The Respiratory System

Respiratory system functions as gas exchange system

for oxygen and carbon dioxide

cellular respiration (energy production)

external vs internal respiration

closely tied to circulatory system

Physiology of Respiration

Pulmonary Ventilation

= External Respiration

we move ~500 ml of air in and out of lungs with each breath

breathing involves 2 processes:

inspiration
expiration

involves moving air down a pressure gradient

Inspiration
an active process
involves contraction of diaphragm

innervated by phrenic nerve
may also involve external intercostals

contraction of diaphragm lowers pressure in thoracic cavity:

outside pressure > pressure in lungs
lungs inflate

outside: 760 mmHg inside: 754 mmHg

Expiration
mainly a passive process

relaxation of diaphragm
volume of chest decreases, forcing air out of lungs
may also involve contraction of internal intercostals

inside: 763 mmHg outside: 760 mmHg

(forced=up to 790 mmHg)

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Factors that affect pulmonary ventilation:

1. Resistance to airflow
in respiratory passages
constriction increases resistance (=drag)
mainly in bronchi and bronchioles

2. Compliance
lungs are >100 x’s more distendable than a balloon
lungs increase in volume passively as chest cavity expands

Pulmonary fibrosis reduces compliance

3. Elasticity of lungs
elasticity = tendency of organ to return to normal position or shape
lungs contain lots of elastin fibers

Emphysema = less elastic and more collagen fibers

requires 3-4x’s more energy to breath
(15-20% vs 5% normal)

4. Reduced Pressure in Thoracic Cavity

pressure in thoracic cavity is kept lower than pressure in outside air

keeps lungs inflated

pneumothorax
opening in chest cavity
eliminates pressure differential
causes lungs to collapse

5. Surface Tension
outer surface of lungs and inner surface of alveoli are covered with thin
film of water
water has a high surface tension (very “sticky”)

on outer surface of lungs:

visceral pleura tends to stick to parietal pleura
creates slight negative intrapleural pressure
helps to inflate lungs during inspiration

on inside of alveoli:

tends to cause the alveoli to collapse upon themselves

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 counteracted by:

a. lungs never completely deflated;

always contain some air

b. secrete surfactant
a lipoprotein
reduces surface tension in alveoli
not produced until 8th month of pregnancy

respiratory distress syndrome

Respiratory Volumes

the volume of air exchanged in breathing is measured with a spirometer

provides information on pulmonary functions

Tidal Volume (TV)

normal volume of air with each breath
small part of total lung capacity (~10%)
~500 ml

Expiratory Reserve Volume (ERV)

additional air one can expire after releaseing tidal volume
use internal intercostals to forcibly expire additional air
~1000-1200 ml

Inspiratory Reserve Volume (IRV)

additional amount of air that can be inspired in addition to tidal volume
use external intercostals to lift rib cage
~3100-3300 ml

Residual Volume
air that cannot be removed from lungs
~1200 ml
removed in pneumothorax

Vital Capacity (VC)

largest volume of air that can be moved into or out of lungs
VC = IRV + TV + ERV

vital capacity is affected by:

a. overall size of individual, gender
size of lungs
b. volume of blood in lungs
eg congestive heart failure
c. excess fluid in pleural or abdominal cavity
d. loss of lung elasticity
eg. emphysema
e. misc health related factors
eg. smoking, exercise, etc
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% Forced Expiratory Volume (%FEV or FEV1)
proportion of Vital Capacity one can exhale in 1 second
usually ~75-85% in healthy individuals

Total Lung Capacity (TLC)

maximum amount of air the lungs can hold
TLC = VC + RV
~5700-6200 ml

Minute Respiratory Volume (MRV)

amount of air that ventilates lungs each minute
is an index of respiratory efficiency
= TV x Breathing rate = ~500 ml x 12
= ~6000 ml/min [6 l/min vs exercise = ~100-200 liters/min]

But of the Tidal Volume (~500 ml)

about 150 ml never gets to alveoli

remains in air passages

Alveolar Ventilation Rate

= ~350 ml x 12
= ~4200 ml/min (~70% of MRV)
= 63 gallons/hr
= 1512 gallons/day
a better index of effective ventilation
eliminates “dead space”
deeper breaths more effective than more frequent breaths

Disorders indicated with pulmonary functions tests:

Restrictive Disorders
diseases that reduce total lung capacity

lowers VC
eg. pulmonary fibrosis
eg. polio, TB, etc

Obstructive Disorders
diseases that increase airway resistance

lowers %FEV
eg. asthma (bronchiole constriction)

normal VC

but lower forced expiratory volume
eg. chronic bronchitis, asthma

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Alveolar Gas Exchange

composition of air:

air entering lungs air exiting lungs

[78% N2]
21% O2 14% O2
0.04% CO2 5.6% CO2

the exchange of gasses in the lungs takes place between alveolar air and
venous blood

gas exchange occurs across the lining of the alveoli and capillaries
(2 cell layers thick)
= respiratory membrane

total surface area ~ 70 (60-80)M2 (=760 ft2 ~20’x38’)

Gas exchange is the result of simple diffusion down oxygen and carbon dioxide
concentration gradients:

concentrations of gasses usually measured in partial pressures

PO2 = 21% of 760 mmHg = 160 mmHg
PCO2 = 0.04% of 760 mmHg = 0.3 mmHg

Alveoli Blood Entering Lungs

PO2 105mmHg 40mmHg
PCO 2 39mmHg 46mmHg

Amount of O2 diffusing into blood depends on:

1. oxygen pressure gradient
alveolar airflow – blood flow coupling
if low O2/high CO2 get

arterial constriction

bronchial dilation
improves gas exchange in alveoli
2. surface area of lungs
3. respiratory rate

Oxygen binds to hemoglobin inside RBC’s = oxyhemoglobin

The exchange of gasses in tissues is also by simple diffusion:

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 Blood leaving lungs Tissues

PO2 104mmHg ≤40mmHg

PCO2 40mmHg ≥45mmHg

The amount of oxygen delivered to tissue cells is affected by:

1. rate of oxygen utilization
regulates the rate of delivery by controlling size of gradient
as conc of O2 in tissues decreases;

the bonds between O2 and Hb weaken
2. Carbon Dioxide concentration
more CO2
more O2 released
3. pH
lower pH
more O2 released
4. temperature
higher temp
more O2 released

Dissociation Curve for Hemoglobin (how easily Hb gives up oxygen):

1st O2 on and off is hardest
other 3 are easier to bind or remove

creates differential release of oxygen to cells needing it most

More oxygen is released to active muscle cells

Myoglobin
has 1 heme group

accepts O2 from Hemoglobin
holds onto O2 longer
“middleman”

Transport of Gasses in Blood

A. Oxygen [O2]

hemoglobin has a very high affinity for O2

almost all hemoglobin in blood going through lungs manages to pick up oxygen

97-99% saturation
versus ~70% saturation in venous blood

only ~1-1.5% of O2 is carried dissolved in plasma

eg. Hyperventilation doesn’t increase PO2 of blood

only slightly increases dissolved O2 concentrations

may deliver a little more O2 to tissues but not much

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the amount of oxygen carried in the blood then is mainly dependent on the
amount of hemoglobin in blood

4 O2/hemoglobin
250 Million Hb/RBC
1 Billion O2/RBC

anemia decreases oxygen transport

Only 20-25% of oxygen is unloaded per circuit of bloodflow

venous reserve
eg. this is why you can “hold breath”
ie. don’t need oxygen continuously

CO binds to Hemoglobin even more strongly than does oxygen

CO poisoning (takes very little, but continuous
exposure)

B. Carbon Dioxide [CO2]

transported in blood three major ways:

1. 7% dissolved in plasma

>20x’s more soluble than O2

2. 20-23% bound to hemoglobin

CO2 binds to amino group of hemoglobin
(O2 binds to heme portion)
=carbaminohemoglobin

3. 70% converted to bicarbonate ions

carbonic anhydrase

CO2 + H2O H2CO3 H+ + HCO3-

carbonic acid bicarbonate ion

this reaction occurs mainly inside RBC’s

bicarbonate ions are then released into the plasma

oxygen release is enhanced by CO2 loading

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Regulation of Respiration

normal breathing is automatic, rhythmic

Skeletal muscles of diaphragm and intercostals are innervated by somatic

motor neurons

controlled by respiratory reflex centers in brainstem

Three reflex centers in brain that regulate breathing:

1. respiratory center: medulla

(medullary rhythmicity area)

establishes basic rhythm of breathing

maintains automatic breathing rate

12-15 breaths/min

a. contain chemoreceptors that are sensitive to changes in CO2

b. chemoreceptors in aorta and carotid sinus also monitor CO2

levels in arterial blood

high blood CO2 faster breathing

c. other chemoreceptors in aorta and carotid sinus also

monitor pH

more acidic faster breathing

d. O2 sensors in aorta and carotid sinus detect slight reductions in

O2 and cause reflex stimulation of respiratory center

more of a backup system

rarely is the most important control

if cells in respiratory become hypoxic they may fail

Hypoxic drive: people with respiratory disease

these O2 receptors become more important

2. apneustic: pons

promotes inspiration, breath holding

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 forceful, prolonged inspiration

3. pneumotaxic center: pons

antagonist to apneustic
inhibits inspiration
fine tunes, prevents overinflation

the two centers in pons insure a smooth transition between inspiration

and expiration

helps maintains rhythmicity of breathing

when connection between medulla and pons are cut breathing becomes
abnormal

gasps

“inflation & deflation reflexes” alternate activity

helps regulate depth of breathing

occurs when stretch receptors in pleura,

bronchioles and alveoli are stimulated during inspiration

prevents overinflation

when stretch receptors are no longer stimulated

prevents further expiration

Hypothalamus
irritant receptors trigger bronchiole constriction, coughing etc

Cerebrum
emotional state, eg fear, pain, can speed up breathing

can voluntarily speed up or slow down breathing

but can’t overpower reflex controls

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 Diseases of
Respiratory System

A. Diseases of inadequate ventilation

1. Pneumothorax
collapsed lung or lungs

2. paralysis of diaphragm muscle

due to injury to respiratory center of brainstem
eg. caused by polio which damages respiratory center
damage to nerves supplying diaphragm (phrenic nerve)

3. bronchial asthma
allergic reaction
excessive mucous secretions and constrictions of bronchioles

4. emphysema
progressive degenerative disease causing destruction of alveolar
walls
may be due to chronic irritation (eg smoking)
loss of tissue elasticity

5. lung cancer
uncontrolled growth of cells
crowd out normal cells

B. Diseases of Poor Gas Exchange

1. emphysema

2. infections
viral or bacterial
eg. hay fever, bronchitis
cause lining of tubes to swell and become inflamed

2. pneumonia
more sever result of respiratory infection
bacterial or viral
alveoli fill with fluids

3. tuberculosis
tubercles formed to wall off bacterial infection
if infection is not controlled may invade more lung tissue causing
fibrosis
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 causes extensive destruction of lung tissue

4. Respiratory Distress Syndrome

collapse of lungs in baby due to lack of surfactants

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