Cardiac Cellular Electrophysiology Flashcards
what is the specialized conduction system
histologic components of the heart that are responsible for conducting electrical impulses throughout the cardiac muscle for rhythmic contraction
what is the path of current conduction in the heart
SA node
internodal tracts
AV node
penetrating bundle of His
L and R bundle branches
purkinje fibers
what makes up the nodal tissue
sinoatrial and atrioventricular nodes
characteristics of nodal action potentials
SLOW - spontaneously generated
depolarization is based on inward CALCIUM current
sinoatrial node
fast nodal tissue
generates APs to set the rhythm of contraction (pacemaker)
atrioventricular node
slow nodal tissue
(does NOT pacemake unless SA node fails)
conducts signal across from atrium to ventricle
what makes up the non-nodal tissue
myocytes (atrial and ventricular)
bundle branches
Purkinje fibers
characteristics of non-nodal action potentials
FAST - cells are waiting to be stimulated by the AP generated by SA node
propagates AP via gap junctions for rapid spread of the signal
depolarization is based on inward SODIUM current
excitation contraction coupling
depolarization of the cell leads to opening of Ca channels –> Ca influx –> release of Ca from SR stores –> high intracellular Ca –> binds troponin C on actin –> contraction
are cell membranes polarized or unpolarized
polarized - membrane potential changes during the cardiac cycle
caused by varied conductance of ions through ion channels
conductance
movement of charge across membrane that is dependent on ion channels opening and closing
high conductance = high ion movement across membrane
what does ion conductance depend on
VOLTAGE
also:
- ligand binding
- NE/epi concentration
- ion concentration (gradients)
phases of the non-nodal action potential
phase 0: depolarization
phase 1: early/rapid repolarization
phase 2: plateau
phase 3: repolarization
phase 4: resting membrane potential
resting membrane potential (RMP)
negative membrane potential maintained during phase 4 (diastole)
RMP of nodal cells
-50 to -60
slow drift - MP slowly increases to threshold due to funny currents
funny currents
I(f)
special Na and K channels in nodal cells open in response to the hyperpolarization that occurs in phase 3 of the cardiac cycle –> causes slow influx of positive ions –> membrane potential slowly increases to reach threshold –> once threshold is reached an action potential is generated
allows nodal cells to be able to spontaneously generate action potentials without a stimuli
RMP of non-nodal cells
-80 to -90
does NOT slow drift - has a stable resting membrane potential
how do non-nodal cells maintain a negative resting membrane potential
leaky K channels
increases extracellular K –> triggers Na/K pump –> 2K in, 3Na out –> RMP remains negative
how do non-nodal cells depolarize
NOT SPONTANEOUS
AP generated by nodal cells –> spreads to non-nodal cells –> opens Na channels –> depolarizes cell –> AP spreads through gap junctions to adjacent cells
what ion drives nodal cell depolarization
calcium
what ion drives non-nodal cell depolarization
sodium
threshold potential
Na channels: -60 to -70 mV
lowest membrane potential that triggers enough voltage Na or Ca channels to opens
yields an “all or nothing” response that generates an action potential
absolute refractory period (ARP)
period following depolarization of a cell during which NO subsequent stimulus arriving at the cell can cause another depolarization
protective mechanism that prevents multiple, compounded APs
occurs during phase 1 and 2
effective refractory period (ERP)
short period after ARP during which a STRONG subsequent stimulus arriving at the cell can cause another depolarization
occurs at the beginning of phase 3
relative refractory period (RRP)
period after ERP during which a moderate subsequent stimulus arriving at the cell can cause another depolarization
occurs the remainder of phase 3
**vulnerable period - stimulus during peak of T wave can induce ventricular fibrillation
class III antiarrhythmics
K channel blockers
prolong refractory period to reduce vulnerability to premature depolarization
ex. sotalol and amiodarone
are sodium channels/current located in nodal or non-nodal cells
non-nodal cells only
function of sodium current
rapid depolarization (phase 0) and spread of conduction in myocytes and Purkinje fibers
mechanism of sodium channels
FAST - opens in response to AP from adjacent cell and closes quickly after
opens at -60 to -70
if RMP is decreased (less negative), how is Na conductance affected
decreases Na conductance
Na channels are less excitable –> slows phase 0 down
if RMP is increased (more negative), how is Na conductance affected
increases Na conductance
Na channels are more excitable –> speeds up phase 0
what class of drugs targets Na channels
class I antiarrhythmics (IA, B, C)
ex. lidocaine - blocks Na channels to decreased excitability of cells and slow conduction
are calcium channels/current located in nodal or non-nodal cells
both
nodal: slows depolarization (phase 0) for regular rhythm
non-nodal: allows Ca influx for contraction and plateau (phase 2)
types of Ca channels/currents
L type and T type
T-type calcium channels
present in nodal cells only
transient/tiny burst; opens at -50 to -60 (more negative MP)
initiates depolarization (phase 0) in nodal cells
L-type calcium channels
present in nodal and non-nodal cells
longer lasting/later; opens at -30 to -40 (more positive MP)
nodal: minor effect; propagates depolarization (phase 0)
non-nodal: important for Ca influx for contraction and plateau
what class of drugs targets Ca channels
catecholamines - increases HR/conduction/contractility
class IV antiarrhythmics - decreases HR/conduction/contractility by blocking L-type Ca channels
class II antiarrhythmics (beta blockers) - decreases HR/conduction/contractility by reducing phosphorylation of Ca channels to indirectly block L-type channels
function of potassium channels/current
keep or return cells to resting membrane potential
types of K channels/currents
I(KI): leaky K channels that maintain RMP in myocytes
I(KR) and I(KS): rapid (R) and slow (S) channels that allow repolarization (phase 3); triggered to open by depolarization
what class of drugs target potassium channels
catecholamines: increase I(KR) and I(KS) to increase rate of repolarization
ADP: (indicates energy depletion); accelerates repolarization to shorten overall AP duration to conserve energy –> reduces contractility
hyperkalemia: reduces leaking in phase 4 –> depolarizes membrane –> increases k conductance to accelerate repolarization
sympathetic effects on nodes
B adrenergic receptors
stimulates I(f), I(CaT), I(CaL), I(K) to increase HR and conduction speed
parasympathetic effects on nodes
acetylcholine
inhibits SNS effects and activates I(Kach) –> hyper polarizes –> prolongs time for funny current to bring membrane potential to threshold –> decreases HR and conduction speed
