lecture 12: cardiovascular system Flashcards
parts of the cardiovascular system
heart
blood
blood vessels (vasculature)
vasculature
blood vessels
veins, arteries, and capillaries
structure of the heart
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
myocardium
heart muscle (what most of it is made out of)
atria made out of this with thinner walls
pulmonary artery
removes waste in the heart
coronary vein
remove waste, CO2, etc. from tissue
coronary artery
bring oxygen and nutrients to the heart tissue
in lungs
blood exchanging oxygen and CO2 with alveoli
pulmonary capillary beds
O2 moves into the blood and CO2 leaves (from tissues)
go from blood to alveoli
pulmonary veins
oxygenated blood gets moved to the heart
return from lungs
aorta
blood moves to the tissues from L atrium and L ventricle
Left atrium
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
artery
blood vessel that moves blood away from the heart
vein
blood vessel that moves blood towards the heart
oxygenated blood
arterial blood with high O2 concentration (L side)
deoxygenated blood
venous blood pumping
how much O2 depends on how much tissues have extracted/metabolic rate (R side)
R atrium
contracts and pushes blood into R ventricle
R ventricle contracts and pushes blood onto pulmonary trunk
pump deoxygenated blood
pulmonary trunk
R ventricle pushes blood onto this
splits into R. and L pulmonary arteries going towards lungs
venae cavae
superior and inferior
empty onto R atrium
superior vena cava
bringing blood to heart from arms, shoulders, head, neck
inferior vena cava
bringing blood to heart from bottom of body
all venous blood
pulmonary arteries
deoxygenated blood being moved away from heart to the lungs
heart valves
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
R ventricle
pushes blood towards lungs
not as thick as L
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
interventricular septum
separating the ventricles
important to not mix blood
need arterial blood to be fully oxygenated
descending aorta
brings oxygenated blood to tissues
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
tricuspid valve
right AV
3 flaps, on R side of heart (between atrium and ventricle)
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
papillary muscles (tense)
during contraction
do not move
fingerlike projections from ventricular wall
prevent valves from prolapsing up and collapsing into atrium
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
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
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
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
chordae tendineae (relaxed) and papillary muscles (relaxed)
both not making valves move
prevent valves from bulging up and prolapsing into atria
prevent backflow
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
types of cardiac muscle
contractile cells
autorhythmic/pacemaker cells
conductive cells
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
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
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
structure of contractile cells
one nucleus
striated
smaller than skeletal muscle and are branched
interconnected through intercalated disks (proteins)
connections that tie all cardiac contractile cells together
- desmosomes —> keep tension and transfer force
- 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
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
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
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
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
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
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
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
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
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
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)
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
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
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
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
skeletal muscle summation
can increase tension and start contraction before muscle relaxes
generate 2nd AP or multiple
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
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
Phase 2 for nodal cells
Ca plateau
Ca leaves cell —> cell repolarizes
LTCC close
VG K channels open
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
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
nodal cells pacemaker potential
no Vrest in pacemaker cells
pacemaker potential
never stays at stable membrane potential
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
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
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
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
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
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
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
mechanism of contraction
- action potential enters cell, travel through membrane of muscle cell to t-tubule
- in t-tubule, VG Ca channels open (DHPR or LTCC), Ca enters the cell
- Ca induces Ca release (90% from SR) through RyR2, DHPR and RyR2 no physically connected (need Ca to activate)
- local release causes Ca spark
- summed Ca sparks create Ca signal
- Ca binds to troponin to initiate contraction, tropomyosin moves, crossbridge and tension
sarcomere shortens (in parallel)
myosin head hydrolyzing ATP, sliding actin filaments
DHPR
if this Ca channel is blocked —-> no cardiac contractile cells, SR cant open
not physically connected to RyR2, need Ca to activate
mechanism of relaxation
- Ca unbinds from troponin
- Ca is pumped back into the SR for storage using SERCA 2 (Ca-ATP pump)
- Ca is exchanged with Na by NCX antiporter (same as in smooth muscle)
- Na gradient is maintained by Na-K pump
