THE MECHANICS OF BREATHING

General Goal: To depict how the conformity and opposition of the respiratory system influence take a breathing under normal conditions and how they may be altered by disease.

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Specific Aims: The pupil should be able to:

define transpulmonary force per unit area, transthoracic force per unit area, and transmural respiratory system force per unit area and discourse how they relate to lung and chest wall kick force per unit area.

describe 2 alone surface tenseness belongingss of wetting agent, depict how these belongingss affect lung conformity, and depict the physiological effects of unnatural surfactant production in IRDS.

define “ dependent lung ” , discuss the mechanism underlying distribution of regional airing in assorted organic structure places.

province whether the lung and chest wall will flinch inward or spring outward at RV, FRC, chest wall unstressed volume ( Vo ) and above 65 % TLC and to place the volume at which lung and thorax wall forces balance.

list 2 major factors which will diminish airway quality and increase airway opposition.

describe why flow is “ attempt independent ” during termination but non inspiration, and discourse the mechanism responsible for greater flow restriction at low lung volumes or in the presence of emphysema.

Resources

Reading: West, JB. Respiratory Physiology-The Essentials ( 4th Ed. ) , Chapter 7.

Taylor, AE, K Rehder, RE Hyatt, JC Parker. Clinical Respiratory Physiology, Chapter 2, 6 and 7. Saunders, 1989.

NORMAL BREATHING

Inspiration is usually active. Termination is usually inactive.

Muscles of respiration

Inspiratory musculuss

Diaphragm. Principle musculus of inspiration.

External intercostals. Lift ribs during inspiration.

Accessary musculuss. Include sternomastoids, scalene musculuss, and alae nasi.

Expiratory musculuss

Abdominal musculuss. Principle musculuss of termination.

Internal intercostals. Pull ribs downward and inward.

Pressures involved in respiration.

Pbs = force per unit area at organic structure surface ( normally

atmospheric )

PM = oral cavity force per unit area ( normally atmospheric )

PPl = intrapleural force per unit area

PALV = alveolar force per unit area

Figure 1

Airway force per unit area gradient PM – PALV. This is the force per unit area gradient driving air flow into the lungs.

Transpulmonary force per unit area PTP = PALV – PPl. This transmural force per unit area across the lungs. Equal to ( i.e. balances ) elastic kick of lungs when there is no air flow. Additions and lessenings with lung volume.

Transchest wall force per unit area PTC = PPl – Pbs. The transmural force per unit area across the thorax. Equal in magnitude to ( i.e. balances ) elastic kick of the chest when there ‘s no air flow. Additions and lessenings with chest volume.

Transmural respiratory system force per unit area PRS = PALV – Pbs. The transmural force per unit area across the full respiratory system ( lungs + thorax ) . This is equal to the net inactive elastic kick force per unit area of the whole respiratory system when air flow is zero.

Balance of forces

Praseodymium

+

PMUS

=

PL

+

PCW

PALV-Pbs

+

PMUS

=

PL

+

PCW

inspiratory

musculus

contraction

Lung

elastic

kick

Chest wall

elastic

kick

Outward Acting forces Inward playing forces

when positive when positive

Three ways to blow up the lungs

Increase alveolar force per unit area. Done when utilizing external positive force per unit area inhalators.

Decrease organic structure surface force per unit area. Done when utilizing the old Fe lungs.

Activate inspiratory musculuss. The normal manner to breath.

Inflation kineticss. Requires that transmural force per unit area development be sufficient to get the better of non merely elastic kick forces but besides airway opposition to flux.

Figure 2

ELASTIC CHARACTERISTICS OF THE LUNG

Lung conformity ( CL ) — step lung volume at assorted transpulmonary force per unit areas. The incline is lung conformity.

Figure 3

Hysteresis. Lung volume at a given transpulmonary force per unit area is higher during deflation than during rising prices. The grounds for this are complex. Often, merely the deflation limb is shown on figures.

Conformity lessenings ( the lung becomes stiffer ) at high lung volumes.

Two major forces contribute to lung conformity: tissue elastic forces and surface tenseness forces.

Saline rising prices eliminates gas-air interface. It takes less transpulmonary force per unit area to blow up the lung with saline. The lung becomes more compliant because merely tissue elastic forces remain.

Surface tenseness in the lung.

At every gas-liquid interface surface tenseness develops.

Laplaces Law. It takes a certain rising prices force per unit area to back up the surface tenseness developed at an air-gas interface.

T=tension ( dyne/cm )

P=transmural force per unit area ( dyne cm2 )

R = radius ( centimeter )

Wetting agent in the lung

Secreted by Type II alveolar cells, surfactant lines the air sac at the gas-liquid interface and has dipalmitoyl lecithin, ( dipolmitoyl phosphotidyl choline=DPPC ) as a major component.

Surfactant has 2 alone surface tenseness belongingss

Figure 4

The mean surface tenseness is low.

Surface tenseness varies with country. Surface tenseness rises as country gets bigger and falls as country gets smaller.

Physiological importance of wetting agent

Additions lung conformity because surface forces are reduced.

Promotes alveolar stableness and prevents alveolar prostration. Decreased surface country lowers surface tenseness. Increased surface country additions surface tenseness. Small air sacs are prevented from acquiring smaller. Large air sacs are prevented from acquiring bigger.

Promotes dry air sac. Alveolar prostration tends to “ suck ” fluid from pneumonic capillaries. Stabilizing air sac ( see B ) prevents transudate of fluid by forestalling prostration.

Infant respiratory disease syndrome ( IRDS )

Surfactant ( DPPC ) production starts tardily in foetal life so premature babies are frequently unable to do surfactant properly.

Babies with unnatural wetting agent have stiff, fluid-filled lungs with atelectatic countries ( alveolar prostration ) . Non-ventilated, collapsed air sac efficaciously do right to go forth shunting of blood.

[ lecithin ] / [ sphingomyelin ] ratio can be analyzed in amnionic fluid to supply an index of gestational adulthood of surfactant production. Sphingomyelin production starts early and remains changeless during gestation and is therefore a marker of entire phospholipid concentration. Sphingomyelin has no surface active belongingss.

Regional lung volume and regional airing

Dependent lung-the lung in the lowest portion of the gravitative field, i.e. , the base when in the unsloped place ; the dorsal part when supine.

Intrapleural force per unit area is higher ( i.e. , less negative ) around dependent parts of the lung because of the weight of the lung.

Figure 5

Transpulmonary force per unit area ( PALV – PPl ) is greater at the vertex ( 0- ( -10 ) than at base ( 0- ( -2.5 ) in unsloped lung. Therefore, the vertex is more hyperbolic ( i.e. , has a higher volume ) at FRC.

Ventilation is greater at the base than the vertex of the unsloped lung because the base is on a steeper part of the force per unit area volume curve. The vertex is on a flatter ( less compliant ) part. The base starts with less air but has greater airing ; the vertex starts with more air volume but has less airing.

Summary. Ventilation is greater in dependent parts of a normal topic ‘s lungs.

Time invariables for emptying. Important regional inhomogeneities in airing can besides be caused by factors which cause regional differences in airway oppositions or elastic features. High opposition and high conformity equal slow voidance.

Specific conformity. Conformity divided by resting lung volume clinically FRC is used ) . This standardization must be done to analyze the elastic features of tissue and their alterations in disease. How would compliance differ in a kid and an grownup, both with normal lungs?

INTERACTIONS BETWEEN LUNGS AND CHEST WALL

The lungs and chest wall operate in series and their conformities add in return to do entire conformity.

The chest wall is like a spring which may be either compressed or distended.

Figure 6

Transthoracic force per unit area is negative at RV and FRC intending the chest wall is smaller than its unstressed volume and its care to spring out. Normal tidal external respiration is wholly in the negative force per unit area scope.

Transthoracic force per unit area is 0 at approximately 65 % of TLC intending the thorax is at its unstressed volume and has no inclination to prostration or expand.

Transthoracic force per unit area is positive at volumes above approximately 65 % TLC. The chest tends to fall in above its unstressed volume.

The lungs are like a spring which may merely be distended.

Figure 7

The lungs are above their unstressed volume ( minimum volume ) even when the system is at residuary volume. The lungs still have some volume at their minimum volume.

Transpulmonary force per unit area is positive from residuary volume to entire lung capacity so the lungs ever tend to prostration.

Functional residuary capacity is the lung volume at which the inclination for the chest wall to jump outward is merely balanced by the inclination for the lungs to flinch inward. The transmural respiratory system force per unit area ( PRS = RALV – Pbs ) is zero at FRC if respiratory musculuss are relaxed.

The secret plan of lung volume against transmural respiratory system force per unit area ( PRS = RALV – Pbs ) with represents the combined consequence of lung and chest wall kick.

Figure 8

A pneumothorax causes lungs and chest wall to alter volume along their curve until their transmural force per unit area is zero. The lungs ever recoil inward. The chest wall springs outward unless it is inflated to beyond 65 % TLC in which instance it besides will flinch inward.

Conformity alterations in disease

Lungs become slightly more compliant with natural aging and go markedly more compliant with emphysema.

Lungs become less compliant ( stiffer ) with pneumonic fibrosis or during hydropss caused by arthritic bosom disease.

Chestwall becomes less compliant ( stiffer ) in status where the chest wall is deformed ( eg. kyphoscoliosis ) . It besides becomes functionally less compliant when abdominal pit alterations cause upward supplanting of the stop ( eg. gestation ) .

AIRWAY RESISTANCE

Air flow is chiefly laminal during quiet external respiration. Resistance is determined by Poiseuille ‘s Law and the force per unit area gradient required is relative to flux.

When air flow additions, as in exercising, some turbulency and eddy flow develops in big air passages and at subdivision points. An excess force per unit area gradient proportional to flux rate squared is necessary.

The major site of opposition is in the larger air passages specifically in the medium size bronchial tube. Merely approximately 20 % of entire air passage opposition is in little air passages ( less than 2 millimeter ) .

Factors taking to cut down airway quality and increased airway opposition.

Contraction of bronchial smooth musculus. Stimulations include: pneumogastric tone, histamine or reduced airway. is peculiarly of import for advancing homogenous airing. When it builds up in a ill ventilated part the air passages to that part tend to distend.

Loss of elastic kick in lung ( i.e. , more compliant lungs ) . Radial grip on bronchial tubes usually helps keep them unfastened.

Lower lung volumes are associated with less elastic kick and slower flow rates.

Loss of elastic tissue in chronic clogging disease ( eg. emphysema ) lower elastic kick forces.

Maximum forced termination consequences in

Figure 9 – Expiratory flow-volume curves.

May be plotted as volume vs. clip or flux vs. volume.

Peak flow occurs early and flow falls as termination continues and lung volume lessenings.

Effort independency. When the maximal flow-volume envelope is reached, flow falls with forced lung volume regardless of get downing volume or attempt.

Mechanism of flow restriction at lower lung volumes during termination.

Figure 10 – Collapse of the air passages during termination: The entire force per unit area in the air sac equals pleural force per unit area + the elastic force per unit area of the lungs. Flow in the air passage requires a force per unit area bead owing to the syrupy opposition of the gas. If the air flow is rapid plenty, or the airway opposition great plenty, this force per unit area bead will go equal to and so greater than the elastic force per unit area, the airway transmural force per unit area becomes zero or less and the air passages will be given to fall in. The point along the air passage where this occurs is called the “ equal force per unit area point ” . With a forced termination the equal force per unit area point moves closer to the air sac because as the flow rate additions so besides the syrupy force per unit area bead additions, but the elastic force per unit area remains the same. Cartilage in the big air passages helps to oppose the inclination to prostration during forced termination.

Alveolar force per unit area = elastic kick force per unit area + intrapleural force per unit area.

Mouth force per unit area = atmospheric force per unit area = 0.

During expiration intrapleural force per unit area is positive ( greater than atmospheric ) .

Equal force per unit area point ( EPP ) . Airway opposition causes a force per unit area bead from air sac to talk. At some point in the bronchial tube the force per unit area has dropped enough that it merely peers environing intrapleural force per unit area. This is the EPP.

Since air passages are collapsable air flow will be relative to the difference between alveolar and EPP force per unit areas and reciprocally relative to the opposition of this section ( retrieve Starling Resistors ) .

Increased attempt will do similar additions in alveolar force per unit area and force per unit area at the EPP. The force per unit area difference and therefore the flow will be unchanged.

Flow restriction at assorted lung volumes during forced termination.

High LUNG VOLUME MEDIUM LUNG VOLUME LOW LUNG VOLUME

Figure 11

Flow restriction in chronic clogging disease ( emphysema ) .

NORMAL LUNGS EMPHYSEMA

Figure 12

Forced inspiration is non attempt independent because intrapleural force per unit area is negative and air passages are held unfastened.

Figure 13 – A household of flow-volume cringles. Each of the four inspiratory and expiratory critical capacity manoeuvres is performed at a different degree of attempt. The manoeuvre with maximum attempt is designated by the figure “ 4 ” . Maneuvers “ 3, 2, and 1 ” are performed with increasingly less and less attempt.

MECHANICS OF BREATHING STUDY QUESTIONS

True or False. The abdominal and internal intercostal musculuss drive expiratory flow during normal external respiration.

What relationship exists between the volume of an elastic construction and its transmural force per unit area?

What transmural force per unit area difference equals the kick force per unit area of the lung? The chest wall? The whole respiratory system?

What 2 forces contribute to lung conformity and must be overcome to blow up a lung? For each force, name a common lung upset in which it is altered?

List two of import surface tenseness belongingss of wetting agent.

List three physiologically important effects of holding surfactant nowadays.

At FRC which part of the lung is most hyperbolic? During inspiration from FRC, which part of the lung is best ventilated?

What is meant by unstressed volume? At what lung volume is the chest wall at its unstressed volume? At what lung volumes are the lungs at their unstressed volume? At what lung volume is the entire respiratory system at its unstressed volume?

During forced termination flow becomes limited. What two force per unit areas add together to do alveolar force per unit area? What force per unit area determines force per unit areas at the equal force per unit area point?

How does maximum forced expiratory flow alteration with lung volume? Why? How does maximal expiratory flow alteration with clogging disease? Why?