- RESPIRATORY SYSTEM
ANATOMY AND MECHANICS
The main function of the respiratory system is gas exchange between atmosphere and blood to provide an adequate amount of O2 and remove by-product of cellar respiration – CO2, as well as pH regulation of our blood.
Air enters the body through the mouth or nose, moves to the pharynx (throat), then passes through the larynx and enters the trachea (a tube which contains rings of cartilages), within lungs air moves through smaller and smaller branches, until it reaches the endpoint – alveoli. Along this way, air adjusts to body temperature, filtered and humidified.
All these structures sited inside two lungs, right and left (right is a bit bigger). Lungs itself is spongy organs, surrounded by membranes (visceral and parietal pleura). The lungs of an average-sized adult weigh approximately 2.3 kg, and volume varies between 4 and 6 liters.
The respiratory system can be divided into conducting and respiratory zone.
Conducting zone includes nasal and mouth cavities, pharynx, trachea, bronchus, and bronchioles. Gas exchange doesn’t take place here and it is often called anatomical dead space.
The respiratory zone is a part of the lungs, where gas exchange takes place. It includes respiratory bronchioles, alveolar ducts, and alveoli. The alveoli are the endpoint of the respiratory system and are small structures (approximately 0.3 mm in diameter) with very thin walls wrapped by pulmonary capillaries. There are more than 500 million alveoli in our lungs with a total area of more than 70 m2. Alveolar tissue receives the largest blood supply of any of the body’s organs.
Alveoli consist of two types of cells. Type one is the alveoli wall itself, through which gas exchange happens, type two produce special substance – surfactant, which prevents lungs from collapsing.
There are four standard lung volumes and four standard lung capacities, which are a combination of two or more lung volumes. A special device – spirometer can be used to measure lung volumes directly (except the residual volume)
Residual Volume (RV) – the amount of air in the lungs at the end of a maximal exhalation.
Tidal Volume (TV) – the volume of air inhaled/exhaled with each breath, during normal breathing.
IRV – Inspiratory Reserve Volume – the volume of air that can be inhaled after a normal inspiration.
ERV – Expiratory reserve volume – the volume of air that can be exhaled after passive exhale.
IC – Inspiratory capacity – the maximal volume of air that can be inspired (IC=TV+IRV).
FRC – functional residual capacity – the volume of air in the lungs at the end of a normal exhalation (FRC=RV+ERV).
Vital Capacity (VC=ERV+TV+IRV): Volume of air that can be exhaled after maximal inspiration
TLC – Total lung capacity (TLC=RV+ERV+TV+IRV): Volume in lungs at the end of a maximal inspiration.
MECHANICS OF PULMONARY VENTILATION
Pulmonary ventilation or breathing is the process of inspiration (air moves into the lung) and exhalation (air moves out from the lung).
At rest, the volume of the lung is a balance between the expansion of the chest wall and the inward elastic recoil of the lungs.
To understand the process of breathing we need to understand the difference between intrapulmonary pressure (pressure inside alveoli) and intrapleural pressure (inside pleural cavity – potential space between visceral and parietal pleura)
Intrapulmonary pressure is equal to atmospheric pressure (760 mmHg) and Intrapleural pressure is a bit less (756 mmHg) due to elasticity of lungs, surface tension, and expansion of chest wall.
This difference helps the lungs to be stick to the thoracic cavity and always follow its movement.
Inspiration begins when the diaphragm and external intercostal muscles of the chest contract in a response of neural impulse from the respiratory center. This causes the diaphragm goes downward toward the abdominal cavity and external intercostal muscles to pull ribs outward. As a result, the thoracic cavity volume will increase. Because the lungs are connected to the chest wall, the lungs expand as well. This expansion will decrease pressure in the lungs below atmospheric pressure, and as a result air from outside flows into the lungs until the pressure becomes equal to atmospheric pressure at the end of inspiration.
Passive exhalation occurs when the diaphragm and external intercostal muscles relax. This is a passive movement and no muscles are involved in it. The lung returns passively (recoil) to its volume at rest because of its elasticity. This decrease in volume will increase the pressure in alveoli, causing air to flow out to the atmosphere.
At the end of a passive exhalation when no air is flowing, pressure in alveoli equals atmospheric pressure.
Forced exhalation also involves abdominal wall muscles and internal intercostal muscles
Gas exchange (external respiration) takes place in alveoli.
Atmospheric air contains mostly nitrogen (79%) and oxygen (21%) with small amounts of other gases, as well as water vapor. At sea level, water vapor is 47 mm Hg.
Partial pressure of O2 (PO2) = 0.21*760 mm Hg = 160 mm Hg.
When inspired, the air becomes humidified as it passes through the nasal passages. Therefore,
PO2 of inspired air = 0.21*(760mm Hg – 47 mm Hg) = 150 mmHg.
PO2 in alveolar air about 104 mmHg
In the blood PO2 is 40 mmHg, therefore O2 moves (diffuse) from alveoli into the blood.
The reverse process happens with CO2 – in a venous blood concentration of CO2 (46 mmHg) is higher compared to alveolar PCO2 (40 mmHg), thus CO2 diffuses from the bloodstream into the alveoli. Despite the relatively small pressure gradient of 6 mmHg for CO2 diffusion, CO2 transfer occurs rapidly because of its high solubility in plasma.
REGULATION OF BREATHING
Breathing is an automatic process and can only be changed temporarily by voluntary efforts. You cannot consciously stop breathing entirely. Breathing is finely tuned to meet metabolic demands, such that during exercise ventilation increases to maintain arterial PO2, PCO2 and pH within a narrow range. To achieve this tight regulation, central and peripheral receptors send information to a respiratory center whose output adjusts initiation, duration, depth, and rate of breathing.
Peripheral chemoreceptors are the carotid receptors and aortic bodies. They are stimulated by
a. a decrease in PaO2 (hypoxia), only if below 60 mmHg
b. an increase in PaCO2 (respiratory acidosis), only if higher than 70-80 mmHg
c. a decrease in pH within the arterial blood (metabolic acidosis).
Central chemoreceptors are widely distributed throughout the brain stem. They respond to an increase in blood PCO2. These receptors actually sense H+ concentration in the interstitial fluid of the brain. They are not affected by changes in arterial pH because the blood-brain-barrier is not permeable to H+ or HCO3-. Instead, CO2 moves across this barrier combine with H2O and form H2CO3, HCO3, and H+, causing a decrease in the interstitial fluid pH. Because the interstitial fluid and the adjoining cerebrospinal fluid contain little protein, they are not well buffered. Hence small changes in PCO2 produce large changes in pH in this area.
Response to low Oxygen
PaO2 must decrease to about 50-60 mm Hg before respiration is increased. It has been suggested that the peripheral carotid chemoreceptors are designed to protect the organism against hypoxia rather than to regulate respiration. This happens for example in a high attitude when O2 partial pressure can be significantly lower than at sea level.
Response to Carbon Dioxide
In contrast with the response to change in PaO2, a very small increase in PaCO2 provides a powerful stimulus to increase respiration, providing tight control of acid-base balance. Of the two sets of receptors involved in this reflex response to elevated PaCO2, the central chemoreceptors are more important accounting for ~70% of the increased ventilation.
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