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Physiology Test III
Respiratory and Muscle Physiology
| Question | Answer |
|---|---|
| describe the flow of blood through the lungs | (1) O2 into lungs and into PC; (2) goes into PV and into heart and into SA; (3) SA goes to SC and O2 exchange with tissues; (4) deoxy blood goes to SV to heart to PA; (5) CO2 out of PC into lungs and out of body |
| what constitutes internal and external respiration? | internal- the giving of O2 from the blood to the mitochondria in tissues which makes ATP, and the giving of CO2 to blood from mitochondria; external- everything else |
| what are other functions of the respiratory system? | behavioral, defense, secretions, metabolic, acid-base balance |
| what is the difference between central and obstructive sleep apnea? | central- brain doesn't tell respiratory muscles to breathe; obstructive- muscles in resp tract relax which blocks airway |
| what do vocal cords do? | they slow release of air coming out of the chest |
| where are things more likely to be lodged in the lung? why? | the right lung because it's straighter than the left lung |
| what is an esophagotracheal fistula? | acid burns through esophagus and smooth muscle causing food to get into lungs |
| what are the divisions of the resp system? | (1) larynx; (2) trachea; (3) primary (lobar) bronchi; (4) secondary bronchi; (5) tertiary bronchi; (6) bronchioles; (7) terminal bronchioles; (8) resp bronchioles; (9) alveolar duct; (10) alveolar sac; (11) alveolus |
| describe the layers of the resp system | (1) mucus layer on top; (2) liquid (sol) layer has cilia which moves mucus |
| what happens in cystic fibrosis? | no chloride is being pumped out into sol layer so water doesn't follow. no sol layer is present so mucus accumulates in lung. they are also very prone to infection |
| why is small airwary disease not so dangerous? | you can lose half of function in small airways and still breathe fine because of the huge cross sectional area |
| what is an acinus composed of? | respiratory bronchiole, alveolar ducts, alveolar sacs, and alveoli |
| what do Type II pneumocytes do? | they secrete surfactant which lowers surface tension |
| what happens in emphysema? | smoking causes holes in the lung; neutrophils release elastase which tear up the lung |
| what is eupnea? | normal breathing in which ventilation matches metabolic demands |
| what is hyperpnea? | increased ventilation which matches increased metabolic demands |
| what is hyperventilation? | inappropriately high ventilation for the metabolic demand; A and a PCO2 decreased, A PO2 increased |
| what is hypoventilation? | inappropriately low ventilation for metabolic demand; A and a PCO2 increase, A O2 decreased |
| what is tachypnea? | increased frequency of breathing |
| what is dyspnea? | subjective sensation of difficult or labored breathing; may not be a gas exchange problem |
| what is apnea? when does it usually occur? | it is the temporary or cessation of breathing (at FRC); usually occurs after hyperventilation of swallowing |
| what happens when neural inputs tells us to breathe? | alveoloar pressure and intrapleural pressure decreases; transpulmonary pressure and lung volume increase |
| what are 3 ways to inflate the lungs? | (1) increase alveolar pressure; (2) decreased body surface pressure; (3) activate inspiratory muscles |
| with increased resistance, what happens to the intrapleural pressure when you inhale and exhale? | inhale- more negative; exhale- more positive |
| what comprises the muscles of respiration? | inspiratory muscles- diaphragm, external and parasternal intercostals, acessory muscles (SCM, scalenes, trapezius); expiratory muscles- abdominal muscles, internal intercostals (only during active expiration) |
| what do the "pump handle" and "bucket handle" examples have to do with respiration? | "pump handle"- motion demonstrates anterior-posterior dimension of rib cage; "bucket handle"- motion demonstrates later dimension |
| what is minute ventilation? | it is the flow moved into or out of the lungs; V.E= VT x f |
| what is the equation for alveolar ventilation? | V.A= (VT - VD) x f |
| what is anatomic dead space? | volume of lung not involved in gas exchange |
| what is alveolar dead space? | poorly ventilated units in alveoli; example- embolus blocks off branch |
| what are the two ways to increase ventilation? which one is more efficient? | (1)increase tidal volume (VA increases, VD unchanged); increase respiratory frequency (VA and VD increase); increasing tidal volume is more efficient |
| if you increase alveolar ventilation, what happens to PCO2? | it decreases |
| what is the formula for opposing force? | Fopp= elastance(length) + resistance(velocity) + inertance(acceleration) |
| what is elastance? compliance? | elastance- tendency to return to initial size after distension; compliance- stretchability or change in volume/change in pressure |
| what is emphysema and fibrosis in terms of elasticity and compliance? | emphysema- low elasticity and high compliance; fibrosis- high elasticity and low compliance |
| what happens to compliance at low and high volumes? | low volumes- steep slope, high compliance; high volumes- shallow slope, low compliance |
| what is the LaPlace equation? | P= 2T/r |
| what happens to compliance when you fill a lung with saline? | the compliance increases |
| what is lung recoil due to? | surface tension and elastic and collagen fibers of lung |
| what does an increased residual volume indicate? | asthma |
| what does a decreased FRC indicate? increased FRC? | decreased FRC- chest wall inverted in more or lung is stiffer; increased FRC- chest wall out more or lung less stiff |
| what CANNOT be measured by a spirometer? | TLC, FRC, and RV |
| what is Ohm's Law? | V= IR |
| what is the equation for flow? | flow= P/R |
| what are the types of flows? | laminar, turbulent, and transitional; laminar is greater than turbulent |
| what happens to resistance when FRC goes to TLC? FRC to RV? | FRC to TLC- resistance decreases; FRC to RV- resistance increases |
| what is hypoxia? hypoxemia? hypocapnia? | hypoxia- low oxygen; hypoxemia- low PO2; hypocapnia- decreased CO2 |
| what are the pressures of O2 and CO2 in atmospheric air, alveolar air, pulmonary veins, systemic arteries, cells, systemic veins, and pulmonary arteries? | atmospheric air- 160 and 0.3; AA, PV, SA- 100 and 40; cells- <40 and >46; SV, PA- 40 and 46 |
| what are normal values for tidal volume, frequency, minute ventilation, alveolar ventilation? | VT- 500 mL; f- 12-20 bpm; VE- 6.0L; VA- 4.2L |
| what are normal values for arterial and venous PO2, PCO2, and pH? | PO2- 95 and 40; PCO2- 40 and 46; pH- 7.4 and 7.37 |
| what happens at the tissue level and lung level with CO2? | (explain it--too difficult to diagram) |
| what are the forms of CO2 in RBCs? | (1) dissolved CO2 (7%); (2) carbamino compounds (23%); (3) bicarbonate in plasma (70%) |
| what are the three ways to express amount of O2 in blood? | (1) O2 partial pressure; (2) O2 content; (3) O2 saturation |
| how do you measure O2 content in blood? ie. what's the equation | CO2= 1.36 [Hb] (%satO2)/(100) + 0.003 (PO2) |
| what happens at tissue and lung level with O2? | lung- O2 goes into blood and joins with Hb; tissue- Hb-O2 dissociate in blood and O2 goes into tissue |
| what are the two forms O2 is carried in the blood? | (1) dissolved in plasma--insignificant; (2) bound to hemoglobin in RBCs |
| how are O2 solubility and and temperature related? | an increase in temperature causes a decrease in O2 solubility |
| how does hemoglobin work? | it has 2 alpha and 2 beta chains and binds 4 molecues for O2; it binds O2 at high PO2 and releases O2 at low PO2 |
| what is the normal hemoglobin concentration? how much can 1 gram of hemoglobin bind? | normal concentration is 15g/100ml; 1g hemoglobin binds 1.36ml O2 |
| what is the critical O2 pressure? | 60mmHg |
| what determines O2 saturation? | PO2 determines it; NOT [Hb] |
| what changes oxyhemoglobin affinity? | increased H+, CO2, temperature, and [2,3-DPG] cause a rightward shift thus giving up O2 |
| what are three things that change O2 carrying capacity? | (1) changes in Hb concentration; (2) presence of carbon monoxide; (3) formation of methemoglobin (due to metabolic disorders) |
| what happens to pressures and blood flow in the different parts of the lung? | zone1- PA>Pa>Pv (no blood flow); zone2- Pa>PA.Pv (some blood flow); zone3- Pa>Pv>PA (alot of blood flow) |
| where does most blood flow and ventilation go in the lung? at low lung volumes? | in the lower regions (zone3); at low volume, the upper lobes receive the most inspired tidal volume |
| what is the ideal V/Q? what happens at increased dead space? increased shunt? | ideal- V/Q=1; DS- V/Q >1 (blood vessel embolism); Shunt- V/Q<1 (obstruction in airways shunts blood away from alveolus) |
| why is diffusion of N2O perfusion limited and CO diffusion limited? | N2O does not bind Hb so it is perfusion limited because it depends on the blood flow; Hb can hold alot of CO so the amount of CO that diffuses is diffusion limit |
| how do you calculate inspired oxygen? | PiO2= (0.21) x (760 - 47 mmHg) = about 150mmHg |
| what is the respiratory quotient? | RQ= (CO2 production)/(O2 utilization) in cell metabolism |
| what is the alveolar gas equation? | PAO2= (PiO2 - PACO2)/R |
| what is V/Q at the top and bottom of the lung? | high V/Q at top of lung, low V/Q at bottom of lung |
| what is V/Q mismatch? how do you cure it? | it is uneven ventilation; give supplemental O2 and it increases PAO2 which increases saturation of O2 |
| how does the body compensate for V/Q mismatch? | (1) hypoxic vasoconstriction decreases degree of contribution from areas where V/Q <1; (2) hyperventilation- can sometimes help in V/Q<1 cases, no help in V/Q>1 |
| where is the respiratory center located? | medulla oblongata |
| what innervates the respiratory system? | stretch receptors- volume; irritant receptors- smoke; J receptors- emboli, muscle spindles; chemoreceptors (from aortic and carotid bodies) |
| what are the different respiratory centers and what are their functions? | DRG- quiet inspiration; VRG- forceful inspiration and active expiration; pneumotaxic center- influences inspiration to shut off; apneustic center- prolongs inspiration |
| what is the main respiratory pacemaker at rest? | DRG |
| what are the 2 types of chemoreceptors and what are their functions? | central- in medulla, more sensitive to changes in PaCO2 due to low pH of CSF; peripheral- in carotid and aortic bodies, stimulated by rise in [H+] in arterial blood |
| what is the effect of increased PaCO2 on minute ventilation? | increased PaCO2 increases minute ventilation |
| as O2 decreases, what happens to ventilation? | ventilation increases sharply due to input from carotid bodies |
| what happens to the oxygen sensors when there's low O2? (below 60mmHg) | low O2 causes KO2 channel to close, K+ decreases causing cell depolarization, depolarization causes exocytosis of dopamine vesicles which creates AP which stimulates AP which signals central chemoreceptors to increase ventilation |
| what is spirometry? | measurement of FVC and FEV1 |
| what are the stages of COPD? | stage 0: normal spirometry; stage 1: FEV1/FVC <70%, FEV1>80%; stage 2: 50%<FEV1<80%; stage 3: 30%<FEV1<50%; stage 4: FEV1<30% |
| what is the FVC? | max amount of air that can be forcefully expired from point of max inspiration |
| what is FEV1? | forced expiratory volume in one second |
| what should the FEV1/FVC ratio be? | about 80% or greater |
| what is PEF? | peak expiratory flow |
| what are the structural components of striated muscle? | (1) whole muscle; (2) muscle fiber; (3) myofibril; (4) sarcomere; (5) myofilaments- thin filament (actin, troponin, tropomyosin, nebulin) and thick filament (myosin, titin) |
| what happens when a muscle is contracted? | only the I-band length shortens! Everything else remains constant |
| describe the crossbridge cycle | (explain it) |
| what is the max velocity determined by? | the ATPase rate |
| what is the max force determined by? | the number of myosin crossbridges |
| what happens when there's Ca present? | it binds to troponin which moves the tropomyosin so that the actin binding site is exposed, allowing myosin to bind |
| what happens when an AP occurs? | AP occurs, transmission along T-tubules, DHPR senses Ca and tell RYR to open Ca channels, Ca diffuses to filaments and initiates contraction, Ca uptake by SR cuases relaxation |
| what is the difference between summation and tetany? | summation- increase in response to second AP that occured during first AP; tetany- max force due to multiple stimuli, also higher [Ca] in cytoplasm for longer period of time |
| what are isometric contractions? | same length generates force but no contractions; passive force increases with increasing length, active force goes up then down |
| what determines the passive force? or what prevents you from overstretching the sarcomere? | collagen (connective tissue) and titin |
| what determines active force? | the attachment of crossbridges (extent of overlap between the thin and thick filaments) |
| what causes the plateau in the filament overlap hypothesis? | the bare zone |
| why don't we want to operate at very long or very short lengths in terms of filament overlap? | too long- not enough crossbridge interaction; too short- causes steric hindrance, blocks binding, and the SR doesn't work very well (reduces Ca release) |
| what are isotonic contractions? | shortening at a constant load |
| how else is max force determined? | preload determines length determines number of crossbridges determines max force |
| with preload set, what allows you to change velocity and force? | afterload |
| what else can change the max velocity? | pH and temperature (decrease temp, decrease Vmax) |
| what is the equation for power? | Power = Force x Velocity |
| what is the difference between Familial Hypertrophic Cardiomyopathy (FHC) and Dilated Cardiomyopathy (DCM)? | both genetic disorders with point mutation of cardiac mysoin gene; FHC- occurs in young sports players, due to enhanced power production; DCM- due to reduced power production |
| what does dystrophin do? | it connects actin to muscle membrane; without it, the membrane is fragile |
| when shortening or lengthening muscle fibers, will the sarcomere length change? why or why not? | the sarcomere length will remain the original length because that's the optimal length; it will add more sarcomeres |
| smooth or skeletal: which has a greater force? greater velocity? better energy consumption? | smooth; skeletal(100x); smooth(300x) |
| what is the myosin structure of smooth muscle? | 2 heavy chains, 4 light chains- essential light chain and regulatory light chain (can be phosphorylated) |
| what happens in smooth muscle contraction? (start with AP) | AP leads to rise in intracellular Ca (from ECF and SR); Ca binds calmodulin; Ca-calmodulin bind MLCK; MLCK phosphorylates regulatory light chain; myosin cycles and attaches to actin |
| where do smooth and skeletal muscle need ATP? | skeletal- crossbridges and Ca ATPase pump; smooth- crossbridges, Ca ATPase pump, and phosphorylate LC |
| what happens during smooth muscle relaxation? | Ca ATPase pumps pump Ca back into SR or in ECF; phosphatases unphosphorylate LC |
Created by:
medchichi
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