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Marieb EN. Human Anatomy andPhysiology 6th ed.
The Respiratory System.Pearson Inc. Cummings: 2004
Presented by: Afadiyanti, A. UNDIP
Slide PPT by:Austin, V. University of Kentucky
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Respiratory System
Consists of the respiratory and conducting zones
Respiratory zone
Site of gas exchange
Consists of bronchioles, alveolar ducts, and alveoli
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Respiratory System
Conducting zone
Provides rigid conduits for air to reach the sites of
gas exchange Includes all other respiratory structures (e.g., nose,
nasal cavity, pharynx, trachea)
Respiratory musclesdiaphragm and other musclesthat promote ventilation
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Respiratory System
Figure 22.1
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Airway to Alveoli
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Alveoli to Red Blood Cell
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Major Functions of the Respiratory System
To supply the body with oxygen and dispose of
carbon dioxide
Respirationfour distinct processes must happen
Pulmonary ventilationmoving air into and out of
the lungs
External respirationgas exchange between the
lungs and the blood
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Major Functions of the Respiratory System
Transporttransport of oxygen and carbon dioxide
between the lungs and tissues
Internal respirationgas exchange between
systemic blood vessels and tissues
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Breathing
Breathing, or pulmonary ventilation, consists of two
phases
Inspirationair flows into the lungs
Expirationgases exit the lungs
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Pressure Relationships in the Thoracic Cavity
Respiratory pressure is always described relative to
atmospheric pressure
Atmospheric pressure (Patm)
Pressure exerted by the air surrounding the body
Negative respiratory pressure is less than Patm Positive respiratory pressure is greater than Patm
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Pressure Relationships in the Thoracic Cavity
Intrapulmonary pressure (Ppul)pressure within the
alveoli
Intrapleural pressure (Pip)pressure within the
pleural cavity
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Pressure Relationships
Intrapulmonary pressure and intrapleural pressure
fluctuate with the phases of breathing
Intrapulmonary pressure always eventually
equalizes itself with atmospheric pressure
Intrapleural pressure is always less thanintrapulmonary pressure and atmospheric pressure
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Pressure Relationships
Two forces act to pull the lungs away from thethoracic wall, promoting lung collapse
Elasticity of lungs causes them to assume smallest
possible size
Surface tension of alveolar fluid draws alveoli to
their smallest possible size
Opposing forceelasticity of the chest wall pulls
the thorax outward to enlarge the lungs
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Pressure Relationships
Figure 22.12
P h
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Pressure changes
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Lung Collapse
Caused by equalization of the intrapleural pressure
with the intrapulmonary pressure
Transpulmonary pressure keeps the airways open
Transpulmonary pressuredifference between the
intrapulmonary and intrapleural pressures(PpulPip)
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Pulmonary Ventilation
A mechanical process that depends on volume
changes in the thoracic cavity
Volume changes lead to pressure changes, which
lead to the flow of gases to equalize pressure
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Intercostals
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Intercostals
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Inspiration
The diaphragm and external intercostal muscles(inspiratory muscles) contract and the rib cage rises
The lungs are stretched and intrapulmonary volume
increases
Intrapulmonary pressure drops below atmospheric
pressure (1 mm Hg)
Air flows into the lungs, down its pressure gradient,
until intrapleural pressure = atmospheric pressure
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Inspiration
Figure 22.13.1
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Expiration
Inspiratory muscles relax and the rib cage descends
due to gravity
Thoracic cavity volume decreases
Elastic lungs recoil passively and intrapulmonaryvolume decreases
Intrapulmonary pressure rises above atmospheric
pressure (+1 mm Hg)
Gases flow out of the lungs down the pressure
gradient until intrapulmonary pressure is 0
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Airway Resistance
As airway resistance rises, breathing movementsbecome more strenuous
Severely constricted or obstructed bronchioles:
Can prevent life-sustaining ventilation
Can occur during acute asthma attacks which stops
ventilation
Epinephrine release via the sympathetic nervous
system dilates bronchioles and reduces air resistance
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Alveolar Surface Tension
Surface tensionthe attraction of liquid moleculesto one another at a liquid-gas interface
The liquid coating the alveolar surface is always
acting to reduce the alveoli to the smallest possible
size
Surfactant, a detergent-like complex, reducessurface tension and helps keep the alveoli from
collapsing
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Surface tension related:
1. Packaging and release of surfactant from type II cells
2. Delivery and spreading of phospholipid at air/water
surface
3. Aggregation of phospholipid at air/water surface4. Removal of sufactant by type II cells and M
Airway defense related:
1. Opsinization of bacteria2. Chemotaxis of leukocytes
3. Stimulation of phagocytosis by macrophages
4. Stimulates production of proinflammatory cytokines
FUNCTIONS OF SURFACTANT
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surfactant concentration
surface area
surface tension
surfactant concentration
surface area
surface tension
Expiration Inspiration
surfactantmolecule
alveolarsurface area
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L C li
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Lung Compliance
The ease with which lungs can be expanded Specifically, the measure of the change in lung
volume that occurs with a given change in
transpulmonary pressure
Determined by two main factors
Distensibility of the lung tissue and surroundingthoracic cage
Surface tension of the alveoli
F t Th t Di i i h L C li
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Factors That Diminish Lung Compliance
Scar tissue or fibrosis that reduces the naturalresilience of the lungs
Blockage of the smaller respiratory passages with
mucus or fluid
Reduced production of surfactant
Decreased flexibility of the thoracic cage or itsdecreased ability to expand
F t Th t Di i i h L C li
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Factors That Diminish Lung Compliance
Examples include:
Deformities of thorax Ossification of the costal cartilage
Paralysis of intercostal muscles
R i t M b
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Respiratory Membrane
This air-blood barrier is composed of:
Alveolar and capillary walls
Their fused basal laminas
Alveolar walls:
Are a single layer of type I epithelial cells
Permit gas exchange by simple diffusion Secrete angiotensin converting enzyme (ACE)
Type II cells secrete surfactant
R i t M b
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Respiratory Membrane
Figure 22.9b
R i t M b
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Respiratory Membrane
Figure 22.9.c, d
S rface Area and Thickness of the Respirator
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Respiratory membranes: Are only 0.5 to 1 m thick, allowing for efficient
gas exchange
Have a total surface area (in males) of about 60 m2(40 times that of ones skin)
Thicken if lungs become waterlogged and
edematous, whereby gas exchange is inadequateand oxygen deprivation results
Decrease in surface area with emphysema, whenwalls of adjacent alveoli break through
Surface Area and Thickness of the RespiratoryMembrane
SPIROMETER
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SPIROMETER
water
nose clip
LUNG VOLUMES
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LUNG VOLUMES
6000
2900
2400
0
1200
volumeml
tidalvolume
inspiratoryreservevolume
expiratoryreservevolume
residualvolume
inspiratorycapacity
functionalresidualcapacity
FRC
vitalcapacity
total lungcapacity
time
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FRC - functionalresidual capacity
inspirationactive
expirationpassive
expirationactive
inspirationpassive
lung
volume
time
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Respiratory Volumes
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Respiratory Volumes
Tidal volume (TV)air that moves into and out of
the lungs with each breath (approximately 500 ml)
Inspiratory reserve volume (IRV)air that can be
inspired forcibly beyond the tidal volume (2100
3200 ml)
Expiratory reserve volume (ERV)air that can be
evacuated from the lungs after a tidal expiration
(10001200 ml)
Residual volume (RV)air left in the lungs after
strenuous expiration (1200 ml)
Respiratory Capacities
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Respiratory Capacities
Inspiratory capacity (IC)total amount of air that
can be inspired after a tidal expiration (IRV + TV)
Functional residual capacity (FRC)amount of air
remaining in the lungs after a tidal expiration
(RV + ERV)
Vital capacity (VC)the total amount of
exchangeable air (TV + IRV + ERV) Total lung capacity (TLC)sum of all lung
volumes (approximately 6000 ml in males)
Dead Space
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Dead Space
Anatomical dead spacevolume of the conducting
respiratory passages (150 ml)
Alveolar dead spacealveoli that cease to act in gasexchange due to collapse or obstruction
Total dead spacesum of alveolar and anatomical
dead spaces
Pulmonary Function Tests
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Pulmonary Function Tests
Spirometeran instrument consisting of a hollowbell inverted over water, used to evaluate respiratory
function
Spirometry can distinguish between:
Obstructive pulmonary diseaseincreased airway
resistance
Restrictive disordersreduction in total lung
capacity from structural or functional lung changes
Pulmonary Function Tests
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Pulmonary Function Tests
Total ventilationtotal amount of gas flow into or
out of the respiratory tract in one minute
Forced vital capacity (FVC)gas forcibly expelledafter taking a deep breath
Forced expiratory volume (FEV)the amount of
gas expelled during specific time intervals of theFVC
Pulmonary Function Tests
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Pulmonary Function Tests
Increases in TLC, FRC, and RV may occur as a
result of obstructive disease
Reduction in VC, TLC, FRC, and RV result from
restrictive disease
Alveolar Ventilation
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Alveolar Ventilation
Alveolar ventilation rate (AVR)measures the flowof fresh gases into and out of the alveoli during a
particular time
Slow, deep breathing increases AVR and rapid,
shallow breathing decreases AVR
AVR = frequency X (TVdead space)
(ml/min) (breaths/min) (ml/breath)
Nonrespiratory Air Movements
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Nonrespiratory Air Movements
Most result from reflex action
Examples include: coughing, sneezing, crying,
laughing, hiccupping, and yawning
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External Respiration: Pulmonary Gas Exchange
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Factors influencing the movement of oxygen and
carbon dioxide across the respiratory membrane
Partial pressure gradients and gas solubilities
Matching of alveolar ventilation and pulmonary
blood perfusion
Structural characteristics of the respiratorymembrane
External Respiration: Pulmonary Gas Exchange
Partial Pressure Gradients and Gas Solubilities
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The partial pressure oxygen (PO2) of venous blood
is 40 mm Hg; the partial pressure in the alveoli is
104 mm Hg
This steep gradient allows oxygen partial pressures
to rapidly reach equilibrium (in 0.25 seconds), and
thus blood can move three times as quickly (0.75
seconds) through the pulmonary capillary and stillbe adequately oxygenated
Partial Pressure Gradients and Gas Solubilities
Partial Pressure Gradients and Gas Solubilities
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Although carbon dioxide has a lower partial pressure
gradient: It is 20 times more soluble in plasma than oxygen
It diffuses in equal amounts with oxygen
Partial Pressure Gradients and Gas Solubilities
Partial Pressure Gradients
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Partial Pressure Gradients
Figure 22.17
Internal Respiration
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The factors promoting gas exchange between
systemic capillaries and tissue cells are the same as
those acting in the lungs
The partial pressures and diffusion gradients are
reversed
PO2 in tissue is always lower than in systemic
arterial blood
PO2 of venous blood draining tissues is 40 mm Hgand PCO2 is 45 mm Hg
Internal Respiration
Oxygen Transport
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Molecular oxygen is carried in the blood:
Bound to hemoglobin (Hb) within red blood cells
Dissolved in plasma
Oxygen Transport
Oxygen Transport: Role of Hemoglobin
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Each Hb molecule binds four oxygen atoms in a
rapid and reversible process The hemoglobin-oxygen combination is called
oxyhemoglobin (HbO2)
Hemoglobin that has released oxygen is called
reduced hemoglobin (HHb)
Oxygen Transport: Role of Hemoglobin
HHb + O2
Lungs
Tissues
HbO2 + H+
Hemoglobin (Hb)
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Saturated hemoglobinwhen all four hemes of the
molecule are bound to oxygen
Partially saturated hemoglobinwhen one to threehemes are bound to oxygen
The rate that hemoglobin binds and releases oxygenis regulated by:
PO2, temperature, blood pH, PCO2, and the
concentration of BPG (an organic chemical)
These factors ensure adequate delivery ofoxygen to tissue cells
Hemoglobin (Hb)
Influence of PO2 on Hemoglobin Saturation
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Hemoglobin saturation plotted against PO2 produces
a oxygen-hemoglobin dissociation curve
98% saturated arterial blood contains 20 ml oxygen
per 100 ml blood (20 vol %)
As arterial blood flows through capillaries, 5 ml
oxygen are released
The saturation of hemoglobin in arterial bloodexplains why breathing deeply increases the PO2 but
has little effect on oxygen saturation in hemoglobin
Influence of PO2 on Hemoglobin Saturation
Hemoglobin Saturation Curve
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Hemoglobin is almost completely saturated at a PO2of 70 mm Hg
Further increases in PO2 produce only smallincreases in oxygen binding
Oxygen loading and delivery to tissue is adequate
when PO2 is below normal levels
Hemoglobin Saturation Curve
Hemoglobin Saturation Curve
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Only 2025% of bound oxygen is unloaded duringone systemic circulation
If oxygen levels in tissues drop:
More oxygen dissociates from hemoglobin and isused by cells
Respiratory rate or cardiac output need not increase
e og ob Satu at o Cu e
Hemoglobin Saturation Curve
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g
Figure 22.20
Other Factors Influencing Hemoglobin
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Temperature, H
+
, PCO2, and BPG Modify the structure of hemoglobin and alter its
affinity for oxygen
Increases of these factors:Decrease hemoglobins affinity for oxygen
Enhance oxygen unloading from the blood
Decreases act in the opposite manner
These parameters are all high in systemic capillarieswhere oxygen unloading is the goal
g gSaturation
Other Factors Influencing Hemoglobin
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Figure 22.21
g gSaturation
Factors That Increase Release of Oxygen by
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As cells metabolize glucose, carbon dioxide isreleased into the blood causing:
Increases in PCO2 and H+ concentration in capillary
blood
Declining pH (acidosis), which weakens thehemoglobin-oxygen bond (Bohr effect)
Metabolizing cells have heat as a byproduct and therise in temperature increases BPG synthesis
All these factors ensure oxygen unloading in thevicinity of working tissue cells
yg yHemoglobin
Hemoglobin-Nitric Oxide Partnership
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Nitric oxide (NO) is a vasodilator that plays a role in
blood pressure regulation
Hemoglobin is a vasoconstrictor and a nitric oxide
scavenger (heme destroys NO)
However, as oxygen binds to hemoglobin:
Nitric oxide binds to a cysteine amino acid on
hemoglobin
Bound nitric oxide is protected from degradation by
hemoglobins iron
g p
Hemoglobin-Nitric Oxide Partnership
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The hemoglobin is released as oxygen is unloaded,
causing vasodilation
As deoxygenated hemoglobin picks up carbon
dioxide, it also binds nitric oxide and carries these
gases to the lungs for unloading
g p
Carbon Dioxide Transport
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Carbon dioxide is transported in the blood in three
forms
Dissolved in plasma7 to 10%
Chemically bound to hemoglobin20% is carried
in RBCs as carbaminohemoglobin
Bicarbonate ion in plasma70% is transported asbicarbonate (HCO3
)
p
Transport and Exchange of Carbon Dioxide
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Carbon dioxide diffuses into RBCs and combines
with water to form carbonic acid (H2CO
3), which
quickly dissociates into hydrogen ions and
bicarbonate ions
In RBCs, carbonic anhydrase reversibly catalyzes
the conversion of carbon dioxide and water to
carbonic acid
p g
CO2 + H2O H2CO3 H+ + HCO3
Carbon
dioxideWater
Carbonic
acid
Hydrogen
ion
Bicarbonate
ion
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Transport and Exchange of Carbon Dioxide
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At the tissues:
Bicarbonate quickly diffuses from RBCs into the
plasma The chloride shiftto counterbalance the outrush
of negative bicarbonate ions from the RBCs,
chloride ions (Cl
) move from the plasma into theerythrocytes
Transport and Exchange of Carbon Dioxide
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At the lungs, these processes are reversed
Bicarbonate ions move into the RBCs and bind
with hydrogen ions to form carbonic acid
Carbonic acid is then split by carbonic anhydrase to
release carbon dioxide and water
Carbon dioxide then diffuses from the blood intothe alveoli
Transport and Exchange of Carbon Dioxide
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Figure 22.22b
Haldane Effect
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The amount of carbon dioxide transported is
markedly affected by the PO2
Haldane effectthe lower the PO2 and hemoglobin
saturation with oxygen, the more carbon dioxide can
be carried in the blood
Haldane Effect
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At the tissues, as more carbon dioxide enters theblood:
More oxygen dissociates from hemoglobin (Bohr
effect)
More carbon dioxide combines with hemoglobin,
and more bicarbonate ions are formed
This situation is reversed in pulmonary circulation
Haldane Effect
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Figure 22.23
Influence of Carbon Dioxide on Blood pH
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The carbonic acidbicarbonate buffer system resistsblood pH changes
If hydrogen ion concentrations in blood begin to
rise, excess H+ is removed by combining withHCO3
If hydrogen ion concentrations begin to drop,
carbonic acid dissociates, releasing H+
Influence of Carbon Dioxide on Blood pH
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Changes in respiratory rate can also:
Alter blood pH Provide a fast-acting system to adjust pH when it
is disturbed by metabolic factors
S mm f s t s t
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Summary of gas transport
Control of Respiration:C
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The dorsal respiratory group (DRG), or inspiratorycenter:
Is located near the root of nerve IX
Appears to be the pacesetting respiratory center
Excites the inspiratory muscles and sets eupnea(12-15 breaths/minute)
Becomes dormant during expiration
The ventral respiratory group (VRG) is involved inforced inspiration and expiration
Medullary Respiratory Centers
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Control of Respiration:M d ll R i C
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Figure 22.24
Medullary Respiratory Centers
Control of Respiration:P R i t C t
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Pons centers:
Influence and modify activity of the medullary
centers
Smooth out inspiration and expiration transitions
and vice versa
The pontine respiratory group (PRG)continuouslyinhibits the inspiration center
Pons Respiratory Centers
Respiratory Rhythm
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A result of reciprocal inhibition of theinterconnected neuronal networks in the medulla
Other theories include
Inspiratory neurons are pacemakers and have
intrinsic automaticity and rhythmicity
Stretch receptors in the lungs establish respiratoryrhythm
Depth and Rate of Breathing
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Inspiratory depth is determined by how actively the
respiratory center stimulates the respiratory muscles
Rate of respiration is determined by how long theinspiratory center is active
Respiratory centers in the pons and medulla are
sensitive to both excitatory and inhibitory stimuli
Medullary Respiratory Centers
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Figure 22.25
Depth and Rate of Breathing: Reflexes
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Pulmonary irritant reflexesirritants promote
reflexive constriction of air passages
Inflation reflex (Hering-Breuer)stretch receptorsin the lungs are stimulated by lung inflation
Upon inflation, inhibitory signals are sent to the
medullary inspiration center to end inhalation andallow expiration
Depth and Rate of Breathing: Higher BrainCenters
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Hypothalamic controls act through the limbic
system to modify rate and depth of respiration
Example: breath holding that occurs in anger
A rise in body temperature acts to increaserespiratory rate
Cortical controls are direct signals from the cerebral
motor cortex that bypass medullary controls
Examples: voluntary breath holding, taking a deep
breath
Centers
Depth and Rate of Breathing: PCO2
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Changing PCO2
levels are monitored by
chemoreceptors of the brain stem
Carbon dioxide in the blood diffuses into the
cerebrospinal fluid where it is hydrated Resulting carbonic acid dissociates, releasing
hydrogen ions
PCO2 levels rise (hypercapnia) resulting in increased
depth and rate of breathing
Depth and Rate of Breathing: PCO2
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Figure 22.26
Depth and Rate of Breathing: PCO2
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Hyperventilationincreased depth and rate ofbreathing that:
Quickly flushes carbon dioxide from the blood
Occurs in response to hypercapnia
Though a rise CO2 acts as the original stimulus,
control of breathing at rest is regulated by thehydrogen ion concentration in the brain
Depth and Rate of Breathing: PCO2
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Hypoventilationslow and shallow breathing due to
abnormally low PCO2
levels
Apnea (breathing cessation) may occur until PCO2
levels rise
Depth and Rate of Breathing: PCO2
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Arterial oxygen levels are monitored by the aortic
and carotid bodies Substantial drops in arterial PO2 (to 60 mm Hg) are
needed before oxygen levels become a major
stimulus for increased ventilation
If carbon dioxide is not removed (e.g., as in
emphysema and chronic bronchitis), chemoreceptors
become unresponsive to PCO2 chemical stimuli
In such cases, PO2 levels become the principal
respiratory stimulus (hypoxic drive)
Depth and Rate of Breathing: Arterial pH
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Changes in arterial pH can modify respiratory rate
even if carbon dioxide and oxygen levels are normal
Increased ventilation in response to falling pH is
mediated by peripheral chemoreceptors
Peripheral Chemoreceptors
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Figure 22.27
Depth and Rate of Breathing: Arterial pH
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Acidosis may reflect:
Carbon dioxide retention
Accumulation of lactic acid
Excess fatty acids in patients with diabetes mellitus
Respiratory system controls will attempt to raise thepH by increasing respiratory rate and depth
Ventilation and work
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Increased work is initially matched by increasedventilation
At low work rates, extra ventilation achieved largely by
increased tidal volume
As work continues to increase, breathing rate begins to
increase, and tidal volume increases more.
At the ventilatory break point, ventilation increases
disproportionately to work.
Respiratory Adjustments: Exercise
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Respiratory adjustments are geared to both theintensity and duration of exercise
During vigorous exercise:
Ventilation can increase 20 fold
Breathing becomes deeper and more vigorous, butrespiratory rate may not be significantly changed(hyperpnea)
Exercise-enhanced breathing is not prompted by anincrease in PCO2 or a decrease in PO2 or pH
These levels remain surprisingly constant duringexercise
Respiratory Adjustments: Exercise
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As exercise begins:
Ventilation increases abruptly, rises slowly, and
reaches a steady state
When exercise stops:
Ventilation declines suddenly, then gradually
decreases to normal
Ventilation during exercise
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Respiratory Adjustments: Exercise
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Neural factors bring about the above changes,
including:
Psychic stimuli
Cortical motor activation
Excitatory impulses from proprioceptors in muscles
Respiratory Adjustments: High Altitude
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The body responds to quick movement to high
altitude (above 8000 ft) with symptoms of acutemountain sicknessheadache, shortness of breath,
nausea, and dizziness
Respiratory Adjustments: High Altitude
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Acclimatizationrespiratory and hematopoietic
adjustments to altitude include:
Increased ventilation2-3 L/min higher than at sea
level
Chemoreceptors become more responsive to PCO2
Substantial decline in PO2 stimulates peripheral
chemoreceptors
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8/3/2019 Faal Paru_ringkas
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