THE RESPIRATORY SYSTEM
Chapter 13
Pgs 436-463
Functional Anatomy Basics
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Nose
Pharynx
Larynx
Trachea
Bronchi
Bronchioles
Alveoli
Detailed Anatomy Upper Respiratory Tract
Homeostatic Imbalance:
Cleft Palate – failure of the bones forming
the palate to fuse medially. Results in
breathing difficulties and oral cavity
functions such as chewing and speaking.
Rhinitis – inflammation of the nasal
mucosa. Causes nasal congestion and
postnasal drop
Sinusitis – sinus inflammation. Difficult to
treat and may cause changes in voice
quality. Blockage of the sinus cavities may
result in sinus headache
Tonisillitis – inflammation of tonsils, often
the pharyngeal tonsil
Choking leading to need for Heimlich
Maneuver or tracheostomy
Anatomy and Functions of Lungs
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Occupy entire thoracic cavity except for the mediastinum
Apex is narrow and superior, base is broad and rests on the
diaphragm
Left lung: two lobes
Right lung: Three lobes
Surface of each lung coated in pulmonary (visceral) pleura and
the walls of the thoracic cavity are lined with the parietal pleura
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Both produce pleural fluid
There is no actual space between membranes but it can exist in
pathological conditions
Homeo. Imbalance: Pleurisy – insufficient or overproduction of
pleural fluid
Anatomy of thoracic cavity
Functional Anatomy of Lungs Cont.
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Respiratory zone includes respiratory bronchioles,
alveolar ducts, alveolar sacs and alveoli. This is the
only location for gas exchange
All other respiratory passages are conducting zone
structures that serve as conduits
Most of the lungs are air space and the stroma is
mostly elastic CT that passively recoils during
exhalation
Respiratory Membrane
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Walls of alveoli are simple
squamous epithelium
Alveolar pores connect
alveoli to provide alternate
air routes
The alveolar surface is
covered with capillaries
The respiratory membrane
(air-blood barrier) is the
alveolar and capillary
walls, their fused BMs and
occasional elastic fibers
Respiratory Membrane
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All gas exchange
via diffusion
Alveolar
macrophages
present in alveoli
Additional
cuboidal cells
produce
surfactant
Lung surface area
~50-70 m2
SE Micrographs of Rat Lung
3D Image of conducting zone and
respiratory zone structures
Respiratory Physiology – 4 Events
Pulmonary ventilation – a.k.a. breathing. Air moves in
and out of lungs for refreshment of air supply
2.
External respiration – gas exchange between alveoli and
pulmonary blood. The lumen of the alveoli are technically
on the body exterior
3.
Respiratory gas transport – blood transport of gases
4.
Internal respiration – gas exchange between systemic
capillaries and tissue
Note: The actual use of oxygen and carbon dioxide production is
part of cellular respiration
1.
Breathing Mechanics
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Basic concept: Volume changes lead to pressure changes,
which lead to the flow of gases to equalize the pressure
Breathing is entirely mechanical:
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When the volume of the space increases, gas particles spread out
to fill the space and pressure drops in the space. Relates to
inspiration
When the volume of the space decreases, gas particles are
compressed together and the pressure in the space increases.
Relates to expiration
Intrapleural pressure, (pressure between visceral and
parietal pleura) is always negative. If it equalizes, the lungs
will collapse completely
Inspiration
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Diaphragm and
external intercostals
contract and
increase the size of
the thoracic cavity
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The height of the
cavity increases
The rib cage lifts
and sternum moves
forward increasing
diameter of cavity
A pressure decrease ensues as the intrapulmonary
volume increases, this sucks air into the lungs like a
vacuum until the pressure equalizes
Expiration
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A passive process
that depends mostly
on elasticity of lung
tissue
As the diaphragm
and intercostals
relax,
intrapulmonary
volume decreases
and pressure
increases above
atmospheric
pressure, thus air
leaves the lungs until
pressure equalizes
Only during forced expiration are the internal
intercostal muscles and abdominal muscles used to
force air out. May be necessary during respiratory
illness
Pressure and Volume Changes
Close up View of Pleura
Intrapleural pressure is negative upon inspiration and positive with expiration
The Interplerual pressure (IPP) is always negative. If it weren’t, the lungs would
collapse
Homeostatic
Imbalance
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Atelectasis – lung collapse
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Occurs when air enters the
pleural space through a chest
would or rupture of the
visceral pleura
Presence of air in the
intrapleural space is
referred to as
pneumothorax
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Lungs reinflate by using chest
tubes in the intrapleural
space to draw out the air
Description of Lung Volume Measurements
Respiratory capacity is affected by:
- Age, body size, sex, physical conditions
Tidal Volume (TV): Normal breathing moves
about 500 mL of air into and out of the lungs
with each breath
Lung Volumes Continued
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Inspiratory reserve volume (IRV) – the amount of air that may be
forcibly inhaled after TV
Expiratory reserve volume (ERV) – amount that may be forcibly
exhaled after TV
Residual volume – the amount that stays in the lungs and may never
be exhaled. Allows continuous gas exchange in between breaths and
keeps alveoli inflated
Vital Capacity – total amount of exchangeable air. TV + IRV + ERV.
~3100 mL in women, 4800 in men
Dead space volume – amount of air stuck in conducting system that
is never involved in gas exchange. About 150 mL in normal tidal
breath. Functional volume (TV) is about 350 mL
Another Idealized tracing of
respiratory volumes
Nonrespiratory Air Movements
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Usually result from reflex activity, though some may be voluntary
Cough – clears lower respiratory passageways. A deep breath followed by
closing of the glottis and a subsequent forceful burst of air passed the glottis
Sneeze – similar to the cough. Clears upper respiratory area. The uvula
depresses and closes pharynx forcing air out through nasal cavities
Crying – inspiration followed by a number of short expirations. Emotionally
induced
Laughing – same as crying movement-wise
Hiccups- sudden inspirations resulting from spasms of the diaphragm;
initiated by irritation of the diaphragm or phrenic nerves
Yawn – deep inspiration with jaws wide open. Ventilates all alveoli
Respiratory Sounds
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Bronchial sounds – produced as air rushes through the
large respiratory passageways
Vesicular breathing sounds – air filling the alveoli.
Very very quiet.
Homeostatic Imbalances: diseased tissue may produce
abnormal sounds in presence of mucus, inflammation or
pus.
 Crackle
– bubbling sound
 Wheezing – whistling sound
 Rales – bronchial sounds produced by presence of mucus or
exudate in the lung passages or by thickening of the
bronchial walls
Gas Exchange
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External respiration –
exchange of gas
between alveoli and
blood
Internal respiration –
exchange between
systemic blood and
tissues
All gas exchange is
based on diffusion
Gas Transport in the Blood
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Oxygen carried in RBCs as
oxyhemoglobin.
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Carbon dioxide mostly transported
as
bicarbonate ion (HCO3 ), which is part of
the blood buffer system
Formation of this molecule occurs in the
RBCs, then the ion diffuses into plasma
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Very small amount is dissolved in plasma
A small amount (20-30%) of CO2 is carried
bound to hemoglobin in the RBCs
For CO2 to be exhaled, the bicarbonate
reaction must be reversed in the RBC and
freed CO2 diffuses from the blood into the
alveoli
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Reversal: H+ ions bind with HCO3- to form
carbonic acid: H2CO3, which quickly splits
into water and CO2
Homeostatic Imbalances
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Hypoxia – impaired oxygen transport.
Skin and mucous membranes take on a bluish hue, a.k.a.:
cyanotic.
 May result from anemia, pulmonary disease, or impaired or
blocked blood circulation
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Carbon monoxide poisoning – CO competes with
oxygen for the same binding sites on hemoglobin, and
binds with higher affinity, thus oxygen can’t be
transported and tissues become hypoxic
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Leading cause of death from fire
Gas Transport in the Blood Cont.
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Internal respiration –
as CO2 diffuses out of
cells, it reacts with
water to form carbonic
acid (H2CO3), with
quickly releases the
bicarbonate ions,
HCO3-, in the RBCs via
carbonic anhydrase
Conversely, oxygen
diffuses out of the
RBCs, through the
plasma and into the
cells
Neural Regulation of Respiration
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The phrenic and intercostal nerves control the basic rhythm of breathing by stimulating the
diaphragm, respiratory muscles and external intercostals.
The neural centers are located in the pons and medulla
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Contains pacemaker called the ventral respiratory group (VRG)
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The medulla also contains a center to modify the pacemaker rhythmically; the pons
smoothes out the basic rhythm
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Normal breathing is called eupnea; 12 – 15 bpm
Bronchioles and alveoli have “stretch receptors” that kick in via vagus nerve when the lung
begins to overinflate
Hyperpnea – vigorous breathing due to increased physical activity
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The rate of breathing may not increase, but the volume of air exchange may
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Respiration becomes more active and abdominal muscles, along with others, may be used
to assist expiration
Homeostatic Imbalance- high doses of central nervous system depressants may inhibit the
respiratory center of the medulla causing death
Breathing control Centers
Nonneural Regulators of Respiration
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Physical factors – talking, coughing, exercising,
increased body temperature, etc.
Volition – conscious control, may be overridden
Emotional factors- gasping, holding breath in
anticipation, breathing quickly from fear, etc.
Chemical factors – the blood buffer system; CO2 levels
rising causes the blood pH to drop and CNS receptors
take notice. Changes in oxygen are picked up by
chemoreceptors in the carotid arteries (carotid bodies)
but are secondary to CO2 concentrations
Homeostatic Imbalances of Regulators
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People who have chronically high levels of CO2, such as
those with emphysema, are not able to use those levels for
regulation, thus low oxygen becomes the stimulus for
breathing
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Patients with these disorders are put on low-oxygen air flow,
otherwise they will cease respiration
Acidosis and alkalosis occur when the blood becomes to
acidic or alkaline
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Hyperventilation – occurs with deep, rapid breathing and is used
to “blow off” extra carbon dioxide (due to increased carbonic
acid) to prevent or correct acidosis
Hypoventilation – shallow, slow breathing allows carbon dioxide
to build up in the blood, lowering pH and prevents or corrects
alkalosis
Respiratory Disorders
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Chronic obstructive pulmonary diseases – exemplified by chronic
bronchitis and emphysema
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Almost always linked to smoking
Dyspnea – difficulty/labored breathing becomes increasingly worse
Cough and frequent pulmonary infections
Most COPD victims are hypoxic, retain CO2, and have respiratory acidosis
Lung cancer
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Squamous cell carcinoma – 25-30% of cases, arises from epithelial linings
Adenocarcinoma- 40%, arises from solitary nodules in bronchial glands and
alveolar cells
Small cell carcinoma – 20%, lymphocyte-like cells that start in main bronchi
and spread aggressively to mediastinum forming grapelike clusters
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Extremely difficult to treat. New therapies include using antibodies to target and/or
deliver toxic drugs to the tumor, 2) cancer vaccines, 3) gene therapy
Developmental Aspects of the
Respiratory System
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It takes about 2 weeks post-birth for the infant respiratory
system to become fully functional due to the production of
surfactant
Necessary for lowering surface tension and preventing lung
collapse between breaths
 Does not develop in sufficient quantity until the 28-30 weeks of
pregnancy
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Premature babies at risk for Infant respiratory distress
syndrome (IRDS)
Cystic fibrosis – the most common lethal genetic disease:
1/2400 births. Oversecretion of mucus due to lack of Cltransporters
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Treatment: Antibiotics, “clapping the chest,” mucus-dissolving
drugs
Homeostatic Imbalances
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Sudden infant death syndrome – exact cause unknown.
Possible causes: problem with neural control of respiration or
reinhalation of expired air
Asthma – chronic inflammation and hypersensitivity of
airways. May be caused by allergens, pathogens,
environmental changes, physiological changes
Sleep apnea – disruption of the pressure in the pharynx,
which is necessary for keeping the glottis open during sleep,
allows the glottis to slide back closing off the trachea,
preventing inspiration until neural gas sensors force
inspiration. Sufferers become hypoxic during sleep and
exhibit a wide array of symptoms during wakeful hours