BIOMECHANICS OF RESPIRATORY ACT

BIOMECHANICS OF RESPIRATORY ACT.

Lungs ventilation

Humans need a continuous supply of oxygen for cellular respiration, and they must get rid of excess carbon dioxide, the poisonous waste product of this process.  Gas exchange supports this cellular respiration by constantly supplying oxygen and removing carbon dioxide.  The oxygen we need is derived from the Earth’s atmosphere, which is 21% oxygen. This oxygen in the air is exchanged in the body by the respiratory surface. In humans, the alveoli in the lungs serve as the surface for gas exchange.

Gas exchange in humans can be divided into five steps:

1.                 Breathing

2.                 External Respiration

3.                 Gas Transport

4.                 Internal Respiration

5.                 Cellular Respiration 

Other factors involved with respiration are:

·                     Adaptations of Diving Mammals

·                     Bohr Shift

·                     Control of Breathing

·                     Partial Pressure

·                     Structure of Respiratory System

Structure of the Human Respiratory System

The Nose – Usually air will enter the respiratory system through the nostrils.  The nostrils then lead to open spaces in the nose called the nasal passages.  The nasal passages serve as a moistener, a filter, and to warm up the air before it reaches the lungs.  The hairs existing within the nostrils prevents various foreign particles from entering.  Different air passageways and the nasal passages are covered with a mucous membrane.  Many of the cells which produce the cells that make up the membrane contain cilia.  Others secrete a type a sticky fluid called mucus.  The mucus and cilia collect dust, bacteria, and other particles in the air.  The mucus also helps in moistening the air.  Under the mucous membrane there are a large number of capillaries.  The blood within these capillaries helps to warm the air as it passes through the nose.  The nose serves three purposes.  It warms, filters, and moistens the air before it reaches the lungs.  You will obviously lose these special advantages if you breath through your mouth.

Pharynx and Larynx – Air travels from the nasal passages to the pharynx, or more commonly known as the throat. When the air leaves the pharynx it passes into the larynx, or the voice box.  The voice box is constructed mainly of cartilage, which is a flexible connective tissue.  The vocal chords are two pairs of membranes that are stretched across the inside of the larynx.  As the air is expired, the vocal chords vibrate.  Humans can control the vibrations of the vocal chords, which enables us to make sounds.  Food and liquids are blocked from entering the opening of the larynx by the epiglottis to prevent people from choking during swallowing.

Trachea – The larynx goes directly into the trachea or the windpipe.  The trachea is a tube approximately 12 centimeters in length and 2.5 centimeters wide.  The trachea is kept open by rings of cartilage within its walls.  Similar to the nasal passages, the trachea is covered with a ciliated mucous membrane.  Usually the cilia move mucus and trapped foreign matter to the pharynx.  After that, they leave the air passages and are normally swallowed.  The respiratory system cannot deal with tobacco smoke very keenly. Smoking stops the cilia from moving.  Just one cigarette slows their motion for about 20 minutes.  The tobacco smoke increases the amount of mucus in the air passages.  When smokers cough, their body is attempting to dispose of the extra mucus.

Bronchi – Around the center of the chest, the trachea divides into two cartilage-ringed tubes called bronchi.  Also, this section of the respiratory system is lined with ciliated cells.  The bronchi enter the lungs and spread into a treelike fashion into smaller tubes calle bronchial tubes.  

Bronchioles – The bronchial tubes divide and then subdivide.  By doing this their walls become thinner and have less and less cartilage.  Eventually, they become a tiny group of tubes called bronchioles.

Alveoli – Each bronchiole ends in a tiny air chamber that looks like a bunch of grapes.  Each chamber contains many cup-shaped cavities known as alveoli.  The walls of the alveoli, which are only about one cell thick, are the respiratory surface.  They are thin, moist, and are surrounded by several numbers of capillaries.  The exchange of oxygen and carbon dioxide between blood and air occurs through these walls.  The estimation is that lungs contain about 300 million alveoli. Their total surface area would be about 70 square meters.  That is 40 times the surface area of the skin.  Smoking makes it difficult for oxygen to be taken through the alveoli.  When the cigarette smoke is inhaled, about one-third of the particles will remain within the alveoli.  There are too many particles from smoking or from other sources of air pollution which can damage the walls in the alveoli.  This causes a certain tissue to form.  This tissue reduces the working area of the respiratory surface and leads to the disease called emphysema.

In order to keep living our cells need the oxygen, available in the air we breath and that the body takes constantly and cycle-wise through breathing. Each cycle is made of two steps:  inhalation, when the air gets into the body full of oxygen, and exhalation, when the air gets out of the body full of carbon dioxide produced through our metabolic process. The air we breath gets out of our body with an average rate of 13/16 cycles per minute. The alternation between inhalation and exhalation is controlled by the respiratory centre, that is located in the medulla oblongata at the base of the skull.

The centre gets signals by the chemoreceptors about the level of carbon dioxide in our body: when such a level increases over a certain amount it gives the impulse to the respiratory apparatus to inhale and exhale again. Let’s briefly see which are the components of the respiratory apparatus following the path of the incoming air. 

I. Common characteristic of breathing. The respiratory system is divided into a respiratory zone, which is the site of gas exchange between air and blood, and a conducting zone, which conducts the air to the respiratory zone. The exchange of gases between air and blood occurs across the walls of tiny air sacs called alveoli, which are only a single cell layer thick to permit very rapid rates of gas diffusion.

The term respiration includes three separate but related functions:

(1) ventilation (breathing);

(2) gas exchange, which occurs between the air and blood in the lungs and between the blood and other tissues of the body; and

(3) oxygen utilization by the tissues in the energy – liberating reactions of cell respiration. Ventilation and the exchange of gases (oxygen and carbon dioxide) between the air and blood are collectively called external respiration. Gas exchange between the blood and other tissues and oxygen utilization by the tissues are collectively known as internal respiration.

Ventilation is the mechanical process that moves air into and out of the lungs. Since the oxygen concentration of air is higher in the lungs than in the blood, oxygen diffuses from air to blood. Carbon dioxide conversely moves from the blood to the air within the lungs by diffusing down its concentration gradient. As a result of this gas exchange, the inspired air contains more oxygen and less carbon dioxide than the expired air. More importantly blood leaving the lungs (in the pulmonary veins) has a higher oxygen and lower carbon dioxide concentration than the blood delivered to the lungs in the pulmonary arteries. This result bring the fact that lungs function is to give gaseous equilibrium between blood and the air.

Intrapulmonary and Intrapleural Pressures

The visceral and parietal pleurae are stuck to each other like two wet pieces of glass. The intrapleural space between them contains only a thin layer of fluid, secreted by the parietal pleura. This fluid is like the interstitial fluid in other organs; it is formed as a filtrate from blood capillaries in the parietal pleura, and it is drained into lymphatic capillaries. The major function of the liquid in the intrapleural space is to serve as a lubricant so that the lungs can slide relative to the

chest during breathing. Since the lungs normally are stuck to the thoracic wall, for reasons described shortly, they expand and contract with the thoracic wall during breathing. The intrapleural space is thus more a potential space than a real

one; it becomes real only if the lungs collapse.

Air enters the lungs during inspiration because the atmospheric pressure is greater than the intrapulmonary, or intraalveolar, pressure. Because the atmospheric pressure does not usually change, the intrapulmonary pressure must fall below atmospheric pressure to cause inspiration. A pressure below that of the atmosphere is called a subatmospheric pressure, or negative pressure. During quiet inspiration, for example, the intrapulmonary pressure may decrease to 3 mmHg below the pressure of the atmosphere. This subatmospheric pressure is shown as − 3 mmHg. Expiration, conversely, occurs when the intrapulmonary pressure is greater than the atmospheric pressure.

During quiet expiration, for example, the intrapulmonary pressure may rise to at least + 3 mmHg over the atmospheric pressure . Because of the elastic tension of the lungs (discussed shortly) and the thoracic wall on each other, the lungs pull

in one direction (they “try” to collapse) while the thoracic wall pulls in the opposite direction (it “tries” to expand). The opposing elastic recoil of the lungs and the chest wall produces a subatmospheric pressure in the intrapleural space

between these two structures. This pressure is called the intra pleural pressure. The intrapleural pressure is lower (more negative) during inspiration because of the expansion of the thoracic cavity than it is during expiration. However, the intrapleural pressure is normally lower than the intrapulmonary pressure during both inspiration and expiration.

FUNDAMENTALS OF BIOMECHANICS

The cyclic alternation of inhalation and exhalation takes place tank to the activity of several muscles working right for the same aim. The most important one is the diaphragm, sinergically working with the ribcage muscles ant not only. The lungs in fact, per definition are passive organs, they cannot move autonomously to let air in and out, but they are expanded during inhalation, by the action of the diaphragm and the thorax inhalation muscles, or they are compressed by the exhalation muscles and by the abdominal muscles in case of forced exhalations.

The diaphragm is essentially an inhalation muscle: when its fibres contract, they lower it taking with them the lower portions of the lungs that expand and let air in.

Just to have an idea of what happens we can think the diaphragm as the piston of a syringe, while it goes down it sucks the air through the respiratory tract that in this example would represent the structure of the syringe.

The diaphragm however does not work alone. During inhalation it works together with the external and middle intercostal muscles that in synergy with other thorax muscles (scalenus, sternocleidomastoideus) are destined to the expansion and the contraction of the ribcage, increasing the thorax volume and by consequence the quantity of air within the lungs.

The rib motions are essentially two: one called “bucket handle”, expanding the thorax, and the other called “pump lever”, raising the ribcage. In the exhalation phase the diaphragm de-contracts going back its original cupola shape, the thorax muscles relax, the ribs lower and the thorax gets back to its original volume. During the exhalation there should not be a massive muscle action as it all happens by relaxation.

However there are some exhalation muscles playing a key role in case of forced exhalation or activities for which an increased air volume is needed. In particular the abdominals during the exhalation can help diaphragm to raise more, compressing the lower portion of the lungs while the thorax muscles (inner intercostals) get the ribs closer reducing the ribcage volume and further compressing the lungs, this way a larger quantity of air gets out during exhalation

Main process of the external respiration. The passage air respiratory systems are divided into two functional zones. The respiratory zone is the region where gas exchange occurs, it includes the respiratory bronchioles (which contain separate outpouchings of alveoli) and the terminal cluster of alveolar sacs.

Gas exchange between the air and blood occurs entirely by diffusion through lung tissue. This diffusion occurs very rapid because there is a large surface area within the lungs and a very short diffusion distance between blood and air.

Phases of respiratory act. Inspiration & Expiration

Pulmonary ventilation consists of two phases: inspiration and expiration. Inspiration (inhalation) and expiration (exhalation) are accomplished by alternately increasing and decreasing the volume of the thorax and lungs.

The thorax must be sufficiently rigid so that it can protect vital organs and provide attachments for many short and powerful muscles. Breathing, or pulmonary ventilation, requires the flexibility of the thorax to function as a bellow during the ventilation cycle. The rigidity and the surfaces for muscle attachment are provided by the bony composition of the rib cage. The rib cage is pliable, because the ribs are separate from one another and most of the ribs (upper ten of the twelve pairs) are attached to the sternum by resilient costal cartilages. The vertebral attachments also provide considerable mobility. The structure of the rib cage and associated cartilages provides continuous elastic tension, so that after stretched by muscle contraction during inspiration, the rib cage can return passively to its resting dimension when the muscles relax. This elastic recoil is greatly aided by the elasticity of the lungs.

Respiratory muscles cause passage of air into the Lung. Between the bony portions of the rib cage are two layers of intercostals muscles: the external intercostal muscles and internal intercostal muscles. Between the costal cartilages, there is only one muscle layer, which its fibers oriented in the same manner to those of the internal intercostal muscle. These muscles may called as the interchondral part of the internal intercostal muscle or parasternal intercostal muscle.

An unforced, or quiet, inspiration primarily results from contraction of the dome– shaped diaphragm, which become lowered and flattened. This increases thoracic volume in a vertical direction. Inspiration is also aided by the parasternal and external intercostal muscles, which raise the ribs when they contract and increase thoracic volume laterally. Other thoracic muscles involved in forced (deep) inspiration. The most important of these is the scalenus muscle, followed by the pectoralis minor muscle, and in extreme cases the sternocleidomastoid muscle. Contraction of these muscles elevates the ribs in an anteroposterior direction; simultaneously, the upper rib cage is stabilized so that the intercostal muscles become more effective.

 

Mechanism of normal quiet inspiration and expiration. Quiet inspiration is an active process. The contraction of the inspiratory muscles and diaphragm increases intrathoracic volume. This stretch the thorax and lungs. Quiet expiration is a passive process. The thorax and lungs recoil when the respiratory muscles relax. due to their elastic tension

Control of Bronchial Tone

The walls of bronchi and bronchioles contain smooth muscle and they are innervated by the autonomic nervous system. In general, sympathetic discharge via Beta-2-adrenergic receptors causes the bronchi to dilate and parasympathetic discharge via the vagus nerves causes them to constrict.. It may be similar to the intrinsic enteric nervous system in the gastrointestinal tract and there is evidence that VIP (Vasoactive intestinal polypeptide) is the mediator secreted by its neurons.

The function of the bronchial muscles is still a matter of debate, but in general, they probably help to maintain an even distribution of ventilation. They also protect the bronchi during coughing. There is a circadian rhythm in bronchial tone, with maximal constriction at about 6 A.M and maximal dilatation at about 6 P.M. Thats why the asthma attacks are more severe in the late night and early morning hours, pi–stimulants such as isoproterenol are effective in asthma because they mimic the effects of sympathetic stimulation. Cooling the airways causes bronchoconstriction, and exercise triggers asthmatic attacks because it lowers airway temperature.

Lung Volumes. The amount of air that moves into the lungs with each inspiration (or the amount that moves out, with each expiration) is called the tidal volume. The air inspired with a maximal inspiratory effort in excess of the tidal volume is the inspiratory reserve volume. The volume expelled by an active expiration effort after passive expiration is the expiratory reserve volume, and the air left in the lungs after a maximal expiratory effort is the residual volume.

The space in the conducting zone of the airways occupied by gas that does not exchange with blood in the pulmonary vessels is the respiratory dead space. The vital capacity, the greatest amount of air that can be expired after a maximal inspiratory effort, is frequently measured clinically as an index of pulmonary function. The fraction of the vital capacity expired in 1 second (timed vital capacity; also called forced expired volume in 1 second, or FEV I”) gives additional valuable information. The vital capacity may be normal but the timed vital capacity can be greatly reduced in diseases such as asthma, in which the resistance of the airways is increased due to bronchial constriction. The amount of air inspired per minute (pulmonary ventilation, respiratory minute volume) is normally about 6 L (500 ml/breath x 12 breaths/min). The maximal voluntary ventilation (MVV), or, as it was formerly called, the maximal breathing capacity, is the largest volume of gas that can be moved into and out of the lungs in 1 minute by voluntary effort. The normal MVV is 125-170 L/min.

Effects of Gravity on the Lung. Because of gravitational forces,the pressure gradient present. Intrapleural pressure at the bases of the lungs is 5 mm Hg greater than at the apexes. Consequently, the transmural pressure (the difference between intrapulmonary and intrapleural pressure) may become negative at the end of forced expiration, causing airways to close. For the same reason, more of the gas inspired during the first part of inspiration goes to the apexes than to the bases.

Gravity also affects the pressure in the pulmonary blood vessels.Dead Space &Uneven Ventilation. Since gaseous exchange in the respiratory system occurs only in the terminal portions of the airways, the gas that occupies the rest of the respiratory system is not available for gas exchange with pulmonary capillary blood. Thus, in a man who weighs 68 kg, only the first 350 ml of the 500 ml inspired with each breath at rest goes through gaseous exchange in the alveoli. Conversely, with each expiration, the first 150 ml expired is the gas that occupied the dead space, and only the last 350 ml is from the alveoli.

It is wise to distinguish between the anatomic dead space (respiratory system volume exclusive of Alveoli) and the total (physiologic) dead space (volume of gas which do not equilibrate with blood and air, e.g waste ventilation). In health, the 2 dead spaces are identical. In disease states that may be no exchange of gas between the alveoli and the blood, and some of the alveoli may be overventilated. The volume of gas in nonperfused alveoli and any volume of air in the alveoli in excess of that necessary to arterialize the b1ood in the alveolar capillaries is part of the dead space (no equilibrating) gas volume. The anatomy dead space can be measured by analysis of the single breath N₂ curves. From mid inspiration,the subject take a deep breath as possible of pure O₂, then exhales steadily while the N₂ content of the expired gas is continuously measured. The initial gas exhaled (phase I) is the gas that filled the dead space and that consequently contains no N₂.

Alveolar Ventilation. Because of the dead space, the amount of air reaching the alveoli (alveolar ventilation) at a respiratory minute volume of 6 L/min is 500 minus 150 ml times 12 breath/min, or 4.2 L/min. because of the dead space, rapid, shallow respiration produces much less alveolar ventilation than slow, deep respiration at the same respiratory minute volume .

Effect of variations in respiratory rate and depth on alveolar ventilation.

During quiet breathing, the intrapleural pressure, which is about – 2.5 mm Hg (relative to atmospheric) at the start of inspiration, decreases to about — 6 mm Hg, the lungs are pulled into a more expanded position. and the pressure in the airway becomes slightly negative, which cause the  air flows into the lungs. At the end of inspiration, the lung recoil pulls the chest back to the expiratory position, where the recoil pressures of the lungs and chest wall become balance. At this time, the pressure in the airway becomes slightly positive, and air flows out of the lungs. Expiration during quiet breathing is passive because no muscles contract which decrease intrathoracic volume. However, there is some contraction of the inspiratory muscles in the early part of expiration. This contraction exerts a braking action on the recoil forces and slows expiration.

Mechanism forced ventilation. Strong inspiratory efforts reduce the intrapleural pressure value as low as —30 mm Hg, producing correspondingly greater degrees of lung inflation. When forced ventilation is increased, the extent of lung deflation is also increased by active contraction of expiratory muscles that decrease intrathoracic volume.

Movement of the diaphragm accounts for 75% of the change in intrathoracic volume during quiet inspiration. This muscle attached around the bottom of the thoracic cage, and it arches over the liver and moves downward like a piston when it contracts.

The other important inspiratory muscles are the external intercostals muscles, which run obliquely downward and forward from rib to rib. The ribs pivot as if hinged at the back, so that when the external intercostals contract they elevate the lower ribs. This pushes the sternum outward and increases the anteroposterior diameter of the chest. The transverse diameter is actually changed little if at all. Either the diaphragm or the external intercostals muscles alone can maintain adequate ventilation at rest. Transaction of the spinal cord above the third cervical segment cause fatal without artificial respiration, but transaction below the origin of the phrenic nerves that innervate the diaphragm (third to fifth cervical segments) is not fatal; conversely, in patients with bilateral phrenic nerve palsy, respiration is somewhat labored, but adequate to maintain life. The scalene and sternocleidomastoid muscles in the neck are accessory inspiratory muscles that they help to elevate the thoracic cage during deep labored respiration.

A decrease in intrathoracic volume and forced expiration result when the expiratory muscles contract. The internal intercostals have this action because they pass obliquely downward and posterior from rib to rib and therefore pull the rib cage downward when they contract. Contractions of the muscles of the anterior abdominal wall also aid expiration by pulling the rib cage downward and inward and by increasing the intraabdominal pressure, which pushes the diaphragm upward.

Change of pressure in pleural cavity in correlation from phases of respiratory act. The lungs and the chest wall are elastic structures. Normally, there is no more than a thin layer of fluid between the lungs and the chest wall. The lungs slide easily on the chest wall but resist being pulled away from it in the same way as 2 moist pieces of glass slide on each other but resist separation. The pressure in the “space” between the lungs and chest wall (intrapleural pressure) is sub atmospheric. The lungs are stretched when they are expanded at birth, and at the end of quiet expiration their tendency to recoil from the chest wall is just balanced by the tendency of the chest wall to recoil in the opposite direction. If the chest wall is opened, the lungs will collapse; and if the lungs lose their elasticity, the chest expands and becomes barrel-shaped.

Movement of blood on venous in correlation from phases of respiratory act.

Contraction of the diaphragm during inhalation also improves venous return. As the diaphragm contracts, it lowers to increase the thoracic volume and decrease the abdominal volume. This creates a partial vacuum in the thoracic cavity (negative intrathoracic pressure) and a higher pressure in the abdominal cavity. The pressure difference thus produced favors blood flow from abdominal to thoracic veins. 

Change of pressure in alveoli. The respiratory muscles cause pulmonary ventilation by alternatively compressing and distending the lungs, which in turn causes the pressure in the alveoli to rise and fall. During inspiration the intra-alveolar pressure becomes slightly negative with respect to atmospheric pressure, normally slightly less than -1 mm Hg, and this causes air to flow inward through the respiratory passageways. During normal expiration, on the other hand, the intra-alveolar pressure rises to slightly less than +1 mm Hg, which causes air to flow outward through the respiratory passageways. Note that, how little pressure is required to move the air into and out of the normal lung, though in most of the time, much pressure is required in some types of lung diseases.

During maximum expiratory effort (with the glottis closed )the intra-alveolar pressure can be increased to as much as 140 mm Hg in the strong, healthy man, and during maximum inspiratory effort it can be reduced to as low as -100 mm Hg.

Recoil Tendency of the Lungs, and the Intrapleural Pressure. The lungs have a continual elastic tendency to collapse and therefore to pull away from the chest wall. This is called the recoil tendency of the lungs, and it is caused by two different factors. First, throughout the lungs are many elastic fibers that are stretched by lung inflation and therefore attempt to shorten. Second, and even more important, the surface tension of the fluid lining the alveoli also causes a continual elastic tendency for the alveoli to collapse. This effect is caused by intermolecular attraction between the surface molecules of the alveolar fluid. That is, each molecule pulls on the next one so that the whole lining sheet of fluid on the alveolar surfaces acts like many small elastic balloons continuously trying to collapse the lung.

Ordinarily, the elastic fibers in the lungs account for about one third of the recoil tendency, and the surface tension phenomenon accounts for about two thirds.

The total recoil tendency of the lungs can be measured by the amount of negative pressure in the pleural space required to prevent collapse of the lungs; this pressure is called the pleural pressure or, occasionally, the lung recoil pressure. It is normally about – 4 mm Hg. This negative pressure (-4 mm Hg) on the outer surfaces of the lungs is required to keep them expanded to normal size. When the lungs are stretched to very large size, such as at the end of deep inspiration, then the pleural pressure required may be as great as -12 to -18 mm Hg.

“Surfactant” in the alveoli, and its effect on the collapse tendency.

A lipoprotein mixture called “surfactant” is secreted by special surfactant-secreting cells (the “type II granular pneumocytes“) which are the component parts of the alveolar epithelium. This mixture, containing especially the phospholipids dipalmitoyl lecithin, decreases the surface tension of the alveolar fluid lining. In the absence of surfactant, lung expansion is extremely difficult, which often requires negative pleural pressures as low as – 20 to – 30 mm Hg to overcome the collapse tendency of the alveoli. This illustrates that surfactant is exceedingly important for minimizing the effect of surface tension which cause the collapse of the lungs.

Gas exchange in the lungs occurs across an estimated 300 million tiny (0.25 to 0.50 mm in diameter) air sacs known as alveoli. Their enormous number provides a large surface area (60 to 80 square meters, or about 760 square feet) for diffusion of gases. The diffusion rate is further increased by the fact that each alveolus is only one cell-layer thick, so that the total “air-blood barrier” is only two cells across (an alveolar cell and a capillary endothelial cell), or about 2 μ m.

There are two types of alveolar cells, designated type I alveolar cells and type II alveolar cells . The type I alveolar cells comprise 95% to 97% of the total surface area of the lung; gas exchange with the blood thus occurs primarily

through type I alveolar cells. These cells are accordingly very thin: where the basement membranes of the type I alveolar

Thoracic Cavity

The diaphragm, a dome-shaped sheet of striated muscle, divides the anterior body cavity into two parts. The area below the diaphragm, the abdominopelvic cavity, contains the liver, pancreas, gastrointestinal tract, spleen, genitourinary tract, and other organs. Above the diaphragm, the thoracic cavity contains the heart, large blood vessels, trachea, esophagus, and thymus in the central region, and is filled

elsewhere by the right and left lungs.

The structures in the central region—or mediastinum —are enveloped by two layers of wet epithelial membrane collectively called the pleural membranes. The superficial layer, or parietal pleura, lines the inside of the thoracic wall. The deep layer, or visceral pleura, covers the surface of the lungs  The lungs normally fill the thoracic cavity so that the visceral pleura covering each lung is pushed against the parietal pleura lining the thoracic wall. There is thus, under normal conditions, little or no air between the visceral and parietal pleura. There is, however, a  potential space”—called the intrapleural space —that can become a real space if the visceral/and parietal pleurae separate when a lung collapses.

The respiratory center is gray matter in the pons and the upper Medulla, which is responsible for rhythmic respiration. This center can be divided into an inspiratory center and an expiratory center in the Medulla, an apneustic center in the lower and midpons and a pneumotaxic center in the rostral-most part of the pons. This respiratory center is very sensitive to the pCO₂ in the arteries and to the pH level of the blood.  The CO₂ can be brought back to the lungs in three different ways; dissolved in plasma, as carboxyhemoglobin, or as carbonic acid. That particular form of acid is almost broken down immediately by carbonic hydrase into bicarbonate and hydrogen ions.  This process is then reversed in the lungs so that water and carbon dioxide are exhaled. The Medulla Oblongata reacts to both CO₂ and pH levels which triggers the breathing process so that more oxygen can enter the body to replace the oxygen that has been utilized.  The Medulla Oblongata sends neural impulses down through the spinal chord and into the diaphragm. The impulse contracts down to the floor of the chest cavity, and at the same time there is a message sent to the chest muscles to expand causing a partial vacuum to be formed in the lungs.  The partial vacuum will draw air into the lungs.      

There are two other ways the Medulla Oblongata can be stimulated. The first type is when there is an oxygen debt (lack of oxygen reaching the muscles), and this produces lactic acid which lowers the pH level.  The Medulla Oblongata is then stimulated.  If the pH rises it begins a process known as the Bohr shift.  The Bohr shift is affected when there are extremely high oxygen and carbon dioxide pressures present in the human body.  This factor causes difficulty for the oxygen and carbon dioxide to attach to hemoglobin.  When the body is exposed to higher altitudes the oxygen will not attach to the hemoglobin properly, causing the oxygen level to drop and the person will black out.  This theory also applies to divers who go to great depths, and the pressure of the oxygen becomes poisonous.  These pressures are known as pO₂ and pCO₂, or partial pressures.  The second type occurs when the major arteries in the body called the aortic and carotid bodies, sense a lack of oxygen within the blood and they send messages to the Medulla Oblongata.