3-Electrophysiology Heart Flashcards
major cell types
- cardiomyocytes- atrial and ventricular
- fibroblasts
- endothelial cells
- pericytes
- smooth muscle cells
- immune cells- myeloid and lymphoid
- adipocytes
- mesothelial cells
- neuronal cells
don’t know all these just cardiomyocytes
cardiac myocytes
characteristics
- well organized, myofibrils syncytium
- connect b/t cells for communication/electrial activity
- intercalated discs, gap junctions
- numerous
- lots of actin and myosin filaments
- NO intrinsic pacemaker activity
- fast response action potentials
optimize contraction
nodal cells
characteristics
- set and coord electrical activity of heart
- pacemaker cells
- intrinsic rhythm generator- rhythmicity + automaticity
- few in number
- cannot detect on ECG
- slow resp action potential
optimize rhythm of heart
functional syncytium
- multinucleate
- have intercalated discs to physically connect indiv fibers + gap junctions for electrochem coupling
- coord spread of electrical signal for muscle contraction- all or nothing AP no matter origin of impluse
membrane potential
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)
resting membrane potential
determined by potassium perm, maintained by Na/K ATPase pump
-hyperkalemia = inc RMP bc makes mem potential less negative, dec magnitude of depolarizing impulse
Na/K ATPase inhibitors
- ouabain
- digoxin
cause RMP be less neg, Na stays in cell longer
cardiac myocyte AP phases
- phase 0 = upstroke, depolar
- phase 1 = initial incomplete repolar
- phase 2 = plateau
- phase 3 = complete repolar
- phase 5 = resting membrane potential RMP
phase 0
- local depolar of mem = open voltage dep Na channels
-is transient so fast/rapid upstroke - threshold potential opens voltage dep Ca channels but no effect on mem until phase 2
voltage dep sodium channel structure
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
absolute refractory period
channel rapidly inactivated, influx of Na stops
-no resp to another impulse,
aka effective period
relative refractory period
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
supranormal refractory period
smaller than normal impulse can gen an AP
-almost all Na channels closed and mem potential back to resting
phase 1
- rapid inact of voltage dep Na channel
- 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)
phase 2
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
phase 3
complete repolar of cell so
-Ca influx reduced
-additional K channels open, as soon as Ca channels close
-membrane pot returns to -85
phase 4
resting membrane potential
-some late Na/Ca exchanger activity
-maintained by K channels and Na/K ATPase
autonomic effects
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)
genetic cardiac ion channelopathies
- long QT syndrome- mutations in K and Na channels, accessory proteins, AP is longer than normal @ ventricular myocytes
- short QT syndrome- mut in K channel (gain of function)
- brugada sydrome- mut in Na channel
nodal cell AP phases
- phase 0 - upstroke, depolar
- phase 3 - repolar
- phase 4 - pacemaker potential
never resting
nodal cell phase 0
- threshold pot met = Ca channels open
- 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
nodal cell phase 3
repolar due to K channels
-K efflux
nodal cell phase 4
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
chronotropy
force/rate of impulse generation from SA node
HCN channel role
important for automaticity
if blocked by ivabradine then see reduced automaticity/dec rate of impulse gen from cells
sympathetics on nodal cell AP
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
parasympathetics on nodal cell AP
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
K channel gain of function mutation
nodal cell AP
will reduce impulse generation
-sustained hyperpolarization of pacemaker cells
-dec HR
determinants conduction velocity
- cell size- cardiomyocytes largest so easier to travel thru/less resistance, nodal small
- strength of impulse- magnitude
- connections b/t cells- gap junctions
sympathetics inc velocity, parasymp dec
will vary thru tissues
gap junctions regional differences
- not many in nodal cells
- oriented in intercalated disks at fiber ends in muscle cells for longitudinal progagation
- regionally different connexin proteins
gap junction modulation
- phosphorylation
- pH
- other??
sinus node impulse initiation
SA node
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
SA node of fit people
will have a slower pacemaker rate bc inc vagal tone and parasympathetics activated
sequence of depolarization
- SA node
- atria
- AV node
- bundle of His
- bundle branches- L and R
- purkinje fibers @endocardial surface
- 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
ectopic focus
if signal generated from wrong spot will spread to receptive tissue aka non-refractory tissue
why need AP different lengths
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
what conduction blocks do
interrupt normal seq, change how impulse travels thru tissue
-can block AV or bundle branches L or R
advantage of diff conduction velocities
coordinate depolarization and contractions to optimize heart function
tissue/cells with highest conduction velocity
purkingje fibers
