Download Expiration-Exhalation

Respiratory System
The body continually uses oxygen for metabolic reactions to release energy from
nutrients and produce ATP. These processes release carbon dioxide which must be
rapidly eliminated as build up of this gas can cause problems. The cardiovascular
and the respiratory systems work together to supply oxygen and remove carbon
dioxide. The respiratory system provided for gas exchange between air and blood
and it moves air to and from the exchange surfaces. The respiratory system also
participates in regulating pH, it contains receptors for smell, it filters inspired air
makes sounds and rids the body of some water and heat in exhaled air.
Anatomy
The respiratory system consists of the nose, pharynx, larynx, trachea, bronchi, and
lungs. These parts can be classified according to structure or to function.
Structurally there are two parts: an upper respiratory system and a lower
respiratory system. The upper system includes the nose, nasal cavity and pharynx.
The lower system includes the larynx, trachea, bronchi, and lungs.
There are also two function zones: the conducting zone and the respiratory zone.
The conducting zone consists of a series of interconnecting cavities, tubes both
outside and within the lungs. It includes the paths from the nasal cavity to the
terminal bronchioles; all rigid conduits for air to reach site of exchange. This
includes the nose, nasal cavity, pharynx, larynx, trachea, bronchi, bronchioles and
terminal bronchioles. This part of the respiratory tract warms, filters and moistens
air as it comes in. The respiratory zone consists of the tubes and tissues within the
lung that serve as the site of gas exchange. It consist of respiratory bronchioles,
alveolar ducts, alveolar sacs and alveoli.
The nose is the primary passage for air to enter system through the external naresnostrils. The external nares are made of hyaline cartilage and is lined by a mucus
membrane. On the undersurface are the external nares. Just inside the nares is the
nasal cavity (the internal part of the nose).This part of the nose has three functions:
it warms, moistens and filters air, it detects olfactory stimuli and it modifies
speech vibrations. Anteriorly the nasal cavity merges with the external nares and
posteriorly it communicates with the pharynx through two openings-the internal
nares. The cavity is divided into a larger, inferior respiratory region and a smaller,
superior olfactory region. The respiratory region is lined with ciliated
pseudostratified columnar epithelium containing goblet cells; it was once called the
respiratory epithelium.
The anterior part of the nasal cavity is called the vestibule. This space is made of
flexible tissue and contained hair or vibrissae which filters particles from air. The
nasal cavity is divided by a vertical partition-the nasal septum. Three shelves
formed by projections of the superior, middle and inferior nasal conchae extend
out of each lateral wall of the nasal cavity. These subdivide each side of the cavity
into a series of groovelike passageways-the superior, middle and inferior meatus.
A mucus membrane lines the cavity and its shelves. Olfactory receptors lie in the
respiratory region making up the olfactory epithelium. The roof is formed by the
ethmoid and sphenoid bones. The floor is called the palate. The soft palate extends
posterior to the hard palate. These are surrounded by the paranasal sinuses found
in each bone surrounding the cavity; these lighten the skull.
The nasal cavity leads into the pharynx, a funnel shaped tube about 13cm long. It
starts at the internal nares and continues to the cricoid cartilage of the larynx. The
wall is comprised of skeletal muscle and is lined with a mucus membrane. The
muscles are arranged in two layers-an outer circular and an inner longitudinal
layer. It has 3 anatomical regions-nasopharynx, oropharynx, laryngopharynx.
The superior part of the pharynx is the nasopharynx. It lies posterior to the nasal
cavity and extends to the soft palate. The posterior wall contains the adenoidsphayngeal tonsils. It is lined with ciliated pseudostratifed columnar epithelium. It
lies above the point where food enters; it is an air passage only. When we swallow
the soft palate and uvula move up closing off nasopharynx.
The oropharynx he intermediate part of the pharynx and lies posterior to oral
cavity. It extends from the soft palate inferiorly to the level of the hyoid bone and
is continuous with the oral cavity through fauces. It is both a food and an air
passage. It is lined with non-keratinized stratified squamous epithelium. The
palatine and lingual tonsils are found here.
The laryngopharynx is the inferior part of the pharynx. It begins at the hyoid bone
and opens into the esophagus posteriorly and the larynx anteriorly. It is a common
passage for air and food.
The larynx-voice box opens into the laryngopharynx and is continuous with the
trachea inferiorly. It provides an open airway and a switching mechanism to route
air and food into proper channels, it is also responsible for voice production. The
larynx onsists of 9 cartilages. The thyroid cartilage is a large, shield shaped
structure resulting from the fusion of 2 cartilage plates. The fusion is marked by
the laryngeal prominence--Adam’s Apple. Inferior to the thyroid cartilage is the
cricoid cartilage. 3 pairs of small cartilages form the lateral and posterior wallsarytenoid, cuneiform and corniculate. The arytenoids influence the postion and
the tension on the vocal folds-true vocal cords. The 9th cartilage is the epiglottis; it
is a flexible elastic cartilage which extends from posterior tongue to anterior rim of
thyroid cartilage and covers the glottis.
Below the larynx is the trachea or windpipe. The trachea is a tubular passageway
for air. It is found anterior to the esophagus. It is patent or open and is kept so by
16 -20 incomplete horizontal rings of c cartilages in its walls. The layers of the
trachea from deep to superficial are: mucosa, submucosa, hyaline cartilage and
adventia. The outer layer is made of a ciliated pseudostratified columnar
epithelium.
The trachea descends from the larynx into the mediastium where it divides into
right and left primary bronchi which enter the right and left lungs at a medial
depression-the hilus. The right and left primary bronchi are unequal in length and
diameter. The right one is wider, shorter and more vertical and therefore it is the
more common site for inhaled objects to lodge.
Upon entering the lungs the primary bronchi divide into the secondary (lobar)
bronchi; one for each lobe. The right lung as three lobes and the left one has two
lobes. The secondary bronchi branch to form smaller bronchi-tertiary (segmental)
bronchi. These break up into smaller bronchioles which branch into terminal
bronchioles. This is the end of the conducting zone. All of this branching looks
like a tree and is called the bronchial tree. Epithelium changes from ciliated
pseudostratified columnar in primary, secondary and tertiary bronchi to ciliated
simple columnar in bronchioles. Terminal bronchioles are lined with simple
cuboidal epithelium. As the branches get smaller and smaller less cartilage is found
in the walls. Each terminal bronchiole feeds into microscopic respiratory
bronchiole which are the thinnest, most delicate branches. These end in spongy,
air-filled sacs-alveoli where gas exchange occurs. Respiratory bronchioles connect
to individual and to multiple alveoli by alveolar ductsend at alveolar sacscommon chamber connected to multiple alveoli. The walls of the alveoli are
simple, squamous cells. There are two types: type I alveolar cells which are the
main sites of gas exchange and type II alveolar cells cells or Septal cells. These
secrete alveolar fluid which contains surfactant, mixture of phospholipids &
lipoproteins. It acts like a detergent and coats alveolar surfaces to reduce surface
tension. Surface tension is the attraction between water molecules at an air-water
boundary. Molecules of liquids are more strongly attached to each other than gas
which produces tension at a liquid’s surface and tends to collapse small bubbles.
Water is the main component of the film coating alveolar walls and acts to reduce
alveoli to their smallest size. Without surfactant alveoli would collapse.
Associated with the alveolar wall are alveolar macrophages or dust cells. These are
phagocytes that remove dust particles and other debris from the alveolar surface.
The Lungs
Each lung is enclosed by a double layered serous membrane-the pleural membrane.
The superficial layers is the parietal pleura and the layer that directly covers the
lung is the visceral pleura. Between these two layers is a space-pleural cavity
containing a small amount of fluid which reduces the friction between the two
membranes.
Respiratory Membrane
Exchange of O2 and CO2 between air spaces in the lung and blood takes place by
simple diffusion and flows from a higher to a lower concentration across the
alveolar and capillary walls. Together these form the respiratory membrane. The
respiratory membrane has four layers. From the alveolar air spaces to the blood
plasma: 1-Type I & Type II alveolar cells along with macrophages, 2-epithelial
basement membrane underlies the alveolar wall, 3- capillary basement membrane
which is often bound to the epithelial basement membrane, and 4- apillary
endothelium.
Respiratory Mucosa
The respiratory mucosa conditions air so that by the time it reaches alveoli foreign
particles and pathogens have been removed. Humidity & temperature have been
brought to acceptable limits. Respiratory mucosa lining the conducting path
consists of psuedostratified ciliated columnar epithelium and many goblet cells.
The goblet cells secrete mucous which helps to intercept and exclude solid matter
in air such as dust, pollen, bacteria, viruses. Particles hit the side wall and are
trapped in the mucus. Once particles have been sidelined by mucus, they have to
be removed and are carried out by cilia.
Respiratory Physiology
The process of gas exchange is called respiration which has three steps: pulmonary
ventilation, external respiration and internal respiration. Pulmonary ventilation is
breathing involving inspiration, taking air into the lungs and expiration, gas
exiting from the lungs. External or pulmonary respiration is the exchange of
gases between the alveoli of the lungs and the blood in the pulmonary capillaries
across the respiratory membrane. Internal or tissue respiration is the exchange of
gases between blood in the systemic capillaries and the tissue cells.
Pulmonary ventilation is mechanical and depends on volume changes in the
thoracic cavity. Volume changes cause pressure changes which cause gases flow
until pressure is equalized. To understand need to understand the physical
principles of gases it is important to learn a couple gas laws.
The relationship between pressure and volume is Boyle’s Law or the Ideal Gas
Law. This law says that when temperature is constant, the pressure of a gas varies
inversely with volume. P1V1=P2V2. P = pressure of gas-mm Hg, V = volumecubic mm. Gases conform to the shape of the container in which they are in and
always fill the container. For large volumes gas molecules are far apart and don’t
bump into each other very much resulting in a low pressure. When the volume is
reduced, the gas molecules compress and they bump into each other more often
causing the pressure to rise. In other words: decrease volume of gaspressure
increases; increase volume of gaspressure decreases.
Inhalation and exhalation involve changes in lung volumes which create pressure
changesmoving air into and out of the lungs. If we think of the thoracic cavity as
a gas filled box with one opening. Each lung is enclosed in a box bounded below
by the diaphragm and on the sides- by the chest wall and mediastium. The parietal
and visceral pleurae of the pleural cavity separated by a thin layer of pleural fluid
can slide past one another but are held together by the fluid between them which
makes the surface of the lungs stick to the inner chest wall and to the diaphragm.
Pressure Changes during Inhalation & Exhalation
Respiratory pressures are described relative to the atmospheric pressure;.
Atmospheric-Patm-pressure is the pressure exerted by the air surrounding the body.
At sea level Patm = 760mm Hg = 1 atm. For air to enter the lungs the pressure
inside the alveoli must become lower than the atmospheric pressure. Inhalation or
quiet inspiration results from contraction of the respiratory muscles- the
diaphragm and external intercostals. The diaphragm is innervated by the phrenic
nerve. When it contracts it flattens increasing the vertical diameter of the
thoracic cavity. It descends about 1 cm, produces a pressure difference of 1 3mmHg and causes inhalation of 500mls of air. During strenuous breathing the
diaphragm may descend 10cm producing a pressure difference of 100mg HG and
inhalation of 2- 3 L of air. Contraction of the diaphragm is responsible for 75% of
the air that enters the lung during quiet breathing. External intercostals elevate the
ribs and is responsible for 25% of the air entering the lungs during normal quiet
breathing.
Movement of the chest wall or the diaphragm changes the volume of the lungs.
Breathing makes the box bigger; movement of the rib cage upwardsincreases
depth and width of thoracic cavity; contraction of diaphragm moves it inferiorly
which increases volume of thoracic cavityalveolar pressure decreases-Pinside <P
outside air rushes in. Air moves in until P inside = P outside.
Pressures in the respiratory system are measured in air spaces of the lung called
alveolar pressure or intrapulmonary pressure and in the pleural fluid between the
parietal and visceral pleurae. This is called intrapleural or intrathoracic pressure.
As the volume of the lungs increase the intrapulmonary pressure drops to 758mm
Hg. Air flows into the lungs since pressure outside is greater than pressure inside.
Air continues to flow into alveoli until pressure inside equalizes with atmospheric
pressure. During this time intrapleural pressure fluid drops to -6mm Hg. The
intrapleural pressure is always subatmospheric (lower than atmospheric pressure).
Negative pressure is important because anytime the intrapleural pressure
equalizes with the intrapulmonary pressurelung collapses. Just before inhalation
this value is 4mm Hg less than atmospheric pressure or 756mm Hg. As the
diaphragm and external intercostals contract and the thoracic cavity increases the
volume of the pleural cavity increasing causing the intrapleural pressure to
decrease to 754mm Hg.
During deep forceful inhalations, accessory muscles increase the size of the
thoracic cavity more than the normal muscles of respiration. These include the
scalenes which elevate the 1st and second ribs, the sternocleidomastoids which
elevate the sternum and the pectoralis minors which elevate the third through the
fifth rib.
Expiration-Exhalation
Exhalation is breathing out. This movement is also due to pressure differences.
Pressure in lungs becomes greater than atmospheric pressure. Normal or quite
exhalation this process is passive; muscle contraction s are not needed. Exhalation
is due to the elastic recoil of the chest wall and the lungs. There are two forces that
contribute to this recoil: 1) elastic fibers that were stretched recoil and 2) surface
tension makes an inward pull. Exhalation begins when the inspiratory muscles
relaxthe diaphragm moves upward and the ribs move back to their original
position decreases volume of thoracic cavity and now P inside is greater (alveolar
pressure increases to 762mm Hg) than P outside and air is forced out. Forced
exhalation requires the contraction of accessory muscles such as the abdominal
muscles which move the ribs inferiorly and compresses the abdominal viscera
forcing the diaphragm to move up. Internal intercostals pull the ribs inferiorly.
The rate of airflow and the amount of effort needed for breathing are also
influenced by alveolar surface tension, compliance of the lungs and airway
resistance. Surface tension of alveolar fluid draws alveoli to their smallest
possible dimension. During breathing this must be overcome to expand the lungs
during inhalation. It also accounts for 2/3rds of the lungs’ elastic recoil which
decreases the size of the alveoli during exhalation. Surfactant works to decrease
surface tension.
Compliance refers to how much effort is required to stretch the lung and the chest
wall. It is an indication of the expandability of the lungs. Lower compliance
greater force is needed to fill and empty the lungs. High compliancelungs
expand easily. A decrease in compliance can be due to scar tissue in the lung, fluid
in lung, not enough surfactant, problem with moving the intercostals muscles.
Airway resistance is the resistance to air flow. Walls of bronchioles offer some
resistance to flow. Larger diameters have less resistance; therefore any condition
that narrows the walls of the bronchioles would increase resistance.
Breathing Types
Air moves due to pressure changes which are direct result of volume changes
which are due to muscle contractions. Quiet inspiration or eupnea (UP-Ne-uh)
refers to the normal pattern of breathing. Breathing can be shallow, deep or
combined. A pattern of shallow breathing is called costal breathing. A pattern of
deep breathing is called diaphragmatic breathing.
Pulmonary Volumes, Rates & Capacities
At rest a healthy adult averages 12 breaths/minute (respiratory rate) moving about
500mls of air into and out of the lungs. This volume is called the tidal volume
(TV). The total volume of air inhaled and exhaled each minute is called minute
volume (MV). It equals respiratory rate times tidal volume = RR X VT . 12 X 500
= 6000ml/minute. The device used to measure this volume of air is called a
spirometer or respirometer. In an adult about 70% of the VT actually reaches the
respiratory zone. The other 30% remains in the conducting pathways which is
called the anatomical ore respiratory. This means that all the MV is not used for
gas exchange.
Alveolar ventilation rate is the volume of air per minute that actually reaches the
respiratory zone. Anatomical dead space is about 150ml therefore 350ml of fresh
air goes to the alveoli. VA = RR X (TV – VD). 12 breaths/min X (500ml/breath –
150ml/breath) = 4200ml/min or 4.2L/min. This rate is a better indicator of
ventilation; it determines the rate of O2 delivery to alveoli.
Total volume of lungs can be divided into volumes and capacities. These values
are important in diagnosis. IRV or inspiratory reserve volume is the additional
amount of air that can be inspired beyond tidal volume. It differs significantly by
gender; lungs of males are larger ERV or expiratory reserve volume is the amount
of air that can be exhaled after normal expiration. RV or residual volume is the
amount of air left after strenuous expiration. This value cannot be directly
measured. It functions to keep alveoli open and prevents lung collapse. Part of RV
is called the minimal volume, the amount of air remaining when lungs collapse.
Lung capacities are the sum of 2 or more lung volumes. IC-inspiratory capacity is
the total amount of aire that can be inspired after tidal expiration = VT + IRV.
FRC-functional residual capacity = RV + ERV. VC-vital capacity-total amount of
exchangeable air = VT + IRV + ERV-amount of air that can be moved into or out
of respiratory system with one breath. TLC-total lung capacity-sum of all lung
volumes = VC + RV. FVC-forced vital capacity is the amount of gas expelled
when take deep breath-then forcibly exhale as maximally as possible..
Gas Exchange
The exchange of O2 and CO2 between pulmonary blood and alveolar air occurs due
to passive diffusion which is governed by two gas laws: Dalton’s Law of Partial
Pressure and Henry’s Law. Gas exchange occurs by diffusion due to
concentration gradients; the differences between O2 and CO2 concentrations which
are measured by partial pressures. The greater the differences in partial
pressuresthe greater the rate of diffusion.
Dalton’s Law of Partial Pressure states that each gas in a mixture exerts its own
pressure as if no other gases were present. This pressure if called it partial pressure
(Px). Air is a mixture of gases including N2, O2, CO2, Ar and water vapor.
Atmospheric pressure is the sum of all the gases present arising from the collision
of all molecules. At any time 78.6% of collisions involve N2; 20.9% involve O2.
Each gas contributes to total pressure in proportion to its relative abundance.
Partial pressure is directly proportional to the % of gas in a mixture. All partial
pressures added = total pressure exerted by a gas mixture =760mm Hg. PN2-parital
pressure nitrogen = 78.6 X 760 mm Hg-597 mm Hg. PO2 20.9 X 760 = 159 mm
Hg.
Henry’s Law states that the quantity of a gas that will dissolve in a liquid is
proportional to its partial pressure and it solubility at a given temperature. More
carbon dioxide is dissolved in plasma because its solubility is 24X that of oxygen.
External & Internal Respiration
External respiration or pulmonary gas exchange is the diffusion of O2 from air in
the alveoli to blood in the pulmonary capillaries and the diffusion of CO2 in the
opposite direction. External respiration in the lungs converts deoxygenated blood
into oxygenated blood. Each gas diffuses independently from the area where its
partial pressure is higher to the area where its partial pressure is lower. Oxygen
diffuses from alveolar air where the PP is 105mm Hg into the blood in pulmonary
capillaries where PO2 is 40 mm Hg. When O2 is diffusing from alveolar air into
deoxygenated blood CO2 is diffusing in the opposite direction. PCO2 of
deoxygenated blood is 45 mm Hg. PCO2 of alveolar air is 40 mm Hg. CO2 diffuses
from deoxygenated blood into the alveoli.
The left ventricle pumps oxygenated blood into the aorta and through the systemic
arteries to the systemic capillaries. Exchange of O2 and CO2 between systemic
capillaries and tissues cells is internal respiration or systemic gas exchange. PO2 of
blood in the systemic capillaries is 100 mmHg and in tissue cells it is 40mm Hg.
As oxygen diffuses out of the capillaries into the tissues the carbon dioxide
diffuses in the opposite direction. PCO2 of cells is 45 mm Hg in the systemic
capillary blood it is 40mm Hg. Tissues use O2 for metabolic activities & generate
CO2.
The rate of diffusion depends on several factors including the PP differences of the
gases, the surface area for gas exchange, the diffusion distance and the molecular
weights and solubility of the gases. There are large PP differences across
membranes. The larger the PP differencethe faster the diffusion. With exercise
and need these become larger. The distances are small; the capillary & alveolar
membranes are fused. The surface are for exchange is huge being 70 square
meters at the alveoli. Oxygen has a lower molecular weight than carbon dioxide. It
can be expected to diffuse across the respiratory membrane 1.2X faster. However
CO2 is 24X more soluble and the newt outward movement of CO2 occurs 20X
faster than inward oxygen diffusion
Gas Transport
O2 has limited solubility in blood. About 1.5% of inhaled O2 is dissolved in blood.
98.5% of oxygen in blood is bound to hemoglobin (Hb) in the red blood cells.
Every 100 ml of blood leaving alveolar capillaries carries about 20ml of O2. At
normal PO2 of alveoli-100ml of blood contains 0.3ml of O2. The amount bound to
Hb is 19.7ml.
Hemoglobin is made of 4 subunits-2 & 2ß globular protein chains. Each chain
has one heme group. Each heme has one ferrous iron. Each Fe can combine with
one O2therefore every Hb can carry 4 O2s. There are 280 X 106 Hb
molecules/RBC. Each RBC could carry a billion O2 molecules. The Fe-O2 bondis
weak and easily broken without altering Hb or O2.Hb + O2 HbO2 oxyhemoglobin. HbO2Hb-deoxyhemoglobin.
The most important factor that determines how much oxygen binds to Hb is P O2.
The higher the PO2 the more oxygen combines with Hb. The percent of heme units
containing a bound O2 at any given moment is Hb saturation. All Hb loaded with
O2100% saturation. If each Hb only had 2 oxygens bound it would be 50%
saturation. The relationship between the percent saturation of Hb & PO2 can be
shown in the O2-Hb dissociation curve. When PO2 is highHb binds with a large
amount of oxygen and is almost 100% saturated. When PO2 is low Hb is only
partially saturated. The graph is not linear; it is S-shaped. There is a steep slope
that flattens into a plateau. It is S shaped because hemoglobin’s subunits interact
so that during successive combination with O2 each combination facilitates the
next. By looking at the curve we can see that when PO2 is between 60 -100mmHG,
Hb is 90% or more saturated with oxygen. Blood picks up nearly a full load of
oxygen from the lungs even when the PO2 of alveolar air is as low as 60mmg Hg.
The curve explains why people can still perform well at high altitudes or when
they have certain cardiac or pulmonary diseases.
Other factors affect the affinity (tightness of bond) of Hb for O2. Certain factors
will shift the curve to the left (higher affinity) and some will shift the curve to the
right (lower affinity). These factors demonstrate how homeostatic mechanisms
adjust body activities to cellular needs. These factors make sense if one remembers
that metabolically active cells need oxygen, make carbon dioxide, generate heat
and make acid.
Hb & pH
Acidity (pH) is one factor that influences the Hb-O2 saturation curve. As acidity
increases and pH goes down the affinity of Hb for O2 decreases and the dissociates
more readily from Hb. Increasing acidity enhances oxygen unloading and when pH
decreases the entire O2-Hb dissociation curve shifts to the right. At any given PO2
Hb is less saturated with oxygen; this change is termed the Bohr Effect. The Bohr
effect works both ways. An increased H+ ion concentration causes O2 to unload
from Hb and the binding of O2 to Hb causes the unloading of H+ from Hb. The
explanation for this is that Hb acts as a buffer for H+ but when H+ bind to amino
acids in Hb they alter its structure slightly decreasing its oxygen carrying capacity
This lowered pH drives oxygen off of the Hb making more oxygen available for
tissue cells. By contrast elevated pH increases the affinity of Hb for O2 which
shifts the O2-Hb dissociation curve to the left.
Hb & CO2
Carbon dioxide also binds to Hb. As PCO2 increases Hb releases oxygen more
readily. PCO2 and pH are related. Low blood pH results from high CO2. In RBC,
carbonic anhydrase catalyzes the following reaction: CO2 + H20H2CO3-carbonic
acid. H2CO3; this is unstable and immediately dissociates H+ + HCO3- hydrogen
and bicarbonate ion. The rate of H2CO3 production increases with an increase in
CO2 in the blood or with PCO2. PCO2 increases as cells metabolize glucose during
glycolysis; they use O2. As H+ diffuse out of RBCdecreases pH of blood. When
the PCO2 decreases, the reaction goes from to the left; H+ go into RBCincreases
pH of blood.
Hb & Temperature
Unloading is increased by raising temperature. Lower temperaturesO2 binds
more to Hb. Exercisegenerate heatincreases temperature at tissuesmore O2
released when it is needed.
Hb & BPG
BPG-2,3 biphosphoglycerate is produced by RBC during glycolysis. It decreases
the affinity of Hb for oxygen. Therefore unloading is increased by raising BPG;
curve shifts to the right. BPG increases with thyroid hormone, GH, epi &
norepinephrine, androgens and high blood pH. All of these improve O2 delivery to
tissues. The amount of BPG generated drops as RBC age; used to determine the
age of blood. If it drops too low, O2 is irreversibly bound to Hb.
CO2 Transport
Each 100 mls of deoxygenated blood contains 53ml of gaseous Co2 . It is carried in
the blood in 3 ways: 1) dissolved in plasma-2 -7&; 2) bound to Hb in RBC-23%
transported as carbaminohemoglobin;Co2 attaches to the –NH2 groups (amino) of
histidine in Hb and 3) converted to carbonic acid-70%. CO2 + H2O H2CO3
carbonic acidH+ + HCO3- . Carbonic acid is unstable and dissociates to
hydrogen and bicarbonate ions. As blood picks ups Co2 , HCO3- accumulates. In
RBCs some HCO3- moves out into the blood down its concentration gradient. In
exchange for one HCO3- -one Cl- moves from the plasma into the RBC. This
maintains electrical neutrality and is called the chloride shift. The net effect is that
Co2 is removed from tissue cells and transported in the blood plasma as HCO3-. As
blood passes through pulmonary capillaries in the lungs these reactions are
reversed and Co2 is exhaled.
Control of Respiration
At rest about 200ml of oxygen is used each minute by body cells. During exercise
the use of oxygen typically increases 15-20 times. Cellular rates of absorption and
generation of gases must be matched by capillary rates of delivery and removal.
Both rates are identical to rate of O2 absorption and CO2 excretion at lungs. If they
become unbalanced, homeostatic mechanisms restore equilibrium. This involves:
changing blood flow and O2 delivery which is locally regulated and changing depth
and rate of respiration which is controlled at the brain’s respiratory centers.
Local Regulation
When peripheral tissues become active O2 demands increase, interstitial PO2
decreases and interstitial PCO2 increases. More O2 dissociates from Hb and more
CO2 is carried off. Local factors coordinate lung perfusion, blood flow to alveoli
with alveolar ventilation or airflow. Adjustments in alveolar blood flow and
bronchiole diameter occur automatically. Blood flows toward alveolar capillaries
directed to where PO2 is high-because alveolar capillaries constrict when local PO2
is low. Smooth muscle bronchiole walls respond to PCO2. Increased PCO2 relaxes
 increases local blood flowbronchiodilation. Reducedbronchioconstriction.
Respiratory Centers of the Brain
Respiratory control has both voluntary and involuntary components. Involuntary
centers regulate activities of respiratory muscles and control respiratory minute
volume by adjusting frequency and depth of pulmonary ventilation. Voluntary
control from cerebral cortical activity affects either output of respiratory centers
in the medulla or pons or motor neurons in the spinal cord that control respiratory
muscles.
There are three areas to the respiratory center one in the medulla and two in the
pons. The medullary rhymicity area is in the medulla control inspiration &
expiration, the pneumotaxic and apneustic areas are in the pons; these influence
rate and depth of ventilation.
The medullary rhymicity area’s function is to control the basic rhythm of
respiration. There is an inspiratory and an expiratory area. During quiet breathing
inhalation lasts about 2 secstimulates inspiratory muscles. Rib cage expands as
diaphragm contracts. During this time inhalation occurs. Nerve impulses generate
the basic rhythm of breathing. Even when all incoming nerve connections to the
inspiratory area are cut the neurons in this area are still rhymically discharging
impulses that cause inhalation.
At the end of the 2 seconds, the neurons stop firing and remain quiet for next 3
secondsinspiratory muscles relaxlung recoils. During this time expiration
occurs. The cycle repeats. Neurons in the expiratory area remain inactive during
quiet breathing.
During forced breathing nerve impulses from the inspiratory area activate the
expiratory area. Impulses from the expiratory area stimulates activate accessory
muscles-the internal intercostals and the abdominal muscles which decrease the
size of the thoracic cavity producing forceful exhalation..
Apneustic & Pneumotaxic Centers
The apneustic and pneumotaxic centers are located in the pons. These adjust output
of the medullary rhymicity centers and help to transition between inhalation and
exhalation. They regulate the respiratory rate and depth of respiration in response
to sensory stimuli or input from other brain centers.
The pneumotaxic centers is in the upper pons. It transmits inhibitory impulses to
the inspiratory area and helps turn off the inspiratory area before the lungs become
too full of air. Increased outputquickens respiration by shortening duration of
each inhalation; breathing rate is more rapid. Decreased outputslows respiratory
pace; depth of respiration increases because apneustic centers are also active.
The apneustic center sends stimulating impulses to the inspiratory area activating it
to produced prolonged inhalation. The result is long, deep inhalations.
Regulation of Respiratory Centers
The basic rhythm of respiration can be modified in response to impulses from other
brain regions, receptors in the peripheral nervous system and other factors.
It is possible to voluntarily alter one’s breathing. Inputs form the cerebral motor
cortex stimulate motor neurons to stimulate respiratory muscles bypassing medulla
centers. This is limited by the buildup of CO2 and O2. When PCO2 and H+ build up
the inspiratory center is stimulatednerve impulses are sent along the phrenic and
intercostals nerves to inspiratory musclesbreathing resumes-forced to inhale.
Nerve impulses from the hypothalamus and limbic system also stimulate the
respiratory center allowing emotional stimuli to alter respiration.
Respiratory Reflexes
The respiratory system functions to maintain the proper levels of CO2 and O2 and is
very responsive to changes in the level of these gases in body fluids. Sensory
neurons sensitive to chemicals in the blood are chemoreceptors. Central
chemoreceptors are found in or near the medulla in the CNS and respond to
changes in pH (H+ions) and PCO2 in cerebral spinal fluid (CSF). Peripheral
receptors are found in aortic bodies-in the wall of the aortic arch and in carotid
bodied found in the common carotid artery. These are sensitive to PCO2 , pH & PO2.
Changes in PCO2 affect ph. PCO2 increase-hypercapnia or hypercarbia. Rise in
arterial PCO2 almost immediately elevates CO2 levels in CSFpH decreases (H+
increase)excites central chemoreceptors stimulates respiratory
centersincreases depth and rate of breathing.
Peripheral chemoreceptors are also stimulated by high PCO2 and rises in H+ .
Peripheral but not central chemoreceptors respond also to lowered O2 levels. When
PO2 falls from 100mm Hg peripheral chemoreceptors are stimulated.
Chemoreceptors participate in negative feedback mechanism to regulate levels of
CO2, O2 and H+. Increases in CO2, and H+ and decreases in P O2 and H+ cause
chemoreceptors to send impulses to the inspiratory area of the brain to become
active and to increase the rate and depth of breathinghomeostasis is restored.
Rapid and deep breathing is hyperventilation. Eventually hyperventilation
hypocapnia or hypocarbia or low PCO2. In this case the central and perihpheral
chemoreceptors are not stimulatedimpulses are not sent to the brain and
therefore the inspiratory center sets its own moderate pace until CO2 accumulates
and the PCO2 rises to 40mm Hg.
Proprioceptors can also stimulate respiration. As soon as one begins to exercise the
rate and depth of breathing increase before there are changes in PO2, PCO2 or H+.
This is due to proprioceptors which stimulate the inspiratory area of the medulla.
Mechanoreceptor reflexes can also stimulate respiration. These are stretch
receptors or baroreceptors which are found in the walls of the bronchi and
bronchioles. They stretch in response to inflation of the lungs. When this happens
nerve impulses are sent over the vagus nerve to the inspiratory and the apneustic
areas. The inspiratory center is inhibited and the apneustic center is inhibited form
activating the inspiratory area and exhalation begins. This is called the HeringBreuer Reflex or the inflation reflex; it prevents over expansion of lung.