TAKING LIFE ONE BREATH AT A TIME.
Breathing is not only so important to staying alive that it has its own center in the Brain dedicated to supervising and regulating breathing, it is the only part of the entire human body that is allowed to influence how much we breath, and exactly how we breath. It is also the only part of the human body that is allowed to influence the work of the respiratory skeletal muscles.
The center responsible for breathing in the body is called the pneumotaxic center of the brain. Pneumo means "air" and taxic means "toxic". Pneumatic machines run on air. The name suggests that we breath according to toxicity levels. Indeed, breathing is first and foremost regulated according to the levels of CO2 in the body, rather than the need for oxygen. Obviously, it is important to address both the needs to dispose of CO2 as it is lethal in high concentration, as well as deliver, extract, and utilize oxygen at the same time.
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With that said and as a matter of principle, too much CO2 will kill you faster than less than perfect volumes of oxygen. Since the first rule of nature (see another post) is survival first, the process of breathing aims to dispose of CO2 first, if we ever had to choose. In reality, we do not have to choose since we can use the same systems in our body to achieve both. Yet, changes to breathing are governed by changes to CO2 far more than the need for oxygen.
Breathing is divided into two major processes: 1) Inhalation or inspiration; 2) Exhalation or expiration. Together, and only together they amount to the process called breathing or air exchange. Exchange take on the meaning of "give and take", where we give to the environment the exhaled air (with increased CO2 and reduced oxygen; getting rid of CO2), and take in air with more oxygen and less CO2.
The prime risk of high levels of CO2 is it tendency to take the place of oxygen, thus acting as an simple asphyxiant. At up to 10%, symptoms may include headache, drowsiness, and convulsions. Above 10%, a person may find themselves in a coma, or even die. At about 40,000 ppm a person will experience CO2 poisoning and can die.
Yet, please don't die so quickly, or at all. Under normal conditions, our body is equipped with the ability to keep CO2 concentrations at a healthy and non-dangerous level. Thus, CO2 poisoning is rare under normal conditions, and normal physiological function. Even during maximal exercise or maximal physiological effort, our body is equipped to deal with the increased creation of CO2, and its disposal and/or buffering. Now we know where the "taxic" part of the brain center's name comes from...
The pneumotaxic center of the brain, uses sensory loops (already explained in one of the previous posts) to supervise and regulate CO2 levels. CO2 levels are the prime substance stimulating the pneumotaxic center of the brain. Naturally, the pneumotaxic center of the brain can make three principle decision regarding breathing: 1) Sustain breathing (keep it the same); 2) Increase breathing (volume and/or pace); 3) Decrease breathing (volume and/or pace).
The overall capacity of the lungs to exchange air (inhale + exhale) is represented by the respiratory system's capacity known as minute ventilation (see separate post about physiological capacities). The tidal volume (mL or L) component of minute ventilation (L/min) represents the extent component, while respiratory rate (breaths per minute; bpm) represents the pace component.
The pneumotaxic center of the brain has complete and sole supervision and regulation of 1) breathing extent; 2) breathing pace; and 3) the breathing pattern. Their are three patterns of breathing in essence: 1) Normo-breathing (normal breathing); 2) Hyper-ventilation; 3) Hypoventilation. Normo-breathing includes the extent, pace, and pattern seen under normal conditions at rest, in a person that is suspected healthy (not diagnosed with a disease and asymptomatic).
Hyperventilation includes a faster pace of breathing (more breathes per minute) combined with a reduced extent of breathing (smaller volumes of air exchanged). Hyper-ventilation is one of the prime physiological solutions in mammals (which include humans) to decreased concentrations of CO2, thus acting as a tool to get rid of CO2, decreasing its levels to normal and/or non-dangerous levels. The number one reason to hyper-ventilate is to get read of CO2. The more CO2 is ridden of to the point of normal and healthy levels, the less hyper-ventilation is required.
Hyporventilation includes a slower pace of breathing (less breathes per minute) combined with an increased extent of breathing (greater volumes of air exchanged). Hypo-ventilation is one of the prime physiological solutions in mammals (which include humans) to increased concentrations of CO2, thus acting as a tool to preserve CO2 in the body, increasing its levels to normal and/or non-dangerous levels. The number one reason to hypo-ventilate is to keep CO2 at its necessary levels. The less CO2 is ridden of to the point of normal and healthy levels, the less hypo-ventilation is required.
The pneumotaxic center of the brain uses both chemical and bio-mechanical information gathered from blood tissue and lung external surface tension, to know what are CO2 levels currently, and how much the lungs are inflated (or not) as an indication for the potential to dispose of CO2, and supply oxygen.
Chemoreceptors (CO2 specific chemical sensors; receptor = sensor) quantify CO2 mostly in venous blood tissue and as early as possible to lengthen the time the pneumotaxic center has to receive information (supervision), analyze information, make a decision, and enforce it (regulation). At the same time, mechanoreceptors (tension specific sensors that sense physical forces) quantify the extent of tension of pleural tissue (how stretched the lungs outer surfaces are).
The receptors "report" to the pneumotaxic center their information or a regular and reoccurring basis, the pneumotaxic center analyzes the chemical and physical information received, makes a decision on the extent, pace, and pattern of breathing needed, and influences the respiratory muscle as needed. The respiratory muscle work the same, more, or less, stimulating the receptor to report to the pneumotaxic center, initiating a new cycle of the sensory loops used to supervise and regulate breathing.
During hyperventilation, we breath fast and shallow. This corresponds with an increased respiratory rate (more breaths per minute) while shallow breathing corresponds with reduces tidal volume. Thus, during hyperventilation, tidal volume decreases while respiratory rate increases, resulting in a decrease in breathing efficiency.
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During hypoventilation, we breath slow and deep. This corresponds with a decreased respiratory rate (less breaths per minute) while deep breathing corresponds with increased tidal volume. Thus, during hypoventilation, tidal volume increases while respiratory rate decreases, resulting in an increase in breathing efficiency.
The normal range for CO2 in the body is usually 40-45 mmHg, above 45 mmHg we regard it as indicative of hypercapnia, also known as hypercarbia, while below 35 mmHg we regard it as indicative of hypocapnia, also known as hyporcarbia. Both cases put the person at risk, thus engaging the body's physiological resources to try and get those CO2 levels back to 40-45 mmHg.
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