The Respiratory Muscles

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Chapter: Anatomy and Physiology for Health Professionals: Respiratory System

As the diaphragm contracts, the external or inspiratory intercostal muscles between the ribs are stimulated to contract.


Organization of the Respiratory System

The upper respiratory tract includes the nose, nasal cavity, paranasal sinuses, and pharynx. The lowerrespiratory tract includes the larynx, trachea, and lungs. The lungs contain the bronchi, bronchioles, and alveoliFIGURE 21-1 shows the structures of the respiratory system.


The Respiratory Muscles

As the diaphragm contracts, the external or inspiratory intercostal muscles between the ribs are stimulated to contract. The ribs raise and the sternum elevates, enlarging the thoracic cavity further. The lungs expand in response to these movements as well as those of the pleural membranes. When the external intercostal muscles move the thoracic wall upward and outward, the parietal pleura also moves as does the visceral pleura. The lungs then expand in all directions.

Expiration occurs because of the elastic recoil of tissues and surface tension. As the diaphragm low-ers, it compresses the abdominal organs below it. The elastic tissues cause the lungs and thoracic cage to return to their original shapes, and the abdominal organs move back into their previous shapes to push the diaphragm­ upward. Surface tension decreases the diameters of the alveoli, increasing alveolar air pressure. Air inside the lungs is forced out, meaning that normal resting expiration is a passive process. If more forceful exhalation is required, the posterior internal or expiratory ­intercostal muscles contract. This pulls the ribs and sternum downward and inward to increase the pressure in the lungs. The abdominal wall muscles squeeze the abdominal organs inward, forcing the diaphragm even higher against the lungs. Accessory respiratory muscles are activated when there is a need for greatly increased respiratory depth and frequency. The accessory respiratory muscles include the internal intercostal, sternocleidomastoid, serratus anterior, pectoralis minor, scalene, transverse thoracis and abdominis, external and internal oblique, and rec-tus abdominis muscles. The processes of expiration and inspiration are shown in FIGURE 21-8A and B.


Muscles Used in Inhalation

The active process of inhalation involves one or more of these three actions:

Diaphragm contraction: This flattens the thoracic cavity floor to increase its volume; air is drawn into the lungs. About 75% of air movement in normal at-rest breathing results from this contraction.

External intercostal muscle contraction: This raises the ribs, contributing about 25% of air volume in the lungs at rest.

Accessory muscle contraction: This assists the exter-nal intercostal muscles in elevation of the ribs; the speed and mount of rib movement is increased.

Muscles Used in Expiration

Based on the level of respiratory activity, expiration (exhalation) is classified as passive or active. When it is active, one or both of the following actions occurs:

The ribs are depressed by the internal intercostal and transversus thoracic muscles. This means that the width and depth of the thoracic cavity is reduced.

The abdominal muscles help the internal intercostal muscles by compressing the abdomen, which forces the diaphragm upward. The abdominal muscles include the external oblique, internal oblique, transversus abdominis, and rectus abdominis.

Modes of Breathing

The volume of air required to be move in or out of the respiratory system influences different combinations of respiratory muscle actions. Respiratory movements are usually classified as either quiet breathing or forced breathing. These classifications are made based on pat-terns of muscle activity within a single respiratory cycle.

Quiet Breathing

Quiet breathing is also known as eupnea. In this type of breathing, muscular contractions are required for inhalation, while exhalation is done passively. Inha-lation usually includes contraction of the diaphragm and external internal intercostal muscles. There are variations in the actions of these muscles:

Deep (diaphragmatic) breathing: Diaphragm contrac tion provides the required thoracic volume change,with air drawn into the lungs as the diaphragm contracts. When it relaxes, air is passively exhaled.

Shallow (costal) breathing: The rib cages changes shape, altering thoracic volume. Contractions of the external intercostal muscles raise the ribs, enlarge the thoracic cavity, and allow inhalation to occur. When these muscles relax, passive exhalation occurs.

The elastic lung fibers are stretched when the lungs expand during quiet breathing. Rib cage ­elevation stretches opposing skeletal muscles as well as elastic fibers in the body walls’ connective tissues. When mus-cles of inhalation relax, there is recoiling of the elastic fibers. The diaphragm, rib cage, or both return to their original positions. This is known aselastic rebound.

Diaphragmatic breathing is used during minimal activity levels. When more air volume is required, the inspiratory movements increase, along with the actions of rib movement. Costal breathing, even while resting, is able to be the dominant form when movements of the diaphragm are restricted, such as by fluids, masses, or abdominal pressure. A good example is during pregnancy, when a woman uses costal breathing on an increased basis as the enlargement of her uterus forces the abdominal organs against the diaphragm.

Forced Breathing

Forced breathing is also called hyperpnea. It involves active movements of inspiration and expiration. The accessory muscles assist with inhalation. The inter-nal intercostal muscles contract during exhalation. When hyperpnea is at maximum level, the abdominal muscles assist in exhalation. When they contract, the contents of the abdomen are compressed and pushed up against the diaphragm. This reduces the thoracic ­cavity volume even further.

Pressure Relationships in the Thoracic Cavity

The force that moves air into the lungs is atmo-spheric pressure, and respiratory pressures are always expressed in relation to this pressure. Atmospheric pressure is defined as the pressure exerted by the gases, which comprise the air that surrounds us. At sea level, normal air pressure is equal to 760 mm Hg. It is exerted on every surface in contact with the air. The pressure on the inside of the lungs and alveoli is almost equal to outside air pressure. Atmospheric pressure may also be expressed in atmospheric units, which means that 760 mm Hg equals 1 atmospheric unit.

A region of the world is lower than atmospheric pressure when there is a negative respiratory pres-sure. For example, a respiratory pressure of –2 mm Hg means the pressure is lower than atmospheric pres-sure by 2 mm Hg. So, 760 mm Hg minus 2 mm Hg leaves 758 mm Hg, which is described as the ­absolute pressure of the given region. A zero respiratory ­pressure is equal to atmospheric pressure. A positive respiratory pressure is higher than atmospheric pressure.

Intrapulmonary pressure is also known asintra-alveolar pressure, abbreviated as “Ppul,” and defined as the pressure inside the alveoli. Ppul increases and decreases during normal breathing but always becomes equalized with atmospheric pressure eventually. The pressure inside the pleural cavity is known as intrapleu-ral pressure, abbreviated as “Pip,” and also increases and decreases during normal breathing. However, Pip is always approximately 4 mm Hg lower than Ppul. It is, therefore, described as always negative to the Ppul.

This occurs because there are opposing forces in the thorax. Two forces pull the visceral pleura of the lungs away from the parietal pleura of the wall of the thorax, causing the lungs to collapse—the natural tendency of the lungs to recoil and the surface tension of the alveolar fluid. Because the lungs are highly elastic, they always form the smallest size they possibly can form. The mol-ecules of the fluid that lines the alveoli are attracted to each other. This causes surface tension, which continu-ally draws the alveoli to their smallest possible dimen-sions. The natural elasticity of the chest wall opposes these lung-collapsing forces. The forces of the chest wall pull the thorax outward, enlarging the lungs.

To have a negative Pip, the amount of pleural fluid in the pleural cavity needs to remain as little as pos-sible. On a continuous basis, pleural fluid is pumped out of the pleural cavity, entering the lymphatics. Oth-erwise, it would accumulate in the intrapleural space and produce a positive pressure in the pleural cavity. The negative pressure in the intrapleural space and the snug joining of the lungs to the wall of the thorax are extremely critical. If a condition equalizes Pip with either intrapulmonary or atmospheric pressure, imme-diate lung collapse occurs. The difference between the intrapulmonary and Pips is called the transpulmonary pressure. This pressure keeps the air spaces in the lungs open, keeping them from collapsing.

Airway Resistance

Friction is the primary nonelastic source of resistance to gas flow. Also referred to as “drag,” it occurs in the respiratory passageways. Gas flow is related to pressure and resistance. Equivalent factors determine gas flow in the respiratory system and blood flow in the cardio-vascular system. Usually, tiny differences in pressure produce significant changes in gas flow volume. During normal, quiet breathing, the average pressure gradient is 2 mm Hg or less. This small amount is able to move 500 mL of air with each breath in and out of the lungs!

Alveolar Surface Tension

Surface tension is a state of tension at a liquid’s surface­ that is produced by unequal attraction. At the boundary of a gas and a liquid, the liquid molecules are attracted to each other more strongly than they are attracted to the gas molecules. Surface tension pulls liquid molecules closer together. It lessens their contact with the gas molecules because they are not similar. Surface tension also resists forces that tend to increase the liquid’s surface area.

H2O is an example of a liquid with very high surface tension. It is made up of highly polar molecules. H2O makes up a major percentage of the liquid film coating the walls of the alveoli. As a result, it helps to reduce the alveoli to their smallest possible size. However, if this film was only made of H2O, the alveoli would collapse between every breath taken. Why does it not collapse?

Surfactant is a mix of lipids and proteins that resembles a detergent in its effects. It is produced by type II alveolar cells. Surfactant makes H2O molecules become less cohesive. This reduces the surface ten-sion of the alveolar fluid. As a result, lower amounts of energy are needed to expand the lungs and keep the alveoli from collapsing. The type II alveolar cells are stimulated to secrete more surfactant by breaths that are deeper than normal.

Respiratory Volumes

There are four distinct respiratory volumes that can be measured by using spirometry, which is also known as pulmonary function testing. Spirometry is used to measure the functional capacity of the lungs (FIGURE 21-9). TABLE 21-2 shows average values of respi-ratory volumes for men and women of normal weight at about 21 years of age. As discussed earlier, about 500 mL of air move in and out of the lungs with each breath during normal, quiet breathing. This is known astidal volume (TV). However, between 2,100 and 3,200 mL of air can be inspired forcibly beyond the TV. This is known as the inspiratory­ reserve volume (IRV).


The amount of air that can be expelled from the lungs after a normal TV expiration is between 1,000 and 1,200 mL. This is known as the expiratory reserve volume (ERV). However, after the most ­strenuous expiration of air, there are still about 1,200 mL remaining in the lungs. Called the residual volume, it helps to prevent lung collapse and keep the alveoli open, which is also referred to as being patent.


1. During inspiration, explain how Ppul decreases.

2. Explain airway resistance and the factors involved.

3. Describe how surfactant keeps the alveoli from collapsing.

4. What is the role of surfactant in the alveoli?

5. Differentiate respiratory volumes from respiratory capacities.

Respiratory Capacities

Respiratory capacities as well as respiratory volumes are useful for diagnosing problems with pulmonary ventilation. On average, adult females have smaller bodies and lung volumes than do adult males, which is why there are gender-related differences regarding respiratory volumes and capacities (TABLE 21-3).


Respiratory capacities include inspiratory, func-tional residual, vital, and total lung capacities. Two or more lung volumes always make up the respi-ratory capacities (FIGURE 21-10 ). The inspiratory capacity is the total air that can be inspired after one normal­ TV expiration. Therefore, TV plus IRV equals inspiratory capacity.


Functional residual capacity (FRC) is the air that remains in the lungs after one normal TV expira-tion. Therefore, residual volume plus ERV equals FRC. Vital capacity (VC) is the total amount of exchange-able air and is made up of the total volume, IRV, and ERV. Total lung capacity (TLC) is the total of all lung volumes added together.

Dead Space

A certain amount of inspired air does not contrib-ute to alveolar gas exchange but fills the conducting respiratory passageways. Anatomic dead space is made up of the volume of these conducting conduits. The dead space is approximately 150 mL. For example, only 350 mL of air are used in alveolar ventilation out of a TV of 500 mL. In conditions of alveolar collapse or mucous obstruction, gas exchange may stop. Then, the alveolar dead space is added to the anatomic dead space, comprising a volume that is not used, known as the total dead space.

Testing Pulmonary Function

Originally, a spirometer was used to test pulmo-nary function. Today, a small electronic measuring device is used instead, into which the patient blows air. Electronic spirometry is used for evaluating lost respiratory function and for studying respiratory dis-ease progression. Although not diagnostic, it can dis-tinguish between obstructive and restrictive diseases of the pulmonary region. Obstructive pulmonary diseases such as chronic bronchitis involve increased airway resistance. The lungs hyperinflate, increasing TLC, FRC, and residual volume. Restrictive diseases involve a reduction in TLC. Because lung expansion is limited, there are decreases in VC, TLC, FRC, and residual volume.

The rate at which gas moves in and out of the lungs is expressed in forced vital capacity (FVC) and forced expiratory volume (FEV). FVC measures how much gas is expelled after taking a deep breath and forcefully, maximally, and rapidly exhaling. FEV determines how much air is expelled during certain time intervals of the FVC test. FEV1 is the volume exhaled during the first second. Healthy people can exhale approximately 80% of their FVC in one second. Obstructive pulmo-nary diseases cause an individual to be unable to exhale anywhere near this percentage. In restrictive diseases, even though there is reduced FVC, the patient can exhale 80% or higher in one second.

1. Explain how TLC is calculated.

2. Describe the importance of surfactant.

3. Explain the diaphragm’s function in respiration.

4. What is the TLC?

Alveolar Ventilation

The total amount of gas flowing into or out of the respiratory tract in one minute is called the minute ventilation. In a healthy individual during normal, quiet breathing, this is approximately 500 mL per breath. At 12 breaths per minute, this is about 6 L of air. The minute ventilation may increase to 200 L/min during vigorous exercise. These values help to assess respiratory efficiency.

A better indicator is the alveolar ventilation rate (AVR) because it includes the air in the dead space. It measures the flow of gases into and out of the alveoli during a certain interval of time. The AVR is calculated by multiplying the frequency of breaths per minute by the TV minus the dead space, both in milliliters of air per breath. The AVR is based on ­millimeters of air per minute.

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