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RESPIRATORY SYSTEM HANDOUT 2012
Respiration involves several components:
Ventilation - the exchange of respiratory gases (O2 and CO2) between the
atmosphere and the lungs. This involves gas pressures and muscle contractions.
External respiration - the exchange of gases between the lungs and the blood.
This involves partial pressures of gases, diffusion, and the chemical reactions
involved in transport of O2and CO2.
Internal respiration - the exchange of gases between the blood and the
systemic tissues. This involves the same processes as external respiration.
Cellular respiration - the includes the metabolic pathways which utilize oxygen
and produce carbon dioxide, which will not be included in this unit.
Quiet inspiration:
Forced inspiration:
The diaphragm contracts, this
causes an increase in volume of the
thorax and the lungs, which causes a
decrease in pressure of the thorax
and lungs, which causes air to enter
the lungs, moving down its pressure
gradient. Air moves into the lungs to fill
the partial vacuum created by the
increase in volume.
Other muscles aid in the increase in thoracic
and lung volumes.
The scalenes - pull up on the first and
second ribs.
The sternocleidomastoid muscles pull up
on the clavicle and sternum.
The pectoralis minor pulls forward on the
ribs.
The external intercostals are especially
important because they spread the ribs
apart, thus increasing thoracic volume.
These muscles produce the "costal
breathing" during rapid respirations.
Quiet expiration:
Forced Expiration:
The diaphragm relaxes. The elasticity
of the muscle tissue and of the lung
stroma causes recoil which returns the
lungs to their volume before
inspiration. The reduced volume
The following muscles aid in reducing the
volume of the thorax and lungs:
The internal intercostals - these compress
causes the pressure in the lungs to
increase thus causing air to leave the
lungs due to the pressure gradient.
the ribs together .
The abdominus rectus and abdominal
obliques: internal obliques, external
obliques- these muscles push the
diaphragm up by compressing the abdomen.
DEAD SPACE- Air in the lungs that does not participate in the gaseous
exchange of O2 and CO2 at the respiratory membrane.
Anatomic dead space- air which fills respiratory passages but does not reach
the alveoli - nose, pharynx, and trachea. On expiration, the air in the dead space
is expired first.
Physiologic dead space - total sum of all the dead spaces (anatomical dead
space + air in the alveoli which cannot perform gaseous exchange (nonfunctional alveoli or due to poor perfusion through the pulmonary capillaries)
In a normal person, the anatomic and physiologic dead spaces are nearly equal
because all alveoli are functional in the normal lung, but in a person with
partially functional or nonfunctional alveoli in some parts of the lungs, the
physiologic dead space is increased.
Respiratory output is determined by the minute volume, calculated by
multiplying the respiratory rate times the tidal volume.
Minute Volume = Rate (breaths per minute) X Tidal Volume (ml/breath)
Rate of respiration at rest varies from about 12 to 15 bpm. Tidal volume averages
500 ml.
Assuming a rate of 12 breaths per minute and a tidal volume of 500, the restful
minute volume is 6000 ml. Rates can, with strenuous exercise, increase to 30 to
40 bpm and volumes can increase to around half the vital capacity.
Not all of this air ventilates the alveoli, even under maximal conditions. The
conducting zone volume is about 150 ml and of each breath this amount does
not extend into the respiratory zone. The Alveolar Ventilation Rate, AVR, is the
volume per minute ventilating the alveoli and is calculated by multiplying the rate
times the (tidal volume-less the conducting zone volume).
AVR = Rate X (Tidal Volume - 150 ml)
For a calculation using the same restful rate and volume as above this yields
4200 ml.
Since each breath sacrifices 150 ml to the conducting zone, more alveolar
ventilation occurs when the volume is increased rather than the rate.
During inspiration the pressure inside the lungs (the intrapulmonary
pressure) decreases to -1 to -3 mmHg compared to the atmosphere. The
variation is related to the forcefulness and depth of inspiration. During expiration
the intrapulmonary pressure increases to +1 to +3 mmHg compared to the
atmosphere. The pressure oscillates around zero or atmospheric pressure.
The intrapleural pressure is always negative compared to the atmosphere. This
is necessary in order to exert a pulling action on the lungs. The pressure varies
from about -4 mmHg at the end of expiration, to -8 mmHg and the end of
inspiration.
The tendency of the lungs to expand, called compliance or distensibility, is due
to the pulling action exerted by the pleural membranes. Expansion is also
facilitated by the action of surfactant in preventing the collapse of the alveoli.
The opposite tendency is called elasticity or recoil, and is the process by which
the lungs return to their original or resting volume. Recoil is due to the elastic
stroma of the lungs and the series elastic elements of the respiratory muscles,
particularly the diaphragm.
Conditions which interfere with compliance or elasticity are called restrictive
disorders. Examples are emphysema , which increases compliance and
decreases elasticity, and fibrosis , which reduces both.
In emphysema the buildup of toxins from cigarette smoke and resulting mucus
production leads to destruction of the alveolar and capillary walls and fibrosis of
the tissue. This produces large thick-walled chambers replacing the normal small
thin-walled alveoli. It results in a larger volume in the lungs but impaired gas
transport and reduced ability to expire the trapped air. Many emphysema
sufferers have the characteristic "barrel chest" as a result. Carbon dioxide tends
to increase in alveolar air and in the blood, in some individuals interfering with
normal respiratory stimuli and responses.
Pulmonary or cystic fibrosis produces thickened mucus secretions which block
the airways and scar tissue often develops in place of the normal elastic stroma.
This is both restrictive and obstructive in its effects.
Restrictive disorders reduce the volume which can be ventilated as seen in a
reduced vital capacity.
In contrast, obstructive disorders such as bronchitis and asthma reduce the
size of the bronchial passages thus interfering with the airflow. [See COPD
below]
In bronchitis an inflammation results from respiratory infection or irritation from
smoke or pollution.
Asthma is like an allergic reaction in which inflammation also occurs together
with a constriction of the bronchial passages.
Purely obstructive disorders do not technically reduce the volume which can be
ventilated but they reduce the rate of ventilation by increasing the resistance to
airflow. They will show a normal vital capacity but a reduced FEV1, (Forced
Expiratory Volume) the percentage of the vital capacity which can be expelled
in the first second. Normal FEV1 is 70-75% or greater.
Many times disorders are both obstructive and restrictive. For example:
obstructive emphysema - in addition to the enlarging and thickening of alveolar
walls many of the passageways collapse producing obstructive effects as well.
COPD Chronic Obstructive Pulmonary Disease - a combination of
emphysema, bronchitis and asthma, has components of each.
Respiratory volumes
Tidal Volume TV: Volume of a single breath, usually at rest.
Inspiratory Reserve Volume IRV: Volume which can be inspired beyond a
restful inspiration.
Expiratory Reserve Volume ERV: Volume which can be expired beyond a
restful expiration.
Residual Volume RV: Volume remaining in the lungs after a maximum
expiration. This volume keeps the alveoli inflated.
Vital Capacity: The vital capacity (VC) is the maximum volume which can be
ventilated in a single breath. VC= IRV+TV+ERV. VC varies with gender, age, and
body build. Measuring VC gives a device for diagnosis of respiratory disorder,
and a benchmark for judging the effectiveness of treatment.
Vital Capacity is reduced in restrictive disorders, but not in disorders which are
purely obstructive.
The FEV1 is the % of the vital capacity which is expelled in the first second. It
should be at least 70-75%. The FEV1 is reduced in obstructive disorders.
Both VC and the FEV1 are reduced in disorders which are both restrictive and
obstructive. (See above)
Basic volumes:
a. Tidal Volume (VT, TV): volume of gas exchanged in each breath -- can change
as ventilation pattern changes
b. Inspiratory Reserve Volume (IRV): maximum volume that can be inspired,
starting from the end inspiratory position -- potential volume at the end of
inspiration
Inspiratory reserve volume; the difference between VC and FRC. This is the
maximal amount of air that can be inspired starting with FRC (functional residual
capacity).
c. Expiratory Reserve Volume (ERV): maximum volume that can be expired,
starting from the end expiratory position -- potential volume at the end of
expiration
d. Residual Volume (RV): volume remaining in the lungs and airways following a
maximum expiratory effort -- lungs cannot empty completely because of (1)
stiffness when compressed and (2) airway collapse and gas trapping at low lung
volumes
2. Capacities: combined volumes
a. Vital Capacity (VC): maximum volume of gas that can be exchanged in a
single breath
VC = TV + IRV + ERV
This is the difference between Total Lung Capacity (TLC) and Residual Volume
(RV); i.e, it is the maximum volume of air which can be exhaled starting at full
lung inhalation.
b. Total Lung Capacity (TLC): maximum volume of gas that the lungs (and
airways) can contain
TLC = VC + RV
= TV + IRV + ERV + RV
= IC + FRC
c. Functional Residual Capacity (FRC): volume of gas remaining in the lungs
(and airways) at the end expiratory position
FRC = RV + ERV
d. Inspiratory capacity (IC): maximum volume of gas that can be inspired from
the end expiratory position
IC = TV + IRV
IC = TV + IRV
VC = IRV + VT + ERV
VC = IC + ERV
TLC = TV + IRV + ERV + RV
TLC = VC + RV
TLC = IC + FRC
FRC = ERV + RV
REGULATION OF RESPIRATION
The respiratory center is composed of several neurons located bilaterally in the
medulla and pons. It is divided into three groups of neurons:
1. dorsal respiratory group- located in the dorsal portion of the medulla
provides the basic rhythm of respiration
2. ventral respiratory group- located in the ventrolateral porton of the medulla
3. pnuemotaxic center- located dorsally in the superior portion of the pons.
DORSAL RESPIRATORY GROUP
This is mainly responsible for inspiration and has the most fundamental role in
the control of respiration. Most of its neurons are located in the nucleus of the
tractus solitarius. The nucleus of the tractus solitarius is also the sensory
termination of the vagus and glossopharyngeal nerves which send signals to the
respiratory center from the peripheral chemoreceptors, the baroreceptors and
several types of receptors in the lung.
The control of inspiration is such that the inspiration is in a ramp fashion in two
seconds, slowly increasing and ceases for 3 seconds. The dorsal respiratory
group controls the rate of increase of the ramp signal as well as the limiting point
at which the ramp suddenly ceases.
PNEUMOTAXIC CENTER
This mainly controls the rate and depth of breathing. Located at the upper pons
in the nucleus parabrachialis, this controls the switch off point of the ramp and
thus controls the duration of the filling phase of the lung cycle. The stronger the
stimulation of the pneumotaxic center, the lesser is the duration of inspiration,
which increases respiratory rate.
The function of the pneumotaxic center is primarily to limit inspiration. This has a
secondary effect of increasing the rate of breathing, because limitation
of inspiration also shortens expiration and the entire period of each respiration. A
strong pneumotaxic signal can increase the rate of breathing to 30 to 40
breaths per minute, whereas a weak pneumotaxic signal may reduce the rate to
only 3 to 5 breaths per minute.
VENTRAL RESIPRATORY GROUP
This group functions in both inspiration and expiration. It is found in the nucleus
ambiguous and nucleus retroambiguus caudally. It remains inactive during
normal quiet breathing.
When the respiratory drive for increased pulmonary ventilation becomes greater
than normal, respiratory signals spill over into the ventral respiratory neurons
from the dorsal respiratory area. As a consequence, the ventral respiratory
area contributes extra respiratory drive as well. Electrical stimulation of a few of
the neurons in the ventral group causes inspiration, whereas stimulation of others
causes expiration. Therefore, these neurons contribute to both inspiration and
expiration.
They are especially important in providing the powerful expiratory signals to the
abdominal muscles during very heavy expiration. This area operates as an
overdrive mechanism when high levels of pulmonary ventilation are required,
especially during heavy exercise.
THE HERING BREUER INFLATION REFLEX
This reflex is mainly a protective mechanism for preventing excess lung inflation.
Nerve signals from the lungs also control respiration. Stretch receptors in the
muscular portions of the walls of the bronchi and bronchioles transmit signals
through the vagi into the dorsal respiratory group when the lungs become
overstretched. This limits inspiration This also increases the rate of respiration.
The Hering-Breuer reflex operates when tidal volume increases to greater than
1.5 liters.
CHEMICAL CONTROL OF RESPIRATION
Excess carbon dioxide or hydrogen ions stimulate the respiratory center
increasing both the inspiratory and expiratory signals to the respiratory center.
Carbon dioxide and hydrogen ions act on the chemosensitive area which is very
sensitive to it. However, hydrogen ions do not cross the blood brain barrier unlike
carbon dioxide. So changes in the hydrogen ions in the blood therefore, have a
less effect in stimulating the chemosensitive neurons than carbon dioxide. Once
carbon dioxide has crossed the blood brain barrier, carbon dioxide reacts with
water in the tissues forming carbonic acid which dissociates into bicarbonate
and hydrogen ions. An increase in the carbon dioxide levels in the blood also
increases the carbon dioxide at the cerebrospinal fluid (CSF) and interstitium of
the medulla Excitation through the CSF has a more immediate (within seconds)
effect than through the interstitium which takes at least a minute.
An increase in the blood carbon dioxide levels has an acute potent effect in the
first few hours. This effect gradually declines in the next 1-2 days because:
1. renal readjustment- the kidneys increase blood bicarbonate that binds to
hydrogen ions at the interstitium and CSF therefore decreasing the hydrogen
ions.
2. bicarbonate diffusion- bicarbonate ions from the blood to the CSF and
interstitium to combine with hydrogen ions.
Changes in blood pH (the inverse logarithmic measure of hydrogen ion
concentration on alveolar ventilation) between 7.3 and 7.5 have a very strong
effect on alveolar ventilation which coincides with normal blood carbon dioxide
levels between 35 and 60 mmHg. The hydrogen ions have a direct potent effect
on the respiratory center however, the changes in blood carbon dioxide affects
the respiratory center more than blood hydrogen levels.
Oxygen doesn't have a significant effect on the respiratory center. It acts on
peripheral chemoreceptors located in the carotid and aortic bodies which transmit
signals for control of respiration. Carbon dioxide is the major controller of
respiration not oxygen.
A change in blood carbon dioxide concentration has a potent acute effect on
controlling respiratory drive but only a weak chronic effect after a few days’
adaptation.
PERIPHERAL CHEMORECEPTOR CONTROL
The largest number of chemoreceptors are in the carotid bodies followed by
aortic bodies.The carotid bodies are located at the bifurcations of the common
carotid arteries and their afferent nerves pass through Hering's nerves to the
glossopharyngeal nerves and then to the dorsal respiratory area. The aortic
bodies are located at the arch of the aorta, their afferent nerves pass through the
Vagi to the dorsal respiratory center.
If arterial hemoglobin saturation with oxygen decreases rapidly (between 60 and
30 mmHg), impulses from the chemoreceptors increase. Tthe peripheral
stimulation from the chemoreceptors is 5 times more rapid than central
stimulation which makes it more important in increasing the rapidity of response
to carbon dioxide at the onset of exercise.
A low arterial oxygen pressure has a paradoxical effect on respiration.
Decrease in blood oxygen
Stimulation from chemoreceptors
Increased respiration
Decrease in carbon dioxide and hydrogen ions that depresses the respiratory
center
Effect of Carbon Dioxide and Hydrogen Ion Concentration on
Chemoreceptor Activity. An increase in either carbon dioxide concentration or
hydrogen ion concentration also excites the chemoreceptors and, in this way,
indirectly increases respiratory activity. These direct effects of both these factors
in the respiratory center itself are more powerful than their effects mediated
through the chemoreceptors (about seven times as powerful). However, the
stimulation by way of the peripheral chemoreceptors occurs as much as five
times as rapidly as central stimulation, so that the peripheral chemoreceptors
might be especially important in increasing the rapidity of response to carbon
dioxide at the onset of exercise.
The effect of a low arterial oxygen in increasing respiration is therefore
counteracted. But there are 2 conditions when the counter effect doesn't
happen:
1. when arterial carbon dioxide and hydrogen ion concentration remain normal
or even increased despite increasing ventilation (in pulmonary conditions with
poor ventilation perfusion)
2. breathing of oxygen at low concentrations for many days. (acclimatization)
Acclimatization results when the respiratory center in the brain loses its
sensitivity within 2-3 days to changes in arterial carbon dioxide and hydrogen
ions. This happens usually among mountain climbers who ascend too quickly on
places with low oxygen pressures causing a decrease in their arterial oxygen. In
a few days, acclimatization occurs which means the decrease in oxygen levels
increases respiratory rate that is not counter acted by a corresponding decrease
in carbon dioxide and hydrogen (as a result of increasing ventilation) despite
increased ventilation because the respiratory center has been rendered
insensitive to carbon dioxide and hydrogen ions. The provides the climber
additional oxygen that is badly needed.
REGULATION OF RESPIRATION DURING EXERCISE
During exercise, the levels of oxygen, carbon dioxide and hydrogen ions don't
change significantly to abnormal levels. What causes an increase in ventilation
during exercise is explained by the following:
1. the brainstem sends collateral signals to the respiratory center while
transmitting impulses to the contracting muscles.
2. body movements alone can increase respiration through joint and muscle
proprioceptors that transmit excitatory impulses to the respiratory center.
At the start of exercise, the increase in ventilation due to the 2 reasons
mentioned even decrease carbon dioxide levels. After 30-40 seconds of
exercise, the carbon dioxide released from the muscles causes now an increase
in respiration. This is said to be a learned response controlled by the cerebral
cortex.
OTHER FACTORS THAT AFFECT RESPIRATION
1. Voluntary Control Of Respiration - the involuntary control is through the
medulla. The voluntary control is mediated from the cerebral cortex to the
spinal nerves innervating the diaphragm.
2. Effect of irritant receptors in the airways - pulmonary irritant receptors
are present at the epithelium of the trachea, bronchi and bronchioles that
may cause coughing and sneezing.
3. Function of the "J" receptors - these "J" receptors are found at the
alveolar walls in juxtaposition with the pulmonary capillaries that are
excited when the pulmonary arteries are congested with blood (especially
during pulmonary edema). Stimulation is said to cause dyspnea.
4. Effect of brain edema- brain edema causes depression of the respiratory
center.
5. Effect of anesthesia- anesthetics and narcotics depending on dosage
depress the respiratory center. Examples of anesthetics that depress the
respiratory center are: sodium pentobarbital, halothane and morphine.
CHEYNE-STOKES BREATHING
During Cheyne-Stokes breathing, the Pco2 of the pulmonary blood changes in
advance of the Pco2 of the respiratory neurons. But the depth of respiration
corresponds with the Pco2 in the brain, not with the Pco2 in the pulmonary blood
where the ventilation is occurring.
This cycle continues over and over again because the supposed damping
mechanisms of the lung don't work in certain conditions such as the following:
1. long delay in the transport of the gases from the lungs to the brainin severe left-sided cardiac failure where there is pulmonary congestion
and blood flow from the left ventricle is very poor.
2. increased negative feedback in the respiratory control areas- the
response to changes in blood carbon dioxide levels is exaggerated. So
even without delay in the blood flow from the lungs to the brain, instead of
a normal 2-3 increase in ventilation when blood carbon dioxide increases
to 3 mm Hg, the increase is 10-20 times more. This happens in braindamaged patients. The Cheyne-Stokes breathing in this case is said to be
a prelude to death.