Download Respiratory System Physiology Dr. Amjed Hassan Al

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Document related concepts

Bag valve mask wikipedia, lookup

Transcript
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
Respiratory physiology
The study of respiratory physiology is important to medicine, because many of
the respiratory diseases (e.g., cystic fibrosis, asthma, emphysema, pulmonary
hypertension, and pneumonia) impact many of the subspecialties, from
pediatrics, to internal medicine, to surgery, and to geriatrics. The human lungs
are so efficiently designed that gas exchange can increase >20-fold to remove
carbon dioxide and to supply oxygen to tissues in order to meet the body’s
energy demands.
Lecture Outline





Functional anatomy
Ventilation
Gas exchange
Gas transport in blood
Regulation of ventilation
Functional anatomy
The respiratory system is composed of the conducting airways and the
respiratory airways.
Figure: respiratory system
Conducting and Respiratory Airways
1
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
The conducting airways include the nose, mouth, pharynx, larynx, trachea,
bronchi, bronchioles, and terminal bronchioles. As their name suggests, these
airways conduct air to the respiratory airways; they do not participate in gas
exchange.
The bronchi are > 1 mm in diameter and have cartilaginous rings that protect
them from collapsing during expiration. They are not embedded in the lung
parenchyma, so their diameter is not dependent on lung volume.
The bronchi branch to form bronchioles that are smaller in diameter and have
no supporting cartilage. They are embedded within lung parenchyma, and their
diameter expands and contracts with lung volume.
Figure: conductive zone
Innervation:
Smooth muscles innervated by autonomic nervous system:
- parasympathetic - muscarinic - bronchoconstriction
- sympathetic - beta2 - receptors – bronchodilation -mainly to adrenalin
The respiratory airways include the respiratory bronchioles (i.e., bronchioles
with alveoli in their walls; and alveolar ducts.
Alveoli: There are ~300 million alveoli in adult lungs, each being ~250μm in
diameter. Their walls are composed of a simple squamous epithelium,
2
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
primarily type I pneumocytes. Each alveolus is encased by pulmonary
capillaries, which are sandwiched between the lumens of adjacent alveoli.
The total surface area available for gas exchange is ~150 m2.
Alveoli first begin to appear on the respiratory bronchioles, marking the start of
the respiratory portion of the lung. These alveoli are isolated initially, then
become more numerous and are collected into sacs. Each sac has a central open
space, or alveolar duct, that is continuous with the lumen of its respiratory
bronchiole. The alveolar walls are composed of squamous epithelium and are
in direct contact with the pulmonary capillaries for gas exchange to occur.
Connective tissue with abundant elastic fibers is found throughout the branches
of the bronchial tree and the alveoli. These contribute substantially to the
elastic recoil of the lungs during expiration.
Figure: respiratory zone
Removal of Inhaled Particles
With its surface area of 50 to 100 square meters, the lung presents the largest
surface of the body to an increasingly hostile environment. Various
mechanisms for dealing with inhaled particles have been developed.
Large particles are filtered out in the nose. Smaller particles that deposit in the
conducting airways are removed by a moving staircase of mucus that
3
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
continually sweeps debris up to the epiglottis, where it is swallowed. The
mucus, secreted by mucous glands and also by goblet cells in the bronchial
walls, is propelled by millions of tiny cilia, which move rhythmically under
normal conditions but are paralyzed by some inhaled toxins.
The alveoli have no cilia, and particles that deposit there are engulfed by large
wandering cells called macrophages. The foreign material is then removed
from the lung via the lymphatics or the blood flow. Blood cells such as
leukocytes also participate in the defense reaction to foreign material.
Pressures in the lungs
To understand the mechanics of ventilation and airflow during breathing, it is
necessary to review the pressure in the lungs.
– Intra-pleural pressure is the pressure in the intra-pleural space.
– Alveolar pressure is the pressure within the alveoli.
– Trans-pulmonary pressure is alveolar pressure minus intra-pleural
pressure.
Intra-pleural pressure is always less than alveolar pressure; therefore, transpulmonary pressure is always positive. It is the positive trans-pulmonary
pressure that keeps the lungs inflated (like a balloon) against the chest wall.
Pleural Pressure and Its Changes
Pleural pressure is the pressure of the fluid in the thin space between the lung
pleura and the chest wall pleura. The normal pleural pressure at the beginning
of inspiration is about –5 centimeters of water, which is the amount of suction
required to hold the lungs open to their resting level. Then, during normal
inspiration, expansion of the chest cage pulls outward on the lungs with greater
force and creates more negative pressure, to an average of about –7.5
centimeters of water.
4
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
Alveolar Pressure
Alveolar pressure is the pressure of the air inside the lung alveoli. When the
glottis is open and no air is flowing into or out of the lungs, the pressures in all
parts of the respiratory tree, all the way to the alveoli, are equal to atmospheric
pressure, which is considered to be zero reference pressure in the airways—that
is, 0 centimeters water pressure. To cause inward flow of air into the alveoli
during inspiration, the pressure in the alveoli must fall to a value slightly below
atmospheric pressure (below 0). during normal inspiration, alveolar pressure
decreases to about –1 centimeter of water. This slight negative pressure is
enough to pull 0.5 liter of air into the lungs in the 2 seconds required for
normal quiet inspiration.
During expiration, opposite pressures occur: The alveolar pressure rises to
about +1 centimeter of water, and this forces the 0.5 liter of inspired air out of
the lungs during the 2 to 3 seconds of expiration.
Trans-pulmonary Pressure: It is the pressure difference between that in the
alveoli and that on the outer surfaces of the lungs, and it is a measure of the
elastic forces in the lungs that tend to collapse the lungs at each instant of
respiration, called the recoil pressure.
Figure: change in pressure during inspiration and expiration
5
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
Ventilation
Ventilation (breathing) is the process by which air enters and exits the lungs.
Respiration is the overall term for ventilation, gas exchange, and utilization in
cells.
Mechanics of Ventilation
Ventilation occurs in a cyclical manner with alternating inspiratory and
expiratory phases.
Inspiration
Inspiration is an active process and is principally mediated by the diaphragm
during quiet breathing.
– Contraction of the diaphragm enlarges the chest cavity, reducing intra-pleural
pressure. This increases the trans-pulmonary pressure and expands the lungs .
Minimal movement of the diaphragm (a few centimeters) is sufficient to move
several liters of gas.
– The external intercostal and accessory muscles are not necessary for resting
respiration, but they contribute substantially to deep respiration during exercise
and respiratory distress.
When the diaphragm moves to the inspiratory position, the ribs are elevated by
the intercostal muscles (chiefly the external intercostals) and scalene muscles.
Because the ribs are curved and directed obliquely downward, elevation of the
ribs expands the chest transversely (toward the flanks) and anteriorly.
Meanwhile, the diaphragm leaflets are lowered by muscle contraction causing
the chest to expand inferiorly. These processes result in overall expansion of
the thoracic volume.
Expiration
Expiration is a passive process during quiet breathing. When the diaphragm
relaxes, air is expelled from the lungs due to the elastic recoil of the lung–chest
wall system. Active expiration (using muscles of expiration) occurs during
exercise or in obstructive lung disease.
6
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
When the diaphragm moves to the expiratory position , the chest becomes
smaller in all dimensions, and the thoracic volume is decreased. This process
does not require additional muscular energy. The muscles that are active during
inspiration are relaxed, and the lung contracts as the elastic fibers in the lung
tissue that were stretched on inspiration release their stored energy, causing
elastic recoil. For forcible expiration, however, the muscles that assist
expiration (mainly the internal intercostal muscles) can actively lower the rib
cage more rapidly and to a greater extent than is possible by passive recoil
alone.
During heavy breathing, however, the elastic forces are not powerful enough to
cause the necessary rapid expiration, so that extra force is achieved mainly by
contraction of the abdominal muscles, which pushes the abdominal contents
upward against the bottom of the diaphragm, thereby compressing the lungs.
Muscles of respiration:
All the muscles that elevate the chest cage are classified as muscles of
inspiration, and those muscles that depress the chest cage are classified as
muscles of expiration. The most important muscles that raise the rib cage are
the external intercostals, but others that help are the (1) sternocleidomastoid
muscles, which lift upward on the sternum; (2) anterior serrati, which lift many
of the ribs; and (3) scaleni, which lift the first two ribs.
The muscles that pull the rib cage downward during expiration are mainly
the (1) abdominal recti, which have the powerful effect of pulling downward
on the lower ribs at the same time that they and other abdominal muscles also
compress the abdominal contents upward against the diaphragm, and (2)
internal intercostals.
7
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
External Respiration
Internal Respiration
Physical Properties of the Lungs
1.Compliance.
2.Elasticity.
3.Surface tension.
1.Compliance of the respiratory system
Lung Compliance
Lung compliance expresses the dispensability of the lungs, that is, how easily
the lungs expand when trans-pulmonary pressure increases. It is expressed by
the following equation:
C = ΔV/ΔP
8
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
where
C = lung compliance
ΔV = increase in lung volume (mL)
ΔP = increase in trans-pulmonary pressure (mm Hg).
– Compliance is inversely related to stiffness.
– Compliance is inversely related to the elastic recoil, or elastance, of the lung.
Recoil causes the lungs to return to their previous volume when stretching
ceases following an increase in trans-pulmonary pressure. It is mediated by
surface tension in the alveoli and by elastic fibers in the lung connective tissue.
Changes in lung compliance in disease states
– Lung compliance is decreased in pulmonary fibrosis because the interstitium
surrounding the alveoli becomes infiltrated with inelastic collagen.
– Lung compliance is increased in emphysema because many small alveoli are
replaced by fewer but larger coalesced air spaces that have less elastic recoil.
– Lung compliance is normal in asthma.
2.Elasticity:
It means tendency to return to initial size after distension. This occurs due to
the high content of elastin proteins present in the lung walls which is very
elastic and resist distension. Elastic tension increases during inspiration and is
reduced by recoil during expiration.
most of elastin proteins present in the lung walls which is very elastic and resist
distension. Elastic tension increases during inspiration and is reduced by recoil
during expiration.
3.Surface Tension in the Alveoli
Surface tension is due to the cohesive forces between water molecules at the
air–water interface in the alveoli of lungs. It acts to contract the alveoli and is a
major contributor to the force of elastic recoil of the lung.
9
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
If there were no opposing force, surface tension would cause the alveoli to
collapse (atelectasis).
However, the collapsing force is opposed by trans-pulmonary pressure, which
is always positive, allowing the alveoli to remain open.
However, surface tension is reduced by pulmonary surfactant, and the
reduction is greater in small alveoli than in larger ones because small alveoli
concentrate the surfactant. Thus, the increased tendency to collapse because of
small radius is just balanced by a greater reduction in surface tension.
Surfactant
Surfactant is a complex substance, consisting of proteins and phospholipids
(mainly dipalmitoyl lecithin), that is produced in type II pneumocytes. It lines
alveoli and lowers surface tension by the same mechanism as detergents and
soaps (i.e., it coats the water surface and reduces cohesive interactions between
water molecules).
As an extension of its role in lowering surface tension, surfactant also produces
the following effects:
– It increases compliance at all lung volumes, which allows for easier lung
inflation and greatly decreases the work of breathing.
– It reduces the otherwise highly negative pressure in the interstitial space,
which reduces the rate of filtration from pulmonary capillaries. This assists in
maintaining lungs without excessive water.
Failure of surfactant production and/or excessive surfactant breakdown occurs
in neonatal respiratory distress syndrome (RDS).
Effect of Alveolar Radius on the Pressure Caused by Surface
Tension
The pressure generated as a result of surface tension in the alveoli is inversely
affected by the radius of the alveolus, which means that the smaller the
alveolus, the greater the alveolar pressure caused by the surface tension. Thus,
10
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
when the alveoli have half the normal radius (50 instead of 100 micrometers),
the pressures noted earlier are doubled. This is especially significant in small
premature babies, many of whom have alveoli with radii less than one quarter
that of an adult person.
Further, surfactant does not normally begin to be secreted into the alveoli until
between the sixth and seventh months of gestation, and in some cases, even
later than that. Therefore, many premature babies have little or no surfactant in
the alveoli when they are born, and their lungs have an extreme tendency to
collapse, sometimes as great as six to eight times that in a normal adult person.
This causes the condition called respiratory distress syndrome of the newborn.
It is fatal if not treated with strong measures, especially properly applied
continuous positive pressure breathing.
The work of inspiration can be divided into three fractions: (1) that required to
expand the lungs against the lung and chest elastic forces, called compliance
work or elastic work; (2) that required to overcome the viscosity
of the lung and chest wall structures, called tissue resistance work; and (3) that
required to overcome airway resistance to movement of air into the lungs,
called airway resistance work.
Airway Resistance
Resistance is inversely proportional to the airway radius to the fourth power,
small changes in diameter cause large changes in resistance.
– The large airways offer little resistance to airflow. The small airways
individually have high resistance, but their enormous number in parallel
reduces their combined resistance to a small value. Therefore, the sites of
highest resistance in the bronchial tree are normally in the medium airways.
Regulation of Airway Resistance:
Airway resistance is primarily regulated by modulation of airway radius by the
parasympathetic and sympathetic nervous systems.
11
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
– Parasympathetic nervous system: Vagal stimulation releases acetylcholine
that acts on muscarinic (M3) receptors in the lungs, leading to
bronchoconstriction. This increases the resistance to airflow.
– Sympathetic nervous system: Postganglionic sympathetic nerves release
norepinephrine that act on β2 receptors, leading to broncho-dilation. This
decreases the resistance to airflow
Lung Volumes and Capacities
– Lung volumes are a way to functionally divide volumes of air that occur
during different phases of the breathing cycle. They are all measured by
spirometry, except for residual volume.They vary with height, sex, and age.
– Lung capacities are the sums of two or more lung volumes.
– Tidal, inspiratory, and expiratory reserve volumes and inspirational and vital
capacities are used in basic pulmonary function tests.
Lung Volumes
– Tidal volume (TV) is the volume of air that moves in or out of the lungs
during one normal, resting inspiration or expiration.
– Inspiratory reserve volume (IRV) is the volume of air that can be inspired
beyond a normal inspiration.
– Expiratory reserve volume (ERV) is the volume of air that can be expired
beyond a normal expiration.
– Residual volume (RV) is the volume of air left in the lungs and airways after
maximal expiration.
Lung Capacities
– Inspirational capacity (IC) is the maximum volume of air that can be
inspired with a deep breath following a normal expiration. It is the sum of TV
and IRV.
12
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
– Functional residual capacity (FRC) is the volume of the lungs after passive
expiration with relaxed respiratory muscles. It is the sum of ERV and RV.
– Vital capacity (VC) or forced vital capacity (FVC): is the maximum
volume of air that can be expired in one breath after deep inspiration. It is the
sum of TV, IRV, and ERV.
– Total lung capacity (TLC) is the total volume of air that can be contained in
the lungs and airways after a deep inspiration. It is the sum of all four lung
volumes: TV, IRV, ERV, and RV.
Note: TLC and FRC cannot be measured by spirometry because residual
volume is needed for their calculation.
Forced Expiratory Volume (FEV1) is the volume of air that can be forcibly
expired in the first second following a deep breath.
It is usually > 70% of the FVC (FEV1/FVC > 70%).
– In obstructive lung disease (e.g., asthma and COPD), FEV1
is reduced proportionally more than FVC; therefore, FEV1 /FVC < 70%.
– In restrictive lung disease (e.g., fibrosis), both FEV1 and FVC are reduced.
This means that FEV1 /FVC is normal or increased.
Figure: old spirometry technique
13
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
Figure: lung volumes and capacities
Dead Space
Dead space is volume within the bronchial tree that is ventilated but does not
participate in gas exchange.
– Anatomical dead space is the volume of the conducting airways (pharynx,
trachea, and bronchi) that do not contain alveoli and therefore cannot
participate in gas exchange. It is ~150 to 200 mL.
– Physiological dead space is the total volume of the bronchial tree that is
ventilated but does not participate in gas exchange.
The total volume exhaled is the forced vital capacity (FVC), and the volume
exhaled in the first second is the forced expiratory volume (FEV1).
14
Respiratory System Physiology
Dr. Amjed Hassan Al-Juboory
lecture 1
– In healthy lungs, physiological dead space is approximately equal to
anatomical dead space.
However, physiological dead space may be increased in lung diseases where
there are mismatches between ventilation (V) and perfusion (pulmonary blood
flow [Q]).
– Physiological dead space can be calculated using Bohr’s equation. This
calculation assumes that the partial pressure of CO2
(Paco2) in the alveoli is the same as that in systemic arterial blood.
Ventilation Rate
Minute ventilation refers to the total ventilation per minute. It is expressed as
Minute ventilation = TV × breaths/min
Alveolar ventilation refers to ventilation of alveoli that participate in gas
exchange per minute. It is expressed as Alveolar ventilation = (TV –
physiological dead space) × breaths/min.
15