alveoli (singular, alveolus The lungs consist mainly of tiny air containing sacs called alveoli (singular, alveolus). The alveoli are the sites of gas exchange with the blood. The airways are all the tubes through which air flows between the external environment and the alveoli. Inspiration (inhalation) is the movement of air from the external environment through the airways into the alveoli during breathing. Expiration (exhalation) is movement in the opposite direction. An inspiration and expiration constitute a respiratory cycle. During the entire respiratory cycle, the right ventricle of the heart pumps blood through the capillaries surrounding each alveolus. At rest, in a normal adult, approximately 4 L of fresh air enters and leaves the alveoli per minute, while 5 L of blood, the entire cardiac output, flows through the pulmonary capillaries. During heavy exercise, the air flow can increase twentyfold, and the blood flow five- to six fold. During inspiration air passes through either the nose (the most common site) or mouth into the pharynx (throat), a passage common to both air and food. The pharynx branches into two tubes, the esophagus through which food passes to the stomach, and the larynx, which is part of the airways. The larynx houses the vocal cords, two folds of elastic tissue stretched horizontally across its lumen. The flow of air past the vocal cords causes them to vibrate, producing sounds. The nose, mouth, pharynx, and larynx are termed the upper airways. The larynx opens into a long tube, the trachea, which in turn branches into two bronchi (singular, bronchus), one of which enters each lung. Within the lungs, there are more than 20 generations of branching, each resulting in narrower, shorter, and more numerous tubes, the names of which are summarized in Figure in the ppt. F= ∆P/R
That is, flow (F) is proportional to the pressure difference (∆P) between two points and inversely proportional to the resistance (R). For air flow into or out of the lungs, the relevant pressures are the gas pressure in the alveoli—the alveolar pressure (Palv)—and the gas pressure at the nose and mouth, normally atmospheric pressure (Patm), the pressure of the air surrounding the body:
F = (Patm _ Palv)/R. (we are not going to discuss about resistance)
A very important point must be made at this point: All pressures in the respiratory system, as in the cardiovascular system, are given relative to atmospheric pressure, which is 760 mmHg at sea, level. For example, the alveolar pressure between breaths is said to be 0mmHg, which means that it is the same as atmospheric pressure.
alveolar pressure is alternately made less than and greater than atmospheric pressure. These alveolar pressure changes are caused, as we shall see, by changes in the dimensions of the lungs. To understand how a change in lung dimensions causes a change in alveolar pressure, you need to learn none more basic concept—Boyle's law. At constant temperature, the relationship between the pressure exerted by a fixed number of gas molecules and the volume of their container is as follows: An increase in the volume of the container (lungs) decreases the pressure of the gas, whereas a decrease in the container volume increases the pressure. It is essential to recognize the correct causal sequences in ventilation: During inspiration and expiration the volume of the "container"—the lungs—is made to change, and these changes then cause, by Boyle's law, the alveolar pressure changes that drive air flow into or out of the lungs. Our descriptions of ventilation must focus, therefore, on how the changes in lung dimensions are brought about. There are no muscles attached to the lung surface to pull the lungs open or push them shut. Rather, the lungs are passive elastic structures—like balloons—and their volume, therefore, depends upon: (1) the difference in pressure—termed the transpulmonary pressure—between the inside and the outside of the lungs; and
(2) How stretchable the lungs are. The rest of this section and the next three sections focus only on transpulmonary pressure; stretchability will be discussed later in the section on lung compliance. The pressure inside the lungs is the air pressure inside the alveoli (Palv), and the pressure outside the lungs is the pressure of the intrapleural fluid surrounding the lungs (Pip). Thus,
Transpulmonary pressure = Palv _ Pip
The situation that normally exists at the end of an unforced expiration—that is, between breaths when the respiratory muscles are relaxed and no air is flowing, the alveolar pressure (Palv) is 0 mmHg; that is, it is the same as atmospheric pressure. The intrapleural pressure (Pip) is approximately 4 mmHg less than atmospheric pressure—that is, _4 mmHg, using the standard convention of giving all pressures relative to atmospheric pressure. Therefore, the transpulmonary pressure (Palv _ Pip) equals [0 mmHg _ (_4 mmHg)] = 4 mmHg. As emphasized in the previous section, this transpulmonary pressure is the force acting to expand the lungs; it is opposed by the elastic recoil of the partially expanded and, therefore, partially stretched lungs. Elastic recoil is defined as the tendency of an elastic structure to oppose stretching or distortion. In other words, inherent elastic recoil tending to collapse the lungs is exactly balanced by the transpulmonary pressure tending to expand them, and the volume of the lungs is stable at this point. As we shall see, a considerable volume of air is present in the lungs between breaths. Inspiration is initiated by the neurally induced contraction of the diaphragm and
the "inspiratory" intercostal muscles located between the ribs. The diaphragm is the most important inspiratory muscle during normal quiet breathing. When activation of the nerves to it causes it to contract, its dome moves downward into the abdomen, enlarging the thorax. Simultaneously, activation of the nerves to the inspiratory intercostals muscles causes them to contract, leading to an upward and outward movement of the ribs and a further increase in thoracic size.
The crucial point is that contraction of the inspiratory muscles, by actively increasing the size of the thorax, upsets the stability set up by purely elastic forces between breaths. As the thorax enlarges, the thoracic wall moves ever so slightly farther away from the lung surface, and the intrapleural fluid pressure therefore becomes even more subatmospheric than it was between breaths. This decrease (increase in negativity) in intrapleural pressure increases the transpulmonary pressure. Therefore, the force acting to expand the lungs—the transpulmonary pressure—is now greater than the elastic recoil exerted by the lungs at this moment, and so the lungs expand further.
inspiration, equilibrium across the lungs is once again established since the more inflated lungs exert a greater elastic recoil, which equals the increased transpulmonary pressure. In other words, lung volume is stable whenever transpulmonary pressure is balanced by the elastic recoil of the lungs (that is, after both inspiration and expiration). Thus, when contraction of the inspiratory muscles actively increases the thoracic dimensions, the lungs are passively forced to enlarge virtually to the same degree because of the change in intrapleural pressure and hence transpulmonary pressure. The enlargement of the lungs causes an increase in the sizes of the alveoli throughout the lungs. Therefore, by Boyle's law, the pressure within the alveoli drops to less than atmospheric, this produces the difference in pressure (Palv _ Patm) that causes a bulk-flow of air from the atmosphere through the airways into the alveoli. By the end of the inspiration, the pressure in the alveoli again equals atmospheric pressure because of this additional air, and air flow ceases. At the end of inspiration, the nerves to the diaphragm and inspiratory intercostal muscles decrease their firing, and so these muscles relax. The chest wall is no longer being actively pulled outward and upward by the muscle contractions and so it starts to recoil inward to its original smaller dimensions existing between breaths. This immediately makes the intrapleural pressure less sub atmospheric and hence decreases the transpulmonary pressure. Therefore, the transpulmonary pressure acting to expand the lungs is now smaller than the elastic recoil exerted by the more expanded lungs, and the lungs passively recoil to their original dimensions. As the lungs become smaller, air in the alveoli becomes temporarily compressed so that, by Boyle's law, alveolar pressure exceeds atmospheric pressure. Therefore, air flows from the alveoli through the airways out into the atmosphere. Thus, expiration at rest is completely passive, depending only upon the relaxation of the inspiratory muscles and recoil of the chest wall and stretched lungs. Under certain conditions (during exercise, for example), expiration of larger volumes is achieved by contraction of a different set of intercostal muscles and the abdominal muscles, which actively decreases thoracic dimensions. The "expiratory" intercostal muscles (again a functional term, not an anatomical one) insert on the ribs in such a way that their contraction pulls the chest wall downward and inward. Contraction of the abdominal muscles increases intraabdominal pressure and forces the relaxed diaphragm up into the thorax. be pictured as air-filled sacs lined with water. At an air-water interface, the attractive forces between the water molecules, known as surface tension, make the water lining like a stretched balloon that constantly tries to shrink and resists further stretching. Thus, expansion of the lung requires energy not only to stretch the connective tissue of the lung but also to overcome the surface tension of the water layer lining the alveoli.
Indeed, the surface tension of pure water is so great that were the alveoli lined with pure water, lung expansion would require exhausting muscular effort and the lungs would tend to collapse. It is extremely important, therefore, that the type II alveolar cells secrete a detergent-like substance known as pulmonary surfactant, which markedly reduces the cohesive forces between water molecules on the alveolar surface.
Therefore, surfactant lowers the surface tension, which increases lung compliance and makes it easier to expand the lungs.
• It's the individual pressure exerted independently by a particular gas within a mixture of gasses. The air we breathe is a mixture of gasses: primarily nitrogen, oxygen, & carbon dioxide. So, the air you blow into a balloon creates pressure that causes the balloon to expand (& this pressure is generated as all the molecules of nitrogen, oxygen, & carbon dioxide move about & collide with the walls of the balloon). However, the total pressure generated by the air is due in part to nitrogen, in part to oxygen, & in part to carbon dioxide. That part of the total pressure generated by oxygen is the 'partial pressure' of oxygen, while that generated by carbon dioxide is the 'partial pressure' of carbon dioxide. A gas's partial pressure, therefore, is a measure of how much of that gas is present (e.g., in the blood or alveoli).
• the partial pressure exerted by each gas in a mixture equals the total pressure times the fractional composition of the gas in the mixture. So, given that total atmospheric pressure (at sea level) is about 760 mm Hg and, further, that air is about 21% oxygen, then the partial pressure of oxygen in the air is 0.21 times 760 mm Hg or 160 mm Hg.
more acidic) pH. So, in active tissues, there are higher levels of CO2, a lower pH, and higher temperatures. In addition, at lower PO2 levels, red blood cells increase production of a substance called 2, 3-diphosphoglycerate. These changing conditions (more CO2, lower pH, higher temperature, & more 2, 3-diphosphoglycerate) in active tissues cause an alteration in the structure of haemoglobin, which, in turn, causes haemoglobin to give up its oxygen. In other words, in active tissues, more haemoglobin molecules give up their oxygen. Another way of saying this is that the oxygen-haemoglobin dissociation curve 'shifts to the right' (as shown with the light blue curve in the graph below). This means that at a given partial pressure of oxygen, the percent saturation for haemoglobin will be lower. For example, in the graph below, extrapolate up to the 'normal' curve (green curve) from a pO2 of 40, then over, & the haemoglobin saturation is about 75%. Then, extrapolate up to the 'right-shifted' (light blue) curve from a PO2 of 40, then over, & the haemoglobin saturation is about 60%. So, a 'shift to the right' in the oxygen-haemoglobin dissociation curve (shown above) means that more oxygen is being released by haemoglobin - just what's needed by the cells in an active tissue!