This text will expertly guide you through cardiopulmonary anatomy and physiology and serves as an ongoing reference throughout your schooling and health profession. Physiology of Respiration. This text explains how the respiratory system functions and provides a framework for understanding many respiratory diseases.
It was developed as a working text with problem-solving exercises for students. The book covers pulmonary anatomy and microstructure, mechanics, gas exchange, acid-base balance, and control mechanisms. Unlike other texts, it strikes a. I hope this textbook conveys the majesty of the human body and its many functions and encourages students to study physiology throughout their careers.
Physiology is the link between basic science and medicine. The great beauty of physiology is that it integrates the individual functions of all the different cells, tissues, and organs of the body into one functional whole, the human body. In fact, the human body is much more than the sum of its parts, and life is based on this total function, not just the function of individual parts of the body isolated from each other.
This brings us to an important question: How do the separate organs and systems coordinate to keep the entire body functioning properly? Fortunately, our bodies are endowed with a vast network of feedback controls that strike the necessary balances without which we could not live. Physiologists call this high level of internal body control homeostasis. In disease states, functional balances are often seriously disturbed and homeostasis is impaired.
And, when even a single disturbance reaches a limit, the whole body can no longer live. When a cardiac impulse passes through the heart, an electrical current also spreads from the heart into the adjacent tissues surrounding the heart. A small portion of the current spreads all the way to the surface of the body. If electrodes are placed on the skin on opposite sides of the heart, electrical potentials generated by the current can be recorded; the recording is known as an electrocardiogram ECG.
Guyton and Hall Physiology Review 11th Edition pdf free. The P wave is caused by electrical potentials generated when the atria depolarize before an atrial contraction begins. The QRS complex is caused by potentials generated when the ventricles depolarize before contraction—that is, as the depolarization wave spreads through the ventricles. Therefore, both the P wave and the components of the QRS complex are depolarization waves. The bronchioles do not normally contain cartilage, glands, or goblet cells.
The sum of the cross-sectional area of the two new airways at each branch point is greater than that of the parent branch. Thus, as you move farther out toward the alveoli, the cross-sectional area of all of the small airways in parallel is quite large, far larger than the trachea Fig. The number of branch points from the trachea to the alveolus ranges from 10 to As you move from conducting airways, tubes through which air flows but no gas exchange takes place, to the alveoli or gas exchange units, you go through what is known as the transitional zone.
This zone consists of airways called respiratory bronchioles, from which a few alveoli originate; thus, there is a transition between the conducting airways and alveoli. Finally, you arrive at the alveolar ducts, which are completely lined by alveoli and are the primary site of gas exchange. The portion of the lung composed of alveoli has been termed the respiratory zone.
As you travel from the mouth to the alveoli, you encounter an increasing number of branch points. As a general principle, at each branch point, the sum of the cross-sectional areas of the new airways is greater than that of the airway from which they originated. The more central airways have cartilaginous support, resulting in some stiffness in their walls. However, the smaller, distal airways are quite compliant and prone to collapse when the pressure outside the airways is greater than the pressure inside.
The size of the conducting airways offers a tradeoff between two competing physiologic demands. On the one hand, the amount of wasted ventilation or dead space needs to be minimized. This would favor conducting airways with very small diameter and volume. On the other hand, the resistance in these airways must also be minimized. Because airway resistance varies inversely with the radius raised to the fourth power see Chapter 4 , the need to minimize the work of breathing suggests that the system should have the largest airway possible.
Hence, you can see the dilemma. Consequently, the velocity of the air moving through the airways decreases as it travels from the trachea to the periphery of the lung. Consider the rapidly moving water in a creek that empties into a large pond; the velocity of the water decreases markedly as it enters the broad pond. Because the total cross-sectional area is a key factor in determining resistance, defined as a pressure decrease divided by flow, most of the resistance in the lungs is in the central airways.
The first six branches of the airways dominate the total resistance of the lung. The bronchioles are generally less than 1 mm in diameter.
As already noted, the bronchioles do not have cartilage in their walls. Thus, they are susceptible to collapse if the pressure in the pleural space is greater than the pressure in the airway.
The bronchioles are located within the connective tissue structure of the lung and are supported by this tissue. As the lung increases in volume during inspiration, the diameter of the bronchioles increases as well. As the lung volume decreases during expiration, so does the diameter of the bronchioles. Emphysema, a disease associated with cigarette smoking, destroys much of the connective tissue support structure within the lung, thereby making these small airways even more susceptible to collapse.
Gas moves from the pharynx to the terminal bronchioles by bulk flow. The driving force during inspiration is the pressure differential between the pharynx and the alveolus alveolar pressure is negative during inspiration because of the action of the inspiratory muscles. Beyond the terminal bronchioles, the cross-sectional area of the millions of respiratory bronchioles and alveolar ducts, all arranged in parallel, becomes enormous and the velocity of the gas entering the gas-exchanging units decreases precipitously see Chapter 4.
In this region of the airways, diffusion is the predominant means for moving gas. The very low velocity of gas in this region of the lung allows particles being carried in the inspired gas to settle out. The low velocity here likely accounts for the fact that this anatomic region is often the site of deposition of very small dust particles and the site of diseases that are associated with these particles Fig.
Because the respiratory bronchioles and alveolar ducts contribute little to the overall resistance of the lungs, the distribution of gas among these units is determined largely by their relative compliance. Compliance is a measure of the stiffness of an object and is equal to the change in volume that occurs in the object for a given change in the pressure across the wall of the object.
In the normal lung, the compliance of a terminal lung unit depends on the volume of the unit—the larger the unit at the beginning of a breath, the less compliant it is see Chapter 3. At the end of exhalation, alveolar units at the apex of the lung are larger than at the bases and, as a result, are less compliant. This accounts partly for the finding that inspired gas is distributed preferentially to the bases of the lungs relative to the apices see Chapter 5.
The distribution of ventilation within the lungs is also affected by microscopic passages called the pores of Kohn, which connect the alveoli within a lobe Fig. These connections permit transfer of gas between alveoli and function to minimize the collapse of lung units if a more central airway is obstructed. As noted previously, however, individual lobes of the lung are fully surrounded by pleura, and cross-ventilation between the lobes can only occur via the airways.
As gas moves from the terminal bronchioles to the respiratory bronchioles and the alveolar ducts, the velocity of the gas decreases markedly. Gas now moves largely by diffusion rather than bulk flow. The decrease in velocity leads to deposition of small, inhaled particles in this region of the lung.
Terminal bronchioles A Normal ventilation B Blockage leading to potential collapse of alveoli C Collateral flow through pores of Kohn works against collapse Pores of Kohn.
Connections between alveoli, called pores of Kohn, allow gas transfer between alveoli within a pulmonary segment. This minimizes the chances that an obstruction within an airway will lead to collapse of alveoli and loss of gas exchanging units. A, The normal flow of gas from the respiratory bronchioles to the alveoli. B, An obstruction forms in a small airway leading to a group of alveoli.
C, The movement of gas into these alveoli from adjacent units via the pores of Kohn prevents collapse of the alveoli downstream from the obstruction. Patients with this syndrome may be infertile cilia line the fallopian tubes, and spermatic function is also affected and typically have respiratory disease.
What parts of the lungs do you think would be affected in this condition? What types of problems might they have? In disease states such as chronic bronchitis, excess production of mucus may reduce the functional diameter of the airways and increase resistance to airflow.
The Gas Exchanger g If the controller and ventilatory pump have accomplished their respective tasks, air arrives at the gas exchanger, which is composed of the alveoli and the pulmonary capillaries. The bulk flow seen in the airways gives way to diffusion as oxygen leaves the alveolus and enters the blood and carbon dioxide moves in the opposite direction.
As with the other components of the respiratory system, nature has constructed a very efficient structure to perform this vital function. In addition, to ensure efficient transfer of gas between the blood and the alveolus, the distance for diffusion must be as short as possible. The gas-exchanging unit, however, must be sufficiently robust to resist collapse during exhalation as the lung volume decreases.
Finally, the system must ensure that perfusion, the term given to blood flow to an organ or tissue bed, goes to the areas of the lung where oxygen is being delivered. To maximize the surface area for gas exchange, millions of gas exchanging units are present at the ends of the respiratory bronchioles. These gas-exchanging units, or alveoli, can be found primarily as part of the alveolar ducts.
The pulmonary capillaries form a fine mesh network around each alveolus to maximize the contact between the two structures and, consequently, the surface area for diffusion of gas. Roughly million alveoli are present in the lung, each of which is less than 0. The total surface area of the gas-exchanging units in the lungs is between 50 and m2.
Because the surface area of the alveoli is large, a comparably large pulmonary capillary surface area is needed to achieve effective transfer of oxygen and carbon dioxide between the two structures. The pulmonary capillaries are literally wrapped around the alveolus in a fine mesh network that produces a virtual sheet of blood for diffusion Fig. As many as pulmonary capillaries come into contact with each alveolus.
The small diameter ensures that the gas has only a minimal distance to travel between the alveolus and the hemoglobin contained within the RBC. Hemoglobin is the primary protein within the RBC and, by virtue of its capacity to bind oxygen, is the major means by which oxygen is transported in the blood.
This percentage is called the oxygen saturation. During the time that an RBC traverses a pulmonary capillary, it may actually come into contact with several alveoli. This means that there is a tremendous reserve capacity for diffusion. For example, when cardiac output is increased, as in exercise, and the speed with which an RBC traverses the alveolus increases, the blood will still be saturated with oxygen by the time it exits the capillary.
Alternatively, if a disease process results in a thickening of the alveolar—capillary interface, there may still be adequate time for the oxygen to diffuse into the RBCs. What would you expect to happen to the oxygen level in the blood when the patient exercises? Under normal conditions, the walls of the alveolus and the capillary are so thin that the pressure within the alveolus can affect blood flow within the capillary.
In some regions of the lung, pressure in the alveolus exceeds that within the capillary, leading to compression or collapse of the capillary more in Chapter 5. The total distance for diffusion of gas from the alveolus to the RBC is approximately 0. The surface across which the gas must diffuse consists of the fluid lining the alveolus, the alveolar wall, the interstitial space between the alveolus and the capillary a space that is negligible in normal individuals but where fluid and inflammatory material may accumulate in disease states , the wall of the capillary, the plasma surrounding the RBC, and the wall of the RBC.
Fluid lining the alveolus 2. Alveolar wall 3. Int Inters tersti titi ti tiall spa space ce 4. Capillary wall 5. Plasma surrounding g the RBC 6. Wal all ll off R RBC BC The wall of the pulmonary capillary is composed of a single layer of squamous epithelium, which minimizes the distance for diffusion. The wall of the alveolus is similarly thin, composed of an epithelium made up of a single layer of cells called type I pneumocytes and an interstitium formed by the fused basal lamina of the alveolar epithelium and the capillary endothelium in some regions, collagen and elastin also contribute to the thickness of the interstitial space.
In healthy people, the thickness of the RBCs forms a significant portion of the distance across which oxygen and carbon dioxide must diffuse. Diffusion is so effective in the lungs, and the reserve time available for diffusion of oxygen into the RBCs is so great, that a low blood oxygen level attributable to diffusion limitation is difficult to demonstrate in the normal lung. In experimental conditions, a low blood oxygen level may occur in a person doing heavy exercise while breathing a mixture of gas with a low partial pressure of oxygen.
Even in disease states, diffusion limitation is rarely a cause of hypoxemia, the term used for low blood oxygen levels at rest see Chapter 5. Alveoli are linked to each other via shared walls and to airways via collagen and elastin. These connections allow forces to be shared among alveoli, and the resulting stabilization makes it difficult for a single alveolus to collapse. Connective tissue, composed of collagen and elastin, is interspersed between the alveoli and the airways.
Use Animated Figure to view how the collapse of a single alveolus is opposed by its connections to surrounding alveoli. Drag one of the alveolar walls and release it to observe how the resulting forces return the collapsing alveolus to its initial state. The wall of one alveolus is often shared by another alveolus. If one alveolus were to collapse, therefore, others would be affected as the adjacent alveoli are pulled down in the same direction.
The phenomenon of atelectasis, or collapse of lung units, is not caused by collapse of individual alveoli; larger lung units must be involved given this degree of interdependence. The pulmonary arteries are located next to the bronchi and branch with them down to the level of the respiratory bronchiole. Here, the arteries divide into capillaries that surround the alveoli, as already described. Arterial smooth muscle cells in pulmonary arterioles respond to hypoxia by contracting.
As ventilation decreases to one alveolus, the partial pressure of oxygen diminishes within that unit. This process leads to an increase in vascular resistance in the vessels perfusing the alveolus and a redirection of blood flow to other regions of lung that are better ventilated and have higher oxygen levels.
This phenomenon maximizes gas exchange by matching ventilation and perfusion within the lung. The arterial walls contain smooth muscle that can contract, thereby changing the resistance of the vessel and the amount of blood flowing through a particular region of lung. Hypoxia is one of the stimuli that cause pulmonary arterial vasoconstriction.
Thus, if one section of lung is not receiving adequate ventilation and local hypoxia develops in that area, the pulmonary artery serving that region will constrict to redirect blood flow to another area that is receiving adequate ventilation Fig. This phenomenon, termed hypoxic pulmonary vasoconstriction, ensures that blood flows to regions of lung receiving the best ventilation.
Use Animated Figure to adjust the airway obstruction and hence the ventilation to the alveolus. Note that as alveolar hypoxia develops i. By matching ventilation and perfusion, the body maximizes the opportunity for diffusion of oxygen and carbon dioxide. Mismatch of ventilation represented. The pulmonary circulation must also be able to handle large changes in blood flow without causing a significant increase in vascular resistance.
When an individual is resting, the volume of blood in the pulmonary capillaries is only one third of the capacity of the vessels, meaning there is a significant reserve capacity.
When cardiac output increases, as during exercise, to meet the metabolic needs of the body, the amount of blood engaging in gas exchange can increase as well.
As more blood enters pulmonary capillaries, additional alveoli are recruited r into the. Thus far, we have focused on the pulmonary circulation, which delivers deoxygenated blood from the right ventricle of the heart to the pulmonary capillaries, where oxygen is transferred to the RBCs and carbon dioxide is transferred to the alveoli.
The bronchial circulation delivers oxygenated blood from the aorta to the lung tissue. The bronchial circulation serves as a major supply of oxygen and nutrients to the trachea, bronchi, and visceral pleura as well as the esophagus.
Together, these structures comprise the extra-alveolar components of the lungs. Bronchial blood flow may be greatly increased in inflammatory conditions of the lung such as bronchiectasis. Erosion of these vessels can lead to intrapulmonary bleeding and hemoptysis i.
Why are most pulmonary emboli not associated with pulmonary infarction death of lung tissue? Type I pneumocytes line the alveolus. Interspersed among these type I pneumocytes are other cells called type II pneumocytes, which produce surfactant, a substance that becomes a component of the liquid layer lining the alveolus.
Surfactant plays a critical role in reducing surface forces within the alveolus, thereby contributing to the stability of the alveoli see Chapter 3. Type II pneumocytes also absorb and recycle surfactant. Mucus traps inhaled foreign material, and the cilia push this material up to the trachea, where it can be expelled. The alveoli also play a part in defending the lungs from infection. Macrophages are found within the alveoli and ingest foreign material that has evaded the airway defenses and managed to enter the gas-exchanging units.
These cells help police the alveoli against infectious agents to minimize damage to the lungs and prevent entry of these organisms into the bloodstream, where they can be carried to the rest of the body. The boy with asthma is allergic to cats, and over the course of an hour, he notes that his breathing is becoming uncomfortable. He feels tightness in his chest and begins to cough. The oxygen saturation of the blood is only slightly down despite the wheezing. What links can you make between the structure and function of the respiratory system in your analysis of this case?
Exposure to the cat dander, an allergen to which the boy was sensitive, led to constriction of the bronchioles and increased production of mucus within the airways. Both of these factors caused airway resistance to increase and diminished ventilation to some rregions of the lung. The respiratory controller sensed changes in the lung via pulmonary receptors and the development of mild hypoxia via the chemoreceptors, as well as the distress the boy was feeling.
The result was an increase in the rate of breathing. To deal with the impairment to the ventilatory pump caused by the constriction of the airways, accessory muscles of ventilation, the sternocleidomastoid muscles, were recruited to serve as ventilatory muscles. The oxygen level was only minimally reduced despite the abnormalities in the airways because the pulmonary capillaries supplying blood to regions of lung most impaired by the bronchoconstriction and mucus constricted in response to localized hypoxia.
Thus, blood was sent to relatively unaffected areas of the lungs, and gas exchange was protected. Consciousness is not required to keep the system in motion, but behavioral factors can modify the rate and depth of breathing.
The accessory muscles normally serve other functions but are recruited to assist the ventilatory pump when the body needs to increase the rate and depth of breathing or when the ventilatory pump is impaired. They also serve an important role in defending the body against infection. Individuals with CCHS do not have a working central pattern generator.
Consequently, when they sleep and all conscious activity ceases, they stop breathing. The condition is generally diagnosed shortly after birth because the infant will have a respiratory arrest when asleep. These people need a permanent tracheostomy, a hole in the trachea that permits the patient to be connected to a mechanical ventilator via a tube placed through the hole. The ventilator must be used to sustain them during sleep. Because the diaphragm receives its neurological signals from nerves that exit the spinal cord between C3 and C5, above the level of the injury, the diaphragm will contract and move normally, leading to the creation of negative intrathoracic pressure see figure below.
The intercostal muscles, however, derive their neurological signals from the thoracic segments of the spinal cord, so these muscles are inactive. Without the action of the intercostal muscles to stabilize the rib cage, the sternum will move inward during inspiration. In essence, the sternum is sucked in by the negative intrathoracic pressure. Innervation of diaphragm C3, C4, C5 intact C7 transection of cord Intercostal muscles no longer innervated Negative intra-thoracic pressure pulls sternum inward Motion of diaphragm on inspiration Lateral view of rib cage With a complete transection of the spinal cord at C7, the diaphragm is still innervated and moves downward during inspiration.
Without the action of the intercostal muscles, however, the negative intrathoracic pressure generated by diaphragm causes the sternum to move inward.
A cholinergic agonist would stimulate the parasympathetic receptors and cause bronchoconstriction. A common way to test for the presence of asthma is to ask the patient to inhale gradually increasing doses of methacholine, a cholinergic agonist.
A diagnosis of asthma is made if the patient develops significant bronchoconstriction at low doses of the inhaled agent. The highest resistance to airflow is found toward the large central airways. The great cross-sectional area of the millions of peripheral airways in parallel leads to low resistance in the periphery of the lung.
As discussed in Chapter 4, one of the major factors in determining the resistance of the airways expressed as the decrease in pressure divided by the flow is the presence or absence of turbulent flow, which depends largely on the velocity of the gas moving through the airway.
As gas moves from a single windpipe to millions of terminal bronchioles, the velocity of the gas decreases tremendously think of water swiftly moving through a creek that empties into a large pond: the velocity of the water slows dramatically as it enters the pond , and resistance falls.
The airways from the trachea to the respiratory bronchioles are lined with cilia. If the cilia do not function normally, the mucus and the foreign material trapped in the mucus are not pushed back up to the trachea to be either swallowed or coughed out.
This abnormality leads to recurrent respiratory infections because one of the key defense mechanisms that prevents bacteria from entering the lungs is disrupted. Recurrent infections and the inflammatory response to them can, over time, lead to dilatation and scarring of the airways, a condition called bronchiectasis. In the patient described, the oxygen level in the blood will decrease when she exercises. The distance for diffusion has been increased because of the scarring of the lung.
Although the reserve capacity of the gas-exchanging unit can compensate for this when the patient is at rest, the increase in cardiac output associated with exercise puts a further strain on the system. The RBC is now speeding through the pulmonary capillary, and the prolonged time required for diffusion, consequent to the pulmonary fibrosis, prevents the hemoglobin from being fully saturated as the RBC exits the capillary.
As a result, the blood oxygen level decreases with exercise. The lung tissue can receive oxygen from multiple sources: the airways, the bronchial circulation, and the pulmonary circulation.
Thus, a blockage of one component of the pulmonary circulation does not necessarily lead to sufficient hypoxia to cause cell death. A year-old college student falls into a pool after consuming large amounts of alcohol. He is unable to swim and sinks to the bottom of the pool.
An alert friend walks by approximately 4 minutes later and dives in after him. He pulls his friend to the surface and begins cardiopulmonary resuscitation. The student is revived and is taken to the hospital, where he is ultimately found to have anoxic brain damage involving his motor cortex bilaterally. He is breathing on a ventilator. Which of the following statements is most likely to be true?
He will never be able to breathe on his own again because of the damage to the motor cortex. He will be able to breathe without the ventilator if he is given a phrenic nerve pacemaker. He will be able to breathe on his own because his brainstem is still intact. He will be able to breathe on his own when he is awake but not when he is asleep.
In the s, there were several severe polio epidemics in the United States. The iron lung was attached to a large vacuum that cycled the pressure inside the iron lung from atmospheric pressure to a negative pressure and then back to atmospheric pressure. This device led to the creation of a negative pressure in the pleural space on each cycle. Which part of the respiratory system was being supplemented primarily by the iron lung? She has had multiple respiratory infections over the past 10 years and was diagnosed with a condition in which the cartilage is weakened in the lungs.
E-Book Description. E-Book Details. Table of Contents. Show more. Show less.
0コメント