Action Potential,Resting Membrane Potential and Conduction System Flashcards
cardiac output
CO = HR x SV
mean arterial pressure
MAP = CO x TPR
types of cardiac cells?
contractile - perform mechanical work
autorhythmic - initiate action potential
order of electrical events?
SA node inter-atrial pathway AV node common AV bundle (bundle of His) right and left bundle branches purkinje fibers
functional syncytium?
myocytes contract as single unit
-due to gap junctions
does cardiac function require neural input?
no
location of SA node
right atrial wall just inferior to opening of superior vena cava
rate at SA node?
60-100 bpm
rate at bundle of His?
40-60 bpm
rate at purkinje fibers?
20-40 bpm
location of AV node?
floor of right atrium immediately behind tricuspid valve and near opening of coronary sinus
location of bundle of His
superior portion of IV septum
location of right and left bundle branches
IV septum
location of purkinje fibers
ventricular myocardium
function of AV node?
receives impulses from SA node and delays relay of impulse to bundle of His
allows time for atria to empty before ventricular contraction
SA node?
normal pacemaker of heart
located at junction between superior vena cava and right atrium
what causes difference in rates of action potentials in pacemaker cells?
different rates of slow depolarization phase
SA node failure?
can result in bradycardia
unmasks slower, latent pacemaker of AV node
internodal pathway?
SA node to AV node
-anterior, middle, and posterior pathways
bachmann’s bundle?
SA node to left atrium
-conduction velocity 1 m/s
AV node location
posteriorly on right side of interatrial septum
near ostium of coronary sinus
three regions of AV junction?
AN region
-transitional between atrium and the node
N region
-midregion of the AV node
NH region
-nodal fibers merge with bundle of His
AV junction?
this is where the signal is slowed
AN region?
longer conduction path
N region
slower conduction velocity
two regions that allow for AV node delay?
AN and N regions
between atria and ventricle delay
why is there a delay between atrial and ventricular excitation?
allows the filling of ventricles before contraction
decremental conduction
signal will peeter out
increase stimulation frequency
decrease conduction velocity
limits rate of conduction to the ventricles from accelerated atrial rhythms
what is more detrimental: atrial or ventricular fibrillation?
ventricular
AV block
purkinje fibers take over (20-40 bpm)
also caused by prolonged nodal delay
wolf-parkinson-white syndrome
common accessory pathway
alternate pathway around AV node
faster than normal AV nodal pathway
-AP conducted directly atria to ventricle
ventricular depolarization is slower than normal
-doesn’t follow normal purkinje fiber pathway
bundle of kent?
alternate pathway around AV node in WPW syndrome
Bundle of His
passes down right side of IV septum
-divides into left and right bundle branches
right bundle branch
branch of bundle of His
-down right side of IV septum
left bundle branch
branch of bundle of His
- thicker than RBB
- perforates IV septum
splits of left bundle branch?
thin anterior and thick posterior division
purkinje fibers
arise from RBB and anterior, posterior LBB
complex network of conducting fibers spread out over subendocardial surfaces of R and L ventrices
arrangement of purkinje fibers?
linearly arranged sarcomeres
- typically lack T tubule system
- largest diameter cardiac cells
fastest conduction in the heart?
purkinje fibers
1-4 m/s
largest diameter***
ventricular muscle depolarization?
1 AV node > bundle branches
2 IV septum depolarizes L-R
3 anteroseptal region depolarizes
4 myocardium depolarizes endocardium > epicardium
5 depolarization apex > base (via purkinje)
6 ventricles fully depolarized
**wave or repolarization - reversed
why contract apex to base?
to “ring” out the blood
early contraction of IV septum?
rigid, anchor point for ventricular contraction
early contraction of papillary muscles?
prevent prolapse of AV valves during ventricular systole
depolarization fro apex to base?
efficient emptying of ventricles into aorta and pulmonary trunk at base
slowest conduction velocity?
AV node (small diameter)
and SA node is quite slow as well
fastest conduction velocity?
purkinje fibers (large diameter)
cardiac muscle
striated mononucleated intercalated disks many mitochondria t-tubules and SR slow speed of contraction (250ms) -skeletal muscle: 100ms
sarcomere
z line to z line
intercalated disks?
gap junctions in cardiac muscle (low resistance)
calcium source in cardiac muscle?
in ECF and SR
- before, it was mainly SR
- now, ECF is important
biomarker for cardiac damage?
cTnT, cTnI
-troponin
CK-MB
creatine kinase isoform specific to cardiac muscle
electrical syncytium
all cardiac muscles contract in synchronous manner
intercalated disks
connect cardiac cells through mechanical junctions and electrical connections
desmosomes
mechanical connections
-prevent cells from pulling apart when they contract
gap junctions
electrical connection (low resistance) allowing AP propagation
conduction of APs in cardiac muscle?
conduction system
cell to cell
widening of QRS complex due to?
ventricular depolarization that spreads only cell to cell via gap junctions
ex/ PVCs, ventricular tachycardia
what forms functional syncytium?
ventrical and atria contract as separate units
all or none law of heart
either all cardiac cells contract or none do
due to functional syncytium and conduction system
no variation in force production via motor unit recruitment
contractility
increased force of contraction independent of initial fiber length, preload
modified by altering sympathetic NS input
-increase in calcium permeability
extracellular calcium and cardiac contraction?
influx of ECF calcium is required for additional release from SR
Ca2+ induced Ca2+ release from SR through Ca2+ release channels (RYR)
amount of Ca2+ from ECF alone is too small to promote actin-myosin binding
Ca2+ release channels remain open longer
relaxation of cardiac contraction?
removal of Ca2+ to ECF
- sarcolemma 3Na+ 1Ca2+ antiporter
- sarcolemma Ca2+ pump (uses ATP)
sequestering Ca2+ into the SR
-SERCA pump, regulated by phospholamban
two ways to remove Ca2+ to ECF of cardiac cells?
sarcolemma Na+/Ca2+ antiporter
-abnormal sodium levels can affect this step
3 Na+ and 1Ca2+
how is Ca2+ sequestered into SR in cardiac cells?
SERCA pump
regulated phospholamban
phospholamban?
regulates SERCA pump in cardiac cells
is there tetanus in cardiac muscle?
no
-because
it would be fatal, because effective pumping would be inhibited
long AP in cardiac muscle results in?
long refractory period
-primarily due to activation of voltage gated L-type Ca2+ channels and slow, delayed K+ channel opening
pacemaker cells?
no resting potential
spontaneus SLOW depolarization phase
phase 4
non-pacemaker cells
true resting potential
-around -80 to -90 mV
phase 4
ion distribution in cardiac cells?
potassium - higher in cell
calcium - higher outside of cell
sodium - higher outside of cell
these are the three primary ions
potassium contribution to RMP in cardiac cells?
relatively permeable to potassium
-large effect on RMP
conductance to potassium is 100x greater than sodium conductance
sodium contribution to RMP in cardiac cells
during AP:
ECF Na+ significantly impacts the max AP upstroke of non-pacemaker cells
RMP:
changes in ECF Na+ do not significantly affect Vm
what does hyperkalemia do?
depolarizes the membrane
slow depolarizing upstroke cells?
SA and AV nodes
fast depolarizing upstroke cells?
atrial myocytes, purkinje fibers, ventricular myocytes
general phases of cardiac action potentials?
0 rapid depolarization 1 early rapid repolarization 2 plateau 3 final rapind repolarization 4 resting potential
stages of fast response?
fast upstroke 0 early, partial repolarization 1 plateau 2 final repolarization 3 resting potential 4
stages of slow response?
gradula upstroke 0
absent early repolarization (no 1)
plateau is less prolonged and flat or absent (2)
transition from plateau to final repolarization is less distinct 3
no true RP 4
RMP in fast vs slow?
more negative in fast
slow has no true RMP
threshold potential fast vs slow?
slow -40 mV
fast -70 mV
fast vs slow?
greater slope of upstroke (phase 0), AP amplitude, extent of overshoot in fast
conduction velocity slow vs. fast?
slow < fast ventricular and atrial < fast purkinje
which has faster recovery from refractory period?
fast response
sodium current?
voltage gated channels
phase 0 of fast AP
calcium current
slow - phase 0 due to calcium
-this is why its slower
fast - plateau phase
potassium current
repolarization of fast and slow cardiomyocytes
pacemaker current?
funny current
responsible for pacemaker activity
influx of primarily sodium
slow depolarization phase of SA and AV nodal cells and sometimes purkinje fibers
phase 0?
slow - if upstroke only due to I-Ca
fast - if upstroke due to I-Na and I-Ca
phase 1?
early, rapid partial repolarization
-in fast only**
minor potassium current (I-to = transient outward)
inactivation of I-Na or I-Ca
phase 2?
plateau phase
-in fast response
continued influx of Ca2+ countered by small K+ current
phase 3?
final repolarization
-depends on I-K in fast and slow cells
phase 4?
electrical diastolic phase
fast - no time-dependent current changes
slow - changes in I-K, I-Ca and I-f produce pacemaker activity in SA and AV nodal cells
voltage gated Na+ channels?
responsible for fast response depolarization
around +30mV inactivation gates close
I-Na
magnitude of sodium current impacts regenerative conduction of APs
depolarization induced by I-Na activates both I-Na in adjacent cells and other currents in the same cell (I-Ca and I-K)
L-type Ca2+ channels
majority
aka long-lived
T-type Ca2+ channels
fewer
aka transient
calcium current vs. sodium?
slower than sodium
nodal cells - slower upstroke vs A an V muscles
APs in nodal cells - slower conduction velocity because smaller I-ca depolarizes adjacent cells more slowly
calcium in slow response ?
I-ca contributes to pacemaker activity
I-ca influx contributes to upstroke
calcium current slower than sodium
calcium in fast response?
adds to depolarization during upstroke (phase 0)
Ca2+ closed at negative RMP
-activate more positive voltages
slower inactivation than sodium channels
calcium and plateau phase?
prolongs plateau via L-type Ca2+ channels
activates release of Ca2+ from SR
potassium role
delayed opening of potassium channels
responsible for repolarization (phase 3) in both fast and slow
no inactivation gates
potassium in SA and AV node
I-K decreases at negative diastolic voltage
contributes to pacemaker activity
fast response APs?
resting potential -90
threshold -70
rising phase - Na+ into cell
plateau phase - slow Ca2+ influx
falling phase - K+ out
potassium?
lots of different types
don’t need to know the specific types, but be aware that there are lots of different types of potassium channels
hypernatremia affect?
will affect maximum upstroke
potassium channel blocker?
ex/ 4-aminopyridine
notch of early repolarization phase is less prominent
what happens if potassium channels blocked?
will get a prolonged AP
atrial muscle AP
sodium, calcium, potassium
AP duration shorter in atrial vs ventricular
-greater efflux of K+ during plateau phase
APs spread directly from cell-to-cell among cardiac myocytes within each atrium
no pacemaker activity in normal atrial muscle
ventricular muscle AP
sodium, calcium, potassium
prolonged plateau phase
AP duration varies among ventricular cells
-difference in delayed rectifier K+ current
purkinje fiber AP
sodium, calcium, potassium AND I-f
from Vm, can produced very slow pacemaker depolarization that depends on I-f
purkinje fibers are unreliable pacemakers due to low rate of pacemaker depolarization (unlikely to reach threshold)
conduction velocity
depends on:
1 amplitude of AP
2 rate of change of potential during phase 0
-slope of depolarization
**how quickly it can be transmitted to adjacent cells
how does Vm impact conduction velocity?
normal AP - depolarization is very fast and inactivations d
hyperkalemia - may have slight depolarization, resulting in inactivated sodium channels
decreased amplitude and slope of depolarization
-slows conduction velocity
effect of hyperkalemia?
slows conduction velocity
depolarization of RMP can result in sodium channel inactivation
decreased amplitude and duration of APs
decreased slope of upstroke
decreased conduction velocity
if potassium high enough, fast response APs begin to look like slow-response
inschemia causes what?
decreased metabolic substrates for Na/K pump
results in hyperkalemic state
-rhythm disruption
myocardial infarction?
infarcted cells release intracellular potassium stores
what can alter conduction velocity?
accessory pathways premature excitation ischemia/hypoxia sympathetic B1 receptors parasympathetic (vagal) M2 receptors
effective refractory period
depolarized cell no longer excitable
subsequent electrical stimulus has no effect
I-Na and I-Ca are largely inactivated by depolarization (inactivation gates)
phase 0 > mid phase 3
relative refractory period
fiber not fully excitable until complete repolarization
before repolarization complete, another AP may be initiated if stimulus strong enough
I-Ca, I-Na inactivation gates open with repolarization
phase 3 - repolarization with increased I-k (efflux)
AP during relative refractory period?
later you go into the RRP, the greater the amplitude and slope of upstroke
therefore, you get faster conduction velocity later into the RRP
role of refractory period?
prevent tetanic contraction
relaxation of cardiac muscle is necessary
- tetanus would result in sustained contraction
- pumping would suck
also, limits extraneous pacemakers from triggering ectopic beats
ectopic foci
generate action potentials that don’t follow normal conduction pathways
cause of most premature contractions
possible causes of ectopic foci?
local area of ischemia
mildly toxic conditions
calcified plaques
cardiac catheterization
ventricular ectopic foci?
wide QRS (PVCs, ventricular tachycardia)
afterdepolarizations?
abnormal depolarizations during relative refractory period
early - during late phase 2 or early phase 3 (early relative refractory)
delayed - late phase 3 or early phase 4
can result in tachycardia
proarrhythmia
amplified during repolarization by increased inward current or decreased outward repolarizing current
long QT syndrome
prolonged APs
EAD
early afterdepolariation
ex/ long QT - torsades de pointes
DAD
delayed afterdepolarization
AP generation during phase 4 replarization
ex/ elevated calcium intracellularly
digoxin toxicity
premature depolarizations?
early in RRP is workse
likely slowed conduction of early impulse
reentry more likely to occur
fibrillation may develop
reentry
aka circus movements
abnormal impulse conduction may re-excite myocardial regions through which an impulse has already passed
responsible for many arrhythmias
requires unidirectional block
-effective refractory period of re-entered region must be shorter than time required for propagation around loop
global reentry?
macroreentry
between atria and ventricles
can cause SVT
ex/ wolff-parkinson-white syndrome
local reentry?
microreentry
within atria or ventricles
causes atrial or ventricular tachycardia
requirements for reentry?
1 partial depolarization of conduction pathway
2 unidirectional block**
3 timing - reentrant current must occur beyond ERP
alterations in autonomic input can promote or block reentry
3 factors promoting reentry in pathologic cardiac conditions?
lengthened conduction pathway
-dilated heart chamber
decreased conduction velocity
-purkinje system block, ischemia, elevated potassium
reduced refractory period
- response to various drugs
- ex/ epinephrine
circus movements
can result in fibrilation
EAD - external automated defibrillator
-strong high-voltage current can promote a re-set by putting all cells in refractory at once, stopping fibrillation
purpose of EAD?
puts all cells into refractory period
importance of slow-response cells?
this is how the body regulates heart rate
**important
I-f
funny current
inward current (mainly sodium) activated during hyperpolarization
via non-specific cation channels
-when Vm reaches around -50mV
slow diastolic depolarization mediated by what?
I-f - influx mainly sodium
I-ca - influx
I-k - efflux
I-ca in slow response?
activated near end of phase 4
impact of ECF calcium on slow-response AP amplitude and upstroke slope
I-k in slow response?
opposes I-f an I-ca during phase 4
opposition decreases and threshold is reached
hyperkalemia?
leads to decreased heart rate
slows phase 4 repolarization
increased AP duration in nodal cells***
delay in reaching hyperpolarization voltage required to activate I-f (sodium influx)
slow response refractory periods?
early in RRP - small amplitudes and shallow upstrokes
can lead to conduction blocks
late in RRP - progressively increasing amplitudes and upstroke slopes
recovery of full excitability is slower than in fast response APs
intrinsic rhythmicity of SA and AV nodes depends on what?
3 major time dependent and voltage gated currents
I-k
I-ca
I-f
intrinsic pacemaker of SA vs AV node?
SA node > AV node
SA fails, AV takes over to drive heart rate**
purkinje fiber currents?
4 time and voltage dependent currents I-na I-ca I-k I-f
also, slowest intrinsic pacemaker
-if AV and SA nodes fail
unreliable pacemaker
tetrodotoxin
blocks fast sodium channels
fast-response can generate slow responses
purkinje APs?
can exhibit both fast and slow response APs
