Respiratory System .pdf

5 functions of the respiratory system • gas exchange -between atmosphere & blood • Homeostatic regulation of pH - equilibrium >keep us healthy & have a lot of buffer • Protection from pathogens • Vocalization -air moving across vocal cords >speech singing communication Thoracic movement at Inspirat...

5 functions of the respiratory system • gas exchange -between atmosphere & blood • Homeostatic regulation of pH - equilibrium >keep us healthy & have a lot of buffer • Protection from pathogens • Vocalization -air moving across vocal cords >speech singing communication Thoracic movement at Inspiration • rib cage elevation Upper ribs • pump handle movement • Anterior & posterior movement Lower Ribs • bucket handle movement • Transverse movement inspiration (breathe in) • need muscles, breathing in is forceful • diaphragm -contraction initiates the breath -without diaphragm breath would be 40% less than normal • external intercostals Accessory muscles needed when SOB • SCM, scalene, traps, pecs, SA, rhomboid, subclavian • Needed to elevate ribs higher Accessory muscles needed when extreme SOB • erector spinae, lats, serratus posterior • Activated if regular accessory msucles need extra help EXPIRATION (breathe out) • passive recoil, only need muscles when force exhaling • forced exhalation; produce quicker/fuller exhalation • Internal intercostal - pull ribs down. • Rectus/transverse abdominis, external/ internal obliques - compress abdomen & push diaphragm up • • • • • • Angle of Louis “Sternal Angle” (2nd rib) where bone is fused (sternum) located at T4/T5 (posteriorly) Where lung & heart auscultation occurs the level of bifurcation of the trachea - into R & L mainstem bronchi -intubation stops right before bifurcation marks the upper Margin of heart Marks the beginning & end of aortic arch Lungs • light spongy tissue - suck in air & fluid • Mostly air-filled • cone shaped • R side larger than Left -heart on left side Apex: top of lung Base: where lung sits on diaphragm Surfaces: costal (by ribs) medial (touch heart) diaphragmatic (sit on diaphragm) Hilum: point where mainstem bronchi penetrate parenchyma Roots: suspend the lungs LUNG LOBES True Ribs: 1-7 • Vertebrosternal ribs -vertebrae to sternum False ribs 8-12 • Vertebrochrondral ribs -vertebrae to cartilage -ribs 8-10 • floating ribs (vertebral) -ribs 11-12 -not attached to sternum Suprasternal notch (jugular notch) • superior border of sternum Manubriumxiphoid joint • joint from manubrium to xhiphoid” Baseline is important because it tells us what is abnormal when pathologies occur WhEn short of breath you want to increase respiratory rate (activating the forced exhalators internal intercostals) Damage to the muscles or innervation of respiration will cause a lower respiratory volume If I don't empty out enough air when Upper Lobe: SOB there's no room for new oxygen • starts: above the clavicle (apex) to come in • ends: 4th rib next to sternum T3 Respiratory muscles never fully shut posteriorly down because you never stop Horizontal fissure breathing • RIGHT SIDE • Slanted downward toward 5th rib @ If one lung is out of commission it can affect lung volume especially if its the midaxillary line right lung • Between upper & middle lobe Middle Lobe If pleurae wasn't lubricated it would • ONLY ON RIGHT SIDE (traingular) hurt (friction) to breathe • starts: under upper lobe at No cartilage in back of throat because • ends: 6th rib midclavicular anteriorly cartilage on esophagus would make it hard to swallow & 5th rib laterally midaxillary • cartilage in front (trachea) for Lower Lobe support • look at from back Tracheostomy will go in • From T3-T10 posteriorly below cricoid cartilage • Lateral basal wraps to anterior basal Collagen=cartilage • • • • • • • Pleurae double-walled continuous sac (ziploc bag) Contains fluid to lubricate lungs/pleurae - holds lungs in partially inflated state - moist for membrane to slide across eachother visceral pleurae: on Lungs Parietal pleurae: touch outside mediastinum -separates one lung from another -helps contain infection intrapleural pressure maintains lung inflation Pleural cavities contain each lung -in between pleural & visceral cavity Tracheobronchial Tree • widest at top & more structured -1 in. at trachea & more cartilage • cartilage disappears at bronchiolar level - c-shaped at top & goes down to irregular plates/rods to nothing • terminal bronchioles -less than 1mm in size - elastic & smooth muscle >squeeze when someone breathes hard > smooth muscle can change airway -no cartilage or goblet cells • Mainstem bronchi Right • vertical, wider, shorter • 25° Angle from trachea • Aspiration is more common -can be shown as right lower lobe pneumonia on CXR • food comes here bc its wider & has more volume Left • horizontal, longer • 40-60° angle from trachea • food get stuck in here bc longer Upper respiratory Tract • above the larynx • Ventilation - air moving through ducts (lungs) 1. Nasal cavities 2. Pharynx (passageway for respiratory & digestive systems) • nasopharynx: nasal cavity • Oropharynx: behind mouth • Laryngopharynx: larynx anterior esophagus posterior 3. Larynx • formed by cricoid & tracheal cartilage • holds the airway open • conduct air between pharynx & trachea • Houses the vocal folds • Contains glottis & epiglottis Conducting zone • anatomical dead space • ventilation ONLY Transitional zone • respiration & ventilation • have respiratory bronchioles with alveoli on outside Respiratory zone only respiration • • alveolar ducts and alveoli Respiratory epithelium Bronchial epithelium Upper conducting airways • psuedostratified: stretched and flattened out layers • columnar: bunched together not uniform • ciliated: sits on top of epithelium to move things along in airway Terminal/Respiratory bronchioles • single layered • Cuboidal: non-striated starts after bronchi. • NON-CILIATED Lower respiration tract • below the larynx -from cricoid cartilage to alveoli • Ventilation & respiration • Tracheobronchial tree - conducting airways -arranged from largest to thinnest structure (trachea to alveoli) 1. Trachea 2. Mainstem bronchi 3. Lobar bronchi 4. Segmental bronchi 5. Bronchioles: conducting bronchioles 6. Terminal bronchioles 7. terminal respiratory unit (Acinar unit) -beginning of respiratory zone >where gas exchange occurs -respiratory bronchioles >alveolar grown on here like fruit -alveolar ducts -alveolar sacs -alveoli Parenchyma • functional issue of lungs • involved in gas exchange - alveoli, ducts & respiratory bronchioles Interstitium • contains support tissues within lungs Epithelium • named for where its located -bronchial , alveolar, & pulmonary capillary • Thin layer outside structures -thin for gas exchange Basement membrane • has stem cells to metabolize & regenerate new tissue • Support epithelium Respiratory Mucosa Respiratory Epithelium • lines respiratory tract • has goblet cells to secrete mucus -moisten & protect airways -saline • bronchial/ alveolar Epiglottis: cartilage that protects Cricoid cartilage sits about the trachea the airway when eating Glottis: opening between vocal Thyroid cartilage: biggest (feel choking here) folds If we didn’t have fluid for air to pass through it would be painful for us to breathe Gag reflex is decreased in older patients • have a harder time coughing up things in airway • • • • Respiratory epithelium Alveolar epithelium efficient gas exchange -thin walls -lots of surface area type I pneumocytes - form surface of alveoli - large flat cells type 2 pneumocytes - ovoid cells: synthesize surfactant >reduces surface tension & prevent air sacs from collapsing in exhalation alveolar macrophages - roam surface & eat pathogens/etc Alveolar capillary unit (Acinus) • site of gas exchange (RESPIRATION) • Both the alveolar surface & capillary endothelium need to work for respiration Alveolar surface • for diffusion • SINGLE layer - epithelial cells, surfactant, macrophages Capillary endothelium • deoxygenated come in & go through come out oxygenated Communication • to allow air to expand & recoil as a unit (collateral ventilation) • Even dispersement of surfactant Though: Lambert's canals • communication between alveoli’s & bronchioles kohn's pores • communication between alveoli • also known as inter-alveolar connection or alveolar pores All phases of coughing must work properly to produce a good cough. Nostril is the best gate keeper for lungs Everything moves from the bottom up If diaphragm or external intercostals aren't Tidal: normal breathing Vital: deep breathing strong enough the volume of breath will not be enough to produce a cough Cilia • muscular hairlike projections Goblet cells • secret mucous -contains immunoglobulins to disable pathogens • Abundant in trachea/large airway Lamina Propria • in alveolar level underneath the bronchial epithelium • Keeps shape of airway Defense mechanisms 1. Physical Barriers 2. Mucociliary transport/escalator 3. Alveolar macrophages Physical barriers FIRST LINE OF DEFENSE • particles (anything you breathe in) • prevent entry of pathogen -nasal hairs >filter large particles -nasal mucosa >hydrate & enlarge particles • reflexes -physically get rid of pathogen -cough, sneeze, gag, bronchospasms Cough phases • inspiratory phase -deep inspiration >60% of vital capacity • compressive phase - glottis closure - increase intraadominal and intrathoracic pressures >more air in thorax • expiratory phase - active forceful contraction of abdominal and intercostal muscles - opening of glottis & forceful expulsion of inspired air Mucociliary transport/escalator • self clearing mechanism between bronchi/larynx -mucus & cilia to trap pathogen/ particles & move to get it out • mucus production increases with inflammation & can be changed by disease • Can be impaired by inhalation of toxic gases, inflammation, infection/disease • Asthma can thicken respiratory mucosa with inflammation or infiltration Alveolar macrophages • look & survey for pathogen on alveoli -ingest and digest pathogens • No mucus because it would slow down oxygen & carbon dioxide exchange • white blood cells (neutrophils-from systemic circulation) can be recruited to help ingest & kill pathogens -wont be needed if macrophages kill pathogen • • • • • • Static lung volumes Residual volume (RV) one unit of measure of how much • minimal volume of air remaining in air is in a space (alveola) lungs after maximal exhalation (1.5L Determined by the balance of 150mL) • Stays in the lung at all times to the lungs elastic properties keep alveoli from collapsing (along (recoil) and the properties of the with surfactant) muscles of the chest wall -mixes with fresh air on next inhale -continuous dynamic • Controlled by expiratory muscle Static lung volume components force Tidal volume (VT) -Occurs when muscle force is Inspiratory reserve volume (IRV) insufficient to reduce chest wall Expiratory reserve volume (ERV) volume further Residual volume (RV) Tidal volume (VT) • Normal value= 0.5L 500mL • the volume of air inhaled/exhaled with a normal breath (quiet breathing) -normal breath in/out • • This includes the air in the alveoli & air in the anatomical dead space (VD =0.15L 150mL) -air in dead space is there so airway doesn’t collapse • • • • How much air participates in gas exchange? alveola can only carry 500mL at all times Tidal volume (500mL) comes in -350mL only can go into alveoli bc of 150mL in VD 150mL (RV) is always left over in the anatomical dead space so that is pushed into alveoli before VT can go into alveola -mix of old & new air the leftover 150mL from VT is the new air (RV) in anatomical dead space Reserve volumes • maximal volume of air that can be moved above or below a normal tidal volume • With exercise reserve levels decrease & Tidal volume increases -alveola reaches it’s capacity & you cannot breathe in or out more Inspiratory reserve volume (IRV) • volume of air that can be inhaled after normal inspiration (3L) • Deep breath in Expiratory reserve volume (ERV) • maximal volume of air that can be exhaled from resting expiratory level (1L) • Deep breath out • • • • • Static lung capacities two or more lung volumes combined Inspiratory capacity (IC) Vital capacity (VC) Functional residual capacity (FRC) Total lung capacity (TLC) Inspiratory capacity (IC) • max volume of air that can be inspired from resting end expiration level (3.5L 350mL) • From the end of a Normal exhale to end of maximal inhale • IC=TV+IRV Vital Capacity (VC) • max volume of air that can be expelled from lung after maximal inspiration (4.5L 450mL) • VC=IRV+TV+ERV Pulmonary function test "spirometry" Measures how air goes in & out of lungs (RV) Decrease in lung volume leads to a shortening of expiratory muscles and a decrease in muscle force and an increased recoil pressure of chest wall. Functional Residual Capacity (FRC) • volume of air in lungs at the end of normal expiration (2.5L 250mL) • FRC=RV+ERV • Allows the stop of the recoil of lungs. Total Lung Capacity (TLC) • amount of air in respiratory system after a max inspiration (6L) • Max volume of air within the lung while chest wall is controlled by muscles of inspiration -occurs when chest wall is unable to generate additional force to further distend the lung and chest wall. • TLC=RV+ERV+TV+IRV Minute ventilation (Ve) • a amount of ventilation (air we transport) per minute • 5-10 L/min @ rest • Ve = RR*VT • there’s a linear relationship between ventilation and increasing levels of activities - 15 to 20 times more during max exercise -with initial/low level exercise VT increases first (deeper breath first) -with high level of activity respiratory rate increases first (faster breath taken first) Alveolar ventilation (VA) • amount of fresh air available for gas exchange -O2 goes in CO2 comes out Hyperventilation • increase in alveolar ventilation exceeding the oxygen demand of metabolism • Hypocapnia: -excessive release of CO2 from body via expired air dropping CO2 below normal limits Hypoventilation • decrease in alveolar ventilation which increases carbon dioxide beyond normal limits (hypercapnia) Mechanics of Breathing Influenced by: • Ventilation is directly proportional to pressure difference • ventilation is Inversely proportional to airway resistance -increasing airway cross sectional area decreases resistance • Affected by physical properties of the lungs: -compliance -elasticity -surface tension >surfactant Upper airway is wider: less resistance Lower airway is smaller: more resistance The lung is a continuous machine that never rests. “resting state”: where all forces neutralize itself At Rest • respiratory muscles at rest & elastic recoil of lung/chest wall are equal but opposite • Intrapleural pressure is subatmospheric -chest wall maintains a stretch @ rest • pressure along Tracheobronchial tree & alveoli are equal to atomospheric pressure -no air flow • air only only flows from higher pressure to lower pressure. • air volume is functional residual capacity (FRC) During inspiration • diaphragm and other muscles contract -compresses abdominal content and decompresses the thorax • intrapleural and alveolar pressure fall becoming subatomospheric (@ same time) • Air flows down the pressure gradient from mouth to alveoli • Lungs & chest expand in volume until thoracic cage stops expanding just before end on inspiration. At end inspiration • equilibrium after inspiration ends & before expiration begins • Pivot moment between inspiration & expiration • Air flows down pressure gradient until alveolar pressure is zero -both equal to atmospheric pressure -gradient ceases to exist (no pressure difference) • lungs/chest fully expand -intrapleural pressure decreases @ top of inhalation. (More negative) • • • • During expiration passive process (respiratory muscles relax) increasing pleasure pressure. -less negative value (natural tendency to recoil) recoil in lungs causes pleural and alveolar pressure to rise (equal amounts) Pressure gradient from alveoli to mouth Lung/chest volume decrease → air comes out causing lung to recoil pressure to fall. -new equilibrium is reached -less tendency to lose air (slows exhalation) More space in lungs because thorax is pulled down causing reduced alveolar & intrapleural pressure causing less resistance for air to come in At end expiration • pleural cavity & alveoli return to pressure relationship at start of inspiration • intrapleural pressure: -5 • Alveolar pressure: 0 Alveolar pressure • rises and falls during inhalation • Starts at 0 Transpulmonary pressure • pressure across organ from alveoli to pleura Intrapleural pressure • starts at -5 • Becomes less negative until next breath Factors affecting alveolar ventilation 1. Pressure 2. Compliance 3. Mechanical resistance 4. Airway resistance 5. Diffusion gradient 6. Barriers 7. Control of pressure Pressure • caused by elastic recoil of lungs & chest wall • Enable gas flow into alveoli • • • • • • • • • • • • • • • • Compliance influenced by interstitum & parenchyma ease at which lungs inflate Low compliance: harder to stretch/inflate High compliance: easier to stretch/inflate Mechanical resistance comes from structure itself Alveoli & bronchioles stretch resulting in drop of pressure -When alveoli expand the bronchioles expand all together airways increase in cross sectional area & decrease in resistance during inhalation. Low lung volumes can cause small airways to completely collapse. -less air flow= alveola doesn’t open -come from pulmonary pathologies Airway resistance Upper airway turbulent airflow leading to high resistance Chaotic airflow in larger airways Airway is wide open but has an irregular shape Lower airway laminar airflow in small airways leading to high resistance Smooth air flow in small airways Air is parallel to its surfaces its traveling through Branching allows many small airways which leads to a reduction of total airflow resistance overall. Resistance is the greatest at 4th-8th bifurcation (middle airway) Gas exchange • respiratory gas exchange take place in the alveoli -type 1 pneumocytes create large surface area • alveolar capillary membrane (covering alveolar surface) is where gas exchange takes place through diffusion -thin for easy gas exchange • • • • • • • • • • • • • Blood supply Pulmonary circulation deliver deoxygenated blood to lungs Returns oxygenated blood to heart Right ventricle → pulmonary arteries →arterioles → alveolar capillary membrane Bronchial circulation aorta → bronchial artery → arterioles→ bronchial glands/walls of respiratory bronchioles delivers oxygenated blood supply to bronchi and connective tissue of the lung NO gas exchange Diffusion occurs through alveolarcapillary membrane from high to low concentration O2 comes from alveolar into blood CO2 from blood to alveolar air Affected by: concentration and solubility -higher=faster membrane thickness -thin membrane surface area -larger when inhaling >fast diffusion -smaller when exhaling >slow diffusion pathology -fibrosis, fluid, edema, sputum Driving pressure • Vessel capacity is 100mmHG of air • Normal transit time <1second Oxygen • PAO2 100mmHg in alveoli →PVO2 40 mmHg in veins • PaO2 100mmHg in arterial blood Carbon Dioxide • PVCO2 46mmHg in veins → PACO2 40 mmHg • PaCO2 40mmHg in arterial blood Fick’s law • Net diffusion rate of gas across fluid membrane -proportional to difference in partial pressure and area of membrane -inversely proportional to thickness of membrane • bi-directional process Diffusion of respiratory gases • oxygen diffuses from alveolar air across tissue barrier & plasma to RBC -combines with hemoglobin • carbon dioxide diffuses from RBC across plasma & tissue barrier to alveolus Tissue Barrier consists of • surfactant, alveolar epithelium, interstitial tissue, capillary endothelium Blood Barrier consists of • plasma & RBC Membrane Pathology affecting diffusion alveolar collapse (atelectasis) Alveolar thickening (alveolar fibrosis) - scar tissue is thicker -cant pass air easily alveolar consolidation - pneumonia >filled with pus (consolidations) frothy secretions (pulmonary edema) - blood smears comes from heart to lung interstitial edema - interstium becomes a barrier alveolar capillary destruction (emphysema) - overall destruction -when alveolar epithelium is broken down the capillary side can then break down • • • • • • O2 transport • lung to tissue • O2 attaches to hemoglobin carried in RBC -hb combines with 4 O2 molecules -normal hb saturation 98% • O2 is dissolved in plasma (partial pressure) Control of breathing • involuntary • central Chemoreceptors respond to acidity of brains ECF -increase in hydrogen ion concentration stimulate ventilation • peripheral chemoreceptor respond to changes in CO2, hydrogen on, & partial pressure of O2 -increase in arterial CO2 & PH or PaO2 below 60mmHg stimulates ventilation (hypoxic drive) CO2 transport • tissue to lungs • CO2 travels in RBC as bicarbonate ions • small amounts of CO2 are dissolved in plasma or bound to Hb (carboxyhemglobin) • • • • • • • Other Sensors stretch receptors in alveoli Proprioceptors in joints/muscles - provide input in breathing -lose abdominal muscles wont compress diaphragm enough emotional input (limbic system) - nerves can make you breathe harder temp Meds -sleepy & stop breathing Anesthesia Disease