Respiratory Super 7 List (1).docx

Respiratory Super 7 List Anatomy and Physiology Review function and lung anatomy; focus on pleura, lobes, major airways Nose: made of cartilage, bone, muscle and skin that supports and protects the anterior portion of the nasal cavity Nasal Cavity: hollow space within the nose and skull Lined wi...

Respiratory Super 7 List Anatomy and Physiology Review function and lung anatomy; focus on pleura, lobes, major airways Nose: made of cartilage, bone, muscle and skin that supports and protects the anterior portion of the nasal cavity Nasal Cavity: hollow space within the nose and skull Lined with hairs and mucus membrane Warm, moisturize and filters air Hairs and mucus lining trap dust, mold, pollen and other environmental contaminants Oral Cavity: can be used to supplement or replace the nasal cavity’s functions when needed Does not warm and moisturize the air entering the lungs as well as the nose The mouth also lacks the hairs and sticky mucus that filter air passing through the nasal cavity The one advantage of breathing through the mouth is that its shorter distance and larger diameter allows more air to quickly enter the body Paranasal Sinus: lightens skull and helps with drainage Pharynx: also known as the throat, is a muscular funnel that extends to the esophagus and larynx. The pharynx is divided into 3 regions: Nasopharynx (Pseudostratified columnar) Oropharynx (Protective stratified squamous epithelium) Laryngopharynx (Stratified squamous) Epiglottis: is a flap of elastic cartilage that acts as a switch between the trachea and the esophagus Ensures that air passes into the trachea by covering the opening to the esophagus During swallowing, the epiglottis moves to cover the trachea to ensure that food enters the esophagus and to prevent choking Larynx: voice box, air way and voice production (cartilage connected by membranes and ligaments) Inferior to the epiglottis is the thyroid cartilage, which is often referred to as the Adam’s Apple as it is most commonly enlarged and visible in adult males. The thyroid holds open the anterior end of the larynx and protects the vocal folds Thyroid cartilage is the ring-shaped cricoid cartilage, holds the larynx open, supports its posterior end In addition to cartilage, the larynx contains special structures known as vocal folds – produce the sound The vocal folds are folds of mucous membrane that vibrate to produce vocal sounds The tensions and vibration speed of the vocal folds can be changed to change the pitch that they produce Trachea: windpipe, long tube made of c-shaped hyaline cartilage Allows trachea to remain open to air Allows esophagus to expand for food moving through Epithelium lining produces mucus that traps dust and other contaminants and prevents it from reaching the lungs Cilia: on the surface of the epithelial cells, move the mucus superiorly towards the pharynx where it can be swallowed and digested in the gastrointestinal tract Bronchus: left and right, known as the primary bronchi Primary bronchi contain many c-shaped cartilage rings, firmly hold the airway open and give the bronchi a cross-sectional shape Secondary bronchi carry air into the lobes Split into many smaller tertiary bronchi within each lobe As the bronchi branch into secondary and tertiary bronchi, the cartilage becomes more widely spaced and more smooth muscle and elastin protein is found in the walls Tertiary bronchi split into many smaller bronchioles Terminal bronchioles (millions) conduct air to the alveoli of the lungs Bronchioles no cartilage Smooth muscles and elastin – more flexible and contractile Have mucus and cilia of their epithelial lining to trap and move dust and other contaminants away from the lungs Lungs: Left and right lungs are slightly different in size and shape due to the heart Left slightly smaller – 2 lobes, oblique fissure b/w superior & inferior Right- 3 lobes, Oblique & horizontal (superior of the two) The interior of the lungs is made up of spongy tissues containing many capillaries and millions of tiny sacs known as alveoli. Alveoli are cup-shaped structures found at the end of the terminal bronchioles, surrounded by capillaries. Thin simple squamous epithelium that allows air entering the alveoli to exchange its gases with the blood passing through the capillaries. Lobes: divided by fissures – 2 in left, 3 in right Lobules: approx. size of penny, large bronchiole & branches serve each lobule Bronchopulmonary segments – separated by connective tissue Rt = 10, Lt = 8-10. Have own artery & veins & segmental bronchus ***Important – confines diseased lung to compartments. Pleura: known as pleural membrane made up of two layers of serous membrane; allow sliding & resists separation with negative pressure. Visceral Pleura: covers the lungs Parietal Pleura: lines the thoracic cavity Pleural Cavity: contains lubricating serous fluid that decreases friction Anatomical and histological differences between types of airways Two types of airway structures and two zones. Upper Respiratory System: nose-pharynx and associated structures Lower Respiratory System: larynx, trachea, bronchi and lungs Conducting Zone: interconnecting cavities and tubes in & outside lungs; nose – terminal bronchioles that filter, warm and moisten air and conduct it to the lungs. As a result, air reaching lungs has less irritants, is warm and damp. Respiratory Zone: consist of tissues within the lung’s bronchioles, alveolar ducts and microscopic alveoli, Site of where gas exchange occurs between the air and the blood. Lung ventilation: how does it happen? Think pressures and Gas laws!! Pulmonary Ventilation: Inspiration & expiration, mechanical process depends on volume change in thoracic cavity. Volume change leads to pressure change to flow of gases. Air molecules in constant friction with one another cause pressure. Decrease pressure, increase volume Inspiration: muscles contract, diaphragm descends, rib cage rises Thoracic cavity volume increases Lungs are stretched – intrapulmonary volume increases and pressure drops (to -1mmHg) Air (gases) flow into lungs down its pressure gradient until intrapulmonary pressure is zero and equal to atmospheric pressure Expiration: Inspiratory muscles relax – diaphragm rises, rib cage descends due to recoil of costal cartilages Thoracic cavity volume decreases Elasticity of lungs recoil passively – intrapulmonary volume decreases Intrapulmonary pressure rises (to =1mmHg) Air (gases) flow out of lungs down its pressure gradient until intrapulmonary pressure is zero Bronchial circuit: Increased pressure, decreased volume Atmospheric pressure (Patm): outside, @ sea level 760mmHG = 1 atmospheric unit or 1 atm Respiratory pressure: always associated with Atmospheric pressure (Patm) – pressure exerted by the air (gases) surrounding the body. Negative respiratory pressure: pressure in region is lower than Patm Intrapulmonary pressure (Ppul): pressure in alveoli Intrapleural pressure (Pip): always negative relative to Ppul Transpulmonary pressure: difference between the two (Ppul – Pip) Boyles Law: Relationship between pressure and volume of gases, P1V2 = P2V2; P = pressure, V = volume, 1&2 = initial & resulting conditions. Decrease volume = increase pressure Daltons Law: The pressure exerted by each gas – its PARTIAL PRESSURE is directly proportional to the percentage of that gas in the gas mixture Henry: When gas is in contact with a liquid, the gas will dissolve in the liquid proportion to its partial pressure. Accordingly, the greater the concentration of a particular gas in the gas phase, the more and the faster that gas will go into solution in the liquid Amount of gas that will dissolve in a liquid depends on: The partial pressure of the gas in contact with the liquid The solubility of the gas in the liquid The temperature of the liquid LaPlace: addresses surface tension – surfactant decrease tension Lung volumes: remember those definitions and what they mean Lung Volumes: Tidal: amount of air inhaled and exhaled with each breath Inspiratory Reserve (IRV): amount of air that can be forcefully inhaled after normal TV inspiration Expiratory Reserve (ERV): amount of air that can be forcefully exhaled after normal TV expiration Residual Volume (RV): amount of air remaining in the lungs after a force expiration Respiratory Capacity (RC): include functional, residual, vita, and total lung capacities. Always consists of 2 or more lung volumes Total Lung Capacity (TLC): max amt. of air contained in lungs after a max inspiratory effort: TV + IRV + ERV Inspiratory Capacity (IC): max amt. of air that can be inspired after normal TV expiration – IC=TV+IRV Functional Residual Capacity (FRC): volume of air remaining in lungs after a normal TV expiration. FRC = ERV+RV Alveolar Dead Space: The sum of the non-useful volumes. Some alveoli cease to act in gas exchange – due to collapse or obstruction by mucous. Anatomical Dead Space: some are inspired filles conducting respiratory passageways and never contributes to gas exchange in the alveoli. The volume of these conducting conduits, make up the anatomical dead space FiO2 = fraction of inspired O2 Pulmonary Function Test: forced vital capacity, forced expiratory volume Minute ventilation: total gas flows in & out in 1 minutes Alveolar ventilation: measures flow of fresh gases in & out of alveoli during a particular time interval. Factors regulating lung recoil: compliance, elasticity and surface tension Compliance – ability to stretch out Increased – COPD/Emphysema, Age Decreased – Tension (pneumo – air pulmonary fibrosis, increased abd. Pressure) Elasticity – ability to come back/with elastin energy Recoil Surface Tension – attraction b/w H20 molecules – resists lung distention Muscle contraction: requires energy = ATP Surface tension 101 and role of surfactant: reduces surface tension, attraction b/w H20 molecules at an air water surface which draws water molecules closer together (i.e. two wet glass slides stuck together…hard to separate with pressure resistance. Force acting to resist lung distension Lung ventilation: how is it regulated? Role of the neurological system? Control of ventilation Lung Contraction: diaphragm flattens (inhalation), lungs expand, less pressure in lungs therefore air enters Relaxation: diaphragm returns to arch position (exhalation), pressure less outside of lung, air moves out. Alveoli: takes up 75sq meters (200-300 alveoli) Muscles involved: 1 - Diaphragm 2 - External intercostal (quiet exhalation 1&2 relax) 3 - Internal intercostal (quiet inhalation 1 & 2 relax) 4 - Sternocleidomastoid (forceful exhalation, labored inhalation) 5 - Abdominal – 5&3 contract Respiratory Centre: medullary smooth rhythmicity respirations, area in medullar oblongata Functions both inspiratory & expiratory Ventral Respiratory Group (VRG) – groups of neurons that fire during inspiration and expiration Dorsal Respiratory Groups (DRG) – peripheral sensory input then modifies VRG Pons: Upper – Pneumotaxic - prevents over inspiration Lower – Apneustic – prevents stopping Theory for respiratory rhythm: Reciprocal inhibition of interconnected neuronal network in medulla 2 sets inhibit each other Factors: Rising CO2 is most powerful stimulant Higher brain centers (cerebral cortex) Increase/Decrease +/- effect – voluntary control – involuntary reflexes Role – adjust depth & rate of ventilation – during normal breathing and increased demands, increased talking Hypothalamus - pain or emotional +/- effect Chemoreceptors: negative feedback – sensory receptors Central: in medulla oblongata Brain Stem = central chemoreceptors – increase CO2, Increase H+ = +effect Peripheral: Aortic & main carotid bodies = chemoreceptors – decrease O2, increase CO2, Increase H+, +effect Proprioceptors: Muscles & joints (increased use) = proprioceptors, + effect Cell Respirations Anatomy of fetal circulation: before and after birth The umbilical vessels as well as the liver and lung bypasses are occluded. Development of the fetal circulation By the end of week 3 the embryo has a system of paired blood vessels, and the two vessels forming the heart have bent into an “S” shape By 3 ½ weeks the miniature heart is pumping blood for an embryo less than a ¼ inch long. Unique cardiovascular modifications seen only during prenatal development include the umbilical arteries and vein and 3 vascular shunts All of these structures are occluded at birth NOTE: keep in mind blood is flowing from and to the fetal heart BUT 02, C02, nutrition and waste exchanges occur at the placenta. The large umbilical vein carries freshly oxygenated blood returning from the placenta into the embryonic body, where it is conveyed to the liver Most of the blood coursing through the umbilical vein enters the ductus venosus – a venous shunt that bypasses the liver sinusoids Both hepatic veins and ductus venosus empty into the inferior vena cava this is where placental blood mixes with deoxygenated blood from the lower parts of fetus’ body - this mixed blood goes directly to the right atrium of the heart Blood flow through the fetal liver is only enough to keep the liver cells healthy, moms body does all the nutrient processing for the fetus Blood in and out of the heart go through two more shunt systems, each allowing to bypass the non-functional lungs Some blood entering the right atrium flows directly into the left atrium through the foramen ovale (oval hole) - hole in the interatrial septum – loosely closed by a flap of tissue. blood that enters the right ventricle is pumped out into the pulmonary trunk The ductus arteriosus transfers most of the blood directly into the aorta, again bypassing the pulmonary circuit (lungs do receive adequate oxygen to facilitate growth) Blood enters the two pulmonary bypass shunts due to the heart vessel/chamber being lower-pressure areas Blood flowing distally through the aorta eventually reaches the umbilical arteries. The deoxygenated blood with metabolic wastes is delivered from here back to the capillaries in the chorionic villi of the placenta Circulation in Fetus and Newborns The umbilical vein carries oxygen and nutrient rich blood from the placenta to the fetus The umbilical arteries carry waste-filled blood from the fetus to the placenta The ductus arteriosus and foramen ovale bypass the non-functional lungs Most of the blood passing through the foramen ovale comes from the inferior vena cava, the ductus venosus allows blood to partially bypass the liver Differences and similarities between fetal and adult hemoglobin The fetus forms a unique hemoglobin, which is hemoglobin F, that has a higher affinity of for O2 than does adult hemoglobin (Hb A). This will enable the fetus to effectively transfer blood from the mother to its self. A fetal hemoglobin contains 2 alpha and 2 gamma subunits polypeptide chains per globin molecule, as opposed to 2 alpha and 2 beta subunits in adult Hb. This difference is important because the beta subunits have 6 positively charged amino acids which attract 2-3 BPG. RBC produce 2-3 BPG as they metabolize glucose and it has a high negative charge. Therefore, the strong positive charge from the 6 amino acids forming a pocket from the beta subunits attracts 2-3 BPG, which results in a decrease in affinity for oxygen. Gamma subunits have a decrease in positive charge only having 4 amino acids, so BPG doesn’t bind as well, therefore increasing the affinity of oxygen. This shifts the oxy-hemoglobin disassociation curve to the left, meaning that at a lower PO2 level the O2 saturation is relatively high. This is important for a fetus because by the time the oxygen reaches the placenta the PO2 decreases so the fetus needs to be able to effectively saturate its hemoglobin for oxygen delivery. Physiology of alveolar gas exchange (pressure) and alveolar wall structure Alveoli are the main site of gas exchange, intimately associated with pulmonary capillaries The respiratory bronchioles lead into the alveolar ducts (smooth muscle, connective tissue fiber) and out pocketing the alveoli The alveolar ducts lead to clusters of alveoli called alveolar sacs. The alveoli are composed of a single layer of squamous epithelial cells called type one alveolar cells, a very flimsy membrane Amongst the type 1 alveolar cells, cuboidal type 2 alveolar cells secrete surfactant that coats gas-exposed alveolar surfaces Surfactant also reduces surface tension and contains antimicrobial proteins that contribute to innate immunity When alveolar pores are open, it equalizes air pressure allowing alternate air routes to collapsed alveoli due to disease The partial pressure of oxygen (O2) and carbon dioxide (CO2) drive the diffusion of these gasses across the respiratory membrane These pressures easily changed by increasing breathing depth and rate Alveolar Ventilation Rate is a better index of effective ventilation In healthy people AVR is usually about 12 breaths per minute Gas exchange occurs due to a steep O2 partial pressure exists in the alveoli causing O2 to diffuse rapidly from the alveoli into the pulmonary capillaries Carbon dioxide diffuses in the opposite direction in a less intense partial pressure gradient, expelling carbon dioxide from the alveoli It is harder to breath (with adequate oxygen exchange) at high altitudes because the partial pressure of oxygen (Po2) and atmospheric pressure are lower. Partial pressure declines in direct proportion to the decrease in atmospheric pressure Alveolar Sacs - are the complete bundle but alveoli are each individual bulbs where the gas exchange occurs Ventilation/Perfusion Ratio: What is it? What does it mean? For optimal gas exchange, there must be a close match between ventilation and perfusion. Ventilation = [tidal volume (500 ml) - dead space (150 ml)] x RR = 4200 ml/min Perfusion (pulmonary capillaries) = Cardiac output (SV x HR) = 5000 ml/min Ratio = 4000/5000 = 0.8 (they take 4000 vs. 4200 for easier math) Apex of lung = increase ventilation (less compliant) and decreased perfusion (gravity) Base of lung = decrease ventilation (more compliant) and increased perfusion Both perfusion and ventilation are controlled by autoregulatory mechanisms that continuously respond to local conditions. The two mechanisms are shown below PCO2 controls ventilation by changing bronchiolar diameter Increase in diameter of blood vessel = decrease resistance to bronchiolar (and vice versa). Example of decrease in resistance would result from exercise and will allow more flow of oxygen and carbon dioxide. An example of increase in resistance could be right-sided heart failure or pulmonary embolism. When the resistance becomes greater in the alveoli with the affected blood vessel it will redirect the blood to other alveoli PO2 controls perfusion by changing arteriolar diameter Oxygen diffuses from endothelial cells into the smooth muscle cells, nitric oxide is produced, then potassium leaves the cell hyperpolarizing it, which in turn vasodilates the blood vessel (from the video). Therefore, increase in ventilation increases perfusion and increases the ratio, and vice versa Transport of oxygen/carbon dioxide in blood: role of hemoglobin, pressures and bicarbonate Oxygen is carried in blood in two ways: bound to hemoglobin within RBC and dissolved in plasma. O2 is not soluble in water well and doesn’t get transported in adequate amounts without the help of hemoglobin Hemoglobin solves this problem by 98.5% of the oxygen is carried from lungs to tissues in a loose chemical combination Hemoglobin is composed of 4 polypeptide chains, bound to an iron-containing heme group. Iron atoms bind oxygen, so each hemoglobin molecule can combine with four molecules of O2 and oxygen loading is rapid and reversible The hemoglobin- oxygen combination, called oxyhemoglobin, is written HbO2. Hemoglobin that has released oxygen is called reduced hemoglobin, or deoxyhemoglobin, and is written HHb. A single reversible equation describes the loading and unloading of O2: After the first O2 molecule binds to iron, the Hb molecule changes shape. When 1,2, or 3 oxygen molecules are bound, a hemoglobin molecule is partially saturated, and when all four of its heme groups are bound to O2, the hemoglobin is fully saturated The unloading of one Oxygen molecule enhances the unloading of the next. This way the affinity (binding strength) of hemoglobin for oxygen changes with the extent of oxygen saturation, and both loading and unloading of oxygen are very efficient The rate at which Hb reversibly binds or releases O2 is regulated by PO2, temperature, blood pH, PcO2, and blood concentration of a chemical called BPG. These factors interact to ensure that adequate oxygen is delivered to tissue cells Carbon Dioxide Transport Active body cells normally produce 200ml of Co2 each minute and the lungs excrete the exact amount Blood transports Co2 from the tissue cells to the lungs in 3 forms: Dissolved in plasma Chemically bound to hemoglobin (dissolved Co2, is bound and carried in the RBCs as carbaminohemoglobin) CO2 + Hb HbCo2 (carbaminohemoglobin) Carbon dioxide transport in RBCs does not compete with oxyhemoglobin transport because carbon dioxide binds directly to amino acids of globin Co2 loading and unloading are directly influenced by the PCO2 and the degree of Hb oxygenation Carbon dioxide readily binds with hemoglobin in the tissues where the PCo2 of alveolar air is lower than that in blood Bicarbonate ions in plasma Most carbon dioxide molecules entering the plasma quickly enter RBCs the reactions that convert carbon dioxide to bicarbonate ions (HCO3) for transport mostly occur inside RBCs. When dissolved CO2 diffuses into RBCs it combines with water, forming carbonic acid (H2CO3). This is unstable and dissociates into hydrogen ions and bicarbonate ions: C02 + H20 H2CO3 H+ + HCO3 This reaction is fast because of the carbonic anhydrase, an enzyme that reversibly catalyzes the conversion of carbon dioxide and water to carbonic acid. HALDANE EFFECT – reflects the greater ability of reduced hemoglobin to form carbaminohemoglobin and to buffer H + by combining with it. Oxyhemoglobin dissociation curve: what is it? what does it mean? why is it important? The oxyhemoglobin depicts the properties of hemoglobin (Hb) and how it affects the binding of oxygen in the lungs and oxygen release in the tissues. Hb is composed of four polypeptide chains, each bound to an iron-containing heme group. Because the iron atoms bind oxygen, each Hb molecule can combine with four molecules of O2, and oxygen loading is rapid and reversible. The hemoglobin-oxygen combination, called oxyhemoglobin, is written HbO2. Hemoglobin that has released oxygen is called reduced hemoglobin, or deoxyhemoglobin, and is written HHb. A single reversible equation describes the loading and unloading of O2: After the first O2 molecule binds to iron, the Hb molecule changes shape. As a result, it more readily takes up two more O2 molecules, and uptake of the fourth is even more facilitated. When one, two, or three oxygen molecules are bound, a hemoglobin molecule is partially saturated. When all four of its heme groups are bound to O2, the hemoglobin is fully saturated. By the same token, unloading of one oxygen molecule enhances the unloading of the next, and so on. In this way, the affinity (binding strength) of hemoglobin for oxygen changes with the extent of oxygen saturation, and both loading and unloading of oxygen are very efficient. The rate at which Hb reversibly binds or releases O2 is regulated by: PO2, temperature Blood pH PCO2 blood concentration of an organic chemical called BPG (RBC produce BPG via metabolism of glucose; BPG binds reversibly with Hb and levels rise when O2 levels are chronically low) These factors interact to ensure that adequate O2 is delivered to tissue cells. All of these factors influence Hb saturation by modifying hemoglobin’s three-dimensional structure, thereby changing its affinity for O2. An increase in temperature, PCO2, H+, or BPG levels in blood lowers Hb’s affinity for O2, enhancing oxygen unloading from the blood. This is shown by the rightward shift of the oxygen-hemoglobin dissociation curve. Conversely, a decrease in any of these factors increases hemoglobin’s affinity for oxygen, decreasing oxygen unloading. This change shifts the dissociation curve to the left. If you give a little thought to how these factors are related, you’ll realize that they all tend to be highest in the systemic capillaries, where oxygen unloading is the goal. As cells metabolize glucose and use O2, they release CO2, which increases the PCO2 and H+ levels in capillary blood. Both declining blood pH (acidosis) and increasing PCO2 weaken the Hb-O2 bond, a phenomenon called the Bohr effect. This enhances oxygen unloading where it is most needed. Heat is a by-product of metabolic activity, and active tissues are warmer than less active ones. A rise in temperature decreases hemoglobin’s affinity for O2 both directly and indirectly (via its influence on RBC metabolism and BPG synthesis). Collectively, these factors see to it that Hb unloads much more O2 in the vicinity of hard-working tissue cells. Pulmonary circulation and regulation of blood flow