Transcript Functions of the Respiratory System 1. 2. 3. 4. 5. Gas Exchange Regulation of blood pH Voice production Olfaction Protection.

Functions of the Respiratory System
1.
2.
3.
4.
5.
Gas Exchange
Regulation of blood pH
Voice production
Olfaction
Protection
Tracheobronchial Tree
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Conducting Zone
Respiratory Zone
– Alveoli
– Type I pneumocytes
– Type II pneumocytes
Thoracic Wall & Muscles of Respiration
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Thoracic wall
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Thoracic vertebrae
Ribs
Sternum
Muscles
Thoracic cavity
– Thoracic wall & Diaphragm
Thoracic Wall & Muscles of Respiration
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Muscles of Respiration
– Muscles of Inspiration
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Diaphragm
External intercostals
Pectoralis minor
Scalenes
– Muscles of Expiration
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Abdominal muscles
Internal intercostals
Pleura
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Each lung is surrounded by a separate pleural
cavity.
Parietal pleura
– Covers the inner layer of the throacic wall.
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Visceral pleura
– Covers the surface of the lung.
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Pleural Cavity
– Filled with pleural fluid.
Pleural Fluid
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Acts as lubricant allowing parietal and visceral
Helps hold the parietal and visceral pleural
membranes together.
Blood Supply
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Blood that has passed through the lungs and
picked up oxygen is called oxygenated blood.
Blood that has passed through the tissues and
released some of its oxygen is called
deoxygenated blood.
Ventilation
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Moving air in & out of the lungs.
Flow of air into the lungs requires a pressure
gradient from the outside of the body to the
alveoli.
If air needs the flow out of the lungs, a
pressure gradient needs to exist in the other
direction.
F = (P1 – P2) / R
Pressure & Volume
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General gas law
– P = nRT / V
– n, R, and T are all constants, therefore pressure is
inversly proportional to volume.
– Called Boyle’s Law.
Airflow into & out of Alveoli
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Inspiration
– Initiated by contraction of diaphragm & external
intercostal muscles.
– Result: increase in the size of the thorax.
– Leads to a drop in alveolar pressure (Boyle’s
Law).
– Palv < PB
– Lung will expand.
Airflow into & out of Alveoli
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Expiration
– At the end of inspiration, the nerves to the
diaphragm and external intercostals stop firing.
– These muscles relax.
– Lungs & chest wall passively return to their
original dimensions.
Airflow into & out of Alveoli
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Expiration
– As lungs decrease in size, the pressure increases
(Boyle’s Law).
– Palv > PB
– Air will flow from the alveoli to the atmosphere.
Forced Expiration
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During exercise, the expiration of larger
volumes is achieved by the contraction of the
internal intercostals and the abdominal
muscles.
Lung Compliance
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Compliance = “stretchability”.
Two determinants:
– Compliance (stretchability of lung tissue)
– Surface tension at the air-water interface of the
alveoli.
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Surfactant
Respiratory Distress Syndrome
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2nd leading cause of death in premature
infants.
Normal maturation of surfactant-synthesizing
cells is facilitated by hormones (particularly
cortisol).
Secretion of cortisol increases late in
pregnancy (7th month).
Respiratory Distress Syndrome
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Premature babies lack mature type II alveolar
cells due to low levels of cortisol.
Treatment:
– Administration of cortisol to mother.
– Administer high pressure, oxygen-rich air to infant.
– Exogenous source of surfactant to infant.
Pleural Pressure
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Normally lower than the alveolar pressure.
This helps keep the alveoli expanded.
If this difference is lost the alveoli will collapse.
e.g. Pneumothorax
Airway Resistance
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F = ΔP / R
Factors that affect R:
– Viscosity
– Length
– Radius
Airway Resistance
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Factors that affect radius:
– Transpulmonary pressure:
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Exerts a distending force.
Increases during inspiration.
– Lateral traction:
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Connective tissue fibers pulling outwards.
– Mucus Accumulation
Airway Resistance
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Factors that affect radius:
– Parasympathetic nerves
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Constriction (ACh)
– Epinephrine
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Dilates
– Histamine
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Constricts
Asthma
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Attacks are characterized by smooth muscle
contraction.
Increases resistance impairing ventilation.
More mucus may also be secreted.
Main defect is inflammation of the airways.
Cause of inflammation varies from person to
person (virus, allergy, etc.).
Asthma
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Smooth muscle can be hyperresponsive to:
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Exercise
Emotional stress
Cold air
Cigarette smoke
Irritants
Certain drugs
Asthma
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Therapy:
– Anti-inflammatory drugs
– Bronchodilators
Chronic Obstructive
Pulmonary Disease
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Examples:
– Emphysema & Chronic Bronchitis
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Emphysema
– Destruction of alveolar walls.
– Impairs gas exchange.
– Destruction of elastic tissue also contributes to
airway collapse (obstruction).
Chronic Obstructive
Pulmonary Disease
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Examples:
– Emphysema & Chronic Bronchitis
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Chronic Bronchitis
– Characterized by excessive mucus production in
bronchi.
– Results in obstruction.
Pulmonary Volumes & Capacities
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Spirometry is the process of measuring
volumes of air moving in & out of the lungs.
Important volumes
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Tidal volume
Inspiratory reserve volume
Expiratory reserve volume
Residual volume
Pulmonary Volumes & Capacities
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Spirometry is the process of measuring
volumes of air moving in & out of the lungs.
Important capacities (= sum of two or more
lung volumes)
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Inspiratory capacity
Functional residual capacity
Vital capacity
Total lung capacity
Pulmonary Volumes & Capacities
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Forced expiratory vital capacity is a simple
clinical pulmonary test.
Forced expiratory volume in one second
(FEV1) is also an important diagnostic value.
Airway obstructions (asthma, emphysema,
chronic bronchitis, etc) cause a decreased
FEV1.
Alveolar Ventilation
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Pulmonary Ventilation
VP = f (VT)
During inspiration, a portion of the inspired air
fills the anatomic dead space before reaching
the alveoli.
This air is not available for gas exchange.
VA = f (VT – VD)
Principles of Gas Exchange
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Dalton’s Law
Partial Pressure
Nitrogen (78.62%)
Oxygen (20.84%)
Sea level
– Total atmospheric pressure = 760 mmHg
– Partial pressure of nitrogen = 597.5 mmHg
– Partial pressure of oxygen = 158.4 mmHg
Inspired air vs. Alveolar air
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Inspired air and alveolar air are different.
– Air entering repiratory system is humidified.
– Oxygen diffuses from alveoli into the blood.
– Carbon dioxide diffuses from pulmonary
capillaries into the alveoli.
– Air in the alveoli is only partially replaced with
atmospheric air during each inspiration.
Diffusion of Gases
Through Respiratory Membrane
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Influenced by:
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Thickness of the membrane.
Diffusion coefficient of the gas.
Surface area of the membrane (70 m2).
Difference of the partial pressures of the gas on
either side of the membrane.
Oxygen & Carbon Dioxide
Transport in the Blood
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Oxygen
– Po2 in alveoli is approx. 104 mmHg.
– Po2 in blood in pulmonary capillaries is approx.
40 mmHg.
– Therefore, O2 diffuses from the alveoli to the
pulmonary capillaries.
Oxygen & Carbon Dioxide
Transport in the Blood
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Oxygen
– Equilibrium is achieved during the first third of the
pulmonary capillary beds.
– Blood leaving the lungs in the pulmonary veins
has a Po2 of approx. 95 mmHg due to mixing with
bronchial veins.
– At the tissues, the Po2 is close to 40 mmHg in the
interstitial space and approx. 20 mmHg in the
individual cells.
Oxygen & Carbon Dioxide
Transport in the Blood
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Carbon Dioxide
– CO2 is continually produced during cellular
respiration.
– The intracellular Pco2 is approx. 46 mmHg
– Interstitial Pco2 is approx. 45 mmHg
– Arterial Pco2 is close to 40 mmHg
– Venous Pco2 is approx. 45 mmHg
– Because the Pco2 is approx. 40 mmHg in the
alveoli, CO2 will diffuse into the alveoli.
Hemoglobin & Oxygen Transport
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Approx. 98.5% of oxygen transported in the
blood is combined with hemoglobin.
The other 1.5% is dissolved in the plasma.
Effect of Po2 on oxygen transport.
– Oxygen-hemoglobin dissociation curve
Hemoglobin & Oxygen Transport
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Effect of pH, Pco2, & temperature on oxygen
transport.
– pH
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Bohr Effect: Decreases in blood pH results in an
decreased ability of Hb to bind to oxygen (decreased
affinity) and vice versa.
– Pco2
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Increases in Pco2 decreases the ability of Hb to bind to
oxygen (decreased affinity) because of the effect of CO2
on pH and vice versa.
Hemoglobin & Oxygen Transport
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Effect of pH, Pco2, & temperature on oxygen
transport.
– Temperature
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Increases in temperature decreases the tendency for
oxygen to remain bound to Hb (decreased affinity).
Transport of Carbon Dioxide
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CO2 is transported in the blood in three
different ways.
1. Dissolved in the plasma (7%)
2. Combined with hemoglobin (23%)
3. As bicarbonate ions (70%)
Transport of Carbon Dioxide
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Dissolved in the plasma (7%)
– CO2 simply dissolves in the plasma.
Transport of Carbon Dioxide
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Combined with hemoglobin (23%)
– CO2 combines with Hb in a reversible fashion.
– Many CO2 molecules can combine with one Hb
molecule.
– Deoxyhemoglobin binds more readily to CO2 than
oxyhemoglobin (Haldane effect).
Transport of Carbon Dioxide
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As bicarbonate ions (70%)
– More than half of the CO2 molecules react with
water (H2O) molecules inside the red blood cell.
CO2 + H20  H2CO3  HCO3- + H+
– As HCO3- accumulates it is exchanged for chloride
ions (Cl-) (chloride shift).
Transport of Carbon Dioxide
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As bicarbonate ions (70%)
CO2 + H20  H2CO3  HCO3- + H+
– Hb binds to H+ ions which decreases the H+
concentration and therefore increases pH.
– Therefore Hb acts as a buffer.
Transport of Carbon Dioxide
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As bicarbonate ions (70%)
CO2 + H20  H2CO3  HCO3- + H+
– The reverse occurs in the lungs.
Carbon Dioxide & Blood pH
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CO2 can also bind with H2O in the plasma.
Therefore, as plasma CO2 levels increase,
hydrogen ion levels increase, and blood pH
decreases.
The respiratory system can regulate the pH of
the blood by changing plasma CO2 levels.
Hyperventilation decreases CO2 levels and
hypoventilation increases CO2 levels.
Rhythmic Ventilation
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The basic rhythm of ventilation is generated
and controlled by the medulla oblongata.
Medullary respiratory center.
– Two dorsal groups
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Primarily responsible for stimulating the contraction of
the diaphragm.
– Two ventral groups
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Primarily responsible for stimulating the external &
internal intercostals, and abdominal muscles.
Chemical Control of Ventilation
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Respiratory system maintains O2 & CO2
concentrations, and blood pH in their normal
range.
If these get out of their normal range they will
have an effect on respiratory movements.
Chemoreceptors
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Respond to hydrogen ion concentration (pH)
or changes in Po2.
Central chemoreceptors
– Located in medulla oblongata
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Peripheral chemoreceptors
– Located in aortic and carotid bodies
Effect of pH
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Blood pH is closely linked to Pco2.
Pco2 levels are monitored by medullary
chemoreceptors.
If Pco2 levels rise, blood pH decreases.
Decreased blood pH values stimulates the
respiratory center resulting in elimination of
CO2.
And vice versa…
Effect of CO2
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Major regulator of respiration during rest and
intense exercise.
An increase in Pco2 of only 5 mmHg can
increase ventilation by 100%!
Hypercapnia = elevated Pco2
Hypocapnia = lowered Pco2
Hypercapnia and hypocapnia affect blood pH
and thereby ventilation.
Effect of O2
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Affects respiration at a relatively minor level.
Hypoxia = reduced Po2 levels
Ventilation will increase, but only after a
marked decrease (50% or more) in Po2.
This is due to the oxygen-Hb saturation curve.
Hering-Breuer Reflex
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Limits inspiration and prevents overinflation of
lungs.
Initiated by stretch receptors in the walls of
bronchi and bronchioles.
Inhibitory influence on the respiratory center.
Effect of Exercise on Ventilation
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Two phases
– Abrupt increase in ventilation
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As much as 50%.
Primarily due to nervous system.
– Gradual increase in ventilation
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Arterial Po2, Pco2, and pH values play a minor role.
Nervous system also plays a role.
pH changes at anaerobic threshold.
Respiratory Adaptations to Exercise
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Training:
– Lead to more efficient cardiovascular and
respiratory systems.
– Slight decrease in residual volume
– Slight increase in vital capacity
– Slight decrease in respiratory rate
– Therefore, little change in minute ventilation.
Respiratory Adaptations to Exercise
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Training:
– However, minute ventilation is greatly increased
during exercise.
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Untrained 120 l/min
Trained 150 l/min
Highly trained 180 l/min
Ventilation in Steady-Rate Exercise
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Light to moderate exercise, ventilation
increases linearly with O2 consumption and
CO2 production.
Averages about 20 - 25 liters of air for every
liter of oxygen consumed.
Also known as ventilatory equivalent (VE/VO2)
Ventilation in Steady-Rate Exercise
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Healthy young adults maintain VE/VO2 of 25
during submax exercise up to approx 55%
VO2max
Children’s values average around 32.
Pulmonary Ventilation During Graded Exercise
160
140
VE (l/min)
120
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80
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20
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2.5
3
Oxygen Consumption (l/min)
3.5
4
4.5
Ventilation in Non-Steady-Rate
Exercise
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At progressively more intense levels of
exercise beyond 55% VO2max, minute
ventilation increases sharply.
Ventilation increases more quickly than O2
consumption.
Therefore, the ventilatory equivalent increases
to values as high as 35 or 40 liters of air per
liter of O2 consumed!
Ventilatory Threshold (VT)
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VT describes the point at which pulmonary
ventilation increases disproportionately with
O2 consumption.
Ventilation is no longer linked with O2
consumption.
Increased ventilation is a result of increases in
CO2 levels.
Ventilatory Threshold (VT)
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Increased CO2 levels come from the buffering
of lactate that accumulates from anaerobic
glycolysis.
Sodium bicarbonate is the buffer in the blood
that buffers almost all of the lactate generated.
Lactic acid + NaHCO3  Na Lactate + H2CO3  H2O + CO2
Respiratory Exchange Ratio (R)
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R is the ratio of CO2 produced and O2
consumed (VCO2/VO2).
In steady-rate exercise the R value remains
less than 1.00.
Excessive CO2 production due to the buffering
of lactate increases R to a value greater than
1.00.
Pulmonary Ventilation During Graded Exercise
160
140
VE (l/min)
120
100
80
60
40
20
0
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0.5
1
1.5
2
2.5
3
Oxygen Consumption (l/min)
3.5
4
4.5
Pulmonary Ventilation During Graded Exercise
160
140
VE (l/min)
120
100
80
60
40
20
0
0
0.5
1
1.5
2
2.5
3
Oxygen Consumption (l/min)
3.5
4
4.5
Pulmonary Ventilation During Graded Exercise
160
140
Point of
ventilatory
threshold
VE (l/min)
120
100
80
60
40
20
0
0
0.5
1
1.5
2
2.5
3
Oxygen Consumption (l/min)
3.5
4
4.5