Post on 01-Jun-2015
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings.
PowerPoint® Lecture Slide Presentation by Robert J. Sullivan, Marist College
RESPIRATIONRESPIRATION
Chapter 37 PULMONARY VENTILATION
DR FARZANA MAJEED
Human Respiratory System
Figure 10.1
Respiratory system extracts oxygen from the atmosphere , and the body utilizes the oxygen and produce CO2 as a result of metabolism.
RESPIRATORY SYSTEM
Basic functions of the respiratory system
1. Breathing (Pulmonary Ventilation) – movement of air in and out of the lungs
• Inhalation (inspiration) draws gases into the lungs.• Exhalation (expiration) forces gases out of the lungs.
Non –pulmonary functions:
2. Gas Conditioning – as gases pass through the nasal cavity and paranasal sinuses, inhaled air becomes turbulent. The gases in the air are
• warmed to body temperature• humidified• cleaned of particulate matter
3. Protects respiratory surfaces4. Site for olfactory sensation 5. Secretes pulmonary alveolar macrophages6. Endocrine functions
7. Immune function8. Vocalization9. Coughing and sneezing to eliminate irritants from respiratory tract10. Production of surfactant
Respiration processes
Components of the Upper Respiratory Tract
Figure 10.2
Passageway for respiration Receptors for smell Filters incoming air to filter larger
foreign material Moistens and warms incoming air Resonating chambers for voice
Upper Respiratory Tract Functions
Components of the Lower Respiratory Tract
Figure 10.3
Functions: Larynx: maintains an open airway, routes food and air appropriately, assists in sound production
Trachea: transports air to and from lungs Bronchi: branch into lungs Lungs: transport air to alveoli for gas exchange
Lower Respiratory Tract
Mechanics of breathing
Pulmonary ventilation is accomplished
by two processes. Inspiration is an active process and
refers to inflow of air into the lungs. This occurs when the intrapulmonary pressure falls below the atmospheric pressure.
Expiration is a passive process and refers to outflow of air from the lungs. This occurs when intrapulmonary pressure exceeds the atmospheric pressure.
Changes in intrapulmonary pressure which govern respiratory cycle are related to the changes in intrapleural pressure.
Changes in intrapleural pressure in turn depend upon the changes in size of thoracic cavity.
Changes in size of thoracic cavity depend upon the respiratory muscles
Muscles of normal quiet inspiration are diaphragm and external intercostal muscles.
Muscles of forceful inspiration are sternocledomastoid, scalenes and parasternals
Normal quiet expiration is due to elastic recoil of lungs
Muscles of forceful expiration are internal intercostals and abdominal recti
movements of inspiration It is an active process Normally produced by descent of
diaphragm and contraction of inspiratory muscles
Therefore diaphragm and external intercostal muscles contract and cause increase in vertical, antroposterior and transverse diameters of thoracic cavity
Role of diaphragm Helps in 70-75% expansion of chest
during normal inspiration During inspiration , diaphragm
contracts and draw the central tendon part downwards by 1.5cm in quiet breathing and 7cm in deep respiration
Cause an increase in vertical diameter of the thorax
Contraction of diaphragm also lifts the lower ribs causing thoracic expansion laterally and anteriorly
(the bucket handle and pump handle movements respectively)
The respiratory muscles
Role of external intercostal muscles Fibers of external intercostal
muscles are attached to vertebral ends of upper and lower ribs
Contraction leads to elevation of ribs causing lateral and antro posterior enlargement of thoracic cavity
Bucket handle and pump handle movements.
movements of expiration Passive phenomenon brought
about by elastic recoil of lungs Decrease in the size of thoracic
cavity by relaxation of diaphragm and external intercostal muscles
mechanism of forced inspiration Forceful contraction of
diaphragm…..decent 7-10 cm as compared to 1-1.5 cm in quiet breathing
Forceful contraction of external intercostal muscles……..increasing transverse and AP diameter of thoracic cavity
Contraction of accessory muscles Sternocledomastoid contracts and
lifts the sternum upwards Anterior serrati and scaleni
muscles contract and lift ribs upwards
mechanism of forced expiration Contraction of abdominal muscles
causes increase in vertical diameter of thoracic cavity
Downward pull on the lower ribs by contraction of internal intercostal muscles decreases AP and transverse diameter of thoracic cavity
Pressure and volume changes during respiratory cycle
Relationship between intrapulmonary pressure and atmospheric pressure determines direction of air flow
In quiet breathing , at end expiration and at end inspiration .no air is going in and out of the lungs as the intrapulmonary pressure and atmospheric pressures are equal i.e. 0 mmHg
Intra ALVEOLAR pressure (IAP)During normal quiet
inspiration IAP decreases to about -1
mmHg which is sufficient to suck in 500 ml of air into lungs within 2 sec.
At the end of inspiration IPP decreases again to 0 mmHg
During expiration IAP swings slightly towards positive
side (+1 mmHg) which forces 500 ml of air out of lungs in 3 sec
At the end of expiration IPP again decreases to 0 mmHg
Significance Negative pressure in alveoli during
inspiration causes the air to enter into alveoli but during expiration IAP becomes positive so air is expelled out of the lungs
Helps in exchange of gasses between air and lungs
Intrapleural pressure
During normal quiet inspiration It is negative pressure At the start of inspiration -5mmHg which is the minimum amount of pressure to
hold the lungs open at resting level During inspiration becomes more negative ( -7.5mmHg)
During expiration All the events are reversed during expiration
significance As it is negative pressure so it
prevents the collapse of lungs after elastic recoil
This also causes dilatation of larger veins and vena cava. So act as suction pump to pull venous blood from lower part of the body to increase venous return.
Transpulmonary pressure / recoil pressure It is the difference between alveolar
pressure and pleural pressure.
SIGNIFICANCE It is the measure of elastic forces of
lungs that tend to collapse the lungs at each instant of respiration
Pressure changes during inhalation and exhalation
Change in lung volume for each unit change in transpulmonary pressure = stretchiness of lungs
Transpulmonary pressure (TPP) is the difference in pressure between alveolar pressure and pleural pressure.
Value of compliance of both lungs in normal human adult =200ml of air/TPP in cm of H2O
LUNG COMPLIANCE(Hysteresis)
There are 2 different curves according to different phases of respiration.
The curves are called :Inspiratory
compliance curveExpiratory
compliance curve
COMPLIANCE DIAGRAM
Shows the capacity of lungs to “adapt” to small changes of transpulmonary pressure.
compliance is seen at low volumes (because of difficulty with initial lung inflation) and at high volumes (because of the limit of chest wall expansion)
The total work of breathing of the cycle is the area contained in the loop.
Two forces try to collapse the lungs
Elastic forces of lungs Thin layer of fluid Two forces prevent collapse of
the lungs Intra pleural pressure surfactant
Major determinants of compliance diagramA. A. Elastic forces of the lung
tissue itself B. Elastic forces of the
fluid that lines the inside walls of alveoli and other lung air passages (surface tension)
Elastic forces of the lungsThis is provided by• Elastin and• Collagen interwoven in lung parenchyma
Deflated lungs: fibers are contracted and in kinked stateInflated lungs: these fibers become stretched and unkinked exerting more elastic forces
Elastic forces caused by surface tension
Is provided by thesubstance called surfactant that is present inside walls of alveoli.
Experiment:
By adding saline solution there is no interface between air and alveolar fluid. (B forces were removed)
surface tension is not present, only elastic forces of tissue (A)
Transpleural pressures required to expand normal lung = 3x pressure to expand saline filled lung.
Conclusion of this experiment:
Tissue elastic forces (A) = represent 1/3 of total lung elasticity
Fluid air surface tension elastic forces in alveoli (B) = 2/3 of total lung elasticity.
Surface tension water molecules are attracted to
one another. The force of surface tension acts in the
plane of the air-liquid boundary to shrink or minimize the liquid-air interface
In lungs = water tends to attract forcing air out of alveoli to bronchi = alveoli tend to collapse
Elastic contractile force of the entire lungs (forces B)
Forces affecting lung compliance Deformities of thorax like Kyphosis Scoliosis Fibrosis Pleural effusion Paralysis of respiratory muscles
Surface agent which tend to decrease surface tension Synthesized by type II alveolar cells Reduces surface tension (prevents alveolar collapse during expiration)Consists of apoproteins +phospholipid (dipalmitoylphosphatidylcholine) + calcium ions
surfactant
Functions Decreases surface tension in alveoli of the lungs Stabilize the alveoli which have tendency to deflate Prevents bacterial invasion Cleans alveoli surface
Plays important role in inflation of lungs during birth. In fetal life it starts producing after 3rd month and completes at 7 months. Till that time lungs remain collapsed. After birth inflation of lungs takes place with initiation of respiration due to CO2 induced activation of respiratory centers. Although respiratory movements are attempted again and again by the new born tend to collapse the lungs.
Effects of deficiency of surfactant Infants: Collapse of the lungs
called Respiratory distress syndrome (RDS) or hyaline membrane disease
Adults: Collapse of the lungs called Adult respiratory distress syndrome (ARDS)
Surface active agent in water = reduces surface tension of water on the alveolar walls
Pure water (surface pressure)
72 dynes/cm
Normal fluid lining alveoli without surfactant (surface pressure)
50 dynes/cm
Normal fluid lining alveoli with surfactant
5-30 dynes/cm
Respiratory volumes and capacities
Lung Volumes and Capacities
Tidal Volume (VT) amount of air
entering/leaving lungs in a single, “normal” breath
500 ml at rest, with activity
IC
FRC
VC
TLC
Lung CapacitiesPrimary Lung
Volumes
IRV
VT
ERV
RVV
olu
me
(ml)
0
6000
Inspiratory Reserve Volume (IRV) additional volume
of air that can be maximally inspired beyond VT by forced inspiration
3000 ml. at rest
IC
FRC
VC
TLC
Lung CapacitiesPrimary Lung
Volumes
IRV
VT
ERV
RVV
olu
me
(ml)
0
6000
Expiratory Reserve Volume (ERV) additional volume
of air that can be maximally expired beyond VT by forced expiration
1100 ml. at rest
IC
FRC
VC
TLC
Lung CapacitiesPrimary Lung
Volumes
IRV
VT
ERV
RVV
olu
me
(ml)
0
6000
Residual Volume (RV) volume of air
still in lungs following forced max. expiration
1200 ml. at rest
IC
FRC
VC
TLC
Lung CapacitiesPrimary Lung
Volumes
IRV
VT
ERV
RVV
olu
me
(ml)
0
6000
Total Lung Capacity (TLC) total amount of air
that the lungs can hold
amt of air in lungs at the end a maximal inspiration
VT + IRV + ERV + RV
5800ml at rest
IC
FRC
VC
TLC
Lung CapacitiesPrimary Lung
Volumes
IRV
VT
ERV
RVV
olu
me
(ml)
0
6000
Vital Capacity (VC) max. amt. air
that can move out of lungs after a person inhales as deeply as possible
VT + IRV + ERV 4600ml at rest
IC
FRC
VC
TLC
Lung CapacitiesPrimary Lung
Volumes
IRV
VT
ERV
RVV
olu
me
(ml)
0
6000
Inspiratory Capacity (IC) max amt. of air that
can be inhaled from a normal end-expiration
breathe out normally, then inhale as much as possible
VT + IRV 3500ml at rest
IC
FRC
VC
TLC
Lung CapacitiesPrimary Lung
Volumes
IRV
VT
ERV
RVV
olu
me
(ml)
0
6000
Functional Residual Capacity (FRC) amt of air remaining
in the lungs following a normal expiration
ERV +RV 2300ml at rest
IC
FRC
VC
TLC
Lung CapacitiesPrimary Lung
Volumes
IRV
VT
ERV
RVV
olu
me
(ml)
0
6000
Forced Expiratory Volume (FEVt)
Amount of air forcibly expired in t seconds
FEVt = (Vt/VC) x 100% Normally…
FEV1 = ~ 80% VC FEV2 = ~ 94% VC FEV3 = ~ 97% VC
Index of air flow through the respiratory air passages
0 1 2 3
5000
4000
3000
2000
1000
0
Time (sec)V
olu
me
(ml)
FEV1 = (5000 ml -1000 ml) / 5000ml= 4000 ml / 5000 ml= 80%
Restrictive and Obstructive Disorders
Restrictive disorder: Vital capacity
is reduced. FVC is normal.
Obstructive disorder: VC is normal. FEV1 is < 80%.
Insert fig. 16.17
Figure 16.17
Air-Flow Disorders Obstructive disorders
obstruction of the pulmonary air passages air flow radius4
slight obstruction will have large in air flow bronchiolar secretions, inflammation and edema
(e.g. bronchitis), or bronchiolar constriction (e.g. asthma)
reduced FEV, normal VC Restrictive disorders
damage to the lung results in abnormal VC test e.g. pulmonary fibrosis
reduced VC, normal FEV
VentilationPULMONARY VENTILATION
ALVEOLAR VENTILATION
Cyclic process by which fresh air enters and leaves the lungs
Air utilized for gaseous exchange
Product of TV and RR Product of TV excluding dead space volume and RR
PV=TV X RR
500ml X 12/min
600ml or 6L/min
AV= (TV-DSV) X RR
(500-150) X 12/min
4.200ml or 4.2 L/min
Dead space Part of respiratory tract where
gaseous exchange doesn’t take place
Types: Anatomical dead space Physiological dead space
ANATOMICAL DEAD SPACE Volume of respiratory tract from
nose up to terminal bronchiole PHYSIOLOGICAL DEAD SPACE Includes anatomical dead space
plus well perfused but non ventilated alveoli and well ventilated but non perfused alveoli
NORMAL VALUE OF DEAD SPACE
Under normal conditions ADS + PDS
So DSV = 150 ml MEASUREMENT BY N2 Wash method
Cough reflex Stimulus irritants in the respiratory
passages Receptors in respiratory passageways Afferents vagus nerve
Centre medulla Efferents neuronal circuits Effectors / response 2.5 ml of air rapidly inspired epiglottis gets closed
vocal cords get approximated so air trapped in
abdominal muscles contract forcefully so that pressure exceeds 100 mmHg or more
Epiglottis suddenly gets open, air under high pressure in lungs exploded out with the velocity of 70-100 miles /hour