BIO 138 Respiratory System II - Lecture Notes PDF

BIO 138 ANATOMY AND PHYSIOLOGY- LECTURE OUTLINE- 2nd LECTURE EXAM RESPIRATORY SYSTEM II -PHYSIOLOGY Chapter 22 pp. 838-865 FACTORS THAT REGULATE AIRFLOW. See fig 22.16 p. 844...

BIO 138 ANATOMY AND PHYSIOLOGY- LECTURE OUTLINE- 2nd LECTURE EXAM RESPIRATORY SYSTEM II -PHYSIOLOGY Chapter 22 pp. 838-865 FACTORS THAT REGULATE AIRFLOW. See fig 22.16 p. 844 1. CHANGES IN LUNG’S VOLUME: Boyle’s law: The pressure of a given quantity of gas is inversely proportional to its volume (at a constant temperature). If the lung’s volume increases (during inspiration), the intrapulmonary pressure ___________________. If the lung’s volume decreases ((during expiration), the intrapulmonary pressure ____________________. PRESSURE: Air flows from areas of higher pressure to areas of lower pressure. 2. Air is a mixture of different gases: Mostly N, O2 and CO2. Each gas has its own partial pressure. pO2, pCO2, etc. Flow of air is directly proportional to the pressure difference (gradient of pressure) between 2 points. Three main pressures: Atmospheric pressure, intrapulmonary pressure, pleural pressure A. Atmospheric pressure: “The weight (pressure) of the air above”. Dalton’s law: The total atmospheric pressure is the sum of the contributions of the partial pressures of individual gases. At sea level: 760 mm Hg = 1 atmosphere. In physiology atmospheric pressure= 0 cm H20 At high altitudes the atmospheric pressure is lower, which means that the partial pressure of gases is lower. This is especially important for pO2 B. Intrapulmonary pressure: pressure of air inside the lungs. See fig 22.16 p. 844. - At rest intrapulmonary pressure = 0 cm H20 - Inhalation: Lung volume increasesàintrapulmonary pressure falls (-1 cm H20) below atmospheric pressureà air moves into the lungs - Exhalation: Lung volume decreasesà intrapulmonary pressure rises (+1 cm H20) above atmospheric pressureà air moves out C. Intrapleural pressure: pressure in the pleural space (space between the visceral and parietal pleurae.) - The small space (pleural space) between parietal and visceral pleura is filled with fluid so these layers stay together. Recoil of lung tissue causes lungs and chest wall to be pulling in opposite directions, thus visceral pleura and parietal pleura pull in opposite directions creating a negative intrapleural pressure. At rest: -5cm H20 - During inspiration: Intrapleural pressure is even more negative:– 8 cm H20, During expiration: Intrapleural pressure is – 5 cmH20. Clinical correlation: 1. Pneumothorax— If the thoracic wall is punctured (gunshot wound, etc)à air goes through the wound into the pleural space. The intrapleural pressure equalizes with the atmospheric pressure. The lung recoilss and collapse. A chest tube becomes necessary to take the air out of the intrapleural space and expand the lung. 3. RESISTANCE TO AIRFLOW: Airflow is inversely proportional to the resistance. Increasing resistance decreases airflow. 2 factors: A. Diameter of the bronchi - Bronchodilation: Due to ____________stimulation à diameter of bronchi increases à airflow increases - Bronchoconstriction: Due to _____________ stimulation, cold air, histamine, etc.à diameter of bronchi decreases à airflow decreases. Correlation: Asthma. Bronchoconstriction of the airway due to multiple factors (airflow decreases). Treatment: bronchodilators B. Pulmonary compliance: “Ease with which the lungs can expand”. Factor that increases compliance: 1. Surfactant: Surfactant disrupts hydrogen bonds between water molecules in alveoli, thus reduces H20 surface tension à Surfactant facilitates lung inflation (increases compliance). Factors that decrease compliance: ). 1. Degenerative lung diseases in which the lungs are stiffened by scar tissue (pulmonary fibrosis). 2. H20 surface tension inside the alveoli 3. Lack of surfactant*. *Clinical correlation: Infant respiratory distress syndrome (IRDS GAS EXCHANGE AND TRANSPORT Anatomical dead space: Conducting division of airway where there is no gas exchange. Nose to terminal bronchioles. If a person inhales 500 mL of air, 150 mL stay in anatomical dead space, only 350 mL reach alveoli (for gas exchange) Gas exchange begins in respiratory bronchioles, it takes place in alveoli of the lungs, referred to as external respiration Gas exchange in the peripheral tissues is referred to as internal respiration. Alveolar ventilation rate (AVR): Air that ventilates alveoli (350 mL) X respiratory rate (12 bpm) = 4,200 mL/min. This measurement is crucially relevant to the body’s ability to get oxygen to the tissues and dispose of carbon dioxide.’ FACTORS THAT AFFECT ALVEOLAR GAS EXCHANGE Alveolar gas exchange depends on: 1. Ventilation–perfusion coupling: Good ventilation (air) in alveolus + good perfusion (blood flow in capillaries). Clinical application: In pulmonary embolism perfusion is affected à less gas exchange. 2. Pressure gradient of the gases: Gradient of pressure contributes to gas diffusion. O2 has a partial pressure PO2 in the alveolus (104 mm Hg) that is higher than the partial pressure PO2 in the blood (40 mmHg). CO2 has a partial pressure PCO2 in blood (46 mmHg) that is higher than the partial pressure PCO2 in the alveolus (40 mmHg). Clinical application: At high altitudes: Low partial pressure of gases à less gas exchange. At high altitudes, the partial pressures of all gases are lower. Pressure gradient difference is less, and less oxygen diffuses into the blood causing hypoxia Hypoxia triggers erythropoiesis 1 3. Film of water and solubility of gases: A film of water covers alveoli, gases dissolve in water. 4. Membrane surface area: Blood in alveolar capillaries, spreads thinly over 70 m2 of alveolar surface area. Clinical application: In emphysema there is alveolar damage à less surface area à less gas exchange. 5. Membrane thickness: Respiratory membrane is normally thin only 0.5 µ thick, so it facilitates diffusion. Clinical application: In pneumonia or pulmonary edema, the membrane is thicker à less gas exchange. EXTERNAL RESPIRATION OR ALVEOLAR GAS EXCHANGE Fig 22.25 p. 855. Swapping of O2 and CO2 across the respiratory membrane. 2 main events: a) Loading of O2 (see red arrow - Fig 22.25 p. 855 O2 diffuses into the capillary (blood) because the PO2 in the alveolus (104 mm Hg) is higher than the PO2 in blood (40 mmHg). - Most of the O2 that enters the capillaries binds to HHb (reduced hemoglobin) to form HbO2 (oxyhemoglobin) b) Unloading of C02: (see blue arrows - Fig 22.25 p. 855) CO2 diffuses into the alveolus because PCO2 in blood (46 mmHg) is higher than the PCO2 in the alveolus (40 mmHg). Most of the CO2 (70%) comes from the dissociation of carbonic acid (H2CO3). H2CO3 -à H2O + CO2. CO2 will be exhaled INTERNAL RESPIRATION OR SYSTEMIC GAS EXCHANGE Fig 22.24 p. 853. Swapping of O2 and CO2 btw capillaries and cells of peripheral tissues. 2 events: a) O2 unloading: (See red arrow - Fig 22.24 p. 853 O2 diffuses from capillaries to cells because PO2 in capillaries is higher than in peripheral tissues. Most O2 (98.5%) that is released to peripheral tissues comes from Oxyhemoglobin (HbO2)). The release requires binding of H+ to form HHb (deoxyhemoglobin) b) CO2 loading: (see blue arrow- Fig 22.24 p. 853 CO2 diffuses from peripheral tissues to capillaries because PCO2 in peripheral tissues is higher than in capillaries. - Most of the CO2 (70%) diffuses into RBC and combines with water to form carbonic acid (H2CO3) CO2 + H2Oà H2CO3 à HCO3− + H+ HCO3− is exchanged for Cl− (“chloride shift”) , H+ lowers blood pH - 23% of CO2 binds to Hb to form carbaminohemoglobin (HbCO2). The affinity of Hb for C02 is higher. This is called a Haldane effect. - 7% of CO2 dissolves in plasma OXYGEN HEMOGLOBIN DISSOCIATION CURVE: Fig 22.26 p. 856 Hemoglobin doesn’t unload the same amount of oxygen to all tissues. Four factors determine how hemoglobin unloads oxygen to tissues: a)PO2: If the PO2 of a tissue is low, HbO2 releases more oxygen. b) Temperature: Elevated temperature promotes oxygen unloading b) pH: H+ promote oxygen unloading (this is called Bohr effect)* c) 2,3 BPG (bisphosphoglycerate): A metabolic intermediate that causes O2 unloading *A shift of the oxygen dissociation curve to the right (thus reducing affinity of O2 for Hb) due to a lower pH is called a Bohr effect. NEURAL CONTROL OF BREATHING Breathing is controlled at two levels of the brain -- One is unconscious and automatic, the other is cerebral and conscious I. Automatic (unconscious) control of breathing: Three respiratory centers in the brain stem coordinate the automatic control of breathing. 1. VRG (ventral respiratory group): In the medulla oblongata. Function: Adjusts the respiratory rhythm (12-20 breaths/min). Inspiratory neurons stimulate: the phrenic nerve (to activate the diaphragm) and intercostal nerves (to activate external intercostal muscles). Expiratory neurons activate internal intercostal muscles. 2. DRG (dorsal respiratory group): In the Medulla Oblongata. Function: Adjusts the depth of breathing depending on input from: a) Peripheral chemoreceptors (from the aortic bodies and carotid bodies that respond to changes in pH or blood CO2 or O2 and send signals via CN IX (glossopharyngeal nerve) and CN X(Vagus nerve) to the DRG. Fig 22.15 p.842. b) Central chemoreceptors in the brain stem that detect changes in the pH of cerebrospinal fluid (reflects the CO2 level in the blood). This is the main stimulus to pulmonary ventilation. c) Stretch receptors: In visceral pleura. Respond to Inflation. A protective Hering-Breuer reflex prevents excessive inflation. d) Irritant receptors in the airway. 3. PRG (pontine respiratory group): In the pons. Function: Adjusts breathing special to special circumstances (sleep, exercise, speech, emotions (crying, laughing, etc) Clinical application: Cervical trauma: Automatic Neural Control of breathing will cease if spinal cord is severed high in neck or if brainstem is damaged. II.Voluntary control of breathing: Impulses from the motor cortex reach the spinal cord, bypassing the brainstem. This mechanism works except in cases in which CO2 levels rise to a point where automatic controls override one’s will. 2