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Block 3 Found Sci > 3-Electrophysiology Heart > Flashcards

3-Electrophysiology Heart Flashcards

1
Q

major cell types

A
  1. cardiomyocytes- atrial and ventricular
  2. fibroblasts
  3. endothelial cells
  4. pericytes
  5. smooth muscle cells
  6. immune cells- myeloid and lymphoid
  7. adipocytes
  8. mesothelial cells
  9. neuronal cells

don’t know all these just cardiomyocytes

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2
Q

cardiac myocytes

characteristics

A
  1. well organized, myofibrils syncytium
  2. connect b/t cells for communication/electrial activity
  3. intercalated discs, gap junctions
  4. numerous
  5. lots of actin and myosin filaments
  6. NO intrinsic pacemaker activity
  7. fast response action potentials

optimize contraction

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3
Q

nodal cells

characteristics

A
  1. set and coord electrical activity of heart
  2. pacemaker cells
  3. intrinsic rhythm generator- rhythmicity + automaticity
  4. few in number
  5. cannot detect on ECG
  6. slow resp action potential

optimize rhythm of heart

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4
Q

functional syncytium

A
  1. multinucleate
  2. have intercalated discs to physically connect indiv fibers + gap junctions for electrochem coupling
  3. coord spread of electrical signal for muscle contraction- all or nothing AP no matter origin of impluse
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5
Q

membrane potential

A

determined by perm to ions and concentration gradient of ions across mem
-expressed as intracellular potential relative to extracellular
-requires threshold potential for voltage dep ionic channels open

depolarize (less neg) or hyperpolarize (more neg)

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6
Q

resting membrane potential

A

determined by potassium perm, maintained by Na/K ATPase pump
-hyperkalemia = inc RMP bc makes mem potential less negative, dec magnitude of depolarizing impulse

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7
Q

Na/K ATPase inhibitors

A
  1. ouabain
  2. digoxin

cause RMP be less neg, Na stays in cell longer

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8
Q

cardiac myocyte AP phases

A
  1. phase 0 = upstroke, depolar
  2. phase 1 = initial incomplete repolar
  3. phase 2 = plateau
  4. phase 3 = complete repolar
  5. phase 5 = resting membrane potential RMP
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9
Q

phase 0

A
  1. local depolar of mem = open voltage dep Na channels
    -is transient so fast/rapid upstroke
  2. threshold potential opens voltage dep Ca channels but no effect on mem until phase 2
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10
Q

voltage dep sodium channel structure

A

alpha subunit
-segment 4 = voltage sensor, will change conform to open channel
-between seg 3/4 = inactivation gate
-between seg 5/6 = selectivity/pore region, activation gate

also has 2 beta subunits

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11
Q

absolute refractory period

A

channel rapidly inactivated, influx of Na stops
-no resp to another impulse,
aka effective period

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12
Q

relative refractory period

A

channel resets with time and voltage changes in phase 3
-recovers from inactivation
-abnormally large impulse can elicit abnormal AP bc not all Na channels are recovered yet

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13
Q

supranormal refractory period

A

smaller than normal impulse can gen an AP
-almost all Na channels closed and mem potential back to resting

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14
Q

phase 1

A
  1. rapid inact of voltage dep Na channel
  2. depolar causes open voltage dep K channels to repolarize with some help from Na/Ca exchanger

transient and incomplete repolar bc efflux of cations (K)

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15
Q

phase 2

A

mem pot steady for extended period of time to extend AP for coord of electric/mechanical events
-aka blood to be ejected/efficient contraction

requires concurrent move opposite to Ca
-sympathetics can effect

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16
Q

phase 3

A

complete repolar of cell so
-Ca influx reduced
-additional K channels open, as soon as Ca channels close
-membrane pot returns to -85

17
Q

phase 4

A

resting membrane potential
-some late Na/Ca exchanger activity
-maintained by K channels and Na/K ATPase

18
Q

autonomic effects

A

norepinephrine binds B1 adrenergic receptor
-Ca channels open enhanced
-Ca cycling from SR enhanced
-speed of cross bridge cycle inc

net effect = inc force contraction (pos inotropy) + greater conduction velocity (pos dromotropy)

19
Q

genetic cardiac ion channelopathies

A
  1. long QT syndrome- mutations in K and Na channels, accessory proteins, AP is longer than normal @ ventricular myocytes
  2. short QT syndrome- mut in K channel (gain of function)
  3. brugada sydrome- mut in Na channel
20
Q

nodal cell AP phases

A
  1. phase 0 - upstroke, depolar
  2. phase 3 - repolar
  3. phase 4 - pacemaker potential

never resting

21
Q

nodal cell phase 0

A
  1. threshold pot met = Ca channels open
  2. slow depolar bc no Na channels and lower magnitude than myocytes

will still reach voltage similar to myocytes bc K channels

-Ca influx

higher magnitude = faster conduction V/V

22
Q

nodal cell phase 3

A

repolar due to K channels
-K efflux

23
Q

nodal cell phase 4

A

pacemaker potential driven slowly by
-progressive dec in K efflux
-progressive inc in Na influx thru HCN channels

also called diastolic depolarization or funny current

hyperpolarization-activated cyclic nucleotide gated cation channel

24
Q

chronotropy

A

force/rate of impulse generation from SA node

25
Q

HCN channel role

A

important for automaticity

if blocked by ivabradine then see reduced automaticity/dec rate of impulse gen from cells

26
Q

sympathetics on nodal cell AP

A

dec time required for threshold to be reached so easier AP/inc automaticity
-threshold is less negative
-pos chronotropic (quicker impulse gen and HR inc)

bc norepinephrine binds B1 adrenergic to inc cAMP and PKA = inc open Ca channels and HCN channels

27
Q

parasympathetics on nodal cell AP

A

inc time required to reach threshold so NEG chronotropy, dec automaticity

Ach binds M2 muscarinic to dec cAMP and delay Ca channel opening, keeps K efflux buffering the funny current so hyperpolarized longer
-max diastolic potential more neg and threshold potential less neg

28
Q

K channel gain of function mutation

nodal cell AP

A

will reduce impulse generation
-sustained hyperpolarization of pacemaker cells
-dec HR

29
Q

determinants conduction velocity

A
  1. cell size- cardiomyocytes largest so easier to travel thru/less resistance, nodal small
  2. strength of impulse- magnitude
  3. connections b/t cells- gap junctions

sympathetics inc velocity, parasymp dec

will vary thru tissues

30
Q

gap junctions regional differences

A
  • not many in nodal cells
  • oriented in intercalated disks at fiber ends in muscle cells for longitudinal progagation
  • regionally different connexin proteins
31
Q

gap junction modulation

A
  1. phosphorylation
  2. pH
  3. other??
32
Q

sinus node impulse initiation

SA node

A

highest pacemaker rate so depolar reaches threshold fastest
-impulse will spread to adjacent muscle cells
-rate is so high that it suppresses other latent lower rate pacemakers but still used as back up

33
Q

SA node of fit people

A

will have a slower pacemaker rate bc inc vagal tone and parasympathetics activated

34
Q

sequence of depolarization

A
  1. SA node
  2. atria
  3. AV node
  4. bundle of His
  5. bundle branches- L and R
  6. purkinje fibers @endocardial surface
  7. ventricles- septum > apex > ventricular free walls

direction down and to left in same order always but AP will change shape

AV node + His = Av junction

35
Q

ectopic focus

A

if signal generated from wrong spot will spread to receptive tissue aka non-refractory tissue

36
Q

why need AP different lengths

A

to ensure readiness of myocytes so the last place to repolarize is first to depolar
-safety mechanism

lengths are different bc diff # of ion channels

37
Q

what conduction blocks do

A

interrupt normal seq, change how impulse travels thru tissue
-can block AV or bundle branches L or R

38
Q

advantage of diff conduction velocities

A

coordinate depolarization and contractions to optimize heart function

39
Q

tissue/cells with highest conduction velocity

A

purkingje fibers

Block 3 Found Sci (60 decks)

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