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MSS - CV Exam 1 > Action Potential,Resting Membrane Potential and Conduction System > Flashcards

Action Potential,Resting Membrane Potential and Conduction System Flashcards

1
Q

cardiac output

A

CO = HR x SV

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2
Q

mean arterial pressure

A

MAP = CO x TPR

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3
Q

types of cardiac cells?

A

contractile - perform mechanical work

autorhythmic - initiate action potential

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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
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5
Q

functional syncytium?

A

myocytes contract as single unit

-due to gap junctions

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6
Q

does cardiac function require neural input?

A

no

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7
Q

location of SA node

A

right atrial wall just inferior to opening of superior vena cava

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8
Q

rate at SA node?

A

60-100 bpm

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9
Q

rate at bundle of His?

A

40-60 bpm

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10
Q

rate at purkinje fibers?

A

20-40 bpm

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11
Q

location of AV node?

A

floor of right atrium immediately behind tricuspid valve and near opening of coronary sinus

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12
Q

location of bundle of His

A

superior portion of IV septum

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13
Q

location of right and left bundle branches

A

IV septum

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14
Q

location of purkinje fibers

A

ventricular myocardium

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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

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16
Q

SA node?

A

normal pacemaker of heart

located at junction between superior vena cava and right atrium

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17
Q

what causes difference in rates of action potentials in pacemaker cells?

A

different rates of slow depolarization phase

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18
Q

SA node failure?

A

can result in bradycardia

unmasks slower, latent pacemaker of AV node

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19
Q

internodal pathway?

A

SA node to AV node

-anterior, middle, and posterior pathways

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20
Q

bachmann’s bundle?

A

SA node to left atrium

-conduction velocity 1 m/s

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21
Q

AV node location

A

posteriorly on right side of interatrial septum

near ostium of coronary sinus

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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

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23
Q

AV junction?

A

this is where the signal is slowed

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24
Q

AN region?

A

longer conduction path

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25
Q

N region

A

slower conduction velocity

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26
Q

two regions that allow for AV node delay?

A

AN and N regions

between atria and ventricle delay

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27
Q

why is there a delay between atrial and ventricular excitation?

A

allows the filling of ventricles before contraction

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28
Q

decremental conduction

A

signal will peeter out

increase stimulation frequency
decrease conduction velocity

limits rate of conduction to the ventricles from accelerated atrial rhythms

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29
Q

what is more detrimental: atrial or ventricular fibrillation?

A

ventricular

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30
Q

AV block

A

purkinje fibers take over (20-40 bpm)

also caused by prolonged nodal delay

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31
Q

wolf-parkinson-white syndrome

A

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

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32
Q

bundle of kent?

A

alternate pathway around AV node in WPW syndrome

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33
Q

Bundle of His

A

passes down right side of IV septum

-divides into left and right bundle branches

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34
Q

right bundle branch

A

branch of bundle of His

-down right side of IV septum

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35
Q

left bundle branch

A

branch of bundle of His

  • thicker than RBB
  • perforates IV septum
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36
Q

splits of left bundle branch?

A

thin anterior and thick posterior division

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37
Q

purkinje fibers

A

arise from RBB and anterior, posterior LBB

complex network of conducting fibers spread out over subendocardial surfaces of R and L ventrices

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38
Q

arrangement of purkinje fibers?

A

linearly arranged sarcomeres

  • typically lack T tubule system
  • largest diameter cardiac cells
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39
Q

fastest conduction in the heart?

A

purkinje fibers
1-4 m/s

largest diameter***

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40
Q

ventricular muscle depolarization?

A

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

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41
Q

why contract apex to base?

A

to “ring” out the blood

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42
Q

early contraction of IV septum?

A

rigid, anchor point for ventricular contraction

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43
Q

early contraction of papillary muscles?

A

prevent prolapse of AV valves during ventricular systole

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44
Q

depolarization fro apex to base?

A

efficient emptying of ventricles into aorta and pulmonary trunk at base

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45
Q

slowest conduction velocity?

A

AV node (small diameter)

and SA node is quite slow as well

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46
Q

fastest conduction velocity?

A

purkinje fibers (large diameter)

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47
Q

cardiac muscle

A 
striated
mononucleated
intercalated disks
many mitochondria
t-tubules and SR
slow speed of contraction (250ms)
-skeletal muscle: 100ms
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48
Q

sarcomere

A

z line to z line

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49
Q

intercalated disks?

A

gap junctions in cardiac muscle (low resistance)

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50
Q

calcium source in cardiac muscle?

A

in ECF and SR

  • before, it was mainly SR
  • now, ECF is important
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51
Q

biomarker for cardiac damage?

A

cTnT, cTnI

-troponin

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52
Q

CK-MB

A

creatine kinase isoform specific to cardiac muscle

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53
Q

electrical syncytium

A

all cardiac muscles contract in synchronous manner

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54
Q

intercalated disks

A

connect cardiac cells through mechanical junctions and electrical connections

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55
Q

desmosomes

A

mechanical connections

-prevent cells from pulling apart when they contract

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56
Q

gap junctions

A

electrical connection (low resistance) allowing AP propagation

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57
Q

conduction of APs in cardiac muscle?

A

conduction system

cell to cell

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58
Q

widening of QRS complex due to?

A

ventricular depolarization that spreads only cell to cell via gap junctions

ex/ PVCs, ventricular tachycardia

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59
Q

what forms functional syncytium?

A

ventrical and atria contract as separate units

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60
Q

all or none law of heart

A

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
Q

contractility

A

increased force of contraction independent of initial fiber length, preload

modified by altering sympathetic NS input
-increase in calcium permeability

62
Q

extracellular calcium and cardiac contraction?

A

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
Q

relaxation of cardiac contraction?

A

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
Q

two ways to remove Ca2+ to ECF of cardiac cells?

A

sarcolemma Na+/Ca2+ antiporter
-abnormal sodium levels can affect this step

3 Na+ and 1Ca2+

65
Q

how is Ca2+ sequestered into SR in cardiac cells?

A

SERCA pump

regulated phospholamban

66
Q

phospholamban?

A

regulates SERCA pump in cardiac cells

67
Q

is there tetanus in cardiac muscle?

A

no
-because

it would be fatal, because effective pumping would be inhibited

68
Q

long AP in cardiac muscle results in?

A

long refractory period

-primarily due to activation of voltage gated L-type Ca2+ channels and slow, delayed K+ channel opening

69
Q

pacemaker cells?

A

no resting potential

spontaneus SLOW depolarization phase

phase 4

70
Q

non-pacemaker cells

A

true resting potential
-around -80 to -90 mV

phase 4

71
Q

ion distribution in cardiac cells?

A

potassium - higher in cell
calcium - higher outside of cell
sodium - higher outside of cell

these are the three primary ions

72
Q

potassium contribution to RMP in cardiac cells?

A

relatively permeable to potassium
-large effect on RMP

conductance to potassium is 100x greater than sodium conductance

73
Q

sodium contribution to RMP in cardiac cells

A

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
Q

what does hyperkalemia do?

A

depolarizes the membrane

75
Q

slow depolarizing upstroke cells?

A

SA and AV nodes

76
Q

fast depolarizing upstroke cells?

A

atrial myocytes, purkinje fibers, ventricular myocytes

77
Q

general phases of cardiac action potentials?

A 
0 rapid depolarization
1 early rapid repolarization
2 plateau
3 final rapind repolarization
4 resting potential
78
Q

stages of fast response?

A 
fast upstroke 0 
early, partial repolarization 1
plateau 2
final repolarization 3
resting potential 4
79
Q

stages of slow response?

A

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
Q

RMP in fast vs slow?

A

more negative in fast

slow has no true RMP

81
Q

threshold potential fast vs slow?

A

slow -40 mV

fast -70 mV

82
Q

fast vs slow?

A

greater slope of upstroke (phase 0), AP amplitude, extent of overshoot in fast

83
Q

conduction velocity slow vs. fast?

A

slow < fast ventricular and atrial < fast purkinje

84
Q

which has faster recovery from refractory period?

A

fast response

85
Q

sodium current?

A

voltage gated channels

phase 0 of fast AP

86
Q

calcium current

A

slow - phase 0 due to calcium
-this is why its slower

fast - plateau phase

87
Q

potassium current

A

repolarization of fast and slow cardiomyocytes

88
Q

pacemaker current?

A

funny current
responsible for pacemaker activity

influx of primarily sodium

slow depolarization phase of SA and AV nodal cells and sometimes purkinje fibers

89
Q

phase 0?

A

slow - if upstroke only due to I-Ca

fast - if upstroke due to I-Na and I-Ca

90
Q

phase 1?

A

early, rapid partial repolarization
-in fast only**

minor potassium current (I-to = transient outward)

inactivation of I-Na or I-Ca

91
Q

phase 2?

A

plateau phase
-in fast response

continued influx of Ca2+ countered by small K+ current

92
Q

phase 3?

A

final repolarization

-depends on I-K in fast and slow cells

93
Q

phase 4?

A

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
Q

voltage gated Na+ channels?

A

responsible for fast response depolarization

around +30mV inactivation gates close

95
Q

I-Na

A

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
Q

L-type Ca2+ channels

A

majority

aka long-lived

97
Q

T-type Ca2+ channels

A

fewer

aka transient

98
Q

calcium current vs. sodium?

A

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
Q

calcium in slow response ?

A

I-ca contributes to pacemaker activity
I-ca influx contributes to upstroke

calcium current slower than sodium

100
Q

calcium in fast response?

A

adds to depolarization during upstroke (phase 0)
Ca2+ closed at negative RMP
-activate more positive voltages

slower inactivation than sodium channels

101
Q

calcium and plateau phase?

A

prolongs plateau via L-type Ca2+ channels

activates release of Ca2+ from SR

102
Q

potassium role

A

delayed opening of potassium channels

responsible for repolarization (phase 3) in both fast and slow

no inactivation gates

103
Q

potassium in SA and AV node

A

I-K decreases at negative diastolic voltage

contributes to pacemaker activity

104
Q

fast response APs?

A

resting potential -90
threshold -70

rising phase - Na+ into cell
plateau phase - slow Ca2+ influx
falling phase - K+ out

105
Q

potassium?

A

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
Q

hypernatremia affect?

A

will affect maximum upstroke

107
Q

potassium channel blocker?

A

ex/ 4-aminopyridine

notch of early repolarization phase is less prominent

108
Q

what happens if potassium channels blocked?

A

will get a prolonged AP

109
Q

atrial muscle AP

A

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
Q

ventricular muscle AP

A

sodium, calcium, potassium
prolonged plateau phase

AP duration varies among ventricular cells
-difference in delayed rectifier K+ current

111
Q

purkinje fiber AP

A

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
Q

conduction velocity

A

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
Q

how does Vm impact conduction velocity?

A

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
Q

effect of hyperkalemia?

A

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
Q

inschemia causes what?

A

decreased metabolic substrates for Na/K pump

results in hyperkalemic state
-rhythm disruption

116
Q

myocardial infarction?

A

infarcted cells release intracellular potassium stores

117
Q

what can alter conduction velocity?

A 
accessory pathways
premature excitation
ischemia/hypoxia
sympathetic B1 receptors
parasympathetic (vagal) M2 receptors
118
Q

effective refractory period

A

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
Q

relative refractory period

A

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
Q

AP during relative refractory period?

A

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
Q

role of refractory period?

A

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
Q

ectopic foci

A

generate action potentials that don’t follow normal conduction pathways

cause of most premature contractions

123
Q

possible causes of ectopic foci?

A

local area of ischemia
mildly toxic conditions
calcified plaques
cardiac catheterization

124
Q

ventricular ectopic foci?

A

wide QRS (PVCs, ventricular tachycardia)

125
Q

afterdepolarizations?

A

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
Q

proarrhythmia

A

amplified during repolarization by increased inward current or decreased outward repolarizing current

127
Q

long QT syndrome

A

prolonged APs

128
Q

EAD

A

early afterdepolariation

ex/ long QT - torsades de pointes

129
Q

DAD

A

delayed afterdepolarization

AP generation during phase 4 replarization

ex/ elevated calcium intracellularly
digoxin toxicity

130
Q

premature depolarizations?

A

early in RRP is workse

likely slowed conduction of early impulse

reentry more likely to occur

fibrillation may develop

131
Q

reentry

A

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
Q

global reentry?

A

macroreentry

between atria and ventricles

can cause SVT
ex/ wolff-parkinson-white syndrome

133
Q

local reentry?

A

microreentry

within atria or ventricles

causes atrial or ventricular tachycardia

134
Q

requirements for reentry?

A

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
Q

3 factors promoting reentry in pathologic cardiac conditions?

A

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
Q

circus movements

A

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
Q

purpose of EAD?

A

puts all cells into refractory period

138
Q

importance of slow-response cells?

A

this is how the body regulates heart rate

**important

139
Q

I-f

A

funny current

inward current (mainly sodium) activated during hyperpolarization

via non-specific cation channels
-when Vm reaches around -50mV

140
Q

slow diastolic depolarization mediated by what?

A

I-f - influx mainly sodium
I-ca - influx
I-k - efflux

141
Q

I-ca in slow response?

A

activated near end of phase 4

impact of ECF calcium on slow-response AP amplitude and upstroke slope

142
Q

I-k in slow response?

A

opposes I-f an I-ca during phase 4

opposition decreases and threshold is reached

143
Q

hyperkalemia?

A

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
Q

slow response refractory periods?

A

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
Q

intrinsic rhythmicity of SA and AV nodes depends on what?

A

3 major time dependent and voltage gated currents
I-k
I-ca
I-f

146
Q

intrinsic pacemaker of SA vs AV node?

A

SA node > AV node

SA fails, AV takes over to drive heart rate**

147
Q

purkinje fiber currents?

A 
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
Q

tetrodotoxin

A

blocks fast sodium channels

fast-response can generate slow responses

149
Q

purkinje APs?

A

can exhibit both fast and slow response APs

MSS - CV Exam 1 (14 decks)

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