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by: Jesse McDonald

Respiratory Biology 204

Jesse McDonald
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Hi Class! I'll be uploading detailed notes for this class all semester for anyone who needs it. I just uploaded my first set of notes. If you sign-up right now you can get them for FREE :-) and y...
Biology of Human Anatomy and Physiology
Dr. David Bridges
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This 4 page Class Notes was uploaded by Jesse McDonald on Monday February 8, 2016. The Class Notes belongs to Biology 204 at Purdue University taught by Dr. David Bridges in Spring 2016. Since its upload, it has received 20 views. For similar materials see Biology of Human Anatomy and Physiology in Biology at Purdue University.


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Date Created: 02/08/16
Respiratory     Lecture 1     Cellular Respiration  ● Requires oxygen for oxidative phosphorylation and produces CO2 from carbon fuels  such as glucose and fatty acids   “Body Respiration”  ● Breathing ­ saturates the blood hemoglobin with O2 which is then delivered to the  metabolizing cells. Also removes excess CO2 from building up within the cells.     ● The trachea and bronchial tree are lined with pseudostratified ciliated epithelium  containing goblet, Clara, and neuroendocrine cells.   ○ This array of cells is called the “muco­ciliary escalator”  ○ Sub epithelial layer has many B­lymphocytes  ● Clara (club) Cells: protect the bronchiolar epithelium.  ○ Not ciliated  ○ Secrete a surfactant­like material   ● The lungs are like elastic foam. The bubbles are air in the alveoli, which are surrounded  by a dense network of capillaries.   ● “Respiratory Membrane”  ○ 1. Thin film of fluid containing pulmonary surfactant (Type II alveolar cells)  ○ 2. Alveolar epithelium (Type I) and its basement membrane  ○ 3. Narrow interstitial space  ○ 4. Walls of pulmonary capillaries  ● RBC’s are 6 micrometers (um) wide and squeeze through the 5um wide capillaries in  contact with the endothelium  ● Therefore oxygen need not to diffuse through the capillary walls  ● The air in the trachea, bronchioles, etc., cannot exchange gases with the blood. This is  DEAD SPACE AIR  ● Alveolar air equilibrates with the blood by diffusion of CO2 and O2 across the respiratory  membrane.  ○ Inspired air (Dead Space air/ lots of O2, little CO2) + Alveolar(More CO2 than DS  air) = Expired Air  ● Inadequate ventilation, adequate perfusion = hypoventilation  ○ Perfusion ­ the process of delivering blood to a capillary bed in the tissue  ● Adequate ventilation, no perfusion = pulmonary embolism  ● Pulmonary edema:  ○ Cardiogenic causes (increased pressure in the left atrium, pulmonary veins,  pulmonary capillaries). Left heart failure or mitral stenosis (narrowing)  ○ Non­cardiogenic causes: Endotoxins or irritant gases  ● Angiotensin­converting enzyme is mainly circulated by the epithelial cells in the lungs. It  can be released after an acute injury which will increase pulmonary vascular  permeability.   ● Dead Space:  ○ Volume of air in trachea, bronchi, bronchioles that cannot exchange with blood  gases.  ○ This is the total volume of the respiratory system without the alveoli  ○ In some diseases, portions the lungs can be poorly ventilated or perfused, which  will increase the volume of dead space.   ● Compliance of the lungs:  ○ The lungs are stretchy. To inflate them, we have to fight their elastic recoil.   ○ In fibrosis or whenever the pulmonary surfactant is lacking, the lungs will be less  stretchy, but will still have the strong elastic recoil, therefore will be more difficult  to inflate.   ○ In emphysema, which is classified as a chronic obstructive pulmonary disease  (COPD), the alveolar walls begin to weaken and eventually rupture. This  decreases the surface area of the alveoli and therefore high compliance occurs  within the lungs.   Lecture 2     Breathing  ● Controls CO2 to prevent dangerous deviations of pH above or below 7.4, the partial  pressure of CO2 must be kept constant  ● Maintains oxygen supply. If partial pressure falls dangerously low, oxidative  phosphorylation cannot proceed and insufficient ATP will be produced  Mechanical Breathing  ● Inspiration:  ○ 1. The diaphragm is innervated by the phrenic nerve.  ○ 2. In more vigorous inspiration the external intercostals and other accessory  muscles (the sternocleidomastoid) may become involved.  ● Expiration (normally passive)  ○ 1. The diaphragm relaxes ­ passive elastic recoil of the lungs expels the air in  them  ○ 2. In forced expiration, the internal intercostals and abdominals muscles (rectus  abdominis) may become involved.  Airway Resistance:  ● In chronic obstructive pulmonary disease COPD = asthma, bronchitis, emphysema.  Airway diameter decreases and resistance to airflow increases.  ● Drugs affect the diameter of the bronchi and bronchioles:  ○ epinephrine = airflow resistance decreases  ○ acetylcholine = constricts so airflow resistance increases  Control of Respirati​ : ● Networks of neurons in the brainstem make up the “Central Controller” of respiration.  ○ Upper pons pneumotaxic center: fine tunes basic rhythm.  ○ Medullary rhythmicity center: controls basic rhythm of breathing.  ● Overridden by the cerebral cortex during speech.  ● These are regulated by sensors for CO2, O2, and H+.  Sensors for O2, CO2, and ​  ● 1. Central: in the medulla: respond to H+ in the CSF, which increases when blood CO2  increases.  ○ They respond to the H+ produced when CO2 crosses into the brain forms  carbonic acid, which then dissociates.   ○ The medullary chemoreceptors are not stimulated by H+ in the plasma because  hydrogen ions cannot cross the blood­brain barrier.   ● 2. Peripheral: carotid and aortic bodies: respond mainly to low oxygen, less importantly,  they will respond to high CO2 and H+  ○ Carotid bodies are small structures that have their own blood supply*  ● Stretch receptors in the smooth muscle of the airways respond to lung distension and  will slow down the breathing rate. This ​ering­Breuer refl​(prominent in babies)  ● Normal CO2 is normally the most important factor in regulating breathing.   ○ If you reduce arterial CO2 by hyperventilating, you destroy the urge to breathe  until the CO2 builds up again.  ○ Hyperventilating DOES NOT change the O2 level in the blood if the levels were  normal beforehand.  ● Arterial oxygen is the next most important:  ○ At high altitudes, partial pressure of oxygen is low, which stimulates the cells in  the carotid and aortic bodies, increasing ventilation.  ○ But this reduces CO2, which puts the brakes on the ventilation increase.  ○ If you slowly allow yourself into the high altitude, your RBC supply will increase.  Hydrogen Ions:  ● Difficult to separate from CO2  ● In metabolic acidosis, there is a fall of blood (plasma) pH, and this stimulates ventilation.   Exercise  ● Increased ventilation is partly caused by increased CO2 production and oxygen  consumption.  Oxygen Toxicit:  ● High oxygen at high pressures can affect the CNS and damage pulmonary capillary  endothelium.  Compression Sickness, Nitrogen Narcosis, Pulmonary Overinflation Syndr: e​ ● Henry’s Law: C=kP (constant temperature)  ● Amount of gas dissolved in liquid C at a given temperature is a function of pressure.  ● When the pressure is reduced, the gas bubbles out.   ● The “bends” ­ at high pressure, nitrogen dissolves in adipose tissue, and is released as  bubbles during decompression when the diver ascends.   ● Nitrogen Narcosis: occurs at 160 ft when a diver as the drunk feeling (“rapture of the  deep”, “martini effect”, “beer buzz”)   ○ Minimized by using helium­oxygen (“heliox”)  ● Pulmonary Overinflation Syndrome:   ○ Boyle’s Law: at constant temperature, volume of a gas is inversely proportional to  the pressure. PV=nRT  ○ If air is not released during a diving ascent, the lungs will expand and rupture  pulmonary tissue and blood vessels.  ○ Asthma and pneumonia lead to trapped pockets of air that can also damage the  lungs during ascent.   ● A diver will often hyperventilate before a breath­hold dive  ○ Hyperventilation lowers you blood CO2: so you can therefore hold your breath  longer.  ● “Shallow Water Blackout”:  ○ Hyperventilation: high O2, low CO2  ○ Underwater: the O2 will slowly decrease, and the CO2 will increase  ○ Ascent: The partial pressure of O2 and CO2 is so low, now the O2 is what is  giving you the urge to breath. This can create cerebral anoxia.  Hemoglobin (Hb) for Oxygen  ● Hb saturated with oxygen in lungs, where pO2 is high  ● Hb releases oxygen in the tissues, where pO2 is low.  ● H+ formed during tissue metabolism bind to hemoglobin, lowering its affinity for O2  (BOhr effect)  ● Elevated temp in the tissue (working muscle) has the same effect.    Hemoglobin Variation​  ● Carboxyhemoglobin (cherry red)  ○ CO from cigarettes, car exhausts, etc, binds tightly to Hb and shuts out oxygen  ○ Blood level >40% carboxyhemoglobin can cause death  ● Myoglobin   ○ Occurs in skeletal muscles  ● HbS:  ○ Causes sickle cell anemia, a gene carried by 2 million in the US, most of whom  are African Americans  ○ HbS seems to confer malarial resistance  ○ Deoxy HbS forms long rods that make red cells regid  ○ Treatment: monthly blood transfusions, hydroxyurea (inhibits change in deoxy  HbS), bone marrow transplants  Carbon Dioxide:  ● Carried by the bloodstream from the tissues to the alveoli in the lungs where it is pushed  out  ● Carried in the blood in three different ways:  ○ Carbamino hemoglobin 5­7%  ○ Dissolved carbon dioxide 3­5%  ○ Bicarbonate 90% 


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