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Respiration II
Anatomy
Ventilation: External Respiration
Gas Transport/Exchange: Internal Respiration
Neural control
Disease/Adaptations
Aside: Epiglottis movement
Respiratory Zone
Terminal bronchioles >
respiratory bronchioles >
alveolar ducts > alveolar
sacs > alveoli (grapes on a
stem) where gas exchange
occurs.
Increase in smooth muscle and
decrease in cartilage as
move to bronchioles and
epithelium thins (changes
from pseudostratified >
columnar > cuboidal at
bronchiole (with no cilia, no
goblet cells, no mucus >
squamous).
Bronchiole ( < 1mm diameter)
smooth muscle is regulated:
sympathetic – NE (dilate),
parasympathetic – Ach
(constrict)
Approximately 300 million
alveoli in the lungs
–
–
Account for most of the
lungs’ volume
Provide tremendous
surface area for gas
exchange
http://mcdb.colorado.edu/courses/2115/units/Other/alveolu
s-circ-animation.swf
Alveoli
Air-filled pockets
within the lungs where
all gas exchange takes
place.
Features:
• Lined by delicate,
simple squamous
epithelium
• septal cells (type II)
that make surfactant
• Pores that connect
alveoli
• Macrophages (dust
cell)
• Rich blood, lymph
supply
• Elastic fibers
THIN (.1 - .5 um)
exchange surface
Figure 23–11
Surfactant
• At air water interface, there is large surface
tension (water is attracted to other waters).
This cohesive force pulls alveoli closed.
• Surfactant breaks apart water bonds, reduces
surface tension and therefore “keeps alveoli
open)
• Surfactant: phospholipids
• Surfactant is made late in pregnancy. Premature
babies do not have much surfactant (IRDS: infant
respiratory distress) and are treated with positive
pressure ventilator, mom given steroid injection,
artificial surfactant
No surfactant
Surfactant
Surfactant: Decreases surface
tension and prevents alveolar
collapse
Respiration
4 integrated processes:
– Pulmonary ventilation – moving air into and
out of the lungs (provides alveolar
ventilation)
– External respiration – gas exchange
between the lungs and the blood
– Transport – transport of oxygen and carbon
dioxide between the lungs and tissues
– Internal respiration – gas exchange
between systemic blood vessels and tissues
Three Gas Laws of Respiratory
Physiology
• Boyle’s Law: The pressure of a given quantity of gas is
inversely proportional to its volume assuming a
constant temperature.
• Dalton’s Law: The total pressure of a gas mixture is
equal to the sum of the partial pressures of the
individual gases
• Henry’s Law: At the air-water interface, the amount
of gas that dissolves in water is determined by its
solubility in water and its partial pressure in the air
(assuming a constant temperature)
Boyle’s Law
The pressure of a given quantity of gas is
inversely proportional to its volume
assuming a constant temperature.
P
1/V
Or
P1V1 = P2V2
In a contained gas (like gas in lungs):
– external pressure forces molecules
closer together
– movement of gas molecules exerts
pressure on container
Respiration: Muscles increase lung volume
creating a pressure gradient for
movement of air into lungs. Higher
pressure in atmosphere than in lungs so
air moves into lungs down pressure
gradient. Process is reversed with exhale
as muscles relax, lungs recoil, volume
inside lungs decrease and thus pressure
increases. Pressure inside lungs is higher
than outside lungs so air moves out.
Henry’s Law
When gas comes into contact with liquid
– Gas dissolves in the liquid until
equilibrium is reached
– The amount of a gas dissolved
in solution is proportional to
the partial pressure of that gas
above the solution.
– If you increase the pressure,
more gas will dissolve in
solution.
– Increase temperature: increase
decrease solubility
– Solubility of gas in water plays
a role: CO2>O2>N2
Example: carbonated beverages. Gas is
dissolved in solution under high
pressures – the gas at the top of
the can is in equilibrium with the gas
in solution. Lid is sealed. When lid
is opened, gas escapes from solution
as it equilibrates with new pressure
(the pressure around everywhere).
Why do we care? Oxygen and carbon
dioxide dissolve in blood until
equilibrium is reached. The partial
pressure of the gases varies within
the body – and thus the
concentration in blood varies.
9
Dalton’s Law
Dalton’s Law: The total pressure of a gas mixture is equal to the sum of the partial
pressures of the individual gases. The partial pressure of the gas depends on
its concentration.
The gas composition of air is: N2=79%, O2=20.9%, H20=.5%, CO2=.04%.
At sea level, the pressure exerted by the gases that make up the atmosphere is 1 atm = 760 mm Hg. (pressure due to gases bumping into
each other)
Use the equation to calculate the partial pressure of O2 = 760 X .209 = 159 mmHg.
At high altitude, (on top of Everest) total atmospheric pressure is less than at sea level (245 mm Hg instead of 760 mm Hg) but the
concentration of oxygen in air is the same. The PO2 on Everest = 245 x .209 = 52 mmHg.
What is the point? The amount of oxygen in solution is proportional to the partial pressure of the gas. If there is less pressure, there is
less concentration in solution.
At high altitude, there is less PO2, therefore less less oxygen in blood. (DETAILS LATER).
More anatomy:
Pleural Cavities
Each lung is housed within a
pleural cavity that is
separated by the mediastinum
The pleural cavity holds a lung and
is lined with a serous
membrane = the pleura
– Consists of 2 layers (balloon
model):
• parietal pleura (attached to the
ribs, spine, diaphragm)
• visceral pleura attached to the
lung
– Intrapleural space filled with
serous fluid that lubricates
space and holds the two layers
together.
The pleural cavity is critical for
keeping lungs inflated. Lungs
have tendency to collapse,
parietal membrane has
tendency to pull open. This
creates negative intrapleural
pressure that effectively
holds lungs open.
Intrapleural Pressure
Intrapleural pressure remains
below Patm throughout
respiratory cycle:
– Elasticity of lungs causes them
to assume smallest possible size
– tendency to shrink
– Surface tension of alveolar fluid
draws alveoli to their smallest
possible size
These forces are resisted by
the bond between the layers
of pleura
Puncture wound that disrupts
the intrapleural pressure
(called pneumothorax) causes
the lungs to deflate.
Pulmonary
Ventilation –
Moving Air into
and out of the
lungs
A Respiratory Cycle Consists
of:
– an inspiration (inhalation)
– an expiration (exhalation)
Air flows from area of higher
pressure to area of lower
pressure (it’s the
pressure difference, or
gradient that matters)
Volume of thoracic cavity
changes (expansion or
contraction of diaphragm
or rib cage) changes the
volume of the lungs and
thus creates changes in
pressure
760 mm Hg
MOVIE
760 mm Hg
Intrapleural
pressure
756 mm Hg
End of expiration:
Alveolar pressure = atmospheric pressure
14
Pressure in lungs
drops to 758 mm Hg
760 mm Hg
Diaphragm
contraction creates
a increase in lung
volume, decrease
in pressure. Air
flows down
pressure gradient
into lungs
Intrapleural pressure
becomes 754 mm Hg
Inspiration takes place
15
Pressures in lungs
760 mm Hg
760 mm
Hg
Inspiration ends when
pressure in lungs =
pressure of atmosphere.
End of inspiration
16
Pressure in the lungs
increases to 763 mm Hg
760 mm Hg
Diaphragm relaxes, lung
volume decreases
creating a pressure
gradient for air to
leave the lungs.
Expiration
17
760 mm Hg
760 mm Hg
Intrapleural
pressure
756 mm Hg
End of expiration:
Alveolar pressure = atmospheric pressure
18
The Respiratory Muscles MOVIE
Inhalation: always active
Diaphragm: contraction
flattens it, expanding
the thorax and drawing
air into lungs, accounts
for 75% of normal air
movement
External intercostal
muscles: assist inhalation
by elevating ribs,
accounts for 25% of
normal air movement
Exhalation: normally
passive
Relaxation of diaphragm
decreases thoracic
volume
Gravity causes rib cage
to descend
Elastic fibers in lungs
and muscles cause elastic
rebound
All serve to raise
intrapulmonary
Active: abdominals,
anternal intercostals
Figure 23–16a, b
Thoracic Wall
and Muscles of Respiration
Compliance
• Measure of the ease with which lungs and thorax
expand
• What would it mean to have a lower-than-normal
compliance?
• Conditions that decrease compliance
– Pulmonary fibrosis: deposition of inelastic fibers in
lung
– Pulmonary edema
– Respiratory distress syndrome
– Increased resistance to airflow caused by airway
obstruction (asthma, bronchitis, lung cancer)
– Deformities of the thoracic wall (kyphosis, scoliosis)
P and V Changes with Inhalation and
Exhalation – note small change in pressure
drive flow
Figure 23–15
Used for health
assessment
Shallow vs. Deep
breathing.
• Tidal volume is
normal inhale and
exhale = 500 ml
• Inspiratory
Reserve Volume =
3000 ml (forceful
inspiration after
TV)
• Expiratory Reserve
Volume: 1100 ml
(forceful
expiration after
TV)
Residual volume:
1200 ml (air
remaining in lungs
after maximal
expiration = DEAD
VOLUME)
Respiratory Volumes
and Capacities
Figure 23–17
Respiratory Rates and Volumes
Vital Capacity = Sum of Tidal, Inspiratory, Expiratory Reserve volumes and
is the maximum amount of air one can forcefully inspire and expire.
Age, sex, body size and training effect (athletes 40% increase in VC).
Respiratory system adapts to changing oxygen demands by varying:
– the number of breaths per minute (respiratory rate)
– the volume of air moved per breath (tidal volume)
Both can be modulated
•
Minute Volume (measures pulmonary ventilation) = respiratory rate
tidal volume
–rest 6L/min (500 ml x 12 breaths/min)
–Exercise 200 L/min
•
•
•
Both RR and TV can be modulated
Only a part of respiratory minute volume reaches alveolar exchange
surfaces
Volume of air remaining in conducting passages is anatomic dead space
Alveolar Ventilation
Alveolar ventilation is the
amount of air reaching
alveoli each minute =
respiratory rate (Tidal
Volume - anatomic dead
space)
– for a given respiratory rate:
• increasing tidal volume
increases alveolar ventilation
rate
– for a given tidal volume:
• increasing respiratory rate
increases alveolar ventilation
• Alveoli contain less O2,
more CO2 than atmospheric
air because inhaled air
mixes with exhaled air
External Respiration: Oxygen into
Blood: MOVIE
Gas
Exchange
Direction and rate of diffusion
of gases across the
respiratory membrane and the
capillaries are determined by
partial pressures and
solubilities of the gas.
http://www.wisconline.com/objects/ViewObject.aspx?ID=AP2404
The path for the
movement of O2
and CO2
What is the ultimate
source of CO2?
What is the ultimate
source of O2?
29
29
O2 and CO2
• Blood arriving in pulmonary arteries has low PO and
2
high PCO
2
• The concentration gradient causes: O2 to enter blood
and CO2 to leave blood
• Blood leaving heart has high PO and lowPCO
2
2
• Interstitial Fluid has low PO = 40 mm Hg and high
2
PCO 45 = mm Hg
2
• Concentration gradient in peripheral capillaries is
opposite of lungs so CO2 diffuses into blood and O2 to
enter tissue
• Although carbon dioxide has a lower partial pressure
gradient (only 5mmHg)
– It is 20 times more soluble in plasma than oxygen
– It diffuses in equal amounts with oxygen
CO2
O2
O2
O2
O2
O2
O2
O2
CO2
Efficiency of Gas
Exchange
The Life Story of an Oxygen Molecule
1. Inspiration: oxygen in air enters nose/nasal cavity & travels down pharynx, larynx,
trachea, bronchus, bronchiole, to the alveoli.
2. At the alveoli the increased levels of oxygen in the alveoli result in a increased
partial pressure of oxygen in the alveoli. This causes the capillaries to dilate and
oxygen diffuses across the respiratory membrane into the capillary.
3. Inside the capillary oxygen binds to hemoglobin where it gets transported through
the bloodstream.
4. Once at the tissue, the metabolic needs of the tissue result in low oxygen levels in
the tissue causing a low oxygen pressure at the tissue. This causes oxygen to
diffuse into the tissues.
5. Once inside the tissues oxygen is used in cellular respiration to make ATP.
The Life Story of Carbon Dioxide
1. Tissues make CO2 as waste from metabolism causing CO2 levels in the tissues to rise.
CO2 diffuses into the bloodstream at the venous end of the capillary.
2. CO2 enters the red blood cell, where it either forms bicarbonate or is bound to
hemoglobin.
3. Bicarbonate then enters the plasma and “transports” the CO2 to the lungs. At the
respiratory membrane, bicarbonate enters RBCs and is converted back into CO2.
4. The CO2 diffuses across the respiratory membrane because the levels of CO2 in the
alveoli are low.
5. CO2 diffusion across the respiratory membrane generates an increase in pressure of
CO2.
6. Expiration: CO2 is expelled out of the airway via bronchiole, bronchus, trachea,
larynx, pharynx, & out the mouth.
Gas Pickup and Delivery
• Red Blood Cells (RBCs): transport O2 to, and CO2 from,
peripheral tissues
• Remove O2 and CO2 from plasma, allowing gases to diffuse
into blood
• Hb carries almost all O2, while only a little CO2 is carried
by Hb
• O2 binds to iron ions in hemoglobin (Hb) molecules in a
reversible reaction
• Each RBC can bind a billion molecules of O2
• Hemoglobin Saturation: the percentage of heme units in a
hemoglobin molecule that contain bound oxygen
Hemoglobin Saturation Curve
Graph relates the
saturation of hemoglobin to
partial pressure of oxygen
• Higher PO results in
2
greater Hb saturation.
• Hemoglobin Saturation:
the percentage of heme
units in a hemoglobin
molecule that contain
bound oxygen
• Graph is not a straight
line because Hb changes
shape each time a
molecule of O2 is bound.
Each O2 bound makes
next O2 binding
• On Everest: PO2 = 53
mmHg
39
Hemoglobin Saturation Curve
Notice that even at PO =
2
40 mm Hg, Oxygen
saturation is at 75%,
therefore each Hb
molecule still has 3
oxygens bound to it. This
reserve is needed when
tissue becomes active
and PO drops to 15 mm
2
Hg
Factors that effect Hb ability
to bind oxygen
• PO of blood
2
• Blood pH
• Temperature
• Metabolic activity within
RBCs (dPG aka bPG)
CO from burning fuels:
Binds irreversibly to
hemoglobin and takes the
place of O2
Figure 23–20 (Navigator)
Bohr Effect
Metabolizing tissue
generates CO2
leads to H+ and
shift of curve to
the right. This
facilitates
unloading of
oxygen at tissues.
EX: Blood arriving at
tissue has PO2 30.
Compare pH 7.2,
7.4, 7.6. Which
will release more
O2?
Right shift of
curve
facilitates Hb
unloading of
O2. (acid, high
temp).
41
Fetal Hemoglobin
Left shift of
fetal Hb
saturation
curve means at
that same
PO2, fetal Hb
is more
saturated with
O2 than adult,
fetal Hb has
higher affinity
for binding
oxygen.
42
Temperature shifts Hb
saturation curve to the right
43
KEY CONCEPTS
• Hemoglobin in RBCs:
– carries most blood oxygen
– releases it in response to low O2 partial
pressure in surrounding plasma
• If PO increases, hemoglobin binds
2
oxygen
• If PO decreases, hemoglobin releases
2
oxygen
• At a given PO hemoglobin will release
2
additional oxygen
if pH decreases or
temperature increases
Control of Respiration
• Ventilation – the amount of gas reaching the
alveoli
• Perfusion – the blood flow reaching the alveoli
• Ventilation and perfusion must be tightly
regulated for efficient gas exchange
• Gas diffusion at both peripheral and alveolar
capillaries maintain balance by:
– changes in blood flow and oxygen delivery
– changes in depth and rate of respiration
Regulation of O2 Transport
• Rising PCO levels in tissues relaxes smooth
2
muscle in arterioles and capillaries, increasing
blood flow there (autoregulation)
• Coordination of lung perfusion (blood) and
alveolar ventilation (air):
– blood flow is shifted to the capillaries serving
alveoli with high PO and low PCO (opposite of
2
2
tissue)
– PCO levels control bronchoconstriction and
2
bronchodilation: high PCO causes bronchodilation
2
(just like with blood in the tissues)
Ventilation-Perfusion Coupling
• In tissue high CO2 causes vasodilation,
in lungs, high CO2 causes vasoconstiction
(Why?)
• In lungs high CO2 causes
bronchodilation (Why?) while low CO2
causes constriction
 Blood goes to alveoli with low CO2 ,
air goes to alveoli with high CO2
Ventilation-Perfusion Coupling
PO2
PCO2
in alveoli
Reduced alveolar ventilation;
excessive perfusion
Pulmonary arterioles
serving these alveoli
constrict
Reduced alveolar ventilation;
reduced perfusion
Pulmonary arterioles
serving these alveoli
dilate
Enhanced alveolar ventilation;
enhanced perfusion
PO2
PCO2
in alveoli
Enhanced alveolar ventilation;
inadequate perfusion
Figure 22.19
Neural
Control of
Respiration
Normal Ventilation rates = 12-20
cycles/minute
Kids: 20 – 40 cycles/sec
Control of respiration – Medulla
Neurons control contraction of
respiratory muscles
• Deeper breathing – more forceful
expansion of lungs (more motor
units)
• More rapid breathing – increased
AP frequency of morot neurons
The Respiratory Rhythmicity Centers
• Respiratory rhythmicity centers in
medulla set the pace of respiration
• Can be divided into 2 groups:
– dorsal respiratory group (DRG)
• Inspiratory center
• Functions in quiet breathing (sets the pace) and
forced breathing
• Dormant during expiration
– ventral respiratory group (VRG)
• Inspiratory and expiratory center
• Functions only in forced breathing
Modifications of Breathing
Coughing
Sneezing
Sighing
Yawning
Sobbing
Sensory Modifiers of Respiratory
Center Activities
• Chemoreceptors are sensitive to:
– PCO , PO , or pH of blood or cerebrospinal
2
2
fluid
• Baroreceptors in aortic or carotid
sinuses:
– sensitive to changes in blood pressure
• Stretch receptors respond to changes
in lung volume
• Irritating physical or chemical stimuli
in nasal cavity, larynx, or bronchial
tree promote airway constriction
Chemoreceptor Reflexes
• Respiratory centers are strongly influenced by
chemoreceptor input from:
– carotid bodies (cranial nerve IX)
– aortic bodies (cranial nerve X)
– receptors in medulla that monitor
cerebrospinal fluid
• All react more strongly to changes in pH and PCO ,
2
to a lesser extent to changes in PO
2
• So in general, CO2 levels, rather than O2 levels,
are primary drivers of respiratory activity
• At rest, it is the H+ ion concentration in
brain CSF (which is a proxy measure of CO2
levels)
Respiratory Disorders
Restrictive disorders: lung cancer,
fibrosis, pleurisy
– Fibrosis: decreases compliance
– harder to inhale
Obstructive disorders: emphysema,
asthma, bronchitis (COPD)
– Loss of elasticity
– Harder to exhale (FRC increased)
COPD – Chronic Obstructive
Pulmonary Disease
• Includes: emphysema,
chronic bronchitis,
asthma. Often, both
emphysema and
bronchitis are present
but in differing
proportions
• Symptoms
– difficult to exhale
– May have barrel
chests due to trapped
air in lungs
– dyspnea (shortness of
breath) accompanied
by wheezing, and a
persistent cough with
sputum
COPD
Emphysema:
• Loss of elastic tissue in the lung alveoli lead to their
enlargement and degeneration of the respiratory membrane
leaving large holes behind
• Suffers are called “pink puffers” because they are thin, usually
maintain good oxygen saturation, and breathe through pursed
lips (Why?)
• Caused by smoking or (rarely) by alpha1 anti-trypsin deficiency –
this is a congenital lack of the gene for alpha1 antitrypsin which
normally protects alveoli from enzyme neutrophil elastase;
without it, elastase eats away the elastic fibers
Bronchitis: Inflammation of airways causes narrowing of
bronchioles and a buildup of mucus, both of which restrict air
flow
• During exhalation, airways collapse
• These patients are often called “blue bloaters” because they
have low oxygen saturation (cyanosis), and often have systemic
edema secondary to vasoconstriction and right-sided heart
failure
• Adaptation of the chemoreceptors occurs especially in the ones
sensitive to CO2
• Thus, their only drive to breathe is provided by low O2 levels!
This is why they are always blue. DO NOT GIVE THESE
PATIENTS O2 ! They will stop breathing totally.
Asthma
•
•
•
•
Reversible, unlike COPD
More common in children than adults
Symptoms: coughing, wheezing, chest tightness, gasping for air
Begins w/ active inflammation of airways- IgE antibodies (stimulated by
TH2 cells) stimulated & recruit inflammatory cells
Obstructive: Emphsema
Emphysema
http://www.yourlunghealth.org/lung_dis
ease/index.cfm
Restrictive: Lung Cancer
•
•
•
•
http://www.medicinenet.com/smokers_
ng_pathology_photo_essay/article.htm
Leading cause of cancer death
in North America
90% of lung cancers result
from smoking
Highly aggressive cancer; high
rate of metastasis; often late
diagnosis
50% die within one year of
diagnosis, only 20% or so
survive 5 years
http://www.airinfonow.org/html/lungattack/lungplay.htm
Other Challenges/Diseases
Respiratory Distress: difficult respiration
– Can occur when septal cells do not produce enough surfactant
– leads to alveolar collapse
Pneumonia: inflammation of the lung tissue
– causes fluid to leak into alveoli
– compromises function of respiratory membrane
Cystic Fibrosis: Recessive genetic disease caused by simple mutation in both
copies of the gene for a chloride transporter.
• Without it, Cl- cannot be pumped onto the lung surface, Na+ doesn’t
follow and neither does water.
• Sticky mucus builds up inside lungs and infections are common. Often
fatal before age 30
Decompression sickness –the bends, nitrogen bubbles exit the blood, enter
the tissues: painful and dangerous
Shallow water blackout: hyperventilation leads to artificially reduced CO2,
allows you to hold your breath to the point of passing out
SIDS: Sudden infant death syndrome
• Disrupts normal respiratory reflex pattern
• May result from connection problems between pacemaker complex and
respiratory centers
Altitude
Altitude sickness: low pressure leads to hypoxia, can
cause cerebral and pulmonary edema
• Normal response to acute high altitude exposure
include:
– Increased ventilation – 2-3 L/min higher than at sea level
due to Increased RR and tidal volume
– Increased HR
– Substantial decline in PO2 stimulates peripheral
chemoreceptors:
– Chemoreceptors become more responsive to PCO2
• Over time
– Increased hematocrit
– Increased BPG causes a right shift in Hb making it easier to
offload oxygen at the tissues