Cardiac Cellular Electrophysiology Flashcards by Jessica Hodson

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

what makes up the nodal tissue

sinoatrial and atrioventricular nodes

How well did you know this?

Not at all

Perfectly

characteristics of nodal action potentials

SLOW - spontaneously generated

depolarization is based on inward CALCIUM current

How well did you know this?

Not at all

Perfectly

sinoatrial node

fast nodal tissue
generates APs to set the rhythm of contraction (pacemaker)

How well did you know this?

Not at all

Perfectly

atrioventricular node

slow nodal tissue
(does NOT pacemake unless SA node fails)

conducts signal across from atrium to ventricle

How well did you know this?

Not at all

Perfectly

what makes up the non-nodal tissue

myocytes (atrial and ventricular)
bundle branches
Purkinje fibers

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

are cell membranes polarized or unpolarized

polarized - membrane potential changes during the cardiac cycle

caused by varied conductance of ions through ion channels

How well did you know this?

Not at all

Perfectly

conductance

movement of charge across membrane that is dependent on ion channels opening and closing

high conductance = high ion movement across membrane

How well did you know this?

Not at all

Perfectly

what does ion conductance depend on

VOLTAGE

also:
- ligand binding
- NE/epi concentration
- ion concentration (gradients)

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

resting membrane potential (RMP)

negative membrane potential maintained during phase 4 (diastole)

How well did you know this?

Not at all

Perfectly

RMP of nodal cells

-50 to -60

slow drift - MP slowly increases to threshold due to funny currents

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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