slide1 l.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Chapter 5 Respiration PowerPoint Presentation
Download Presentation
Chapter 5 Respiration

Loading in 2 Seconds...

play fullscreen
1 / 70

Chapter 5 Respiration - PowerPoint PPT Presentation


  • 87 Views
  • Uploaded on

Chapter 5 Respiration. When you can not breath, nothing else matters Slogan of the American Lung Association. Respiration is the process by which the body takes in and utilizes oxygen (O 2 ) and gets rid of carbon dioxide (CO 2 ). An Overview of Key Steps in Respiration.

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Chapter 5 Respiration' - flo


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
chapter 5 respiration
Chapter 5 Respiration

When you can not breath, nothing else matters

Slogan of the American Lung Association

slide3

Respiration is the process by which the body takes in and utilizes oxygen (O2) and gets rid of carbon dioxide (CO2).

slide5

Respiration can be divided into four major functional events

  • Ventilation: Movement of air into and out of lungs
  • Gas exchange between air in lungs and blood
  • Transport of oxygen and carbon dioxide in the blood
  • Internal respiration: Gas exchange between the blood and tissues
slide6

Respiratory System Functions

  • Gas exchange: Oxygen enters blood and carbon dioxide leaves
  • Regulation of blood pH: Altered by changing blood carbon dioxide levels
  • Voice production: Movement of air past vocal folds makes sound and speech
  • Olfaction: Smell occurs when airborne molecules drawn into nasal cavity
  • Protection: Against microorganisms by preventing entry and removing them
  • Metabolism: Synthesize and metabolize different compounds (Nonrespiratory Function of the Lung)
slide8

Ventilation

  • Occurs because the thoracic cavity changes volume
  • Insipiration uses external intercostals and diaphragm
  • Expiration is passive at rest, but uses internal intercostals and abdominals during severe respiratory load
  • Breathing rate is 10-20 breaths / minute at rest, 40 - 45 at maximum exercise in adults
slide12

Pleural fluid produced by pleural membranes

    • Acts as lubricant
    • Helps hold parietal and visceral pleural membranes together
slide14

Conducting

Airways

Lungs

Gas Exchange

Pleural Cavity

Very small space

Maintained at negative pressure

Transmits pressure changes

Allows lung and ribs to slide

Chest Wall

(muscle, ribs)

Diaphragm

(muscle)

Pleural CavityImaginary Space between

Lungs and chest wall

Principles of Breathing

Functional Unit: Chest Wall and Lung

Follows Boyle’s Law:Pressure (P) x Volume (V) = Constant

slide15

CW

Principle of Breathing

Follows Boyle’s Law: PV= C

At Rest with mouth open Pb = Pi = 0

Pb

Airway Open

A

Pi

PS

D

1

slide16

Principle of Breathing

Follows Boyle’s Law: PV= C

  • At Rest with mouth open Pb = Pi = 0
  • Inhalation:
  • Increase Volume of Rib cage
  • Decrease the pleural cavity pressure- Decrease in Pressure inside (Pi) lungs

Pb

Airway Open

A

Pi

PS

CW

D

2

slide17

Principle of Breathing

Follows Boyle’s Law: PV= C

  • At Rest with mouth open Pb = Pi = 0
  • Inhalation:
  • Pb outside is now greater than Pi- Air flows down pressure gradient
  • Until Pi = Pb

Pb

Airway Open

A

Pi

CW

PS

D

3

slide18

Principle of Breathing

Follows Boyle’s Law: PV= C

  • At Rest with mouth open Pb = Pi = 0
  • Exhalation: Opposite Process
  • Decrease Rib Cage Volume

Pb

Airway Open

A

Pi

CW

PS

D

4

slide19

Principle of Breathing

Follows Boyle’s Law: PV= C

  • At Rest with mouth open Pb = Pi = 0
  • Exhalation: Opposite Process
  • Decrease Rib Cage Volume
  • Increase in pleural cavity pressure - Increase Pi

Pb

Airway Open

A

Pi

CW

PS

D

5

slide20

Principle of Breathing

Follows Boyle’s Law: PV= C

  • At Rest with mouth open Pb = Pi = 0
  • Exhalation: Opposite Process
  • Decrease Rib Cage Volume
  • Increase Pi
  • Pi is greater than Pb
  • Air flows down pressure gradient
  • Until Pi = Pb again

Pb

Airway Open

A

Pi

CW

PS

D

6

slide21

Rib Cage

Contract

IntercostalsContractto Lift

Spine

Rib

Diaphragm

Volume

Volume

Ribs

Mechanisms of Breathing: How do we change the volume of the rib cage ?

  • To Inhale is an ACTIVE process
    • Diaphragm
  • External Intercostal Muscles

Both actions occur simultaneously – otherwise not effective

ii resistance of the ventilation
II Resistance of the Ventilation
  • Elastic Resistance
  • Inelastic Resistance
slide24

1. Elastic Resistance

  • A lung is an elastic sac.
  • The thoracic wall is also an elastic element.
  • So during inspiration
    • the inspiratory muscles must expand the thoracic cage
      • which are together with the elastic resistance.
slide25

The elastic forces can be divided into two parts:

    • Caused by the elastic tissue of the lung and the thoracic wall
    • 2) Caused by surface tension of the fluid that lines the inside wall of the alveoli.
  • The elastic forces caused by surface tension are much more complex.
  • Surface tension accounts for about two thirds of the total elastic forces in a normal lungs.
slide26
Surface tension (表面张力): a measure of the attraction force of the surface molecules per unit length of the material to which they are attached
slide27

Surface Tension

  • Force exerted by fluid in alveoli to resist distension
  • Lungs secrete and absorb fluid, leaving a very thin film of fluid.
    • This film of fluid causes surface tension..
  • H20 molecules at the surface are attracted to other H20 molecules by attractive forces.
    • Force is directed inward, raising pressure in alveoli.
slide28

At surface

Unbalanced forces

Generate Tension

Within Fluid

All forces balance

What is Surface Tension ?

slide29

Surface Tension

  • Law of Laplace:
    • Pressure in alveoli is directly proportional to surface tension; and inversely proportional to radius of alveoli.
    • Pressure in smaller alveolus would be greater than in larger alveolus, if surface tension were the same in both.

Insert fig. 16.11

slide30

AirFlow

Expand

Collapse

Effect of Surface Tension on Alveoli size

slide31

Surfactant (表面活性物质)

  • Phospholipid produced by alveolar type II cells.
  • Lowers surface tension.
    • Reduces attractive forces of hydrogen bonding
    • by becoming interspersed between H20 molecules.
      • Surface tension in alveoli is reduced.
slide32

Low S/unit Area

Slider - Change Surface Area

Increase Area

DecreaseArea

Surfactant

High S/unit Area

Area

Saline

Saline

Tension

Area dependence of Surfactant action

slide34

Normal (with surfactant)

Saline Filled

Volume L

6

3

Without surfactant

RV

Pleural Pressure

0

0

- 15

- 30 cm H2O

Volume-pressure curves of lungs filled with saline and with air (with or without surfactant)

physiology importance of surfactant
Physiology Importance of Surfactant
  • Reduce the work of breathing
  • Stabilize alveoli
    • Prevent collapse and sticking of alveoli
  • Maintain the dryness of the alveoli
    • Prevent the edema of the alveoli
slide36

Compliance

  • Distensibility (Stretchability, Elasticity):
    • Ease with which the lungs can expand.
    • The compliance is inversely proportional to elastic resistance
  • Change in lung volume per change in transpulmonary pressure.
  • DV/DP
  • 100 x more distensible than a balloon.
  • Specific compliance (比顺应性, CL): the compliance per unit volume
  • CL = pulmonary compliance/residual volume
slide37

2. Inelastic Resistance

  • The inelastic resistance comprises
    • airway resistance (friction)
    • pulmonary tissue resistance (viscosity and inertia).
  • Of these the airway resistance is by far the more important both in health and disease.
    • It account for 80%-90% of the inelastic resistance.
slide38

Airway Resistance

  • Airway resistance is the resistance to flow of air in the airways and is due to :
      • internal friction between gas molecules
      • 2) friction between gas molecules and the walls of the airways
slide40

Laminar flow

  • … is when concentric layers of gas flow parallel to the wall of the tube.
  • The velocity profile obeys Poiseuille’s Law
slide41

Poiseuille and Resistance

  • Airway Radius or diameter is KEY.
  •  radius by 1/2  resistance by 16 FOLD - think bronchodilator here!!
slide42

The gas flow in the larger airways (nose, mouth, glottis, and bronchi) is turbulent

  • Gas flow in the smaller airway is laminar
  • Breath sounds heard with a stethoscope reflect the turbulent airflow
  • Laminar flow is silent
slide43

Airway Resistance

  • Any factor that decreases airway diameter, or increases turbulence will increase airway resistance, eg:
    • Rapid breathing: because air velocity and hence turbulence increases
    • Narrowing airways as in asthma (哮喘), parasympathetic stimulation, etc.
    • Emphysema (肺气肿), which decreases small airway diameter during forced expiration
  • Increase of the density and viscosity of the inspired gas also increase the airway resistance
slide44

Control of Airway Smooth Muscle

  • Neural control
    • Adrenergic beta receptors causing dilatation
    • Parasympathetic-muscarinic receptors causing constriction
    • NANC nerves (non-adrenergic, non-cholinergic)
      • Inhibitory release VIP and NO  bronchodilitation
      • Stimulatory  bronchoconstriction, mucous secretion, vascular hyperpermeability, cough, vasodilation “neurogenic inflammation”
slide45

Control of Airway Smooth Muscle

  • Local factors
    • histamine binds to H1 receptors-constriction
    • histamine binds to H2 receptors-dilation
    • slow reactive substance of anaphylaxis (过敏反应)- constriction-allergic response to pollen
    • Prostaglandins (前列腺速) E series - dilation
    • Prostaglandins (前列腺素)F series - constriction
slide46

Control of Airway Smooth Muscle

(cont)

  • Environmental pollution
    • smoke, dust, sulfur dioxide, some acidic elements in smog
  • Elicit constriction of airways
    • mediated by:
      • parasympathetic reflex
      • local constrictor responses
slide50

Pulmonary Volumes

  • Tidal volume (潮气量)
    • Volume of air inspired or expired during a normal inspiration or expiration (400 – 500 ml)
  • Inspiratory reserve volume (补吸气量)
    • Amount of air inspired forcefully after inspiration of normal tidal volume (1500 – 2000 ml)
  • Expiratory reserve volume (补呼气量)
    • Amount of air forcefully expired after expiration of normal tidal volume (900 – 1200 ml)
  • Residual volume (残气量,RV)
    • Volume of air remaining in respiratory passages and lungs after the most forceful expiration (1500 ml in male and 1000 ml in female)
slide52

Pulmonary Capacities

  • A Capacity is composed of two or more volumes
  • Inspiratory capacity (深吸气量)
    • Tidal volume plus inspiratory reserve volume
  • Functional residual capacity (功能残气量, FRC)
    • Expiratory reserve volume plus the residual volume
  • Vital capacity (肺活量, VC)
    • Sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume
  • Total lung capacity (肺总量, TLC)
    • Sum of inspiratory and expiratory reserve volumes plus the tidal volume and residual volume
slide54

RV/TLC

  • Normally less than 0.25
  • Increase by the obstructive pulmonary disease (RV)
  • Increase during the restrictive lung disease (TLC)
slide55

Minute and Alveolar Ventilation

  • Minute ventilation: Total amount of air moved into and out of respiratory system per minute
  • Respiratory rate or frequency: Number of breaths taken per minute
  • Anatomic dead space: Part of respiratory system where gas exchange does not take place
  • Alveolar ventilation: How much air per minute enters the parts of the respiratory system in which gas exchange takes place
slide56

Dead Space

  • Area where gas exchange cannot occur
  • Includes most of airway volume
  • Anatomical dead space (=150 ml)
    • Airways
  • Physiological dead space
    • = anatomical + non functional alveoli
slide57

A tube = Airway (Trachea – Bronchi – Bronchioles)

VD

A thin walled Sac = Alveolus

VA

GAS EXCHANGE

OCCURS HERE

Blood Vessels

Basic Structure of the Lung

NO GAS EXCHANGE

DEAD SPACE

Formula: Total Ventilation = Dead Space + Alveolar Space VT = VD + VA

slide58

VD

  • Anatomical Dead Space = Airways (constant)

VA

Physiological =Anatomical Dead Space Dead Space +

Additional Dead Space

BlockedVessel

Similar Concept: Physiological Dead Space

Healthy Lungs:

Diseased lungs:

slide60

FVC - forced vital capacity (cont)

  • Defines maximum volume of exchangeable air in lung (vital capacity)
    • forced expiratory breathing maneuver
    • requires muscular effort and some patient training
  • Initial (healthy) FVC values approx 4 liters
    • slowly diminishes with normal aging
slide61

FVC - forced vital capacity (cont)

  • Significantly reduced FVC suggests damage to lung tissue
    • restrictive lung disease (fibrosis,纤维化)
    • constructive lung disease
    • loss of functional alveolar tissue
    • FVC volume reduction trend over time (years) is key indicator
  • Intra-subject variability factors
    • age
    • sex
    • height
    • ethnicity
slide62

FEV1 - forced expiratory volume

(1 second)

  • Defines maximum air flow rate out of lung in initial 1 second interval
    • forced expiratory breathing maneuver
    • requires muscular effort and some patient training
  • FEV1/FVC ratio
    • normal FEV1 about 3 liters
    • FEV1 needs to be normalized to individual’s vital capacity (FVC)
    • typical normal FEV1/FVC ratio = 3 liters/ 4 liters = 0.75
slide63

FEV1 - forced expiratory volume (1 second)

  • Standard screening measure for obstructive lung disease
    • FEV1/FVC reduction trend over time (years) is key indicator
    • calculate % predicted FEV1/FVC (age and height normalized)
  • Reduced FEV1/FVC suggests obstructive damage to lung airways
    • episodic, reversible by bronchodilator drugs
      • probably asthma (哮喘)
    • continual, irreversible by bronchodilator drugs
      • probably COPD (chronic obstructive pulmonary disease,慢性阻塞性肺病)
slide64

Spirometry

1 sec

Volume (litres)

Forced Expiratory Volume in 1 sec - FEV1

Time (sec)

Total Lung Capacity

Forced Vital Capacity - FVC

Residual Volume

slide65

Normal Lung Volume

Lung Volume in Restrictive Disease

3. Assessment of RESTRICTIVE Lung Diseases

These are diseases that reduce the effective surface area available for gas exchange

eg fibrosis / pulmonary oedema

slide66

Spirometry

RESTRICTIVE lung disease

Total Lung Capacity

Vital Capacity

REDUCED

Volume (litres)

Residual Volume

Time (sec)

slide67

Normal Airway Calibre

Airway Calibre in Obstructive Disease

Assessment of OBSTRUCTIVE Lung Diseases

These are diseases that reduce the diameter of the airways and increase airway resistance -

remember Resistance increases with 1/radius 4

eg asthma / bronchitis

slide68

Forced Vital Capacity - FVC

FEV1 > 80% of FVC

is Normal

or in words - you should be able to forcibly expire more than 80% of your vital capacity in 1 sec.

Forced Expiratory Volume in 1 sec - FEV1

slide69

Spirometry

1 sec

Total Lung Capacity

Volume (litres)

Forced Expiratory Volume in 1 sec - FEV1

Forced Vital Capacity - FVC

Residual Volume

Time (sec)

OBSTRUCTIVE lung disease

FEV1 < 80% of FVC