1) myogenic- electrical activity originates with in the heart itself

2) electrical syncitium- the entire heart behaves as if it were one cell

3) Electrically coupled by low resistance gap junctions located at the intercalated disc at the ends of the cells and the nexus points on the sides.  Gap junctions are formed by conexins

4) APD are much longer in cardiac muscle (up to 400ms)

1) SA node: located in the R atrium near the SVC, spontaneous AP spread over the atria in all directions at a rate of ≈1m/s (atrial specialized conduction system)

2) AV node: electrical link between atria and ventricle, located at the endocardial floow of the R atrium, Conduction is very slow (0.01-0.05 m/sec) so AV delay- allows time for filling before the ventricle contracts

3) Ventricular Conducting system: Bundle of HIS, bundle branches, and then Purkinje fibers to the ventricular muscle.  Conductio  velocity in the HIS purkine system is the fastest in the heart (2-4m/sec)- this allows contraction to proceed from the apex to base

4) Conductio  in the ventricular muscle proceeds at 1m/s

In the atria, ventricle, and PKJ Em is normally constant during phase 4.  This is determined by the K gradient.  Changes in serum K alter Em.

Decreased K the cell hyperpolarizes except if you decrease below 2-2.5 PKJ depolarize.

Increased serum K causes depolarization.   Nodes are insensitive until >20mM

1) Em is -85 everywhere except the nodes where it is -60

2) APD ranges from 150ms-500ms

PKJ>Vent>atria>nodes

3) Upstroke is rapid except in the nodes (100fold faster)

4) Nodes do not have a phase 1 and phase 2/3 run together

I_ion=g_ion (Em-E_ion)

g=conductance= how easy is it for ion to cross

driving force=how far are you from where you want to be, you must use the nernst equation to determine

E_ion=61/z (logi/o) answer in mV

positive I are outward, negative I are inward

Phase 4: inward and outward currents are equal, g_K1 is high and keeps E_m close to E_K and therefore repolarized

Phase 0: depolarization causes Na channels to open and because the driving force is so high large influx of Na causes rapid depolarization high I_Na. This is regenerative and E_m approaches E_Na.  By the end I_Na decreases because driving force decreases and inactivation of Na channels so decrease in g_Na.

Phase 1: I_K1 slightly increased, I_TO increased in ventricle and PKJ

Phase 2: activation then deactivation of g_Ca L type channels and slow activation of g_K. responsible for plateau

Phase 3: everything resets, g_k1 rapidly increases and g_K slowly turns off- repolarization

I_Ca is responsible for phase 0 depolarization.  Amplitude is smaller and rate of depolarization is smaller.  T type channels present in SAN

I_f=pacemaker current, slowly turned on by hyperpolarization in phase 4- slowly depolarizes cell to TP and then another AP can be elicited (responsible for automaticity)- in absence of a sinus beat also present in PKJ

1) I_Ca provides balancing inward current

2) decrease in g_K1 upon depolarization limits outward current and makes it easier to maintain plateau

intrinsic ability to spontaneously depolarize in phase 4

1) SAN 2) AVN 3)bundle of HIS 4) Bundle branches 5)PKJ

pacemaker rates decrease as you go further down the conduction

everything after the SAN are considered latent pacemakers because they are normally under overdrive suppression (suppressed by HR faster than they would choose to go)  also called ectopic pacemakers (originated outside SAN)

NOT ADP

1) Threshold potential: usually moves in the same direction as E_m more positive harder to fire AP, more negative easier to fire AP

related to Na/Ca channels

Absolute Refractory Perdiod: stimulation is NOT possible

Relative Refractory Period: stimulation is possible at a higher threshold- begining will not conduct, end will conduct

Effective Refractory Period: longer than ARP, conducted AP can not be elicited

Supranormal Period: TP returns to normal just before repolarization is complete

Recovery of excitability depends on Na/Ca channels.  Na channels require repolarization to go back to the closed state so excitability closely follows repolarization.  Excitability return is slower in the nodes due to Ca.

Conduction velocity is not effected by APD.

1) larger amplitude of current=faster CV'

2) Increased gap resistance (R_i) causes electrical uncoupling and slows CV

3) increased excitability speeds CV- think responsiveness relationship

-Maximum rate of rise (dV/dt or Vmax) depends on resting E_m

-dV/dt is a rough measure of amplitude of inward current

-The more negative the resting potential the more ion channels are in the closed state and therefore able to elicit an AP upon depolarization- more channels means more influx/higher amplitude

-So, dV/dt is proportional to excitability and CV