IB TOPIC 6.4 GAS EXCHANGE CARDIOPULMONARY SYSTEM CARDIOPULMONARY SYSTEM Branch from the pulmonary artery (oxygen-poor blood) Branch from the pulmonary vein (oxygen-rich blood) Terminal bronchiole Nasal cavity Pharynx Left lung Alveoli 50 µm Larynx Esophagus Trachea 50 µm Right lung Bronchus Bronchiole Diaphragm Heart SEM Colorized SEM
GAS EXCHANGE ventilation alveoli capillaries partial pressure compare: ventilation, gas exchange, cellular respiration 6.4.U1 ventilation maintains concentration gradients of O2 & CO2 between air in alveolar sacs and blood flowing through adjacent capillaries A CLOSER LOOK PARTIAL PRESSURES LUNG CAPACITY What is your vital capacity?
GAS EXCHANGE - CELL SPECIALIZATION 6.4.U2 Type 1 pneumocytes are thin alveolar cells that are adapted to carry out gas exchange pneumocyte surfactant 6.4.U3 Type 2 pneumocytes secrete a surfactant solution: keeps surface moist prevents internal adhesion of alveolus adhesion surface tension CLOSER LOOK: PULMONARY SURFACTANT Phospholipoprotein produced by Type 2 pneumocytes it facilitates hydrophyllic adsorption in water on alveolar surface hydrophobic region orients towards air reduces surface tension, easing inflation and resisting collapse of alveolus GAS EXCHANGE - STRUCTURE AND FUNCTION trachea bronchi bronchioles 6.4.U4 Air is carried to the lungs in the trachea and bronchi and then to the alveoli in the bronchioles
BREATHING USES DIFFERENT MUSCLES FOR INSPIRATION AND EXPIRATION GAS EXCHANGE - STRUCTURE AND FUNCTION thorax inspiration expiration intercostal diaphragm antagonistic 6.4.U5 Muscle contractions cause pressure changes inside the thorax that force air in and out of lungs to ventilate them 6.4.U6 Different are required for inspiration and expiration because only do work when they contract GAS EXCHANGE - STRUCTURE AND FUNCTION inspiration expiration intercostal diaphragm antagonistic 6.4.A3 Ventilation uses antagonistic muscle groups Principal of inspiration: diaphragm (flattens and moves down) external intercostals (move rib cage up and out) neck (pull up) Principal of expiration: abdominal wall (e.g. rectus abdominis (6pack) internal intercostals
GAS EXCHANGE - DISORDERS IRDS: Infant Respiratory Distress Syndrome insufficient surfactant production during last part of gestation incidence: 50% of infants born at 26-28 weeks, 25% at 30-31 weeks #1 cause of death of premature birth infants treated with breathing tube + surfactant (synthetic or from animal) O2 DISSOCIATION CURVES D.6.U1 Oxygen dissociation curves show hemoglobin s affinity for Oxygen RBCs have hemoglobin (Hb) Hb = 4 polypeptide chains, ea. w/ a heme group carrying Iron (Fe) ea. heme group reversibly binds to one O2 molecule As each O2 binds, Hb affinity for the next O2 increases thus high affinity for O2 in lungs (=loading) thus low affinity for O2 in (=unloading) TRANSPORT OF CO2 CO2 is carried in plasma and by Hb CO2 in the RBCs is turned into carbonic acid most CO2 is carried in RBC Hb buffers the ph by absorbing H+ ions
O2 DISSOCIATION CURVES D.6.U5 Chemoreceptors are sensitive to blood ph CO2 in plasma may combine with H2O to form carbonic acid (H2CO3) Chemoreceptors (in medulla) detect ph and trigger body responses to keep homeostasis lungs: change respiratory rate kidneys: control reabsorption/excretion of bicarbonate (HCO3) blood ph is buffered by plasma proteins normal range: 7.35-7.45 O2 DISSOCIATION CURVES D.6.U4 The Bohr shift explains the increased unloading of O2 in respiring tissues increased respiration makes more CO2 what happens to ph in RBC? lower ph decreases Hb affinity for O2 CHALLENGES C AN YOU SKETC H: Dissociation curves for: fetal Hb? Llama Hb? myoglobin? Hb at higher temp?
HYPERVENTILATION WHY DO PEOPLE GET LIGHTHEADED? Normally: approx. 10% of air exchanged w/ ea. breath hyperventilation exchanges more gas with air, thus: less CO2 in body and less in blood Normally: if high CO2 in blood, low O2 and blood vessels in brain dilated (why?) If low CO2 (eg. hyperventilation) then b.v. constricted. result: less O2, fainting GAS EXCHANGE - DISORDERS cancer metastasis 6.4.A1 Causes and consequences of lung cancer abnormal growth of lung tissue tumors may metastasize initial causes include: smoking asbestos air pollution genetics GAS EXCHANGE - DISORDERS 6.4.A3 Causes and consequences of emphysema alveolar walls lose elasticity alveoli enlarge; effect on surface area? decreases holes may develop between alveoli major cause: smoking phagocytes brought to lungs enzyme elastase breaks down walls