Chapter 13
Lecture Outline*
Respiratory Physiology
Eric P. Widmaier
Boston University
Hershel Raff
Medical College of Wisconsin
Kevin T. Strang
University of Wisconsin - Madison
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Organization of the Respiratory System
Fig. 13-1
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The Respiratory System
• The main function of the respiratory system is to
supply the body tissues with oxygen and dispose of
carbon dioxide generated by cellular metabolism.
• Respiration is collectively made up of 4 processes:
1. Pulmonary ventilation (breathing)
2. External respiration (movement of O2 from lungs into
blood; CO2 from blood to lungs)
3. Transport of respiratory gases in the blood
4. Internal respiration (movement of O2 from blood into
tissue cells; CO2 from cells into blood)
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The Airways and Blood Vessels
Fig. 13-2
Fig. 13-3
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The Airways
• The structures that comprise the system are:
– Nose, nasal cavity, pharynx, larynx, trachea, bronchi,
lungs, alveoli
• These can be divided into the respiratory zone (where
the gas exchange happens) and the conducting zone
(everything else).
• The trachea is also known as the “windpipe.” It has 3
layers and the mucosa has the goblet cells and cilia.
• Smoking kills the cilia. So coughing is the only way
to keep mucus from accumulating in the lungs. (hence
the chronic cough seen in many long-term smokers)
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Site of Gas Exchange: The Alveoli
• The alveoli are tiny, hollow sacs whose open ends are continuous
with the lumens of the airways .
• Most of the air-facing surfaces of the wall are lined by a
continuous layer, one cell thick, of flat epithelial cells termed
type I alveolar cells.
• Type II alveolar that produce a detergent-like substance called
surfactant.
• The total surface area of alveoli is very large and this permits the
rapid exchange of large quantities of oxygen and carbon dioxide
by diffusion.
• In some of the alveolar walls, pores permit the flow of air
between alveoli.
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Site of Gas Exchange: The Alveoli
Fig. 13-4
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Relation of the Lungs to the Thoracic Wall
Fig. 13-5
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Pleurae
• The pleurae form a thin double-layered serosa. The parietal
pleura covers the thoracic wall and superior face of the
diaphragm. The visceral pleural covers the external surface of
the lung.
• The pleural fluid that they form lives in the pleural cavity. This
provides lubrication of the lung to prevent friction while
breathing.
• Pleurisy is an infection or inflammation of the pleura and often
results from pneumonia. This results in a roughening of the
pleura, which creates friction and a stabbing pain with each
breath. As the disease progresses there is a build-up of fluid,
which hinders breathing.
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Steps of
Respiration
Fig. 13-6
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Ventilation and Air Flow
• Ventilation is defined as the exchange of air
between the atmosphere and alveoli.
• F = ΔP/R
• Remember that flow is proportional to the
pressure difference (Δ P) between two points
and inversely proportional to the resistance
(R).
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Ventilation
• Remember that a volume change leads to a pressure
change and that pressure changes lead to the flow of gases
to equalize the pressure.
• Boyle’s law says that at a constant temperature the
pressure of a gas varies inversely with its volume.
• P1V1=P2V2
• Remember that gases always fill their container. So in a
large container the molecules in a given amount of gas
will be far apart (low pressure). In a smaller container
that same amount of gas will have molecules close
together (high pressure).
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Pressure Measurements
• The respiratory pressures are always relative to
atmospheric pressure!
• We measure this in mm Hg or atmospheres
(atm).
• At sea level this is 760 mm Hg or 1 atm.
• If you were to go to higher altitudes (i.e., up in
the Andes Mountains), then the pressures would
be different.
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Lung volumes depend on two factors
• Transpulmonary pressure
• Elasticity and strechebility of the lung
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Intrapulmonary Pressure
• Palv is the pressure in the alveoli.
• It rises and falls with breathing, but it
ALWAYS equalizes with the atmospheric
pressure.
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Intrapleural Pressure
• Pip is the pressure in the pleural cavity.
• It also fluctuates with breathing, but it is
always 4 mm Hg less than Palv.
• IF THE Pip EVER = to Ppul THE LUNGS WILL
IMMEDIATELY COLLAPSE!
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Transpulmonary Pressure
• Transpulmonary pressure = Palv – Pip
• Transpulmonary pressure is the transmural pressure
that governs the static properties of the lungs.
• Transmural means “across a wall” and is represented
by the pressure in the inside of the structure (Pi)
minus the pressure outside the structure (PO).
• Inflation of a balloon-like structure like the lungs
requires an increase in the transmural pressure such
that Pi increases relative to PO.
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Ventilation and Lung Mechanics
Fig. 13-7
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How is a Stable Balance Achieved
Between Breaths?
Fig. 13-10
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Inspiration
Fig. 13-12
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Expiration
Fig. 13-15
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Lung Compliance
• Compliance can be considered the inverse of stiffness.
• The greater the lung compliance, the easier it is to
expand the lungs at any given change in
transpulmonary pressure.
• There are two major determinants of lung compliance:
1. The stretchability of the lung tissues
2. The surface tension at the air-water interfaces within the
alveoli
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Lung Compliance
Fig. 13-16
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Lung Compliance and Surfactant
• The type II alveolar cells secrete the detergentlike substance known as surfactant.
• Surfactant markedly reduces the cohesive
forces between water molecules on the
alveolar surface.
• Therefore, surfactant lowers the surface
tension, which increases lung compliance and
makes it easier to expand the lungs.
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Clinical Interest
• A lack of surfactant is a huge problem for babies, especially
those born prematurely. Infant respiratory distress syndrome
(IRDS) also known as respiratory distress syndrome of the
newborn (RDSN).
• Too little surfactant allows the alveoli to collapse and then they
have to re-inflate every time. This is a huge energy drain.
• Normally surfactant isn’t made until the last two months in
utero. If a baby is being born too early they can now administer
some steroids to help stimulate production. But in most
emergency births this isn’t possible so the baby is put on a
ventilator. We can now give some artificial surfactant to help.
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Airway Resistance
• Airway resistance is normally very small, but
changes in airway resistance follow changes in
airway radii.
• Airway radii may change in response to
physical, neural, and chemical factors.
• The greatest resistance is found in the medium
sized bronchi.
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Asthma
• Asthma is a disease characterized by intermittent episodes in
which airway smooth muscle contracts strongly, markedly
increasing airway resistance.
• The basic defect in asthma is chronic inflammation of the
airways, the causes of which vary from person to person and
include, among others, allergy, viral infections, and sensitivity to
environmental factors.
• The underlying inflammation makes the airway smooth muscle
hyperresponsive and causes it to contract strongly in response to
such things as exercise (especially in cold, dry air), cigarette
smoke, environmental pollutants, viruses, allergens, normally
released bronchoconstrictor chemicals, and a variety of other
potential triggers.
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Asthma
• The first aim of therapy for asthma is to reduce the chronic
inflammation and airway hyperresponsiveness with antiinflammatory drugs, particularly leukotriene inhibitors and
inhaled glucocorticoids.
• The second aim is to overcome acute excessive airway smooth
muscle contraction with bronchodilator drugs, which relax the
airways.
• For example, one class of bronchodilator drugs mimics the
normal action of epinephrine on beta-adrenergic (beta-2)
receptors. Another class of inhaled drugs block muscarinic
cholinergic receptors, which have been implicated in
bronchoconstriction.
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Chronic Obstructive Pulmonary Disease
• The term chronic obstructive pulmonary disease refers to
emphysema, chronic bronchitis, or a combination of the two.
• These diseases cause severe difficulties not only in ventilation,
but in oxygenation of the blood.
• Emphysema is caused by destruction and collapse of the smaller
airways.
• Chronic bronchitis is characterized by excessive mucus
production in the bronchi and chronic inflammatory changes in
the small airways. The cause of obstruction is an accumulation of
mucus in the airways and thickening of the inflamed airways.
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Pathophysiology
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Lung Volumes and Capacities
Fig. 13-18
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Lung Volumes
& Capacities
Fig. 13-18
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Alveolar Ventilation
Fig. 13-19 44
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Dead space
• Anatomic dead space
• Alveolar dead space
• Functional dead space
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Exchange of Gases in Alveoli and Tissues
Fig. 13-20
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Partial Pressures of Gases
Fig. 13-21
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factors that determine the value of
alveolar PO2
(1)the PO2 of atmospheric air
(2) the rate of alveolar ventilation
(3) the rate of total-body oxygen
consumption
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• Hyperventilation: when there is a decrease in
the ratio of carbon dioxide production to
alveolar ventilation
• Hypoventilation: there is an increase in the
ratio of carbon dioxide production to alveolar
ventilation.
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Alveolar Gas Pressures
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Gas Exchange Between Alveoli and Blood
Fig. 13-23
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Matching of Ventilation and Blood Flow in Alveoli
Fig. 13-24
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Transport of Oxygen in Blood
Oxygen is transported
in the blood bound to
hemoglobin.
Fig. 13-25
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What Is the Effect of PO2 on Hemoglobin Saturation?
Fig. 13-26
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Oxygen delivery to tissues
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Oxygen Movement in Lungs and Tissues
Fig. 13-28
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Effects of
Blood PCO2,
H+
Concentration,
Temperature,
and DPG
Concentration
on Hemoglobin
Saturation
Fig. 13-29
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Transport of Carbon Dioxide in Blood
Fig. 13-30
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Transport of Hydrogen Ions Between Tissues
and Lungs
Fig. 13-31
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Neural
Generation
of
Rhythmical
Breathing
An overdose of
morphine,
barbituates or
alcohol suppresses
the neurons in the
ventral respiratory
group and stops
respiration.
Fig. 13-32
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Baroreceptors
Fig. 13-33
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Hyperventilation
Fig. 13-35
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Reflexively Induced Hyperventilation and
H+ Concentration
Fig. 13-39
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Control of Ventilation by PO2, PCO2, and H+
Concentration
Fig. 13-40
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Control of Ventilation During Exercise
Fig. 13-43
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Hypoxia
• Hypoxia is defined as a deficiency of oxygen
at the tissue level.
• causes of hypoxia:
1. Hypoxic hypoxia
2. anemic or carbon monoxide hypoxia
3. ischemic hypoxia
4. hypoxia, in which the cell is unable to utilize
the oxygen because a toxic agent—cyanide,
for example—has interfered with the cell’s
metabolic machinery.
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Cyanide
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Cyanide
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Why Do Ventilation-Perfusion Abnormalities
Affect O2 More than CO2?
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Sleep Apnea
Fig. 13-44
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Other Ventilatory Responses
• Protective reflexes: coughing, sneezing
• Voluntary control of breathing: holding your
breath, laughing
• Reflexes from J receptors
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Hypoxia
• Hypoxia is an inadequate oxygen delivery to tissues.
1. Anemic hypoxia: poor O2 delivery because of too few
RBCs or abnormal hemoglobin.
2. Ischemic hypoxia: blood circulation is impaired.
3. Histotoxic hypoxia: the body’s cells are unable to use O2
(cyanide causes this).
4. Hypoxemic hypoxia: reduced arterial O2
(can be caused by lack of oxygenated air, pulmonary
problems, lack of ventilation-perfusion coupling).
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Carbon Monoxide Poisoning
• This is a type of hypoxemic hypoxia. It is the leading
cause of death from fire.
• CO is an odorless, colorless gas that competes with O2 for
the binding sites on the hemoglobin. It has a 200-times
greater affinity for hemoglobin than O2 does.
• The symptoms are confusion, respiratory distress, the skin
becomes cherry red. NO CYANOSIS is detectable.
• To treat it, hyperbaric treatment or 100% oxygen is used.
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