HSF 2 - Unit 2 Physiology: Pulmonary Physiology Flashcards
what are the functions of the lung?
control pH, humidify the air we breathe in, defense, filter the airways
how does the lung maintain pH?
through the CO2/HCO3- buffer system: CO2 + H2O –> H2CO3 –> HCO3- + H+ all through carbonic anhydrase
what causes respiratory acidosis? alkalosis?
acidosis: hypoventilation; not getting rid of enough CO2 so pushes equation to the right giving more H+ ions, more acidic pH
alkalosis: hyperventilation; getting rid of too much CO2 through fast breathing so pushes equation towards the left and higher pH
how do we humidify air?
through the sinuses (nasal especially), this also warms it before it reaches the lower respiratory system
how are the airways filtered? what can be a problem with this in smokers and people with CF?
through mucus from goblet cells in the trachea; mucus layer traps the particles from dust or other inhaled things and underneath is a watery saline layer to allow the goblet cells’ cilia to move the mucus towards the pharynx. we end up swallowing most of this unconsciously and it is ultimately eliminated in the stool. CF: thick and sticky mucus so cannot be moved out, more prone to infections because bacteria colonizes in the mucus. smokers: tar in cigarettes make the cilia unable to move while also introducing carcinogens into the body, unable to remove these and also mucus effectively
what are various cell products that defend our respiratory system?
Mast: IgE, heparin, proteases, histamine, prostaglandins, chemotactic factors for the immune response
Goblet: mucus, prostaglandins, heparin, histamine
what does IgE do?
immune response, amount is in the teens
what do proteases from ______ cells do?
Mast/basophil; destroy proteins of foreign bacteria but not selective so other proteins are also destroyed, resulting in damaged lung tissue following an infection; this is a problem with chronic inflammation
what does histamine do?
bronchoconstriction and vasodilation (transport of immune factors is faster); BP crashes and leakage of fluid into the tissues but airways close so prevent access by the foreign invaders further into the respiratory system
what does heparin do?
prevents blood clotting; if blood clots it could get stuck in the pulmonary arteries
what makes up the lower respiratory tract?
trachea, bronchi, bronchioles, respiratory bronchioles, alveoli
what happens as you move lower into the respiratory tract? why can this be an issue but is also necessary?
slowly lose the hyaline cartilage rings, problematic because little support so the lungs could close up but necessary to allow gas exchange
what is bronchiectasis? what can cause it?
remodeling and thickening of the walls (smooth muscle gets replaced by fibroblasts and scar tissue) of the large airways making the lumen smaller, irreversible, thus reducing airflow and making it harder to remove mucus - promotes infection; caused by recurrent infection and inflammation, which can happen with diseases such as CF, immune deficiency, TB, chronic bronchitis, primary ciliary dyskinesia
what are alveoli composed of?
single layer of epithelial cells: type I and type II
what are type I cells?
thin cells in the alveoli for gas exchange
what are type II cells?
cells in the alveoli that secrete surfactant
what are the chemical properties of the contents of alveoli?
holds water, which has 2 dipoles, one neg and one pos, hydrogen bonding causes surface tension and a tendency for the alveoli to close, so surfactant reduces the hydrogen bonding between the water molecules and thus reduces surface tension to keep the alveoli open
what causes respiratory distress syndrome? how can we help ease the symptoms?
lack of surfactant, so the alveoli recoil and collapse because of the surface tension of the water within the alveoli; can be treated with positive pressure breathing or administration of surfactant
what is atelectasis? what causes it?
collapsing of the airways; caused by pressure on the outside of the lung (buildup of fluid), blockage of the air passages (complete mucus plugs), lack of surfactant, anesthesia
what surrounds alveoli? how is this compromised in certain diseases?
extensive and redundant network of capillaries and elastic fibers; when diseases destroy these you lose air and blood vessels, resulting in a higher BP; seen in emphysema with pulmonary hypertension because there is no where for the blood to go
how big is the gap for gas exchange?
0.1-1.5 micrometers between the alveoli and the capillaries; separated by a very small interstitial space
what is Boyle’s law?
P1V1 = P2V2; decreasing volume increases the rate of collisions of oxygen molecules with the lung interior and increases pressure
what happens to the volume and pressure of the lungs during inspiration? expiration?
inspiration: volume increases so pressure decreases; atmospheric pressure is greater than the alveolar pressure so air follows the gradient and moves in
expiration: volume decreases so pressure increases; atmospheric pressure is less than the alveolar pressure so air follows the gradient and moves out
what are the pleural membranes?
visceral and parietal, separated by an intrapleural space that is filled with pleural fluid that provides lubrication between the 2 membranes and is also cohesive so they stick together and move fluidly during breathing
what is the pressure in the intrapleural space?
negative; due to the thoracic cavity’s tendency to go out and the lungs tendency to recoil in
what are the Pip changes during breathing?
starts at -4 (4 under atmospheric) because of opposite pulling of the lungs and the thoracic cavity and the lymphatics draining the area; continues to go more negative during inspiration because no air going into the cavity but air coming into alveoli - can’t equalize; during expiration volume goes back down so the pressure goes back to -4
what are the PA changes during breathing?
goes down at first during chest expansion as air comes in, at the end of inspiration it equalizes then goes back up
what happens during a pneumothorax?
the cohesion is broken between the parietal and visceral membranes, so it equalizes to atmospheric pressure and the lung collapses due to its elastic recoil tendency
what happens during a hemothorax?
aka tension pneumothorax; causes more intense pain and pressure in the lung, pulling in more air and cannot expel it; building up pressure in the lung so must be punctured to release it, then seal and provide positive pressure for reinflation
what is an example of positive pressure breathing?
mechanical ventilation, CPAP for people with sleep apnea to keep airways open
what is compliance work?
(inspiration) distensibility or stretchiness of the lung and its ability to move; elastic work
what is airway resistance work?
(expiration) overcome tissue and airway resistance (obstructions), flow is proportional to change in pressure/resistance : increase change in pressure you increase the flow and an increase resistance you decrease flow
what are the 2 types of work during breathing?
compliance and airway resistance
what are the determining factors of lung compliance?
property of the tissue (stretchable, scar tissue), volume of the lung, surfactant, obesity (abdominal fat makes it harder on the diaphragm to move downward and reduces compliance so have to work harder)
what is the compliance equation?
change in volume over the change in pressure (slope of the line in transpulmonary pressure versus volume graph)
what is emphysema? what are its causes?
effects the alveoli, get destruction of them so lose elastic recoil and can get narrowing of the bronchioles,, causing air trapping, V/Q mismatch, reduced DLCO, and loss of capillaries; caused by smoking (chronic irritants and infection; smoke leads to neutrophils and macrophages which leads to proteases and inflammation and ROS) or alpha 1 antitrypsin (protease inhibitor) deficiency; all results in a loss of surface area in the alveoli and total lung, lowered ability to exchange gas and increased compliance because fewer alveoli to oppose opening of the lung
what is pulmonary fibrosis?
thickened alveolar membrane slows gas exchange, lowering lung compliance and decreasing alveolar ventilation; fibrous scar tissue (stiff lung), DLCO reduced; can be caused by inhalation of particulates (asbestos, coal dust, silica, etc.) which leads to repetitive alveolar injury and thus increased production of fibroblasts and collagen (ECM)
how is resistance determined?
length of the respiratory system, viscosity, and radius of the tubes
what is Poiseulle’s law?
R = 8nl/pi*r^4 R=resistance n=viscosity l=length r=radius
what are the determining factors for the radius of the respiratory tubes?
1) mechanical connections (connective tissues and alveoli)
2) physical (mucus)
3) neural control (autonomic nervous system)
4) paracrine and endocrine agents (CO2, histamine, prostaglandins, leukotrienes, etc.)
what are the different lung volumes?
tidal volume, inspiratory reserve volume, expiratory reserve volume, residual volume
what are the different lung capacities?
vital capacity, inspiratory capacity, functional residual capacity, total lung capacity
