Module 9 Pulmonary PDF

1 The primary function of the pulmonary system is the exchange of gases between the environmental air and the blood. Three steps are involved in this process: 1. ventilation (the movement of air into and out of the lungs) 2. diffusion (the movement of gases between air spaces in the l...

1 The primary function of the pulmonary system is the exchange of gases between the environmental air and the blood. Three steps are involved in this process: 1. ventilation (the movement of air into and out of the lungs) 2. diffusion (the movement of gases between air spaces in the lungs and the bloodstream) 3. perfusion (movement of blood into and out of the capillary beds of the lungs to the body organ and tissues)  this requires an intact cardiovascular system 2 To carry out these functions the pulmonary system is made up of: A set of conducting airways (upper and lower) deliver air to each section of the lung  provide a passage for movement of air into and out of the gas- exchange portion of the lungs Upper conducting airways consists of nasopharynx and oropharynx which also help filter and moisturize the air that is inhaled Larynx connects upper and lower airways  it’s supporting cartilage prevent collapse of larynx during inspiration and expiration and swallowing Lower conducting airways begin at the level of the trachea connects larynx to bronchi and then divides into the two main airways (or bronchi) 3 There is continued branching of the conducting airways  known as generations  at the end of the 16th division is the smallest of the conducting airways…known as the terminal bronchioles. Remember, no gas exchange occurs in the conducting airways. From the terminal bronchioles there is continued divisions of respiratory bronchioles to the alveolar ducts. Gas exchange is possible starting at the level of the respiratory bronchioles but the primary gas exchange units of the lung are the aveoli. 4 The alveoli are the primary gas-exchange units of the lung where oxygen enters the blood and CO2 is removed. The lung contains ~ 25 million alveoli at birth & 300 million by adulthood. There are two major type of epithelial cells that appear in alveolus: Type I provide structure (elastin) Type II  secrete surfactant, a lipoprotein that coats the inner surface of the alveoli. This facilitates expansion of the alveoli during inspiration and allows for establishment of FRC (functional residual capacity) The alveoli also contain Alveolar macrophages  ingest foreign material that reaches the alveolus & prepare it for removal through the lymphatics 5 Pulmonary Circulation facilitates: Gas exchange Delivers nutrients to lungs Acts as a reservoir for the left ventricle (everything that the lungs sees the left ventricle will see) Serves as filtering system that removes clots, air, debris from circulation Pulmonary circulation participates in gas exchange and entire cardiac output from right ventricle goes into lungs… but…pulmonary circulation has lower pressure & resistance than systemic circulation. Mean pulmonary artery pressure is 18 mmHg…mean aortic is 90 mmHg. FYI: the bronchial circulation is part of the systemic circulation supplying nutrients to conducting airways, nerves, lymph nodes, large pulmonary vessels and membranes…and does not participate in gas exchange. 6 The shared alveolar and capillary walls compose the alveolo-capillary membrane (also referred to as the respiratory membrane). Gas exchange occurs over this membrane. Any disorder that thickens the membrane impairs gas exchange (examples would include interstitial edema, pulmonary edema, fibrosis). 7 So, there are four major factors that determine how rapidly a gas (O2 or CO2) will pass thru the membrane are: 1). Thickness of membrane  will increase d/t edema in the interstitial space or in the alveoli. Gasses now not only have to diffuse thru membrane but also thru the fluid. Pulmonary diseases that cause fibrosis of the lungs are another example of a disorder that increase thickness of membranes thereby affecting the diffusion of gases across the membrane. 2). Surface area of membrane  refers to the expanse of alveolar and capillary membranes available for gas exchange. Surface are is normally high in the lungs. But, it can be decreased by many conditions, for example in emphysema many of the alveoli coalesce with dissolution of alveolar walls. The new chambers are much larger than original alveoli but the total surface area of the respiratory membrane is decreased as much as fivefold with loss of the alveolar walls. 3). Diffusion coefficient of the gas  depends on its solubility in the membrane Carbon dioxide diffuses thru the membrane about 20 times as rapidly as oxygen Oxygen diffuses about twice as rapidly as nitrogen 4). Pressure difference between the two sides of the membrane  is the difference between the partial pressure of the gas in the alveoli and the pressure of the gas in the blood. Gases will move from areas of higher to lower concentration …so as alveolar oxygen concentration reflects atmospheric oxygen and pulmonary capillary oxygen concentration reflects the oxygen concentration of the systemic venous blood (which has a low oxygen concentration as much of the oxygen has been used by the cells of the body), oxygen will move for the alveolar to the pulmonary side. 8 When looking at the functional component of the respiratory system we initially said it dealt with ventilation. What is the ventilation and what are some factors that affect ventilation? Ventilation  is just the mechanical movement of gas (air) into & out of lung. ventilation is often misnamed (or used interchangeably) with the term “respiration” but, in physiology respiration refers to the diffusion of gases between an alveolus and the capillary which perfuses it so, when we count someone’s respirations we’re actually looking at their ventilation Alveolar ventilation  can not be determined by observation of vent rate, pattern or effort. An arterial blood gas analysis must be performed to measure PaCO2 9 Ventilation is controlled by the respiratory center in the lower brain stem  control respiration thru the transmission of impulses to the respiratory muscles based on combination information of peripheral chemoreceptors and several receptors in the lung. What’s the difference and how do they function…next slide. 10 Lung receptors  three types of lung receptors send impulses from the lungs to the dorsal respiratory group (neurons located in the brain stem): 1). Irritant receptors Found on epithelium of the conducting airways Sensitive to noxious stimuli (pollens, smoke, perfume, etc). Ever stand behind an elderly woman at the grocery store who’s spritzed herself with an entire bottle of perfume and you start coughing  well, your irritant receptors have been stimulated. Initiate cough reflex, increase respiratory rate in attempts to protect and rid the body of the noxious stimuli Cause bronchoconstriction  as a protective mechanism trying to prevent the irritant from going into the respiratory track (however, bronchoconstriction causes problem in itself  2). Stretch receptors Are located in smooth muscles of airways Sensitive to increases in size and volume of lungs When stimulated they decrease the rate and volume (amount) of air inhaled known as Hering-Breuer expiratory reflex, a protective mechanism to protect against excess lung inflation (reflex active only at high tidal volumes) 3). J-receptors (juxtapulmonary capillary receptors) Located on alveolar capillaries 11  Sensitive to increases pulmonary capillary pressure – basically they are sensing “blood pressure” within the pulmonary circulation Stimulates lungs to initiate rapid, shallow respiration  why? What’s the purpose?  think – what happens to CO2 when you breathe rapid, shallow respirations  it decreases  what happens to pH when CO2 decreases?  pH increases (causing an alkalosis)…so… Alkalosis induces pulmonary vasculature dilation  leading to a decrease in pulmonary pressure 11 Central chemoreceptors in the brain respond to changes in the hydrogen ion concentration of the CSF. They monitor the arterial blood indirectly by sensing the pHof the cerebrospinal fluid. They are located in the respiratory center (in the medulla) & are very sensitive to small changes in the pH of CSF. Hydrogen ion concentration usually reflects carbon dioxide concentration Therefore, when CO2 levels rise, hydrogen ions rise, stimulating an increase in respiratory rate & then when CO2 levels and H+ ions decrease the respiration slows (see the critical thinking activity) Peripheral chemoreceptors are located in aortic bodies, the aortic arch & carotids. They are primarily sensitive to changes in pO2. Have to drop to below pO2 60 before they “kick-in” and increase respiratory rate in attempts to bring in more O2. 12 Alveolar ventilation (or distension) is made possible by surfactant by lowering surface tension. Surface tension refers to the tendency of water molecules to pull toward each other and to collapse a sphere. Because each alveolus is lined with a thin water layer, this increases surface tension… because of surface tension, the net tendency of the lung is to reduce the alveolar surface to its minimum area  in other words to collapse the alveoli. The mechanism to reduce surface tension is the role of surfactant. It acts by forming a monomolecular layer @ the interface between the fluid lining the alveoli & air in the alveoli. Surfactant’s primary function is to stabilize the alveoli at low lung volumes on expiration so that alveolar collapse does not occur. It’s ability to do this is known as…alveolar stability also called functional residual capacity (FRC) Basically on expiration there is also a little amount of air that is still present in the alveoli so the alveoli does not collapse completely and the alveoli is easy to open with the next breath. Think of it as blowing up a balloon –a new balloon is completely collapsed and you have to take a good breath to start to inflate it – but once you get that initial air in the balloon – subsequent breathes are easier to inflate balloon. That little bit of air in there initially is FRC and surfactant prevents the alveoli from collapsing completely so that each of our subsequent breathes are easy. 13 Surfactant also prevents high surface tension pulmonary edema from developing. And, it has a role in host defense – some of the proteins that make up surfactant bind to bacteria and then “present” them to the alveolar macrophages for removal. 13 Properties of lung and chest wall also influence ventilation: Compliance  measure of lung and chest wall distensibility. It is the ease in which these structures can be stretched and is determined by alveolar surface tension and elastic recoil of the lung & chest wall. Increased compliance lungs or chest wall is abnormally easy to inflate & has lost some elastic recoil. This is seen in emphysema, resulting in chronic overinflation of the lungs Decreased compliance  lungs stiff or difficult to inflate. Decreased compliance can be seen in pneumonia, edema, fibrosis, or adult respiratory distress syndrome (ARDS) 14 Many of the pulmonary diseases that our patients exhibit result in hypoxia and/or hypoxemia hypoxia is reduced oxygenation of cells in tissues hypoxemia is reduced oxygenation of arterial blood There are many causes of hypoxemia, such as: Inadequate oxygenation of lungs due to extrinsic reasons (high altitudes, hypoventilationneuromuscular disorders) Pulmonary disease (hypoventilation, abnormal V/Q) Shunting of blood Inadequate oxygen transport by blood to tissues (anemias, abnl hgb, tissue edema) Inadequate tissue capability of using oxygen (poisoning –cyanide; vitamin deficiencies) An abnormal V/Q (ventilation-perfusion) ratio is the most common cause of hypoxemia Ventilation refers to air moving into and out of the lungs Perfusion is the blood passing through the pulmonary circulation to be oxygenated The ventilation-perfusion ratio, the V/Q, is the ration of airflow into the lungs divided by the pulmoanry blood flow. A decreased (or low) V/Q may occur when delivery of air to some alveoli is obstructed (for example, with mucus or alveoli may collapse d/t atelectasis)… so the blood flowing past these underventilated alveoli will not be oxygenated Sometimes you can see high V/Q – alveoli (ventilation) is normal but capillary perfusion is compromised. Examples of this can be pulmonary embolus. A myocardial infarct would also cause decreased perfusion of the alveoli. 15 When evaluating pulmonary diseases … they can be placed into two major patterns Obstructive patterns Restrictive patterns 16 Fundamental physiologic problem in obstructive diseases is increased resistance to airflow as a result of caliber reduction in conducting airways. Obstruction is worse with expiration with dyspnea & wheezing as the most common signs and symptoms Examples of common obstructive disorders are: Asthma Emphysema Chronic bronchitis Individuals who have long-standing emphysema also usually have chronic bronchitis and demonstrate indications of both diseases. This condition is referred to as COPD (chronic obstructive pulmonary disease). Chronic asthma in association with either emphysema or chronic bronchitis may also result in COPD. 17 Hallmark of obstructive disease is decreased in expiratory flow rate. Fundamental physiologic problem in obstructive diseases is increased resistance to airflow as a result of caliber reduction in conducting airways. This increased resistance can be caused by processes within: Lumen  luminal obstruction are increased secretions seen in asthma & chronic bronchitis Airway wall airway wall thickening & narrowing can result from the inflammation seen in both asthma & bronchitis. Also, the bronchial smooth muscle contraction in asthma narrows the airway increasing resistance Supporting structures surrounding the airways emphysema is the classic example of obstruction d/t loss of support from the destruction of lung elastic tissue In obstructive disease total lung capacity (TLC) is normal or increased  maximum volume to which the lungs can be expanded (can get air in – can’t get it out) RV (volume of air remaining in lungs after most forceful expiration) is elevated due to trapping of air during expiration 18 Asthma is an obstructive alteration characterized by spastic contraction of smooth muscle of bronchioles. Reported to occur in 3 – 5 % of all people at some time in their life. Usual cause is hypersensitivity of bronchioles to foreign substances in the air: in younger patients (