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Cardiovascular

Costanzo-Cardiovascular Physiology

QuestionAnswer
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