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Respiratory Physiology


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Title: Respiratory Physiology

Breakdown of Topics in Respiratory Physiology
Ventilation, Gas Exchange, Control of Respiration
Respiratory Physiology
Functions of the Respiratory System
  • Respiration
  • Acid-base balance
  • Enabling vocalization
  • Defense against pathogens and foreign particles
  • Route for water and heat losses

General Concepts of Respiration
  • Ventilate bring the oxygen to the blood
  • Gas exchange diffusion of gasses from alveoli
    into blood then gasses go to/from erythrocytes
    to /from Hemoglobin
  • O2 utilization Mitochondria need the oxygen to
    make ATP (cellular respiration)

  • Ventilation is the process of bringing air into
    and out of the lungs.
  • Lungs are the only organs that do not have smooth
    muscle in them. They are just elastic tissue.
  • The lungs cannot inflate on their own. They need
    to be tethered to muscles in order to get volume
    changes, which causes pressure changes, which
    regulate air flow.
  • There are pressure gradients from the partial
    pressures of gasses. If the partial pressure of a
    gas is increased, the concentration of that gas
    increases, too.
  • Your lungs also contain millions of macrophages,
    so they are a good line of defense against
    pathogens. They also get rid of the dust and
    other debris that accumulates in the lungs.
  • They are also a route of heat and water loss.
    When you exhale, you lose water vapor and heat.
    90 of the heat lost from your body is from

Gas Exchange
  • In the lungs, oxygen moves into the blood, driven
    by pressure gradients, which are similar to
    concentration gradients.
  • Oxygen will diffuse down its concentration
    gradient (from the lungs, into the plasma, and
    into the cells) while CO2 moves down its
    concentration gradient (from the cells, into the
    plasma, and into the lungs).
  • These two gas exchanges are called external

Oxygen Utilization
  • When oxygen enters the cells, some of it enters
    the mitochondria, which uses oxygen as an
    electron acceptor (the mitochondria places
    hydrogen ions on the oxygen and turns it into
    water). This excess water leaves the cell and
    enters the tissues.
  • The removal of oxygen from the plasma and the
    addition of water in the tissues creates a
    driving force (known as the Starling principle)
    to continuously draw oxygen into the tissues,
    since the water in the tissues has diluted the
    number of particles there, and oxygen, as a
    particle, will be sucked into the tissues.
  • The gas exchange that occurs at the tissue
    capillary beds is called internal respiration.
  • The actual use of oxygen as a final electron
    acceptor(during a process called oxidative
    phosphorylation) is called cellular respiration.

General Concepts Airway Anatomy
Surface area 70 sq meters- each lung (size of a
large lecture hall)! Barrier/ thickness to
diffusion 0.2 microns
Carbon Monoxide
  • This is an odorless, colorless gas from
    incomplete burring of fuels.
  • Carbon monoxide binds to hemoglobin 200x more
    strongly than oxygen, so it drives the O2 from
    the hemoglobin, and attaches in its place and
    stays there. Carbon monoxide decreases the amount
    of oxygen that can be transported by hemoglobin
  • The person dies from suffocation it makes the
    lips cherry red.
  • Cyanide poisoning kills in the same way, but the
    lips are blue (cyanosis).

CO2 Transport
  • When oxygen is on the hemoglobin molecule, it is
    called oxyhemoglobin.
  • Dissociation of oxyhemoglobin is when the oxygen
    is released and enters the tissues.
  • This dissociation increases as the pCO2 levels
  • In other words, when the carbon dioxide levels
    rise, oxygen will jump off the hemoglobin and
    into the tissues. Therefore, the most effective
    stimulus to the respiratory center is an increase
    in pCO2.
  • The waste product of cellular respiration is
    carbon dioxide.
  • CO2 will then attach onto the hemoglobin and be
    taken to the lungs to be expelled.

CO2 Transport
  • CO2 is carried to the lungs on the hemoglobin,
    after the oxygen has left to enter the tissues.
  • The carbon dioxide reacts with water in the RBC
    to form carbonic acid, which then breaks apart
    into a hydrogen ion (which lowers blood pH) and a
    bicarbonate ion (which raises blood pH).
  • CO2 H2O ? H2CO3 ? H
  • This reaction is reversible, and would go mainly
    to the right in the tissues and to the left in
    the lungs.
  • CO2 is transported in the blood predominately in
    the form of bicarbonate.
  • The number of H ions in the blood depends partly
    on the amount of CO2 in the blood. The more CO2
    in the blood, the more H in the blood, which
    makes the blood acidic. If the blood is too
    acidic, bicarbonate ions are absorbed to raise
    the pH. If the blood is to alkaline, bicarbonate
    ions are excreted by the kidneys.

Respiratory System Contribution to pH Balance in
the Blood
  • If a person has excess H ions in the blood
    (acidosis), they will breathe more rapidly.
  • If the person has an airway obstruction (such as
    asthma), they cannot exhale the excess CO2.
  • Because the H are building up, the carbonic acid
    will also build up, causing a drop in pH
    (acidosis) in the blood.
  • Enzymes in the body cannot work outside of their
    optimal pH range, so chemical reactions come to a
  • Hyperventilation results in too little CO2 in the
    blood, so the person has a high pH (alkalosis),
    which also denatures enzymes.

Control of Respiration
  • Changes in lung volume, and thus ventilation, are
    dependent upon the change in thoracic cavity
  • Alterations in the space inside the thoracic
    cavity are the result mainly of the contraction
    of the diaphragm, intercostal muscles.
  • These muscles are innervated by neurons in the
    respiratory centers of the brain stem (medulla
    and pons).

Respiratory Centers Medulla oblongata and Pons
  • Pons (Pneumotaxic Center)
  • decreases respiratory rate
  • Medulla
  • Dorsal respiratory group
  • Increases inspiration rate
  • Ventral Respiratory Group
  • Inactive during quiet respiration
  • Active during forced respiration

Figure 41-1 Guyton Hall
  • Carbon Dioxide, Hydrogen Ions
  • Central chemosensitive area of medulla senses
    levels in CSF
  • Oxygen
  • Peripheral chemoreceptors sense oxygen levels in
  • Aortic chemoreceptors (CN X)?
  • Carotid chemoreceptors (CN IX)?

Respiratory Chemoreceptors
  • In the cardiovascular lecture, we learned about
    baroreceptors detecting blood pressure in the
    aortic arch and carotid sinus.
  • The respiratory system has chemoreceptors in
    those areas, too. They function to detect the O2,
    CO2, and pH levels of the blood.
  • The medulla oblongata also has chemoreceptors
    that monitor pH. This information is sent to the
    other parts of the respiratory centers (pons and
    other areas in the medulla oblongata) to allow
    them to alter breathing rate to maintain proper
    blood pH.

Control of Respiration
  • Relaxed breathing only requires the diaphragm to
    contract for inspiration, and for the diaphragm
    to relax for expiration.
  • Forced breathing requires the diaphragm plus
    muscles that raise and lower the ribs (external
    intercostals for inspiration, internal
    intercostals for expiration).
  • The respiratory centers are most sensitive to the
    level of CO2 in the blood, rather than the levels
    of oxygen.

Control of Gas at Cellular Level
  • The flow of blood through capillaries is
    controlled by sphincters on the arterioles and
    capillary beds to adjust the amount of blood
    flowing to particular tissues.
  • Cells and tissues that are undergoing increased
    aerobic activity have less oxygen and more CO2,
    lower pH, and increased temperature.
  • When CO2 levels in the tissues are too high, the
    smooth muscle sphincters relax to allow more
    blood flow to increase gas exchange.

Inspiration (inhalation) Expiration (exhalation)
Normal inhalation, normal exhalation Forced
inhalation, forced exhalation
  • Concepts
  • Pressure gradient created by volume changes
    (Boyles Law)
  • Anatomy of lung and chest wall

Inhalation and Exhalation vs. Force
  • Ventilation requires ATP during inhalation, but
    normal exhalation does not require ATP.
  • Some people with respiratory problems need to
    work at exhalation as well by using skeletal
    muscle, and this means that they need to use more
    ATP. Lungs are not muscular structures. They
    need the skeletal muscles in the thoracic cage to
    change the thoracic volume, which changes the
    pressure gradients.
  • Air flows from high pressure to low pressure.

  • Boyle's Law P1V1P2V2
  • Pressure and volume are inversely related (if
    other variables are kept constant.)

Boyles Law assumes normal circumstances, not a
person who is in high altitude or who has
variation in body temperature.
Air Pressure in Lungs
  • Every time a molecule strikes the wall of a
    container, it causes pressure. In a larger
    container with fewer molecules, it takes a while
    to strike the wall randomly, so there is less
  • The number of impacts on a container wall is the
  • The lungs must have a volume change to create a
    pressure change, which is required to have air
    move into and out of the lungs.

Air Pressure in Lungs
  • The diaphragm is the muscle that mostly
    contributes to the volume change. When it
    contracts, it pulls downward, and the volume of
    the thoracic cavity increases.
  • The external intercostals elevates the ribcage,
    giving the lungs more room, so they also increase
    the lung volume.
  • Those two muscles cause increased volume.

Air Pressure in Lungs
  • Because the lungs are tethered to the thoracic
    cavity, when your chest wall expands, your lungs
    expand with it. The lungs are stuck to the chest
    wall because the serous fluid in the pleural
    cavity makes the lungs stick to the chest wall
    like two pieces of wet glass stuck together.
  • When the lungs expand, their volume expands. That
    means there is less pressure in the lungs than
    there is in the outside air. Since air moves from
    high to low pressure, air flows into the lungs.
  • As air flows in, the alveoli expand, so the
    volume in each air sac expands, so the pressure
    in the alveoli lowers. Air in the conducting
    passages (bronchi) is at higher pressure, so it
    will move from high to low pressure areas.
    Therefore, air will move into the alveoli.

Air Pressure in Lungs
  • Air has weight atmospheric pressure is 760 mmHg
    at sea level (much less weight and pressure at
    high altitudes).
  • Since air will flow from higher pressure to lower
    pressure areas, to get the air to flow into our
    lungs, we need to have a lower pressure in our
  • We can decrease the pressure in our lungs by
    expanding the volume. As we expand the volume of
    our thoracic cavity (taking a breath), the
    pressure in the lungs drops, and air flows into
    the lungs.
  • It is a small pressure difference, but it is
    enough to get 500 ml of air to come into your
  • At higher altitudes, even though the amount of
    oxygen is the same (21) there is less air
    pressure. At 8,000 feet in elevation, there is ¼
    less pressure. This makes it harder to breathe.
  • When you exhale, you simply relax the muscles,
    and if the lungs are not being pulled open any
    more, the elastic tissue there will recoil,
    making the lung volume smaller, so the pressure
    there increases.

Lung Compliance
  • Lung Compliance is how much the lung volume
    changes when the pressure changes.
  • Compliance can be considered the opposite of
  • A low lung compliance would mean that the lungs
    would need a greater than average change in
    pressure to change the volume of the lungs.
    Instead of needing only 10 mmHg pressure
    difference between the outside air and the lungs,
    would now need a 20 mm difference.
  • A high lung compliance would indicate that little
    pressure difference is needed to change the
    volume of the lungs.
  • More energy is required to breathe in a person
    with low lung compliance. Persons with low lung
    compliance due to disease therefore tend to take
    shallow breaths and breathe more frequently.

Gases move down pressure gradients
P atm 760 torr
Flow Rule Patm Palv Resistance
How are the pressure gradients changed? According
to Boyles law we will need to create volume
p alveolar 758 torr
Air moves from high to low pressure
Air Pressure in Lungs
  • We are looking at two types of air pressures
    atmospheric pressure, and the pressure of air
    deep in the lungs, called the alveolar
    (pulmonary) pressure.
  • As long as there is a difference in pressure
    between these two, there will be a pressure
    gradient, and air will flow.
  • If they equal each other (such as during a
    punctured lung, called a pneumothorax), air will
    not flow.

Air Pressure in Lungs
  • Take a breath in and stop. Enough air has come in
    now so that the air pressure in the alveoli
    equals the atmosphere, so you no longer get more
    air flowing in.
  • When you relax, the lungs recoil, air comes out,
    and when the two pressures equal each other, air
    stops flowing out.
  • You will get zero pressure differences upon
    maximum inhalation and exhalation.

Oxygen-Hbg Dissociation Curve
  • X-axis is partial pressure of oxygen (pO2)
  • Y-axis is saturation of Hgb with O2
  • The partial pressures of respiratory gases found
    in arterial blood correspond most closely to
    those partial pressures found in the alveoli.

Oxygen-Hbg Dissociation Curve
  • Hgb in the blood leaving the lungs is about 98
    saturated with O2.
  • This graph demonstrates that 98 of Hbg is still
    saturated when pO2 is only 70 mm (when it first
    arrives in the tissues).
  • By the time pO2 reaches 100mm (in the lungs), Hbg
    is already 100 saturated.

  • In the lungs, pO2 is 100 mm Hg. Hemoglobin is
    still 100 saturated at this pO2 level.
  • In the body cells, pO2 is 40 mm Hg. Hemoglobin is
    still about 75 saturated at this low pO2 level.
  • The difference of 25 saturation means that
    hemoglobin gives up only about 25 of its O2 to
    body cells as it passes by.

Left shift
CAUSE pH decreased CO2 increased Temperature
CAUSE pH increased CO2 decreased Temperature
Right shift
CAUSE pH increased CO2 decreased
CAUSE pH decreased CO2 increased
  • A left shift will increase oxygen's affinity for
  • In a left shift condition (alkalosis,
    hypothermia, etc.) oxygen will have a higher
    affinity for hemoglobin (it wont leave!).
  • This can result in tissue hypoxia even when there
    is sufficient oxygen in the blood.
  • A right shift decreases oxygen's affinity for
  • In a right shift (acidosis, fever, etc.) oxygen
    has a lower affinity for hemoglobin. Blood will
    release oxygen more readily.
  • This means more O2 will be released to the cells,
    but it also means less oxygen will be carried
    from the lungs in the first place.

Vacuum in Lungs
  • There is another anatomical structure you need to
    remember the plural cavity. Each lung is
    surrounded by a parietal and visceral serousal
  • The serousal cells make a lubricating fluid so
    the lungs dont rub against the thoracic cavity,
    causing heat generation, which can denature
  • This fluid has cohesive properties. If you put
    two pieces of wet glass together, you have to use
    more force to pull them apart than if they were
    dry. You have to break the vacuum.

Vacuum in Lungs
  • The surface of the lungs are tightly stuck to the
    surface of the thoracic wall.
  • If they are disengaged, they will recoil like
    deflated balloons.
  • If the vacuum in the pleural cavity is broken,
    the lung will collapse.
  • They need to be reinflated by the administration
    of oxygen.

Mechanics of Ventilation
  • Normal Inspiration
  • Is an active process (Its work! It uses ATP)
  • Contract Diaphragm and it moves inferiorly to
    increase thoracic volume -60-75 of volume change
  • Contract external intercostals
  • Forced Inspiration
  • Accessory muscles needed
  • Sternocleidomastoid
  • Scalenes
  • Serratus anterior
  • Others (erector spinae)

When the chest wall moves, so do the lungs! Why
are the lungs right up against the chest wall?
  • Pleural Space or Cavity
  • a vacuum (contains no air)
  • pleural fluid (water) has surface tension

Result? Lung moves with the chest wall
Lungs are not muscular organs, they cannot
actively move. They move with the chest wall.
What happens if the lung dissociates from the
chest wall?
  • Pneumothorax air in the pleural cavity
  • Hemothorax blood in the pleural cavity
  • How?
  • Injury (Gun shot, stabbing)
  • Spontaneous (tissue erosion, disease lung)
  • Bleeding wound
  • Chest wall recoils outward (barrel chest)
  • Lung recoils inward (atelectasis alveolar, lung

Mechanics of Ventilation
  • Normal Expiration-
  • A Passive process
  • Simply relax the muscles of inspiration
  • Rely on the elastic properties of lung (like a
    balloon deflating on its own)
  • Forced Expiration
  • Relax muscles of inhalation AND
  • Contract internal intercostals
  • Contract Abdominal muscles
  • Internal and external obliques
  • Transverse abdominis
  • Rectus abdominis

  • COPD (chronic obstructive pulmonary disease) is
    emphysema plus chronic bronchitis.
  • Emphysema is generally caused by smoking.
  • The alveoli have broken, leaving spaces where gas
    exchange cannot take place.
  • Compliance decreases, so It is difficult to expel
    the air in the lungs.
  • Each inhalation is a forced inspiration also.
  • When the ribs are continually raised with each
    breath, they eventually remain in the upright
    position, causing a barrel chest.

Exhalation Problem COPD
  • Normal exhalation is passive, requires no ATP.
    But forced expiration (such as emphysema patient)
    recruits abdominal muscles. The muscles enlarge
    with time, creating a barrel-shaped chest,
    typical of emphysema patients and COPD.

  • In everyone, the midsized bronchioles do not have
    cartilage rings to hold them open, and during
    exhalation, the sides of the bronchioles collapse
    and touch each other.
  • If there is not enough surfactant, they stick to
    each other with greater strength (like two wet
    pieces of glass), and the person has to
    forcefully exhale with each breath to overcome
    the cohesiveness of the fluid.
  • Surfactant is like adding soap to the fluid so
    the surfaces come apart easier.

  • Giving oxygen in high concentration helps get air
    into their lungs, but it reduces the drive for
    them to breathe. CO2 is a powerful driving force
    for ventilation. When a person has COPD, they
    have less CO2, and oxygen becomes the driving
  • If we give them oxygen, the drive for them to
    breathe becomes diminished. They eventually wind
    up on a positive pressure ventilator, but the
    disease progresses, and they die from
  • A continuous positive airway pressure machine is
    called a CPAP machine.

CPAP Machine
Both the Lung and Chest Wall are Elastic
  • Both lung and chest wall have the tendency to
  • What is recoil? Tendency to snap back to resting
  • (like a stretched rubber band recoils when
    youlet go of one end)

The chest wall recoils outward (springs out) The
lung recoils inward (ie. it collapses!)
  • Increase in lung volume decreases intra-alveolar
    pressure (we now have a pressure gradient) air
    goes in.
  • Decrease in lung volume raises intra-alveolar
    pressure above atmosphere air goes out.

When the pressure at the alveoli are at 0 (no
difference between their pressure and atmospheric
pressure), no air flows in or out of the lungs.
Patm and Palv create the pressure gradient that
drives ventilation
  • Atmospheric Pressures (Patm)- pressure of the
    outside air (760mmHg760 torr 1 atm).
  • Intra-alveolar pressure (Palv) pressure within
    the alveoli of the lungs. Equal to Patm (0mmHg)
    at rest, but varies during phases of ventilation.
  • Intra-pleural pressure (Pip) pressure in the
    intra-pleural space.
  • Pressure is negative because of the lack of air
    in the intrapleural space, lymph drainage, and
    opposing forces of lung and chest wall.

Air Flow
  • If atmospheric pressure is greater than alveolar
    pressure, air flows into the lungs.
  • If atmospheric pressure is less than alveolar
    pressure, air flows out of the lungs.
  • Transpulmonary pressure is the difference between
    the alveolar and intra-pleural pressures.

Positive Pressure breathing
Negative Pressure breathing
Iron Lung
  • This chamber is an iron lung, invented for polio
    patients, whose respiratory nerves were
    paralyzed. When we are normally breathing, we are
    changing thoracic volume, so we are using
    negative pressure breathing. But a paralyzed
    person cannot move their respiratory muscles.
  • It works like a reverse vacuum. There is less air
    pressure in the tank, so there is less pressure
    on the chest, so the chest recoils more, to help
    get air in. The vacuum then reverses, increases
    pressure on the chest, air flows out.

Acute Mountain Sickness(Altitude Sickness)
  • When you visit someone in a high elevation (5,000
    m) you might get acute mountain sickness.
  • Symptoms
  • Severe headache, fatigue, dizziness, palpitation
    and nausea.
  • Cause
  • Pulmonary edema.
  • Why do you get pulmonary edema?
  • High elevations have lower pO2 levels.
  • This causes hypoxia (lack of oxygen) in the
    pulmonary capillaries
  • This causes increased pulmonary arterial and
    capillary pressures (pulmonary hypertension)
  • That causes the pulmonary edema

Respiratory Cycle
Ventilation Volume
  • When you breathe in, you inhale about 500 ml. You
    exhale about 500 ml. Therefore, 500 ml is your
  • Not all 500 ml gets down deep to your alveoli.
    About 150 ml of it stays in the conductive zone
    (bronchi and trachea). About 350 ml reaches the
    alveoli. That is considered your alveolar
    ventilation volume.
  • That is the amount of air that can undergo gas
    exchange. If you want to calculate how much air
    moves in and out per minute, take the tidal
    volume and multiply it by breathing rate (about
    12 breaths per minute for adult, 20 for
  • 500 x 12 total ventilation
  • Tidal volume 150 x 12 alveolar ventilation

Lung function tests
  • Lung volumes are assessed by spirometry.
  • Subject breathes into a closed system in which
    air is trapped within a bell floating in H20.
  • The bell moves up when the subject exhales and
    down when the subject inhales.
  • Spirometry
  • Static lung tests
  • Volumes and capacities
  • No element of time involved, ie. How long does it
    take you to push the air out? Normal expiration
    takes 2-3 x longer than inspiration
  • Dynamic lung tests
  • Time element, rate of exhale
  • How much, how quickly?

Spirometry measures lung volumes
  • The tidal volume, vital capacity, inspiratory
    capacity and expiratory reserve volume can be
    measured directly with a spirometer.
  • Most air (80) is exhaled during the first second
    of exhalation. You take a maximum inhale, then a
    maximum exhale (vital capacity). The pen moves
    down the paper, showing time.
  • You can calculate how much air you blew out
    (vital capacity), and the amount of air you blew
    out in one second (expiratory reserve volume in
    one second).
  • Expiratory reserve volume divided by vital
    capacity should be 80. If you are less than 80,
    it is suggestive of an obstructive pulmonary

Dynamic Lung Tests
Someone with COPD takes longer than one second
to exhale 80.
Obstructive Lung Diseases
  • Obstructive lung diseases are characterized by
    inflamed and easily collapsible airways,
    obstruction to airflow, and frequent
  • Examples
  • Asthma
  • Bronchitis
  • Chronic obstructive pulmonary disease (COPD)

Restrictive Lung Diseases
  • These are extrapulmonary or pleural respiratory
    diseases that restrict lung expansion, resulting
    in a decreased lung volume (rapid, shallow
    breathing), an increased work of breathing, and
    inadequate ventilation and/or oxygenation.
    Decreased vital capacity.
  • Cystic Fibrosis
  • Infant Respiratory Distress Syndrome
  • Weak respiratory muscles
  • Pneumothorax

Capacities are two or more volumes added together
Capacities are two or more volumes added together
These are measured with a
spirometer This is estimated, based on
height and age These are
calculated FRC ERV RV TLC
Quiz yourself (color version)
Quiz yourself (what the test will look like)
  • You dont need to memorize the normal numbers,
    just the definitions
  • Respiratory Cycle A single cycle of inhalation
    and exhalation
  • Respiratory rate number of breaths per minute
    (usually about 12-18 children higher 18-20).
  • Tidal Volume normal breath in and out. Usually
    about 500 ml.
  • Inspiratory Reserve Volume take in a normal
    breath, stop, now inhale as much more as you can.
    In other words, this is the amount of air that
    can be forcefully inhaled after a normal
    inhalation. This is your tidal volume in plus
    your inspiratory volume.
  • Expiratory Reserve Volume (Expiratory capacity)
    take a normal breath in, a normal breath out,
    then breathe out the most you can. In other
    words, this is the amount of air that can be
    forcefully exhaled after a normal exhalation.
    This is the air needed to perform the Heimlich
    maneuver. The maneuver decreases the thoracic
    cavity volume, causing increased pressure in
    lungs. That causes forced air with high pressure
    to be expelled from the lungs.
  • Residual volume The amount of air left in your
    lungs after you exhale maximally. This air helps
    to keep the alveoli open and prevent lung
    collapse. This is estimated based on height and

Capacities are two or more volumes added together
  • You dont need to memorize the normal numbers,
    just the definitions
  • Vital capacity The volume of air a patient can
    exhale maximally after a forced inspiration.
    Maximum deep breath in, then exhale as much as
    possible. It can be used to determine if problems
    are obstructive (normal) or restrictive
    (reduced). Vital capacity divided by expiratory
    reserve volume should be 80.
  • Total Lung Capacity (TLC) the sum of all lung
  • Inspiratory Capacity amount of air for a deep
    breath in after normal exhalation
  • Functional residual capacity amount of air left
    in your lungs after a normal exhale. You have to
    calculate this
  • FRC ERV residual volume.
  • In COPD, their FRC increases.
  • They have a barrel chest
  • The lungs dont have as much recoil, have
    decreased tidal volume, cannot exhale enough

Capacities are two or more volumes added together
  • You dont need to memorize the normal numbers,
    just the definitions
  • Dead Space Area where air fills the passageways
    and never contributes to gas exchange. Amounts to
    about 150 ml.
  • Minute Respiratory Volume (MRV) tidal volume x
    respiratory rate. This calculation does not take
    into account the volume of air wasted in the dead
    space. A more accurate measurement of respiratory
    efficiency is alveolar ventilation rate.
  • Alveolar Ventilation Rate (AVR)
  • AVR (TV Dead Space) x Respiratory Rate

Summary of lung calculations
Dead Space) x RR
You DO need to know these formulas.
Lung Capacity and Disease Summary
  • Obstructive Disease
  • Decreased VC
  • Increased TLC, RV, FRC.
  • FEV1/VC is less than 80
  • Restrictive Disease
  • Decreased VC
  • Decreased TLC, RV, FRC
  • So FEV1/VC ratio normal

FRC ERV RV. Why is this important? Its the
volume of air in your lungs at the end of a
normal exhale. It represents the normal
equilibrium position of your chest wall trying to
spring out and lung to recoil, but forced
together due to pleural cavity.
Sample Questions
  • Minute Respiratory Rate is the volume of air that
    enters the airways (passes the lips) each min.
  • MRV Tidal volume x rate of breathing
  • (500 ml/breath) x 12 breaths/min
  • 6,000 ml/min
  • Alveolar ventilation rate is the volume of air
    that fills all the lungs respiratory airways
    (alveoli) each min. In a normal, healthy lung,
    this might be
  • AVR (tidal volume dead space volume) x rate
    of breathing
  • (500 ml/breath 150 ml) x 12
  • (350 ml/breath) x 12 breath/ min
  • 4, 200 ml/min
  • In a diseased, poorly perfused lung, this value
    may well be much lower.
  • Then, is panting an example of hyper, normal, or

Hyper and Hypo Ventilation
  • The deeper regions of your lungs get more blood
    flow and the upper regions have more air flow.
  • If you hyperventilate, the rate and depth of
    ventilations increases, so more air gets to
    alveoli. After voluntary hyperventilation, apnea
    (no breathing) may occur b/c the arterial blood
    contains less carbon dioxide
  • Hypoventilation is dealing only with conductive
    zone. When you pant, you are just shifting air in
    the conducting zone. You are not increasing air
    to the alveoli. Panting is hypoventilation.

Respiratory vs. Metabolic Acidosis and Alkalosis
    blood pH which is caused by abnormal breathing
    rates. It is not necessarily a disease, since
    hyperventilating from stress is not a disease.
  • Respiratory alkalosis is caused by
    hyperventilation. This increases the amount of
    CO2 that you are exhaling. CO2 is an acid, so if
    you hyperventilate, you are exhaling a lot of
    acid, so your blood plasma pH will increase
  • Respiratory acidosis is caused by
    hypoventilation. This decreases the amount of CO2
    that you are exhaling. If you hypoventilate, you
    are not exhaling enough acid, so your blood
    plasma pH will decrease (acidosis). Respiratory
    acidosis can also be caused by interference with
    respiratory muscles by disease, drugs, toxins.
    blood pH which is not caused by abnormal
    breathing rate.
  • Metabolic acidosis can be caused by
  • Salicylate (aspirin) overdose
  • Untreated diabetes mellitus (leading to
  • Metabolic alkalosis can be caused by
  • excessive vomiting (loss of acid from stomach)

Compensations for Respiratory vs. Metabolic
Acidosis and Alkalosis
  • Respiratory alkalosis can be compensated by
  • excreting an alkaline urine
  • Cannot hypoventilate since hyperventilation is
    the problem in the first place!
  • Respiratory acidosis can be compensated by
  • excreting an acidic urine
  • Cannot hyperentilate since hypoventilation is the
    problem in the first place!
  • Metabolic acidosis can be compensated by
  • excreting an acidic urine
  • hyperventilation
  • Metabolic alkalosis can be compensated by
  • Excreting an alkaline urine
  • Hypoventilation

Acid-Base Conditions
  • Excessive diarrhea
  • Causes the problem of low HCO3
  • Leads to ?pH in blood (acidosis)
  • Lungs Compensate by
  • ?pCO2 (hyperventilation, which decreases the
  • content in the blood,
    thereby removing acid
  • from the blood)

Acid-Base Conditions
  • Ingesting excessive stomach antacids
  • Causes the problem of high HCO3
  • Leads to ?pH in blood (alkalosis)
  • Lungs Compensate by
  • ?pCO2 (hypoventilation, which increases the CO2
  • content in the blood,
    thereby adding acid
  • from the blood)

Acid-Base Conditions
  • Aspirin overdose
  • Causes the problem of high acid, low
    HCO3 (bicarbonate)
  • Leads to ?pH in blood (acidosis)
  • Lungs Compensate by
  • ?pCO2 (hyperventilation, which decreases the
  • content in the blood,
    thereby removing acid
  • from the blood)

Acid-Base Conditions
  • Anxiety or hysteria with panting
  • The patient hypoventilates
  • Causes the problem of high pCO2
  • Leads to ? pH in blood (acidosis)
  • Lungs Compensate by
  • ? HCO3 (by hyperventilation, which decreases
    the CO2
  • content in the blood,
    thereby removing acid
  • from the blood)

Pulmonary Embolism
  • Pulmonary Embolism blockage of the pulmonary
    artery (or one of its branches) by a blood clot,
    fat, air or clumped tumor cells. The most common
    form of pulmonary embolism is a thromboembolism,
    which occurs when a blood clot, generally in a
    vein, becomes dislodged from its site of
    formation, travels to the heart, goes into a
    pulmonary artery, and becomes lodged in the
    smaller artery in the lungs, blocking blood flow
    and oxygen to that region of the lung.
  • Symptoms may include difficulty breathing, pain
    during breathing, and possibly death. Treatment
    is with anticoagulant medication.
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