Elements of cardiac excitation Aug10, 2013 Dr.

Dominguez
ELEMENTS OF CARDIAC EXCITATION
I) CARDIAC ACTION POTENTIAL
PHASE
4

FAST RESPONSE
- atria, ventricles, purkinje fibers
Resting membrane potential due
to outward diffusion of potassium
(via voltage gated channels)
- electrolytes are found in areas
where they are not originally
found

SLOW RESPONSE
- SA node & AV node
Slow depolarization
Pacemaker activity or
automaticity activity due to
inward movement of sodium (via
funny channels) and Ca (via Ttype calcium channels)

- slow upstroke
- pacemaker activity
0

Depolarization due to influx of

sodium via fast sodium channels

Depolarization caused by
increased inward calcium current
(L-type calcium channels)

- rapid upstroke
- in hyponatremia, lesser
amplitude at phase 0, cell
depolarization is slower
1
2

Initial repolarization due to

transient efflux of potassium
Plateau phase due to entry of
calcium (via L-type Calcium
channels)

None
None

- allow ventricles to fill in with

blood
- Ca channel blockers verapamil
and diltiazem(specifically that
affect the heart) slows the heart
rate
- Beta blockers prevent the entry
of Ca
- efflux of K but balanced by
entry of Na
3

Repolarization due to efflux of

potassium

Repolarization due to efflux of

potassium

- Class III anti arrhythmics- delay

repolarization

- Class III anti arrhythmics- delay

repolarization

** RESTORATION OF IONIC CONCENTRATIONS via Na-K-ATPase pump and 3Na-1Ca

antiporter
** Check out Figures 16-1 and 16-3, Berne and Levy
CLINICAL CORRELATION:
1. Class Ia antiarrhythmics control heart rate by blocking Na influx
(Phase 0 for fast response, Phase 4 for slow response)

2. Class II (beta blockers) and Class IV (calcium-channel blockers like

3.

verapamil and diltiazem) antiarrhythmics block calcium entry (Phase 2 for

fast response, Phase 0 for slow response)
With myocardial ischemia or infarction, activity of Na-K-ATPase pump is
impaired
** Na-K-ATPase pump - 3Na ions in exchange for 2K ions
** Ischemia, decrease O2 Na remains in, K remains out
heart doesnt contract properly

FACTORS AFFECTING CONDUCTION VELOCITY

1. Amplitude of action potential: the greater the action potential amplitude, the
more rapidly is the wave of depolarization propagated
2. Rate of change of potential during phase 0: the more gradual the rate of
change of potential in phase 0, more time required to reach threshold, slower
conduction velocity
3. Resting membrane potential (RMP): the more negative the RMP, the harder it is
to reach threshold, decreases amplitude of action potential and slope of upstroke,
slower conduction velocity
CARDIAC EXCITABILITY
1. Absolute or effective refractory period: No matter how strong stimulus is,
another action potential cannot be generated; prevents sustained, tetanic
contraction of cardiac muscle
2. Relative refractory period (RRP): another action potential can be generated
in presence of stronger stimulus; the later in the RRP that the fiber is
stimulated, the greater the increase in amplitude of response and slope of
upstroke, thus the propagation velocity also increases
Early relative refractory period- very small amplitude is
generated.
Prone to development of arrhythmia ( re entry phenomenon
in ventricular fibrillation
Late relative refractory period- amplitude increases
** Check out Figure 16-15
II) CARDIAC CONDUCTION
- one-way conduction: SA node to AV node to AV bundle (bundle of his) to
right and left bundle branches to Purkinje fibers
heart is a inverted triangle, base is up and apex is down
- Spread of depolarization is from endocardium to epicardium, apex to base
- Automaticity self-excitation; ability to initiate its own beat
- Rhythmicity regularity of pacemaking activity
- Right ventricle contracts first because it is less muscular

1. SA node (fires at normal heart rate 60-100 bpm)

a. Pacemaker of the heart- controls rate of beating of the entire heart
b. With greatest automaticity and rhythmicity (highest firing rate)
Sympathetic response:
Steeper phase 4
SA node more permeable to sodium and calcium, increased heart
rate
Faster conduction velocity
Less negative membrane potential- reach threshold easily

Threshold potential is same with normal

Vagal response:
Reduced slope in phase 4
SA node more permeable to potassium, decreased heart rate
Reach threshold slowly- slower firing rate
Anti arrythmics increase threshold SA node fire slowly
Phase 4 determinants
1. rate of depolarization during phase 4
2.
maximal negativity during phase 4
3. threshold potential