The Respiratory System

The Respiratory System

• Cells continually use O2 & release CO2

• Respiratory system designed for gas exchange

• Cardiovascular system transports gases in blood

• Failure of either system– rapid cell death from O2

starvation

Nose•lined with a nasal mucosa•entrance – external nares• two nasal cavities with bony outgrowths called nasal conchae • nasal cavities separated by nasal septum•superior most region of the cavity – site for olfactory epithelium - olfactory receptors for odors (smell)•nasal cavities communicate with cranial sinuses (air-filled chambers within the skull)• nasal cavities connect with the nasopharynx - upper portion of the pharynx•connection between nasal cavity and nasopharnyx – internal naresfunctions: warm, moisten, and

filter incoming air

mucosasubmucosa

Nasopharynx

• From internal nares to soft palate

– Anatomical Landmark: openings of auditory (Eustachian) tubes from middle ear cavity

– adenoids or pharyngeal tonsil in roof

• Passageway for air only

• From soft palate to epiglottis– Anatomical Landmark: behind the uvula– palatine tonsils found in side walls,

lingual tonsil in tongue• Common passageway for food & air

OropharynxLaryngopharynx• Extends from epiglottis to cricoid

cartilage• Anatomical Landmark: the epiglottis• Common passageway for food & air

& ends as esophagus inferiorly

The Pharynx

Tortora & Grabowski 9/e 2000 JWS

The Larynx

• triangular box = “voicebox”• top of the larynx is a hole = glottis • covered with the epiglottis• contains the vocal cords - mucosal folds supported by elastic ligaments•Epiglottis---leaf-shaped piece of elastic cartilage

–during swallowing, larynx moves upward bringing the glottis up to the epiglottis–epiglottis bends slightly to cover glottis

• Laryngeal cartilages:• 1. thyroid cartilage (Adam’s apple)• 2. cricoid cartilage• 3. arytenoid cartilage – for the attachment of true vocal cords and arytenoideus muscles

• filters, moistens, vocal production

Vocal Cords• False vocal cords (ventricular

folds) found above the true vocal cords

• True vocal cords attach to arytenoid cartilages

• True vocal cord contains both skeletal muscle and an elastic ligament (vocal ligament)

• When intrinsic muscles of the larynx contract they move the arytenoid cartilages & stretch the true vocal cords tighter

• When air is pushed past the tightened cords, sound is produced


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Larnyx and Vocal Cords• true vocal cords vibrate upon passage of air ->

speech• thickness determines frequency of vibration

and timber of sound thicker the cords – slower they vibrate – lower

the pitch thinner the cords – faster they vibrate – higher

the pitch• thickness also controlled by testosterone

• pitch can also be controlled by tightening the vocal cords voluntarily

tighter the cords – faster they will vibrate

Trachea

• flexible cylindrical tube - Size is 5 in long & 1 in diameter• sits anterior (in front of) the esophagus • splits into right and left primary bronchi – enter the lungs• held open by “C” rings of hyaline cartilage = tracheal cartilage

–16 to 20 incomplete rings • layers:

– innermost layer (mucosa) = pseudo-stratified columnar with cilia & goblet cells (similar to nasal mucosa)–outer layer (submucosa) = loose connective tissue & mucous glands

•functions: conducts air into the lungs, filtration, moistens

Trachea and Bronchial Tree

• Primary bronchi supply each lung• Secondary bronchi supply each lobe of the lungs (3 right + 2 left)• Tertiary bronchi splits into successive sets of Intralobular bronchioles that supply each

bronchopulmonary segment ( right = 10, left = 8)• IL bronchioles split into Terminal bronchioles -> these split into Respiratory Bronchioles• each RB splits into multiple Alveolar ducts which end in an Alveolar sac

Pleural Membranes & Pleural Cavity

• Visceral pleura covers lungs • Parietal pleura lines ribcage & covers upper surface of

diaphragm• Pleural cavity is space between the two pleura

– contains a small amount of fluid


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

• Blood vessels & airways enter lungs at hilus

• Forms root of lungs• Covered with pleura

(parietal becomes visceral) Tortora & Grabowski 9/e 2000 JWS

Alveoli

• Respiratory bronchioles branch into multiple Alveolar ducts• Alveolar ducts end in a grape-like cluster = alveolar sac or lobule

-each grape = alveolus

terminal

Alveoli• site of gas exchange by simple diffusion• deoxygenated blood flows over the alveolus & picks up O2 via diffusion

because the alveolar wall is very thin• Type I alveolar cells

– simple squamous cells where gas exchange occurs• Type II alveolar cells (septal cells)

– free surface has microvilli– secrete alveolar fluid containing surfactant

• Alveolar dust cells– wandering macrophages remove debris

• from heart (right ventricle)-> Pulmonary artery multiple branches ending as the Pulmonary arteriole Capillary bed over Alveolus Pulmonary venule multiple veins Pulmonary vein heart (left atrium)

Respiration• internal respiration: cellular

respiration• external respiration –

exchange of O2 and CO2 between the external environment and the lungs– three steps:

• 1. Ventilation or breathing– act of moving the air

• 2. Exchange – O2 and CO2 are exchanged

between alveolar air and pulmonary blood

• 3. Transport

Non –respiratory functions• 1. route for water loss and heat elimination

– inhaled air is humidified and warmed before it is expired• 2. enhances venous return

– respiratory pump – act of muscular contraction drives blood back to the heart

• 3. maintains normal acid-base balance of the blood– removal of CO2 in expired air decreases the total amount of carbonic

acid• 4. enables speech, singing and other vocalizations• 5. smell/olfaction• 6. removes, modifies, activates or inactivates materials passing

through the pulmonary circulation


to understand external respiration – you need to understand the pleural membranes in relation to the lungs


• air moves into the lungs because of a pressure gradients• three different pressures need to be considered:

– 1. atmospheric (barometric) pressure• caused by the weight of air on objects on the Earth’s surface

– 2. intra-alveolar (intrapulmonary) pressure• pressure within the alveolus• alveolus are directly connected to the outside through the respiratory tubes• therefore air moves due to a pressure gradient difference between IAP and AP

Respiratory pressures

– 3. intrapleural (intrathoracic) pressure• pressure within the pleural sac• at rest – subatmosperic pressure


• in breathing:• AP equilibrates with intra-alveolar pressure – this equilibration is what

moves air in and out of the lungs• IP does not equilibrate with IAP or AP because there is no direct

connection with the outer pleural cavity and the inside of the lungs or the atmosphere


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Intrapleural fluid & TPG

• the pleural cavity is larger than the unstretched lungs• so the lungs are stretched slightly to try and fill this cavity• HOW?• two forces stretch the lungs within the pleural cavity• 1. Transmural Pressure Gradient• 2. Intrapleural fluid cohesion


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TPG

– 1. transmural pressure gradient (TPG)

• when breathing - intra-alveolar pressure always equilibrates with AP (760 mm Hg) and both pressure are greater than intra-pleural pressure (756 mm Hg)

• net pressure difference = transmural pressure gradient

• TPG is a pressure is pushing outward across the lung wall (air pushing from “ inside out”) and also a pressure pushing inward across the thoracic wall (air pushing in on the chest)

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Intrapleural fluid & TPG

– 1. transmural pressure gradient (TPG)

• chest wall has a tendency to “spring” outwards – the TPG pushing in on the chest wall counteracts this and compresses the chest wall in

• the lung also has a tendency to collapse - the TPG pushing from within the lung outwards counteracts this force and keeps the lung inflated

because of these TPG forces- the pleural cavities are slightly enlargened & the lungs are kept slightly inflated within them

Tortora & Grabowski 9/e 2000 JWS 23-22

• because of TPG – the pleural cavities are slightly stretched up and out

• BUT what keeps the lungs from “pulling away” from these pleural cavities and collapsing????


• 2. intrapleural fluid cohesiveness• thin layer of pleural fluid is found between the parietal and

visceral pleural membranes• water molecules resist being pulled apart – results in

cohesiveness in thin layers of water-based fluids• the cohesion between visceral and parietal pleura caused by

the intrapleural fluid keeps the lungs “attached” to the thoracic wall


• 2. intrapleural fluid cohesiveness• IP fluid also plays are role in changing lung volume in breathing

– as the thoracic wall expands – the parietal pleura is pulled along with the chest wall

– this pulls the visceral pleura with it– expands the volume of the lungs


• TPG and the cohesiveness of the intrapleural fluid prevent the lungs and chest wall from separating

• if the self-contained nature of the pleural cavities is disturbed (puncture) – air can rush in and equilibrate the intra-pleural pressure with atmospheric = pneumothorax– no transmural pressure gradient

exists across the lung wall or the chest wall because AP, IAP and IP now equal


Mechanism of Breathing: Boyle’s Law• flow of air in and out of the

lung occurs due to cyclical changes in IAP relative to AP

• IAP can be changed by altering the volume of the lungs

• described in Boyle’s law• As the size of closed

container decreases, pressure inside is increased

• As the size of a closed container increases, pressure decreases

Mechanism of Breathing

Inspiration:

-at rest: pressure inside lung = pressure outside lungs (IAP=AP)-inhale - diaphragm contracts and drops, external intercostal muscles swing the ribcage up and out-increase in thoracic cavity volume results, increase in lung volume increases also-IAP drops = Boyle’s Law-air rushes in to equalize-muscles of inspiration do not act directly on the lungs but act to change the volume of the pleural cavities-due to the cohesiveness of intrapleural fluid – lung volume changes-increase in lung volume decreases the IAP directly

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Mechanism of Breathing

Expiration: PASSIVE-occurs because of the elasticity of the lungs -in addition: relaxation of diaphragm and intercostal muscles returns thoracic and pleural cavity volume to normal-IAP increases over AP- air leaves lungs to equalize

Lung Elasticity

Expiration:-elasticity of the lung has two components: elastic recoil & compliance-elastic recoil – provided by the elastic nature of the connective tissue and the surface tension in the alveolus

-alveolar surface tension: created by a thin film of fluid produced by the type I cells – coats the inside of the alveolus-the water molecules at an air-water interface are strongly attracted to one another = surface tension-the pressure of surface tension is directed inward alveolar collapse-therefore alveoli are coated with a surfactant to reduce surface tension-however, when an alveolus fills with air – surface tension does increase – this is what helps “deflate” the lungs

-compliance: how much effort is required to stretch or distend the lungs

-e.g. how hard you have to work to blow up a balloon

-the less compliant a lung, the higher the TPG has to be to stretch the lung so it can expand enough to give a normal inspiration

-increased TPG can only be accomplished through greater expansion of the thorax/pleural cavities and a more vigorous contraction of the inspiratory muscles

-requires active inspiration and expiration – brings other muscles into play

Compliance

Summary of Breathing

• Alveolar pressure decreases & air rushes in

• Alveolar pressure increases & air rushes out


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• Forced expiration– abdominal mm force diaphragm up– internal intercostals depress ribs

• Forced inspiration– sternocleidomastoid, scalenes &

pectoralis minor lift chest upwards as you gasp for air

Airway resistance and air flow

• amount of air moved into the lungs is not only determined by the pressure differences (IAP, AP) but by the resistance the air meets as it flows through the bronchial tubes

• remember flow rate??– F = ΔP/R

• F = flow rate• ΔP = pressure gradient• R = resistance

• primary determinant for airflow just like blood flow is vessel resistance ®

Bronchioles • surrounded by “ring” of bronchiolar smooth

muscle that can control the diameter of the bronchiole

23-35smooth muscle

Airway resistance and air flow• normal individuals have large enough bronchial tubes so that R is

negligible • BUT bronchiole diameter can be dramatically influenced by the

contraction or relaxation of the smooth muscle layer found within the bronchial tubes– bronchodilation and bronchocontriction

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Bronchiolar Smooth Muscle• sensitive to changes in local environment – specifically to CO2

levels• the flow of blood to the alveolus must be carefully balanced to

match airflow– cardiac output to the alveolar capillaries can be controlled – by adjusting R of the blood vessels

Lung Volumes

• normal breathing only requires 3% of total energy expenditure if compliance is kept high and surface tensions are minimized

• during quiet breathing the lungs are only at 50% of their maximum capacity

• measurement of lung volumes – using a spirometer

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Respiratory Volumes and Capacities

• tidal volume (TV) = amnt of air that enters or exits the lungs500 ml per inhalation

• inspiratory capacity (IC) = max. amnt of air taken in after a normal exhalation, 3500 ml • inspiratory reserve volume (IRV) = IC - TV, 3000 ml

• total lung capacity = VC + RV

Respiratory Volumes and Capacities

•residual volume (RV) = amnt of air left in lungs after forced expiration = 1200 ml• expiratory reserve volume (ERV) = amnt of air forcefully exhaled, 1100 ml• functional residual capacity = ERV + RV, 2300 ml• vital capacity = max. amntof air capable of inhaling,IRV + TV + ERV = 4600 ml

• total lung capacity = VC + RV

Alveolar ventilation

• changes in lung volume are one factor in the overall determination of pulmonary ventilation = amount of air breathed in and out in one minute

• another factor is respiratory rate– Pulmonary ventilation (PV) = Tidal Volume (TV) x Respiratory

rate (RR)• not all inspired air reaches the alveolus – part remains in

the conducting airways = anatomical dead-space– greatly affects the efficiency of pulmonary ventilation– SO: amount of atmospheric air exchanged between the

atmosphere and the alveoli per minute= Alveolar Ventilation– AV = [TV-dead space] x RR

Alveolar ventilation

Internal Respiration: Gas Exchange & Dalton’s Law

• Each gas in a mixture of gases exerts its own pressure = partial pressure– pressure as if all other gases were not present– partial pressures denoted as p– Air = 21% O2, 79% N2 and .04% CO2

• Total pressure is sum of all partial pressures– atmospheric pressure (760 mm Hg) = pO2 + pCO2 + pN2 +

pH2O– to determine partial pressure of O2-- multiply 760 by % of air

that is O2 (21%) = 160 mm Hg


Gas Exchange

1. External Respiration: exchange between air and blood in the pulmonary circuit•blood plasma entering the pulmonary capillaries has a lower pO2 (40 mm Hg) than air in the alveoli (105 mm Hg)•SO: oxygen diffuses into the plasma, then into the RBC

-opposite it true for CO2

•blood entering the pulmonary capillaries has a higher pCO2 (45 mm Hg) than air in the alveoli (40 mm Hg)•therefore CO2 diffuses out of the blood into the air of alveoli


2. Internal respiration: exchange of gases between the blood and tissues• diffusion of oxygen into tissues results because pO2 is lower in the tissues (40 mm Hg vs. 100 mm Hg in the blood plasma)

Gas Exchange


Gas Exchange

Other determinants of gas exchange

• effect of surface area – during exercise, the surface are for exchange can be increased to enhance the rate of gas transfer

• effect of thickness between blood plasma and air – according to Fick’s law, increase thickness of a membrane decreases diffusion rates– increase thickness of the exchange surface in the lung can

occur through• 1. pulmonary edema • 2. pulmonary fibrosis • 3. pneumonia - accumulation of fluid due to inflammatory response

Other determinants of gas exchange

• effect of diffusion coefficient – rate of gas transfer is proportional to a diffusion coefficient (D) – D is related to the solubility of the gas and its molecular weight– D for CO2 is 20 times that of O2 – CO2 is more soluble in body

tissues and blood plasma– therefore rate of CO2 transfer is 20X that of O2– offset by the partial pressure gradient for O2 which results in

equal amounts of O2 and CO2 exchanged at the lungs



Gas transport: Hemoglobin

• O2 as a molecule dissolves poorly in the plasma of blood

• oxygen is carried in the blood by hemoglobin = oxyhemoglobin-this does not directly contribute to the pO2 of the blood-the pO2 of the blood is a measure of the dissolved O2 in the plasma – which is related to the pO2 in the inhaled air

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Gas transport: Hemoglobin• Hb has a definite binding capacity - affected by the amount of O2

dissolving in the blood• in the pulmonary capillaries on top of the alveolus - the concentration of O2

in the blood plasma (the pO2) increases – promotes the binding of O2 to Hb• in the systemic capillaries of the tissues – blood plasma pO2 decreases –

reaction is driven the opposite direction to form Hb + O2


• 100 mmHg of pO2 in the blood plasma translates into 98% saturation of Hb• if blood plasma pO2 falls below 100 mmHg there is little change in the saturation

level of Hb until you get to about 60 mm Hg (~90% saturation)• 40 mm Hg (~75% saturation)• plateau phase provides a margin of safety

- generally 98% of the Hb in blood is saturated with oxygen in the capillaries of the lungs

- 60-70% saturated in the capillaries of tissues at sea level


• saturation level can be affected by temperature (increase temp, decrease saturation)• saturation level can be affected by atmospheric pressure (decrease pressure, decrease

saturation)• saturation level can be affected by blood pH (decrease pH, decrease saturation)

• saturation level can be affected by CO2 concentration/plasma pH (decrease pH, decrease saturation)

• shift in the saturation curve of Hb to the right (decrease saturation) = Bohr Shift• HOWEVER – these shifts do not dramatically change Hb saturation!!!


Significance of Hb

• so pO2 is the dissolved amount of O2 in the blood – creates the pressure gradient that drives O2 exchange with the lungs and at the tissues

• Hb is a storage depot for O2

• when the blood enters the pulmonary capillaries on top of an alveolus – the pO2 is considerably lower than alveolar pO2 diffusion of O2 from the lungs into the blood

• as diffusion takes place - blood pO2 increases temporarily – drives the loading onto the Hb

• the plasma pO2 then drops down to its original level – allows more diffusion from alveolar air into blood plasma

• so the Hb soaks up the diffusing O2 – allows more diffusion at the lungs!!!!

• at the tissues – O2 released from the Hb and moves into the plasma – temporary increase in pO2 – drives the movement into the tissues

• CO2 is carried by the blood in 3 ways:1. 90% of the CO2 combines with water in the RBC to

form carbonic acid which immediately dissociates into bicarbonate and H+ ions (binds to Hb)

• catalyzed by the RBC enzyme called carbonic anhydrase

2. some CO2 can dissolve in the plasma as carbonic acid H+ and bicarbonate

3. CO2 can combine with hemoglobin to form carbaminohemoglobin

• in the lungs – Hb releases the H+ ion – it combines with the HCO3- to reform carbonic acid

• carbonic acid breaks up into H2O and CO2• CO2 is also released by Hb• CO2 diffuses into the alveolar air and is breathed out

Body tissue

Capillarywall

Interstitialfluid

Plasmawithin capillary

CO2 transport

from tissuesCO2 produced

CO2

CO2

CO2

H2O

H2CO3 HbRedbloodcell Carbonic

acid

Hemoglobin (Hb)picks up

CO2 and H+.

H+HCO3

Bicarbonate

HCO3

HCO3

To lungs

CO2 transport

to lungs

HCO3

H2CO3

H2O

CO2

H+

HbHemoglobin

releases

CO2 and H+.

CO2

CO2

CO2

Alveolar space in lung

CO2 transport

Respiration Rate: controlled by a respiratory center made up of a Medullary rhythmicity area in the medulla and two nuclei in the pons

-MRA -group of neurons with an automatic, rhythmic discharge-groups are called the dorsal and ventral respiratory groups-controls rate and depth of breathing-dorsal group is called the inspiratory center which send signals via

the motor neurons of the phrenic nerve and intercostal nerves that supply the inspiratory muscles (diaphragm and external intercostals)

-ventral group contains expiratory neurons – inactive during normal quiet breathing but called into play with forced, active breathing

Respiratory Center

• Respiration also controlled by neurons in pons

• Pneumotaxic Area– constant inhibitory impulses to

inspiratory area to limit breath in

• Apneustic Area– stimulatory signals to inspiratory

area to prolong inspiration

-breathing rhythm is altered by concentrations of O2, CO2 and H+

-changes in concentration are detected by chemoreceptors -additional chemoreceptors : carotid bodies

aortic bodies-respond to changes in O2 by releasing neurotransmitters that stimulate ANS neurons leading to the MRA

O2

Role of PCO2 in ventilation• Negative feedback control of

breathing

• Increase in arterial pCO2

• Stimulates receptors

• Inspiratory center

• Muscles of respiration contract more frequently & forcefully

• pCO2 Decreases

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The Respiratory System