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Chapter 22, Respiratory System 1

22

The Respiratory System

Anatomy

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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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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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Function of the Nose

The only externally visible part of the respiratory

system that functions by:

Providing an airway for respiration

Moistening (humidifying) and warming theentering air

Filtering inspired air and cleaning it of foreign

matter

Serving as a resonating chamber for speech

Housing the olfactory receptors

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Structure of the Nose

The nose is divided into two regions

The external nose, including the root, bridge,

dorsum nasi, and apex

The internal nasal cavity

Philtruma shallow vertical groove inferior to the

apex The external nares (nostrils) are bounded laterally

by the alae

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Figure 22.2a

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Figure 22.2b

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Nasal Cavity

Lies in and posterior to the external nose

Is divided by a midline nasal septum

Opens posteriorly into the nasal pharynx via internal

nares

The ethmoid and sphenoid bones form the roof

The floor is formed by the hard and soft palates

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Nasal Cavity

Vestibulenasal cavity superior to the nares

Vibrissaehairs that filter coarse particles from

inspired air

Olfactory mucosa

Lines the superior nasal cavity Contains smell receptors

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Nasal Cavity

Respiratory mucosa

Lines the balance of the nasal cavity

Glands secrete mucus containing lysozyme and

defensins to help destroy bacteria

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Nasal Cavity

Figure 22.3b

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Nasal Cavity

Inspired air is:

Humidified by the high water content in the nasalcavity

Warmed by rich plexuses of capillaries

Ciliated mucosal cells remove contaminated mucus

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Nasal Cavity

Superior, medial, and inferior conchae:

Protrude medially from the lateral walls

Increase mucosal area

Enhance air turbulence and help filter air

Sensitive mucosa triggers sneezing when stimulatedby irritating particles

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Functions of the Nasal Mucosa and Conchae

During inhalation the conchae and nasal mucosa:

Filter, heat, and moisten air

During exhalation these structures:

Reclaim heat and moisture

Minimize heat and moisture loss

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Paranasal Sinuses

Sinuses in bones that surround the nasal cavity

Sinuses lighten the skull and help to warm and

moisten the air

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Pharynx

Funnel-shaped tube of skeletal muscle that connects

to the:

Nasal cavity and mouth superiorly

Larynx and esophagus inferiorly

Extends from the base of the skull to the level of thesixth cervical vertebra

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Pharynx

It is divided into three regions

Nasopharynx

Oropharynx

Laryngopharynx

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Oropharynx

Extends inferiorly from the level of the soft palate to

the epiglottis

Opens to the oral cavity via an archway called the

fauces

Serves as a common passageway for food and air

The epithelial lining is protective stratified

squamous epithelium

Palatine tonsils lie in the lateral walls of the fauces

Lingual tonsil covers the base of the tongue

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Laryngopharynx

Serves as a common passageway for food and air

Lies posterior to the upright epiglottis

Extends to the larynx, where the respiratory and

digestive pathways diverge

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Larynx (Voice Box)

Attaches to the hyoid bone and opens into the

laryngopharynx superiorly

Continuous with the trachea posteriorly

The three functions of the larynx are:

To provide a patent airway

To act as a switching mechanism to route air andfood into the proper channels

To function in voice production

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Framework of the Larynx

Cartilages (hyaline) of the larynx

Shield-shaped anterosuperior thyroid cartilage with

a midline laryngeal prominence (Adams apple)

Signet ringshaped anteroinferior cricoid cartilage

Three pairs of small arytenoid, cuneiform, and

corniculate cartilages

Epiglottiselastic cartilage that covers the

laryngeal inlet during swallowing

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Framework of the Larynx

Figure 22.4a, b

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Vocal Ligaments

Attach the arytenoid cartilages to the thyroid

cartilage

Composed of elastic fibers that form mucosal foldscalled true vocal cords

The medial opening between them is the glottis

They vibrate to produce sound as air rushes up from

the lungs

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Vocal Ligaments

False vocal cords

Mucosal folds superior to the true vocal cords

Have no part in sound production

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Vocal Production

Speechintermittent release of expired air while

opening and closing the glottis

Pitchdetermined by the length and tension of thevocal cords

Loudnessdepends upon the force at which the airrushes across the vocal cords

The pharynx resonates, amplifies, and enhances

sound quality

Sound is shaped into language by action of thepharynx, tongue, soft palate, and lips

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Movements of Vocal Cords

Figure 22.5

S i i f

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Sphincter Functions of the Larynx

The larynx is closed during coughing, sneezing, and

Valsalvas maneuver

Valsalvas maneuver

Air is temporarily held in the lower respiratory tractby closing the glottis

Causes intra-abdominal pressure to rise whenabdominal muscles contract

Helps to empty the rectum

Acts as a splint to stabilize the trunk when liftingheavy loads

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T h

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Trachea

Figure 22.6a

C d ti Z B hi

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Conducting Zone: Bronchi

The carina of the last tracheal cartilage marks the

end of the trachea and the beginning of the right andleft bronchi

Air reaching the bronchi is:

Warm and cleansed of impurities

Saturated with water vapor

Bronchi subdivide into secondary bronchi, eachsupplying a lobe of the lungs

Air passages undergo 23 orders of branching in thelungs

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C d ti Z B hi l T

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Conducting Zone: Bronchial Tree

Bronchioles

Consist of cuboidal epithelium

Have a complete layer of circular smooth muscle

Lack cartilage support and mucus-producing cells

R i t Z

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Respiratory Zone

Defined by the presence of alveoli; begins as

terminal bronchioles feed into respiratorybronchioles

Respiratory bronchioles lead to alveolar ducts, then

to terminal clusters of alveolar sacs composed ofalveoli

Approximately 300 million alveoli:

Account for most of the lungs volume

Provide tremendous surface area for gas exchange

R i t Z

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Respiratory Zone

Figure 22.8a

R i t Z

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Respiratory Zone

Figure 22.8b

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

Al eoli

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Alveoli

Surrounded by fine elastic fibers

Contain open pores that:

Connect adjacent alveoli

Allow air pressure throughout the lung to be

equalized

House macrophages that keep alveolar surfacessterile

I nterActive Physiology:

Respiratory System: Anatomy Review: Respiratory StructuresPLAY

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Figure 22.9b


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Figure 22.9.c, d

Gross Anatomy of the Lungs

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Gross Anatomy of the Lungs

Lungs occupy all of the thoracic cavity except the

mediastinum

Rootsite of vascular and bronchial attachments

Costal surfaceanterior, lateral, and posteriorsurfaces in contact with the ribs

Apexnarrow superior tip

Baseinferior surface that rests on the diaphragm

Hilusindentation that contains pulmonary and

systemic blood vessels

Lungs

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Lungs

Cardiac notch (impression)cavity thataccommodates the heart

Left lungseparated into upper and lower lobes by

the oblique fissure

Right lungseparated into three lobes by the

oblique and horizontal fissures

There are 10 bronchopulmonary segments in each

lung

Gross Anatomy of Lungs

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Gross Anatomy of Lungs

Base, apex (cupula), costal surface, cardiac notch

Oblique & horizontal fissure in right lung results in 3 lobes

Oblique fissure only in left lung produces 2 lobes

Mediastinal Surface of Lungs

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Mediastinal Surface of Lungs

Blood vessels & airways enter lungs at hilus

Forms root of lungs

Covered with pleura (parietal becomes visceral)

Blood Supply to Lungs

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Lungs are perfused by two circulations: pulmonary

and bronchial

Pulmonary arteriessupply systemic venous blood

to be oxygenated

Branch profusely, along with bronchi

Ultimately feed into the pulmonary capillary

network surrounding the alveoli

Pulmonary veinscarry oxygenated blood from

respiratory zones to the heart


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Bronchial arteriesprovide systemic blood to thelung tissue

Arise from aorta and enter the lungs at the hilus

Supply all lung tissue except the alveoli

Bronchial veins anastomose with pulmonary veins

Pulmonary veins carry most venous blood back to

the heart

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Pleurae

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Pleurae

Visceral, or pulmonary, pleura

Covers the external lung surface

Divides the thoracic cavity into three chambers

The central mediastinum

Two lateral compartments, each containing alung

Breathing

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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

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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

Pressure Relationships

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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 than

intrapulmonary 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

Lung Collapse

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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)

Pulmonary Ventilation

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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

Boyles Law

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Boyle s Law

Boyles law the relationship between the pressureand volume of gases

P1V1= P2V2

P = pressure of a gas in mm Hg

V = volume of a gas in cubic millimeters

Subscripts 1 and 2 represent the initial and resulting

conditions, respectively

Inspiration

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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

Inspiration

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Inspiration

Figure 22.13.1

Expiration

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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

Expiration

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p o

Figure 22.13.2

Physical Factors Influencing Ventilation:

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Friction is the major nonelastic source of resistance

to airflow

The relationship between flow (F), pressure (P), and

resistance (R) is:

y g

Airway Resistance

P

RF =

Physical Factors Influencing Ventilation:

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The amount of gas flowing into and out of the

alveoli is directly proportional to P, the pressure

gradient between the atmosphere and the alveoli

Gas flow is inversely proportional to resistance with

the greatest resistance being in the medium-sized

bronchi

y g

Airway Resistance

Airway Resistance

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y

As airway resistance rises, breathing movements

become 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

Alveolar Surface Tension

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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 possiblesize

Surfactant, a detergent-like complex, reduces

surface tension and helps keep the alveoli from

collapsing

Lung Compliance

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g p

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 surrounding

thoracic cage

Surface tension of the alveoli

Factors That Diminish Lung Compliance

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g p

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

Factors That Diminish Lung Compliance

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g p

Examples include:

Deformities of thorax

Ossification of the costal cartilage

Paralysis of intercostal muscles


Respiratory System: Pulmonary VentilationPLAY
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22

The Respiratory System

Physiology

Respiratory Volumes

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p y

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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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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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 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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Most result from reflex action

Examples include: coughing, sneezing, crying,

laughing, hiccupping, and yawning

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What is Composition of Air?

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Air = 21% O2, 78% N2 and .04% CO2

Alveolar air = 14% O2, 78% N2 and 5.2% CO2

Expired air = 16% O2, 78% N2 and 4.5% CO2

Observations

alveolar air has less O2 since absorbed by blood

mystery-----expired air has more O2 & less CO2 than

alveolar air?

Anatomical dead space = 150 ml of 500 ml of tidal volume

Basic Properties of Gases: Henrys Law

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When a mixture of gases is in contact with a liquid,

each gas will dissolve in the liquid in proportion toits partial pressure

The amount of gas that will dissolve in a liquid also

depends upon its solubility

Various gases in air have different solubilities:

Carbon dioxide is the most soluble

Oxygen is 1/20thas soluble as carbon dioxide

Nitrogen is practically insoluble in plasma

Hyperbaric Oxygenation

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Clinical application of Henrys law

Use of pressure to dissolve more O2

in the blood

treatment for patients with anaerobic bacterial infections (tetanus and

gangrene)

anaerobic bacteria die in the presence of O2

Hyperbaric chamber pressure raised to 3 to 4 atmospheres so that

tissues absorb more O2

Used to treat heart disorders, carbon monoxide poisoning,

cerebral edema, bone infections, gas embolisms & crush injuries

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External Respiration: Pulmonary Gas

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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

Exchange

Partial Pressure Gradients and Gas

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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

Solubilities

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Partial Pressure Gradients

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Figure 22.17

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Oxygenation of Blood

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Chapter 22, Respiratory System 91Figure 22.18

Ventilation-Perfusion Coupling

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Ventilationthe amount of gas reaching the alveoli

Perfusionthe blood flow reaching the alveoli

Ventilation and perfusion must be tightly regulatedfor efficient gas exchange

Changes in PCO2in the alveoli cause changes in thediameters of the bronchioles

Passageways servicing areas where alveolar carbondioxide is high dilate

Those serving areas where alveolar carbon dioxideis low constrict

Ventilation-Perfusion Coupling

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Surface Area and Thickness of the Respiratory

M b

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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 andedematous, whereby gas exchange is inadequate

and oxygen deprivation results

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

Membrane

Th f i h b

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

PO2in tissue is always lower than in systemic

arterial blood

PO2of venous blood draining tissues is 40 mm Hgand PCO2is 45 mm Hg


Respiratory System: Gas ExchangePLAY
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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 calledreduced hemoglobin (HHb)

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 three

hemes 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

Influence of PO2on Hemoglobin Saturation

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Chapter 22, Respiratory System99

Hemoglobin saturation plotted against PO2produces

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 PO2but

has little effect on oxygen saturation in hemoglobin

Hemoglobin Saturation Curve

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Hemoglobin is almost completely saturated at a PO2of 70 mm Hg

Further increases in PO2produce only smallincreases in oxygen binding

Oxygen loading and delivery to tissue is adequate

when PO2is 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


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Figure 22.20

Other Factors Influencing Hemoglobin

Saturation

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Temperature, H+, PCO2, and BPG

Modify the structure of hemoglobin and alter itsaffinity 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

Saturation

Factors That Increase Release of Oxygen by

Hemoglobin

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As cells metabolize glucose, carbon dioxide is

released into the blood causing:

Increases in PCO2and 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

Hemoglobin

Hemoglobin and Oxygen Partial Pressure

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Blood is almost fully saturated

at pO2 of 60mm

people OK at high

altitudes & with somedisease

Between 40 & 20 mm Hg, large

amounts of O2 are released

as in areas of need like

contracting muscle

lungsmuscle tissues

pCO2 & Oxygen Release

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As pCO2 rises with

exercise, O2 is released

more easily

CO2 converts to carbonic

acid & becomes H+ and

bicarbonate ions &

lowers pH.

Acidity & Oxygen Affinity for Hb

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As H+ increases (decrease

in pH), O2 affinity for

Hb decreases

Bohr effect allows the bloodto unload oxygen

H+ binds to hemoglobin &

alters it

O2 left behind in needy

tissues

Temperature & Oxygen Release

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As temperatureincreases, more O2 is

released

Metabolic activity &heat increases

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

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

Carbon Dioxide Transport

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Carbon dioxide is transported in the blood in threeforms

Dissolved in plasma7 to 10%

Chemically bound to hemoglobin20% is carried

in RBCs as carbaminohemoglobin

Bicarbonate ion in plasma70% is transported asbicarbonate (HCO3

)

C b di id diff i RBC d bi

Transport and Exchange of Carbon Dioxide

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Carbon dioxide diffuses into RBCs and combines

with water to form carbonic acid (H2CO3), which

quickly dissociates into hydrogen ions and

bicarbonate ions

In RBCs, carbonic anhydrase reversibly catalyzesthe conversion of carbon dioxide and water to

carbonic acid

CO2 + H2O H2CO3 H+

+ HCO3

Carbon

dioxideWater

Carbonic

acid

Hydrogen

ion

Bicarbonate

ion


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Figure 22.22a


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Chapter 22, Respiratory System

114

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 the

erythrocytes


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115

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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Haldane Effect

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117

The amount of carbon dioxide transported is

markedly affected by the PO2

Haldane effectthe lower the PO2and hemoglobin

saturation with oxygen, the more carbon dioxide can

be carried in the blood

Haldane Effect

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118

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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119Figure 22.23

Influence of Carbon Dioxide on Blood pH

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120

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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121

Changes in respiratory rate can also:

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

is disturbed by metabolic factors


Respiratory System: Gas TransportPLAY

Control of Respiration:

Medullary Respiratory Centers
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122

The dorsal respiratory group (DRG), or inspiratory

center:

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

edu y esp o y Ce e s



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y p y


Pons Respiratory Centers

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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

p y

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 medullaare

sensitive to both excitatory and inhibitory stimuli


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Depth and Rate of Breathing: Reflexes

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Pulmonary irritant reflexesirritants promote

reflexive constriction of air passages

Inflation reflex (Hering-Breuer)stretch receptors

in 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 Brain

Centers

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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

Depth and Rate of Breathing: PCO2

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Changing PCO2levels 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

PCO2levels rise (hypercapnia) resulting in increaseddepth and rate of breathing


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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 CO2acts 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 PCO2levels

Apnea (breathing cessation) may occur until PCO2

levels rise

Arterial oxygen levels are monitored by the aortic


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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 PCO2chemical stimuli

In such cases, PO2levels 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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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 the

pH by increasing respiratory rate and depth

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Respiratory Adjustments: Exercise

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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

Respiratory Adjustments: 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 System: Control of RespirationPLAY

Respiratory Adjustments: High Altitude
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The body responds to quick movement to high

altitude (above 8000 ft) with symptoms of acute

mountain sicknessheadache, shortness of breath,

nausea, and dizziness

Respiratory Adjustments: High Altitude

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Acclimatizationrespiratory and hematopoieticadjustments to altitude include:

Increased ventilation2-3 L/min higher than at sea

level

Chemoreceptors become more responsive to PCO2

Substantial decline in PO2stimulates peripheralchemoreceptors

Pneumothorax Pleural cavities are sealed

iti t t th

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cavities not open to theoutside

Injuries to the chest wallthat let air enter theintrapleural space

causes a pneumothorax

collapsed lung on sameside as injury

surface tension and recoilof elastic fibers causesthe lung to collapse

Smokers Lowered Respiratory Efficiency

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Smoker is easily winded with moderate exercise

nicotine constricts terminal bronchioles

carbon monoxide in smoke binds to hemoglobin

irritants in smoke cause excess mucus secretion

irritants inhibit movements of cilia

in time destroys elastic fibers in lungs & leads to emphysema

trapping of air in alveoli & reduced gas exchange

Every thirteen seconds someone dies from a smoking-related

disease.

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Chronic Obstructive Pulmonary Disease(COPD)

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Exemplified by chronic bronchitis and obstructive

emphysema

Patients have a history of:

Smoking

Dyspnea, where labored breathingoccurs and getsprogressively worse

Coughing and frequent pulmonary infections

COPD victims develop respiratory failureaccompanied by hypoxemia, carbon dioxideretention, and respiratory acidosis

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Pathogenesis of COPD

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Characterized by dyspnea wheezing and chest

Asthma

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Characterized by dyspnea, wheezing, and chest

tightness

Active inflammation of the airways precedes

bronchospasms

Airway inflammation is an immune response caused

by release of IL-4 and IL-5, which stimulate IgE and

recruit inflammatory cells

Airways thickened with inflammatory exudates

magnify the effect of bronchospasms

Tuberculosis

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Infectious disease caused by the bacterium

Mycobacterium tuberculosis

Symptoms include fever, night sweats, weight loss,a racking cough, and splitting headache

Treatment entails a 12-month course of antibiotics

Accounts for 1/3 of all cancer deaths in the U.S.

Lung Cancer

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90% of all patients with lung cancer were smokers

The three most common types are:

Squamous cell carcinoma (20-40% of cases)arises

in bronchial epithelium

Adenocarcinoma (25-35% of cases)originates inperipheral lung area

Small cell carcinoma (20-25% of cases)containslymphocyte-like cells that originate in the primary

bronchi and subsequently metastasize

Olfactory placodes invaginate into olfactory pits byh

Developmental Aspects

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the 4thweek

Laryngotracheal buds are present by the 5thweek

Mucosae of the bronchi and lung alveoli are presentby the 8thweek

By the 28thweek, a baby born prematurely canbreathe on its own

During fetal life, the lungs are filled with fluid andblood bypasses the lungs

Gas exchange takes place via the placenta

Respiratory System Development

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Figure 22.29

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