Respiratory Physiology PDF

SYSTEMS PHYSIOLOGY Respiratory  Outlines Organization of the Respiratory System Ventilation and Lung Mechanics Exchange of Gases in Alveoli and Tissues Transport of Oxygen in Blood Transport of Carbon Dioxide in Blood Transport of Hydrogen Ion Between Tissues and Lungs Co...

SYSTEMS PHYSIOLOGY Respiratory  Outlines Organization of the Respiratory System Ventilation and Lung Mechanics Exchange of Gases in Alveoli and Tissues Transport of Oxygen in Blood Transport of Carbon Dioxide in Blood Transport of Hydrogen Ion Between Tissues and Lungs Control of Respiration Hypoxia Nonrespiratory Functions of the Lungs Organization of the Respiratory System The Airways and Blood Vessels.  Organization of the Respiratory System The Airways and Blood Vessels. Functions of the Conducting Zone of the Airways Provides a low-resistance pathway for airflow. Resistance is physiologically regulated by changes in contraction of bronchiolar smooth muscle and by physical forces acting upon the airways. Defends against microbes, toxic chemicals, and other foreign matter. Cilia, mucus, and macrophages perform this function. Warms and moistens the air. Phonates (vocal cords).  Organization of the Respiratory System Site of Gas Exchange: The Alveoli What consequences would result if inflammation caused a buildup of fluid in the alveoli and interstitial spaces? Relation of the Lungs to the Thoracic (Chest) Wall  Ventilation and Lung Mechanics Understanding the forces that control the inflation and deflation of the lung and the flow of air between the lung and the environment requires some knowledge of several fundamental physical laws. Ventilation is defined as the exchange of air between the atmosphere and alveoli. – Like blood, air moves by bulk flow from a region of high pressure to one of low pressure. – Bulk flow can be described by the equation: F=ΔP/R  Ventilation and Lung Mechanics A very important point must be made here: – All pressures in the respiratory system, as in the cardiovascular system, are given relative to atmospheric pressure, which is 760 mmHg at sea level but which decreases in proportion to an increase in altitude. – During ventilation, air moves into and out of the lungs because the alveolar pressure is alternately less than and greater than atmospheric pressure (Figure).  Ventilation and Lung Mechanics To understand how a change in lung dimensions causes a change in alveolar pressure, you need to learn one more basic physical principle described by Boyle’s law, which is represented by the equation P 1 V 1 = P 2 V 2.  Ventilation and Lung Mechanics 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 on other factors. – The first of these is the difference in pressure between the inside and outside of the lung, termed the transpulmonary pressure ( P tp ). – The second is how stretchable the lungs are, which determines how much they expand for a given change in P tp. The pressure inside the lungs is the air pressure inside the alveoli ( P alv ), and the pressure outside the lungs is the pressure of the intrapleural fluid surrounding the lungs ( P ip ). Thus, Transpulmonary pressure – Ptp= Palv-Pip  Ventilation and Lung Mechanics How Is a Stable Balance Achieved Between Breaths? The transmural pressures of the respiratory system at rest—that is, at the end of an unforced expiration when the respiratory muscles are relaxed and there is no airflow. At rest, when there is no airflow and P alv = 0, P ip must be negative, providing the force that keeps the lungs open and the chest wall in. What are the forces that cause P ip to be negative? At rest, all of these transmural pressures balance each other out. It is clear that the subatmospheric. (negative) intrapleural pressure ( P ip ) is the essential factor keeping the lungs partially expanded between breaths. An extremely important question is, “What is the reason for a subatmospheric (‘negative’) P ip ?”  Ventilation and Lung Mechanics How Is a Stable Balance Achieved Between Breaths? The importance of the transpulmonary pressure in achieving this stable balance can be seen when, during surgery or trauma, the chest wall is pierced without damaging the lung. – Atmospheric air enters the intrapleural space through the wound, a phenomenon called pneumothorax, and the intrapleural pressure increases from -4 mmHg to 0 mmHg. How can a collapsed lung be re-expanded in a patient with a pneumothorax? – That is, P ip increases from 4 mmHg lower ( Hint: What changes in P ip and P tp would be than P atm to a P ip value equal to P atm. needed to re-expand the lung?) – The transpulmonary pressure acting to hold the lung open is thus eliminated, and the lung collapses.  Ventilation and Lung Mechanics Inspiration/Expiration  Ventilation and Lung Mechanics Inspiration Inspiration is initiated by the neurally induced contraction of the diaphragm and the external intercostal muscles located between the ribs.  The diaphragm is the most important inspiratory muscle that acts during normal quiet breathing. 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. When contraction of the inspiratory muscles actively increases the thoracic dimensions, the lungs are passively forced to enlarge.  The enlargement of the lungs causes an increase in the sizes of the alveoli throughout the lungs.  Ventilation and Lung Mechanics Expiration At the end of inspiration, the motor neurons to the diaphragm and inspiratory intercostal muscles decrease their firing and so these muscles relax. As the lungs become smaller, air in the alveoli becomes temporarily compressed so that, by Boyle’s law, alveolar pressure exceeds atmospheric pressure. Under certain conditions, such as during exercise, expiration of larger volumes is achieved by contraction of a different set of intercostal muscles and the abdominal muscles, which actively decrease thoracic dimensions.  Ventilation and Lung Mechanics Inspiration/Expiration  Ventilation and Lung Mechanics Lung Compliance To repeat, the degree of lung expansion at any instant is proportional to the transpulmonary pressure, P alv - P ip. But just how much any given change in transpulmonary pressure expands the lungs depends upon the stretchability, or compliance, of the lungs. – Lung compliance ( C L ) is defined as the magnitude of the change in lung volume (Δ V L ) produced by a given change in the transpulmonary pressure: – CL = ΔVL/ΔPtp – Thus, the greater the lung compliance, the easier it is to Premature infants with inadequate expand the lungs at any given change in transpulmonary surfactant have decreased lung pressure. compliance (respiratory distress syndrome of the newborn). If surfactant is not available to administer Compliance can be considered the inverse of stiffness. for therapy, what can be done to inflate the lung?  Ventilation and Lung Mechanics Lung Compliance Determinants of Lung Compliance. There are two major determinants of lung compliance. – One is the stretchability of the lung tissues, particularly their elastic connective tissues. Thus, a thickening of the lung tissues decreases lung compliance. – Two the presence of the Surfactant which is a mixture of both lipids and proteins, Some Important Facts About Pulmonary Surfactant – Pulmonary surfactant is a mixture of phospholipids and protein. – It is secreted by type II alveolar cells. – It lowers the surface tension of the water layer at the alveolar surface, which increases lung compliance, thereby making it easier for the lungs to expand. – Its effect is greater in smaller alveoli, thus reducing the surface tension of small alveoli below that of larger alveoli. This stabilizes the alveoli. – A deep breath increases its secretion by stretching the type II cells. Its concentration decreases when breaths are small. – Production in the fetal lung occurs in late gestation and is stimulated by the increase in cortisol (glucocorticoid) secretion that occurs then.  Ventilation and Lung Mechanics Airway Resistance The volume of air that flows into or out of the alveoli per unit time is directly proportional to the pressure difference between the atmosphere and alveoli and is inversely proportional to the resistance to flow of the airways. The factors that determine airway resistance are analogous to those determining vascular resistance in the circulatory system. Physical, neural, and chemical factors affect airway radii and therefore resistance. – One important physical factor is the transpulmonary pressure, which exerts a distending force on the airways, just as on the alveoli. – A second physical factor holding the airways open is the elastic connective-tissue fibers that link the outside of the airways to the surrounding alveolar tissue. Why are we concerned with all the physical and chemical factors that can influence airway resistance when airway resistance is normally so low that it poses no impediment to airflow?  Ventilation and Lung Mechanics Lung Volumes and Capacities  Ventilation and Lung Mechanics Alveolar Ventilation The total ventilation per minute—( V˙E )—is equal to the tidal volume multiplied by the respiratory rate: Minute ventilation (mL/min)= Tidal volume(mL/breath)*Respiratory rate(breaths/min) – VE=Vt* f Dead Space The total volume of fresh air entering the alveoli per minute is called the alveolar ventilation ( V˙ A ): Alveolar ventilation (mL/min) = Tidal volume (mL/breath) – Dead space (mL/breath) * Respiratory rate (breaths/min) What would be the effect of breathing through a plastic tube with a length of 20 VA = (Vt - VD) * f cm and diameter of 4 cm? Alveolar ventilation, rather than minute ventilation, is the more ( Hint: Use the formula for the volume of important factor in the effectiveness of gas exchange. a perfect cylinder.)  Ventilation and Lung Mechanics Alveolar Ventilation Dead Space This generalization is demonstrated readily by the data in Table 13.4. In this experiment, subject A breathes rapidly and shallowly, B normally, and C slowly and deeply. Each subject has exactly the same minute ventilation; that is, each is moving the same amount of air in and out of the lungs per minute. Yet, when we subtract the anatomical-dead-space ventilation from the minute ventilation, we find marked differences in alveolar ventilation. Subject A has no alveolar ventilation and would become unconscious in several minutes, whereas C has a considerably greater alveolar ventilation than B, who is breathing normally.  Ventilation and Lung Mechanics Alveolar Ventilation Dead Space The anatomical dead space is not the only type of dead space. Some fresh inspired air is not used for gas exchange with the blood even though it reaches the alveoli because some alveoli may, for various reasons, have little or no blood supply. This volume of air is known as alveolar dead space. It is quite small in healthy persons but may be very large in persons with several kinds of lung disease. As we shall see, local mechanisms that match air and blood flows minimize the alveolar dead space. The sum of the anatomical and alveolar dead spaces is known as the physiological dead space. This is also known as wasted ventilation because it is air that is inspired but does not participate in gas exchange with blood flowing through the lungs.  Exchange of Gases in Alveoli and Tissues Oxygen must move across the alveolar membranes into the pulmonary capillaries, be transported by the blood to the tissues, leave the tissue capillaries and enter the extracellular fluid, and finally cross plasma membranes to gain entry into cells. Carbon dioxide must follow a similar path, but in reverse. The balance depends primarily upon which nutrients are used for energy, because the enzymatic pathways for metabolizing carbohydrates, fats, and proteins generate different amounts of CO 2. – The ratio of CO 2 produced to O 2 consumed is known as the respiratory quotient ( RQ )  Exchange of Gases in Alveoli and Tissues Partial Pressures of Gases Gas molecules undergo continuous random motion. As Dalton’s law states, in a mixture of gases, the pressure each gas exerts is independent of the pressure the others exert. The sum of the partial pressures of all these gases is called atmospheric pressure, or barometric pressure. Diffusion of Gases in Liquids – When a liquid is exposed to air containing a particular gas, molecules of the gas will enter the liquid and dissolve in it. – Another physical law, called Henry’s law, states that the amount of gas dissolved will be directly proportional to the partial pressure of the gas with which the liquid is in equilibrium. – A corollary is that, at equilibrium, the partial pressures of the gas molecules in the liquid and gaseous phases must be identical.  Exchange of Gases in Alveoli and Tissues Alveolar Gas Pressures Typical alveolar gas pressures are PO2 = 105 mmHg and PCO2 5 40 mmHg. Alveolar PCO2 is higher than atmospheric PCO2 because carbon dioxide enters the alveoli from the pulmonary capillaries. The factors that determine the precise value of alveolar PO2 are – (1) the PO2 of atmospheric air, – (2) the rate of alveolar ventilation, and – (3) the rate of total-body oxygen consumption.  Exchange of Gases in Alveoli and Tissues Alveolar Gas Pressures Hypoventilation exists when there is an increase in the ratio of carbon dioxide production to alveolar ventilation. In other words, a person is hypoventilating if the alveolar ventilation cannot keep pace with the carbon dioxide production. The result is that alveolar PCO2 increases above the normal value. Hyperventilation exists when there is a decrease in the ratio of carbon dioxide production to alveolar ventilation, that is, when alveolar ventilation is actually too great for the amount of carbon dioxide being produced. The result is that alveolar PCO2 decreases below the normal value.  Exchange of Gases in Alveoli and Tissues Gas Exchange Between Alveoli and Blood The blood that enters the pulmonary capillaries is systemic venous blood pumped to the lungs through the pulmonary arteries. The differences in the partial pressures of oxygen and carbon dioxide on the two sides of the alveolar-capillary membrane result in the net diffusion of oxygen from alveoli to blood and of carbon dioxide from blood to alveoli. The net diffusion of these gases ceases when the capillary partial pressures become equal to those in the alveoli.  Exchange of Gases in Alveoli and Tissues Gas Exchange Between Alveoli and Blood In a healthy person, the rates at which oxygen and carbon dioxide diffuse are high enough and the blood flow through the capillaries slow enough that complete equilibrium is reached well before the blood reaches the end of the capillaries. Many of the pulmonary capillaries at the apex (top) of each lung are normally closed at rest. During exercise, these capillaries open and receive blood, thereby enhancing gas exchange. What is the effect of The mechanism by which this occurs is a simple physical one; exercise on PO2 at the end of – the pulmonary circulation at rest is at such a low blood a capillary in a normal pressure that the pressure in these apical capillaries is region of the lung? inadequate to keep them open, In a region of the lung with diffusion limitation due to – but the increased cardiac output of exercise increases disease? pulmonary vascular pressures, which opens these capillaries.  Exchange of Gases in Alveoli and Tissues Matching of Ventilation and Blood Flow in Alveoli The major disease-induced cause of inadequate oxygen movement between alveoli and pulmonary capillary blood is not a problem with diffusion but, instead, is due to the mismatching of the air supply and blood supply in individual alveoli. The lungs are composed of approximately 300 million alveoli, each capable of receiving carbon dioxide from, and supplying oxygen to, the pulmonary capillary blood. To be most efficient, the correct proportion of alveolar airflow (ventilation) and capillary blood flow (perfusion) should be available to each alveolus. Any mismatching is termed ventilation–perfusion inequality. – The major effect of ventilation–perfusion inequality is to decrease the PO2 of systemic arterial blood.  Exchange of Gases in Alveoli and Tissues Matching of Ventilation and Blood Flow in Alveoli There are several local homeostatic responses within the lungs that minimize the mismatching of ventilation and blood flow and thereby maximize the efficiency of gas exchange. The net adaptive effects of vasoconstriction and bronchoconstriction are to – (1) supply less blood flow to poorly ventilated areas, thus diverting blood flow to well-ventilated areas; and – (2) redirect air away from diseased or damaged alveoli and toward healthy alveoli. – These factors greatly improve the efficiency of pulmonary gas exchange, but they are not perfect even in the healthy lung. – There is always a small mismatch of ventilation and perfusion, which, as just described, leads to the normal alveolar-arterial O2 gradient of about 5 mmHg.  Transport of Oxygen in Blood Each liter normally contains the number of oxygen molecules equivalent to 200 mL of pure gaseous oxygen at atmospheric pressure. The oxygen is present in two forms: – (1) dissolved in the plasma and erythrocyte cytosol and – (2) reversibly combined with hemoglobin molecules in the erythrocytes. As predicted by Henry’s law, the amount of oxygen dissolved in blood is directly proportional to the PO2 of the blood. hemoglobin can exist in one of two forms—deoxyhemoglobin ( Hb ) and oxyhemoglobin ( HbO 2 ). In a blood sample containing many hemoglobin molecules, the fraction of all the hemoglobin in the form of oxyhemoglobin is expressed as the percent hemoglobin saturation. The denominator in this equation is also termed the oxygen-carrying capacity of the blood.  Transport of Oxygen in Blood What factors determine the percent hemoglobin saturation? By far the most important is the blood PO2. However, it must be stressed that the total amount of oxygen carried by hemoglobin in the blood depends not only on the percent saturation of hemoglobin but also on how much hemoglobin is in each liter of blood. – A significant decrease in hemoglobin in the blood is called anemia. What Is the Effect of PO2 on Hemoglobin Saturation? It is evident that increasing the blood PO2 should increase the combination of oxygen with hemoglobin. The quantitative relationship between these variables is called an oxygen–hemoglobin dissociation curve.  Transport of Oxygen in Blood What Is the Effect of PO2 on Hemoglobin Saturation? We now retrace our steps and reconsider the movement of oxygen across the various membranes, this time including hemoglobin in our analysis.  Transport of Oxygen in Blood What Is the Effect of PO2 on Hemoglobin Saturation? Let us now apply this analysis to capillaries of the lungs and tissues.  Transport of Oxygen in Blood What Is the Effect of PO2 on Hemoglobin Saturation? Effect of Carbon Monoxide on Oxygen Binding to Hemoglobin Carbon monoxide is a colorless, odorless gas that is a product of the incomplete combustion of hydrocarbons, such as gasoline. – It is one of the more common causes of sickness and death due to poisoning, both intentional and accidental. – Its most striking pathophysiological characteristic is its extremely high affinity—210 times that of oxygen—for the oxygen-binding sites in hemoglobin. – For this reason, it reduces the amount of oxygen that combines with hemoglobin in pulmonary capillaries by competing for these sites. – It also exerts a second deleterious effect: It alters the hemoglobin molecule so as to shift the oxygen–hemoglobin dissociation curve to the left, thus decreasing the unloading of oxygen from hemoglobin in the tissues. – The situation is worsened by the fact that persons suffering from carbon monoxide poisoning do not show any reflex increase in their ventilation.  Transport of Oxygen in Blood Effects of CO 2 and Other Factors in the Blood and Different Isoforms on Hemoglobin Saturation Researchers are developing blood substitutes to meet the demand for emergency transfusions. What would be the effect of artificial blood in which binding of O 2 is not altered by acidity?  Transport of Carbon Dioxide in Blood Remember that CO 2 is a waste product that has toxicity in part because it generates H+.  Transport of Hydrogen Ion Between Tissues and Lungs As blood flows through the tissues, a fraction of oxyhemoglobin loses its oxygen to become deoxyhemoglobin, while simultaneously a large quantity of carbon dioxide enters the blood and undergoes the reactions that generate HCO3- and H+. What happens to this H1? Deoxyhemoglobin has a much greater affinity for H+ than does oxyhemoglobin, so it binds (buffers) most of the H+. When deoxyhemoglobin binds H, it is abbreviated HbH.  Control of Respiration The control of breathing at rest, altitude, and during and after exercise has intrigued physiologists for centuries. It is a wonderful example of several general principles of physiology, including how homeostasis is essential for health and survival, and how physiological functions are controlled by multiple regulatory systems, often working in opposition. Neural Generation of Rhythmic Breathing The diaphragm and intercostal muscles are skeletal muscles and therefore do not contract unless motor neurons stimulate them to do so. Thus, breathing depends entirely upon cyclical respiratory muscle excitation of the diaphragm and the intercostal muscles by their motor neurons. Destruction of these neurons or a disconnection between their origin in the brain stem and the respiratory muscles results in paralysis of the respiratory muscles and death, unless some form of artificial respiration can be instituted. Inspiration is initiated by a burst of action potentials in the spinal motor neurons to inspiratory muscles like the diaphragm. Then the action potentials cease, the inspiratory muscles relax, and expiration occurs as the elastic lungs recoil. In situations such as exercise when the contraction of expiratory muscles facilitates expiration, the neurons to these muscles, which were not active during inspiration, begin firing during expiration.  Control of Respiration Neural Generation of Rhythmic Breathing By what mechanism are impulses in the neurons innervating the respiratory muscles alternately increased and decreased? – The respiratory rhythm generator is located in the pre- Bötzinger complex of neurons in the upper part of the VRG – The medullary inspiratory neurons receive a rich synaptic input from neurons in various areas of the pons, the part of the brainstem just above the medulla. – Another cutoff signal for inspiration comes from pulmonary stretch receptors, which lie in the airway smooth muscle layer and are activated by a large lung inflation. This is called the Hering–Breuer reflex. – The arterial chemoreceptors also have important input to the respiratory control centers. – A final point about the medullary inspiratory neurons is that they are quite sensitive to inhibition by drugs such as barbiturates and morphine.  Control of Respiration Control of Ventilation by PO2, PCO2 , and H+ Concentration Several decades ago, removal of the carotid bodies was tried as a treatment for asthma. It was thought that it would reduce shortness of breath and airway hyperreactivity. What would be the effect of bilateral carotid body removal on someone taking a trip to the top of a mountain (an altitude of 3000 meters)?  Control of Respiration Control of Ventilation by PO2, PCO2 , and H+ Concentration Control by PO2  Control of Respiration Control of Ventilation by PO2, PCO2 , and H+ Concentration Control by PCO2  Control of Respiration Control of Ventilation by PO2, PCO2 , and H+ Concentration Control by Changes in Arterial H+ Concentration That Are Not Due to Changes in Carbon Dioxide  Control of Respiration Control of Ventilation by PO2, PCO2 , and H+ Concentration  Control of Respiration Control of Ventilation During Exercise During exercise, the alveolar ventilation may increase as much as 20-fold. On the basis of our three variables— PO2, PCO2, and H+ concentration—it may seem easy to explain the mechanism that induces this increased ventilation. This is not the case, however, and the major stimuli to ventilation during exercise, at least moderate exercise, remain unclear.  Control of Respiration Control of Ventilation During Exercise Other Factors A variety of other factors play some role in stimulating ventilation during exercise. These include: (1) reflex input from mechanoreceptors in joints and muscles, (2) an increase in body temperature, (3) inputs to the respiratory neurons via branches from axons descending from the brain to motor neurons supplying the exercising muscles (central command), (4) an increase in the plasma epinephrine concentration, (5) an increase in the plasma potassium concentration due to movement of potassium out of the exercising muscles, and (6) a conditioned (learned) response mediated by neural input to the respiratory centers.  Control of Respiration Control of Ventilation During Exercise The existence of chemoreceptors in the pulmonary artery has been suggested. Hypothesize a function for peripheral chemoreceptors located on and sensing the PO2 and PCO2 of the blood in the pulmonary artery.  Hypoxia Hypoxia is defined as a deficiency of oxygen at the tissue level. There are many potential causes of hypoxia, but they can be classified into four general categories: – (1) hypoxic hypoxia (also termed hypoxemia ), in which the arterial PO2 is reduced; – (2) anemic hypoxia or carbon monoxide hypoxia, in which the arterial PO2 is normal but the total oxygen content of the blood is reduced because of inadequate numbers of erythrocytes, deficient or abnormal hemoglobin, or competition for the hemoglobin molecule by carbon monoxide; – (3) ischemic hypoxia (also called hypoperfusion hypoxia ), in which blood flow to the tissues is too low; – (4) histotoxic hypoxia, in which the quantity of oxygen reaching the tissues is normal but the cell is unable to utilize the oxygen because a toxic agent— cyanide, for example— has interfered with the cell’s metabolic machinery.  Hypoxia Why Do Ventilation–Perfusion Abnormalities Affect O 2 More Than CO 2 ? Ventilation–perfusion inequalities often cause hypoxemia without associated increases in PCO2. The explanation for this resides in the fundamental difference between the transport of O 2 and the transport of CO 2 in the blood. An increase in PO2 above 100 mmHg does not add much oxygen to hemoglobin that is already almost 100% saturated. The situation for CO 2 , however, is very different. The CO 2 content curve is relatively linear because CO 2 is transported in the blood mainly as highly soluble HCO3- , which does not reach saturating levels at physiological concentrations. The net result, as blood mixes in the pulmonary vein in this case, is essentially normal arterial CO 2 content and PCO2. Thus, clinically significant ventilation–perfusion mismatching can lead to low arterial PO2 with normal PCO2.  Hypoxia Emphysema The pathophysiology of emphysema, a major cause of hypoxia, offers an instructive review of many basic principles of respiratory physiology. Emphysema is characterized by a loss of elastic tissue and the destruction of the alveolar walls leading to an increase in compliance. Acclimatization to High Altitude Atmospheric pressure progressively decreases as altitude increases. – Therefore, the alveolar and arterial PO2 must decrease as persons ascend unless they breathe pure oxygen. The effects of oxygen deprivation vary from one individual to another, but most people who ascend rapidly to altitudes above 10,000 ft experience some degree of mountain sickness (altitude sickness). Over the course of several days, the symptoms of mountain sickness usually disappear, although maximal physical capacity remains reduced. Acclimatization to high altitude is achieved by the compensatory mechanisms.  Non-respiratory Functions of the Lungs The lungs perform a variety of functions in addition to their roles in gas exchange and regulation of H+ concentration. Most notable are the influences they have on the arterial concentrations of a large number of biologically active substances. In contrast, the lungs may also produce new substances and add them to the blood. Finally, the lungs also act as a sieve that traps small blood clots generated in the systemic circulation, thereby preventing them from reaching the systemic arterial blood where they could occlude blood vessels in other organs.  Functions of the Respiratory System Conclusion – Provides oxygen – Eliminates carbon dioxide – Regulates the blood’s hydrogen ion concentration (pH) in coordination with the kidneys – Forms speech sounds (phonation) – Defends against microbes – Influences arterial concentrations of chemical messengers by removing some from pulmonary capillary blood and producing and adding others to this blood – Traps and dissolves blood clots arising from systemic veins such as those in the legs