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Cardiovascular
Costanzo-Cardiovascular Physiology
| Question | Answer |
|---|---|
| atrioventricular (AV) valves | one-way valves connecting atrium=>ventricle tricuspid valve (right heart) mitral valve (left heart) |
| systemic circulation | left heart, systemic arteries, capillaries, veins left ventricle pumps blood to all organs except lungs |
| pulmonary circulation | right heart, pulmonary arteries, capillaries, veins |
| cardiac output | rate blood pumped out from either ventricle per unit time CO=SV x HR in steady state right heart CO= left heart CO |
| venous return | rate blood returned to atria from veins in steady state CO=venous return |
| circuitry | LV=>aorta=>organs=>veins=>RA=>RV=>pulmonary artery=>lungs=>pulmonary vein=>LA=>LV |
| semilunar valve | pulmonic valve (right heart) aortic valve (left heart) |
| arteries | functions to deliver oxygenated blood to organs thick-walled-->receive high pressure blood (stressed volume) extensive elastic tissue, smooth muscle, connective tissue aorta the largest artery-->medium and small-sized arteries branch from it |
| arterioles | smallest branches of arteries site of highest resistance to blood flow=>can be changed by alteration of SNS activity, circulating catecholamines, vasoactive substances contains alpha1-adrenergic and beta2-adrenergic receptors |
| alpha1-adrenergic receptors | commonly found in several vascular beds-->constricts smooth muscle-->increases resistance to blood flow |
| beta2-adrenergic receptors | found in arterioles of skeletal muscle=>dilates sooth muscle=>↓ resistance to blood flow |
| capillaries | thin-walled structures lined with single layer of endothelial cells surrounded by basal lamina not all perfused with blood with blood all the time=>depends on metabolic needs site of exchange |
| veins and venules | thin-walled structures with endothelial cell layer surrounded by basal lamina very large capacitance=>capacitance changes with contraction of smooth muscle holds largest % of blood=>unstressed vol (low press) |
| velocity of blood flow | v=Q/A highest in aorta lowest in capillaries |
| pressure difference | driving force for blood flow |
| resistance | impediment to flow major mechanism to change blood flow thru changing blood vessel resistance in arterioles |
| blood flow | Q=(delta)P/R used to measure TPR and resistance in single organ direction of blood flow always from high to low |
| total peripheral resistance (TPR) | total resistance of entire systemic vasculature |
| Poiseuille equation | R=8nl/(3.14r^4) factors that determine resistance of blood flow R=resistance n=viscosity of blood l=length of blood vessel r^4=radius of blood vessel |
| series resistance | total resistance= to sum of individual resistances total flow thru each level the same press ↓ progressively as blood flows thru each sequential component arrangement of blood vessels within an organ |
| parallel resistance | total resistance less than any individual resistance=>adding more resistance ↓ total resistance *increasing one individual resistance ↑ total resistance no loss of press in major arteries seen in aortic branching |
| laminar flow | streamlined blood flow=>parabolic profile=>velocity highest at center and lowest toward vessel walls |
| turbulent flow | lamina flow disrupted to streams mixing radially and axially=>seen in valves or sites with blood clots more energy required to drive flow often accompanied by murmurs |
| Reynold's number | used to predict laminar or turbulent flow <2000 laminar >3000 turbulent NR=pdv/n NR=Reynold's number p=density of blood d=diameter of blood vessel v=velocity of blood flow* n=viscosity of blood* |
| anemia and Reynold's number | ↑ Reynold's number due to 1)↓ blood viscosity 2)high CO |
| thrombi and Reynold's number | ↑ Reynold's number 1)narrows blood vessel diameter 2)↑ blood velocity at site of thrombus |
| capacitance | describes vol of blood a vessel can hold at a given press C=V/P C=compliance V=volume P=pressure higher compliance=>more vol it can hold at given press veins most compliant and contain unstressed vol |
| changes in compliance of veins | leads to redistribution of blood between veins and arteries ↑ compliance shifts blood from arteries=>veins ↓ compliance shifts blood from veins=>arteries |
| compliance of arteries and aging | walls get stiffer, less distensible, less compliant arteries hold less blood=>why elderly have higher BP |
| pressures in cardiovascular system-systemic | aorta=100 large arteries=100(120/80) arerioles=50 capillaries=20 vena cava=4 right atrium=0-2 |
| pressures in cardiovascular system-pulmonary | pulmonary artery=15(25/8) capillaries=10 pulmonary vein=8 left atrium=2-5 |
| aorta and BP | largest artery=>medium and small-sized arteries branch from it mean press very high 1)large vol pump from left ventricle into aorta 2)low compliance of arterial wall |
| large arteries and BP | high mean press because high elastic recoil of arterial walls pulsations greater here than aorta=>higher systole and lower diastole |
| small arteries and BP | where arterial press begins to ↓ pulse press ↓ in small arteries and absent in arterioles most significant ↓ in arterioles because has highest resistance to flow |
| capillaries and BP | press ↓ further from arterioles 1)frictional resistance to flow 2)filtration of fluid |
| venules and veins and BP | press ↓ further from capillaries because compliance is very high |
| pulsations | reflect pulsatile activity of heart: ejecting blood during systole=>resting dring diastole=>ejecting blood=>resting each pulsatile cycle coincides with one cardiac cycle |
| diastolic pressure | lowest arterial press measured during cardiac cycle press in artery during ventricular relaxation=>no blood being ejected from left ventricle |
| systolic pressure | highest arterial press measured during cardiac cycle press in artery after blood ejected from left ventricle during systole |
| dicrotic notch | "blip" in arterial press curve produced when aortic valve closes=>produces brief period of retrograde flow=>↓ aortic press below systolic value |
| pulse pressure | difference between systolic and diastolic press=>magnitude reflects SV will change if SV changes |
| stroke volume | vol of blood ejected from left ventricle on a single beat |
| mean arterial pressure (MAP) | average press in a complete cardiac cycle=>the driving force for blood flow in arteries MAP=diastolic press + 1/3 pulse press *diastolic press used because greater fraction of each cardiac cycle spent in diastole than systole |
| dampening of pulse pressure | 1)resistance of blood vessels=>particularly arterioles 2)compliance of blood vessels=>particularly veins |
| arteriosclerosis | plaque deposits in arterial walls ↓ diameter of arteries=>makes them stiffer and less compliant ↓ compliance=>SV prod greater ∆ in arterial press ↑ systolic press, pulse press, and mean press |
| aortic stenosis | aortic valve is narrowed SV ↓=>less blood enters aorta ↓ systolic press, pulse press, and mean arterial press |
| aortic regurgitation | when aortic valve incompetent=>one-way flow disrupted |
| contractile cells | working cells of heart=>majority of atrial and ventricular tissues AP in these cells lead to contraction and generation of force or press |
| conducting cells | constitute tissues of SA node, atrial internodal tracts, AV node, bundle of His, and Purkinje system specialized muscle cells=>function to rapidly spread AP over entire myocardium *can generate AP spontaneously=>normally suppressed except for SA n |
| SA node | serves as pacemaker |
| spread of excitation within heart | SA node=>atrial internodal tracts=>atria=>AV node=>bundle of His=>Purkinje system=>ventricles |
| AV node | slow conduction here ensures ventricles have sufficient time to fill with blood before they are activated and contract ↑ conduction leads to ↓ 1)ventricular filling 2)SV 3)cardiac output |
| His-Purkinje system | conduction is extremely fast=>rapidly distributes AP to ventricles=>important for efficient contraction and ejection of blood |
| normal sinus rhythm | pattern and timing of electrical activation of heart normal 1)AP must originate in SA node 2)SA nodal impulses must be regular (60-100 per min) 3)activation of myocardium must occur in correct sequence, timing, and delays |
| resting membrane potential | determined primarily by K+ in cardiac cells=>conductance to K+ at rest is high=>resting membrane potential close to K+ equilibrium potential |
| AP basis for ventricles, atria, and Purkinje system | 1)long duration=>long refractory period 2)stable resting membrane potential 3)plateau=>sustained period of depolarization=>explains long duration of AP and refractory period |
| phases of AP for ventricles, atria, and Purkinje system | 1)phase 0, upstroke 2)phase 1, initial depolarization 3)phase 2, plateau 4)phase 3, repolarization |
| AP-phase 0 | upstroke=>rapid depolarization by transient ↑ in Na+ conductance (inward current) |
| AP-phase 1 | initial depolarization=>brief period of repolarization from inactivation of Na+ channels and outward K+ current |
| AP-phase 2 | plateau=>long period of stable, depolarized membrane potential result of ↑ in Ca2+ conductance=>slow inward current of Ca2+ through L-type channels balanced by outward K+ current *initiates Ca2+-induced Ca2+ release |
| AP-phase 3 | repolarization=>begins gradually then rapidly with ↑ outward K+ current and ↓ Ca2+ inward current outward K+ current ↓ as membrane potential fully repolarizes |
| AP-phase 4 | resting membrane potential=>membrane potential stable again |
| L-type channels | inhibited by Ca2+ channel blockers=>nifedipine, diltiazem, verapamil |
| AP in SA node | 1)phase 0, upstroke 2)phase 3, repolarization 3)phase 4, spontaneous depolarization |
| SA node AP-phase 0 | upstroke=>result of ↑ in Ca2+ conductance and inward current thru T-type Ca2+ c hannels *upstroke not as sharp as in ventricules, atria, and Purkinje upstroke |
| SA node AP-phase 3 | repolarization=>from ↑ in K+ conductance and outward K+ current |
| SA node AP-phase 4 | spontaneous depolarization=>from "funny" inward Na+ current turned on by previous repolarization=>ensures each AP in SA node followed by another AP longest portion of SA node AP rate of this phase sets heart rate |
| latent pacemakers | myocardial cells other than SA node that have intrinsic automaticity AV node, bundle of His, and Purkinje fibers=>not expressed due to overdrive suppression |
| overdrive suppression | suppression of latent pacemakers by driving their heart rate ex)when SA node drives heart rate fastest potential pacemaker set the heart rate=>suppresses other by driving their firing rate |
| ectopic pacemaker | latent pacemakers that become the pacemaker occurs when 1) SA node suppressed or 2)conduction of its AP blocked or 3)latent pacemaker faster than SA node |
| firing rate of SA node and latent pacemakers | SA node=70-80 AV node=40-60 Bundle of His=40 Purkinje fibers=15-20 |
| AV delay | conduction velocity slowest in AV node=>ensures ventricles have time to fill with blood from atria requires approx. 1/2 total conduction time through myocardium |
| conduction velocity | speed AP propagates thru tissue depends on size of inward current during upstroke and cable properties (gap junctions) |
| excitability | capacity of myocardial cells to generate AP in response to inward depolarizing current *amount of inward current require to bring myocardial site to threshold potential |
| refractory period | when no upstroke can occur due to closed inactivation gates=>no upstroke no AP |
| absolute refractory period | cell completely refractory to fire another AP=>incapable of generating a 2nd AP no matter how large the stimulus |
| effective refractory period | 2nd AP can be generated a conducted AP cannot be generated |
| relative refractory period | 2nd AP can be generated with a stimulus greater-than-normal but will have 1)abnormal configuration 2)shortened plateau phase |
| supranormal period | cell more excitable than normal during this period=>less inward current required to depolarize cell to threshold potential |
| chronotropic effects | effects of ANS on heart rate sympathetic stimulation ↑ heart rate parasympathetic stimulation ↓ heart rate |
| positive chronotropic effects | ↑ heart rate=>SNS stimulate beta1 receptors in SA node=>↑ conduction of "funny" channels=>↑ phase 4 depolarization |
| negative chronotropic effects | ↓ heart rate=>PNS stimulates M2 receptors in SA node 1)↓ conduction of "funny" channels=>↓ phase 4 depolarization 2)↑ conductance of K+-Ach channel=>enhances outward K+ current=>hyperpolarizes SA nodal cells |
| dromotropic effects | effects of ANS on conduction velocity |
| positive dromotropic effects | SNS ↑ conduction velocity thru AV node=>↑ rate AP conducted from atria to ventricles mechanism thru ↑ Ca2+ conduction and inward current |
| negative dromotropic effects | PNS ↓ conduction velocity thru AV node=>↓ rate AP conducted from atria to ventricles 1)↓ Ca2+ conduction and inward current 2)↑ conduction of K+-Ach channel and outward K+ current can produce heart block |
| heart block | AP potentials not conducted at all from atria to ventricles different degrees where conduction is slowed or severe cases where AP not conducted to ventricles at all |
| ECG- P wave | depolarizaton of atria duration correlates with conduction time thru atria |
| ECG- PR interval | time from initial depolarizatoin of atria to initial depolarization of ventricles includes P wave and PR segment PR segment and interval corresponds to AV node conduction |
| ECG- QRS complex | represents depolarization of ventricles short duration because conduction velocity takes place in His-Purkinje system |
| ECG- T wave | repolarization of ventricles |
| ECG- QT interval | represents first ventricular depolarization to last ventricular repolarization |
| ECG- ST segment | part of QT interval=>correlates with plateau of ventricular AP |
| ECG- heart rate | number of QRS complexes |
| ECG- cycle length | R-R interval |
| arrhythmias | abnormal heart rhythms ↑ heart rate a factor |
| myocardial cell structure | composed of sarcomeres thick filaments composed of myosin thin filaments composed of actin, tropomyosin, and troponin contraction thru sliding filament model contains T tubules (continuous with cell membrane) and sarcoplasmic reticulum |
| actin | globular protein with myosin-binding site |
| tropomyosin | runs along groove of twisted actin strands and blocks myosin-binding site |
| troponin | globular complex of 3 subunits=>troponin C subunit binds Ca2+ and changes conformationally to remove tropomyosin from myosin-binding site |
| Ca2+ release from sarcoplasmic reticulum | determined by 1)amount of Ca2+ previously stored 2)size of inward Ca2+ current during plateau of action potential |
| cross-bridges | formed between actin and myosin during contraction to produce tension cross-bridge cycling continues as long as intracellular [Ca2+] high enough to bind troponin C |
| muscle relaxation | occurs when [Ca2+] ↓ to resting levels 1)reaccumulated in sarcoplasmic reticulum=>Ca2+-ATPase 2)extruded from cell=>Ca2+ ATPase and Ca2+-Na+ exchange |
| inotropism | intrinsic ability of myocardial cells to develop force at given muscle cell length |
| positive inotropic effects | SNS=>beta1 receptors=>pathway phosphorylates sarcolemmal Ca2+ channels and phospholamban 1)↑ peak tension 2)↑ rate of tension development 3)faster rate of relaxation=>shorter contraction=>longer filling time |
| sarcolemmal Ca2+ channels | when phosphorylated 1)↑ inward Ca2+ current during plateau phase 2)↑ Ca2+ trigger=>↑ Ca2+ released from sarcoplasmic reticulum |
| phospholamban | protein that regulates Ca2+ ATPase in sarcoplasmic reticulum when phosphorylated stimulates Ca2+ ATPase=>greater uptake and storage of Ca2+in sarcoplasmic reticulum leads to 1)faster relaxation 2)↑ amount of stored Ca2+ for future release |
| negative inotropic effects | PNS=>muscarinic receptors=>negative effect on ATRIA=>inhibitory pathway ↓ contractility 1)ACh ↓ inward Ca2+ current during plateau 2)ACh ↑ K+-Ach conduction=>shortens AP duration=>↓ inward Ca2+ current |
| heart rate and contractility | ↑ HR ↑ contractility and vice versa=>Ca2+ the underlying concept 1)greater influx of Ca2+ during AP=>greater accumulation of Ca2+=>↑ total amount of trigger Ca2+ 2)↑ HR caused by SNS=>phospholamban phosphorylated |
| cardiac glycosides | positive inotropic agents=>inhibit Na+-K+ ATPase=>alters Ca2+-Na+ exchanger fxn=>[Na+] equilibrates [Ca2+] ↑=>↑ tension derived from foxglove plan=>Digitalis purpurea=>used to treat CHF ex) digoxin, digitoxin, ouabain |
| muscle length and Ca2+ (length-tension relationship) | increasing muscle length 1)↑ troponin C's Ca2+ sensitivity 2)↑ Ca2+ release from sarcoplasmic reticulum |
| preload | LVEDV=>resting length from which muscle contracts |
| afterload | aortic press=>velocity of shortening cardiac muscle maximal when afterload=0 |
| stroke volume | vol of blood ejected by ventricle on each beat SV=(EDV) - (ESV) |
| ejection fraction | fraction of EDV ejected in each SV=>meas of ventricular efficiency EF=SV/EDV |
| Frank-Starling relationship/law of the heart | vol of blood ejected by ventricle depends on vol present in ventricle at end of diastole EDV depends on venous return law underlies and ensures CO=venous return if VR ↑=>EDV ↑=>SV ↑ |
| width of PV-loop | vol of blood ejected=SV |
| ventricular pressure loop phases | 1)isovolumetric contraction 2)ventricular ejection=>aortic valve opens; press reaches highest point 3)isovolumetric relaxation 4)ventricular filling=>mitral valve opens |
| PV loop-increased preload | ↑ VR=>↑ preload=>↑ SV ↑ SV based on Frank-Starling relationship |
| PV loop-afterload | ↑ aortic press=>SV ↓=>EDV ↑ *ventricular press must rise to greater-than-normal level during isovolumetric contraction |
| PV loop-increased contractility | ↑ contractility=>↑ tension and press=>↑ SV and EF *EDV ↓ |
| myocardial oxygen consumption | press work (internal work) more costly than vol work |
| aortic stenosis and myocardial O2 consumption | myocardial O2 consumption greatly ↑=>extra press work from ventricle to develop high press to pump blood thru stenosed aortic valve *CO reduced |
| strenuous exercise and myocardial O2 consumption | myocardial O2 consumption ↑ from ↑ vol work |
| law of Laplace | greater wall thickness=>greater developed press *explains ventricular wall hypertrophy=>but too much thickness can lead to ventricular failure |
| Fick principle | CO of left and right ventricles equal |
| cardiac cycle | 1)atrial systole 2)isovolumetric ventricular contraction 3)rapid ventricular ejection 4)reduced ventricular ejection 5)isovolumetric ventricular relaxation 6)rapid ventricular filling 7)reduced ventricular filling |
| cardiac cycle-atrial systole | preceded by P wave=>depol of atria=>artrial contraction=>↑ atrial press reflected in veins=>a wave mitral valve open=>ventricles filling *blip in ventricular press. during contraction=>active filling S4 heard in ventricular hypertro |
| cardiac cycle-isovolumetric ventricular contraction | begins during QRS complex=>electrical activation of ventricles mitral valve closes when L ventricular press>L atrial press; tricuspid valve closes in R heart; *S1 heard=>splits bc mitral closes before tricuspid press ↑ but vol constant |
| cariac cycle-rapid ventricular filling | ventricular press reaches highest value=>aortic valve opens *MOST SV ejected=>aortic press ↑ atrial filling begins for ejection in next cycle ends with beginning of T wave (end of ventricular contraction) |
| cardiac cycle-reduced ventricular ejection | reduced ejection=>aortic valve still open without any ventricular contraction=>ventricular press falls aortic press falls because blood running off into arterial tree ventricles begin to repolarize=>beginning of T wave |
| cardiac cycle-isovolumetric ventricular relaxation | begins after ventricles fully repolarized=>end of T wave left ventricular press ↓ dramatically=>aortic valve closes(dicrotic notch)=>S2=>splits bc inspiration delays pulmonic valve closure |
| cardiac cycle-dicrotic notch | point in aortic press curve where aortic valve closes |
| cardiac cycle-rapid ventricular filling | ventricular press falls to lowest level(remains low bc relaxed)=>mitral valve opens=>ventricles start to fill rapidly=>S3 S3 normal in children-not adults=>only heard when in CHF(vol overload), advanced mitral/tricuspid regurgitation |
| cardiac cycle-reduced ventricular filing | longest phase of cardiac cycle end of this phase marks end of diastole |
| mean systemic pressure | mean circulatory press if heart stopped=>press same throughout vasculature and equal to mean systemic press=>no blood flow=0 venous return influences 1)blood vol 2)distribution of blood between stressed and unstressed vol |
| stressed volume | vol of blood that produces press by stretching elastic fibers in blood vessels=>vol in arteries |
| unstressed volume | vol of blood that produces no press=>blood in veins when full ↑ blood vol moves into stressed vol can hold |
| decrease in TPR and venous return | ↓ resistance ↑ venous return=>makes blood flow back to heart easier |
| increase in TPR and venous return | increases arterial press-->increases afterload-->decreases CO increased resistance decreases venous return-->makes blood flow back to heart harder |
| mean arterial pressure | approx. 100 mmHg=>driving force for blood flow |
| baroreceptor reflex | fast and neurally mediated 1)BP sensors 2)afferent neurons=>carry info to brain 3)brain stem centers=>process info and coordinate response 4)efferent neurons=>direct changes in heart and blood vessels keeps arterial press constant |
| baroreceptors | press sensors in 1)carotid sinus=>sensitive to ↑ and ↓ of arterial press 2)aortic arch=>sensitive to ↑ in arterial press *more sensitive to rate of change in press |
| parasympathetic outflow effect on heart | vagus nerve ↓ heart rate via SA node |
| sympathetic outflow effect on heart | 1)↑ HR via SA node 2)effects cardiac muscle=>↑ contractility and SV 3)effects arterioles=>vasoconstriction and ↑ TPR 4)effects veins=>venoconstriction and ↓ of unstressed vol |
| hemorrhage and baroreceptor reflex response | hemorrhage ↓ arterial press=>↓ stressed vol reflex tries to ↑ arterial presure 1)↓ PNS activity in heart 2)↑ SNS activity to heart and blood vessels =>↑ TPR and CO |
| valsalva maneuver | expiring against closed epiglottis (ex.coughing, defecation, heavy lifting) ↑ intrathoracic press=>↓ venous return=>↓ CO=>↓ arterial press *HR should ↑ if baroreceptor reflex intact |
| RAA system | hormonally regulates blood vol=>arterial press mechanoreceptors in afferent arterioles sense ↓ in renal perfusion press in kidneys prorenin=>renin acts on angiotensinogen=>ATI(via ACE)=>ATII stimulates secretion of aldosterone and A |
| angiotensin II | acts on adrenal cortex=>stimulates synthesis and secretion of aldosterone causes arteriolar vasoconstriction=>↑ TPR acts on hypothalamus=>↑ thirst and secretion of ADH stimulates Na+-H+ exchange in renal proximal tubule |
| aldosterone | secreted by zona glomerulosa cells of adrenal cortex acts on principal cells of renal distal tubule and collecting ducts-->increase Na+ reabsorption-->increase ECF volume and blood volume |
| ADH | secreted by posterior pituitary=>secretion stimulates 1)increasing serum osmolarity 2)↓ in BP V1 receptors in vascular smooth muscle=>vasoconstriction V2 receptors in principal cells of renal collecting ducts=>↑ water reabsorptio |
| O2 peripheral chemoreceptors | located in carotid bodies and aortic bodies 1)sensitive to ↓ in Po2=>arteriolar vasoconstriction 2)sensitive to increasing Pco2 and ↓ pH |
| central chemoreceptors | located in medulla=>sensitive to changes in Pco2 and pH brain intolerant of ↓ in blood flow ↑ sympathetic outflow=>intense arteriolar vasoconstriction and ↑ in TPR=>blood redirected to brain |
| Cushings reaction | ↑ ICP ↓ perfusion to brain=>stim central chemoreceptors=>↑ sympathetic outflow to blood vessels 1)↑ TPR 2)dramatically ↑ arterial press(can be life-threatening levels) |
| cardiopulmonary (low-pressure) baroreceptors | located in veins, atria, pulmonary arteries=>sense high blood vol 1)↑ secretion of ANP 2)secretion of ADH inhibited 3)renal vasodilation 4)↑ HR=>↑ CO=>↑ renal perfusion=>↑ Na+ and water excretion |
| atrial natriuretic peptide (ANP) | secreted by atria in response to ↑ atrial press 1)vasodilation and ↓ TPR 2)↑ Na+ and water excretion in kidneys=>↓ total body Na+ content, ECF vol, and blood vol |
| Starling equation | Jv=Kf[(Pc-Pi)-(πc-πi)] (+) filtration (-) absorption |
| Starling pressures | 1)capillary hydrostatic press=>favors filtration=>declines along length of capillary 2)interstitial hydrostatic press=>opposes filtration 3)capillary oncotic press [protein]=>opposes filtration 4)interstitial oncotic press=>favors filtration |
| lymphatic capillaries | lie in interstitial fluid close to vascular capillaries have one-way valves=>interstitial fluid and protein enter only=>drain in thoracic duct=>empties in large veins smooth muscle walls and muscle compression =>aids in flow back to thoracic du |
| edema | ↑ in interstitial vol that exceeds ability of lymphatics to return it to circulation result of 1)lymph nodes surgically removed or irradiated 2)filariasis 3)parasitic infection of lymph nodes 4)lack of muscular activity |
| local control of blood flow | primary mechanism utilized to match blood flow with metabolic needs of tissue exerted thru direct action of local metabolites on arteriolar resistance 1)autoregulation 2)active hyperemia 3)reactive hyperemia |
| neural or hormal control of blood flow | 1)SNS on vascular smooth muscle 2)vasoactive substances-histamine, bradykinin, prostaglandins |
| autoregulation of local blood flow | maintenance of constant blood flow to organ despite changing arterial press 1)achieved by immediate compensatory vasodilation of coronary arterioles 2)↓ resistance of coronary vasculature |
| active hyperemia | blood flow ↑ proportionately to meet ↑ metabolic demand |
| reactive hyperemia | blood flow ↑ in response to or reacting to a prior period of ↓ blood flow |
| myogenic hypothesis | explains autoregulation 1)when arterial press ↑=>arterioles stretch then contract=>maintains constant flow in face of ↑ press 2)when arterial press ↓=>arterioles relax and resistance ↓=>maintains constant flow |
| metabolic hypothesis | explains all local control of blood flow basic premise: O2 delivery to tissue matches O2 consumption=>metabolic activity produces vasodilator metabolites (CO2, H+, K+, lactate, adenosine) |
| histamine | released in response to trauma=>powerful vascular effects 1)dilates arterioles 2)constricts venules *large ↑ in capillary hydrostatic press=>↑ filtration=>edema |
| bradykinin | 1)dilation of arterioles 2)constriction of venules *large ↑ in capillary hydrostatic press=>↑ filtration=>edema |
| serotonin | released in response to blood vessel damage=>local vasoconstriction=>reduce blood flow and blood loss |
| prostaglandins | various effects 1)prostacyclin and prostaglandin-E series=>vasodilators 2)thromboxane A2 and prostaglandin-F series=>vasoconstrictors |
| coronary circulation local blood flow control | almost entirely controlled by local metabolites *most important local metabolic factors 1)hypoxia 2)adeosine mechanical compression of blood vessels causes brief periods of occlusion during systole in cardiac cycle=>reactive hyperemia |
| cerebral circulation local blood flow control | almost entirely controlled by local metabolites exhibits autoregulation, active and reactive hyperemia *CO2 the most important local vasodilator |
| pulmonary circulation local blood flow control | controlled by O2=>hypoxia causes vasoconstriction=>shunts blood away from poorly ventilated areas where blood flow would be "wasted" and toward well-ventilated areas where gas exchange can occur |
| renal circulation local blood flow control | tightly autoregulated=>flow constant even when renal perfusion changes result of myogenic properties of arterioles and tubuloglomerular feedback |
| skeletal muscle circulation local blood flow control | 1)at rest-sympathetic innervation; alpha1-vasoconstriction; beta2-vasodilation (predominates) 2)during exercise-local metabolites (ex. lactate, adenosine, K+); autoregulation, active and hyperactive hyperemia exhibited |
| skin circulation local blood flow control | contains dense sympathetic innervation=>alters blood flow to skin to regulate body temperature vasoactive substances have effects (ex. histamine) |
| thyroid hormones | thermogenic hormones 1)stimulate Na+-K+ ATPase 2)↑ O2 consumption 3)↑ metabolic rate 4)↑ heat production |
| SNS generating heat mechanism | activated by cold temp and stim 1)brown fat=>↑ metabolic rate and heat production 2)alpha1 receptors=>vasoconstriction to reduce blood flow to surface of skin=>reduces heat loss |
| mechanism for dissipating heat | coordinated in anterior hypothalamus 1)↓ sympathetic activity in skin blood vessels=>heat loss 2)↑ activity of sweat glands |
| fever | abnormal elevation of body temp produced by pyrogens=>↑ hypothalamic set-point temp pyrogens ↑ prod of IL-1=>↑ PG prod=>↑ set-point temp reduced by aspirin |
| aspirin and fever | reduces fever=>inhibits cyclooxygenase enzyme necessary to synthesize prostaglandins=>disrupts raise of set-point temperature |
| heat exhaustion | consequence of body's response to elevated environmental temperatures excessive sweating can result in ↓ ECF vol, ↓ blood vol, ↓ arterial press, and fainting |
| heat stroke | body temperature ↑ to point of tissue damage heat not properly dissipated=>core temperature ↑ to dangerous levels |
| malignant hyperthermia | massive ↑ in metabolic rate, ↑ O2 consumption, ↑ heat prod in skeletal muscle=>head dissipating mechanisms can't keep up can be fatal if untreated can be caused by inhalation anesthetics |
| orthostatic hypotension | occurs when someone stands up too quickly=>↓ in arterial blood press upon standing=>blood pools in the veins of lower extremities=>venous return and CO ↓=>↓ in mean arterial press can cause light-headedness, fainting, edema |
| first degree heart block | slowing in AV conduction=>prolonged PR interval each P wave does succeed in conducting through the AV conducting system to activate the ventricle |
| second degree heart block | only some P waves conduct through the AV junction=>ventricles don't get excited=>heart skips a beat |
| third degree heart block | complete block=>no P waves go thru AV conduction system to depolarize the ventricle if block at AV node a focus lower in the AV junction becomes pacemaker=>rate is usually less than a normal sinus rate. |
Created by:
kphom001
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