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