Respiratory physi ology
Jan 12, 2016
Respiratory physiology
Respiration is the process by which the body takes in and utilizes oxygen (O2) and gets rid of carbon dioxide (CO2).
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
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
Section 1 Pulmonary Ventilation
Pulmonary ventilation means the inflow and outflow of air between the atmosphere and the lung alveoli, which is determined by the activity of the airways, the alveolus and the thoracic cage.
I Functions of the Respiratory Passageways
Respiratory System Divisions
• Upper tract– Nose, pharynx
and associated structures
• Lower tract– Larynx, trachea,
bronchi, lungs
Conducting Zone• All the structures air
passes through before reaching the respiratory zone.
• Cartilage holds tube system open and smooth muscle controls tube diameter
• Warms and humidifies inspired air.
• Filters and cleans:
Insert fig. 16.5
Respiratory Zone
• Region of gas exchange between air and blood.
• Includes respiratory bronchioles and alveolar sacs.
Airway branching
Bronchioles and Alveoli
Thoracic Walls and Muscles of Respiration
• 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
Breathing
Thoracic Volume
Pleura
•Pleural fluid produced by pleural membranes
–Acts as lubricant
–Helps hold parietal and visceral pleural membranes together
Ventilation
• Movement of air into and out of lungs
• Air moves from area of higher pressure to area of lower pressure
• Pressure is inversely related to volume
Alveolar Pressure Alveolar Pressure Changes During Changes During RespirationRespiration
Chest WallChest Wall(muscle, ribs)(muscle, ribs)
Principles of BreathingPrinciples of BreathingFunctional Unit: Chest Wall and Lung Functional Unit: Chest Wall and Lung
ConductingConductingAirwaysAirways
DiaphragmDiaphragm(muscle)(muscle)
LungsLungsGas ExchangeGas Exchange
Follows Boyle’s Law:Follows Boyle’s Law:Pressure (P) x Volume (V) = ConstantPressure (P) x Volume (V) = Constant
Pleural CavityPleural CavityImaginary Space betweenImaginary Space betweenLungs and chest wallLungs and chest wall
Pleural CavityPleural CavityVery small space Very small space Maintained at negative pressureMaintained at negative pressureTransmits pressure changes Transmits pressure changes Allows lung and ribs to slideAllows lung and ribs to slide
CWCW
Follows Boyle’s Law: PV= CFollows Boyle’s Law: PV= C
At Rest with mouth open PAt Rest with mouth open Pbb = P = Pi i = 0= 0
DD
PPii
AA
PSPS
PPbb
Airway OpenAirway Open
Principle of BreathingPrinciple of Breathing
1
CWCW
Follows Boyle’s Law: PV= CFollows Boyle’s Law: PV= C
At Rest with mouth open PAt Rest with mouth open Pbb = P = Pi i = 0= 0Inhalation: Inhalation: - Increase Volume of Rib cageIncrease Volume of Rib cage- Decrease the pleural cavity pressureDecrease the pleural cavity pressure- Decrease in Pressure inside (P- Decrease in Pressure inside (Pii) lun) lungsgs
DD
PPii
AA
PSPS
PPbb
Airway OpenAirway Open
Principle of BreathingPrinciple of Breathing
2
CWCW
Follows Boyle’s Law: PV= CFollows Boyle’s Law: PV= C
At Rest with mouth open PAt Rest with mouth open Pbb = P = Pii = 0 = 0Inhalation: Inhalation:
- PPbb outside is now greater than P outside is now greater than Pii
- Air flows down pressure gradient- Air flows down pressure gradient- Until Pi = PbUntil Pi = Pb
DD
PPii
AA
PSPS
PPbb
Airway OpenAirway Open
Principle of BreathingPrinciple of Breathing
3
CWCW
Follows Boyle’s Law: PV= CFollows Boyle’s Law: PV= C
DD
PPii
AA
PSPS
PPbb
Airway OpenAirway Open
At Rest with mouth open PAt Rest with mouth open Pbb = P = Pii = 0 = 0
Exhalation: Opposite ProcessExhalation: Opposite Process- Decrease Rib Cage VolumeDecrease Rib Cage Volume
Principle of BreathingPrinciple of Breathing
4
CWCW
Follows Boyle’s Law: PV= CFollows Boyle’s Law: PV= C
At Rest with mouth open PAt Rest with mouth open Pbb = P = Pii = 0 = 0
Exhalation: Opposite ProcessExhalation: Opposite Process- Decrease Rib Cage VolumeDecrease Rib Cage Volume- Increase in pleuralIncrease in pleural
cavity pressure cavity pressure - Increase P - Increase Pii
DD
PPii
AA
PSPS
PPbb
Airway OpenAirway Open
Principle of BreathingPrinciple of Breathing
5
CWCW
Follows Boyle’s Law: PV= CFollows Boyle’s Law: PV= C
At Rest with mouth open PAt Rest with mouth open Pbb = P = Pii = 0 = 0
Exhalation: Opposite ProcessExhalation: Opposite Process- Decrease Rib Cage VolumeDecrease Rib Cage Volume- Increase PIncrease Pii
- Pi is greater than PPi is greater than Pbb
- Air flows down pressure gradientAir flows down pressure gradient- Until PUntil Pii = P = Pbb again again
DD
PPii
AA
PSPS
PPbb
Airway OpenAirway Open
Principle of BreathingPrinciple of Breathing
6
Mechanisms of Breathing: Mechanisms of Breathing: How do we change the volume of the rib cage ?How do we change the volume of the rib cage ?
To Inhale is an ACTIVE processTo Inhale is an ACTIVE process• DiaphragmDiaphragm
Rib CageRib Cage
ContractContract
DiaphragmDiaphragmVolumeVolume
•External Intercostal Muscles External Intercostal Muscles
IntercostalsIntercostalsContractContract
to Liftto LiftRibRib
SpineSpine
RibsRibs VolumeVolume
Both actions occur simultaneously – otherwise not effectiveBoth actions occur simultaneously – otherwise not effective
II Respiratory Resistance
Including Elastic Resistance and Inelastic resistance
Elastic Resistance
A lung may be considered as an elastic sac. The thoracic wall also can be considered as an elastic element.
So during inspiration the inspiratory muscles must expand the thoracic cage which are together with the elastic resistance.
Elasticity
• Tendency to return to initial size after distension.
• High content of elastin proteins.– Very elastic and resist distension.
• Recoil ability.
• Elastic tension increases during inspiration and is reduced by recoil during expiration.
Compliance
• Distensibility (stretchability):– Ease with which the lungs can expand.– The compliance is inversely proportional to
elastic resistance
• Change in lung volume per change in transpulmonary pressure.
V/P• 100 x more distensible than a balloon.
0
100
50
0 30
Lungvolume(%TLC)
Transpulmonary pressure (cmH2O)
Static lung compliance C = V/P
inflation
deflation
normal breathing
The elastic forces can be divided into two parts:
1) the elastic forces of the lung tissue itself
2) the elastic forces 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.
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.
What is Surface What is Surface Tension ?Tension ?
Within Fluid Within Fluid All forces balanceAll forces balance
At surfaceAt surfaceUnbalanced forces Unbalanced forces Generate TensionGenerate Tension
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
CollapseCollapse
ExpandExpand
Effect of Surface Tension on Alveoli sizeEffect of Surface Tension on Alveoli size
AirAir FlowFlow
Surfactant• 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.
• As alveoli radius decreases, surfactant’s ability to lower surface tension increases.
Area dependence of Surfactant actionArea dependence of Surfactant action
TensionTension
AreaAreaSurfactantSurfactant
Increase AreaSalineSaline
Slider - Change Surface AreaSlider - Change Surface Area
SalineSaline
DecreaseArea
Low S/unit Area
High S/unit Area
Surfactant prevents alveolar collapse
Volume LVolume L
RVRV
Pleural PressurePleural Pressure00
66
00- 30 cm H- 30 cm H22OO- 15- 15
33
Factors Contributing to ComplianceFactors Contributing to Compliance- Hysteresis- Hysteresis
Normal (with surfactant)Normal (with surfactant)Saline FilledSaline Filled
Without surfactant
Inelastic Resistance
The inelastic resistance comprises the airway resistance (friction) and 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.
Airway Resistance
• Airway resistance is the resistance to flow of air in the airways and is due to :
• 1) internal friction between gas molecules
• 2) friction between gas molecules and the walls of the airways
Types of Flow
Laminar flow
• … is when concentric layers of gas flow parallel to the wall of the tube. The velocity profile obeys Poiseuille’s Law (pg 43:11)
Poiseuille and Resistance
• Airway Radius or diameter is KEY. radius by 1/2 resistance by 16 FOLD - think
bronchodilator here!!
Airway resistance increase
• 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, parasympathetic stimulation, etc.
• Emphysema, which decreases small airway diameter during forced expiration
Control of Airway Smooth Muscle
• Neural control– Adrenergic beta receptors causing dilatation– Parasympathetic-muscarinic receptors causing co
nstriction– NANC nerves (non-adrenergic, non-cholinergic)
• Inhibitory release VIP and NO bronchodilitation• Stimulatory bronchoconstriction, mucous secretion,
vascular hyperpermeability, cough, vasodilation “neurogenic inflammation”
Control of Airway Smooth Muscle (cont.)
• Local factors– histamine binds to H1 receptors-constriction
– histamine binds to H2 receptors-dilation
– slow reactive substance of anaphylaxsis-constriction-allergic response to pollen
– Prostaglandins E series- dilation
– Prostaglandins F series- constriction
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
III Pulmonary Volume and Capacity
Pulmonary Volumes• Tidal volume
– Volume of air inspired or expired during a normal inspiration or expiration (400 – 500 ml)
• Inspiratory reserve volume– Amount of air inspired forcefully after inspiration of nor
mal tidal volume (1500 – 2000 ml)
• Expiratory reserve volume– Amount of air forcefully expired after expiration of norm
al tidal volume (900 – 1200 ml)
• Residual volume– Volume of air remaining in respiratory passages and lung
s after the most forceful expiration (1500 ml in male and 1000 ml in female)
Pulmonary Capacities• Inspiratory capacity
– Tidal volume plus inspiratory reserve volume
• Functional residual capacity– Expiratory reserve volume plus the residual volume
• Vital capacity – Sum of inspiratory reserve volume, tidal volume, and exp
iratory reserve volume
• Total lung capacity– Sum of inspiratory and expiratory reserve volumes plus t
he tidal volume and residual volume
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
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
Basic Structure of the LungBasic Structure of the Lung
VVDD
A tube = Airway A tube = Airway (Trachea – Bronchi – Bronchioles) (Trachea – Bronchi – Bronchioles)
NO GAS EXCHANGENO GAS EXCHANGE
DEAD SPACEDEAD SPACE
A thin walled Sac = AlveolusA thin walled Sac = Alveolus
Blood VesselsBlood Vessels
GAS EXCHANGEGAS EXCHANGEOCCURS HEREOCCURS HERE
VVAA
Formula: Total Ventilation = Dead Space + Alveolar SpaceFormula: Total Ventilation = Dead Space + Alveolar Space V VTT = V = VD D + V+ VA A
Physiological =Physiological = Anatomical Dead SpaceAnatomical Dead Space Dead Space Dead Space + +
Similar Concept: Physiological Dead SpaceSimilar Concept: Physiological Dead Space
Diseased Diseased lungs:lungs:
Healthy Lungs:Healthy Lungs:
BlockedBlockedVesselVessel
Additional Dead SpaceAdditional Dead Space
• Anatomical Dead SpaceAnatomical Dead Space = Airways (constant) = Airways (constant)
VVAA
VVDD
FVC - forced vital capacity• defines maximum volume of exchangeable air in lung (vital capacit
y)– forced expiratory breathing maneuver– requires muscular effort and some patient training
• initial (healthy) FVC values approx 4 liters– slowly diminishes with normal aging
• significantly reduced FVC suggests damage to lung parenchyma– restrictive lung disease (fibrosis)– constructive lung disease– loss of functional alveolar tissue (atelectasis)– FVC volume reduction trend over time (years) is key indicator
• intra-subject variability factors– age– sex– height– ethnicity
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
• standard screening measure for obstructive lung disease (COPD) – 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– continual, irreversible by bronchodilator drugs
• probably COPD
Vol
um
e (l
itre
s)
Time (sec)
Forced Vital Capacity - FVC
Total Lung Capacity
Residual Volume
Spirometry
Forced Expiratory Volume in 1 sec - FEV1
1 sec
eg fibrosis / pulmonary oedema
Assessment of RESTRICTIVE Lung Diseases
These are diseases that reduce the effective surface area available for gas exchange
Normal Lung Volume Lung Volume in Restrictive Disease
REDUCED
Vol
um
e (l
itre
s)
Time (sec)
Vital Capacity
Total Lung Capacity
Residual Volume
Spirometry
RESTRICTIVE lung disease
eg asthma / bronchitis
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
Normal Airway Calibre Airway Calibre in Obstructive Disease
Forced Vital Capacity - FVC
Forced Expiratory Volume in 1 sec - FEV1
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 Vital Capacity - FVC
Vol
um
e (l
itre
s)
Time (sec)
Total Lung Capacity
Residual Volume
Spirometry
Forced Expiratory Volume in 1 sec - FEV1
1 sec
FEV1 < 80% of FVC
OBSTRUCTIVE lung disease