turning cogs

Mechanics of Breathing

 

I. Introduction

A.    P = x R. To move air into or out of the lungs we must create pressure differences between the atmosphere and the alveoli.

B.     To move air into the alveoli we must make alveolar pressure less than atmospheric pressure (except during positive pressure ventilation). (Levitzky Table 2-1).

C.     Alveoli expand passively in response to an increased transmural pressure gradient. As they expand, their elastic recoil increases (Levitzky Fig.2-1).

D.    Alveolar pressure = intrapleural pressure + alveolar elastic recoil pressure.

 

II. Muscles of Breathing

A.    Inspiration - expansion of thoracic cavity lowers intrathoracic pressure, which decreases alveolar pressure below atmospheric. "Negative pressure." Normally no true intrathoracic space. Only about 15-25 ml pleural fluid; 10-30µ thick.

1. The Diaphragm. The diaphragm is the primary muscle of inspiration. During supine eupneic breathing it is responsible for at least 2/3 of the tidal volume. The muscle fibers of the diaphragm are inserted into the sternum and the lower ribs, and into the vertebral column by the two crura. The other ends of these muscle fibers converge to attach to the fibrous central tendon. During eupnea, contraction of the approximately 250 cm2 diaphragm causes its dome to descend 1 to 2 cm into the abdominal cavity, with little change in its shape, except that the area of apposition decreases in length. This elongates the thorax and increases its volume. These small downward movements of the diaphragm are possible because the abdominal viscera can push out against the relatively compliant abdominal wall. (Levitzky Fig.2-3). During a deep inspiration the limit of the compliance of the abdominal wall is reached and the indistensible central tendon becomes fixed against the abdominal contents. After this point contraction of the diaphragm against the fixed central tendon elevates the lower ribs.

a.  Nerve supply: 2 Phrenic nerves - emanate from C- 3, C- 4, and C - 5.

b.  "Paradoxical" upward movement if one hemidiaphragm is paralyzed.

2.   External and Parasternal Intercostal Muscles - contraction pulls ribs up. Increases antero-posterior diameter of the chest. Innervation from T -1 to T-11.

3.  Accessory muscles - not involved in eupnea but may be called into action during exercise, cough, sneeze, chronic obstructive pulmonary diseases, etc. Include sternocleidomastoid and others. Act to raise the upper ribs and the sternum.

B.  Expiration

1. Expiration during eupneic breathing is passive. Relaxation of the inspiratory muscles allows the increased alveolar elastic recoil to decrease the volume of the alveoli, increasing alveolar pressure above atmospheric pressure.

2. The muscles of expiration are involved in active expiration: exercise, speech, cough, sneeze, forced expiration, etc.

a. Internal intercostals - Perpendicular to external intercostals. Action pulls rib cage down and inward.

b. Muscles of abdominal wall - raise intra-abdominal pressure. Displace diaphragm upward into thorax. Includes rectus abdominis, internal and external oblique muscles, and transversus abdominis. (Levitzky Fig.2-4).

3. During expiration there is a "braking action" of the inspiratory muscles at high lung volumes.

4. Although all of the respiratory muscles are usually considered to be completely relaxed at the FRC, diaphragmatic tone probably plays an important role.

 

III. Pressure and Volume in the Lung: Compliance and Elastic Recoil

A.    Changes in lung volume, alveolar and intrapleural pressures and airflow during the respiratory cycle (Levitzky Fig.2-5). During eupneic breathing expiration is longer than inspiration.

B.     Pressure - volume curves (Levitzky Fig.2-6): Alveoli expand passively in response to an increased transmural pressure gradient.

1. Normally negative intrapleural pressure expansion of the lungs, but pressure difference is the important factor, not whether "negative" or "positive" pressure respiration (for excised lungs). Transmural pressure gradient (alveolar distending pressure) = alveolar pressure minus intrapleural pressure.

2. Hysteresis (the difference between the inflation curve and the deflation curve) indicates energy loss.

3. Each individual alveolus will have its own pressure-volume characteristics. However, we can consider each alveolus as being somewhere on the pressure-volume curve for the whole lung.

4.  The slope of the pressure-volume curve represents compliance.

5. Compliance ( V/ P) may be a useful diagnostic tool. Compliance is inversely proportional to elastic recoil or elastance. Must consider transmural pressures for P. Measurement of compliance - esophageal balloon used to indicate intrapleural pressure.

6. Total compliance of the respiratory system (that is, of the lung and the chest wall, which   are in series) is normally about 0.1 L/cm H2O.

a. Compliances in series add as reciprocals:

b. Compliances in parallel (e.g. the two lungs) add directly.

c. Static compliance (calculated when no air is flowing):

7. Compliance is decreased by: Fibrosis, atelectasis, pneumothorax, pulmonary vascular congestion, lack of pulmonary surfactant, and pulmonary edema decrease the compliance of the lungs. Obesity and kyphoscoliosis decrease the compliance of the chest wall.  Decreased compliance increases the work of inspiration (Levitzky Fig.2-7).

8. Compliance is increased by: emphysema.

9. Compliance is volume dependent
            Specific compliance = compliance/volume

10. Dynamic compliance = compliance calculated during breath.

11. Elastic recoil of the lung (inversely proportional to pulmonary compliance) is due to:

a. Elastic fibers in pulmonary parenchyma

b. Surface tension of the liquid film lining the alveoli

12. Surface tension (dynes/cm). Occurs at a gas-liquid interface: can abolish with saline inflation of the lung.

a. T = Pr; P = T/r (Law of Laplace) (Levitzky Fig.2-9).

b. At the same surface tension, smaller alveoli should empty into larger alveoli because pressure would be greater inside smaller alveoli than inside larger. Why doesn't this occur? (Levitzky Fig.2-10)

c. The alveolar fluid lining has a lower surface tension than would be predicted by a plasma-air interface. (This increases pulmonary compliance and lowers pulmonary work).

d. The alveolar liquid lining surface tension changes with the size of the alveoli: the smaller the area the lower the surface tension. (This is not true if we lower the surface tension of water with a detergent). This stabilizes the alveoli. (Levitzky Fig.2-12)

e. This due to a substance known as pulmonary surfactant that is secreted by type II alveolar cells.

f. Advantages of pulmonary surfactant are that it lowers surface tension of alveolar lining-decreases the inspiratory work of breathing and it preferentially lowers surface tension in small alveoli-stabilizes alveolar units. (This also aided by "interdependence" of alveoli). Therefore a relative decrease in the functional surfactant present in the lung can greatly increase the effort necessary to expand the lung and may also lead to diffuse spontaneous atelectasis. This shifts the static pulmonary compliance curve to the right. Hypoxia and/or hypoxemia lead to decreased surfactant production. This may be a contributing factor in acute respiratory distress syndrome.

g. Surfactant is not produced by the fetal lung until approximately the fourth month of gestation and may not be fully functional until the seventh month or later. This is a major factor in infant respiratory distress syndrome.

 

IV.  Mechanical Interaction of the Lung and the Chest Wall - at the FRC, the chest wall is pulled in by the elastic recoil of the lung; the lung is pulled out by the elastic recoil of the chest wall. (The intrapleural liquid between them has a negative pressure because it is between these two opposing forces.)They are mechanically interdependent. This may be what really opens the alveoli during inspiration (Levitzky Fig.2-2).

A. Summary of elastic recoil of the lung: the relaxation pressure-volume curve of the lung and chest wall. (Levitzky Fig.2-14). Can separate the contributions of the lung and chest wall if determine the intrapleural pressure.

1. At the Functional Residual Capacity, the elastic recoil of lung (inward) is balanced by the elastic recoil of the chest wall (outward). Relaxation pressure is 0. Interaction of the lung and chest wall determine the FRC.

2. Below the FRC the relaxation pressure is negative because the recoil of the chest wall (outward) is greater than the recoil of the lung (inward).

3. Above the FRC the relaxation pressure is positive because the elastic recoil of the lung (inward) is greater than the outward elastic recoil of the chest wall. In fact, at high lung volumes the elastic recoil of the chest wall is also inward.

4. Changes in body position affect the outward elastic recoil of the chest wall. Thus, in the supine position the lung has less outward elastic recoil and the FRC is decreased (Levitzky Fig.2-15).

 

V.  Resistance and breathing

A. Frictional resistance of lung tissues and chest wall ("tissue resistance"). Normally less than 20% of total respiratory system resistance.

B. Resistance to air flow ("airways resistance"). Resistances in series add directly; resistances in parallel add as reciprocals.

1. Characteristics of air flow (Levitzky Fig.2-16).

a. Laminar flow: Delta P proportional to Flow x R1 (Poiseuille's Law)

where R1 = (8 x viscosity x length)/ ¶ x radius4
     Gas in the center of the tube moves faster than that closer to the wall of the tube or vessel.

b.   Turbulent flow: P 2 x R2. (The driving pressure required to generate the same air flow is proportional to 2). Density is more important than viscosity during turbulent flow. Turbulent flow occurs if Reynold's number is greater than (approximately) 2,000

c. Reynold's number = (density x linear velocity x diameter) /  viscosity

d.  In the airways there is usually a combination of both laminar and turbulent flow ("transitional flow"), depending on Reynold's number for the particular segment of airway.

e. True laminar flow probably only occurs in the smallest airways, where linear velocity is very low. (Remember that linear velocity is inversely proportional to cross-sectional area for any given flow).

2. Distribution of airways resistance:

a.    Approximately 40% of total airways resistance resides in the upper airways (oro-and nasopharynx, larynx, etc.) when breathing through the nose and about 25% of the total when breathing though the mouth.

b.   Tracheo-bronchial tree: Although resistance to air flow is greatest in individual small airways, the total resistance to air flow contributed by the small airways taken together is very low because they represent a huge number of parallel pathways. Therefore under normal circumstances the greatest resistance to air flow resides in the medium-sized bronchi.

3. Factors contributing to airways resistance

a.  "Active" factors - Autonomic nervous system

Parasympathetic - stimulation causes broncho- constriction (and increased glandular secretion of mucus). There is normally some parasympathetic tone of the airways. Parasympathetically mediated reflex constriction in response to irritants, arterial chemoreceptor stimulation, etc.

Sympathetic - ß2 stimulation causes bronchodilation(and inhibits glandular secretion of mucus);stimulation may cause bronchoconstriction (and increased glandular secretion of mucus). Circulating ß2 agonists are probably more important than sympathetic innervation of the airways. There is normally little or no sympathetic tone of the airways.

Local responses - increased local PCO2 or decrease local PO2 causes dilation of small airways; decreased local PCO2 causes constriction of small airways.

b. "Passive" factors - airways resistance is inversely related to lung volume - airways resistance is low at high lung volumes and high at low lung volumes (Levitzky Fig.2-17). Airway collapse is most likely to occur in small airways with no cartilaginous support. Two reasons for this:

Traction by alveolar septa inserted into small airways (Levitzky Fig.2-18). Higher lung volumes cause greater alveolar elastic recoil and increase the traction on small airways, distending them and decreasing airways resistance.

Transmural pressure gradient is very positive as breathe to high lung volumes and negative during forced expiration to low volumes. Dynamic compression of small airways when intrapleural pressure becomes positive during forced expiration (Levitzky Fig.2-19).

4. Assessment of airways resistance

a.    Forced vital capacity (FVC); forced expiratory volume in first second (FEV1); forced expiratory flow rate between 25 and 75% of the vital capacity (FEF25 - 75%). Resistance takes time to overcome. FEV1/FVC <80% indicates airway obstruction.) (Levitzky Fig.2-21).

b.   Body pleythysmograph technique.

c.    Isovolume pressure - flow curve - individual points taken as subject passes through a particular lung volume during forced expirations of varying intensities (Levitzky Fig.2-22).

When intrapleural pressure becomes positive, increasing the effort (i.e. intrapleural pressure) causes no further increase in air flow. This effort independence indicates that resistance to air flow is increasing as intrapleural pressure increases (dynamic compression).

At the same intrapleural pressure air flow is greater at greater lung volumes. This is a result of greater alveolar elastic recoil:

More traction on the small airways.

Greater driving pressure for air flow (see below).

d.  Flow-volume curves (Levitzky Fig.2-23).

Effort - dependent portion at high lung volumes

Effort - independent portion at low lung volumes

Normally no effort independence in inspiratory curve if breathing through mouth

e.  Explanation - the equal pressure point hypothesis (Levitzky Fig.2-19).

The equal pressure point is the point at which pressure inside the airway equals pressure outside (intrapleural pressure). Above the equal pressure point there is a tendency for airway collapse (which is opposed by cartilaginous support in larger airways and traction by alveolar elastic recoil in smaller airways).

During a forced expiration, when intrapleural pressure is positive, the effective driving pressure for airflow is alveolar pressure minus intrapleural pressure, (which equals alveolar elastic recoil pressure).

During the course of a forced expiration the equal pressure point moves toward the alveoli and collapsible small airways. The lung volume decreases, leading to smaller alveoli with less alveolar elastic recoil. As elastic recoil decreases, the effective driving pressure for air flow decreases and the traction on the small airways decreases (Levitzky Fig.2-20)..

f.  Flow-volume curves as a diagnostic tool (Levitzky Figs.2-24 and 2-25).

Dynamic compliance changes usually indicate elevated airflow resistance in small airways.

VI. Work of breathing: W = P x V

A."Elastic work" (Restrictive lung diseases)

1.   Surface tension

2.   Elastic recoil of pulmonary parenchyma

3.   Elastic recoil of muscles of respiration and rib cage

B. "Resistive work" (Obstructive lung diseases)

1.Tissue resistance

2.Airways resistance

C. O2 cost of eupneic breathing is normally less than 5% of total body O2 consumption. Can increase to 30% in maximal exercise.

 


Copyright © 2000 M. G. LEVITZKY


Last updated: Wednesday July 3, 2013


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