B4-099 Overall View of the Heart's Function Flashcards
which layer of the heart wall…
ejection of blood from the heart
myocardium
which layer of the heart wall…
protection of the heart from mechanical trauma
pericardium
which layer of the heart wall…
stabilize the heart within the thoracic cavity
pericardium
which layer of the heart wall…
functions as a lubricant to decrease friction
pericardium
which layer of the heart wall…
prevent excessive dilation of the heart
pericardium
which layer of the heart wall…
provides a smooth surface for blood flow
endocardium
which layer of the heart wall…
releases substances that control heart development
endocardium
the closure of the AV valves is heard as a
lub
S1
closure of AV valves
the closure of SL valves is heard as a
dub
S2
closure of SL valves
the mitral valve has […] cusps
2
capacity to respond to an electrical impulse
excitability
ability to initiate electrial impulse
automatism
capacity to maintain
rhymicity
ability to transmit the electrical stimulus to all areas of the heart
conductivity
transient lack of the cardiac cells to respond to stimulus
refractoriness
capacity of heart muscle to contract
contractility
difference in voltage between the intracellular compartment and the external medium
resting membrane potential
cardiac cells can trigger a change in membrane potential, which will lead to
cardiac contraction
- depolarization to repolarization
- all or none response
action potential
return to the cell resting potential
repolarization
rapid change in resting membrane potential
depolarization
how is cardiac action potential different from skeletal muscle?
- is it self generating
- it can be conducted directly from cell to cell
- it has relatively long duration
atrial and ventricular cardiomyocytes and purkinje fibers have a […] response
fast
action potential
SA and AV nodes have a […] response
slow
action potential
phase 4
pre action potential
phase 0
upstroke of action potential
phase 1
transient repolarization
phase 2
plateau phase
phase 3
repolarizing phase
in the SA and AV nodes, the action potential only has […] phases
3
4, 0, 3
in ventricular myocytes, the action potential has […] phases
all 5
different in nodal and myocardial ventricular cells
depolarizing current
in the SA and AV nodes, the depolarizing current is the
calcium current
in ventricular myocytes, the depolarizing current is the
sodium current
important for excitation-contraction of the heart
calcium current
the repolarizing current in all areas of the heart is the
potassium current
sodium channels are […] gated
voltage
slow response action potential is […] dependent
calcium
SA and AV node
fast response action potential is […] dependent
sodium
cardiomyocytes, bundle of His, perkinje fibers
cardiac chronotropism
- automatism
- the capacity of the heart to produce electical impulses
automatism depends on the
SA node
does not have a stable resting potential
SA node
name the phase/location:
- slow depolarization
- pacemaker potential due to increased Na+ conductance
- funny sodium current is responsible for heart’s automaticity
phase 4
SA node
name the phase/location:
upstroke of action potential due to inward calcium current
phase 0
SA node
name the phase/location:
not present in nodal cells
phase 1/2
name the phase/location:
- repolarizing phase
- caused by increased K+ conductance
- leads to outward K+ current
phase 3
SA node
- most negative potential in SA node
- normally about 50mV
MDP
maximum diastolic potential
if the SA node is no longer function, cardiac excitation will be driven by
AV node
the action potential of AV node is similar to SA node, but the slope of phase […] is less steep
4
determines the conduction velocity of the action potential moving through the AV node
magnitude of calcium current
responsible for sodium entrance and phase 0 depolarization
funny sodium channels
activated during phase 0 to cause depolarization
L-type calcium channels
repolarization during phase 3 occurs due to
K+ channels
name the phase/location:
- stable resting potential
- inward rectifier potassium channels
phase 4
myocardial cells
name the phase/location:
upstroke due to voltage gated sodium current
phase 0
myocardial cells
name the phase/location:
- transient repolarization due to K+ moving out of cells
- decrease in Na+ conductance
phase 1
myocardial cells
name the phase/location:
- plateau phase due to balance between Ca+ and K+ currents
- delayed rectifier K+ channels
phase 2
myocardial cells
name the phase/location:
repolarization phase due to K+ outward current driven by delayed rectifier potassium cells
phase 3
myocardial cells
- responsible for phase 0 depolarization
- very transient current
voltage gated sodium channels
- activated during phase 0
- little change in membrane potential in phase 2
- Ca+ inactivation gates close near end of phase 2
L-type Ca+ channels
repolarization during phase 3 occurs due to
K+ channels
normal sinus rhythm
60-100 bpm
what channel contributes to diastolic depolarization in SA and AV nodes?
funny sodium channel
what channel is active during phase 0 of action potential?
voltage gated sodium channel
what channels are open during phase 2 of action potential?
- L-type calcium channel
- K+ delayed rectifier channel
what channel maintains high K+ permeability during phase 4 of action potential?
K+ inward rectifier channel
what channel contributes to phase 1 of action potential?
K+ transient outward channel
the funny sodium channel opens with
repolarization
Na+ channels open in response to
depolarization
voltage gated sodium channels have 3 main conformational states
- closed
- open
- inactivated
Na+ channels have two separate gates
- activation gate
- inactivation gate
at resting membrane potential, the voltage gated sodium channel is
closed
[…] opens the activation gate of the voltage gates sodium channel
depolarization
at full depolarization, the [….] gate of the voltage gated sodium channel closes
inactivation
the activation gate opens [fast or slow]
fast
the inactivation gate opens [fast or slow]
slow
in hyperkalemia, the resting membrane potential is more positive than normal.
This causes
- decreased voltage gated sodium current
- decreased excitability of heart cells
the magnitude of the voltage gated sodium current in the cardiac myocytes will determine
- threshold potential
- amplitude of action potential
- rate of rise of action potential
- conduction velocity
the L type Ca+ channel has activation and inactivation curves that overlap called
calcium window
the magnitude of L-type calcium current in the SA and AV nodes will determine
- threshold potential
- amplitude of action potential
- rate of rise of action potential
- conduction velocity
conduction velocity in the AV node will determine the
duration of PR segment on ECG
K+ delayed rectifier cells open upon
depolarization
very slow to allow depolarization to finish
lowest conduction velocity
AV node
cardiac muscle cells are rectangular shaped cells connected by
intercalated discs
- protein lined tunnels
- allow direct transmission of the depolarizing current from cell-to-cell so they contract in unison
gap junctions
because of the way gap junctions function, cardiac muscle cells are said to be
electrically coupled
period in which the cardiac cells is unable to intiate anothe action potential
refractory period
refractory period allows for
complete emptying of the heart
heart muscle contraction is reffered to as
inotropism
process by which the electrical activation of the cardiac myocytes leads to the activation of contraction
cardiac excitation contraction coupling (ECC)
increases inotropy and stroke volume
calcium
Frank-Starling’s Law
the energy of contraction is proportional to the initial length of the cardiac muscle fiber
stroke volume increases when
preload is increased
as preload increases, sarcomere length
increases
allows more cross bridging during systole
increased sarcomere length allows
more cross bridges to form during systole
increasing EDV allow more overlap of
thick and thin filaments
more crosslinking
- all cardiac valves are closed with no blood flow
- pressure in ventricles is low
isovolumic relaxation
diastole
mitral and tricuspid valves open, pulmonic valves are closed
ventricular filling
diastole
during ventricular filling, the pressure in the ventricles drops below
that of the atria
- all cardiac valves are closed with no blood flow
- ventricular pressure raises
- atrial pressure raises
isolvolumic contraction
systole
aortic and pulmonic valves are open; mitral and tricuspid are closed
ejection
systole
when the heart rate is high, […] is shortened the most
diastole
the AV node will not conduct beyond
230 bpm
Ejection fraction=
stroke volume/
EDV
normal value for EDV
120-140 mL
normal value for ESV
40-60 mL
normal value for SV
60-100 mL
normal value for ejection fraction
0.5-0.7
normal value for cardiac output
5.0-6.0 L/min
normal value for cardiac index
2.6-4.2 L/min/m2 of body surface area
way to normalize values for cardiac output to differences in body size
cardiac index
myocardial action potential
- rapid upstroke and depolarization
- voltage gated Na+ channels open
phase 0
myocardial action potential
- initial repolarization
- inactivation of voltage gated Na+ channels
- voltage gated K+ channels begin to open
phase 1
myocardial action potential
- Ca+ influx through voltage gated Ca+ channels balances K+ efflux
- Ca+ influx triggers Ca+ release from sarcoplasmic reticulum and myocyte contraction
phase 2
Ca+in =K out causes platwo
myocardial action potential
- rapid repolarization
- massive. K+ efflux due to opening of delayed rectifier K+ channels
- closure of voltage gated K+ channels
phase 3
myocardial action potential
- resting potential
- high K+ permeability through K+ channels
phase 4
myocardial action potential occurs in all cardiac myocytes except
SA and AV node
pacemaker action potential
- upstroke
- opening of L type Ca+ channels
- results in slow conduction velocity
phase 0
pacemaker action potential
- repolariztion
- inactivation of Ca+ channels
- increased activation of K+ channels
- increase K+ efflux
phase 3
pacemaker action potential
- slow spontaneous diastolid depolarization due to funny sodium current
phase 4
neurotransmitters that decrease the rate of diastolic depolarization and HR
- ACh
- adenosine
neurotransmitters that increase depolarization and HR
chatecholamines
increases the chance that funny sodium channels are open and thus increases HR
sympathetic stimulation