RISBIROTARY-1

7/30/2019 RISBIROTARY-1

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Mee Wah Ng RSO Dubai 2002

BASICSof

RESPIRATORY

FUNCTION


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Ventilation:

The moving of Oxygen and Carbon Dioxide in and out of

our body. Commonly termed breathing

Respiration:

Metabolic process that occurs in the lungs and cells of the

body breaking down organic substances to simpler productsto release energy


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VENTILATION

Moving of gas from the atmosphere to the lung alveoli

by convection or bulk flow through conducting airways

due to a pressure gradient


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Air enters the RESPIRATORY SYSTEM through

1.The nose and mouth( filtrated, warmed and moistened )

2. then passes down the

throat (pharynx)

and

through the voice box (larynx).

( The entrance to thelarynx is covered by a

small flap of musculartissue (epiglottis)

that closes whenswallowing, thuspreventing food fromentering the airways.

3.The largest airway is the

windpipe (trachea), which

branches into

4. Two smaller airways

(bronchi) to supply the two

lungs.

5. The bronchi themselves

divide many times beforeevolving into smaller

airways (bronchioles).

These are the narrowest airways--one

fiftieth of an inch across.

6. At the end of each bronchiole are

dozens of bubble-shaped, air-filled

cavities (alveoli) that is surrounded by

a dense network of capillaries. Theextremely thin walls of the alveoli

allow oxygen to move from the alveoli

to the capillaries and carbon dioxide

to move from the capillaries into the

alveoli.

(Tiny hairs called cilia help remove

dirt and microbes. )


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Breathing in and out is known asinhalationand exhalation

(inspirationandexpiration)

Due to changes in the volume of the thoracic cavity.

Leads to pressure changes which cause air to enter or leave the lungs.

The diaphragm which is a sheet of muscle under the lungs

The intercostal muscles which connect the ribs.

There are two sets. The internal intercostal muscles and the

external intercostal muscles.

The main components facilitating the lung volume change are:


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Expiration

Diaphragm relaxes

The external intercostal muscles relax

allowing the ribs to drop back down

Lungs recoil inwards

Air is forced out

Alveolar pressure equals atmosphericpressure

Air will flow from an area of higher pressure to one of lower pressure

( pressure gradient )

Inspiration

Diaphragm contracts

The external intercostal

muscles contract moving the

ribs upwards and outwards.

Chest expands

Lungs are pulled outwards

Alveolar pressure decreases


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PRESSURE AND FLOW

Three pressures determine airflow and volume of the lungs

ATMOSPHERIC PRESSURE (PATM)

Barometric pressure

ALVEOLAR PRESSURE (PALV

)

The pressure in the lung.

PLEURAL PRESSURE (PPLU

)

The pressure in the pleura, between the lung and thoracic wall.


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(PATM - PALV) = TRANSAIRFLOW PRESSURE

The pressure dif ference between the atmosphere and alveoli whi ch

determines air f low.

DeltaP = (PATM - PALV) = (Airflow) x (Resistance)

The higher the flow, the higher the pressure;

the higher the resistance for an equivalent flow,

the higher the pressure required to overcome that resistance.

(PALV - PPLU) = TRANSPULMONARY PRESSURE

Transpulmonary pressure determines the volume of the lung

and is therefore dependent on the compliance of the lung.

The lower the compliance of the lung, the higher the

transpulmonary pressure necessary to achieve an

equivalent tidal volume.

PRESSURE AND FLOW


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BEGINNING OF INSPIRATION: no movement of air.

alveolar pressure is 0 (the same as atmospheric pressure) Pleural Pressure is -5 cm H2O

FORCED INSPIRATION

Rapid or forced inspiration causes pleural pressure to become much

more negative than usual.

FORCED EXPIRATION

The pleural pressure can actually become positive as air is forced out of lungs

During INSPIRATION

pleural pressure changes from -5 to about -8 cm H2O

Air flows into the lungs and lung volume increases

Amount of pressure changes is dependent on the compliance of the lung.

EXPIRATION

Normal expiration is simple relaxation of the diaphragm ------> lung-volume decreases due to its natural elasticity.

PRESSURE AND FLOW


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This relationship between lung volume and pressure determine

compliance of the lung.

Compliance

Compliance is related to

1. the elasticity

2. Surface tension

Compliance is a measure of

change in volume in response to a change in pressure.

Affects: Chest wall

Lungs - alveoli

Diaphragm

High compliancethoracic wall and lungs expand easily

Low compliancethoracic wall and lungs resist expansion


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Compliance decreases with lung volume.

an empty lung has a higher compliance than a filled lung.

This is consistent with the P/V curve leveling off as it approaches Total

Lung Capacity.

Compliance

La PLACE relationship

PRESSURE required to keep alveoli inflated

=(2 Surface Tension) / r

The higher the surface tension,the more pressure required to inflate

alveolus. The lower the radius (size) of the alveolus,

the more pressure required to inflate alveolus.

the bigger (r), the less pressure is needed to hold them open

the smaller (r) , the more pressure will be needed


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ELASTANCE

Refers to the tendency of an object to resist deformation and theability to return to its original shape after deformation

( elastic recoil. )

Two factors explain the lung's desire to return to end expiration volume.1. elastic fibres located throughout lung parenchyma which, when

stretched by lung inflation, attempts to recoil.

2. A very thin coating of fluid lines the inner surface of alveoli

which serves to enhance recoil properties of the lung.

3. This fluid, called surfactant encourages lung recoil when fully

inflated yet serves to prevent collapse of alveoli when the lungs

are near end expiration.


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Static Recoil Pressure or Pst

the elastic like tendency of the lung to return to its end expiration volume is due to

static recoil pressure

Which unlike pleural pressure, is positive relative to atmospheric pressure.

Static recoil pressure is in direct opposition to pleural pressure

Elastance is Relative to Compliance

As Compliance ; Elastance As Compliance : Elastance


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Compliance decreases with conditions that

Destroys lung tissues

Causes it to become fluid filled

Produces a deficiency in surfactant In any way impedes lung expansion or

contraction

Lung volume measurements reflect the stiffness or elasticity of the

lungs and the rib cage.

Disorders that cause stiff lungs or that reduce the movement of the

rib cage are called restrictive disorders.

Compliance


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HIGH COMPLIANCE

as in Obstructive Lung Disease

The lungs have trouble deflating because they have lost their elasticity

destruction of elastic fibers in lung

great difficulty in exhaling but not inhaling.

LOW COMPLIANCE

As in Restrictive Lung Disease.

great difficulty in inhaling, expanding the lung.

lack of surfactant as in Infant Respiratory Distress

Syndrome ( IRDS )

Compliance


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Compliance

"Static" Compliance is a measure of the "stiffness" or elasticity oflung and chest wall

"Dynamic" compliance includes the extra pressure needed to

overcome resistance to airflow, inertia of chest wall, and

viscoelasticity of tissues.

Total compliance varies from person to person and from time to time.

Lung compliance is an important consideration for manytherapeutics routinely carried out in the critical care setting.

influences how best to ventilate critically ill patients


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RESISTANCE

Defined as the Force ( Pressure ) necessary to maintain a

specific flow in a particular system

It is a measure of the change in pressure per unit change in flow

Resistance in a system is affected by

Lumen of systemLength of system

Type of flow in system

Branching of system

PA-PB

VmbarL/s

R =


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Law of Hagen - Poiseulle

The most important determinantof airway resistance in a single

tube system is theradiusof the

tube

Under laminar conditions,

resistance is a function of lengthdivided by radius to the fourth

power

Reduction in radius by one half

would require a sixteenfold

driving pressure to maintain thesame flowrate of gas per unit

time

R ~1

r4


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airway resistance is lower during inspiration due to effects of changes in

intrapleural pressure on airway diameter.

During inspiration, pleural pressure becomes negative,

a distending pressure is applied across the lung.

which increases airway diameter as well as alveolar diameter

decreases the resistance to gas flow.

During expiration, pleural pressure increases and airways are compressed.

When intrapleural pressure is high during active expiration, airways may

collapse and gas may be trapped in the lung.

Resistance to gas flow arises because of:

airway resistancefriction between gas molecules and the walls of airway

viscous tissue resistancefriction between the tissues of the lung and the chest wall

Resistance is inversely proportional to lung volume.

RESISTANCE


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the region of greatest resistance Highest resistance always occurs in the nose and nasopharynx..

The terminal bronchioles have low resistance because they have

the highest total cross-sectional area.

AIRWAY RESISTANCE

Rtotal can be partitioned into two components

Rperipheral (gen. 7 - gen. 23): low resistance (laminar & diffusive zones)

Rcentral (nose - gen. 6): high resistance (turbulent flow zone)

Rcentral >>> Rperipheral (50% of resistance in nasal passages alone)

Airway resistance represents approximately

80% of the total resistance of the respiratory system.


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Flow rate measurements reflect the degree of narrowing or

obstruction of the airways. This type of disorder is called an

obstructive disorder.

The higher the pressure difference required to maintain flow, the higher the

airway resistance.

Normal response to increased resistance is increased effort

Chronic obstructive pulmonary disease such as bronchitis, asthma and

emphysema have some degree of obstruction of the airway which

increases airway resistance

AIRWAY RESISTANCE


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inertial work- work to overcome:acceleration and deceleration of air (negligible

due to low mass of air)

acceleration and deceleration of chest wall and

lungs (negligible due to overdamping)

Work of Breathing

Components of Work

elastic work- work to overcome:

lung elastic recoil

thoracic cage displacement

abdominal organ displacement

frictional work- work to overcome:

air-flow resistance (major)

viscous resistance (lobe friction, minor )


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Graphical Representation of the Major Components of Work

work = force * distance pressure * volume / 2

elastic work - area a-b-c-a

inspiratory flow-resistive work - area a-i-b-a

expiratory flow-resistive work - area a-b-e-a

passive recoil of lungs overcomes the work of expiratory flow-resistance


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RESPIRATION

External Respiration

Exchange of oxygen and carbon dioxide between the alveoli

of the lung and pulmonary blood capillaries

Internal Respiration

Exchange of oxygen and carbon dioxide between tissue bloodcapillaries and tissue cells


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Gas exchange by "diffusiondue to partial pressure gradient

1. to supply oxygen to the blood for distribution to the cells of the body,

2. to remove carbon dioxide from the blood that has been collected from the

cells of the body.

External Respiration

Gas exchange in the lungs occurs only in the smallest airways and the alveoli.


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Physiologic

Region

PO2

(mm Hg)

PCO2

(mm Hg)

inspired air 159 0.23

trachea 149 0.21

alveolus 100 40

pulmonaryvein 95 40

pulmonaryartery

40 46

Partial pressure difference


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DEAD SPACEinspired air that is not perfused by blood

thus "wasted" as it does not contribute to gas exchange.

ANATOMICAL DEAD SPACE + ALVEOLAR DEAD SPACE

= PHYSIOLOGICAL DEAD SPACE

ANATOMICAL DEAD SPACE

The volume of air occupying the upper airways where there are no alveoli.

ALVEOLAR DEAD SPACEThe volume of air that reaches the alveoli but doesn't get perfused by blood.

In HEALTHY Individuals

Alveolar Dead Space should be virtually zero,

so physiological dead space = anatomical dead space.


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DEAD SPACE: VA/Q TOO HIGH.

Normally dead space should only be anatomical dead space (20- 30% of tidalvolume).

Any dead space in excess is physiological.

Alveolar air that is not perfused has the same O2concentration as atmospher ic

air, 147 mm Hg

So, an alveolar PAO2 of close to 147 is indicative of too much dead space.

SHUNTED BLOOD: VA/Q TOO LOW.

Shunted blood is defined as blood that goes through pulmonary

circulation without getting ventilated (i.e. without taking up O2).

This occurs when there is too little ventilation (hypoventilation) relative to

perfusion.

More shunted blood ------> lower PCap

O2------> arterial gas composition (both

CO2and O

2) approaches the levels of venous blood.

. .

. .


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ideally, ventilation and perfusion must be exactly matched

ventilation must be distributed to perfused areasperfusion must be distributed to ventilated areas

the ratio of ventilation to perfusion (V A/Q ) is the critical factor governing gas

exchange

regions of high ventilation should have high blood flows (base of lung)

regions of low ventilation should have low blood flows (apex of lung)

one lung is represented by many regional V A/Q ratios, not a single V A/Q value

Concept of Ventilation/Perfusion Matching

. .

. . . .


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Regional Variation in Lung Ventilation

EFFECTS OF GRAVITY ON FRC

Ventilation within the lungs is greatest near

the bases, in the upright position.

This is probably mainly due to variation in intra-pleural pressure

As we move from apex to base - pressure is more negative near the apex.

Effectively, this probably causes more expansion of the apices at FRC.

During inhalation, it is easier to expand the bases, as these are less

distended than the apices!


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Regional Variations in Ventilation, Perfusion and Vent/Perf Ratio

APEX OF LUNG: Relatively less air and less blood go to the apex.

low V A, lower Q , high V A/Q > 1 (wasted ventilation)

high PAO2 & low PACO2 due to high V A/Q > 1

BASE OF LUNG: Relatively more air and more blood go to the base of the

lung, primarily due to gravity.

high V A, higher Q , low V A/Q < 1 (wasted perfusion)

Low PAO2 & High PACO2 due to low V A/Q


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shunt alveolar unit: :VA/Q = 0, PAO2 = 40 mm Hg, PACO2 = 46 mm Hg

Q >> V A (wasted perfusion)

dead space alveolar unit: V A/Q = infinity, PAO2 = 150 mm Hg, PACO2 = 0 mm Hg

Q


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COMPENSATORY BRONCHOCONSTRICTION

The converse of above.

If there is low blood flow to a region of lung, the corresponding

bronchioles will bronchoconstrict.

Local low blood flow ------> local low PCO2 ------> Regional

bronchoconstriction ------> decreased ventilation to region

VA/Q Balance Compensatory Mechanisms

HYPOXIC PULMONARY VASOCONSTRICTION

Low PO2in the pulmonary circulation indicates poor ventilation.

If we have poor ventilation, we don't want blood to flow to that region.

Thus Poor venti lation ------> Low PO2locally ------> local

vasoconstr iction diverts blood elsewhere.

This is the exact oppositeof the systemic circulation, where lowPO

2in tissues leads to vasodilation to increase local flow.

. .


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Gravity and Positioning

ProneSupine


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Raised Position

Diseased subject

FRC improved

Reduce WOB

spontaneous

breathing is

encouraged

Healthy subject

FRC reduction

of approx. 1 Ltr.

90

45


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Internal Respiration

How much pO2 blood can hold depends on:

the amount of haemoglobin1 gm Hb can hold 1.34 mls of O2

type of haemoglobin

Temperature

Acidity

Transport of gases between the lungs and body tissues

is a function of blood and cardiac output


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Histotoxic hypoxia

Although there is adequate delivery of oxygen to tissues, the tissues are

unable to utilise it properly eg as in cyanide poisoning

HYPOXIA

Differential causes of hypoxia

Hypoxic hypoxia - low pO2 in arterial blood due to: Intrinsic lung problems

Fluid in the lungs

High altitude

Anaemic Hypoxia - Low level of haemoglobin as aresult of:

Haemorrhage Anaemia

Failure of Hb to carry its normal complement of O2 as incarbon monoxide poisoning

Stagnant Hypoxiainability of blood to carry O2 to tissues fastenough for their needs

Heart failure

Circulatory shock


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Breathing is usually automatic, controlled subconsciously by the respiratory

center at the base of the brain known as the respiratory centre.

Control of Breathing

The respiratory centre is functionally divided into three areas:

Medullary rythmicity area controls the basic rhythm of breathing

Normal inspiration time 2 secs

Expiration 3 seconds

Pnuemotaxic area co-ordinate transition between inspiration and expiration

Inhibits inspiratory phase ( as to prevent overinflation )

Apneustic AreaAnother part that co-ordinates transition between inspiration and expiration

Prolongs inspiration when pneumotaxic area is inactive


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Regulation of Respiratory Centre Activity

Cortical Influences:Cerebral cortex connects with respiratory centre allowing

voluntary control of pattern of breathing.Emotional stimuli such as crying

Inflation reflex:

Stretch receptorssend messages along the vagus nerves to inspiratoryarea

Located in walls of bronchi and bronchiolesStimulates the start of expirationKnown as the inflation ( Hering - Breur ) reflex

Evidence that this reflex is mainly a protective mechanism for preventingoverinflation of the lungs

Chemical Regulation:The brain and small sensory organs in the aorta and carotid arteries sense when oxygenlevels are too low or carbon dioxide levels are too high, and the brain increases the speedand depth of breathing.

Hypercapnia ( High pCO2 ) results in increased respiratory rate

Hypocapnia ( Low pCO2 ) results in decreased respiratory rate

Controlled by 3 main factors:


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Summary of stimuli that affect ventilation rate and depth

Stimuli that Increase Rate and Depth

of Ventilation

Stimuli that Decrease Rate and Depth

of Ventilation

Increase in arterial blood H+ level or

pCO2 > 40 mm Hg

Decrease in arterial blood H+ level or

pCO2< 40 mm Hg

Decrease in arterial blood pO2 from

105 to 50 mm Hg

Decrease in arterial blood pO2 > 50

mm Hg

Decrease in blood pressure Increase in blood pressure

Increase in body temperature Decrease in body temperature

Prolonged pain Severe pain causes apnoea

Irritation of pharyns or larynx by

touch or chemicals causes apnoea
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Normal Respiratory Mechanics Values

Parameter AdultRange Neonatal Range

Respiratory Rate 10-15 breaths/minute 30-40 breaths/minute

Tidal Volume 7-10 ml/kg 5-7 ml/kg

Minute Ventilation 5-10 liters/minute 200-300 ml/kg/min

Dynamic Compliance 25-50 ml/cmH2O 1-2 ml/cmH2O/kg

Airway Resistance 2-5 cmH2O/L/S 25-50 cmH2O/L/S

Work of Breathing(Insp.) 0.3-0.6 joules/liter

Intrinsic PEEP 0 cmH2O

Respiratory Drive P0.1 2-4 cmH2O
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