 This video will cover the following objective from respiratory physiology, outline the forces that allow for air movement into and out of the lungs, describe the mechanisms that drive breathing, discuss how pressure volume and resistance are related, discuss the meaning of respiratory volumes and capacities, distinguish between restrictive and obstructive pulmonary disorders and define respiratory rate. To understand pulmonary ventilation, which is the process of drawing air in and out of the lungs, we must first understand the relationship between pressure and volume. There's an inverse relationship between pressure and volume. If we have a constant amount of air molecules and the volume that they're contained in increases the pressure of that air will decrease. In contrast, if we decrease the volume, it will cause an increase in the pressure. The muscles that stimulate inspiration or the breathing in of air are known as the primary muscles of inspiration. And so the primary muscles of inspiration are the diaphragm and the external intercostal muscles and when these muscles contract, it causes the volume of the thoracic cavity to increase and this increase volume causes the pressure of the air inside of the lungs to decrease. This decreased pressure inside the lungs is what will drive the movement of air into the lungs. Air flows from areas of higher pressure to lower pressure. So when the thoracic volume increases, the pressure inside of the lungs decreases. The pressure inside the lungs is known as the intra-alveolar pressure and if the intra-alveolar pressure is lower than the atmospheric pressure, air will flow into the lungs. Then if the intra-alveolar pressure is above the atmospheric pressure, air will flow out of the lungs. And so although the atmospheric pressure is equal to 760 millimeters of mercury or approximately 760 millimeters of mercury at sea level, we will refer to respiratory pressures, the pressures inside of the lungs relative to the atmospheric pressure. So the intra-alveolar pressure will call zero millimeters of mercury when there's no air flowing in or out of the lungs. Then a positive intra-alveolar pressure causes air to flow out of the lungs and a negative intra-alveolar pressure will cause air to flow into the lungs. So we can see that Ohm's law describes the relationship between flow, pressure, and resistance. So air flows in response to the change in pressure between the atmospheric pressure and the intra-alveolar pressure. And that airflow rate is also dependent upon the airway resistance. And airway resistance depends on the diameter of the airways. Airway resistance is the opposition to airflow resulting from friction of the air along the airways. The lungs are surrounded by two membranes known as the pleural membranes. The outer of these is known as the parietal pleura that lines the walls of the thoracic cavity. The inner layer is the visceral pleura that lines the surface of the lungs. And in between these two membranes is a fluid filled space known as the pleural cavity. The pleural cavity normally has a negative pressure known as the intra-pleural pressure. And that helps to create a force that holds the lungs open known as the trans-pulmonary pressure. So the trans-pulmonary pressure is the difference between the intra-alveolar pressure and the intra-pleural pressure in response to changes in the volume of the thoracic cavity, the changes of the intra-alveolar pressure will drive airflow into and out of the lungs during inspiration and expiration. The rate of airflow over time is what we call pulmonary ventilation. So the volume of air that moves in and out of the lungs with one breath is what we call the tidal volume. So the tidal volume is the typical volume of a breath, usually around 500 milliliters in a healthy male. And the respiratory rate is how many breaths a person takes in a minute. So for example, if the respiratory rate is 12 breaths per minute and the tidal volume is 500 milliliters per breath, then the pulmonary ventilation rate would be 6,000 milliliters per minute. And so we can regulate pulmonary ventilation by increasing the rate of respiration, increasing the respiratory rate by breathing more rapidly, or we could increase the pulmonary ventilation rate by increasing the depth of breath, increasing the tidal volume. If air was able to enter the pleural cavity, for example, if there was trauma to the chest wall and air was able to enter through damage to the chest wall, this could cause an increase in the intra-pleural pressure. As air enters the pleural cavity, the intra-pleural pressure would increase, and the trans-pulmonary pressure would decrease. This causes the lungs to collapse and is what we know as a pneumothorax. And so a traumatic pneumothorax would be a type of pneumothorax resulting from air being forced into the pleural cavity. This could happen during a car accident, for example, or some other kind of traumatic incident. If fluid were to fill the pleural cavity, if excess fluid were to flow into the pleural cavity, this could also cause the lungs to collapse. And when blood, when there's bleeding into the pleural cavity, and blood causes the lungs to collapse, it's called a hemothorax. Inspiration is breathing in, and in contrast, expiration is the act of breathing out. Inspiration is an active process where we have to contract the muscles of inspiration. We have to contract the diaphragm and external intercostal muscles, which cause the thoracic cavity to increase, causing the intra-alveolar pressure to decrease so that air will flow into the lungs, the lungs will expand. In contrast with expiration, the diaphragm and external intercostal muscles can just relax, and as those muscles relax, the thoracic cavity volume decreases, and the intra-alveolar pressure increases, causing the air to flow out of the lungs. And so the act of inspiration is an act of process, and expiration is a passive process, although there are accessory muscles that can be contracted in order to have a more forceful expiration. If you contract your abdominal muscles, you can breathe out more forcefully, such as when you're blowing bubbles or playing the trumpet or something like that. So how easily the lungs can expand during inspiration is what we call compliance. So compliance is a measurement of the ease of expansion, and the compliance of the lung could be imperative if the lung becomes scarred, if you have pulmonary fibrosis, or if the lung linings are swelling, if you have edema, if you have pleurisy, or edema, this could cause it to be more difficult for the lung to stretch. So the compliance is decreased. If pulmonary compliance is decreased, this is a type of pulmonary disorder, or restrictive pulmonary disorder, where the ability to inflate the lungs is impaired. So the ability of the lungs to return to their size after expanding, so to recoil after stretching, is the elasticity of the lungs. And so the lungs have both compliance and elasticity, and ideally they'll be able to stretch out to a large, maximal volume, what we call the vital capacity when you breathe in with your full inspiratory reserve volume. And then elasticity will help force the air rapidly out during expiration. Surface tension as a result of the attraction of water molecules on the surface of the alveoli is a force that stimulates the alveoli to collapse. And so the epithelium of the alveoli, the cells that form the alveoli produce molecules known as surfactant, which help to reduce the surface tension in order to prevent the wall of the alveoli from collapsing. Bronchoconstriction is a decrease in the diameter of the airways as a result of contraction of smooth muscle lining the wall of the airways. Bronchoconstriction is stimulated under an intrinsic control mechanism where low carbon dioxide levels detected inside of the lungs stimulates bronchoconstriction. It's also stimulated by extrinsic control mechanisms. The parasympathetic nervous system releases acetylcholine from postganglionic fibers into the smooth muscle of the bronchioles to cause bronchoconstriction. Similarly, inflammatory mediators like histamine released from leukocytes like the basal fills and mast cells that are activated during inflammation. These inflammatory mediators are stimulating bronchoconstriction which contributes to asthma and allergies. Bronchodilation is an increase in the diameter of the airways leading to decreased resistance and increased airflow. Bronchodilation is stimulated by an intrinsic control mechanism when a high carbon dioxide concentration is detected inside of the lungs that stimulates bronchodilation. An extrinsic control mechanism also stimulates bronchodilation. In response to activation of the sympathetic nervous system, epinephrine is released from the adrenal medulla. Epinephrine then stimulates bronchodilation when epinephrine is traveling through the blood and binds to the beta-adrenergic receptors in the smooth muscle of the bronchioles. Because epinephrine stimulates bronchodilation, we can also use adrenergic agonists medically as bronchodilators. Albuterol is a beta-adrenergic receptor agonist that stimulates bronchodilation as a way of decreasing airway resistance to help treat asthma and other obstructive pulmonary disorders where the airways become too constricted. So, bronchoconstriction which is stimulated by inflammation and parasympathetic activity can become excessive causing health problems and then bronchodilators are used medically in order to activate the adrenergic receptors and open up the airways. Here we see a normal spirogram, a measurement of respiratory volumes. The tidal volume is the amount of air in a normal breath, typically around 500 milliliters in a healthy male. The amount of air that can be brought into the lungs under a maximal inspiration, the amount that you can bring in beyond the tidal volume, is known as the inspiratory reserve volume. That's typically a little larger than 3,000 milliliters in a healthy male. So, the tidal volume plus the inspiratory reserve volume is called the inspiratory capacity. The amount of air that you can force out beyond a tidal volume is the expiratory reserve volume and that's typically around a thousand milliliters. So, the sum of the inspiratory reserve volume, the tidal volume, and the expiratory reserve volume is the vital capacity which is the largest breath that you could take. So, you can add together the respiratory volumes to calculate a respiratory capacity, like the inspiratory capacity is IRV plus tidal volume, the vital capacity is IRV plus tidal volume plus ERV, or the expiratory capacity would be tidal volume plus ERV. The vital capacity is typically a little bit under 5,000 milliliters but the total lung capacity is larger. It's closer to 6,000 milliliters and so after a maximal expiration there's always some air that remains in the lungs. This is what we call the residual volume, the amount of air that remains in the lungs after maximal expiration and so we cannot really measure the total lung capacity using a spirometer. All we can measure is the vital capacity. There's also a term for the amount of air that remains in the lungs after a tidal volume expiration. This is the functional residual capacity. So, the functional residual capacity is your expiratory reserve volume plus your residual volume, ERV plus residual volume, or it's the amount of air remaining in the lungs after a normal expiration. Pulmonary function tests include a forced vital capacity measurement which is useful for distinguishing between two major types of lung disease. Obstructive lung disease is a type of lung disease where the resistance of the airways increases. An example would be asthma, bronchitis, or also in emphysema. These conditions involve excess inflammation, stimulating bronchoconstriction, leading to increased resistance when the patient is asked to breathe their entire vital capacity rapidly. We'll analyze the volume of air, breathe during the first second as the forced expiratory volume one, and then analyze the ratio of the entire forced vital capacity. What percentage of the forced vital capacity can the patient force out in one second? In a healthy patient that's typically around 80% but a patient with obstructive lung disease will have a greatly decreased FEV to FVC ratio. In contrast, a restrictive lung disease causes a decrease in pulmonary compliance, making it more difficult for the lungs to expand, causing a greatly decreased vital capacity, decreased inspiratory reserve volume. However, the forced expiratory volume, the FEV1 to FEVC ratio, is not decreased and is often greater than 80% in a restrictive pulmonary disorder. And so we'll focus on using this pulmonary function test to distinguish between obstructive and restrictive lung disease. However, there's several other pulmonary function tests we can see here. For example, you could do a maximum voluntary ventilation where the patient is asked to breathe in and out as rapidly and deeply as possible for a minute and to see if their maximum voluntary ventilation capacities increased or decreased. And also we could use a blood gas analyzer to measure the concentration of oxygen and carbon dioxide in the blood. Let's see what a spirogram from pulmonary function testing of a patient with obstructive lung disease would look like. Here we see a typical size of a tidal volume. They took one normal breath, then a maximal inspiration followed by maximal expiration, and they were asked to force that breath out quickly, and their vital capacity was 3,200 milliliters. The expiratory reserve volume of 500 milliliters is slightly small, and the expiratory reserve volume of 2,200 milliliters is also slightly small. So many of these lung volumes are slightly decreased in it, obstructive lung disease. However, what really has the most prominent and diagnostic characteristic in this spirogram is the rate of airflow. If we look at the FEV1 to FVC ratio in obstructive lung disease, this will be less than 80 percent because resistance, excess resistance, slows the rate of airflow. There's a decreased rate of airflow, and that is what is distinguishing the obstructive lung disease in this graph. Now let's contrast that with a restrictive lung disease. If we have a patient with restrictive lung disease, we'll see that there's a greatly decreased vital capacity. So 2,800 milliliters is much less than the normal vital capacity of around 5,000 milliliters, and the inspiratory reserve volume of 1,300 milliliters is also much less than a typical inspiratory reserve volume of around 3,000 milliliters. So less than half of the typical inspiratory reserve volume in this greatly reduced IRV suggests a restrictive lung disease. So we see a typical expiratory reserve volume, but what will also confirm that this is a restrictive lung disease rather than an obstructive lung disease is analyzing the rate of airflow. If we look at the ratio of FEV1 to FVC, we can see that it's greater than 80%, and so with a decreased vital capacity and inspiratory reserve volume, but an increased FEV1 to FVC ratio, we can confirm that this spirogram is a a spirogram of a patient with restrictive lung disease.