Term
| *B lymphocytes differentiate into ___________ with lots of ER to make antibodies |
|
Definition
|
|
Term
| antibodies are... [macromolecule] |
|
Definition
|
|
Term
| Antibodies provide __________ immunity |
|
Definition
| humoral (humors are body fluids) |
|
|
Term
| *Antibodies circulate in the... |
|
Definition
|
|
Term
| *Cytotoxic T cells destroy by ____________ interaction & are responsible for ____________ immunity |
|
Definition
| cell-to-cell, cell-mediated |
|
|
Term
| *Helper T cells secrete _______ to help regulate immune responses |
|
Definition
cytokines
("master switch") |
|
|
Term
|
Definition
supply lymphatic organs w/ mature lymphocytes
bone marrow & thymus (near sternum) |
|
|
Term
| *Where do B & T cells mature? |
|
Definition
B = Bone marrow
T = Thymus |
|
|
Term
|
Definition
| ability to recognize antigens & fight invaders |
|
|
Term
| How do B & T cells make millions of receptors for possible antigens? |
|
Definition
| random DNA cutting/pasting |
|
|
Term
| *secondary lymphoid organs |
|
Definition
where processed/mature lymphocytes take up residence & where cells activated by antigen confront invaders
move between organs (lymphocyte trafficking) to inc. chance to meet spec./own antigen
lymph nodes, tonsils, spleen, lymphocyte clusters near body linings (ex. GI, urogenital) |
|
|
Term
| spleen is like a lymph node for the... |
|
Definition
|
|
Term
| *What lymphocyte do we not know if or where are processed? |
|
Definition
|
|
Term
|
Definition
arise after antigen binds to B cell receptor (activation)
secrete antibodies that travel in blood to invader |
|
|
Term
|
Definition
protein messengers secreted from immune cells, esp. helper Ts
regulate immune responses, allow norm. B & cytotoxic T fxn. |
|
|
Term
| *draw flow chart for lymphocytes after antigen binds to spec receptors |
|
Definition
|
|
Term
| Antibodies are _________ shaped proteins called ____________ |
|
Definition
|
|
Term
|
Definition
Y-shaped proteins
globulins
plasma proteins
secreted into blood by plasma cells
spec for particular antigen that stimulates its secretion
2 long/heavy chains, 2 short/light chains
Fc=stem, constant for all antibodies in a class
Fab=antigen-binding fragments, "prongs", diff for each
tag/mark invader, act as opsonin, activate complement, neutralize toxins, prevent virus from entering cells, or activate NK cells
see notes & pg 251 |
|
|
Term
|
Definition
| Antigen bind to BCR & helper T cytokine interaction-> activation-> division into clones-> plasma cells that secrete antibodies & memory cells which respond later to antigen |
|
|
Term
|
Definition
activate lymphocytes
recognizable part of invader
often on surface |
|
|
Term
|
Definition
location diff!
antibodies in blood
BCRs on membrane
both are immunoglobulins w/ same antigen binding sites |
|
|
Term
|
Definition
IgA/D/G/M/E
IgG is most abundant
IgE are involved in allergies |
|
|
Term
| *What does a clone of plasma cells secrete? |
|
Definition
| a spec antibody that looks like receptors of the clone of Bs |
|
|
Term
| The non-spec immune response of inflammation makes vessels leaky to _________, including ________- so these will get out of the blood into the ________. |
|
Definition
| proteins, antibodies, ISF |
|
|
Term
|
Definition
hold microbe in place for phagocyte to eat
Fc/stem binds phagocyte
Fab/prongs bind antigen on invader |
|
|
Term
| *antibodies activating complement |
|
Definition
activation of complement sys (collection of proteins) w/ cascade-like rxn (like + feedback)
C1 & C3b
"complement" what antibody does |
|
|
Term
|
Definition
binds Fc of antibody that is bound to antigen->cascade->proteins form membrane attack complex (MAC)-> inserts into cell membrane of invader (holes/pores)-> inc. ions & water in cell-> death
can also be non-spec, produce MAC w/o antibodies involved |
|
|
Term
|
Definition
| cascade-> activated C3b-> acts as opsonin (promotes phagocytosis) by linking invader to phagocyte |
|
|
Term
| Antibodies can bind toxins & viruses in the... |
|
Definition
|
|
Term
| *antibodies bound to toxins or viruses |
|
Definition
antibody-toxin & antibody-virus complexes can be phagocytized
neutralizes toxin by preventing interaction w/ cells that lead to damage
prevents virus from entering cell |
|
|
Term
| *antibodies binding to NKs |
|
Definition
| Fc bind to NK & Fab bind to antigen-> NK secrete chemicals to kill cell (esp. perforin) |
|
|
Term
|
Definition
secreted by NKs to create pores in bact
like MAC |
|
|
Term
|
Definition
differentiated from activated Bs
don't secrete antibodies initially
quickly respond if same antigen reappears
large secondary response
vaccines
T cells also have memory cells |
|
|
Term
| *primary & secondary responses |
|
Definition
primary= antibody response to 1st exposure to antigen
secondary= " " subsequent exposure, faster & larger
see notes & pg 255 |
|
|
Term
| *vaccines & explain figure |
|
Definition
have antigens that cause production of memory cells
allows a quick & lg secondary response when actually exposed
fig. on notes & pg 256 |
|
|
Term
| TCRs cannot bind to antigen unless antigen is bound to a "_______" protein on cell membrane |
|
Definition
|
|
Term
| *antigen-presenting cells |
|
Definition
have an antigen "presented" on protein on cell membrane
recognized by TCRs
process & present antigens |
|
|
Term
|
Definition
macrophages, dendritic cells (similar to macrophages, have projections), & B cells
dendritic cell engulfs bact-> bact broken down by lysosomes-> antigenic peptides produced-> ER-Golgi complex makes MHC molecule-> antigenic peptides bind MHCs-> antigen displayed on cell surface as bound to MHC
Bs take in antigen by receptor-mediated endocytosis while performing plasma cell fxn as well-> present antigen-> CD4 coreceptor on helper T links T & B-> helper T secretes cytokines-> inc B cell activation
have Class II MHCs |
|
|
Term
| Major Histocompatibility Complex proteins |
|
Definition
MHCs
"self" proteins/"identity tags"
focus in tissue matching
only identical twins have same |
|
|
Term
| Only APCs with Class _____ MHCs can be recognized by helper Ts |
|
Definition
|
|
Term
| Helper Ts are ____+ T cells |
|
Definition
|
|
Term
|
Definition
cluster designation
spec cluster of membrane proteins
on T cells
bind to MHCs |
|
|
Term
|
Definition
presents antigens to cytotoxic Ts
found in all cells w/ nucleus (not RBCs)
for "endogenous" antigens |
|
|
Term
| Cytotoxin Ts are ____+ T cells |
|
Definition
|
|
Term
|
Definition
| virus or cancer-> abnormal proteins produced in cell-> endogenous antigen-> presented by Class I MHCs-> bind to cytotoxic Ts-> T & APC linked by CD8 coreceptor-> activated (by helper T cytokines) can destroy body cell w/ perforin (pore-forming protein) |
|
|
Term
|
Definition
arise/are made inside body cells
means cell is infected w/ virus (host cell makes viral proteins) or has abnormal proteins from cancer
all cells w/ nucleus (not RBCs) |
|
|
Term
| *Why do cytotoxic Ts kill virus-infected body cells? |
|
Definition
kill before virus can enter nucleus and replicate OR if virus has replicated and is released-> can be phagocytized
sacrifice host cells to get rid of invader
usually few die, but if a lot damaged then can affect organ/tissue fxn (ex. Type 1 diabetes- destruction of insulin-secreting cells) |
|
|
Term
| *NK cells & activated macrophages |
|
Definition
NKs= lymphocyte
activated macrophages= activated by helper T cytokines, "angry macrophages"
secrete chems to destroy target cells (virus-infected or cancerous)
nonspecific
can deal w/ bad cells before specific immune response "kicks in" |
|
|
Term
| *Antibodies protect against _________ antigens found in the __________, and cytotoxic Ts protect against ________ antigens found in the _________ |
|
Definition
| exogenous, ECF, endogenous, cells w/ nuclei |
|
|
Term
| Like skeletal muscle, cardiac muscle needs an _____________ to cause contraction, but unlike skeletal muscle, cardiac muscle generates its own |
|
Definition
|
|
Term
| The ____________ & __________ arteries bump blood ________ from heart |
|
Definition
|
|
Term
| heart's "guaranteed period of relaxation": AP has ______ refractory period, so ____________ is not possible & heart must relax |
|
Definition
|
|
Term
| cardiac cycle is ____ complete heartbeat w/ ________ contracting & relaxing, then _________ contracting & relaxing |
|
Definition
|
|
Term
| _______________ measures flow out of the heart in liters per min, out of either ventricle |
|
Definition
|
|
Term
| _________ & __________ determine cardiac output |
|
Definition
| heart rate (beats per min), stroke volume (vol per beat) |
|
|
Term
| when heart muscle dies due to lack of coronary artery blood flow |
|
Definition
| myocardial infarctions/heart attacks |
|
|
Term
|
Definition
| vessel shunt/s are sewn in to bypass an obstruction so blood will travel to coronary artery |
|
|
Term
|
Definition
| inflation of a balloon inside blocked vessel to open it |
|
|
Term
|
Definition
| inserted lattice to prevent closure of vessel |
|
|
Term
|
Definition
1. myocardium: thick muscle
2. endocardium: inner layer continuous w/ endothelium (flat cells that line vascular sys) of blood vessels
3. epicardium: aka visceral ("viscera"= organs) pericardium, outer layer ("peel of apple")
see notes or pg 266 |
|
|
Term
|
Definition
1. parietal ("parietal"= wall) pericardium: outside epicardium, lines 2
2. fibrous pericardium: fibrous sac around wall |
|
|
Term
| *fxn of serous fluid between parietal & fibrous pericardium |
|
Definition
aka pericardial fluid
lubricant
allows heart to beat in sac w/o friction |
|
|
Term
| heart operates as 2 pumps in... |
|
Definition
|
|
Term
| *pulmonary & systemic circulation |
|
Definition
P: right side of heart pumps blood to lungs
S: left side pumps blood to rest of body
septum separates R/L sides |
|
|
Term
|
Definition
1. atria: receiving chambers, blood flows passively w/o contraction, but there is a contraction which pushes a sm amount of blood into ventricles
2. ventricles: pumping chambers, blood out of heart into arteries
valves between
on R & L side |
|
|
Term
| *blood flow thru heart & body |
|
Definition
sup & inf vena cavae-> R atrium-> R AV valve (tricuspid)-> R ventricle-> ventricle contracts-> pulmonary semilunar valve-> pulmonary arteries-> picks up O2 & loses CO2 in lungs (air sacs/alveoli)-> pulmonary veins-> L atrium-> L AV valve (bicuspid/mitral)-> L ventricle-> ventricle contracts-> aortic semilunar valve-> aorta-> rest of body (inc. heart muscle)-> [repeat]
see notes or pg 269 |
|
|
Term
|
Definition
V: carry blood to heart
A: carry blood from heart |
|
|
Term
|
Definition
| blood in aorta-> coronary arteries (openings just past aortic semilunar valve)-> heart muscle-> coronary sinus-> R atrium->... |
|
|
Term
|
Definition
between atria & ventricles
R: tricuspid
L: bicuspid, mitral
larger than semilunar valves |
|
|
Term
|
Definition
pulmonary: between R ventricle & pulmonary arteries
aortic: between L ventricle & aorta
smaller than AV valves
when open, cusps look like half-moons ("semilunar") |
|
|
Term
| *Why can't heart muscle get nutrients by diffusion from blood in heart chambers? |
|
Definition
muscle is too thick (diffusion is very slow across distances >a few mm)
must rely on coronary arteries for nutrients & O2 |
|
|
Term
|
Definition
myocardial infarction
coronary artery blocked-> heart muscle deprived of O2-> muscle cells die |
|
|
Term
|
Definition
allow only 1 way/unidirectional/forward flow of blood
close to prevent backward flow
when pressure is greater behind valve-> opens
when pressure greater in front-> closes |
|
|
Term
|
Definition
| fibrous cords ("strings") attached to edges of cuspid valves restrain edges from going up into atria when vesicles contract |
|
|
Term
|
Definition
3 cusps
R AV, aortic, & pulmonary semilunar valves |
|
|
Term
|
Definition
aka mitral valve
2 cusps
L AV valve |
|
|
Term
| *The heart is a double pump- pumps blood thru _______ & _________ circuits |
|
Definition
|
|
Term
| *Where do heart impulses originate? |
|
Definition
In heart itself
spontaneously generates own impulses to cause contraction |
|
|
Term
|
Definition
small connecting tunnels between cells
allows AP to go from cell to cell- current (+ ions) flows
muscle contracts as a unit
"functional syncytium" |
|
|
Term
|
Definition
merging/connected cells act tg electrically & mechanically
single unit smooth muscle
facilitated by gap junctions |
|
|
Term
| *functional syncytium in heart |
|
Definition
1: in atria
2: in ventricles
separated by heart's fibrous skeleton |
|
|
Term
| *heart's fibrous skeleton |
|
Definition
fibrous rings surround valves
provides attachment for valves & muscle fibers
does not conduct impulses
connective tissue
separates functional syncytium of atria & ventricles |
|
|
Term
| *"link to the ventricles" |
|
Definition
only pt where syncytial aren't separated
part of heart's conduction system
AV node |
|
|
Term
| *Does heart muscle require APs to cause contraction? |
|
Definition
|
|
Term
| *heart vs skeletal muscle contraction |
|
Definition
Both: need AP
H: doesn't require neural stimulation, AP originate in heart from pacemaker pot
S: need neural stimulation for APs |
|
|
Term
| *Can a heart removed from the body beat on its own? |
|
Definition
Yes
Ringer's solution can make it beat for hours
heart can rhythmically initiate own APs w/o neural stimulation |
|
|
Term
|
Definition
heart excites itself rhythmically
initiates own APs
created by ion permeability changes
slow depolarization (pacemaker potential ramps to threshold) followed by self-induced AP |
|
|
Term
|
Definition
100bpm
HR if heart is "in your hand" w/ nothing affecting HR except heart itself |
|
|
Term
| *Why doesn't inherent rate equal normal/resting rate? |
|
Definition
IR=100bpm
NR=70bpm
PS NS is dominant at rest-> slows HR |
|
|
Term
| *effects of ANS divisions on pacemaker pot |
|
Definition
| PS: dec slop of pacemaker pot (PP), longer to reach threshold, dec HR ( |
|
|
Term
|
Definition
SA node
pacemaker of norm heart
node's IR is faster than other parts of heart- gets to threshold fastest/first
"leader"-fires first in norm hearts, other parts follow its pace
near opening of sup vena cava
mass of specialized cardiac muscle cells
auto rhythmic 100bpm (70bpm w PS impulses) |
|
|
Term
|
Definition
other area can take over as pacemaker, but slower rate
if AV node takes over, NR=50bpm
in complete heart block: SA node incorrect fxn & AV node non-functional (no "link to ventricle")-> purkinje fiber/ventricular autorhythmic tissue takes over-> atria at 70bpm & ventricles at 30bpm |
|
|
Term
| *effect of ectopic focus/pacemakeer w/ faster rate than SA node |
|
Definition
"ectopic"= in the wrong place
heart driven by area (entropic focus) other than SA node, which is going abnormally fast
whole HR driven by ectopic focus, HR is fast |
|
|
Term
|
Definition
rate of both & overall HR at 30-40bpm b/c auto rhythmic Purkinje fibers become pacemaker
probably unconscious bc low brain blood flow |
|
|
Term
| *Cardiac muscle AP is [short/long] & _____ from the _______ enters the cell during the AP |
|
Definition
|
|
Term
| *refractory period in cardiac muscle |
|
Definition
refractory period of the membrane is long
prevents prolonged/tetanic contraction in heart bc pumping blood requires contraction AND THEN relaxation so heart can fill with blood
ARP= contraction t
no new AP/contraction until 1st over
twitch- contraction lasts certain amount of t |
|
|
Term
| *skeletal vs cardiac refractory period |
|
Definition
S: short compared to contraction duration, 2nd contraction can be stimulated before 1st over (summation-> tetanus)
C: AP lasts as long as contraction (longer), ARP= contraction t, no summation/tetanus, twitch (1 AP= 1 contraction)
see notes or pg 277 |
|
|
Term
|
Definition
AP of working cell in ventricle has plateau
1. depolarization: rising phase, open volt-gate Na+ channels (like neurons)
2. Na+ channels close/inactivate
3. plateau: membrane remains depol at ~0mV b/c K+ permeability decreases & Ca++ perm increases (slow/L/long-lasting channels) [so, Na+ has gone in, K+ is not going out, Ca++ begins going in-> + inside]
4. repolarization: Ca++ & K+ perms revert-> K+ perm inc.-> + charge out (& less + in from Ca++) |
|
|
Term
| *effect of Ca++ entering cell during cardiac AP |
|
Definition
Ca++ in ECF-> into cell during plateau-> more Ca++ released from ST (Ca-induced Ca release)-> lg amount of Ca++ can bind to troponin-> tropomyosin pulled out of way (activation of contractile machinery)
inc Ca++ in cytosol-> inc contraction strength b/c more Ca++ means can bind more troponin sites |
|
|
Term
| *how epi, NR, & digitalis inc contraction strength |
|
Definition
inc Ca++ in cytosol from ECF (-> inc SR release-> inc troponin bind-> strong contraction)
digitalis: drug used to treat heart failure (heart doesn't pump enough blood), improves symptoms but doesn't prolong life |
|
|
Term
| *effect of Ca channel blockers on heart |
|
Definition
block Ca channels on heart-> less Ca++ in cytosol from ECF-> less Ca++ release from SR-> less troponin bound-> weaker contraction
can also affect channels on smooth muscle of blood vessels |
|
|
Term
| What would happen in experiment that blocked all Ca++ channels on heart muscle? |
|
Definition
No contraction
would never block all channels in patient, use therapeutic dose (some blocked) instead |
|
|
Term
| *Heart's conduction sys makes cardiac contraction... |
|
Definition
|
|
Term
|
Definition
specialized cardiac muscle cells transmit impulse/AP to cause contraction
faster transmission than regular cells thru gap junctions
impulse brought quickly to ventricles (then some norm cell-to-cell conduction)- ventricles need conduction sys bc thick
atria is mostly norm cell-to-cell conduction
1. atrial contraction: SA node pacemaker pot reaches threshold-> generates AP-> AP spreads thru atrial myocardium via gap junctions-> depol-> atria contract tg-> atria squeeze blood into ventricles
2. link to ventricles: AV node gets impulse (delayed)
3. conduction to ventricles: bundle of His (AV bundle) gets impulse-> R & L branches
4. ventricle contraction: Purkinje fibers get impulse-> thick myocardium-> norm cell-to-cell conduction-> depol-> ventricles contract tg-> blood out of heart |
|
|
Term
|
Definition
AV bundle
conductive tissue in ventricular septum
branches into L & R
carries AP to Purkinje fibers
see notes or pg 279 |
|
|
Term
| *Where is impulse delayed in conduction sys? |
|
Definition
at AV node
~0.1s
gives atria time to contract & squeeze blood into ventricles before ventricles contract |
|
|
Term
| *Depol causes _________ of the myocardium. With repol, ___________ occurs. |
|
Definition
|
|
Term
| *When would a patient need an artificial pacemaker? |
|
Definition
when SA node not fxn properly or for heart block
electrically stimulates heart
some pace atria, some ventricles, some both |
|
|
Term
| *EKGs to diagnose disease |
|
Definition
evaluates electrical events in heart
changes in electrical events can indicate disease
depol (- outside) & repol (+ out) of myocardium causes current in body fluids outside of heart-> tiny current flow can be detected on surface of body
electrodes on skin detect current |
|
|
Term
|
Definition
specific arrangement of electrodes for EKG
12
on chest, arms, & legs
cardiologist knows typical wave forms for a given lead |
|
|
Term
|
Definition
1. P wave: depol of atria
2. QRS complex: depol of ventricles (repol of atria occurs at this t but does not cause QRS)
3. T wave: repol of ventricles
see notes or pg 281 |
|
|
Term
|
Definition
EKG between end of P wave to begin of QRS
measure of AV nodal delay |
|
|
Term
|
Definition
some impulses don't get thru AV node
some P waves not followed by QRS & T wave |
|
|
Term
| *complete heart block EKG |
|
Definition
no impulses get thru AV node
no correlation between P wave & QRS
ventricle beating on its own
part of conducting sys of ventricle acts as its pacemaker- ventricular rate 30-40bpm so person is unconscious
treat w/ pacemaker that paces ventricles |
|
|
Term
|
Definition
| variation from norm heart rhythm |
|
|
Term
|
Definition
HR >100bpm
norm hearts during exercise or disease (ex. hyperthyroidism) |
|
|
Term
|
Definition
HR <60bpm
athletes can have if pump more per beat
occurs in complete heart block |
|
|
Term
|
Definition
HR >200bpm but regular
not enough t to fill w blood
if occurs in ventricles >30s-> need med intervention |
|
|
Term
|
Definition
"cardiac chaos"
cells/myocardium fail to contract tg
chamber is squirming/quivering- contracting & relaxing indep
fibrillating chambers can't pump blood
atrial: common (~10% ppl over 70), tire easily w exercise bc lose atrial "kick" that "tops of" filling of ventricle
ventricular: life-threatening, not pumping blood out of heart, need to defibrillate to re-est norm rhythm |
|
|
Term
|
Definition
re-est norm rhythm from ventricular fibrillation
expose myocardium to strong electric current-> depol all cells at once-> (hopefully) norm sinus rhythm (norm SA node as pacemaker & norm impulse conduction) |
|
|
Term
|
Definition
1 complete heart beat
systole + diastole
SA node PP gets to threshold-> AP thru atrial myocardium (P wave)-> contraction (atrial "kick")-> blood to ventricles (already 70-80% full before atrial contraction)-> AV node impulse-> bundle of His-> branches-> Purkinje fibers-> depol ventricular myocardium (QRS)-> contraction-> AV valve closes (b/c high ventricular pressure) for 1st heart sound-> ventricular pressure continues to rise-> ventricular pressure > aortic pressure-> aortic (or pulmonary) semilunar valve opens-> blood ejected-> ventricle repol (T wave)-> relaxation-> ventricular pressure falls-> aortic (or pulmonary) semilunar valve closes (2nd heart sound)-> AV valve opens-> ventricle begins filling->...
see notes or pg 285 |
|
|
Term
|
Definition
S: contraction
D: relaxation
usually refers to what ventricles are doing |
|
|
Term
| *pressure changes during cardiac cycle |
|
Definition
| arterial: rises during contraction, falls when emptied
ventricular: rises during contraction-> causes AV valve close (V>Art) then semilunar valve open (V>Aort), falls when emptied & during repol-> causes semilunar valve close (V |
|
|
Term
| *ventricular volume changes during cardiac cycle |
|
Definition
filling to 70-80% capacity while AV valve open-> inc. when atria contracts to "top off" ventricle-> same until pressure opens semilunar valve-> dec. as blood ejected to aorta & repol
some blood still left over after systole b/c some blood flowed back before semilunar valve closed, this is end systolic vol
vol in ventricle at end of diastole= end diastolic vol |
|
|
Term
|
Definition
SV=EDV-ESV
70m/s is norm resting
force of contraction |
|
|
Term
| *EKG during cardiac cycle |
|
Definition
P wave: AP spread thru atrial myocardium for depol (-> AV node impulse-> etc)
QRS: depol & contraction of ventricles (-> AV valve closes-> etc)
T wave: repol & relaxation of ventricles (-> semilunar valves close-> etc) |
|
|
Term
| *heart sounds during cardiac cycle |
|
Definition
1st: AV valve closes when ventricular P > atrial P, vibration of heart walls w/ reverberating blood
2nd: semilunar valve closes when ventricular P < aortic P, vibration of vessels & heart walls w/ reverberating blood |
|
|
Term
| *When & why do valves close & open? |
|
Definition
valves close due to inc forward P, allows only unidirectional flow
VP>arterial P-> AV valve close
VP semilunar valve close
VP>aortic P-> semilunar valve open
VP AV valve open |
|
|
Term
| *how elasticity of arteries maintains a P during diastole |
|
Definition
expand w/ vol of blood
stretch & recoil "like rubber band" (compliant)
expand during systole
clamp down on blood to maintain pressure to drive blood thru tissues when ventricles relaxing (diastole)
have flow thru tissues throughout cardiac cycle
if not stretchable, blood would only flow when heart contracting |
|
|
Term
|
Definition
BP=systolic/diastolic P in mmHg
aortic BP is ~equal (w/in a couple mmHg) to P in other arteries |
|
|
Term
| *cardiac cycle in R vs L side of heart |
|
Definition
R has lower Ps- pulmonary circuit is low resistance (BP~24/8mmHg) so don't need as much P to cause blood flow
R heart wall is thinner bc doesn't need to generate as much P
BUT eject same amount of blood |
|
|
Term
|
Definition
abnormal heart sounds
caused by turbulent flow of blood
1. stenosis: narrowed valve doesn't open completely, rapid blood flow
2. regurgitation/insufficient/leaky valve: don't close completely, blood flows backward against forward flow
3. blood flowing thru hole in septum |
|
|
Term
| *laminar vs turbulent flow |
|
Definition
L: layers slide over each other, norm, quiet
T: layers break up, sound from vibrating nearby structures |
|
|
Term
| What murmurs would occur during systole? |
|
Definition
| stenotic semilunar or insufficient AV |
|
|
Term
| What murmurs would occur during diastole? |
|
Definition
| stenotic AV or insufficient semilunar |
|
|
Term
| *Cardiac output is determined by... |
|
Definition
| volume of blood pumped per beat & HR (bpm) |
|
|
Term
| *Cardiac output changes with... |
|
Definition
|
|
Term
|
Definition
amount of blood pumped by either ventricle per min
flow thru systemic OR pulmonary circulation (usually 5L/min for each circuit)
CO= HR (bpm)xSV(blood pumped by 1 contraction, norm 70mL/s) |
|
|
Term
| *CO during rest, moderate activity, & exercise |
|
Definition
R= 5L/min (entire blood vol thru 1 circuit in 1 min)
MA= 7L/min
E= 20-40L/min (dep. on athleticism) |
|
|
Term
|
Definition
ANS:
1. PS fibers travel in Vagus to SA node, AV node, & atrial myocardium, secrete ACh to dec HR, dec conduction thru AV node & inc. AV nodal delay
2. cardiac sympathetic nerves innervate SA node, AV node, atrial myocardium & ventral myocardium, secrete NE to inc HR, inc conduction thru AV node & dec AV nodal delay
Epi: inc HR by acting on Beta-1 receptors
Temp: hypothermia dec. HR, fever inc. HR
Electrolytes: ECF [K+] abnormalities cause arrhythmias
Thyroid hormones: inc # Beta-1 receptors on heart, inc sensitivity to NE & epi, in HR |
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Term
| *HR is mostly determined by... |
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Definition
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Term
| *SV is changed by _________ control of ________ nerves or __________ control of how much __________ |
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Definition
| extrinsic, sympathetic, intrinsic, blood fills heart before contraction |
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Definition
always possible bc always blood left in ventricle
1. intrinsic (inherent to heart): inc EDV (inc cardiac fiber length)-> inc SV so when ventricle fills w more blood then more blood is ejected bc filling P inc, Starling (reservoir experiment)
2. extrinsic (coming from outside): sympathetic nerves innervate entire myocardium, NE acts on Beta-1 receptors to inc contractility indep of EDV,
Also, hypertension (high BP) can dec SV |
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Term
| *Frank-Starling Law of the Heart (draw curve) |
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Definition
inc venous return-> inc blood in atrium-> inc ventricular filling P-> inc EDV & cardiac fiber length-> inc SV
curve in notes or pg 293 |
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Term
| *Starling's Law vs skeletal muscle length-tension relationship |
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Definition
skeletal T-L relationship is a hill
cardiac is normally on the rising part of the curve (length inc = contraction inc) |
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Definition
amount of blood flowing into heart from veins per t (min)
inc venous return-> inc EDV & SV |
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Term
| *venous return during exercise |
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Definition
| inc. venous return-> inc CO (due to Starling's Law) |
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Term
| *How does heart automatically adjust SV to amount in ventricle? |
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Definition
inc. flow to ventricle-> inc amount pumped out
blood doesn't back up |
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Term
| *How & why does Starling's Law keep the output of L&R ventricles equal? |
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Definition
inc SV from one side-> inc venous return to other side
makes sure blood doesn't accumulate on 1 side of circulatory sys |
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Term
| *left-sided heart failure |
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Definition
L side can't pump as well as R
blood backs up behind L side in lungs-> pulmonary edema (excess ISF)-> problems w gas exchange bc respiratory membrane too thick for norm diffusion of gases |
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Term
| *PS vs sympathetic innervation of myocardium |
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Definition
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Term
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Definition
inc F of contraction NOT due to EDV
causes more ejection of EDV
inc. w/ sympathetic stimulation (extrinsic) |
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Term
| *When you move up/down a single curve, it's due to _____________. When you shift to a new curve, it's due to ______________ |
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Definition
| Starling's Law, change in contractility w/ sympathetic stimulation |
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Term
| *Why does inc. contractility cause dec. ESV? |
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Definition
| inc contractility-> more EDV ejection-> less ESV |
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Term
| *Draw figure summarizing control of CO |
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Definition
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Term
| Contraction of arterioles would _____ upstream artery P |
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Definition
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Term
| Most fluid is pulled back into capillaries by... |
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Definition
| osmotic effect of plasma proteins |
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Term
| With substantial blood loss- HR inc, skin pales, & become cold due to inc. _________ activity caused by the __________ reflex response to drop in arterial BP |
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Definition
| sympathetic, baroreceptor |
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Term
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Definition
1. inner layer/tunica intima: single layer of flattened squamous cells called endothelium, has valves in some veins to prevent back flow, only layer in capillaries
2. middle layer/tunica media: smooth muscle w elastin, thicker in arteries than veins
3. outer layer/tunica adventitia: connective tissue w collagen |
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Term
| *blood vessel structure & fxn |
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Definition
1. arteries: blood at high P so lg middle layer w/ elastin to swell w/ SV
2. veins: blood at low P so thinner walls bc inelastic
3. capillaries: sites of nutrient/waste exchange between blood & ISF, so thin walls with only inner layer |
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Term
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Definition
wastes in cell-> ISF-> capillary
nutrients in capillary-> ISF-> cell
diffusion down conc. gradient |
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Term
| *_______ of arterioles controls resistance |
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Definition
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Term
| *blood thru cardiovascular sys |
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Definition
| heart contraction-> BP-> arteries-> arterioles-> capillaries-> venues-> veins |
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Definition
blood flows "down a P gradient" (high->low P)
pressure diff ([delta]P) in mmHg
flow proportional to P gradient |
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Definition
Flow = vol/t
ex. CO is L/min
F = [delta]P/R (P=pressure, R=resistance) where R=n*L*8/r^4*pi (n=viscosity, L=vessel length, r=radius) |
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Definition
impedes flow, friction
proportional to blood viscosity & vessel length
radius has big effect (r^4)-> inc. r = dec. R |
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Term
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Definition
friction of molecules of adjacent layers of flowing fluid (laminar flow)
determined by hemocrit (# RBCs)- anemia has dec RBC so dec viscosity & inc flow, polycythemia has inc RBC |
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Term
| *What is controlled to control flow resistance? |
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Definition
radius
inc r-> dec R
if r x2-> R -x16
arteriole r affects F thru capillaries |
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Term
| *When ventricle ejects blood, arterial P _________. When ventricle relaxes, arteries recoil, which ___________ P during diastole |
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Definition
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Term
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Definition
lg r, low R
P = aortic P
supply blood to all organs at same P regardless of distance
maintains blood flow during diastole/relaxation by dilation ("pressure reservoir")
stretched during systole bc more blood enters than leaves, so high P
max P during systole = systolic P
min P before systole = diastolic P
arteriole BP = systolic/diastolic |
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Definition
diff between systolic & diastolic P
PP = SP - DP
each pulse throb is caused by inc P from each systole, so pulse rate = HR |
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Term
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Definition
avg P driving blood into tissues throughout cardiac cycle
MAP = DP + 1/3PP bc heart spends more time (2/3) in diastole
normally 93mmHg |
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Term
| *__________ diameter controls blood flow thru an organ |
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Definition
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Term
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Definition
small r, lg R
big drop in BP (90->35mmHg)
dec PP
can dilate & constrict to change R |
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Term
| *control of arteriolar tone |
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Definition
1. intrinsic/local: w/in organ, active hyperemia & flow auto regulation, "selfish"
2. extrinsic: nerves (sympathetic) & hormones, homeostasis |
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Term
| *"juggling" blood flow during exercise |
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Definition
| inc CO & dilation of skeletal muscle arterioles-> inc flow, esp to muscles & heart (intrinsic control); dec flow to GI, kidneys, & bone (extrinsic SNA) |
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Term
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Definition
intrinsic arteriolar R control
"above blood"
inc activity/metabolism-> inc CO2, H+, K+, adenosine, & osmolarity; dec O2-> act directly on arteriolar smooth muscle or cause release of paracrine (ex. NO) from endothelial cells-> relax smooth muscle (inc r)-> dec R-> inc flow
reverses to norm when stop exercising |
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Term
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Definition
intrinsic control of arteriolar R
dec flow-> not delivering enough O2, not removing enough metabolites-> inc flow
imp in kidney |
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Term
| *What is the most imp extrinsic control of arteriolar R? |
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Definition
| sympathetic nerve activity |
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Term
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Definition
neural tone is maintained
intrinsic tone + SNA |
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Term
| *SNA effects on arteriole tone |
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Definition
dec SNA-> inc r-> dec R-> inc flow
inc SNA-> dec r |
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Term
| *extrinsic arteriole control & homeostasis |
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Definition
| SNA for reflex control of R- controls arterial BP as driving P of flow, maintaining flow to whole body for homeostasis |
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Term
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Definition
F = [delta]P/R becomes CO = MAP/TPR (TPR is total peripheral R)
MAP = CO*TPR |
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Term
| *How does arteriolar r change TPR & MAP? |
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Definition
inc constriction (dec r)-> inc TPR-> inc MAP (BP)
increased R means less blood flowing out from arteries, so higher P |
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Term
| *extrinsic control of arteriolar R during hemorrhage |
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Definition
hemorrhage: lose blood
dec blood vol-> dec MAP-> baroreflex response inc TPR via extrinsic arteriolar control-> inc MAP to norm |
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Term
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Definition
sites of exchange
slowest velocity of flow to allow t for exchange w/ ISF
slow b/c have the largest total cross-sectional area, flow must be equal in all segments of circulatory sys at steady st |
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Term
| *solute exchange in capillaries |
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Definition
through diffusion
nutrients, gases, & wastes |
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Term
| *lipid soluble vs lipid insoluble diffusion thru capillaries |
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Definition
LS: diffuse thru endothelial cells, O2 & CO2
LI: diffuse thru capillary pores (where adjacent endothelial cells come close tg, intercellular cleft is a pore), Na+ & K+ & glucose & AAs |
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Term
| *protein movement thru capillaries |
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Definition
only "exchangeable proteins" like protein hormones- plasma proteins are not exchangeable & can't get thru
thru vesicular transport (endo- & exocytosis)
proteins are too big for pores & lipid insoluble |
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Definition
NOT diffusion
movement of fluid & dissolved substances tg (in bulk)
thru capillary wall is plasma minus proteins- wall is a filter
affects distribution of the ECF (ISF & plasma outside capillary)
capillaries have pores (endothelial cell junctions/intercellular clefts)
no net solute exchange bc solutes going out = solutes going in |
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Term
| *Capillary wall acts like a __________ which lets in __________ minus proteins |
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Definition
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Term
| *In bulk flow, fluid is reabsorbed at the ____________ end of the capillary, and the ___________ sys picks up filtered fluid that is not reabsorbed |
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Definition
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Term
| *inward & outward forces for fluid movement thru capillary walls |
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Definition
1. capillary hydrostatic P: blood is under P, pushes fluid out of capillary, higher on arteriole than venule end
2. plasma colloid ("colloid"=lg molecules) osmotic P: osmotic P due to plasma proteins (can't get out), draws fluid into capillary
3. interstitial fluid hydrostatic P: very low, if/when positive (+1mmHg) pushes fluid in
4. interstitial fluid colloid osmotic P: low, ~3mmHg, due to proteins in ISF |
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Term
| *calculating net filtration P |
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Definition
| subtract mmHg of inward forces (interstitial fluid hydrostatic P + plasma colloid osmotic P) from outward forces (capillary hydrostatic P + interstitial fluid colloid osmotic P) |
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Term
| *filtration vs reabsorption at capillaries |
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Definition
F: outward, at arteriole end ("ultra filtrate" of plasma bc only ultra sm stuff), overall more than reabsorption (3-4L/day)
R: inward, at venule end |
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Term
| *lymphatic sys & excess fluid |
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Definition
lymphatic sys picks up filtered fluid that is not reabsorbed by capillaries
lymphatic capillaries are permeable proteins
drains into venous sys of heart
also picks up leaked proteins |
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Term
| *effect of dec plasma colloid osmotic P |
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Definition
kidney disease (proteins lost in urine), liver disease (dec synthesis), protein deficiency in diet-> dec plasma proteins-> less F for reabsorption-> inc ISF-> edema (swelling of tissues)
liver makes plasma proteins
Kwashiorkor= bloated belly edema, inc ISF in abdomen |
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Term
| *effect of inc interstitial fluid colloid osmotic P |
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Definition
| burns (capillary damage), allergic response (histamine inc permeability to proteins)-> leaky capillaries let proteins out bc bigger pores-> inc movement out-> inc ISF-> edema |
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Term
| *effect of inc capillary hydrostatic P |
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Definition
| pregnancy (restrict flow from veins), heart failure-> inc venous P-> less [delta] P to move blood out of capillaries-> inc capillary P-> inc filtration-> edema |
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Term
| *effect of dec capillary hydrostatic P |
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Definition
| hemorrhage-> inc reabsorption-> replace lost plasma w/ tissue fluid |
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Definition
surgical removal of lymph nodes (ex. in mastectomy) disrupts/blocks lymph flow
causes edema |
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Term
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Definition
| parasite blocks lymph vessels/drainage-> extreme swelling of blocked area |
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Term
| *veins are ______ P vessels |
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Definition
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Term
| *P due to ___________ causes pooling of blood in veins |
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Definition
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Term
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Definition
low P (~15mmHg at venule end of capillary, 10mmHg at larger veins before vena cavae)
small [delta] P, skeletal muscle contraction, respiratory movements, and venous constriction drive blood to heart
compliant
thin-walled |
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Term
| *fxn of skeletal muscle contractions for veins |
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Definition
squeezes blood forward in veins, valves in peripheral veins prevent back flow
interrupts columns of blood- completely empties sections of veins, reduces effect of gravity |
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Term
| *standing vs walking venous P |
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Definition
S: no leg muscle contractions-> inc venous P-> inc capillary P-> inc filtration-> edema
W: less edema bc muscle contractions break up columns to dec venous P, no edema |
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Term
| *fxn of respiratory movements for veins |
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Definition
| breathe in-> inc chest size (diaphragm lowers)-> dec P of chest veins, inc abdominal P-> inc P gradient-> promotes flow to chest |
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Term
| *fxn of venous constriction |
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Definition
sympathetic impulses-> smooth muscle of veins contracts-> dec r-> inc venous P-> inc [delta]P between veins & heart (atrial P = 0mmHg)-> inc venous return
does not inc R b/c veins so lg |
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Term
| *What happens when you stand w/ your knees locked? |
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Definition
little muscle contractions-> lose skeletal muscle pump in legs-> dec venous return, dec SV, dec CO, dec MAP
could faint
inc capillary P-> inc filtration-> inc ISF-> edema |
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Term
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Definition
compliance: measure of stretchability
veins much more than arteries
can hold a lot of blood w/o much P change, act as reservoirs when capillaries closed at rest by moving blood slowly
C=[delta]V/[delta]P
high compliance means big vol change w/ sm P change |
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Term
| *How much blood in normally in veins? |
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Definition
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Term
| *How does the body utilize blood in veins when needed? |
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Definition
| hemorrhage-> dec MAP-> baroreflex response inc sympathetic impulses-> vein constriction (dec diameter, dec C)-> inc venous P-> inc venous return-> inc SV & CO-> raises MAP |
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Term
| *Long-term regulation of bp involves __________ & _________ balance |
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Definition
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Term
| *Short-term regulation of bp involves minute to minute ___________ control of CO & _______ |
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Definition
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Term
| *factors that affect arterial bp |
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Definition
1. blood vol: dec Na+-> dec water in plasma-> dec ECF/blood vol-> dec MAP, long-term regulation, Na+ & water balance changes ECF (blood is a part) vol, kidneys involved in Na+ & water retention/loss
2. CO & TPR: MAP = CO + TPR, inc HR or inc SV (thru intrinsic or extrinsic control)-> inc CO (if not too high HR bc would dec filling t)-> inc MAP, dec r of arterioles-> inc R-> less blood flow out of arteries-> inc MAP, short-term regulation thru baroreflex (sensory stretch receptors in arteries- carotid sinus & aortic arch- stop firing when MAP crashes low, effectors are heart & vessels, homeostatic - FB) |
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Term
| *baroreflex response when you get up in the morning |
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Definition
| stand-> inc gravity P-> inc venous P-> veins distended-> blood "pools" in veins-> dec venous return, dec SV, dec CO-> dec MAP-> baroreceptors fire less-> baroreflex inc CO or TPR-> inc MAP |
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Term
| *baroreflex w/ bedridden patients |
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Definition
don't have vol-retaining effects of gravity
can have reduced baroreflex response & faint when get up |
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Term
| *explain cardiovascular events during hemorrhage |
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Definition
see notes or pg 342
similar response to standing, but needs long-term mechanisms- kidneys retain Na+ & water, inc thirst, liver replaces plasma proteins, RBCs replaced
SV, CO, & MAP directly dec due to hemorrhage restored toward norm
HR & TPR go above pre-hemorrhage lvl due to reflex response |
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Term
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Definition
| lose too much blood, weak heart, vasodilation from bact toxins or allergic rxn or dec. sympathetic activity-> dec CO a LOT-> damage heart & brain-> more dec CO-> patient dies |
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Term
| draw flow hart of autonomic CV sys control |
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Definition
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Term
| blood returning to the heart from the lungs enters the... |
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Definition
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Term
| if the SA node was damaged so cells couldn't reach threshold, HR would... |
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Definition
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Term
| ARP of cardiac muscle lasts... |
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Definition
| about as long as contraction |
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Term
| cardiac impulse is delayed 0.1s at... |
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Definition
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Term
| in complete heart block, there is no correlation between... |
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Definition
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Term
| HR>250bpm could occur during... |
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Definition
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Term
| 1st heart sound is due to closing of _________ valves |
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Definition
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Term
| chord tendineae __________ valves |
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Definition
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Term
| during ventricular systole, blood vol in the ventricle... |
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Definition
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Term
| aortic semilunar valve closes when ventricular P is _____ than aortic P |
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Definition
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Term
| normal aortic diastolic BP |
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Definition
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| R ventricle wall is _____ than L ventricle |
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Definition
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Term
| inc PS impulses to heart _______ HR |
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Definition
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Term
| inc venous return _________ EDV |
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Definition
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Term
| Starling's Law is _________ control of SV |
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Definition
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Term
| changes in contractility is ___________ control of SV |
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Definition
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Term
| sympathetic NS is __________ control of SV |
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Definition
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Term
| The tunica media of vessel walls is... |
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Definition
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Term
| inc pressure gradient will _______ flow |
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Definition
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Term
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Definition
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Term
| in active hyperemia, inc metabolic activity in an organ causes arteriolar __________ which ____ flow thru the organ |
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Definition
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Definition
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Definition
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Term
| velocity of flow is slowest in... |
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Definition
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Term
| _______ molecules move thru the capillary wall by diffusion thru endothelial cells. __________ molecules move thru by diffusion thru intercellular clefts. |
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Definition
| lipid soluble, lipid insoluble |
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Term
| Filtration is _________ reabsorption in total capillary action |
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Definition
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Term
| __________ plasma proteins would cause edema |
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Definition
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Term
| arterioles have the _____ resistance of all vessels |
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Definition
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Term
| sympathetic stimulation of veins _______ venous P & ________ venous return |
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Definition
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Term
| when a standing person begins waking, pressure of veins in foot will... |
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Definition
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