Mechanics of Respiration Physiology Notes

Respiratory Movements Introduction

• During normal quiet breathing, inspiration is the active process involving contraction of diaphragm and external intercostals muscles.
• On the contrary, expiration is the passive process involving elastic recoiling of the lungs and thoracic cage.
• During inspiration, the thoracic cage enlarges and the lungs expand so that air enters the lungs easily.
• During expiration, the thoracic cage and lungs decrease in size and attain the pre-inspiratory position so that air leaves the lungs easily.

Read And Learn More: Medical Physiology Notes

Muscles Of Respiration

• Respiratory muscles involved in inspiratory movements are known as inspiratory muscles and the muscles involved in expiratory movements are called expiratory muscles.

However, the respiratory muscles are generally classified into two types:

1. Primary or major respiratory muscles
2. Accessory respiratory muscles.

Primary Respiratory Muscles

• Primary respiratory muscles are the muscles, which are responsible for changes in size of the thoracic cage during normal quiet breathing.

Accessory Respiratory Muscles

• Accessory respiratory muscles are the muscles that help primary respiratory muscles during forced respiration.

Inspiratory Muscles

Primary inspiratory muscles:

• Primary inspiratory muscles are the diaphragm, which is supplied by the phrenic nerve (C3 – C5), and external intercostal muscles, supplied by intercostal nerves OWh).
• Respiratory System and Environmental Physiology

Accessory inspiratory muscles

• Sternocleidomastoid, scalene, anterior serrate, elevators of scapulae, and pectorals are the accessory inspiratory muscles.

Expiratory Muscles

Primary expiratory muscles

• Primary expiratory muscles are the internal intercostal muscles, which are innervated by intercostal nerves.

Accessory expiratory muscles

• Accessory expiratory muscles are the abdominal muscles.

Movements Of Thoracic Cage

• Inspiration causes enlargement of thoracic cage. Thoracic cage enlarges because of increase in all diameters, viz.
• anteroposterior, transverse, and vertical diameters. An increase in anteroposterior and transverse diameters occurs due to the elevation of ribs.
• The vertical diameter of thoracic cage is increased by the descent of the diaphragm.
• In general, the change in the size of thoracic cavity occurs because of the movements of four units of structures.

1. Thoracic lid
2. Upper costal series
3. Lower costal series
4. Diaphragm.

Movements Of Thoracic Lid

• Movement of thoracic lid increases the anteroposterior diameter of thoracic cage.
• The thoracic lid is formed by manubrium sterni and the first pair of ribs. It is also called the thoracic operculum.
• Due to the contraction of scaleni muscles, the first ribs move upwards to a more horizontal position.
• This increases the anteroposterior diameter of the thoracic cage.

Upper Costal Series:

Movement of the upper costal series increases the anteroposterior and transverse diameter of the thoracic cage.

Pump handle movement:

• The upper costal series is constituted by the second to sixth pair of ribs. The contraction of external intercostal muscles causes elevation of these ribs and upward and forward movement of the sternum.
• This movement is called pump handle movement.
  Pump handle movement increases the anteroposterior diameter of the thoracic cage.

Bucket handle movement:

• Simultaneously, the central portions of these ribs (arches of ribs) move upwards and outwards to a more horizontal position.
• This movement is called bucket handle movement and it increases the transverse diameter of the thoracic cage.

Lower Costal Series

Movement of the lower costal series increases the transverse diameter of the thoracic cage.

Bucket handle movement

• Bucket handle movement is formed by the seventh to tenth pair of ribs. These ribs also show bucket handle movement by swinging outward and upward. This movement increases the transverse diameter of the thoracic cage.
• The eleventh and twelfth pairs of ribs are the floating ribs, which are not involved in changing the size of the thoracic cage.

Lower Costal Series Diaphragm:

• Movement of diaphragm increases the vertical diameter of the thoracic cage. Normally, before inspiration, the diaphragm is dome-shaped with convexity facing upwards.
• During inspiration, due to the contraction, the muscle fibers are shortened. But, the central tendinous portion is drawn downwards so the diaphragm is fattened.
• Flattening of the diaphragm increases the vertical diameter of the thoracic cage.

Movements Of Lungs

• During inspiration, due to the enlargement of the thoracic cage, the negative pressure is increased in the thoracic cavity.
• Movement of Lungs causes the expansion of the lungs. During expiration, the thoracic cavity decreases in size to the inspiratory position.
• The pressure in the thoracic cage also comes back to the pre-inspiratory level. It compresses the lung tissues so that, the air is expelled out of the lungs.

Collapsing Tendency of Lungs:

• During expiration when air is expelled out, the lungs are expected to collapse. But it does not happen.
• The lungs are under constant threat to collapse even under resting conditions because of certain factors.

Factors causing Collapsing Tendency of Lungs

Two factors are responsible for the collapsing tendency of the lungs

• Elastic property of lung tissues
• Surface tension.

1. Elastic property of lung tissues: The elastic tissues in the lungs show a constant recoiling tendency and try to collapse the lungs.
2. Surface tension: It is the tension exerted on the surface of the alveolar membrane by the fluid secreted from the alveolar epithelium.

Fortunately, there are some factors that save the lungs from collapsing.

Factors Preventing Collapsing Tendency of Lungs

• In spite of the elastic property of the lungs and the surface tension in the alveoli of the lungs, the collapsing tendency of the lungs is prevented by two factors:
• Intrapleural pressure: It is the pressure in the pleural cavity which is always negative (see below). Because of negativity, it keeps the lungs expanded and prevents the collapsing tendency of lungs produced by the elastic tissues
• The surfactant: It is a substance secreted in the alveolar epithelium. It reduces surface tension and prevents the collapsing tendency produced by surface tension.

Factors Preventing Collapsing Surfactant

• Surfactant is a surface-acting material or agent that is responsible for lowering the surface tension of a fluid.
• The surfactant that lines the epithelium of the alveoli in the lungs is known as pulmonary surfactant and it decreases the surface tension on the alveolar membrane.

Source of secretion of pulmonary surfactant

The pulmonary surfactant is secreted by two types of cells

Type 2 alveolar epithelial cells in the lungs, which are called surfactant-secreting alveolar cells or pneumocytes.

• The characteristic feature of these cells is the presence of microvilli on their alveolar surface.
• Clara cells, which are situated in the bronchioles. These cells are also called bronchiolar exocrine cells.

Factors Preventing Collapsing Chemistry

Surfactant is a lipoprotein complex formed by lipids, especially phospholipids, proteins, and ions.

1. Phospholipids: The phospholipids form about 75% of the surfactant. The major phospholipid present in the surfactant is dipalmitoylphosphatidylcholine (DPPC).
2. Other lipids: The other lipid substances of sur-factant are triglycerides and phosphatidylglycerol (PG).
3. Proteins: The proteins of the surfactant are called specific surfactant proteins. There are four main surfactant proteins, called SP-A, SP-B, SP-C, and SP-D. SP-A and SP-D are hydrophilic, while SP-B and SP-C are hydrophobic.
4. Surfactant proteins are vital components of surfactants, and the surfactant becomes inactive in the absence of proteins.
   Ions: Ions present in the surfactant are mostly calcium ions.

Factors Preventing Collapsing Formation

Type 2 alveolar epithelial cells and Clara cells have a special type of membrane-bound organelles called lamellar bodies which form the intracellular source of surfactant.

• Laminar bodies contain surfactant phospholipids and surfactant proteins.
• These materials are synthesized in the endoplasmic reticulum and stored in laminar bodies.
• By means of exocytosis, the lipids and proteins of lamellar bodies are released into the surface fluid lining the alveoli.
• Here, in the presence of surfactant proteins and calcium, the phospholipids are arranged into a lattice (meshwork) structure called tubular myelin.
• Tubular myelin is in turn converted into surfactant in the form of a film that spreads over the entire surface of alveoli.
• Most of the surfactant is absorbed into the type 2 alveolar cells, catabolized and the products are loaded into lamellar bodies for recycling.

Factors necessary for the formation and spreading of surfactant

1. The formation of surfactants requires many substances. Formation of tubular myelin requires DPPC, PG, and the hydrophobic proteins, SP-B and SP-C.
2. Formation of surfactant film requires SP-B, SP-C, and PG.
3. Type 2 alveolar epithelial cells occupy only about 5% of the alveolar surface.
4. However, the surfactant must spread over the entire alveolar surface. It is facilitated by PG and calcium ions.
5. Glucocorticoids play an important role in the formation of surfactants.

Functions of surfactant

1. The surfactant reduces the surface tension in the alveoli of the lungs and prevents the collapsing tendency of the lungs.
2. Surfactant acts by the following mechanism: The phospholipid molecule in the surfactant has two portions. One portion of the molecules is hydrophilic.
3. This portion dissolves in water and lines the alveoli. The other portion is the hydrophobic portion which is directed toward the alveolar air.
4. This surface of the phospholipid along with other portions spreads over the alveoli and reduces the surface tension. SP- B and SP-C play an active role in this process.
5. The surfactant is responsible for the stabilization of the alveoli, which is necessary to withstand the collapsing tendency.
6. It plays an important role in the inflation of the lungs after birth. In the fetus, the secretion of surfactant begins after the third month.
7. Until birth, the lungs are solid and not expanded. Soon after birth, the first breath starts because of the stimulation of respiratory centers by hypoxia and hypercapnia.
8. Although respiratory movements are attempted by the infant, the lungs tend to collapse repeatedly.
9. And, the presence of surfactant in the alveoli prevents the lungs from collapsing.
10. Another important function of surfactant is its role in defense within the lungs against infection and inflammation.
11. The hydrophilic proteins SP-A and SP-D destroy the bacteria and viruses by means of opsonization. These two proteins also control the formation of inflammatory mediators.

Effect of deficiency of surfactant

• In infants, the collapse of the lungs occurs due to the lack or absence of surfactant. This condition is called respiratory distress syndrome or hyaline membrane disease.
• The deficiency of surfactant occurs in adults also and it is called adult respiratory distress syndrome (ARDS).
• In addition, the deficiency of surfactants increases the susceptibility to bacterial and viral infections.

Respiratory Pressures

Two types of pressures are exerted in the thoracic cavity and the lungs during the process of respiration:

1. Intrapleural pressure or intrathoracic pressure
2. Intra-alveolar pressure or intrapulmonary pressure.

Intrapleural Pressure Definition

• The intrapleural pressure is the pressure existing in the pleural cavity, that is, in between the visceral and parietal layers of the pleura.
• It is exerted by the suction of the fluid that lines the pleural cavity.
• It is also called intrathoracic pressure since it is exerted in the whole of the thoracic cavity.

Normal Values

• Respiratory pressures are always expressed in relation to atmospheric pressure which is 760 mm Hg.
• Under physiological conditions, the intrapleural pressure is always negative.

The normal values are:

• At the end of normal inspiration: -6’mm Hg (760 – 6 = 754 mm Hg)
• At the end of normal expiration: -2 mm Hg (760 – 2 = 758 mm Hg)
• At the end of forced inspiration: -30 mmHg
• At the end of forced inspiration with closed glottis (Muller’s maneuver): – 70 mm Hg
• At the end of forced expiration with closed glottis (Valsalva maneuver): + 50 mm Hg

Cause for Negativity of Intrapleural Pressure

The pleural cavity is always lined by a thin layer of fluid that is secreted by the visceral layer of the pleura.

• This fluid is constantly pumped from the pleural cavity into the lymphatic vessels. The pumping of fluid creates negative pressure in the pleural cavity.
• Intrapleural pressure becomes positive in the Valsalva maneuver and in some pathological conditions such as pneumothorax, hydrothorax, hemothorax, and pyothorax.

Measurement:

Intrapleural pressure is measured by direct method and indirect method.

• Directly, the intrapleural pressure is determined by introducing a needle into the pleural cavity and connecting the needle to a mercury manometer.
• In the indirect method, the intrapleural pressure is measured by introducing the esophageal balloon, which is connected to a manometer.
• The intrapleural pressure is considered as equivalent to the pressure existing in the esophagus.

Significance of Intrapleural Pressure

Throughout the respiratory cycle, intrapleural pressure remains lower than intra-alveolar pressure. This keeps the lungs always inflated.

The intrapleural pressure has two important functions:

• Since the intrapleural pressure is always negative, it prevents the collapsing tendency of the lungs, which is caused by the elastic recoiling of lung tissues
• Because of the negative pressure in the thoracic region, the larger veins and vena cava are enlarged, i.e. dilated.
• Also, the negative pressure acts like a suction pump and pulls the venous blood from the lower part of the body towards the heart against gravity.
• Thus, intrapleural pressure is responsible for venous return. So, it is called the respiratory pump for venous return.

Intra-Alveolar Pressure

Definition:

Intra-alveolar pressure is the pressure existing in the alveoli of the lungs. It is also known as intrapulmonary pressure.

Normal Values:

• Normally, intra-alveolar pressure is equal to the atmospheric pressure, which is 760 mmHg.
• It becomes negative during inspiration and positive during expiration.

The normal values are:

1. During normal inspiration: – 1 mm Hg (760 – 1 = 759 mm Hg)
2. During normal expiration: + 1 mm Hg (760 + 1 = 761 mm Hg)
3. At the end of inspiration and expiration: Equal to atmospheric pressure (760 mm Hg)
4. During forced inspiration with closed glottis (Muller’s maneuver): – 80 mm Hg
5. During forced expiration with closed glottis (Valsalva maneuver): + 100 mm Hg

Measurement:

Intra-alveolar pressure is measured by using plenty- Cosmograph.

Significance of Intra-alveolar Pressure

The significance of the intra-alveolar pressure:

1. The intra-alveolar pressure causes a flow of air in and out of the alveoli. During inspiration, the intra- alveolar pressure becomes negative, so the atmospheric air enters the alveoli.
2. And, as the intra-alveolar pressure becomes positive during expiration, the air is expelled out of alveoli
3. The intra-alveolar pressure also helps in the exchange of gases between the alveolar air and the blood.

Transpulmonary Pressure:

• Transpulmonary pressure is the pressure difference between alveoli and the outer surface of the lungs or the difference between intra-alveolar pressure and intrapleural pressure.
• It is the measure of elastic forces in the lungs, which is responsible for the collapsing tendency of the lungs.

Compliance

Compliance Definition:

• Compliance is the ability of the lungs and thorax to expand or it is the expansibility of lungs and thorax.
• It is defined as the change in volume per unit change in pressure.

Significance of Determining Compliance:

Determination of compliance is useful as it is the measure of the stiffness of the lungs. The stiffer the lungs, the less the compliance.

Normal Values:

The compliance is expressed in two ways:

• In relation to intra-alveolar pressure
• In relation to intrapleural pressure.

Compliance in Relation to Intra-alveolar Pressure:

• Compliance is the volume increase in lungs per unit increase in the intra-alveolar pressure.
• Compliance of lungs and thorax together: 130 mL/1 cm H20 pressure.
• Compliance of lungs alone: 220 mL/1 cm H20 pressure.

Compliance in Relation to Intrapleural Pressure:

Compliance is the volume increase in lungs per decrease in intrapleural pressure.

• Compliance of lungs and thorax together – ICO mU 1 cm H20 pressure.
• Compliance of lungs alone = 200 mL/1 cm H20 pressure.
• Thus, if the lungs are removed from the thorax, the expansibility (compliance) of the lungs alone is doubled.
• It is because of the absence of inertia and the restriction exerted by the structures of the thoracic cage, which interfere with the expansion of the lungs.

Specific Compliance:

• The term specific compliance is introduced to assess the stiffness of lung tissues more accurately.
• Specific compliance is the compliance per liter of lung volume. It is usually reported for expiration at functional residual capacity.
• It is the compliance divided by functional residual capacity.

• Functional residual capacity is the volume of air present in the lungs at the end of normal expiration.

Types Of Compliance:

Compliance is of two types:

1. Static compliance
2. Dynamic compliance

Static Compliance:

• Static compliance is the compliance measured under static conditions, i.e. by measuring pressure and volume when breathing does not take place (see below).
• Static compliance is the pressure required to overcome the elastic resistance of the respiratory system for a given tidal volume under zero flow (static) conditions.

Dynamic Compliance

Dynamic compliance is the compliance measured during dynamic conditions, i.e. during breathing.

Static Compliance vs Dynamic Compliance:

• In healthy subjects, there is little difference between static and dynamic compliance.
• In patients with stiff lungs, dynamic compliance decreases while little change occurs in static compliance.

Measurement Of Compliance:

Measurement of Static Compliance:

• To measure static compliance, the subject is asked to inspire air periodically at regular steps from a spirometer.
• In each step, a known volume of air is inspired. At the end of each step, the intrapleural pressure is measured by means of an esophageal balloon.
• Then, the air is expired in steps until the volume returns to the original pre-inspiratory level. The intrapleural pressure is measured at the end of each step.
• The values of volume and pressure are plotted to obtain a curve. The curve is called the pressure-volume curve.
• From this curve, compliance can be calculated. The graph shows a difference in inspiration and expiration.

Measurement of Dynamic Compliance:

• Dynamic compliance is measured during normal breathing.
• It is measured by determining the lung volume and esophageal pressure (intrapleural pressure) at the end of inspiration and expiration when the lungs are apparently stationary.

Dynamic compliance Applied Physiology:

Increase in Compliance:

Compliance increases in physiological and pathological conditions.

Old Age (physiological):

In old age, lung compliance increases due to the loss of elastic properties of lung tissues.

Emphysema (Pathological)

• In emphysema, because of the loss of walls (membrane) of many alveoli and loss of elastic tissue, the lungs become loose and floppy.
• So lung compliance increases and low pressure is enough to increase the volume.

Decrease in Compliance:

Compliance decreases in several pathological conditions such as

• Deformities of the thorax like kyphosis and scoliosis
• Fibrotic pleurisy (inflammation of the pleura resulting in fibrosis)
• Paralysis of respiratory muscles
• Pleural effusion
• Abnormal thorax (pneumothorax, hydrothorax, hemothorax, and pyothorax.

Work Of Breathing

The work done by the respiratory muscles during breathing to overcome the resistance in the thorax and respiratory tract is known as work of breathing.

Work Done By Respiratory Muscles:

• During the respiratory processes, inspiration is an active process and the expiration is a passive process.
• So, during quiet breathing, the respiratory muscles perform the work only during inspiration and not during expiration.

Utilization Of Energy:

During the work of breathing, the energy is utilized to overcome three types of resistance:

1. Airway resistance
2. Elastic resistance of lungs and thorax
3. Nonelastic viscous resistance.

Airway Resistance:

• Airway resistance is the resistance offered to the passage of air through respiratory tract.
• The resistance increases during bronchiolar constriction which increases the work done by the muscles during breathing.
• The work done to overcome the airway resistance is called airway resistance work.

Elastic Resistance of Lungs and Thorax:

• The energy is required to expand the lungs and thorax against the elastic force.
• The work done to overcome this elastic resistance is called compliance work.

Nonelastic Viscous Resistance:

• Energy is also required to overcome the viscosity of the lung and tissue of the thoracic cage. The work done to overcome this viscous resistance is called tissue resistance work.
• The above factors are explained by the curve that shows the relation between lung volume and pleural pressure.