends

due to gravity

Thoracic cavity volume decreases

Elastic lungs recoil passively and intrapulmonaryvolume decreases

Intrapulmonary pressure rises above atmospheric

pressure (+1 mm Hg)

Gases flow out of the lungs down the pressure

gradient until intrapulmonary pressure is 0


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Airway Resistance

As airway resistance rises, breathing movementsbecome more strenuous

Severely constricted or obstructed bronchioles:

Can prevent life-sustaining ventilation

Can occur during acute asthma attacks which stops

ventilation

Epinephrine release via the sympathetic nervous

system dilates bronchioles and reduces air resistance


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Alveolar Surface Tension

Surface tensionthe attraction of liquid moleculesto one another at a liquid-gas interface

The liquid coating the alveolar surface is always

acting to reduce the alveoli to the smallest possible

size

Surfactant, a detergent-like complex, reducessurface tension and helps keep the alveoli from

collapsing


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Surface tension related:

1. Packaging and release of surfactant from type II cells

2. Delivery and spreading of phospholipid at air/water

surface

3. Aggregation of phospholipid at air/water surface4. Removal of sufactant by type II cells and M

Airway defense related:

1. Opsinization of bacteria2. Chemotaxis of leukocytes

3. Stimulation of phagocytosis by macrophages

4. Stimulates production of proinflammatory cytokines

FUNCTIONS OF SURFACTANT


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surfactant concentration

surface area

surface tension

surfactant concentration

surface area

surface tension

Expiration Inspiration

surfactantmolecule

alveolarsurface area


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L C li


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Lung Compliance

The ease with which lungs can be expanded Specifically, the measure of the change in lung

volume that occurs with a given change in

transpulmonary pressure

Determined by two main factors

Distensibility of the lung tissue and surroundingthoracic cage

Surface tension of the alveoli

F t Th t Di i i h L C li


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Factors That Diminish Lung Compliance

Scar tissue or fibrosis that reduces the naturalresilience of the lungs

Blockage of the smaller respiratory passages with

mucus or fluid

Reduced production of surfactant

Decreased flexibility of the thoracic cage or itsdecreased ability to expand

F t Th t Di i i h L C li


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Factors That Diminish Lung Compliance

Examples include:

Deformities of thorax Ossification of the costal cartilage

Paralysis of intercostal muscles

R i t M b


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Respiratory Membrane

This air-blood barrier is composed of:

Alveolar and capillary walls

Their fused basal laminas

Alveolar walls:

Are a single layer of type I epithelial cells

Permit gas exchange by simple diffusion Secrete angiotensin converting enzyme (ACE)

Type II cells secrete surfactant

R i t M b


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Figure 22.9b

R i t M b


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Figure 22.9.c, d

S rface Area and Thickness of the Respirator


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Respiratory membranes: Are only 0.5 to 1 m thick, allowing for efficient

gas exchange

Have a total surface area (in males) of about 60 m2(40 times that of ones skin)

Thicken if lungs become waterlogged and

edematous, whereby gas exchange is inadequateand oxygen deprivation results

Decrease in surface area with emphysema, whenwalls of adjacent alveoli break through

Surface Area and Thickness of the RespiratoryMembrane

SPIROMETER


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SPIROMETER

water

nose clip

LUNG VOLUMES


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LUNG VOLUMES

6000

2900

2400

0

1200

volumeml

tidalvolume

inspiratoryreservevolume

expiratoryreservevolume

residualvolume

inspiratorycapacity

functionalresidualcapacity

FRC

vitalcapacity

total lungcapacity

time


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FRC - functionalresidual capacity

inspirationactive

expirationpassive

expirationactive

inspirationpassive

lung

volume

time


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Respiratory Volumes


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Respiratory Volumes

Tidal volume (TV)air that moves into and out of

the lungs with each breath (approximately 500 ml)

Inspiratory reserve volume (IRV)air that can be

inspired forcibly beyond the tidal volume (2100

3200 ml)

Expiratory reserve volume (ERV)air that can be

evacuated from the lungs after a tidal expiration

(10001200 ml)

Residual volume (RV)air left in the lungs after

strenuous expiration (1200 ml)

Respiratory Capacities


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Respiratory Capacities

Inspiratory capacity (IC)total amount of air that

can be inspired after a tidal expiration (IRV + TV)

Functional residual capacity (FRC)amount of air

remaining in the lungs after a tidal expiration

(RV + ERV)

Vital capacity (VC)the total amount of

exchangeable air (TV + IRV + ERV) Total lung capacity (TLC)sum of all lung

volumes (approximately 6000 ml in males)

Dead Space


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Dead Space

Anatomical dead spacevolume of the conducting

respiratory passages (150 ml)

Alveolar dead spacealveoli that cease to act in gasexchange due to collapse or obstruction

Total dead spacesum of alveolar and anatomical

dead spaces

Pulmonary Function Tests


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Spirometeran instrument consisting of a hollowbell inverted over water, used to evaluate respiratory

function

Spirometry can distinguish between:

Obstructive pulmonary diseaseincreased airway

resistance

Restrictive disordersreduction in total lung

capacity from structural or functional lung changes



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Total ventilationtotal amount of gas flow into or

out of the respiratory tract in one minute

Forced vital capacity (FVC)gas forcibly expelledafter taking a deep breath

Forced expiratory volume (FEV)the amount of

gas expelled during specific time intervals of theFVC



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Increases in TLC, FRC, and RV may occur as a

result of obstructive disease

Reduction in VC, TLC, FRC, and RV result from

restrictive disease

Alveolar Ventilation


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Alveolar Ventilation

Alveolar ventilation rate (AVR)measures the flowof fresh gases into and out of the alveoli during a

particular time

Slow, deep breathing increases AVR and rapid,

shallow breathing decreases AVR

AVR = frequency X (TVdead space)

(ml/min) (breaths/min) (ml/breath)

Nonrespiratory Air Movements


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Nonrespiratory Air Movements

Most result from reflex action

Examples include: coughing, sneezing, crying,

laughing, hiccupping, and yawning


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External Respiration: Pulmonary Gas Exchange


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Factors influencing the movement of oxygen and

carbon dioxide across the respiratory membrane

Partial pressure gradients and gas solubilities

Matching of alveolar ventilation and pulmonary

blood perfusion

Structural characteristics of the respiratorymembrane

External Respiration: Pulmonary Gas Exchange

Partial Pressure Gradients and Gas Solubilities


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The partial pressure oxygen (PO2) of venous blood

is 40 mm Hg; the partial pressure in the alveoli is

104 mm Hg

This steep gradient allows oxygen partial pressures

to rapidly reach equilibrium (in 0.25 seconds), and

thus blood can move three times as quickly (0.75

seconds) through the pulmonary capillary and stillbe adequately oxygenated




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Although carbon dioxide has a lower partial pressure

gradient: It is 20 times more soluble in plasma than oxygen

It diffuses in equal amounts with oxygen


Partial Pressure Gradients


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Partial Pressure Gradients

Figure 22.17

Internal Respiration


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The factors promoting gas exchange between

systemic capillaries and tissue cells are the same as

those acting in the lungs

The partial pressures and diffusion gradients are

reversed

PO2 in tissue is always lower than in systemic

arterial blood

PO2 of venous blood draining tissues is 40 mm Hgand PCO2 is 45 mm Hg

Internal Respiration

Oxygen Transport


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Molecular oxygen is carried in the blood:

Bound to hemoglobin (Hb) within red blood cells

Dissolved in plasma

Oxygen Transport

Oxygen Transport: Role of Hemoglobin


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Each Hb molecule binds four oxygen atoms in a

rapid and reversible process The hemoglobin-oxygen combination is called

oxyhemoglobin (HbO2)

Hemoglobin that has released oxygen is called

reduced hemoglobin (HHb)

Oxygen Transport: Role of Hemoglobin

HHb + O2

Lungs

Tissues

HbO2 + H+

Hemoglobin (Hb)


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Saturated hemoglobinwhen all four hemes of the

molecule are bound to oxygen

Partially saturated hemoglobinwhen one to threehemes are bound to oxygen

The rate that hemoglobin binds and releases oxygenis regulated by:

PO2, temperature, blood pH, PCO2, and the

concentration of BPG (an organic chemical)

These factors ensure adequate delivery ofoxygen to tissue cells

Hemoglobin (Hb)

Influence of PO2 on Hemoglobin Saturation


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Hemoglobin saturation plotted against PO2 produces

a oxygen-hemoglobin dissociation curve

98% saturated arterial blood contains 20 ml oxygen

per 100 ml blood (20 vol %)

As arterial blood flows through capillaries, 5 ml

oxygen are released

The saturation of hemoglobin in arterial bloodexplains why breathing deeply increases the PO2 but

has little effect on oxygen saturation in hemoglobin

Influence of PO2 on Hemoglobin Saturation

Hemoglobin Saturation Curve


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Hemoglobin is almost completely saturated at a PO2of 70 mm Hg

Further increases in PO2 produce only smallincreases in oxygen binding

Oxygen loading and delivery to tissue is adequate

when PO2 is below normal levels




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Only 2025% of bound oxygen is unloaded duringone systemic circulation

If oxygen levels in tissues drop:

More oxygen dissociates from hemoglobin and isused by cells

Respiratory rate or cardiac output need not increase

e og ob Satu at o Cu e



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g

Figure 22.20

Other Factors Influencing Hemoglobin


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Temperature, H

+

, PCO2, and BPG Modify the structure of hemoglobin and alter its

affinity for oxygen

Increases of these factors:Decrease hemoglobins affinity for oxygen

Enhance oxygen unloading from the blood

Decreases act in the opposite manner

These parameters are all high in systemic capillarieswhere oxygen unloading is the goal

g gSaturation

Other Factors Influencing Hemoglobin


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Figure 22.21

g gSaturation

Factors That Increase Release of Oxygen by


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As cells metabolize glucose, carbon dioxide isreleased into the blood causing:

Increases in PCO2 and H+ concentration in capillary

blood

Declining pH (acidosis), which weakens thehemoglobin-oxygen bond (Bohr effect)

Metabolizing cells have heat as a byproduct and therise in temperature increases BPG synthesis

All these factors ensure oxygen unloading in thevicinity of working tissue cells

yg yHemoglobin

Hemoglobin-Nitric Oxide Partnership


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Nitric oxide (NO) is a vasodilator that plays a role in

blood pressure regulation

Hemoglobin is a vasoconstrictor and a nitric oxide

scavenger (heme destroys NO)

However, as oxygen binds to hemoglobin:

Nitric oxide binds to a cysteine amino acid on

hemoglobin

Bound nitric oxide is protected from degradation by

hemoglobins iron

g p

Hemoglobin-Nitric Oxide Partnership


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The hemoglobin is released as oxygen is unloaded,

causing vasodilation

As deoxygenated hemoglobin picks up carbon

dioxide, it also binds nitric oxide and carries these

gases to the lungs for unloading

g p

Carbon Dioxide Transport


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Carbon dioxide is transported in the blood in three

forms

Dissolved in plasma7 to 10%

Chemically bound to hemoglobin20% is carried

in RBCs as carbaminohemoglobin

Bicarbonate ion in plasma70% is transported asbicarbonate (HCO3

)

p

Transport and Exchange of Carbon Dioxide


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Carbon dioxide diffuses into RBCs and combines

with water to form carbonic acid (H2CO

3), which

quickly dissociates into hydrogen ions and

bicarbonate ions

In RBCs, carbonic anhydrase reversibly catalyzes

the conversion of carbon dioxide and water to

carbonic acid

p g

CO2 + H2O H2CO3 H+ + HCO3

Carbon

dioxideWater

Carbonic

acid

Hydrogen

ion

Bicarbonate

ion


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At the tissues:

Bicarbonate quickly diffuses from RBCs into the

plasma The chloride shiftto counterbalance the outrush

of negative bicarbonate ions from the RBCs,

chloride ions (Cl

) move from the plasma into theerythrocytes



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At the lungs, these processes are reversed

Bicarbonate ions move into the RBCs and bind

with hydrogen ions to form carbonic acid

Carbonic acid is then split by carbonic anhydrase to

release carbon dioxide and water

Carbon dioxide then diffuses from the blood intothe alveoli



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Figure 22.22b

Haldane Effect


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The amount of carbon dioxide transported is

markedly affected by the PO2

Haldane effectthe lower the PO2 and hemoglobin

saturation with oxygen, the more carbon dioxide can

be carried in the blood

Haldane Effect


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At the tissues, as more carbon dioxide enters theblood:

More oxygen dissociates from hemoglobin (Bohr

effect)

More carbon dioxide combines with hemoglobin,

and more bicarbonate ions are formed

This situation is reversed in pulmonary circulation

Haldane Effect


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Figure 22.23

Influence of Carbon Dioxide on Blood pH


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The carbonic acidbicarbonate buffer system resistsblood pH changes

If hydrogen ion concentrations in blood begin to

rise, excess H+ is removed by combining withHCO3

If hydrogen ion concentrations begin to drop,

carbonic acid dissociates, releasing H+

Influence of Carbon Dioxide on Blood pH


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Changes in respiratory rate can also:

Alter blood pH Provide a fast-acting system to adjust pH when it

is disturbed by metabolic factors

S mm f s t s t


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Summary of gas transport

Control of Respiration:C


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The dorsal respiratory group (DRG), or inspiratorycenter:

Is located near the root of nerve IX

Appears to be the pacesetting respiratory center

Excites the inspiratory muscles and sets eupnea(12-15 breaths/minute)

Becomes dormant during expiration

The ventral respiratory group (VRG) is involved inforced inspiration and expiration

Medullary Respiratory Centers


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Control of Respiration:M d ll R i C


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Figure 22.24


Control of Respiration:P R i t C t


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Pons centers:

Influence and modify activity of the medullary

centers

Smooth out inspiration and expiration transitions

and vice versa

The pontine respiratory group (PRG)continuouslyinhibits the inspiration center

Pons Respiratory Centers

Respiratory Rhythm


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A result of reciprocal inhibition of theinterconnected neuronal networks in the medulla

Other theories include

Inspiratory neurons are pacemakers and have

intrinsic automaticity and rhythmicity

Stretch receptors in the lungs establish respiratoryrhythm

Depth and Rate of Breathing


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Inspiratory depth is determined by how actively the

respiratory center stimulates the respiratory muscles

Rate of respiration is determined by how long theinspiratory center is active

Respiratory centers in the pons and medulla are

sensitive to both excitatory and inhibitory stimuli



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Figure 22.25

Depth and Rate of Breathing: Reflexes


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Pulmonary irritant reflexesirritants promote

reflexive constriction of air passages

Inflation reflex (Hering-Breuer)stretch receptorsin the lungs are stimulated by lung inflation

Upon inflation, inhibitory signals are sent to the

medullary inspiration center to end inhalation andallow expiration

Depth and Rate of Breathing: Higher BrainCenters


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Hypothalamic controls act through the limbic

system to modify rate and depth of respiration

Example: breath holding that occurs in anger

A rise in body temperature acts to increaserespiratory rate

Cortical controls are direct signals from the cerebral

motor cortex that bypass medullary controls

Examples: voluntary breath holding, taking a deep

breath

Centers

Depth and Rate of Breathing: PCO2


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Changing PCO2

levels are monitored by

chemoreceptors of the brain stem

Carbon dioxide in the blood diffuses into the

cerebrospinal fluid where it is hydrated Resulting carbonic acid dissociates, releasing

hydrogen ions

PCO2 levels rise (hypercapnia) resulting in increased

depth and rate of breathing



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Figure 22.26



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Hyperventilationincreased depth and rate ofbreathing that:

Quickly flushes carbon dioxide from the blood

Occurs in response to hypercapnia

Though a rise CO2 acts as the original stimulus,

control of breathing at rest is regulated by thehydrogen ion concentration in the brain



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Hypoventilationslow and shallow breathing due to

abnormally low PCO2

levels

Apnea (breathing cessation) may occur until PCO2

levels rise



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Arterial oxygen levels are monitored by the aortic

and carotid bodies Substantial drops in arterial PO2 (to 60 mm Hg) are

needed before oxygen levels become a major

stimulus for increased ventilation

If carbon dioxide is not removed (e.g., as in

emphysema and chronic bronchitis), chemoreceptors

become unresponsive to PCO2 chemical stimuli

In such cases, PO2 levels become the principal

respiratory stimulus (hypoxic drive)

Depth and Rate of Breathing: Arterial pH


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Changes in arterial pH can modify respiratory rate

even if carbon dioxide and oxygen levels are normal

Increased ventilation in response to falling pH is

mediated by peripheral chemoreceptors

Peripheral Chemoreceptors


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Figure 22.27

Depth and Rate of Breathing: Arterial pH


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Acidosis may reflect:

Carbon dioxide retention

Accumulation of lactic acid

Excess fatty acids in patients with diabetes mellitus

Respiratory system controls will attempt to raise thepH by increasing respiratory rate and depth

Ventilation and work


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Increased work is initially matched by increasedventilation

At low work rates, extra ventilation achieved largely by

increased tidal volume

As work continues to increase, breathing rate begins to

increase, and tidal volume increases more.

At the ventilatory break point, ventilation increases

disproportionately to work.

Respiratory Adjustments: Exercise


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Respiratory adjustments are geared to both theintensity and duration of exercise

During vigorous exercise:

Ventilation can increase 20 fold

Breathing becomes deeper and more vigorous, butrespiratory rate may not be significantly changed(hyperpnea)

Exercise-enhanced breathing is not prompted by anincrease in PCO2 or a decrease in PO2 or pH

These levels remain surprisingly constant duringexercise



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As exercise begins:

Ventilation increases abruptly, rises slowly, and

reaches a steady state

When exercise stops:

Ventilation declines suddenly, then gradually

decreases to normal

Ventilation during exercise


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Neural factors bring about the above changes,

including:

Psychic stimuli

Cortical motor activation

Excitatory impulses from proprioceptors in muscles

Respiratory Adjustments: High Altitude


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The body responds to quick movement to high

altitude (above 8000 ft) with symptoms of acutemountain sicknessheadache, shortness of breath,

nausea, and dizziness

Respiratory Adjustments: High Altitude


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Acclimatizationrespiratory and hematopoietic

adjustments to altitude include:

Increased ventilation2-3 L/min higher than at sea

level

Chemoreceptors become more responsive to PCO2

Substantial decline in PO2 stimulates peripheral

chemoreceptors

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