Gas Exchange: Topic 6.4 and D.6 Flashcards
Describe how the structure of the alveoli is adapted to its function (make sure to include type I and type II pneumocytes as well).
ALVEOLI (TRIM):
Thin walls – surrounded by a single layer of epithelial cells (minimizes diffusion distance) - capillary walls only one cell thick too (endothelial cells)
Rich capillary network surrounding each alveolus – maintains high concentration gradient (O2/ CO2) between lungs and blood for diffusion
Increased SA:V ratio – small, spherical shape increases surface area while decreasing volume
Moist – cells lining each alveolus secrete fluids to allow gases to dissolve (dissolved oxygen diffuses easier into blood) and prevent alveoli from collapsing on themselves/ sticking together
TYPE I PNEUMOCYTES:
Squamous (flattened) and extremely thin to minimize diffusion distance and increase surface area for gas exchange
TYPE II PNEUMOCYTES:
cuboidal with granules (store components to make surfactant); function is to secrete pulmonary surfactant - a liquid substance that reduces/ decreases surface tension (ensuring all alveoli expand at the same rate and none of them collapse in on themselves due to unequal pressure)
Identify type I and type II pneumocytes and red blood cells in electron micrographs of the alveoli.
- Type I pneumocytes are the flattened cells right up against the alveolar space
- Type II pneumocytes are the less flattened (sort of cuboidal but mostly just less flattened) cells up against the alveolar space
- Red blood cells are not right up against the alveolar space
Distinguish cellular respiration, ventilation, and gas exchange.
Cellular Respiration - The release of ATP from organic molecules (enhanced by oxygen – aerobic respiration)
Ventilation - The exchange of air between lungs and atmosphere (through breathing)
Gas Exchange - The exchange of oxygen and carbon dioxide in the alveoli (lungs) and in the bloodstream (by diffusion)
Explain the process of gas exchange in the alveoli of the lungs and the role of the ventilation system in maintaining concentration gradients of CO2 and O2 between the alveoli and the capillaries surrounding them.
- Because gas exchange is a passive process (diffusion),
the lungs function to continually cycle fresh air into the alveoli (high O2 in alveoli allows diffusion of O2 into the blood and low CO2 in alveoli allows diffusion of CO2 out of blood and into alveoli) - Ventilation system maintains a high concentration of O2 AND a low concentration of CO2 in the alveoli in the lungs
- Ensures that O2 diffuses from the lungs through the alveoli walls INTO the blood (capillaries) and CO2 diffuses OUT of the blood (capillaries) through the alveoli walls and into the lungs (most cell respiration is aerobic – requires O2 and produces CO2)
- A ventilation system allows continual cycling of the air in the lungs with the air in the atmosphere to maintain concentration gradients between the alveoli and the capillaries for gas exchange
Outline the processes of inspiration/ inhalation and exhalation (including the roles of antagonistic muscles)
Ventilation (exchange of air between lungs and atmosphere through breathing) involves the internal and external intercostal muscles (between ribs), the diaphragm (below lungs) and abdominal wall muscles, and it is driven by a negative pressure mechanism
Inspiration (breathing in)
a. Diaphragm muscles contract (flatten downwards) and external (on outside) intercostal muscles contract (pull ribs up and out)
b. Thoracic cavity volume and lung volume increase (pressure of air in lungs drops below atmospheric pressure – air rushes in through mouth or nasal passage to equalize)
Expiration (breathing out)
a. Diaphragm muscles relax (curves upward), abdominal wall muscles contract (pushing diaphragm up), external intercostal muscles relax (ribs fall), and internal (on inside) intercostal muscles contract (pulling ribs back down)
b. Thoracic cavity volume and lung volume decrease (pressure of air in lungs rises above atmospheric pressure – air rushes out to equalize)
Outline the causes and consequences of emphysema and lung cancer (and the treatments of emphysema too).
Emphysema is a chronic/progressive disease where the walls of the alveoli are damaged and lose their elasticity (feeling of shortness of breath) - a form of COPD (chronic obstructive pulmonary disease)
* Causes: SMOKING/ tobacco/marijuana/fumes/coal dust/air pollution (irritants cause damage, then phagocytes (WBC’s) come to “help” damaged tissue/ secrete elastase, which breaks down elastic fibers in alveolar walls) - Note that in rare cases, hereditary gene mutation causes deficiency in elastase enzyme inhibitor (which causes hereditary emphysema)
* Consequences: Healthy alveoli break down/ rupture, turn into large, irregularly shaped structures with gaping holes, ↓ elasticity (so ↑total lung volume at rest), ↓ SA, ↓O2 can reach the bloodstream
* Treatments: No cure, but certain treatments can help alleviate symptoms/ delay disease = bronchodilators (improve airflow by relaxing bronchial muscles), inhaled steroids (reduce inflammatory response/ phagocytes), oxygen supplementation, elastase enzyme inhibitors, surgery (remove damaged tissue/ lung transplant)
Lung cancer is a cancerous growth (uncontrolled cell division) within the lungs.
* Causes: carcinogens (smoking, asbestos)/air pollution/ certain infections/genetic predispositions
* Malignant cancer cells can take over healthy tissues of the bronchioles & alveoli – then eventually spread (metastasize) to the brain/bones/liver/adrenal gland
* Lung tissues become dysfunctional, can lead to internal bleeding, coughing up blood, wheezing, respiratory distress and weight loss
Explain the effects of increased exercise (changes in CO2/ pH) on ventilation rate (and tidal volume), and explain how ventilation rate is controlled.
The rate of ventilation is controlled by the respiratory control center in the medulla oblongata and during exercise the rate of ventilation changes in response to the amount of CO2 in the blood
- Exercise increases metabolism (cell respiration rate)
- This increases CO2 in the blood, which
DECREASES the pH of the blood (becomes more
acidic) - normal range = 7.35-7.45 (~7.4 average) - Chemoreceptors in the carotid artery (neck) and the aorta (heart) detect CO2/ O2 levels and blood pH; Chemoreceptors in the medulla detect CO2 changes (as pH changes in cerebrospinal fluid)
- Chemoreceptors send impulses to the respiratory/ breathing center (in medulla oblongata)
- Medulla sends impulses to the diaphragm and intercostal muscles to increase rate of contraction (increasing ventilation rate/ hyperventilation)
- As ventilation rate increases, CO2 levels in blood decrease, pH rises and is restored
- As CO2 levels drop and pH is restored, breathing rate decreases
- As breathing rate decreases, CO2 levels rise again, pH drops again and the cycle continues
Outline how to use a spirometer to measure ventilation rate.
Spirometer measures volume of gas inhaled/ expelled per breath - Note: changes in volume are shown as increasing (breathing in) or decreasing (breathing out) over time on a graph and each breath is one “wave” (shows tidal volume - amount of O2 in or out in in one breath)
Calculate ventilation rate and tidal volume using spirometer data and make conclusions using that data.
Look at worksheets!
Describe how the structure of hemoglobin and myoglobin are related to their functions and their oxygen dissociation curves.
Hemoglobin (oxygen-binding protein in red blood cells)
- Composed of FOUR polypeptide chains (quaternary structure!)
- Each chain has an iron-containing heme group that is able to REVERSIBLY bind with oxygen
- Binding of oxygen to hemoglobin is cooperative – one molecule (of O2) binding changes the shape so it’s easier for another oxygen to bind, which changes the shape again so it’s even easier for another molecule to bind and so forth (up to four O2 per hemoglobin = HbO8). This means that hemoglobin has a HIGHER affinity for O2 (binds more readily to it) in oxygen-rich areas (lungs), promoting oxygen loading
- The opposite of this is also true! As O2 molecules are released from hemoglobin, the shape changes, making it easier for other O2 molecules to be unloaded as well (this means hemoglobin has a LOWER affinity for O2 in oxygen-starved areas (respiring tissues/ muscles), promoting oxygen unloading
Myoglobin (oxygen-binding protein in skeletal muscles)
- Composed of only ONE polypeptide chain with an iron-containing heme group (able to bind reversibly with oxygen – NO cooperative binding though b/c only one heme group, so binds only one oxygen molecule at a time)
- Binds to O2 and stores it IN muscle cells (acts as an “oxygen reserve”)
- Able to provide O2 to muscle cells when O2 in blood is very low; delays anaerobic respiration
Diagram and explain the oxygen dissociation curves for adult hemoglobin, fetal hemoglobin, and myoglobin.
Myoglobin is furthest to the left, then fetal hemoglobin, then adult hemoglobin
The further left, the higher the oxygen affinity
Adult hemoglobin:
* Shows a sigmoidal (S-shaped) curve (due to its cooperative binding of oxygen molecules)
* High saturation at high pressures (pO2)/ lungs = oxyhemoglobin forms when high pO2; Low saturation at low pressures/ concentrations (pO2)/ respiring tissues = oxyhemoglobin dissociates (unbinds/ breaks apart) at low pO2
Fetal hemoglobin: (Understand that fetal hemoglobin is different from adult hemoglobin, allowing the transfer of oxygen in the placenta onto the fetal hemoglobin)
* Fetal hemoglobin molecules have slightly different shape (molecular structure) than adult hemoglobin, making them have a HIGHER AFFINITY for oxygen (they bind it more readily/ easily - binds O2 more readily at lower pO2)
* Sigmoid shape dissociation curve but shifted LEFT (b/c it has a higher oxygen affinity)
* Higher affinity for oxygen ensures that oxygen moves from adult (mom’s) hemoglobin to fetal hemoglobin in the capillaries of the placenta
Myoglobin: (Skill: Analysis of oxygen dissociation curves for hemoglobin and myoglobin)
* Higher affinity for oxygen than hemoglobin (saturated at extremely low O2 concentrations, so able to store oxygen in muscle cells no matter what concentrations are in body) – NOT an S-shaped curve b/c NO cooperative binding, like in hemoglobin. Only binds ONE O2 molecule at a time (only one heme group per myoglobin)
* Releases oxygen to muscle cells when levels of O2 in blood are extremely low (from intense exercise), allowing aerobic respiration to continue/ delaying anaerobic respiration/ lactic acid formation!
Diagram and explain the Bohr shift (remember that “explain” means you include the REASONS/ WHY’s in an answer too).
Understand that the Bohr Shift explains the increased release of oxygen by hemoglobin in respiring tissues.
Respiring tissues release MORE CO2 into the blood, which LOWERS the pH of the blood (it becomes more acidic)
↓in pH shifts the oxygen dissociation
curve to the RIGHT (Bohr shift/ effect),
causing ↓affinity of hemoglobin for
oxygen = MORE O2 is released to respiring cells/ tissues! How?
* Excess CO2 diffuses into RBC’s and is
converted into carbonic acid
* Carbonic acid dissociates into H+ ions and HCO3- ions
* H+ ions in the RBC bind to hemoglobin (causing it to change shape and have a LOWER affinity for oxygen, so O2 is released)
* MORE O2 is released at the same partial pressure due to Bohr effect
The Bohr shift ENSURES that respiring tissues have enough O2 when they need it the most (during ↑ physical activity/ exercise)!
Explain WHY and how the body adapts to gas exchange at high altitudes (including pros and cons of high altitude training).
- As altitude ↑ atmospheric pressure ↓ (less O2 because less air overall = lower partial pressure of O2)
- Lower pO2 makes it more difficult for hemoglobin to take up and transport oxygen (lower pO2 = lower % Hb saturation in the lungs/ alveoli) – tissues and cells receive LESS oxygen (Symptoms of low oxygen intake/ hypoxia = breathlessness, headache, fatigue, rapid pulse, nausea - note that increased ventilation rate causes ↑ loss of H2O too)
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Over time, the body IS able to acclimate to lower O2 in the air! HOW?
1. RBC production increases (more RBC’s = more hemoglobin = more O2 transport) - this causes kidneys to excrete excess fluid though = more urination = dehydration (so need more H2O)
2. RBCs are produced with more hemoglobin molecules in them (these also have a slightly different structure which gives them a higher affinity for oxygen - shifts oxygen dissociation curve to the left - ↑ % saturation of Hb at lower pO2)
3. Vital capacity increases (more air in/out per breath = increased rate of gas exchange)
4. Muscles produce more myoglobin (capillaries become more dense too – more O2 diffusion into cells and binding by myoglobin)
5. Kidneys secrete alkaline urine (remove excess HCO3- to improve buffering of blood pH)
6. Greater lung surface area/ larger chest size – if living permanently at high altitude
High Altitude Training
BENEFITS:
Improved performance/ endurance (at lower oxygen levels, and when returning to lower altitude maintain benefits temporarily)
Due to:
* Higher concentration of hemoglobin/ RBC’s/ increased affinity of Hb for O2 = more O2 transported
* Improved gas exchange/ vital capacity (↑ lung surface area)
* Increased capillaries/ myoglobin in skeletal muscles
RISKS:
Altitude sickness/ lowered immunity/ stroke/ increased breakdown of muscle tissue
Effects only temporary/ require lengthy training time to achieve and may be unfair advantage to other competitors
Describe the different ways that carbon dioxide is carried in the blood.
Carbon dioxide is carried in the blood (from the tissues to the lungs) in one of three ways:
- Bound to hemoglobin (HbCO2 - binds to globin, not heme, so does not compete with oxygen)
- Dissolved in the blood plasma (in water portion - forms carbonic acid/ bicarbonate ions)
- In erythrocytes (RBC’s) as carbonic acid (~75% of CO2 carried this way!):
a. CO2 diffuses into erythrocyte
b. CO2 combines with water to form carbonic acid, which is more soluble (H2CO3) – this reaction is catalyzed by carbonic anhydrase
c. Carbonic acid dissociates into H+ ions and bicarbonate ions (HCO3-)
d. Chloride shift: Bicarbonate ions are pumped OUT of erythrocytes and Cl- ions are pumped in (ensures overall charge remains the same)
e. Bicarbonate ions in blood plasma combine with sodium ions in the blood plasma(NaHCO3) – these are carried to the lungs
f. H+ ions in the erythrocyte lower the pH, causing hemoglobin to release oxygen (to respiring cells/ tissues)
g. Hemoglobin absorbs/ binds excess H+ ions to buffer/ maintain pH in the erythrocyte
h. In lungs, HCO3- pumped back into RBC’s and entire process reversed
Outline how blood pH is maintained (and know the range of “normal” pH in the body).
Chemoreceptors are sensitive to changes in blood pH, and pH of blood is regulated to stay within the (VERY) narrow range of 7.35 to 7.45 (to avoid the onset of disease)
Chemoreceptors (such as those in the aorta/ carotid artery and medulla) detect changes in blood pH and can trigger body responses to maintain balanced pH in the blood:
* Changes in ventilation rate in lungs helps regulate CO2 in blood
* Kidneys control reabsorption of HCO3- (from filtered blood contents - called filtrate) back into blood; excess HCO3- excreted/ not reabsorbed
pH in blood is also maintained by plasma proteins:
* Plasma proteins act as pH buffers by removing excess H+ ions (that would ↑ acidity) or by removing excess OH- ions (that would ↑ alkalinity)
* Amino acids (building blocks of proteins) are zwitterions (both positive and negative charges) - Amine groups take on H+ ions (removing them from blood), carboxyl groups release H+ (adding them to blood where they combine with OH- ions to form water, removing excess OH- ions from blood)
