Study BIOL 472 Topic 11 Flash Cards
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Pile Management Card
BIOL 472 Topic 11
BIOL 472 Topic 11
| 3 types of capillaries |
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1. continuous: leaky junctions, muscle, brain, connective tissue -blood/brain barrier has tight junctions 2. fenestrated: large pores to help volume exchange between plasma and interstilial (kidney, intestines) 3. sinusoid: (not a capillary) 5x wider, fenestrations (liver) |
| prostaglanin role |
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prostacyclin: endothelial wall; decreases platelet aggregation; vasodilator thromboxane: increase platelet clot aggregation aspirin: general COX inhibitor; prevents clotting |
| mast cells |
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vasodilation reactive hyperemia |
| reactive hyperemia |
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-mast cells -tissues produce vasoactive compounds Histamine, bradykinins -occurs in response to increase in blood flow to an organ after being occluded. -shortage of oxygen -build-up of metabolic waste |
| Sympathetic ANS control of BP |
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-increases HR -increases force of contraction -alpha receptors: vaso constrict w/ NE ???????????? |
| active hyperemia |
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-metabolic demand of tissue causes vasodilation (skeletal muscle, digestive tract) -increased blood flow that occurs when tissue is active -blood vessels compensate for active metabolism by dilatation -allows more blood to reach the tissue. -prevents deprivation -ex: erections and nitric oxide |
| beta receptos |
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-greater affinity for E B1: stimulates heart contractility and rate, kidney, fat lyposis B2: inhibits (relaxes) smooth muscle in lungs, heart, skeletal muscles |
| alpha receptors |
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-greater affinity for NE a1: stimulates contraction of smooth muscle a2: same + inhibition of preganglionic nerve endings |
| treatment of high blood pressure |
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-diuretics -beta blockers (B1 receptor) -calcium chanel blockers (prevent contraction of smooth muscles) -ACE inhibitors (angio cycle) |
| lymphatic system |
| -excess tissue fluid and proteins that accumulate can be shunted back into circulation via lymphatic system |
| net filtration eq |
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net filtration rate= K[(Pc-Pi)-(pi c- pi i)] -arterial side tend to froce blood out -venous side tend to reabsorb -summation of both arterial and venous yields net outward force |
| pi i |
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-oncotic pressure of intersitial fluid proteins -filtration force -froces fluid out of capillary |
| osmotic pressure (oncotic?) |
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-determined by solute concentration of a compartment -main diff b/w plasma and interstial fluid is due to proteins -proteins in plasma, not intersitial |
| pi c |
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-determined by solute concentration of a compartment -oncotic pressure of capillary plasma proteins -reabsorption force -tends to force fluid into capillaries |
| Pi |
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-hydrostatic pressure of interstitial fluid -0 or filtration force -weak -0 to negative in value -always directed out -essentially 0 |
| Pc |
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-hydrostatic pressure in capillary -(filtration force) -varies -primary outward force -tends to force fluid out of capillary -decreases along pathway -higher at arterial end |
| 4 starling forces |
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1. Pc= hydrostatic pressure in capillary 2. Pi= hydrostatic pressure of interstial fluid 3. pi c= oncotic pressure of capillary plasma protein 4. pi i= oncotic pressure of interstial fluid proteins -determine fluid mvt in capillaries -most capillaries show net filtration at arterial end and net reabsorption at venous end |
| effect of temp |
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increase: vasodilation decrease: vasoconstriction |
| chemoreceptors |
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-more important at lower pressures, at tissue supply level vasodilation -increase pCO2--> H+ -decreases pH -decreases pO2 (less important) |
| metabolic theory |
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-tissues produce vasaodilators -decrease flow, vasodilators accumulate -increase flow, vasodilators wash away -local control of arteriole resistance -individual tissues regulate own blood supply -local regulation accomplished by paracrines |
| autoregulation of blood flow |
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1. myogenic theory 2. metabolic theory -vascular muscle has ability to regulate own state of contraction |
| myogenic theory |
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-smooth muscle's reaction to stretch is contraction -as BP increases, vessels contract -autoregulates |
| Atrial natriuretic peptide/factor |
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-released by increase in stretch in atrial wall (increased BP) -vasodilation -increases kidney Na+, water secretion -opposite of aldosterone -hormone |
| epinephrin |
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-dilator in heart, liver, skeletal muscles -B2 receptors |
| histimine |
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-vasodilation -allergic reactions |
| bradykinin |
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-peptide that causes blood vessels to enlarge -blood pressure to lower -endothelium-dependent -pain |
| EDRF |
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-endothelium-derived relaxing factor -NO -via cGMP -arginine is NO precursor -relaxes vascular smooth muscle -nitroglycerine action -erection/Viagra |
| endothelins |
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-potent vasoconstrictor -local effects -proteins that constrict blood vessels and raise blood pressure |
| ADH |
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-anti diuretic hormone -vasopressin: peptide hormone (stored in the posterior pituitary to be released into the blood stream) |
| vasodilators |
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EDRF: NO bradykinin kistamine Epinephrine atrial natriuretic peptide/factor protaglanin |
| vasocontrictors |
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NE- sympathetic ADH- vasopressin renal hormone cascade endothelins |
| hormones |
| - |
| Val Salva maneuver |
| -contract abs against closed glottis (Victorian women in corsetts) |
| thorasic pump inhalation |
|
-negative pressure -mvt of thorax while breathing in -when inhaling, thoracic cavity expands -subatm pressure -decreases pressure in inferior vena cava in thorax (it expands) -draws blood into vena cava |
| skeletal muslce pump |
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-when muscles (like in calf) contract, they compress the vein -force blood upward past valves |
| venous valves |
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-venous system at low pressure -collapse of valves results in varicose veins -one-way -blood passing can't flow backwards -pushed along by continuous mvt of cappillaries |
| frank starling law |
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-venous return is major determining factor of CO -aka heart pumps what it receives |
| venous return |
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Frank starling law 3 factors: 1. venous valves 2. skeletal mucle as pump 3. throasic pump inhalation |
| renin-angiotensin-aldosterone system |
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-liver constantly produces angiotensinogen in plasma -JG apparatus decrease in renal BP -granular kidney cells produce renin -acts on angiotensinogen already in system from liver -ANG I = enzyme -ANG II = vasoconstrictor -triggers aldosterone release from adrenal cortex -increase Na+ reabsorption -increase water reabsorption in distal tubule -increase blood volume and pressure -angiotensin III = vasoconstrictor pg. 655 |
| renal BP control |
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-important for long term reg -renin-angiotensin-aldosterone system |
| orthostatic hypotension |
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-pressure compensation from laying to standing -low blood pressure that occurs when going from laying down to standing up |
| vagal center |
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-vagus nerve -carries sensory info and efferent signals to many internal organs, including the heart |
| carotid sinus |
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-contains numerous baroreceptors -"sampling area" for maintaining blood pressure -internal carotide artery in throat |
| baroreceptors |
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-most important short term regulator -rapid -carotid sinus -aorta operates at higher pressure -increase BP, increase receptor firing rate -excites vagal centers (decreased HR) -inhibits medullary vasoconstriction centers -not good at long term BP reg because receptors reset after several days to prevailing BPs -orthostatic hypotension |
| vasoconstriction |
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-mst important flow regulator -restricts flow to non-essential organs |
| medullary ischemia |
| -O2 starved brain can increase BP |
| parasympathetic ANS control of BP |
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-decrease HR via vagus nerve -ACh -no effect on contraction -ACh is a vasodilator but not a force in BP regulation |
| ANS control of BP |
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-vasomotor center/baroreceptors linked to medulla -sym -para -medullary ischemia |
| blood pressure regulators |
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1. ANS 2. baroreceptors 3. renal 4. venous return 5. hormones 6. autoregulation 7. chemoreceptors 8. temp |
| Bernoulli principle |
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-lower pressure in small diameter tube w/ faster velocity -but, capillaries have slowest flow b/c of huge total area -fastest flow in small-diameter arterial system |
| Batista Procedure |
| -remove part of ventricular wall in enlarged heart, reduce r, less tension needed to maintain BP |
| Law of Laplace |
| pressure= (wall tension)/radius |
| shunting |
|
1. liver, digestive tract 2. skeletal muscle 3. kidneys |
| capillaries |
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-exchange vessels -O2, nutrients, CO2, hormones -5L of blood, but 8-10L of capillary space -football field surface area |
| venules and veins |
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-capacitance vessels -volume storage -54% of blood in venous system |
| arterioles |
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-main site of variable resistance to blood flow -contribute to 60% of total resistance -variable b/c of huge amts of smooth muscle -changes radius readily |
| Total peripheral resistance |
| MAP= CO x TPR |
| heart flow |
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-MAP/resistance -resistance= 1/radius^4 -aka MAP x radius^4 |
| Mean arterial pressure |
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-represents driving pressure for blood flow -1/3(pulse pressure) + diastolic pressure -1/3[2(Diastolic+ Systolic)] |
| pulse pressure |
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systolic-diastolic -measure of strength of the pressure wave |
| sound of Korotkoff |
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-pressure where Korotkoff sound is 1st heard is highest pressure in artery -when it disappears, lowest pressure in artery -systolic/diastolic |
| angioplasty |
| -balloon tube passed into coronary artery is inflated to open up the blockage |
| coronary bypass |
| -veins from other parts of the body are grafted onto the heart arteries to provide bypass channels around blocked regions |
| angina pectoris |
| heart pain that results from constricted blood vessels |
| atherosclerosis |
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-hardening of the arteries -fatty deposits form inside arterial blood vessels -elevated serum cholesterol and triglycerides also cause it |
| Fick Principle |
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-measures cardiac output in living subjects -application of law of conservation of mass -estimated w/ O2 consumption, with arterial pulmonary and venous values for O2 CO= (O2 consumed in mL/min)/(O2arterial-O2venous) CO= (mg dye injected x 60 sec)/(avg dye [] (mg/L) x duration of curve in sec) |
| Ca++ channel blockers |
|
-Verapamil -smooth muscle antagonist -dilates smooth muscle -lowers BP (afterload) -Ca++ channels in smooth muscle of blood vessels -block Ca++, dilates blood vessels -treats hypertension and angina |
| nitroglycerine |
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-cardiac vasodilator -used to treat angina (heart pain from constricted blood vessels) |
| digitalis |
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-enhances intracellular Ca++ entry -enhances contracility -slows Ca++ removal from cytosol -does not occur w/o drug |
| volume balance b/w ventricles |
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-left heart failure: congestive fluid in liquids -right heart failure: leads to endema in tissues |
| if heart rate >170... |
| ...decreases cardiac output due to insufficient filling time |
| max HR |
| 220-age |
| how to decrease heart rate? |
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-parasymapthetic inhibits -block nerves that slow heart rate -atropine blocks ACh |
| how to increase heart rate? |
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-smpathetic stimmulates -E, NE |
| chronotropes |
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-may change the heart rate by affecting the nerves controlling the heart -sympathetic stimulates (E, NE) -parasympathetic inhibits (vagus nerv via ACh; atropine blocks ACh) |
| muscle length in heart |
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-resting heart muscle shorter than optimal -increase end disatolic volume, increase muscle to optimal length |
| Heart contractility info |
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-a muscle can stay at 1 length and still increase contractility -increasing sarcomere length makes cardiac muscles more sensitive to Ca++, linking contractility to muscle length |
| Digitalis |
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-increase Ca++ flow -enhance contracility -positive inotropic effect |
| positive inotropes |
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1. increase Ca++ flow (Digitalis) 2. increase cAMP (Ca++ channels via epinephrine, caffeine) |
| positive inotropes |
| -a chemical that increases force of contraction in heart |
| Ejection fraction |
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(stroke volume)/(EDV) x100% normally 60-70% pg. 493 |
| Frank Starling Law |
|
-heart has intrinsic ability to change SV in response to input (venous return) -aka "heart pumps what it receives" |
| stroke volume |
| end diastolic volume- end stroke volume |
| cardiac output formula |
| cardiac output= heart rate x stroke volume |
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