May 12, 2025 • 52 mins
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This episode features a full reading of “Respiratory Physiology” from Update in Anaesthesia, Volume 24, Number 2.
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(00:02):
Updates in Anaesthesia, volume 24 #2 Respiratory Physiology by
Fred Roberts and Ian Kersten. Summary This article covers the
(00:27):
main areas of respiratory Physiology that are important to
anaesthetists. Examples relevant to anaesthesia
and pathological states of the respiratory system are used when
possible. Further detail is included in
(00:49):
the following articles on oxygendelivery and carbon dioxide
transport. Some areas are covered in more
than one article but are included since alternative
explanations from different authors may enhance
understanding of more difficult aspects of this subject.
(01:17):
Introduction The main function of the lungs is to provide
continuous gas exchange between inspired air and the blood in
the pulmonary circulation, supplying oxygen and removing
carbon dioxide, which is then cleared from the lungs by
(01:42):
subsequent exploration. Survival is dependent on this
process being reliable, sustained and efficient, and
even when challenged by disease or an unfavourable environment.
Evolutionary development has produced many complex mechanisms
(02:06):
to achieve this, several of which are compromised by
anaesthesia. A good understanding of
respiratory Physiology is essential to ensure patient
safety during anaesthesia. Mechanism of breathing A
(02:31):
pressure gradient is required togenerate air flow in spontaneous
respiration. Inspiratory flow is achieved by
creating a sub atmospheric pressure in the alveoli that is
of the order of -5 centimetres of water during quiet breathing
(02:55):
by increasing the volume of the thoracic cavity under the action
of the inspiratory muscles. During expiration, the intra
alveolar pressure becomes slightly higher than atmospheric
pressure and gas flow to the mouth results motor pathways.
(03:25):
The main muscle generating the negative intra thoracic pressure
that produces inspiration is thediaphragm, A muscular tendinous
sheath separating the thorax from the abdomen.
Its muscular part is peripheral,attached to the ribs and lumbar
(03:48):
vertebrae with a central tendon.Innervation is from the phrenic
nerves, that is, C3 to five, with contraction moving the
diaphragm downwards, forcing theabdominal contents down and out.
(04:12):
Additional inspiratory efforts are produced by the external
intercostal muscles, that is innervated by their intercostal
nerves T1 to 12, and the accessory muscles of
respiration, that is, stenomastoids and scalenes,
although the latter only become important during exercise or
(04:37):
respiratory distress During quiet breathing, expiration is a
passive process relying on the elastic recoil of the lung and
chest wall. When ventilation is increased,
(04:57):
such as during exercise, expiration becomes active with
contraction of the muscles of the abdominal wall and the
internal intercostals. Central control The mechanism by
(05:18):
which respiration is controlled is complex.
There is a group of respiratory centres located in the brainstem
producing automatic breathing activity.
This is then regulated mainly byinput from chemo receptors.
(05:40):
This control can be overridden by voluntary control from the
cortex. Breath holding, panting or
sighing at will are examples of this voluntary control.
The main respiratory centre is in the floor of the 4th
(06:03):
ventricle with inspiratory that is dozo, an expiratory that is
ventral neuron groups. The inspiratory neurons fire
automatically but the expiratoryones are used only during forced
(06:24):
expiration. The two the two other main
centres are the apnostic centre,which enhances inspiration, and
the pneumotoxic centre, which terminates inspiration by
inhibition of the dorsal neuron group above.
(06:49):
The chemoreceptors that regulaterespiration are located both
centrally and peripherally. Normally, control is exercised
by the central receptors locatedin the medulla, which respond to
the cerebrospinal fluid. Hydrogen ion concentration in
(07:14):
turn determined by carbon dioxide, which diffuses freely
across the blood brain barrier from the arterial blood.
The response is both quick and sensitive to small changes in
arterial PCO two, that is, PA CO2.
(07:39):
In addition, there are peripheral chemoreceptors
located in the carotid and aortic bodies, most of which
respond to fall in oxygen, but some also to a rise in arterial
carbon dioxide. The degree of hypoxia required
(08:04):
to produce significant activation of oxygen receptors
is such that they are not influential under normal
circumstances, but will do so ifprofound hypoxia that is PAO 2
less than 8 kilopascals or causefor example, at high altitude
(08:29):
when breathing air. See later in special
circumstances. It also happens when the
response to carbon dioxide is isimpaired, which can occur if the
PA CO2 is chronically elevated, leading to a blunting of the
(08:51):
central receptor. Sensitivity.
Respiratory process. Respiratory values.
The various terms used to describe long excursion or
(09:12):
movement during quiet and maximal respiration are shown in
Figure 1 below. Next we get to figure one with a
famous diagram explaining long volumes in an adult male
measured with a spirometer during quiet breathing with one
(09:37):
maximum breath referring to the residual volume, inspiratory
reserve volume, functional residual capacity, vital
capacity, total long capacity, tidal volume, and expiratory
(10:00):
reserve volume. Kindly pause the recording and
take some time to go through this figure.
The tidal volume 500 mils multiplied by the respiratory
rate 14 breaths per minute is the minute volume. 7000 meals
(10:26):
per minute, that is TV Times RR is equals to MV.
Not all of the tidal volume takes part in respiratory
exchange, as this process does not start until the air or gas
(10:48):
reaches the respiratory bronchioles Division 17 of the
respiratory tree. Above this level, the Airways
are solely for conducting their volume, being known as the
anatomical Dead Space. The volume of the anatomical
(11:14):
Dead Space is approximately 2 mils per kilogramme, or 150 mils
in an adult, roughly 1/3 of the tidal volume.
The part of the tidal volume which does take part in
(11:35):
respiratory exchange multiplied by the respiratory rate is known
as the alveolar ventilation, which is approximately 5000
meals per minute. Let's take a step back and just
(11:55):
go through the standard volumes in Figure 1.
The standard long volumes, functional residual capacity,
2500 mills. Residual volume 1000 mills,
(12:21):
vital capacity, 5000 mills. Expiratory reserve volume 1500
mills, Inspiratory reserve volume 3000 mills, Tidal volume
(12:47):
500 mills and finally total longcapacity 6000 mills.
Let's continue. Functional residual capacity.
FRC is the volume of air in the lungs at the end of a normal
(13:15):
expiration. The point at which this occurs,
and hence the FRC value, is determined by a balance between
the inward elastic force forces of the lung and the outward
forces of the respiratory cage, mostly due to muscle tone.
(13:37):
FRC falls with lying, supine obesity, pregnancy and
anaesthesia, though not with age.
The functional residual capacityis of particularly importance to
anaesthetics because during apnea it is the reservoir to
(14:02):
supply oxygen to the blood. As it falls, the distribution of
ventilation within the lungs changes leading to mismatching
with pulmonary blood flow and ifit falls below a certain volume
that is the closing capacity, airway closure occurs leading to
(14:28):
a shunt resistance and compliance.
In the absence of respiratory efforts, the long will come to
lie at the point of the functional residual capacity.
(14:49):
Remember it is 2500 mills. To move from this position and
generate respiratory movement, 2aspects need to be considered
which oppose lung expansion and air flow and therefore need to
be overcome by respiratory muscle activity.
(15:14):
These are the airway resistance and the compliance of the lung
and chest wall resistance of theAirways.
Describes the obstruction to airflow provided by the conducting
Airways, resulting largely from the larger Airways, that is down
(15:36):
to division 6 to 7 + A contribution from tissue
resistance produced by friction as tissues of the lungs slide
over each other during respiration.
An increase in resistance resulting from airway narrowing,
(15:57):
such as bronchospasm, leads to obstructive Airways disease.
In obstructive Airways disease, it might be expected that
airflow should be improved by greater respiratory efforts,
that is, increasing the pulse gradient to overcome the
(16:19):
increase in Airways resistance. Whilst this is normally due and
true for inspiration, it is not necessarily the case during
expiration as the increase in intrapurial pressure may act to
(16:41):
compress Airways proximal to thealveoli, leading to further
obstruction with no increase in expiratory flow and air trapping
distally. This is shown in Figure 2 and
(17:01):
demonstrates why expiration is usually the major problem during
an asthmatic attack. Compliance denotes
distensibility, that is, stretchiness, and in a clinical
setting refers to the lung and chest wall combined being
(17:25):
defined as the volume change by unit pressure change, that is, V
/ P. When compliance is low, the
lungs are stiffer and more effort is required to inflate
the alveoli. Conditions that worsen
(17:49):
compliance, such as pulmonary fibrosis, produce restrictive
lung disease. Compliance also varies within
the lung according to the degreeof inflation as shown in Figure
2. Poor compliance is seen at low
(18:13):
volumes because of difficulty with initial lung inflation and
at high volumes because of the limits of chest wall expansion
with best compliance in the mid expansion range.
(18:37):
Next we get to Figure 2 explaining compliance.
The compliance curve showing compliance within the lung at
different levels of inflation atfunctional reserve capacity in
the young healthy individual. The AP CS are well inflated,
(18:58):
that is towards the top of the curve and therefore less
ventilated than the mid zones and bases which are on the lower
steeper part of the compliance curve.
Walk of breathing. Of the two barriers to
(19:22):
respiration, airway resistance and lung compliance, it is only
the first of these which requires actual work to be done
to overcome it. Airway resistance to flow is
present during both inspiration and expiration, and the energy
(19:45):
required to overcome it, which represents the work of
breathing, is dissipated as heat.
Although energy is required to overcome compliance in expanding
the lung, it does not contributeto the actual work of breathing
(20:07):
as it is not dissipated but converted to potential energy.
In the distended elastic tissues, some of this stored
energy is used to do the work ofbreathing produced by Airways
resistance during expiration. The work of breathing is best
(20:32):
displayed on a PROS on a pressure volume curve of 1
respiratory cycle, which shows the different pathways for
inspiration and expiration knownas hysteresis.
The total work of breathing of the cycle is the area contained
(20:56):
in the loop with high respiratory rates.
Faster air flow rates are required, increasing the
fictional forces frictional forces.
This is more marked in obstructive Airways disease and
(21:17):
such patients therefore generally minimise the work of
breathing by using a slow respiratory rate and large tidal
volumes. In contrast, patients with
restrictive lung disease, that is, poor compliance, reach the
(21:38):
unfavourable upper part of the compliance curve soon as the
tidal volume increases. The pattern of breathing seen in
such patients usually involves small tidal volumes and a fast
respiratory rate. Next we get to Figure 3,
(22:01):
explaining the work of breathing, shown in a longer
pressure volume, that is compliance curve surfactant.
Any liquid surface exhibits surface tension, A tendency for
(22:25):
the molecules on the surface to pull together.
This is why when water lies on the surface, it forms rounded
droplets. If the surface tension is
reduced, for example by adding asmall amount of soap, the
(22:46):
droplets collapse and the water becomes a thin film.
When a liquid surface is spherical, it acts to generate a
pressure within the sphere according to Laplace's law,
(23:07):
which is pressure is equals to two times surface tension
divided by the radius of the sphere.
The film of liquid lining the alveoli exhibits surface tension
in such a manner to increase thepressure in the alveoli with a
(23:29):
greater rise in small alveoli than in large ones.
Surfactant is a substance secreted by type 2 alveolar
epithelial cells which lowers the surface tension of this
respiratory surface liquid markedly, mainly consisting of a
(23:55):
phospholipid that is dipamitol lecithin.
It's physiological benefits are a reduction in the fluid leak
from pulmonary capillaries into the alveoli as the surface
tension forces. As the surface tension forces
(24:18):
act to increase the hydrostatic pressure gradient from capillary
to alveolus, an increase that isimprovement in overall lung
compliance and a reduction in this tendency for small alveoli
(24:38):
to empty into large ones, reducing the tendency for the
lung to collapse. Diffusion of oxygen.
The alveoli provide an enormous surface area for gas exchange
(25:00):
with pulmonary blood that is between 50 to 100 metre square
with a thin membrane across which gases must diffuse.
The solubility of oxygen is suchthat is diffusion across the
normal alveolar capillary membrane is an efficient and
(25:23):
rapid process. Under resting conditions, the
pulmonary capillary blood is in contact with the alveolus for
about 0.75 seconds in total and is fully equilibrated with
alveolar oxygen after only about1/3 of the way along this
(25:47):
'cause. If lung disease is present which
impairs diffusion, there is therefore still usually
sufficient time for full equilibration of oxygen when at
rest. During exercise, however, the
(26:09):
pulmonary blood flow is quicker,shortening the time available
for gas exchange, and so those with lung disease are unable to
oxygenate the pulmonary blood fully and thus have a limited
ability to exercise. For carbon dioxide, which
(26:34):
diffuses across the alveolar capillary membrane 20 times
faster than oxygen, the above factors are less liable to
compromise to compromise transfer from blood to alveoli,
(26:54):
ventilation, perfusion and shunt.
In an ideal situation, the ventilation delivered to an area
of lung would be just sufficientto provide full exchange of
oxygen and carbon dioxide, with the blood perfusing that area in
(27:20):
the normal setting, Whilst neither ventilation nor
perfusion is distributed evenly throughout the lung, their
marching is fairly good, with the bases receiving
substantially more of both than the A PCs.
(27:42):
Next we get to Figure 4, describing the distribution of
ventilation, that is V, and perfusion, that is Q in the
lung. Take a while to go through this.
For perfusion, the distribution throughout the lung is largely
(28:06):
due to the effects of gravity. Therefore, in the upright
position, this means that the perfusion pressure at the base
of the lung is equal to the meanpulmonary artery pressure, that
is 15 millimetres of mercury or 20 centimetres of water, plus
(28:30):
the hydrostatic pressure betweenthe main pulmonary artery and
lung base, that is approximately15 centimetres of water.
At the AP CS, the hydrostatic pressure difference is
subtracted from the pulmonary artery pressure, with the result
(28:53):
that the perfusion pressure is very low and may at times even
fall below the pressure in the alveoli, leading to vessel
compression and intermittent cessation of blood flow.
The distribution of ventilation across the lung is related to
(29:17):
the position of each area of thecompliance curve at the start of
a normal tidal inspiration. That is the point of the FRC.
Because the bases are on a more favourable part of the
compliance curve than the EP CS,they gain more volume change
(29:43):
from the pressure change appliedand thus receive a greater
degree of ventilation. Although the inequality between
bases and AP CS is less marked for ventilation than for
perfusion, overall there is still good V stroke Q matching
(30:07):
an efficient oxygenation of blood passing through the lungs.
Note that this traditional explanation of the relationship
between ventilation and perfusion has recently been
challenged. There is still increasing
evidence that physiological matching of ventilation and
(30:28):
perfusion, despite considerable apparent heterogeneity in both,
is achieved by a common pattern of asymmetric branching of the
Airways and blood vessels. Disturbance of this distribution
(30:51):
can lead to a VQ mismatching. C Figure 5.
For an area of low V stroke Q ratio, the blood flowing through
it will be incompletely oxygenated, leading to a
reduction in the oxygen level inarterial blood.
(31:16):
That is, hypoxemia providing some ventilation is occurring in
the area of low VQ. The hypoxemia can normally be
corrected by increasing the FI O2, which restores the alveolar
oxygen delivery to a level sufficient to oxygenate the
(31:38):
blood fully. Next we get to the ventilate.
Figure 5. Talking about the ventilation
stroke perfusion mismatch. Take a while to go through this
figure. VQ mismatch occurs very commonly
(32:03):
during anaesthesia because the functional residual capacity
falls, leading to a change in the position of the lung on the
compliance curve. The APCS therefore move to the
most favourable part of the curve while the bases are
(32:24):
located on a less favourable path at the bottom of the curve.
At the extremes of VQ mismatch, an area of lung receiving no
perfusion will have AVQ ratio ofInfinity and is referred to as
(32:47):
alveolar Dead Space which together with the anatomical
Dead Space makes up the physiological Dead Space.
Ventilating the Dead Space is ineffect wasted ventilation but is
(33:07):
unavoidable. So, just as a recap, Alvula
displays Dead Space plus anatomical Dead Space is equals
to the physiological Dead Space.In contrast, in an area of lung
(33:31):
receiving no ventilation owing to airway closure or blockage,
the VQ ratio will be 0 and the area will be designated as a
shunt. Blood will emerge from an area
of shunt with APO 2 Onyx unchanged from the venous level,
(33:55):
that is 5.3 kilopascals and produced marked arterial
hypoxemia. This hypoxemia cannot be
corrected by increasing the FIO 2 even to 1 as the area of shunt
receives no ventilation at all. The well ventilated parts of the
(34:21):
lung cannot compensate for the area of shunt because
haemoglobin is fully saturated at a normal PO2.
Increasing the PO2 of this bloodwill not increase the oxygen
content substantially in the case of shunt.
(34:44):
Therefore, adequate oxygenation can only be re established by
restoring ventilation to these areas using measures such as
physiotherapy, PEEP or CPAP, which clear blocked Airways and
(35:04):
reinflate areas of collapsed lung.
Because closing capacity that isCC increases progressively with
age and is also higher in neonates, these patients are at
particular risk during anaesthesia as the functional
(35:26):
residual capacity may fall belowclosing capacity causing airway
closure. A physiological mechanism exists
which reduces the hypoxemia resulting from areas of low VQ
ratio by producing local vessel constriction in these areas and
(35:52):
diverting blood to other beta ventilated parts of the lung.
These effects known as hypoxic pulmonary vasoconstriction.
HPV is mediated by unknown localfactors.
(36:16):
The protective action of HPV is,however, inhibited by various
drugs, including inhalational anaesthetic agents.
Control of respiration, anaesthesia effects respiratory
(36:38):
function in different ways. Knowledge of respiratory
Physiology is necessary to understand these effects.
Physiological control systems involving the nervous system
usually have 3 components. These are a central controlling
(37:03):
area, an afferent pathway and anefferent pathway.
The neurons, that is, nerve cells of the controlling area
integrate the information from other parts of the body and
(37:23):
produce a coordinated response. This response from the central
controlling area is carried to the various organs and muscles
along inferent pathways. The input to the central
controlling area is from the various sensors via the afferent
(37:47):
pathways. Central controlling area The
central controlling area for breathing, called the
respiratory centre, is in the lower part of the brain stem.
(38:08):
In the medulla oblongata. There are inspiratory neurons
which are active during inspiration and inactive during
expiration. Other neurons are active during
expiration but not inspiration. The expiratory neurons.
(38:35):
These two groups of neurons automatically maintain a
rhythmic cycling pattern of inspiration and expiration.
This automatic rhythm can be modified by afferent
information. Afferent supply can central
(39:04):
chemoreceptors. Chemoreceptors are cells that
respond to chemical stimuli. There are cells on the floor of
the front ventricle that is partof the brain stem that respond
to the acidity of the cerebrospinal fluid CSF, and the
(39:28):
output from these cells influences breathing.
The acidity of any fluid is measured by the pH.
This is related to the number ofhydrogen ions in the solution.
The normal pH of the body is 7.4.
(39:52):
A higher pH than this representsalkaline conditions in the body
with a lower hydrogen ion concentration.
Aph less than 7.4 represents acidic conditions with a higher
hydrogen or ion concentration. Aph.
(40:18):
Sorry. The cells in the floor of the
4th ventricle respond to the pH of the CSF.
An acidic CSF causes hyperventilation.
This is the reason for dyspnea with conditions such as diabetic
(40:40):
ketoacidosis. An alkaline CSF inhibits the
respiratory centre. Carbon dioxide in the blood can
rapidly diffuse across into the CSF, and there is a balance
(41:01):
between the level of carbon dioxide, hydrogen ions and
bicarbonate ions in the CSF. If the carbon dioxide in the
blood increases, for example following exercise, then the
carbon dioxide, hydrogen ion andbicarbonate ion concentrations
(41:24):
increase correspondingly in the CSF.
This increase in CSF acidity causes hyperventilation, which
lowers the carbon dioxide concentration in the blood.
A low blood carbon dioxide levelthat is hypocarbia has the
(41:48):
opposite effect and may occur, for example, following
controlled ventilation during anaesthesia.
This may delay the return of spontaneous breathing at the end
of surgery. Peripheral chemoreceptors.
(42:15):
The carotid and aortic bodies are small pieces of tissue that
contain chemoreceptors which responds to the oxygen and
carbon dioxide concentrations inarterial blood.
The carotid body is the more important of the two and is
(42:36):
situated at the division of the common carotid artery into the
external and internal carotid arteries.
In the neck. The aortic body is found on the
aortic arc. The information from the carotid
body is carried along the glossopharyngeal nerve that is
(43:01):
the 9th cranial nerve and the information from the aortic body
is along the vagus nerve that isthe 10th cranial nerve to the
respiratory centre. The output from the carotid body
is thought to provide information to allow immediate
(43:23):
regulation of breathing breath by breath by the respiratory
centre. In normal people, if the
arterial blood reaching the carotid body has a partial
pressure of oxygen of 10 kilopascals, that is 80
(43:43):
millimetres of mercury, or a carbon dioxide partial pressure
of more than approximately 5 kilopascals, that is 40
millimetres of mercury, then there is an immediate and marked
increase in breathing. These limits can be modified by
(44:06):
disease or age. For example, people with chronic
bronchitis may tolerate an increased concentration of
carbon dioxide or a decreased concentration of oxygen in the
blood. Brain breathing can be
(44:32):
influenced by other parts of thebrain.
We can all consciously breathe deeply and more rapidly, called
hyperventilation, and this can happen for example before
starting strenuous exercise. Intensely emotional situations,
(44:57):
for example distressing sites, will also cause
hyperventilation. Hyperventilation is also part of
the response to a massive blood loss.
This response is coordinated by the autonomic system in the
(45:18):
hypothalamus and the vasomotor centre in the brainstem lung.
There are various receptors in the lung that modify breathing.
Receptors in the wall of the bronchi respond to irritant
(45:41):
substances and cause coughing, breath holding, and sneezing.
In the elastic tissues of the lung and chest wall are
receptors that respond to stretch.
The exact function of these receptors is not fully
(46:05):
understood, but is thought to beresponsible for various reflexes
that have been discovered in laboratory studies of animals.
There are stretch responses thatoccur when the lung and chest
wall are distended and inhibit further inspiration.
(46:30):
This is an obvious safety mechanism to avoid
overdistension. Conversely, when the lung volume
is low, then there are opposite reflexes.
A small increase in lung size may stimulate stretch receptors
(46:52):
to cause further inspiration. This can sometimes be seen in
anaesthetized patients who have been given an opioid.
Spontaneous breathing may be absent or very low slow, but if
the patient is given a small positive pressure breath by the
(47:12):
anaesthetist, then inspiration is stimulated and the patient
takes a deep breath. This reflex may also have some
function in newborn babies just after delivery, when small
breaths may stimulate further inspiration.
(47:34):
There are also stretch receptorsin the blood vessels in the
lung. If these are stretched, as in
heart failure, the response is to hyperventilate.
The information from these receptors in the lung is carried
to the respiratory centre along the vagus nerve.
(48:00):
Inferent supply. The inferent nerves from the
respiratory centre pass down thespinal cord to the diaphragm,
intercostal muscles and accessory muscles of
respiration. In the neck, the diaphragm is
(48:25):
supplied by the phrenic nerve that is formed in the neck from
the spinal nerves C 3-4 and five.
The intercostal muscles are supplied by the segmental
intercostal nerves that leave the spinal cord between T1 and
(48:45):
T12. The accessory muscles in the
neck are supplied from the cervical plexus during normal
breathing. Inspiration is an active
muscular process. Expiration is passive and relies
(49:07):
on the natural elasticity of thetissues to deflate the lung.
The most important muscle for inspiration is the diaphragm.
Any disease that affects the inferent pathways from the
respiratory centre to C 3-4 and five and then the phrenic nerve
(49:31):
to the diaphragm may cause severe difficulty in breathing.
Trauma to the cervical cord above C3 is normally fatal for
this reason. Anaesthetic drugs and
(49:53):
respiration Opioid drugs such asmorphine or fentanyl depress the
respiratory centre response to hypercarbia.
These effects can be reversed bynaloxone.
(50:14):
Volatile anaesthetic agents depress the respiratory centre
in a similar fashion, although ether has less effect on
respiration than the other agents.
Volatile agents also alter the pattern of blood flow in the
lungs, resulting in increased ventilation, stroke, perfusion
(50:37):
mismatch and decreasing the efficiency of oxygenation.
Nitrous oxide has only minor effects on respiration.
The depressant effects of opioids and volatile agents are
(50:57):
additive, and close monitoring of respiration is necessary when
they are combined. When oxygen is not available,
respiration should always be supported during anaesthesia.
Non respiratory lung functions Whilst the main function of the
(51:26):
lung is for respiratory gas exchange, it has several other
important physiological roles including a reservoir of blood
available for circulatory compensation, a philtre for
circulating microaggregates, activation of angiotensin 2 from
(51:52):
angiotensin one by angiotensin, converting enzyme, inactivation
of several substances such as norepinephrine and bradykinin,
and an immunological function bysecreting immunoglobulin A into
(52:14):
bronchial mucus.
Updates in Anaesthesia, volume 24 #2 Respiratory Physiology by
Fred Roberts and Ian Kersten. Summary This article covers the
(00:27):
main areas of respiratory Physiology that are important to
anaesthetists. Examples relevant to anaesthesia
and pathological states of the respiratory system are used when
possible. Further detail is included in
(00:49):
the following articles on oxygendelivery and carbon dioxide
transport. Some areas are covered in more
than one article but are included since alternative
explanations from different authors may enhance
understanding of more difficult aspects of this subject.
(01:17):
Introduction The main function of the lungs is to provide
continuous gas exchange between inspired air and the blood in
the pulmonary circulation, supplying oxygen and removing
carbon dioxide, which is then cleared from the lungs by
(01:42):
subsequent exploration. Survival is dependent on this
process being reliable, sustained and efficient, and
even when challenged by disease or an unfavourable environment.
Evolutionary development has produced many complex mechanisms
(02:06):
to achieve this, several of which are compromised by
anaesthesia. A good understanding of
respiratory Physiology is essential to ensure patient
safety during anaesthesia. Mechanism of breathing A
(02:31):
pressure gradient is required togenerate air flow in spontaneous
respiration. Inspiratory flow is achieved by
creating a sub atmospheric pressure in the alveoli that is
of the order of -5 centimetres of water during quiet breathing
(02:55):
by increasing the volume of the thoracic cavity under the action
of the inspiratory muscles. During expiration, the intra
alveolar pressure becomes slightly higher than atmospheric
pressure and gas flow to the mouth results motor pathways.
(03:25):
The main muscle generating the negative intra thoracic pressure
that produces inspiration is thediaphragm, A muscular tendinous
sheath separating the thorax from the abdomen.
Its muscular part is peripheral,attached to the ribs and lumbar
(03:48):
vertebrae with a central tendon.Innervation is from the phrenic
nerves, that is, C3 to five, with contraction moving the
diaphragm downwards, forcing theabdominal contents down and out.
(04:12):
Additional inspiratory efforts are produced by the external
intercostal muscles, that is innervated by their intercostal
nerves T1 to 12, and the accessory muscles of
respiration, that is, stenomastoids and scalenes,
although the latter only become important during exercise or
(04:37):
respiratory distress During quiet breathing, expiration is a
passive process relying on the elastic recoil of the lung and
chest wall. When ventilation is increased,
(04:57):
such as during exercise, expiration becomes active with
contraction of the muscles of the abdominal wall and the
internal intercostals. Central control The mechanism by
(05:18):
which respiration is controlled is complex.
There is a group of respiratory centres located in the brainstem
producing automatic breathing activity.
This is then regulated mainly byinput from chemo receptors.
(05:40):
This control can be overridden by voluntary control from the
cortex. Breath holding, panting or
sighing at will are examples of this voluntary control.
The main respiratory centre is in the floor of the 4th
(06:03):
ventricle with inspiratory that is dozo, an expiratory that is
ventral neuron groups. The inspiratory neurons fire
automatically but the expiratoryones are used only during forced
(06:24):
expiration. The two the two other main
centres are the apnostic centre,which enhances inspiration, and
the pneumotoxic centre, which terminates inspiration by
inhibition of the dorsal neuron group above.
(06:49):
The chemoreceptors that regulaterespiration are located both
centrally and peripherally. Normally, control is exercised
by the central receptors locatedin the medulla, which respond to
the cerebrospinal fluid. Hydrogen ion concentration in
(07:14):
turn determined by carbon dioxide, which diffuses freely
across the blood brain barrier from the arterial blood.
The response is both quick and sensitive to small changes in
arterial PCO two, that is, PA CO2.
(07:39):
In addition, there are peripheral chemoreceptors
located in the carotid and aortic bodies, most of which
respond to fall in oxygen, but some also to a rise in arterial
carbon dioxide. The degree of hypoxia required
(08:04):
to produce significant activation of oxygen receptors
is such that they are not influential under normal
circumstances, but will do so ifprofound hypoxia that is PAO 2
less than 8 kilopascals or causefor example, at high altitude
(08:29):
when breathing air. See later in special
circumstances. It also happens when the
response to carbon dioxide is isimpaired, which can occur if the
PA CO2 is chronically elevated, leading to a blunting of the
(08:51):
central receptor. Sensitivity.
Respiratory process. Respiratory values.
The various terms used to describe long excursion or
(09:12):
movement during quiet and maximal respiration are shown in
Figure 1 below. Next we get to figure one with a
famous diagram explaining long volumes in an adult male
measured with a spirometer during quiet breathing with one
(09:37):
maximum breath referring to the residual volume, inspiratory
reserve volume, functional residual capacity, vital
capacity, total long capacity, tidal volume, and expiratory
(10:00):
reserve volume. Kindly pause the recording and
take some time to go through this figure.
The tidal volume 500 mils multiplied by the respiratory
rate 14 breaths per minute is the minute volume. 7000 meals
(10:26):
per minute, that is TV Times RR is equals to MV.
Not all of the tidal volume takes part in respiratory
exchange, as this process does not start until the air or gas
(10:48):
reaches the respiratory bronchioles Division 17 of the
respiratory tree. Above this level, the Airways
are solely for conducting their volume, being known as the
anatomical Dead Space. The volume of the anatomical
(11:14):
Dead Space is approximately 2 mils per kilogramme, or 150 mils
in an adult, roughly 1/3 of the tidal volume.
The part of the tidal volume which does take part in
(11:35):
respiratory exchange multiplied by the respiratory rate is known
as the alveolar ventilation, which is approximately 5000
meals per minute. Let's take a step back and just
(11:55):
go through the standard volumes in Figure 1.
The standard long volumes, functional residual capacity,
2500 mills. Residual volume 1000 mills,
(12:21):
vital capacity, 5000 mills. Expiratory reserve volume 1500
mills, Inspiratory reserve volume 3000 mills, Tidal volume
(12:47):
500 mills and finally total longcapacity 6000 mills.
Let's continue. Functional residual capacity.
FRC is the volume of air in the lungs at the end of a normal
(13:15):
expiration. The point at which this occurs,
and hence the FRC value, is determined by a balance between
the inward elastic force forces of the lung and the outward
forces of the respiratory cage, mostly due to muscle tone.
(13:37):
FRC falls with lying, supine obesity, pregnancy and
anaesthesia, though not with age.
The functional residual capacityis of particularly importance to
anaesthetics because during apnea it is the reservoir to
(14:02):
supply oxygen to the blood. As it falls, the distribution of
ventilation within the lungs changes leading to mismatching
with pulmonary blood flow and ifit falls below a certain volume
that is the closing capacity, airway closure occurs leading to
(14:28):
a shunt resistance and compliance.
In the absence of respiratory efforts, the long will come to
lie at the point of the functional residual capacity.
(14:49):
Remember it is 2500 mills. To move from this position and
generate respiratory movement, 2aspects need to be considered
which oppose lung expansion and air flow and therefore need to
be overcome by respiratory muscle activity.
(15:14):
These are the airway resistance and the compliance of the lung
and chest wall resistance of theAirways.
Describes the obstruction to airflow provided by the conducting
Airways, resulting largely from the larger Airways, that is down
(15:36):
to division 6 to 7 + A contribution from tissue
resistance produced by friction as tissues of the lungs slide
over each other during respiration.
An increase in resistance resulting from airway narrowing,
(15:57):
such as bronchospasm, leads to obstructive Airways disease.
In obstructive Airways disease, it might be expected that
airflow should be improved by greater respiratory efforts,
that is, increasing the pulse gradient to overcome the
(16:19):
increase in Airways resistance. Whilst this is normally due and
true for inspiration, it is not necessarily the case during
expiration as the increase in intrapurial pressure may act to
(16:41):
compress Airways proximal to thealveoli, leading to further
obstruction with no increase in expiratory flow and air trapping
distally. This is shown in Figure 2 and
(17:01):
demonstrates why expiration is usually the major problem during
an asthmatic attack. Compliance denotes
distensibility, that is, stretchiness, and in a clinical
setting refers to the lung and chest wall combined being
(17:25):
defined as the volume change by unit pressure change, that is, V
/ P. When compliance is low, the
lungs are stiffer and more effort is required to inflate
the alveoli. Conditions that worsen
(17:49):
compliance, such as pulmonary fibrosis, produce restrictive
lung disease. Compliance also varies within
the lung according to the degreeof inflation as shown in Figure
2. Poor compliance is seen at low
(18:13):
volumes because of difficulty with initial lung inflation and
at high volumes because of the limits of chest wall expansion
with best compliance in the mid expansion range.
(18:37):
Next we get to Figure 2 explaining compliance.
The compliance curve showing compliance within the lung at
different levels of inflation atfunctional reserve capacity in
the young healthy individual. The AP CS are well inflated,
(18:58):
that is towards the top of the curve and therefore less
ventilated than the mid zones and bases which are on the lower
steeper part of the compliance curve.
Walk of breathing. Of the two barriers to
(19:22):
respiration, airway resistance and lung compliance, it is only
the first of these which requires actual work to be done
to overcome it. Airway resistance to flow is
present during both inspiration and expiration, and the energy
(19:45):
required to overcome it, which represents the work of
breathing, is dissipated as heat.
Although energy is required to overcome compliance in expanding
the lung, it does not contributeto the actual work of breathing
(20:07):
as it is not dissipated but converted to potential energy.
In the distended elastic tissues, some of this stored
energy is used to do the work ofbreathing produced by Airways
resistance during expiration. The work of breathing is best
(20:32):
displayed on a PROS on a pressure volume curve of 1
respiratory cycle, which shows the different pathways for
inspiration and expiration knownas hysteresis.
The total work of breathing of the cycle is the area contained
(20:56):
in the loop with high respiratory rates.
Faster air flow rates are required, increasing the
fictional forces frictional forces.
This is more marked in obstructive Airways disease and
(21:17):
such patients therefore generally minimise the work of
breathing by using a slow respiratory rate and large tidal
volumes. In contrast, patients with
restrictive lung disease, that is, poor compliance, reach the
(21:38):
unfavourable upper part of the compliance curve soon as the
tidal volume increases. The pattern of breathing seen in
such patients usually involves small tidal volumes and a fast
respiratory rate. Next we get to Figure 3,
(22:01):
explaining the work of breathing, shown in a longer
pressure volume, that is compliance curve surfactant.
Any liquid surface exhibits surface tension, A tendency for
(22:25):
the molecules on the surface to pull together.
This is why when water lies on the surface, it forms rounded
droplets. If the surface tension is
reduced, for example by adding asmall amount of soap, the
(22:46):
droplets collapse and the water becomes a thin film.
When a liquid surface is spherical, it acts to generate a
pressure within the sphere according to Laplace's law,
(23:07):
which is pressure is equals to two times surface tension
divided by the radius of the sphere.
The film of liquid lining the alveoli exhibits surface tension
in such a manner to increase thepressure in the alveoli with a
(23:29):
greater rise in small alveoli than in large ones.
Surfactant is a substance secreted by type 2 alveolar
epithelial cells which lowers the surface tension of this
respiratory surface liquid markedly, mainly consisting of a
(23:55):
phospholipid that is dipamitol lecithin.
It's physiological benefits are a reduction in the fluid leak
from pulmonary capillaries into the alveoli as the surface
tension forces. As the surface tension forces
(24:18):
act to increase the hydrostatic pressure gradient from capillary
to alveolus, an increase that isimprovement in overall lung
compliance and a reduction in this tendency for small alveoli
(24:38):
to empty into large ones, reducing the tendency for the
lung to collapse. Diffusion of oxygen.
The alveoli provide an enormous surface area for gas exchange
(25:00):
with pulmonary blood that is between 50 to 100 metre square
with a thin membrane across which gases must diffuse.
The solubility of oxygen is suchthat is diffusion across the
normal alveolar capillary membrane is an efficient and
(25:23):
rapid process. Under resting conditions, the
pulmonary capillary blood is in contact with the alveolus for
about 0.75 seconds in total and is fully equilibrated with
alveolar oxygen after only about1/3 of the way along this
(25:47):
'cause. If lung disease is present which
impairs diffusion, there is therefore still usually
sufficient time for full equilibration of oxygen when at
rest. During exercise, however, the
(26:09):
pulmonary blood flow is quicker,shortening the time available
for gas exchange, and so those with lung disease are unable to
oxygenate the pulmonary blood fully and thus have a limited
ability to exercise. For carbon dioxide, which
(26:34):
diffuses across the alveolar capillary membrane 20 times
faster than oxygen, the above factors are less liable to
compromise to compromise transfer from blood to alveoli,
(26:54):
ventilation, perfusion and shunt.
In an ideal situation, the ventilation delivered to an area
of lung would be just sufficientto provide full exchange of
oxygen and carbon dioxide, with the blood perfusing that area in
(27:20):
the normal setting, Whilst neither ventilation nor
perfusion is distributed evenly throughout the lung, their
marching is fairly good, with the bases receiving
substantially more of both than the A PCs.
(27:42):
Next we get to Figure 4, describing the distribution of
ventilation, that is V, and perfusion, that is Q in the
lung. Take a while to go through this.
For perfusion, the distribution throughout the lung is largely
(28:06):
due to the effects of gravity. Therefore, in the upright
position, this means that the perfusion pressure at the base
of the lung is equal to the meanpulmonary artery pressure, that
is 15 millimetres of mercury or 20 centimetres of water, plus
(28:30):
the hydrostatic pressure betweenthe main pulmonary artery and
lung base, that is approximately15 centimetres of water.
At the AP CS, the hydrostatic pressure difference is
subtracted from the pulmonary artery pressure, with the result
(28:53):
that the perfusion pressure is very low and may at times even
fall below the pressure in the alveoli, leading to vessel
compression and intermittent cessation of blood flow.
The distribution of ventilation across the lung is related to
(29:17):
the position of each area of thecompliance curve at the start of
a normal tidal inspiration. That is the point of the FRC.
Because the bases are on a more favourable part of the
compliance curve than the EP CS,they gain more volume change
(29:43):
from the pressure change appliedand thus receive a greater
degree of ventilation. Although the inequality between
bases and AP CS is less marked for ventilation than for
perfusion, overall there is still good V stroke Q matching
(30:07):
an efficient oxygenation of blood passing through the lungs.
Note that this traditional explanation of the relationship
between ventilation and perfusion has recently been
challenged. There is still increasing
evidence that physiological matching of ventilation and
(30:28):
perfusion, despite considerable apparent heterogeneity in both,
is achieved by a common pattern of asymmetric branching of the
Airways and blood vessels. Disturbance of this distribution
(30:51):
can lead to a VQ mismatching. C Figure 5.
For an area of low V stroke Q ratio, the blood flowing through
it will be incompletely oxygenated, leading to a
reduction in the oxygen level inarterial blood.
(31:16):
That is, hypoxemia providing some ventilation is occurring in
the area of low VQ. The hypoxemia can normally be
corrected by increasing the FI O2, which restores the alveolar
oxygen delivery to a level sufficient to oxygenate the
(31:38):
blood fully. Next we get to the ventilate.
Figure 5. Talking about the ventilation
stroke perfusion mismatch. Take a while to go through this
figure. VQ mismatch occurs very commonly
(32:03):
during anaesthesia because the functional residual capacity
falls, leading to a change in the position of the lung on the
compliance curve. The APCS therefore move to the
most favourable part of the curve while the bases are
(32:24):
located on a less favourable path at the bottom of the curve.
At the extremes of VQ mismatch, an area of lung receiving no
perfusion will have AVQ ratio ofInfinity and is referred to as
(32:47):
alveolar Dead Space which together with the anatomical
Dead Space makes up the physiological Dead Space.
Ventilating the Dead Space is ineffect wasted ventilation but is
(33:07):
unavoidable. So, just as a recap, Alvula
displays Dead Space plus anatomical Dead Space is equals
to the physiological Dead Space.In contrast, in an area of lung
(33:31):
receiving no ventilation owing to airway closure or blockage,
the VQ ratio will be 0 and the area will be designated as a
shunt. Blood will emerge from an area
of shunt with APO 2 Onyx unchanged from the venous level,
(33:55):
that is 5.3 kilopascals and produced marked arterial
hypoxemia. This hypoxemia cannot be
corrected by increasing the FIO 2 even to 1 as the area of shunt
receives no ventilation at all. The well ventilated parts of the
(34:21):
lung cannot compensate for the area of shunt because
haemoglobin is fully saturated at a normal PO2.
Increasing the PO2 of this bloodwill not increase the oxygen
content substantially in the case of shunt.
(34:44):
Therefore, adequate oxygenation can only be re established by
restoring ventilation to these areas using measures such as
physiotherapy, PEEP or CPAP, which clear blocked Airways and
(35:04):
reinflate areas of collapsed lung.
Because closing capacity that isCC increases progressively with
age and is also higher in neonates, these patients are at
particular risk during anaesthesia as the functional
(35:26):
residual capacity may fall belowclosing capacity causing airway
closure. A physiological mechanism exists
which reduces the hypoxemia resulting from areas of low VQ
ratio by producing local vessel constriction in these areas and
(35:52):
diverting blood to other beta ventilated parts of the lung.
These effects known as hypoxic pulmonary vasoconstriction.
HPV is mediated by unknown localfactors.
(36:16):
The protective action of HPV is,however, inhibited by various
drugs, including inhalational anaesthetic agents.
Control of respiration, anaesthesia effects respiratory
(36:38):
function in different ways. Knowledge of respiratory
Physiology is necessary to understand these effects.
Physiological control systems involving the nervous system
usually have 3 components. These are a central controlling
(37:03):
area, an afferent pathway and anefferent pathway.
The neurons, that is, nerve cells of the controlling area
integrate the information from other parts of the body and
(37:23):
produce a coordinated response. This response from the central
controlling area is carried to the various organs and muscles
along inferent pathways. The input to the central
controlling area is from the various sensors via the afferent
(37:47):
pathways. Central controlling area The
central controlling area for breathing, called the
respiratory centre, is in the lower part of the brain stem.
(38:08):
In the medulla oblongata. There are inspiratory neurons
which are active during inspiration and inactive during
expiration. Other neurons are active during
expiration but not inspiration. The expiratory neurons.
(38:35):
These two groups of neurons automatically maintain a
rhythmic cycling pattern of inspiration and expiration.
This automatic rhythm can be modified by afferent
information. Afferent supply can central
(39:04):
chemoreceptors. Chemoreceptors are cells that
respond to chemical stimuli. There are cells on the floor of
the front ventricle that is partof the brain stem that respond
to the acidity of the cerebrospinal fluid CSF, and the
(39:28):
output from these cells influences breathing.
The acidity of any fluid is measured by the pH.
This is related to the number ofhydrogen ions in the solution.
The normal pH of the body is 7.4.
(39:52):
A higher pH than this representsalkaline conditions in the body
with a lower hydrogen ion concentration.
Aph less than 7.4 represents acidic conditions with a higher
hydrogen or ion concentration. Aph.
(40:18):
Sorry. The cells in the floor of the
4th ventricle respond to the pH of the CSF.
An acidic CSF causes hyperventilation.
This is the reason for dyspnea with conditions such as diabetic
(40:40):
ketoacidosis. An alkaline CSF inhibits the
respiratory centre. Carbon dioxide in the blood can
rapidly diffuse across into the CSF, and there is a balance
(41:01):
between the level of carbon dioxide, hydrogen ions and
bicarbonate ions in the CSF. If the carbon dioxide in the
blood increases, for example following exercise, then the
carbon dioxide, hydrogen ion andbicarbonate ion concentrations
(41:24):
increase correspondingly in the CSF.
This increase in CSF acidity causes hyperventilation, which
lowers the carbon dioxide concentration in the blood.
A low blood carbon dioxide levelthat is hypocarbia has the
(41:48):
opposite effect and may occur, for example, following
controlled ventilation during anaesthesia.
This may delay the return of spontaneous breathing at the end
of surgery. Peripheral chemoreceptors.
(42:15):
The carotid and aortic bodies are small pieces of tissue that
contain chemoreceptors which responds to the oxygen and
carbon dioxide concentrations inarterial blood.
The carotid body is the more important of the two and is
(42:36):
situated at the division of the common carotid artery into the
external and internal carotid arteries.
In the neck. The aortic body is found on the
aortic arc. The information from the carotid
body is carried along the glossopharyngeal nerve that is
(43:01):
the 9th cranial nerve and the information from the aortic body
is along the vagus nerve that isthe 10th cranial nerve to the
respiratory centre. The output from the carotid body
is thought to provide information to allow immediate
(43:23):
regulation of breathing breath by breath by the respiratory
centre. In normal people, if the
arterial blood reaching the carotid body has a partial
pressure of oxygen of 10 kilopascals, that is 80
(43:43):
millimetres of mercury, or a carbon dioxide partial pressure
of more than approximately 5 kilopascals, that is 40
millimetres of mercury, then there is an immediate and marked
increase in breathing. These limits can be modified by
(44:06):
disease or age. For example, people with chronic
bronchitis may tolerate an increased concentration of
carbon dioxide or a decreased concentration of oxygen in the
blood. Brain breathing can be
(44:32):
influenced by other parts of thebrain.
We can all consciously breathe deeply and more rapidly, called
hyperventilation, and this can happen for example before
starting strenuous exercise. Intensely emotional situations,
(44:57):
for example distressing sites, will also cause
hyperventilation. Hyperventilation is also part of
the response to a massive blood loss.
This response is coordinated by the autonomic system in the
(45:18):
hypothalamus and the vasomotor centre in the brainstem lung.
There are various receptors in the lung that modify breathing.
Receptors in the wall of the bronchi respond to irritant
(45:41):
substances and cause coughing, breath holding, and sneezing.
In the elastic tissues of the lung and chest wall are
receptors that respond to stretch.
The exact function of these receptors is not fully
(46:05):
understood, but is thought to beresponsible for various reflexes
that have been discovered in laboratory studies of animals.
There are stretch responses thatoccur when the lung and chest
wall are distended and inhibit further inspiration.
(46:30):
This is an obvious safety mechanism to avoid
overdistension. Conversely, when the lung volume
is low, then there are opposite reflexes.
A small increase in lung size may stimulate stretch receptors
(46:52):
to cause further inspiration. This can sometimes be seen in
anaesthetized patients who have been given an opioid.
Spontaneous breathing may be absent or very low slow, but if
the patient is given a small positive pressure breath by the
(47:12):
anaesthetist, then inspiration is stimulated and the patient
takes a deep breath. This reflex may also have some
function in newborn babies just after delivery, when small
breaths may stimulate further inspiration.
(47:34):
There are also stretch receptorsin the blood vessels in the
lung. If these are stretched, as in
heart failure, the response is to hyperventilate.
The information from these receptors in the lung is carried
to the respiratory centre along the vagus nerve.
(48:00):
Inferent supply. The inferent nerves from the
respiratory centre pass down thespinal cord to the diaphragm,
intercostal muscles and accessory muscles of
respiration. In the neck, the diaphragm is
(48:25):
supplied by the phrenic nerve that is formed in the neck from
the spinal nerves C 3-4 and five.
The intercostal muscles are supplied by the segmental
intercostal nerves that leave the spinal cord between T1 and
(48:45):
T12. The accessory muscles in the
neck are supplied from the cervical plexus during normal
breathing. Inspiration is an active
muscular process. Expiration is passive and relies
(49:07):
on the natural elasticity of thetissues to deflate the lung.
The most important muscle for inspiration is the diaphragm.
Any disease that affects the inferent pathways from the
respiratory centre to C 3-4 and five and then the phrenic nerve
(49:31):
to the diaphragm may cause severe difficulty in breathing.
Trauma to the cervical cord above C3 is normally fatal for
this reason. Anaesthetic drugs and
(49:53):
respiration Opioid drugs such asmorphine or fentanyl depress the
respiratory centre response to hypercarbia.
These effects can be reversed bynaloxone.
(50:14):
Volatile anaesthetic agents depress the respiratory centre
in a similar fashion, although ether has less effect on
respiration than the other agents.
Volatile agents also alter the pattern of blood flow in the
lungs, resulting in increased ventilation, stroke, perfusion
(50:37):
mismatch and decreasing the efficiency of oxygenation.
Nitrous oxide has only minor effects on respiration.
The depressant effects of opioids and volatile agents are
(50:57):
additive, and close monitoring of respiration is necessary when
they are combined. When oxygen is not available,
respiration should always be supported during anaesthesia.
Non respiratory lung functions Whilst the main function of the
(51:26):
lung is for respiratory gas exchange, it has several other
important physiological roles including a reservoir of blood
available for circulatory compensation, a philtre for
circulating microaggregates, activation of angiotensin 2 from
(51:52):
angiotensin one by angiotensin, converting enzyme, inactivation
of several substances such as norepinephrine and bradykinin,
and an immunological function bysecreting immunoglobulin A into
(52:14):
bronchial mucus.
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