Saturday, 25 January 2020

Respiration and Pulmonary Ventilation |Mechanics of Pulmonary Ventilation|Lungs Compliance |Pulmonary Volumes and Capacities |Dead Space |Functions of the Respiratory Passageways|

             Physiology Gyton Hall Chapter Respiration.

 Respiration and Pulmonary Ventilation |Mechanics of Pulmonary Ventilation|Lungs Compliance |Pulmonary Volumes and Capacities |Dead Space |Functions of the Respiratory Passageways|


Pulmonary Volumes and Capacities |Dead Space |Functions of the Respiratory Passageways|
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Respiration :


The process in which oxygen is supplied to the tissues while carbon dioxide removes through the respiratory system called respiration. The main functional events of respiration include
(1) pulmonary ventilation, which is that the movement of air in and out of the alveoli;
(2) diffusion of oxygen and carbon dioxide between the blood and alveoli;
(3) transport of oxygen and CO2 to and from the peripheral tissues; and
(4) regulation of respiration. This chapter provides a discussion of pulmonary ventilation.

Mechanics of Pulmonary Ventilation



Muscles That Cause Lung Expansion and Contraction ;

Lungs Volume Increases and Decreases as the Thoracic Cavity Expands and Contracts any time the length or thickness of the chest cavity increases or decreases, simultaneous changes in lung volume occur. • Normal quiet breathing is accomplished with the diaphragm.

During the inspiration process, the diaphragm contract and pulls the lower surfaces of the lungs downward. During expiration, the diaphragm relaxes and therefore elastic recoil of the lungs, chest wall, and abdominal structures compress the lungs.

 During the heavy breathing process, the elastic forces are not sufficiently powerful to cause rapid expiration. The extra force is mainly achieved by the contraction of the abdominal muscles, which pushes the abdominal contents upward against the diaphragm.


Raising and Lowering the Rib Cage Causes the Lungs to Expand and Contract ;


Due to the elevation of the rib cage, the ribs project almost directly forward and the sternum also moves forward and away from the spine, increasing the anteroposterior thickness of the chest.

Muscles that raise the rib cage are muscles of inspiration Contraction of the external intercostals causes the ribs to move upward and forward in a “bucket handle” motion. Accessory muscles include the sternocleidomastoid muscles, the anterior serrati, and the scaleni.

 Muscles that depress the rib cage are muscles of expiration, including the internal intercostals and the abdominal recti. The other muscles of abdomen compress the abdominal contents upward toward the diaphragm.

Due to the movement of air in and out of the lungs and the Pressures That Cause the Movement.


Pleural Pressure Is the Pressure of the Fluid in the Space between the Lung Pleura and Chest Wall Pleura.

At the beginning of inspiration, the normal pleural pressure is about −5 cm of water, which is the amount of suction required to hold the lungs at their resting volume.

 During inspiration, the chest cage pulls the surface of the lungs with still greater force and creates still more negative pressure due to its expansion, averaging about −7.5 cm of water. Alveolar Pressure Is the Air Pressure Inside the Lung Alveoli.

When the glottis is open and there is no movement of air, the pressures in all parts of the respiratory tree are equal to the atmospheric pressure, which is considered to be 0 cm of water.

    • During inspiration, the pressure in the alveoli decreases to about −1 cm of water, which is sufficient to move about 0.5 L of air into the lungs within the 2 seconds required for inspiration. 

• During expiration, opposite changes occur: The alveolar pressure rises to about +1 cm of water, which forces the 0.5 L of inspired air out of the lungs during the 2 to 3 seconds of expiration.


Lungs Compliance ;


Lung Compliance Is the Change in Lung Volume for each Unit Change in Transpulmonary Pressure.


Transpulmonary pressure is the difference between the alveolar and pleural pressures. The normal total compliance of both lungs together in the average adult is about 200 mL/cm of water. 

Compliance is dependent on the following elastic forces: 

  • Elastic forces of the lung tissues are determined mainly by the elastin and collagen fibers.
 • Elastic forces caused by surface tension in the alveoli account for about two-thirds of the total elastic forces in normal lungs.

SurfactantSurface Tension
, and Collapse of the Lungs
Water Molecules Are Attracted to One Another;

The water surface lining the alveoli attempts to contract as the water molecules pull toward one another. This attempts to force air out of the alveoli, causing the alveoli to attempt to collapse. The net effect is to cause an elastic contractile force of the entire lung, called the surface tension elastic force.

Surfactant Reduces the Work of Breathing (Increases Compliance) by Decreasing Alveolar Surface Tension

Surfactant is secreted by type II alveolar epithelial cells of the lungs. Its most important component is the phospholipid dipalmitoylphosphatidylcholine. The presence of a surfactant on the alveolar surface reduces the surface tension to one-twelfth to one half of the surface tension of a pure water surface. Smaller 

Alveoli Have a Greater Tendency to Collapse;

Note from the following formula (Law of Laplace) that the collapse pressure generated in the alveoli is inversely related to the radius of the alveolus. This means that the smaller the alveolus the greater is the collapse pressure:

Surfactant, “Interdependence,” and Lung Fibrous Tissue Are Important for “Stabilizing” the Size of the Alveoli

If some of the alveoli were small and others were large, theoretically the smaller alveoli would tend to collapse and cause expansion of the larger alveoli. This instability of alveoli does not occur normally for the following reasons:

 • Interdependence. The adjacent alveoli, alveolar ducts, and other air spaces have the ability to support each other in such a way that a large alveolus usually cannot exist adjacent to a small alveolus because they share common septal walls.                                       

Fibrous tissue. The lung is constructed of about 50,000 functional units, each of which contains one or a few alveolar ducts and their associated alveoli. All of them are surrounded by fibrous septa that act as additional supports. 

• Surfactant. Surfactant reduces surface tension, allowing the interdependence phenomenon and fibrous tissue to overcome the surface tension effects. When an alveolus becomes smaller, the surfactant molecules on the alveolar surface-became squeezed together and increasing their concentration and thereby reducing the surface tension still further.

Pulmonary Volumes and Capacities :


Most pulmonary volumes and capacities can be measured with a spirometer. The total lung capacity, functional residual capacity, and residual volume cannot be measured with a spirometer. The recording was made using an apparatus called a spirometer.

 The Pulmonary Volumes Added Together Equal the Maximum Volume to Which the Lungs Can Be Expanded

The four pulmonary volumes are;
• Tidal volume (Vt) is the volume of air (about 500 mL) inspired and expired with each normal breath. 
• Inspiratory reserve volume (IRV) is the extra volume of air (about 3000 mL) that can be inspired over and above the normal tidal volume.
• Expiratory reserve volume (ERV) is the extra amount of air (about 1100 mL) that can be expired by forceful expiration after the end of a normal tidal expiration. 
Residual volume (RV) is is the volume of air (about 1200 mL) remaining in the lungs after the most forceful expiration. Pulmonary Capacities Are Combinations of Two or More Pulmonary Volumes

The pulmonary capacities are   described as follows:

 • Inspiratory capacity (IC) equals the tidal volume plus the inspiratory reserve volume. This is the amount of air (about 3500 mL) a person can breathe beginning at the normal expiratory level and distending the lungs to the maximum amount.

 • Functional residual capacity (FRC) equals the expiratory reserve volume plus the residual volume. This is the amount of air that remains in the lungs at the end of a normal expiration (about 2300 mL). 

• Vital capacity (VC) equals the inspiratory reserve volume plus the tidal volume plus the expiratory reserve volume. This is the maximum amount of air a person can expel from the lungs after first filling the lungs to their maximum extent and then expiring to the maximum extent (about 4600 mL).

 • Total lung capacity (TLC) is the maximum volume to which the lungs can be expanded with the greatest possible inspiratory effort (about 5800 mL); it is equal to the vital capacity plus the residual volume.

Minute Respiratory Volume and Alveolar Ventilation;


The Minute Respiratory Volume Is the Total Amount of New Air That Is Moved Into the Respiratory Passages Each Minute. 
It is equal to the tidal volume multiplied by the respiratory rate.

 The normal tidal volume is about 500 mL, and the normal respiratory rate is about 12 breaths per minute; therefore the minute respiratory volume normally averages about 6 L/min.

Alveolar Ventilation Is the Rate at which New Air Reaches the Gas Exchange Areas of the Lungs

During inspiration, some of the air never reaches the gas exchange areas but, instead, fills respiratory passages; this air is called dead space air. Because alveolar ventilation is the total volume of new air that enters the alveoli, it is equal to the respiratory rate multiplied by the amount of new air that enters the alveoli with each breath:
where, 
              Pressure =cocentration of dissolved gas
                                                   Solubility Coefficient 

A is the volume of alveolar ventilation per minute, Freq is the frequency of respiration per minute, Vt is the tidal volume, and Vd is the dead space volume. Thus with a normal tidal volume of 500 mL, a normal dead space of 150 mL, and a respiratory rate of 12 breaths per minute, alveolar ventilation equals 12 × (500 − 150), or 4200 mL/min.

Dead Space :

There Are Three Types of Dead Space Air ;


• Anatomical dead space is the air in the conducting airways that do not engage in gas exchange.

 • Alveolar dead space is the air in the gas exchange portions of the lung that cannot engage in gas exchange; it is nearly zero in normal individuals.

Physiological dead space is the sum of the anatomic dead space and the alveolar dead space (i.e., the total dead space air).

Functions of the Respiratory Passageways;


Trachea, Bronchi, and Bronchioles


Air Is Distributed to the Lungs by Way of the Trachea, Bronchi, and Bronchioles.

The trachea is the first-generation passageway, and two main right and left bronchi are the second-generation passageways. Each division thereafter is an additional generation. There are between 20 and 25 generations before the air reaches the alveoli.

The Walls of the Bronchi and Bronchioles Are Muscular

The walls are composed mainly of smooth muscle in all areas of the trachea and bronchi not occupied by cartilage plates. 

The walls of the bronchioles are almost entirely smooth muscle, except for the most terminal bronchioles (respiratory bronchioles), which have only a few smooth muscle fibers.

 Many obstructive diseases of the lung result from narrowing of the smaller bronchi and bronchioles, often because of excessive contraction of the smooth muscle itself.

The Greatest Resistance to Air Flow Occurs in the Larger Bronchi, Not in the Small, Terminal Bronchioles.

The reason for this high resistance is that there are relatively few bronchi in comparison with about 65,000 parallel terminal bronchioles, each of which pass only a minute amount of air. However, under disease conditions, the smaller bronchioles often play a greater role in determining airflow resistance for two reasons: 

(1) they are easily occluded because of their small size and

 (2) they constrict easily because they have a greater proportion of smooth muscle fibers in their walls.

Epinephrine and Norepinephrine Cause Dilation of the Bronchiole Tree,


Direct control of the bronchioles by sympathetic nerve fibers is relatively weak because few of these fibers penetrate as far as the central portions of the lung. 
The bronchial tree, however, is
exposed to circulating norepinephrine and epinephrine released from the adrenal gland medullae.

 Both of these hormones, especially epinephrine because of its greater stimulation of βadrenergic receptors, cause dilation of the bronchial tree.

 The Parasympathetic Nervous System Constricts the Bronchioles


A few parasympathetic nerve fibers derived from the vagus nerve penetrate the lung parenchyma. These nerves secrete acetylcholine, which causes mild to moderate constriction of the bronchioles.
 When a disease process such as asthma has already caused some constriction, parasympathetic nervous stimulation often worsens the condition. When this occurs, the administration of drugs that block the effects of acetylcholine, such as atropine, can sometimes be used to relax the respiratory passages sufficiently to relieve the obstruction. 

Mucous Lining the Respiratory Passageways; Action of Cilia to Clear the Passageways



All the Respiratory Passages Are Kept Moist with a Layer of Mucus,

The mucus is secreted in part by individual goblet cells in the epithelial lining of the passages and in part by small submucosal glands. In addition to keeping the surfaces moist, the mucus traps small particles from the inspired air. The mucus itself is removed from the passages by the actions of ciliated epithelial cells. The Entire Surface of the Respiratory Passages Is Lined with Ciliated Epithelium.

 Physiology Gyton Hall Chapter Respiration.

Other topics :


Surfactants and Surface Tension| Surfactants Source Of Secretion | Law Of Laplace | Surfactants in Alveoli| Formation of Surfactants | PULMONARY SURFACTANT | Functions of Surfactants |




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