Chapter 23: THE RESPIRATORY SYSTEM
Cells produce energy for maintenance, growth, defense, division and need ATP via aerobic respiration
cells use
and produce
can go without oxygen for
minutes.
Respiratory System Functions to:
1. Pulmonary Ventilation:
2. External Respiration: exchange of gasses b/w alveoli and pulmonary capillaries
3. Internal Respiration: exchange of gasses b/w tissue cells and systemic capillaries
4. Protect respiratory tract from dehydration, temperature changes and pathogens
5. Sound
6. Olfaction
Organization of the Respiratory System:
Upper respiratory system: nose - pharynx
Lower respiratory system: larynx - alveoli
Respiratory Tract: Functionally: 2 zones
1. Conducting Zone:
2. Respiratory Zone:
Respiratory Mucosa:
pseudostratified ciliated columnar epithelial tissue with goblet cells:
lamina propria:
Respiratory Defense System
Goblet cells and mucous glands secrete mucus
Cilia: (mucus escalator)
Filtration in nasal cavity:
Alveolar Macrophages (Dust Cells)
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Anatomy of the Respiratory System
1. Nose and nasal cavity:
External nares (nostrils)
Hair and mucus
Olfaction:
Paranasal sinuses:
Nasal septum: ethmoid and vomer bones
divides R, L nasal cavities
Hard palate: formed by:
Soft palate:
Nasal conchae: projections from the lateral side of each nasal cavity
Meatuses: air passageways that spiral through conchae
Helps warm, filter and humidify incoming air
Nasal mucosa: filters incoming air
Many blood vessels in lamina propria to warm and humidify air
epistaxis: nosebleed
2. Pharynx
nasophyarynx: contains pharyngeal tonsil
oropharynx:
laryngopharynx:
pharyngitis:
tonsilitis:
3. Larynx
• glottis: opening b/w pharynx and larynx
• formed from cartilage (laryngeal prominence or Adam's apple)
Thyroid Cartilage, Cricoid & Arytenoid Cartilage & Epiglottis
• epiglottis: forms lid over glottis
during swallowing epiglottis folds over glottis to prevent food/drink from entering
respiratory tract
Aspiration:
Choking: Heimlich maneuver
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Ligaments of the Larynx
Vestibular ligaments and vocal ligaments (covered by epithelium termed folds)
Sound Production
Air passing through glottis
Vibrates vocal folds/cords
Produces sound waves
Laryngitis:
4. Trachea
• 1 " diameter formed by C-shaped hyaline cartilage rings (tracheal cartilages)
• transports air to bronchial tree
• tracheostomy:
5. Bronchial tree:
• begins with R and L primary bronchi
R primary bronchus has larger diameter
• enter at hilum
• once inside lungs each primary bronchus subdivides into secondary
bronchi (lobar bronchi) to tertiary bronchi (segmental bronchi) etc. etc. to 23 orders
air passageway <1 mm diameter are called:
the amount of smooth muscle increases as passageways become
respiratory zone:
bronchodilation: caused by sympathetic stimulation
bronchoconstriction: caused by parasympathetic stimulation
bronchitis:
bronchoscopy:
6. The Lungs
• occupy entire thoracic cavity
• located in pleural cavity
• base: inferior portion
• apex & root
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• costal surface
• right lung 3 lobes: Superior, Middle & Inferior: oblique & horizontal fissures
left lung 2 lobes: Superior & Inferior: oblique fissure only
• lungs consist of elastic connective tissue termed stroma
pneumonia: lung infection
viral, bacterial or fungal infection
S/S: cough (green/yellow mucus), fever, chest pain
7. Alveoli:
respiratory bronchioles connect to alveolar ducts which lead to alveolar sacs to alveoli
alveoli surrounded by pulmonary capillaries
walls of alveoli consist of simple squamous epithelial tissue known as type I cells (pneumocytes
type I)
type II cells (septal cells or pneumocytes): secrete surfactant (phospholipid)
surfactant lines each alveolus and functions to
Dust cells: alveolar macrophages
Respiratory Distress: Difficult respiration (S/S: rapid, shallow breathing, cyanosis, nasal flaring)
ARDS: (Adult Respiratory Distress Syndrome):
● Lung capillaries become leaky, decreases lungs ability to expand for inhalation
● caused by decreased surfactant (chemicals), lung inflammation from aspiration,
pneumonia, injury to chest
IRDS: (neonatal respiratory distress or hyaline membrane disease)
● due to lack of surfactant
Respiratory Membrane: 3 parts (pg. 828 figure 23-11)
1. type I cells of alveolus (squamous epithelial cells)
2. endothelium of capillary
3. basement membranes of both
very thin to facilitate diffusion
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Blood Supply to Lungs:
pulmonary artery: enter at hilus and branch with bronchi
pulmonary arterioles
pulmonary capillaries: gas exchange
also make ACE
pulmonary venules
pulmonary vein
Capillaries supplied by bronchial arteries
 Provide oxygen and nutrients to tissues of conducting passageways of lung
 Venous blood bypasses the systemic circuit and flows into pulmonary veins
Pulmonary embolism: one or more pulmonary arteries/arterioles blocked
BP in pulmonary circuit 30 mmHg or less
easy for clots and air bubbles to block blood vessels
typically clot originates from DVT
Risk Factors: prolonged immobility, surgery, age, smoking, heart disease, family history, being
overweight
S/S: sudden unexplained shortness of breath, chest pain
Tx: anticoagulant therapy, surgery
Pleura (serous membranes)
visceral pleura
parietal pleura
pleural fluid
pleurisy = rough dry surface, pain
Respiratory Physiology
External Respiration:
Internal Respiration:
Hypoxia
Anoxia
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Boyle's Law: when temperature is constant the pressure is inversely related to volume.
So if the volume of the thoracic cage increases, pressure will:
and if the volume of the thoracic cage decreases the pressure will:
Pressure & Airflow to the lungs:
Air flows from area of higher pressure to area of lower pressure
Respiratory Cycle: inspiration & expiration
So – volume changes lead to pressure changes which causes air to move
A. Pressure Relationships in Thoracic Cavity and Pulmonary Ventilation
Atmospheric pressure (Patm): 760 mmHg at sea level
altitude decreases this pressure
diving increases this pressure
Intrapulmonary pressure (Ppul) = pressure within lungs or alveoli
depends on volume changes in thoracic cavity (758 - 762 mmHg
rises & falls but always equalizes with Patm
Intrapleural pressure (Pip) = pressure within pleural cavity
always negative pressure to Patm and Ppul
why is it always negative?
elasticity of lungs
important to have negative intrapleural pressure to keep the visceral pleura attached to
parietal pleura
any condition which causes intrapleural pressure to equalize or intrapulmonary will result
in immediate lung collapse (atelectasis)
Pneumothorax: presence of air in interpleural space – lung collapse
1. Primary spontaneous pneumothorax: blebs: small sac on lung ruptures
2. Secondary spontaneous pneumothorax: occurs in individuals with pre-existing lung
disorder (emphysema)
3. Traumatic pneumothorax:
Hemothorax: presence of blood in interpleural space
Lung Collapse S/S: sudden sharpt chest pain, shortness of breath, rapid HR, anxiety
Tx: chest tube to drain blood/air, reinflation
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Inspiration: active phase (pg. 833 figure 23-15)
diaphragm contracts which increases the volume of the thoracic cavity
so pressure inside thoracic cavity (intrapulmonary) decreases (758-759 mmHg)
(note intrapleural pressure also falls & becomes more negative)
now atmospheric pressure exceeds intrapulmonary pressure: air rushes into lungs until
equilibrium is reached (760 mmHg)
external intercostals and
inspiration
other accessory muscles:
are the accessory muscles which assist with forced
Lung Compliance
ease with which lungs can be expanded: high compliance means less work necessary to
inflate the lungs.
compliance diminished by any factor that:
1. decreases natural resilience of lungs
2. blocks respiratory passageways
3. increases surface tension in alveoli
4. impairs flexibility of thoracic cage
Expiration: passive phase
diaphragm relaxes (AND lungs recoil) which decreases the volume of the thoracic cavity
so intrapulmonary pressure increases (761 or 762 mmHg) to exceed atmospheric
pressure and air flows out of lungs
Lung Elasticity: lung recoil essential for normal expiration
forced expiration occurs when
muscles contract.
note: changes in intrapulmonary pressure are small, only 1-2 mmHg
this normal breathing (quiet breathing) is called the tidal volume (VT) – 500 ml/breath
Breathing Types:
eupnea: 12-18 breaths/minute
hyperpnea: forced breathing
dyspnea:
apnea:
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Physical Factors Influencing Pulmonary Ventilation:
A. Respiratory Passageway Resistance mainly due to friction in passageway
R due to diameter of conducting tubes not very significant
significant factor is smooth muscle of bronchiole walls
parasympathetic & inflammatory chemicals = bronchoconstriction, increase R
sympathetic= epinephrine, dilates bronchioles = bronchodilation (NE binds to β2 receptor)
respiratory disease: sources of R
Gas Laws: Composition of Air: N2 (78/6%), O2 (20.9%), H2O (.5%), CO2 (.04%)
Basic Properties of Gases:
Dalton's Law of Partial Pressures: total pressure exerted by a mixture of gases
is the sum of the pressures exerted independently by each gas in the mixture.
partial pressure: pressure exerted by each gas (table 23-2 pg. 839)
% of gas X 760 mmHg = PP
O2 makes up 20.9% of room air, what is the PO2 in air?
21% x 760 mmHg = 159 mmHg
CO2 makes up .04% = PCO2=.3 mm
Henry's Law:
At a given temperature the amount of a particular gas in solution is directly proportional to the
partial pressure of that gas. (The pressure contributed by each gas in the atmosphere)
the greater the concentration of a particular gas, the greater the partial pressure
The volume of gas dissolved also depends on its solubility
CO2 is 20X more soluble than O2
Hyperbaric conditions
Hyperbaric Oxygen
Decompression Sickness “the bends” (pg. 840)
Gas Exchange Between Blood, Lungs, & Tissues
I. External Respiration:
several factors influence diffusion of O2 & CO2 across respiratory membrane
1. partial pressure gradients & gas solubilities
2. structural characteristics of respiratory membrane
3. functional aspects of matching blood flow to air
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1. Partial Pressure & Gas Solubilities
External Respiration
PO2 of blood in pulmonary artery/capillaries =
PO2 of alveoli=
PO2 in pulmonary vein=
RBC has .75 seconds to exchange gasses and
reaches PO2 of 100 mmHg in .25 sec.
(has extra .5 seconds if it needs it)
Blood leaves the lungs in the pulmonary vein
oxygenated.
Hb is 98% saturated with O2 and each 100 ml of
blood contains 20 ml of O2
CO2 moves in opposite direction
PCO2 in pulmonary artery/capillaries=
PCO2 in alveoli=
PCO2 in pulmonary vein:
Internal Respiration:
PO2 of systemic arteries:
PO2 of tissue cells:
so O2 leaves blood and enters cells
PO2 of systemic veins
PCO2 of systemic arteries:
PCO2 of tissue cells:
so CO2 leaves cells and enters blood
PCO2 of systemic veins:
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2. Respiratory membrane
.5 - 1 micrometer thick - allows for rapid diffusion
large surface area
the greater the surface area of respiratory membrane, the faster the diffusion
Fick's law: diffusion rate is directly proportional to surface area and inversely proportional to
membrane thickness
3. Matching blood with air or Ventilation-Perfusion Coupling
ventilation = amount of gas reaching alveoli
perfusion = blood flow in pulmonary capillaries
When an area of the lung isn't healthy the alveolar ventilation is inadequate, the PO2 in that region
is
therefore the pulmonary vessels
so blood is redirected to areas where O2
pickup can be more efficient.
(matching the blood to the best ventilation - O2)
Or when alveolar ventilation is maximum, pulmonary vessels to that region will:
Changes in PCO2 = changes in diameters of bronchioles
if have poor ventilation CO2levels increase, therefore the bronchioles removing
CO2 will
to increase its removal.
Transport of Respiratory Gases by Blood
I. Oxygen Transport: 2 ways
1. bound to hemoglobin (Hb) within RBC (98.5%)
2. dissolved in plasma (1.5%)
Association & Dissociation of O2 & Hb:
- Hb can combine with
molecules of O2
reduced hemoglobin= HHb
oxyhemoblobin= HBO2
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Rate at which Hb binds/releases O2 is regulated by: PO2, Temp, blood pH, PCO2 & DPG.
1. Hb & PO2
Oxygen-hemoglobin dissociation curve
• O2 binding to Hb depends on the PO2, the
higher the PO2 the more O2 bound/carried by Hb
• normally each 100 ml of systemic blood
contains 20 ml of O2 & Hb is 98% saturated with
O2.
Curve is NOT linear: large changes in PO2 can
occur with only small changes in Hb’s O2saturation
• arterial blood unloads aprx. 5 ml of O2 per 100
ml into tissue cells so Hb saturation drops to
75% (tissue PO2 is 40 mmHg)
•arterial blood contains 20 ml O2/100 ml &
venous blood contains 15 ml/100 ml blood.
2.) Hb and O2 binding & Temperature
•This is the (a-v)O2 difference or arterial venous oxygen difference.
At rest it is 5 ml/100 ml/blood
When the temperature
increases, Hb is less saturated
with O2.
Hb's affinity for O2 decreases
so at any given PO2 Hb is less
saturated with O2
therefore the (a-v)O2 difference
increases
more O2 is unloaded to the tissue
cells
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3.) Hemoglobin and pH
H+ weaken the Hb-O2 bond.
The Bohr Effect: when H+ concentration
increases or pH
Hb's affinity for
O2 decreases.
Therefore more O2 is unloaded to the tissue
cells.
The (a-v)O2 difference will
.
These "shifts" of the Hb-O2 dissociation curve
are termed right shifts.
4.) Hb & BPG
2,3-biphosphoglycerate (BPG) is a by-product of glycolysis
when metabolic rate of RBC increases, 2,3-BPG levels increase which decreases Hb's affinity
for oxygen.
This would cause a
shift of the O2-dissociation curve
Fetal vs. Adult Hb:
At same PO2 fetal Hb binds more O2 than adult Hb
Impairments of O2 Transport
hypoxia:
anemic hypoxia
stagnant (ischemic) hypoxia
hypoxemic hypoxia
hypobaric hypoxia
Carbon monoxide (CO) poisoning: CO is an odorless, colorless gas
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2. Carbon Dioxide Transport: 3 ways
Generated as by-product of aerobic metabolism
1. Dissolved in plasma: 7-10%
2. Carbaminohemoglobin: 20-25% binds to protein (amine) portion of Hb
CO2 + HHb  HbCO2 + H+
rapid reaction
loading/unloading influenced by:
1. PCO2
2. Degree of oxygenation of Hb
3. Bicarbonate ion in plasma (HCO3): 70% travels this way
C.A
.
carbonic anhydrase enzyme only found in RBC so reactions occurs faster in RBC than in
plasma
when it happens in RBC the HCO3- ion leaves the RBC and enters the plasma to work as a
buffer.
The negative charge is replaced by a Cl- which enters the RBC.
This is called the Cl- shift
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CA
CA
Haldene Effect:
the more CO2 released into blood, the more O2 unloaded which then allows more CO2 to
combine with HHb
(CO2 loading forms more H+ ions which increases O2 unloading to the cells which frees up more
HHb to pick up even more CO2)
reversed in pulmonary circulation
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Influence of CO2 on blood pH
Typically H+ released during carbonic acid dissociation are buffered by Hb
HCO3 generated in RBC exits and enters the plasma where it can also buffer H+
But changes in respiratory rate or depth can cause changes in blood pH by modifying amount
of carbonic acid in blood.
CO2 + H2O  H2CO3  H+ + HCO3-slow, shallow respiration: retain CO2, PCO2 increases
-rapid deep breathing: eliminate CO2 too quickly, PCO2 decreases
Control of Respiration: (pages 850 – 851)
Neural Mechanisms:
I. Respiratory Centers in Medulla Oblongata
1. Inspiratory center (dorsal resp. group DRG)
neurons spontaneously depolarize and send nerve impulse to phrenic nerve which
innervates the
.
this makes the
contract = inspiration
cyclic activity: “on” for 2 seconds
2. Expiratory center (ventral resp. group VRG)
stimulates accessory muscles for forced inspiration and expiration
II. Pons Respiratory Center
1. Pneumotaxic center
send inhibitory impulses
can shorten
2. Apneustic:
continuously stimulates DRG
prolongs inspiration
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Respiratory Reflexes
1. Pulmonary Irritant Reflexes:
2. The Hering-Breuer Reflex:
stretch receptors
3. Voluntary Control by cerebral cortex:
4. Chemoreceptor Reflexes
most important factors are levels of CO2, O2, & H+ ions in arterial blood
chemoreceptors: located in 2 major sites
1. central chemoreceptors
2. peripheral chemoreceptors:
carotid bodies send info via glossopharyngeal nerve
aortic bodies send info via vagus nerve
A. Influence of PCO2:
40 mm Hg (37-43 mmHg) normal range
increased CO2 levels affect pH
CO2 passes through blood-brain barrier and forms H+ which to lower the pH of the CSF. This
directly stimulates the central chemoreceptors.
this results in an increased rate and depth of breathing to eliminate the CO2
hypercapnia: increased CO2
elevation of PCO2 of only 5 mmHg
hypocapnia: caused by hyperventilating
B. Influence of PO2:
peripheral chemoreceptors respond to PO2 levels
normally effects of decreasing PO2 levels increases sensitivity
of central receptors to CO2 levels
arterial levels of O2 must decrease substantially (50 mmHg) before O2 becomes the stimulus for
breathing.
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pulmonary disease: retain CO2 therefore the P CO2 is chronically
elevated and chemoreceptors become unresponsive to CO2
C. Influence of arterial pH
H+ ions poorly diffuse into cerebrospinal fluid and pH changes stimulate peripheral
chemoreceptors
Effects of High Altitude:
decrease in PO2 levels
Acclimatization: modifications to increase oxygen delivery to tissues
Respiratory Changes:
Cardiovascular Changes:
Hematologic:
Metabolic:
1. Smoking and the Respiratory System
paralyze cilia causes frequent respiratory infections
increases risk for CV disease and cancer
long term effects from smoking:
2.) COPD: Chronic Obstructive Pulmonary disease
Main causes: smoking, pollution, rarely α1 trypsin deficiency
Characterized by bronchial irritation/inflammation & breakdown of elastic tissue
S/S: dyspnea, frequent infections, air trapped in lungs (↑ FRC), hypoxemia
-emphysema:
-chronic bronchitis:
3.) Lung Cancer:
leading cancer killer in men and women
smoking, radon and asbestos exposure increase risk
stage 1 5 yr. survival rate is 47%, stage 4 is 2%
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3 main types:
1.) squamous cell carcinoma
2.) adenocarcinoma
3.) small cell carcinoma
Other:
Valsalva Maneuver: If strain while glottis is closed increases peritoneal pressure can cause alveolar rupture or
hernia.
If exhale against a closed glottis compresses aorta and vena cavae which may collapse = drop in venous
return and cardiac output
BP decreases which causes increased HR and vasoconstriction of blood vessels
Tuberculosis (TB): (pg. 817)
#1 killer of all infectious diseases (54 million become infected each year)
50% fatality rate for untreated cases
multi-drug resistant TB has been found in 43 states
Latent vs. Diseased
Asthma:
Wheezing, chest tightness, breathlessness
Often triggered by environmental “triggers”: dust mites, smoke, pollution, pets, mold
Inflammation & bronchoconstriction of bronchioles
Tx:
Changes in Respiratory System at Birth
1. Before birth:
 pulmonary vessels are collapsed
 lungs contain no air

2. During delivery:
 placental connection is lost
 blood PO2 falls
 PCO2 rises
3. At birth:
 newborn overcomes force of surface tension to inflate bronchial tree and alveoli and take
first breath
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4. Large drop in pressure at first breath:
 pulls blood into pulmonary circulation
 closing foramen ovale and ductus arteriosus
 redirecting fetal blood circulation patterns

5. Subsequent breaths:
 fully inflate alveoli
Three Effects of Aging on the Respiratory System
1. Elastic tissues deteriorate:
 altering lung compliance
 lowering vital capacity
2. Arthritic changes:
 restrict chest movements
 limit respiratory minute volume
3. Emphysema:
 affects individuals over age 50
 depending on exposure to respiratory irritants (e.g., cigarette smoke)
Coordination of Respiratory and Cardiovascular Systems
 Improves efficiency of gas exchange by controlling lung perfusion
 Increases respiratory drive through chemoreceptor stimulation
 Raises cardiac output and blood flow through baroreceptor stimulation
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