Flashcards in Cardiac Electrical Activity (Part 1) Deck (25)
The cardiac myocytes exhibit a range of electrical properties such as..
Fast Response cells (fast APs) are?
Fast parts of the specialised conduction system
What are the steps of Fast response, and what is the resting and threshold potentials
Phase 0: Depolarisation
Phase 1 : small repolarisation
Phase 2: Plateau
Phase 3: Repolarisation
Phase 4: Resting
Resting Potential = ~-90mV
Threshold Potential = ~-70mV in ventricles (-30 to -60 in atria)
Rapid Depolarisation (Upstroke)
-Very fast increase in Na+ permeability, fast inward sodium current
-Electrical AND conc gradients both inwards
-Membrane approaches Nernst potential for sodium
Early repolarisation (to near 0mV)
-transient outward K+ current
- Na+ channels inactive hence cell is refractory, inward and outwards currents nearly balanced
1) Slow inward calcium current: L-type Ca channels & release of Ca from SR (ca dependent ca release)
2) Outward K+ current
Both currents decline across the plateau.
Outward K+ current
1) iK switched on after a delay (time-dependent)
2) Reactivation of iK1 as membrane potential drops (voltage-dependent)
** other smaller channels
3) iK,ATP (a decrease in intracellular ATP activates iK,ATP)
4) iK,Ach (incr Ach activates)
iK1 : High potassium conductance defines and sets resting potential
What's always going on in the background and setting the potenital?
1) Calcium pump - outward current
2) Na/Ca exchanger - ongoing 3Na in for 1Ca out, so electrogenic (inward/depolarising)
3) Na/K ATPas - 3Na out for 2K in, electrogenic (outward, repolarising)
Draw the fast response with its channels..
Cells with a slow response. Why is Na+ not responsible?
Upstroke is not as rapid, and is due to Calcium ions current reaching TP. Their influx is not as intense and depolarisation not as rapid.
Slow response cells have a higher Resting potential. At this RP (~-55mV), the sodium channels have already been activated, opened and then closed.
Slow Response Cells are found in?
Some diseased cells
May be pacemaker or non-pacemaker type
What are slow response RP and phases? Draw the slow response AP
Phases: 0, (2), 3, 4
Phase 0: slow upstroke, slow inward Ca current
Absolute (effective) Refractory Period
Time when membrane cannot be re-excited. This is essential for cardiac function to avoid tetanus, in order for contraction/relaxation function.
Relative refractory Period
Need a larger then normal stimulus to get a propagated AP (slow propagation)
Get propagated AP from weaker then normal stimulus (slow propagation)
Full Recovery Time
May extend beyond return to RP (time dependence)
As HR increases, most of this change is due to decreasing the diastolic phase. BUT some is from the active phase. Therefore as HR increases the AP shortens.
What does it mean that cardiac cells are NOT neurogenic
-They do NOT contract in response to a neural signal
-They are MYOGENIC, signal begins within the heart itself
-Electrical activation spreads through the myocardium from cell to cell, as each cell is electrically coupled to several neighbours.
As one depolarizes, current spreads to those cells
How does the electrical signal spread between cardiac myocytes.
Cells branch and connect to neighbours via intercalated disks, the sites of electrical and mechanical coupling.
These cells are in a laminar structure, and the myocardium is NOT a uniformly continuous syncitium.
Automaticity? Where is this found?
Ability of cells to initiate an electrical impulse through their own pacemaker activity or diastolic depolarisation.
Some cells around AV node
How does automaticity occur?
A combination of decreasing outward currents and increasing inward currents
OUTWARD currents decrease: iK
INWARD currents increase: if (funny current, iCa (slow inward calcium current)
Mechanisms for altering the intrinsic rate of pacemaker discharge
-alter rate of depolarization (slope)
-alter threshold potential
-alter maximum diastolic potential
How is the heart rate regulated?
By the Autonomic Nervous System
1) PNS slows HR: by release of Ach at vagal endings in the heart. @ SA node Ach increases K+ permeability of cells (iK,Ach)
-> hyperpolarized, decrreased pacemaker slope
PNS also slows conduction through AV node. Very strong vagal stimulation can stop the SA/AV node
2) SNS increases HR: By release of noradrenaline at SA node
- increase pacemaker depolarisation slope