Chapter 23: The Respiratory System BIO 211 Lecture Instructor: Dr. Gollwitzer 1.
-
Upload
jody-mcdowell -
Category
Documents
-
view
234 -
download
2
Transcript of Chapter 23: The Respiratory System BIO 211 Lecture Instructor: Dr. Gollwitzer 1.
Chapter 23: The Respiratory System
BIO 211 LectureInstructor: Dr. Gollwitzer
1
• Today in class we will:– Describe the functions of the organs and anatomical
structures of the respiratory system– Distinguish between external respiration and internal
respiration• Describe the key steps in external respiration
– Define pulmonary ventilation and begin to describe the general roles of pressure changes, muscle movement and respiratory rates and volumes• Pressure changes
– Discuss the general relationship between gas pressure, volume and airflow into/out of the lungs
– Define respiratory cycle, inhalation/inspiration and exhalation/expiration– Define intrapulmonary pressure and intrapleural pressure
» Discuss how intrapulmonary pressure and intrapleural pressure change during the respiratory cycle
2
Energy• Produced by cells for:– Maintenance– Growth – Defense – Replication
• Usually obtained through aerobic mechanisms– Requires O2 and produces CO2
– O2 and CO2 exchange occurs in lungs• CVS = link between exchange surfaces of
lungs and interstitial fluids3
Functions of the Respiratory System
• Provides large area for gas exchange between air and blood
• Moves air to/from exchange surfaces of lungs (alveoli)
• Protects respiratory surfaces– From dehydration, temperature changes, invasion
by pathogens• Produces sounds, e.g., speaking, singing• Provides olfactory sensations to CNS– From olfactory epithelium in nasal cavity
4
Respiratory Physiology
• Respiration = 2 integrated processes• Internal (cellular, mitochondrial) respiration
(see Chapter 25)– O2 uptake and CO2 production by individual cells
• External respiration– Exchange of O2 and CO2 between interstitial fluids
and the external environment– Involves the respiratory system
5
External Respiration
6Figure 23-12
3 Processes of External Respiration
• Pulmonary ventilation = breathing– Physical movement of air into/out of lungs
• Gas diffusion (O2 and CO2)– Across respiratory membrane (between alveolar air
spaces and alveolar capillaries)– Across capillary walls in peripheral tissues
• Transport of O2 and CO2
– Between alveolar capillaries and capillary beds in other tissues
7
3 Processes of External Respiration
• Any abnormality in one of these processes affects:– Gas concentration of interstitial fluids– Cellular activity
• If O2 declines, affected tissue oxygen-starved (hypoxia)
• If supply cut off entirely, results in anoxia
8
Pulmonary Ventilation
• Physical movement of air into/out of lungs• Primary function– To maintain adequate alveolar ventilation (air
into/out of alveoli)
• Ensures continuous supply of O2
– Keeps pace with absorption by bloodstream
• Prevents build up of CO2 in alveoli
• Process governed by basic principles/laws
9
Law of Gas Volume and Pressure (Boyle’s Law)
• Inverse relationship between gas volume and pressure– If you decrease volume of a gas, its pressure rises– If you increase the volume of a gas, its pressure
falls
• Air flows from area of higher pressure to area of lower pressure (down a gradient)
• Provides basis for pulmonary ventilation
10
Figure 23-13, 7th edition
Gas Volume and Pressure
11
Respiratory Cycle• Consists of:– An inspiration/inhalation– An expiration/exhalation
• Volume of thoracic cavity changes– With expansion/contraction of diaphragm or rib
cage• Causes volume changes in lungs that create
changes in pressure• Creates pressure gradients that move air
into/out of the respiratory tract
12
Mechanisms ofPulmonary Ventilation
• Volume of thoracic cavity changes when:– Diaphragm changes position• Forms floor of thoracic cavity• Relaxed shape is dome that projects superiorly into
thoracic cavity• Contracted shape flattens and moves inferiorly
– Rib cage (ribs and sternum) moves• Elevated• Lowered
13
Figure 23-14, 7th edition 14
Mechanisms ofPulmonary Ventilation
• Volume of thoracic cavity increases when:– Diaphragm contracts (flattens and moves
inferiorly)– Rib cage is elevated (increases depth and width)
• Volume of thoracic cavity decreases when:– Diaphragm relaxes and returns to dome shape– Rib cage is lowered
15
Mechanisms ofPulmonary Ventilation
• Process of breathing– At start of breath:• Pressures inside and outside thoracic cavity are the
same• No air moving in or out of lungs
– When thoracic cavity enlarges, pleural cavities and lungs expand to fill additional space
– Expansion of lungs lowers pressure inside lungs
16
Mechanisms ofPulmonary Ventilation
• Process of breathing (continued)– Air enters RT because pressure inside is lower
than outside (atmospheric pressure)– Air continues to enter until volume stops
increasing and internal pressure = outside pressure
– When thoracic cavity decreases in size, pressure rises inside lungs, forcing air out of RT
17
Mechanisms ofPulmonary Ventilation
• Direction of air flow determined by relationship between:– Atmospheric pressure (760 mm Hg)– Intrapulmonary pressure (= intra-alveolar
pressure) • When lungs expand (inhalation)
– Pressure decreases (to 759 mm Hg) in alveoli– Air moves in
• When lungs contract (exhalation)– Pressure increases (to 761 mm Hg)– Air moves out
18
Figure 23-15 19
Mechanisms ofPulmonary Ventilation
• Size of pressure gradient increases when breathing heavily– -30 mm Hg during inhalation (730 mm Hg)– +100 mm Hg straining with glottis closed (860 mm
Hg)
• When lifting weights, exhale because this keeps intrapulmonary and peritoneal pressures from climbing so high that alveolar rupture or hernia could occur
20
Pulmonary Ventilation
• Respiratory cycle– Single cycle of inhalation and exhalation
• Tidal volume (TV)– Amount of air moved into/out of lungs during
single cycle– Approx 500 mL
• Amount in (inhalation) = amount out (exhalation)
21
Pleural Cavity• Contains lung• Parietal and visceral pleura separated by thin film of
pleural fluid• Pleurae can slide along each other but great force
needed to pull apart– Fluid bond exists between parietal and visceral pleurae– Pulling apart creates suction (like wet glass on smooth
surface)
• RESULT: surface of lung sticks to inner wall of chest and superior surface of diaphragm
22
Intrapleural Pressure• = pressure in the pleural cavity– Measured in space between parietal and visceral pleurae
• Always lower than atmospheric pressure throughout normal cycles of inhalation/ exhalation– Elastic fibers in lungs pull visceral pleura away from
parietal pleura– Pull increases intrapleural space and lowers intrapleural
pressure• Average = -4 mm Hg (756 mm Hg)– Decreases to -6 mm Hg during inhalation– Increases to -2.5 mm Hg during exhalation
• Cyclical changes operate respiratory pump– Aids in venous return to heart
23
Pneumothorax
• Injury to chest wall that allows air into pleural cavity– Breaks fluid bond between pleurae– Allows elastic fibers to recoil– RESULT = atelectasis (collapsed lung)
• Treatment– Remove as much air as possible and seal opening– Lowers intrapleural pressure and reinflates lung
24
• Today in class we will:– Define pulmonary ventilation and continue our description of the general
roles of pressure changes, muscle movement and respiratory rates and volumes• Discuss muscle movement
– The mechanics of breathing– Define compliance and identify the factors that affect it
• Discuss respiratory rates and volumes– Define respiratory rate, respiratory minute volume, alveolar ventilation and
anatomic dead space– Distinguish between various pulmonary volumes, such as tidal volume, expiratory
reserve volume, residual volume and inspiratory reserve volume• Define vital capacity and total lung capacity
– Discuss gas exchange• Define partial pressure and describe the partial pressures of O2 and CO2 in alveolar air
and capillaries, the systemic circuit and interstitial fluid.• Principles that govern the diffusion of gases into and out of the blood• Describe the important structural features and function of the respiratory membrane
25
Mechanics of Breathing
• Inhalation– Always active
• Exhalation– Active or passive
26
Modes of Breathing• Respiratory muscles used in various
combinations, depending on volume of air to be moved into/out of system
• 2 modes of breathing– Eupnea• Quiet breathing
– Hyperpnea• Forced breathing
27
Modes of Breathing: Eupnea• Inhalation active (uses muscular contractions)• Exhalation passive• Costal/shallow breathing– External intercostals contract– Elevate ribs and enlarge thoracic cavity
• Diaphragmatic/deep breathing– Diaphragm contracts– Increases thoracic volume
28
Figure 23-16 29
Modes of Breathing: Hyperpnea• An abnormal increase in rate and depth of
breathing• Active inhalation and exhalation• Involves accessory muscles– Internal intercostals– Pectoralis minor– Sternocleidomastoid– Serratus anterior
30
Apnea• Cessation of breathing• Often occurs during sleep• Signaled by snoring followed by tiredness
next day• Can lead to: heart disease, high BP, clots,
stroke• Important to treat, e.g., continuous pressure
air pump (CPAP) that keeps airways open
31
Compliance• = expandability; the ability of the lungs to tolerate
changes in volume (how easily the lungs expand)• Lower compliance requires more force to fill the lungs• Greater compliance requires less force to fill the lungs• Factors affecting compliance:– Connective tissue (Ct) of lungs
• Loss of supporting Ct due to alveolar damage increases compliance
– Level of surfactant production• Inadequate surfactant can cause alveoli to collapse upon exhalation
– Mobility of thoracic cage• Arthritis and other skeletal disorders can affect expandability of
ribcage
32
Respiratory Terminology/Values• Respiratory rate = number of breaths/min– Normal, resting adult = 12-18– Child = 18-20
• Tidal volume (TV) = amount of air moved in and out of lungs in single respiratory cycle– 500 mL/breath– 350 mL travels along passageways and enters
alveoli– 150 mL remains in conducting passages; never
gets further than passageways = anatomic dead space
33
Respiratory Terminology/Values• Respiratory minute volume = amount of air moved
(L/min)– = respiratory rate (breaths/min) X tidal volume (L/breath)– At rest = 12 breaths/min X 500 mL/breath = 6000 mL/min
or 6L/min– Can be increased by increasing respiratory rate and/or
tidal volume• Alveolar ventilation = amount of air reaching alveoli
each minute– = respiratory rate X (TV – anatomic dead space)– At rest = 12 breaths/min X 350 mL = 4.2 L/min– Can be increased by increasing the respiratory rate and/or
TV
34
Fig. 23-17
Respiratory Volumes/Capacities
35
Respiratory Volumes• Inspiratory reserve volume (IRV)– = Amount of air you can take in over and above TV
• Expiratory reserve volume (ERV)– = Amount of air expelled after a complete and
normal respiratory cycle• Residual volume (RV)– = Amount of air that remains in lungs after
maximum exhalation
36
Respiratory Volumes• Vital capacity (VC)– = absolute maximum amount of air you can move
into or out of lungs in a single respiratory cycle
– = TV + IRV + ERV
• Total lung capacitance (TLC) = total volume of lungs– = VC + RV
37
Pulmonary Function Tests• Measure rate/volumes of air movements• Use spirometer, peak flow meter,
pneumotachometer• Values abnormal in:– Asthmatics (asthma = reversible constriction of
smooth muscle around respiratory passageways)– Smokers
38
Gas Diffusion/Exchange at Respiratory Membrane
• Pulmonary ventilation ensures alveoli are supplied with O2, removes CO2
• Gas exchange– Occurs between blood and alveolar air spaces
across respiratory membrane– Depends on:• Partial pressures of gases• Diffusion of molecules between gas and liquid
39
Gas Laws• Diffusion occurs in response to:– Concentration gradients– Pressure gradients
• Pressure gradients– Cause gases to move from high pressure to low pressure– Cause gases to move in and out of solution
• Rate of diffusion depends on physical principles or gas laws, e.g., gas volume and diffusion
• Also determined by:– Law of Partial Pressures (Dalton’s Law)– Law of Solubility and Pressure (Henry’s Law)
40
Law of Partial Pressures(Dalton’s Law)
• Air we breathe is mixture of gases– N2 (Nitrogen) = 78.6%– O2 (Oxygen) = 20.9%– H2O (water) = 0.5%– CO2 (Carbon dioxide)= 0.04%
• Atmospheric pressure = 760 mm Hg– = Combined effects of different molecules colliding in air– Each gas contributes a partial pressure (P) to the total
• Because we know the percentage for each gas, we can calculate the P for each– PN2
+PO2 +PH2O+PCO2 = 760 mm Hg
– 597+159+4+0.3 = 760.3 mm Hg
41
Law of Solubility and Pressure (Henry’s Law)
• Amount of a gas in solution:– Is directly proportional to partial pressure of that gas (at a given
temperature)• When gas under pressure comes in contact with liquid:
– Pressure forces gas molecules into solution until equilibrium reached• At equilibrium, molecules that diffuse in = molecules that
diffuse out• If P increases, more gas molecules go in
– e.g. soda can (CO2 put in under pressure and can sealed)
• If P decreases, more gas molecules come out of solution– e.g., open soda can, CO2 starts coming out until totally gone ( flat
soda)
42
Figure 23-18, 7th edition 43
Decompression Sickness
• Caused by sudden drop in atmospheric pressure• Because N2 has a high partial pressure it– Comes out of solution– Forms bubbles in joint cavities, CSF, bloodstream (like
shaken soda can)• Causes great pain curl up “bends”• Affects:– Scuba divers (breathing air under greater than normal
pressures)– People in airplanes with sudden loss of cabin pressure
44
Gas Diffusion/Exchange at Respiratory Membrane
• Site of gas exchange• Very efficient• Rapid diffusion because:– Gases lipid soluble, travel
easily across membrane– Substantial differences in P
across respiratory membrane
– Distances very small– Large total surface area
45Figure 23-11c
Gas Diffusion/Exchange at Respiratory Membrane
• Blood flow and air flow coordinated– Blood flow greatest around alveoli with highest PO2
values
• Coordination lost when one part impaired– Blood flow impairment, e.g., pulmonary embolism– Air flow impairment, e.g., pulmonary obstruction
46
Figure 23-19
Partial Pressures
47
Blood Gas Analysis
• Measurement of pH, PCO2, PO2
• Useful in monitoring:– Heart attack victims– Asthmatics (COPD = chronic obstructive
pulmonary disease)
48
• Today in class we will:– Discuss O2 and CO2 transport
• O2 transport– Describe how O2 is transported in the blood– Describe a normal oxygen-hemoglobin saturation curve and the
effects of pH and temperature on that curve• CO2 transport
– Describe how CO2 is transported in the blood– Discuss the effects of carbon monoxide (CO)
– Discuss control of respiration• Describe how changes in blood flow and O2 delivery are regulated
at the local level• Name the 3 respiratory centers, their locations and their basic
functions– Discuss the respiratory reflexes and describe their role in
respiration49
Transport of O2 and CO2
• O2 and CO2 have limited solubility in plasma
• Problem solved by RBCs– Remove O2 from plasma and bind to hemoglobin
– Remove CO2 from plasma and convert to soluble compounds
• Reactions are temporary and completely reversible– If tissue gases high, excess removed by RBCs– If too low, RBCs release stored reserves
50
O2 Transport• In blood leaving alveolar capillaries:– 1.5 % of O2 in solution
– Rest bound to Fe ions in center of heme units of hemoglobin molecules
• Each Hb can bind 4 molecules of O2 oxyhemoglobin
• Hb + O2 HbO2
(reversible reaction)• > 1 billion O2 molecules/RBC!
51
Figure 19-3, 7th edition 52
Hemoglobin Saturation
• O2 carrying capacity of Hb– = % of total heme units bound to O2
• Presented in a graph• Curved (vs. straight) line because:– Hb changes shape each time O2 molecule bound
– Each O2 bound makes next O2 binding easier • Factors that affect saturation– Blood PO2
– Blood pH– Temperature
53
Hemoglobin Saturation
• Blood PO2
– High PO2 % saturation of hemoglobin increases
• e.g., at PO2 = 100 mm Hg, Hb sa = 98%
– Low PO2 % saturation of hemoglobin decreases
• e.g., at PO2 = 40 mm Hg, Hb sa = 75%
– Automatically regulates O2 delivery
54
Figure 23-20 55
Hemoglobin Saturation• Blood pH– Active tissues generate acids that lower pH of
interstitial fluid and blood• CO2 HCO3 H+ + HCO3
-
• When PCO2 increases, H+ increases, pH decreases (more
acidic)
– Decreased blood pH • Change in shape of hemoglobin releases O2 more
readily• % Hb saturation decreases
– “ Bohr Effect”56
Figure 23-21, 7th edition 57
Hemoglobin Saturation
• Temperature– Increase in temp Hb releases more O2
– Decrease in temp Hb binds O2 more tightly
– Significant only in active tissues where heat is generated, e.g., skeletal muscles
58
CO2 Transport
• After entering bloodstream, CO2 is:– Converted to carbonic acid (70%) – Bound to Hb inside RBCs
carbaminohemoglobin (23%)– Remains dissolved in plasma (7%)
• Completely reversible reactions
59
Figure 23-23 60
Figure 23-24 61
CO (Carbon Monoxide) Poisoning• CO produced from burning fuels, e.g.,
combustion in engines, space heaters, etc.• CO competes with O2 for binding sites on Hb
• CO “wins” because has greater affinity than O2
• Very strong attachment• Makes Hb unavailable for O2
• Treatment– Administer pure O2 to force CO off and O2 on Hb
– Transfuse RBCs
62
Control of Respiration• O2 absorption and delivery =
CO2 production and removal
• If unbalanced, homeostatic mechanisms restore equilibrium
• Mechanisms involved– Local factors• Control blood flow and O2 and CO2 exchange and
transport
– Respiratory centers• Control depth and rate of respiration
63
Control of Respiration:Local Factors
• Regulate O2 delivery to and CO2 removal from tissues– Active tissues dec PO2
and inc PCO2
– Inc PCO2 relaxed smooth muscle in arterioles and
capillaries vasodilation inc blood flow– More PO2
delivered, more CO2 carried away• Coordinate alveolar blood flow– Low alveolar PO2
alveolar capillaries constrict– Blood flows toward alveolar capillaries where PO2
is high• Coordinate alveolar airflow– Inc PCO2
in bronchioles relaxed smooth muscle in bronchioles bronchodilation inc air flow out of lungs; dec PCO2
bronchoconstriction
64
Control of Respiration:Respiratory Centers
• In brain stem (i.e., pons, medulla oblongata)– Body’s autopilot– Also has centers for HR, BP, temp
• 3 pairs of nuclei that regulate respiratory muscles – Respiratory rhythmicity centers (in medulla
oblongata) – set rate– Apneustic centers (in pons) – cause inspiration– Pneumotaxic centers (in pons) – inhibit apneustic
and promote exhalation
65
Respiratory Centers and Reflex Controls
Figure 23–26, Part 4 66
Control of Respiration:Respiratory Reflexes
• Baroreceptors• Chemoreceptors
67
Control of Respiration:Baroreceptor Reflexes
• Baroreceptors– Monitor amount of stretch in walls of• Arteries• R atrium
– Located in• Carotid sinuses (expanded chambers near base of
internal carotid arteries) (Fig 21-22)• Aortic sinuses (sac-like dilations at base of ascending
aorta) (Fig 20-8b)– Respond to changes in BP (see Chapter 21)• Affect respiratory rhythmicity centers
– Inc BP dec respiratory rate– Dec BP inc respiratory rate
68
69Figure 21-22
70Figure 20-8b, 7th edition
Control of Respiration:Chemoreceptor Reflexes
• Chemoreceptors– Respond to inc CO2, dec pH, dec O2 in arteries or
CSF– Located in• Carotid bodies (near carotid sinuses)• Aortic bodies (near aortic arch)
– Stimulate respiratory rhythmicity centers (in medulla oblongata), e.g., inc CO2 • Inc respiratory rate• Inc elimination of CO2 at alveoli• Dec PCO2
71
Control of Respiration:Voluntary Control
• Conscious and unconscious thought processes also affect respiration– Fear stimulates sympathetic system
bronchodilation and inc respiratory rate– Relaxation has opposite effect
• Cannot override respiratory center activity or chemoreceptor reflexes by holding breath– When PCO2
increases to critical level, forced to breathe
72
Aging and the Respiratory System
• Respiratory system less efficient in elderly• Elastic tissue deteriorates dec vital
capacity of lungs• Chest movements restricted by:– Arthritic changes– Decreased flexibility of costal cartilages
• Some degree of emphysema usually present
73
Emphysema
• Chronic, progressive condition• Characterized by shortness of breath and
inability to tolerate physical exertion• Alveoli expand, merge larger air spaces
supported by fibrous tissue without capillaries• Loss of respiratory surface restricts O2
absorption• Associated with cigarette smoke and aging
74
Figure 23-28
Respiratory Performance
75
Lung Cancer• Aggressive cancer• Originates in epithelial cells of bronchioles or
alveoli• Diagnosis usually delayed until tumor masses
restrict airflow• Signs/symptoms: chest pain, shortness of
breath, cough/wheeze, weight loss• Treatment: surgery, radiation exposure,
chemotherapy• Associated with smoking
76