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Physiology Test III

Respiratory and Muscle Physiology

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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