platelet aggregation, contraction of SM at wound site
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serotonin
vascular constriction at wound site
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blood flow circulation
Left ventricle, aorta, arteries, arterioles, capillaries, venueles, veins, right atrium
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filling ventricles
AV - open SL - closed PA>PV
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isovolumetric contraction
AV - closed SL - closed PA < PV < Paorta
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ejection
ventricles open PA
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preload
directly related to ventricular filling
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afterload
pressure the heart must work against to eject blood during systole
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TPR
related to BP
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preload decreases
Ventricles fill less so less stretch, less stretch = less overlap of myosin heads with actin sites for myosin binding so less force of contraction (decrease SV and CO)
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heart muscle AP
1. Na channels open 2. Na channels inactivate, K opens 3. L-type Ca channel opens 4. L-type closes 5. K closes
pooling blood in lower extremities decrease CO blood accumulates in the legs and venous return decrease, drops EDV (preload) and SV decreases, results in decrease in CO which drops BP
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drop in BP
drop in SV by drop in venous return, EDV drop in HR cause drop in CO (para) drop in TRP
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sympathetic activates
Gs phosophorlate Na channel and they open faster
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parasympathetic activates
Gi inhibits adreylate cyclase and cAMP production and beta gamma binds to K channels, slow the closing of these channels
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edema
low albumin (decrease in plasma protein which decreases osmotic pressure) leakage of protein into interstitial fluid
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conducting zone
regulate air flow to alveoli smooth muscle
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conducting zone cleans with
ciliated cells and mucous cells
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partial pressure
% of gas x total pressure
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take a breath
-intrapleural space expands -pressure drops -lung expands -lung volume increases so alveolar pressure drops relative to Atm pressure -air moves into the lungs
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surfactant
does not increase elasticy increases compliance
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muscles involved in quiet breathing
diaphrgram and external intercostal muscles contract
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inspiratory reserve volume
deep breath, the volume taken in
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expiratory reserve volume
blowing air out forcefully
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vital capacity
TV + IRV + ERV
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inspiratory capacity
TV + IRV
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passive diffusion
O2 and CO2 can move across membrane by
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CO2 normal condition
high in capillaries and flow from cap to aveoli
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chloride shift
1. CO2 released to aveoli and exhaled 2. CO2 converted to HCO3 at tissues to be carried by blood 3. shift allows for conversion of CO2 to HCO3 at tissue 4. shift of HCO3 to CO2 in lungs
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in lungs
shift of HCO3 to CO2 takes place in
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in tissue
shift of CO2 to HCO3 takes place in
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decrease affinity
decrease CO2
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decrease affinity
decrease pH
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hemoglobin
wants less affinity
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these decrease affinity
increase temp, acid, CO2, DPG
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go up in altitude
-immediatly O2 drops -hyperventilate and lower CO2 so affinity for O2 increases -after a few days DPG levels increase and O2 affinity decreases
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H2O + CO2 (CA) = H2CO3 = H + HCO3
equation for alkalosis
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Aeolus poorly ventilated
O2 down, CO2 high then constrict this capillary blood vessel to limit blood flow to this alveolus
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no blood flow
O2 levels in that alveoli high CO2 low, we constrict the smooth muscle of the alveolus that is not perfused and relax the other
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if lungs are not functioning
hyperventilate, CO2 builds up and move to the right of eq to get more H+ acidosis
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metabolic acidosis
lungs are fine you are acidic, lungs want to hyperventilate to lower H+ so PCO2 levels are low
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pheriphreal chemoreceptors
carotid bodies measure pH and O2 aortic bodies measure only pH can measure metablic acids
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central chemoreceptors
measure pH indirectly only CO2 crosses BBB and then you measure change in pH