Action Potential,Resting Membrane Potential and Conduction System Flashcards
(149 cards)
1
Q
cardiac output
A
CO = HR x SV
2
Q
mean arterial pressure
A
MAP = CO x TPR
3
Q
types of cardiac cells?
A
contractile - perform mechanical work
autorhythmic - initiate action potential
4
Q
order of electrical events?
A
SA node inter-atrial pathway AV node common AV bundle (bundle of His) right and left bundle branches purkinje fibers
5
Q
functional syncytium?
A
myocytes contract as single unit
-due to gap junctions
6
Q
does cardiac function require neural input?
A
no
7
Q
location of SA node
A
right atrial wall just inferior to opening of superior vena cava
8
Q
rate at SA node?
A
60-100 bpm
9
Q
rate at bundle of His?
A
40-60 bpm
10
Q
rate at purkinje fibers?
A
20-40 bpm
11
Q
location of AV node?
A
floor of right atrium immediately behind tricuspid valve and near opening of coronary sinus
12
Q
location of bundle of His
A
superior portion of IV septum
13
Q
location of right and left bundle branches
A
IV septum
14
Q
location of purkinje fibers
A
ventricular myocardium
15
Q
function of AV node?
A
receives impulses from SA node and delays relay of impulse to bundle of His
allows time for atria to empty before ventricular contraction
16
Q
SA node?
A
normal pacemaker of heart
located at junction between superior vena cava and right atrium
17
Q
what causes difference in rates of action potentials in pacemaker cells?
A
different rates of slow depolarization phase
18
Q
SA node failure?
A
can result in bradycardia
unmasks slower, latent pacemaker of AV node
19
Q
internodal pathway?
A
SA node to AV node
-anterior, middle, and posterior pathways
20
Q
bachmann’s bundle?
A
SA node to left atrium
-conduction velocity 1 m/s
21
Q
AV node location
A
posteriorly on right side of interatrial septum
near ostium of coronary sinus
22
Q
three regions of AV junction?
A
AN region
-transitional between atrium and the node
N region
-midregion of the AV node
NH region
-nodal fibers merge with bundle of His
23
Q
AV junction?
A
this is where the signal is slowed
24
Q
AN region?
A
longer conduction path
25
N region
slower conduction velocity
26
two regions that allow for AV node delay?
AN and N regions
between atria and ventricle delay
27
why is there a delay between atrial and ventricular excitation?
allows the filling of ventricles before contraction
28
decremental conduction
signal will peeter out
increase stimulation frequency
decrease conduction velocity
limits rate of conduction to the ventricles from accelerated atrial rhythms
29
what is more detrimental: atrial or ventricular fibrillation?
ventricular
30
AV block
purkinje fibers take over (20-40 bpm)
also caused by prolonged nodal delay
31
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
32
bundle of kent?
alternate pathway around AV node in WPW syndrome
33
Bundle of His
passes down right side of IV septum
| -divides into left and right bundle branches
34
right bundle branch
branch of bundle of His
| -down right side of IV septum
35
left bundle branch
branch of bundle of His
- thicker than RBB
- perforates IV septum
36
splits of left bundle branch?
thin anterior and thick posterior division
37
purkinje fibers
arise from RBB and anterior, posterior LBB
complex network of conducting fibers spread out over subendocardial surfaces of R and L ventrices
38
arrangement of purkinje fibers?
linearly arranged sarcomeres
- typically lack T tubule system
- largest diameter cardiac cells
39
fastest conduction in the heart?
purkinje fibers
1-4 m/s
largest diameter***
40
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
41
why contract apex to base?
to "ring" out the blood
42
early contraction of IV septum?
rigid, anchor point for ventricular contraction
43
early contraction of papillary muscles?
prevent prolapse of AV valves during ventricular systole
44
depolarization fro apex to base?
efficient emptying of ventricles into aorta and pulmonary trunk at base
45
slowest conduction velocity?
AV node (small diameter)
and SA node is quite slow as well
46
fastest conduction velocity?
purkinje fibers (large diameter)
47
cardiac muscle
```
striated
mononucleated
intercalated disks
many mitochondria
t-tubules and SR
slow speed of contraction (250ms)
-skeletal muscle: 100ms
```
48
sarcomere
z line to z line
49
intercalated disks?
gap junctions in cardiac muscle (low resistance)
50
calcium source in cardiac muscle?
in ECF and SR
- before, it was mainly SR
- now, ECF is important
51
biomarker for cardiac damage?
cTnT, cTnI
| -troponin
52
CK-MB
creatine kinase isoform specific to cardiac muscle
53
electrical syncytium
all cardiac muscles contract in synchronous manner
54
intercalated disks
connect cardiac cells through mechanical junctions and electrical connections
55
desmosomes
mechanical connections
| -prevent cells from pulling apart when they contract
56
gap junctions
electrical connection (low resistance) allowing AP propagation
57
conduction of APs in cardiac muscle?
conduction system
| cell to cell
58
widening of QRS complex due to?
ventricular depolarization that spreads only cell to cell via gap junctions
ex/ PVCs, ventricular tachycardia
59
what forms functional syncytium?
ventrical and atria contract as separate units
60
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
61
contractility
increased force of contraction independent of initial fiber length, preload
modified by altering sympathetic NS input
-increase in calcium permeability
62
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
63
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
64
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+
65
how is Ca2+ sequestered into SR in cardiac cells?
SERCA pump
regulated phospholamban
66
phospholamban?
regulates SERCA pump in cardiac cells
67
is there tetanus in cardiac muscle?
no
-because
it would be fatal, because effective pumping would be inhibited
68
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
69
pacemaker cells?
no resting potential
spontaneus SLOW depolarization phase
phase 4
70
non-pacemaker cells
true resting potential
-around -80 to -90 mV
phase 4
71
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
72
potassium contribution to RMP in cardiac cells?
relatively permeable to potassium
-large effect on RMP
conductance to potassium is 100x greater than sodium conductance
73
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
74
what does hyperkalemia do?
depolarizes the membrane
75
slow depolarizing upstroke cells?
SA and AV nodes
76
fast depolarizing upstroke cells?
atrial myocytes, purkinje fibers, ventricular myocytes
77
general phases of cardiac action potentials?
```
0 rapid depolarization
1 early rapid repolarization
2 plateau
3 final rapind repolarization
4 resting potential
```
78
stages of fast response?
```
fast upstroke 0
early, partial repolarization 1
plateau 2
final repolarization 3
resting potential 4
```
79
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
80
RMP in fast vs slow?
more negative in fast
| slow has no true RMP
81
threshold potential fast vs slow?
slow -40 mV
| fast -70 mV
82
fast vs slow?
greater slope of upstroke (phase 0), AP amplitude, extent of overshoot in fast
83
conduction velocity slow vs. fast?
slow < fast ventricular and atrial < fast purkinje
84
which has faster recovery from refractory period?
fast response
85
sodium current?
voltage gated channels
phase 0 of fast AP
86
calcium current
slow - phase 0 due to calcium
-this is why its slower
fast - plateau phase
87
potassium current
repolarization of fast and slow cardiomyocytes
88
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
89
phase 0?
slow - if upstroke only due to I-Ca
| fast - if upstroke due to I-Na and I-Ca
90
phase 1?
early, rapid partial repolarization
-in fast only**
minor potassium current (I-to = transient outward)
inactivation of I-Na or I-Ca
91
phase 2?
plateau phase
-in fast response
continued influx of Ca2+ countered by small K+ current
92
phase 3?
final repolarization
| -depends on I-K in fast and slow cells
93
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
94
voltage gated Na+ channels?
responsible for fast response depolarization
around +30mV inactivation gates close
95
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)
96
L-type Ca2+ channels
majority
aka long-lived
97
T-type Ca2+ channels
fewer
aka transient
98
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
99
calcium in slow response ?
I-ca contributes to pacemaker activity
I-ca influx contributes to upstroke
calcium current slower than sodium
100
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
101
calcium and plateau phase?
prolongs plateau via L-type Ca2+ channels
activates release of Ca2+ from SR
102
potassium role
delayed opening of potassium channels
responsible for repolarization (phase 3) in both fast and slow
no inactivation gates
103
potassium in SA and AV node
I-K decreases at negative diastolic voltage
contributes to pacemaker activity
104
fast response APs?
resting potential -90
threshold -70
rising phase - Na+ into cell
plateau phase - slow Ca2+ influx
falling phase - K+ out
105
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
106
hypernatremia affect?
will affect maximum upstroke
107
potassium channel blocker?
ex/ 4-aminopyridine
notch of early repolarization phase is less prominent
108
what happens if potassium channels blocked?
will get a prolonged AP
109
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
110
ventricular muscle AP
sodium, calcium, potassium
prolonged plateau phase
AP duration varies among ventricular cells
-difference in delayed rectifier K+ current
111
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)
112
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
113
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
114
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
115
inschemia causes what?
decreased metabolic substrates for Na/K pump
results in hyperkalemic state
-rhythm disruption
116
myocardial infarction?
infarcted cells release intracellular potassium stores
117
what can alter conduction velocity?
```
accessory pathways
premature excitation
ischemia/hypoxia
sympathetic B1 receptors
parasympathetic (vagal) M2 receptors
```
118
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
119
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)
120
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
121
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
122
ectopic foci
generate action potentials that don't follow normal conduction pathways
cause of most premature contractions
123
possible causes of ectopic foci?
local area of ischemia
mildly toxic conditions
calcified plaques
cardiac catheterization
124
ventricular ectopic foci?
wide QRS (PVCs, ventricular tachycardia)
125
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
126
proarrhythmia
amplified during repolarization by increased inward current or decreased outward repolarizing current
127
long QT syndrome
prolonged APs
128
EAD
early afterdepolariation
ex/ long QT - torsades de pointes
129
DAD
delayed afterdepolarization
AP generation during phase 4 replarization
ex/ elevated calcium intracellularly
digoxin toxicity
130
premature depolarizations?
early in RRP is workse
likely slowed conduction of early impulse
reentry more likely to occur
fibrillation may develop
131
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
132
global reentry?
macroreentry
between atria and ventricles
can cause SVT
ex/ wolff-parkinson-white syndrome
133
local reentry?
microreentry
within atria or ventricles
causes atrial or ventricular tachycardia
134
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
135
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
136
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
137
purpose of EAD?
puts all cells into refractory period
138
importance of slow-response cells?
this is how the body regulates heart rate
**important
139
I-f
funny current
inward current (mainly sodium) activated during hyperpolarization
via non-specific cation channels
-when Vm reaches around -50mV
140
slow diastolic depolarization mediated by what?
I-f - influx mainly sodium
I-ca - influx
I-k - efflux
141
I-ca in slow response?
activated near end of phase 4
impact of ECF calcium on slow-response AP amplitude and upstroke slope
142
I-k in slow response?
opposes I-f an I-ca during phase 4
opposition decreases and threshold is reached
143
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)
144
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
145
intrinsic rhythmicity of SA and AV nodes depends on what?
3 major time dependent and voltage gated currents
I-k
I-ca
I-f
146
intrinsic pacemaker of SA vs AV node?
SA node > AV node
SA fails, AV takes over to drive heart rate**
147
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
148
tetrodotoxin
blocks fast sodium channels
fast-response can generate slow responses
149
purkinje APs?
can exhibit both fast and slow response APs
