lecture 12: cardiovascular system Flashcards

1
Q

parts of the cardiovascular system

A

heart
blood
blood vessels (vasculature)

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2
Q

vasculature

A

blood vessels
veins, arteries, and capillaries

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3
Q

structure of the heart

A

circulation maintains heart works properly by pumping blood continuously
apex and base
Right side: R. atrium, R. ventricle, superior vena cava
Left side: Aorta, pulmonary artery, L. atrium, L. ventricle, coronary artery and vein

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4
Q

myocardium

A

heart muscle (what most of it is made out of)
atria made out of this with thinner walls

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5
Q

pulmonary artery

A

removes waste in the heart

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6
Q

coronary vein

A

remove waste, CO2, etc. from tissue

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7
Q

coronary artery

A

bring oxygen and nutrients to the heart tissue

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8
Q

in lungs

A

blood exchanging oxygen and CO2 with alveoli

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9
Q

pulmonary capillary beds

A

O2 moves into the blood and CO2 leaves (from tissues)
go from blood to alveoli

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10
Q

pulmonary veins

A

oxygenated blood gets moved to the heart
return from lungs

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11
Q

aorta

A

blood moves to the tissues from L atrium and L ventricle

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12
Q

Left atrium

A

blood from pulmonary veins comes into here
contracts and pushes it to L ventricle
L ventricle pushes to aorta and all arteries and systemic circuit tissues

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13
Q

artery

A

blood vessel that moves blood away from the heart

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14
Q

vein

A

blood vessel that moves blood towards the heart

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15
Q

oxygenated blood

A

arterial blood with high O2 concentration (L side)

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16
Q

deoxygenated blood

A

venous blood pumping
how much O2 depends on how much tissues have extracted/metabolic rate (R side)

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17
Q

R atrium

A

contracts and pushes blood into R ventricle
R ventricle contracts and pushes blood onto pulmonary trunk
pump deoxygenated blood

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18
Q

pulmonary trunk

A

R ventricle pushes blood onto this
splits into R. and L pulmonary arteries going towards lungs

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19
Q

venae cavae

A

superior and inferior
empty onto R atrium

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20
Q

superior vena cava

A

bringing blood to heart from arms, shoulders, head, neck

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21
Q

inferior vena cava

A

bringing blood to heart from bottom of body
all venous blood

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22
Q

pulmonary arteries

A

deoxygenated blood being moved away from heart to the lungs

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23
Q

heart valves

A

2 atrioventricular (in between atria and ventricles)
2 semilunar (between ventricles and outflow vessels)
blood flow is unidirectional in heart, never goes back BECAUSE OF THESE
separation of chambers, do not want to mix blood

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24
Q

R ventricle

A

pushes blood towards lungs
not as thick as L

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24
L ventricle
wants to produce lots of contraction, overcome gravity lots thicker than R pushes blood to whole systemic circulation, including the head overcome gravity pushing blood up contracts more forcefully
24
interventricular septum
separating the ventricles important to not mix blood need arterial blood to be fully oxygenated
25
descending aorta
brings oxygenated blood to tissues
26
AV (mitral valves)
atriventricular prevent blood from backflow to atrium formed by thin flaps of connective tissue joined at base by ring of connective tissue very flimsy, delicate can be tricuspid or bicuspid open towards the ventricles dont "move" since theres no muscle, open and close due to pressure changes between the chambers and/or out flow vessels happens passively
27
tricuspid valve
right AV 3 flaps, on R side of heart (between atrium and ventricle)
28
mitral or bicuspid valve
2 flaps left AV, between L atrium and L ventricle prolapse can sometimes happen here because L ventricle contracts more forcefully not opening completely damage to valve itself or chordae tendineae
29
papillary muscles (tense)
during contraction do not move fingerlike projections from ventricular wall prevent valves from prolapsing up and collapsing into atrium
30
chordae tendineae (tense)
tense connective tissue during contraction at "tips" of flaps (holds edge together) of tricuspid and bicuspid valves like a guitar string connect to papillary muscles prevent valves from prolapsing
31
ventricular contraction
ventricle contracts ---> pushes blood up ---> contracts from bottom to top ---> catches edge of mitral/tricuspid valve flaps ---> causes them to close ---> L atrium has little blood and pressure
32
semilunar valves
between the ventricles and outflow vessels L ventricle and aorta R ventricle and pulmonary arteries open towards pulmonary artery/aorta prevent blood that has entered the arteries from flowing back into the ventricles during ventricular relaxation
33
heart murmurs
usually happen due to problems with valves backflow into ventricles or aorta valves arent working properly constantly taking blood into heart chambers (constant leakage) valves can become calcified
34
chordae tendineae (relaxed) and papillary muscles (relaxed)
both not making valves move prevent valves from bulging up and prolapsing into atria prevent backflow
35
ventricular relaxation
pressure in arteries higher (full of blood) blood tends to back up but catches at back of semilunar valve flaps flaps close valves themselves do not contract or relax because they dont have muscle open and close due to changes in pressure between outflow vessels and ventricles
36
types of cardiac muscle
contractile cells autorhythmic/pacemaker cells conductive cells
37
myogenic
characteristic of the heart means it contracts on its own without hormones (endocrine system) or without signals (nervous system) ANS modulates/regulates function of the heart due to pacemaker cells constant input from parasympathetic branch
38
contractile cardiac cells
myocardium most muscle cells striated fibers organized into sarcomeres like skeletal one nucleus like smooth muscles force of contraction pressure to cause blood flow
39
pacemaker cells
1% of heart, few and smaller signal for contraction, set the rhythm for HR can spontaneously depolarize/ generate MAP AP goes to contractile cells to depolarize and generate MAP ---> contraction smaller and fewer contractile fibers compared to contractile cells do not have organized sarcomeres, dont participate in generating tension/pressure/contraction determine bpm heart goes through
40
structure of contractile cells
one nucleus striated smaller than skeletal muscle and are branched interconnected through intercalated disks (proteins)
41
connections that tie all cardiac contractile cells together
1. desmosomes ---> keep tension and transfer force 2. gap junctions ---> cytoplasm of one cell connects to another cell's cytoplasm, AP propagation ---> muscle cells contract/depolarize all at the same time ---> push of blood happens quickly and effectively
42
orientation of cardiac muscle fibers
have to contract in more than one direction to push blood to various places striated ---> only contract along their long axis, can still be organized in parallel and on same longitudinal axis with sliding of filaments fibers wrap around to squeeze the blood out contraction in two axis
43
nodal or pacemaker cells
depolarize at faster rate than other pacemaker cells sinoatrial node (SA) at top of R atrium atrioventricular node (AV) between the atria and ventricles both nodes connected by internodal pathways signal for contraction, set the rhythm specialized to start depolarization conduction velocity ---> 0.02 m/sec
44
conductive cells
bundle of His (also pacemaker cells), right after AV node branch in L and R Purkinje fibers (huge relative to other fibers) specialized to spread depolarization do not contract conduction velocity ---> 3.4 m/secrt
45
conducting system of the heart
SA and AV node connected to each other by internodal pathways SA node ---> AP will move to cardiocontractile cells through gap junctions ----> internodal pathways ----> conduct signal faster than cardiac contractile cells do, highway ----> AV node ----> bundle branches which are huge and conduct AP/electrical signal faster ----> less resistance for current/flow of ions ---> Purkinje fibers ---> go deep into muscle
46
AV node connection
cells from atria not connected to cells from ventricle by gap junctions NEED to be connected through AV node there is connective tissue separating atria from ventricles AP from cardiac contractile cells in atrium cannot jump to cardiac contractile cells in ventricle ---> brake in AV node bundle of Beckman goes from SA node to L atrium
47
action potentials of cardiac contractile cells
Phase 4: Resting membrane potential Phase 0: fast depolarization Phase 1: small repolarization Phase 2: Ca plateau Phase 3: Repolarization
48
Phase 4 for contractile cells
resting membrane potential Vrest ~ - 90 mV (more negative than neuron) no hyperpolarization of the cell VG K channels may not be completely closed (slow to open/close) but -90 mV = Ek efflux of K stops no undershot like with neuron cell not becoming MORE negative, stopping at -90 mV
49
Phase 0 for contractile cells
increase in permeability of Na fast depolarization VG Na channels activate --> open relatively quickly compared to LTCC Na moves into cell down conc gradient cell less negative diffuse really fast
50
Phase 1 for contractile cells
small repolarization decrease in Na permeability, stops /decreases, G Na channels inactivate small increase in K permeability ---> VG K channels open fast, K goes out of cell with conc gradient
51
Phase 2 for contractile cells
Ca plateau VG Ca channels activate (open due to depolarization event), LTCC, slow to open increase in Ca permeability matches K efflux makes AP much longer than for skeletal muscle cells (which rely on VG Na channels only)
52
Phase 3 for contractile cells
repolarization decrease in Ca permeability, increase in K permeability VG K channels activate (open a bit slower, slower than Phase 1 channels) Ca stops moving in, no LTCCs open
53
difference between skeletal and cardiac action potentials
skeletal muscle ---> MAP: 1-5 msecs, 2-3 msecs cardiac muscle ----> AP: 200-300 msecs lasts much longer 200 = ventricular, 300 = atrial VG Ca channels in cardiac muscle extend depolarization phase
54
refractory period in cardiac muscle action potentials
time we cannot generate a 2nd AP with same stimulus, not until you reach repolarization ends almost at the same time as muscle twitch ends(contraction) muscle almost completely relaxes before having second AP chamber can fill with blood again next contraction can eject blood effectively can initiate muscle twitch right after and have 2nd AP prevent tetanus in the heart long AP due to Ca plateau prevents summation
55
cannot summate for cardiac muscle contraction
summation of tension without letting heart completely relax before contraction prevents complete ventricular filling of blood wont effectively eject enough blood
56
skeletal muscle summation
can increase tension and start contraction before muscle relaxes generate 2nd AP or multiple
57
nodal (pacemaker) cells action potential
slow spontaneously depolarize and generate AP dont need nervous system to generate AP heart beats on its own even without signal Phase 0: slow depolarization Phase 2: Ca plateau Phase 3: Repolarization Phase 4: Reach membrane threshold
58
Phase 0 for nodal cells
increase in Ca permeability LTCC open slow depolarization slope sets the conduction velocity of AP steeper slope ---> faster depolarization, propagation of AP, conduction velocity
59
Phase 2 for nodal cells
Ca plateau Ca leaves cell ---> cell repolarizes LTCC close VG K channels open
60
Phase 3 for nodal cells
repolarization decrease in Ca permeability, increase in K permeability moving out til -60 mV in the cell sets the AP duration steeper slope = shorter AP duration
61
Phase 4 for nodal cells
Funny current channels (If) open K and Na move through Na depolarizes the cell autorrhythmic reach Vt ---> cell becoming less negative (pacemaker potential) increase in K and Na, opening of transient type Ca channels when TTCC open ---> If channels close (closer to Phase 0) sets the AP firing frequency steeper slope = faster AP frequency, reach Vt faster while pacemaker potential is getting more negative
62
nodal cells pacemaker potential
no Vrest in pacemaker cells pacemaker potential never stays at stable membrane potential
63
T-Type Ca channels
transient type VG open/close fast lower threshold than LTCC Ca moves into cell brings cell to threshold ---> activate LTCC initiate phase 0
64
funny current (If) channels
allow Na and K to move through moving more Na in than K out hyperpolarization (-60 mV) cyclic nucleotide activated channels activate, deactivate, @ -60 mV activate again
65
what determines AP firing frequency
membrane potential ---> determines how long it takes to get to depolarization increase in Vm ----> reach Vt faster if Vm is more negative than -60 mV, it takes longer to reach Vt
66
pacemakers of the heart
SA node ----> 80-100 depolarizations per minute , sets pace of the heart (fastest) AV node -----> 45 bpm Bundle of His -----> 30 bpm Purkinje fibers are not autorhythmic, just these 3 AV and Bundle of His can act as pacemakers under some conditions if SA node is injured, but the heart pumps very slowly
67
spread of depolarization in myocardial cells
pacemaker cells spontaneously depolarize spread to adjacent contractile cells through gap junctions contraction by the time AV node can depolarize ---> signal has already arrived through internodal pathways to AV node ----> cause depolarization after
68
AV node and delay
routes the direction of electrical signals, to ensure that the heart contracts from apex to base AV node delay, smaller cells compared to His fibers slower conductional signals through nodal cells ensures atria depolarize and contract before ventricles fibers need to be brought to threshold signal has time to go to bottom of apex, depolarize bottom to top causes MAP/contraction to go from bottom to top accumulate Ca through LTCC in AV node ----> bring bundle of His to threshold ---> impedance imbalance no connection/gap junctions between atrium contractile cells and ventricular contractile cells ---> connective tissue dividing the two, signal can ONLY go through AV node first
69
electrical conduction system of the heart
sets HR to contact ----> need electrical event/MAP 1. signal begins in SA node which depolarizes faster 2. spontaneous depolarization to L atrium 3. goes to AV node, atria is completely depolarized 4. go past AV node, signal goes through Bundle of His quickly 5. signal moves towards apex of heart
70
mechanism of contraction
1. action potential enters cell, travel through membrane of muscle cell to t-tubule 2. in t-tubule, VG Ca channels open (DHPR or LTCC), Ca enters the cell 3. Ca induces Ca release (90% from SR) through RyR2, DHPR and RyR2 no physically connected (need Ca to activate) 4. local release causes Ca spark 5. summed Ca sparks create Ca signal 6. Ca binds to troponin to initiate contraction, tropomyosin moves, crossbridge and tension sarcomere shortens (in parallel) myosin head hydrolyzing ATP, sliding actin filaments
71
DHPR
if this Ca channel is blocked ----> no cardiac contractile cells, SR cant open not physically connected to RyR2, need Ca to activate
72
mechanism of relaxation
1. Ca unbinds from troponin 2. Ca is pumped back into the SR for storage using SERCA 2 (Ca-ATP pump) 3. Ca is exchanged with Na by NCX antiporter (same as in smooth muscle) 4. Na gradient is maintained by Na-K pump