The document discusses membrane potential, its functions, and its impact on supernormal conduction in cardiac tissue. It explains how variations in membrane potential affect excitability and conduction velocity, particularly during premature stimulation and certain physiological phenomena. Additionally, the text outlines mechanisms behind supernormal conduction and excitability, emphasizing the significance of refractory periods and dual A-V nodal pathways.

1. Supernormal
ConduCtion
Dr. VIKAS MEDEP

2. 
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Membrane potential (also transmembrane potential or
membrane voltage) is the difference in electric potential
between the interior and the exterior of a biological cell.
With respect to the exterior of the cell, typical values of
membrane potential range from –40 mV to –80 mV.
All animal cells are surrounded by a membrane
composed of a lipid bilayer with proteins embedded in it.
The membrane serves as both an insulator and a
diffusion barrier to the movement of ions.

3. 
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Ion transporter/pump
are electrically equivalent to a set of batteries and
resistors inserted in the membrane, and therefore create
a voltage difference between the two sides of the
membrane.
All eukaryotic cells maintain a non-zero transmembrane
potential, with a negative voltage in the cell interior as
compared to the cell exterior ranging from –40 mV to –
80 mV.

5. 
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The membrane potential has two basic functions.
First, it allows a cell to function as a battery, providing
power to operate a variety of "molecular devices"
embedded in the membrane.
Second, in electrically excitable cells such as neurons
and muscle cells, it is used for transmitting signals
between different parts of a cell

6. 
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In non-excitable cells, and in excitable cells in their
baseline states, the membrane potential is held at a
relatively stable value, called the resting potential
For neurons, typical values of the resting potential range
from –70 to –80 millivolts.

7. 
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The opening and closing of ion channels can induce a
departure from the resting potential.
This is called a depolarization if the interior voltage
becomes more positive (say from –70 mV to –60 mV),
Or a hyperpolarization if the interior voltage becomes
more negative (say from –70 mV to –80 mV).

8. 
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In excitable cells, a sufficiently large depolarization can
evoke an action potential, in which the membrane
potential changes rapidly and significantly for a short
time often reversing its polarity.
Action potentials are generated by the activation of
certain voltage-gated ion channels
The threshold potential is the critical level to which the
membrane potential must be depolarized in order to
initiate an action potential

10. Supernormal Conduction
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DEFINITION
Supernormal conduction implies conduction that is better than
anticipated or conduction that occurs when block is expected.
It should be emphasized that most of the cases of so-called
supernormal conduction described in humans have been
associated with baseline disturbances of A–V conduction.

11. 
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Therefore, the term supernormal has been referred to
improved conduction but not to conduction that is better
than normal
Mackenzie‘ in1913. 1925,Lewis,
In man, "supernormal"conduction is recorded only in
abnormally functioning cardiac tissue.

12.  Effects
of Membrane Potential on
Supernormal Excitability and Conduction.
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In 1955,Weidmann demonstrated the relationship
between the amplitude and voltage time Course of
Purkinje fiber actionpotentials evoked at different levels
of membrane potential by means of premature
stimulation.
Impulses resulting from premature stimulation were
thought to propagate at reduced velocity until they
encountered fully repolarized tissue, at which time
conduction velocity was thought to return to normal.

13. 
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Impulses elicited by stimuli applied immediately after the
end of repolarization, and thus at the maximum level of
membrane potential, display a greater rate Of rise and
amplitude of the actionpotential
Propagate more rapidly than those initiated later at a
somewhat lower level of membrane potential.

14. 
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Premature beats evoked early during the repo-larization
phase of the action potential often reached the more
distant electrode earlier than did later responses evoked
at membrane potentials closer to maximum resting
potentials.
The apparent conduction time between two recording
electrodes often decreased with increasing prematuity,.

15. 
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Purkinje fibers exhibit supernormal conduction and
supernormal excitability while His-bundle and ventricular
muscle fibers do not.
In an experiment where 3 microelectrodes were
simultaneously impaled along a canine Purkinje fiber.
Weidmann found that the Period of supemormal
excitability was due to the rapid recovery of excitability

16. 
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The time Course of two
simultaneously recorded
Purkinje Transmembrane AP
are displayed together with the
threshold current required to
Evoke a conducted response.
The graph at the right Of the
transmembrane potentials
displays the threshold current
required to evoke conducted
responses During the
repolarization phase.
It can be noted that there is a
decreased current requirement
associated with repolarization
in Purkinje fibers

17.  During
this
supemormal
phase of
excitability, there
also is a
corresponding
decrease in
conduction time

18. 
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The supernormal phase of conduction has several
outstanding features;
A pro-longed refractory period, either in the His–Purkinje
system or AV accessory pathways, appears to be one of
the prerequisite requirements for its occurrence.
According to Levi et al., SNC occurs at a relatively
constant position within the cardiac cycle,
Namely close to the end of the T wave.
However, it occurs earlier at faster heart rates (i.e.,
shorter cycle lengths) and later in longer cycle
lengths/slower heart rates.

19. Supernormal Conduction

Physiologic mechanisms explaining apparent
supernormal conduction include
1.
2.
3.
4.
5.
6.
Supernormal excitability in phase 3
Diastolic Phase4 Depolarization
The gap phenomenon.
Dual A–V nodal pathways.
Peeling back refractoriness
The shortening of refractoriness by changing the
preceding CL.

20. 7. The Wenckebach phenomenon in the bundle
branches.
8. Summation of sub threshold impulses.
9. Wendensky facilitation.
10. Bradycardia-dependent blocks.

21. Supernormal excitability
 During the super normal
period excitation is
possible in otherwise
subthreshold stimulus .
 Possible explanations are
1. Availability of fast Na
channels
2. Proximity of membrane
potential to threshold
potential
1.

22.  2.
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Diastolic Phase 4 Depolarization
The presence of diastolic depolarization (phase4depolarization) can also lead to apparent supernormal
excitability and conduction.
Premature beats that arrive early when the
membranepotential Is within the potential range of the
supernormal period of excitability will conduct more
rapidly than earlier or later premature beats.

23. 3. The Gap Phenomenon
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The term gap in A–V conduction was originally used by
Moe and his associates to define a zone in the cardiac
cycle during which PAC failed to evoke ventricular
responses, while PAC of greater and lesser prematurity
conducted to the ventricles.
The gap phenomenon was attributed to functional
differences of conduction and/or refractoriness in two or
more regions of the conducting system.

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The physiologic basis of gap phenomenon in most
instances depended on a distal area with a long
refractory period and a proximal site with a shorter
refractory period
During the gap phenomenon, initial block occurs distally.
With earlier impulses, proximal delay is encountered,
which allows the distal site of early block to recover
excitability and resume conduction.

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When the A V node is excited early by conduction from
the PAC , prepotential occurs, preceding the all-or-none
AV N actionpotential.
The AVN pre-potential results in a delay in conduction
through the A V node ,allowing the BB actionpotential to
recover to a potential closer to the RMP.
Accordingly, the BB can be excited and a Propagated
response to the ventricles

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Premature A response develops later ,allowing
conduction to reach the A V node when it is excitable.
The all-or- none AVN AP results in conduction to BB fiber
when the BB has not repolarized to a sufficient
membranepotential to permit an all-or-none response .
Conduction to the ventricles fails.
Is the most accepted theory

28.  4.
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Dual A–V nodal pathways
Dual A V pathways can also allow earlier PAC to
propagate over the slower A V pathway, resulting in early
PAC being propagated to ventricles.
Later PAC that propagate over the fast A V pathway are
blocked since they reach the A V nodal cells when they
are still refractory .

29. 
This demonstration of fast
pathway conduction during
slow pathway conduction
adds strong evidence for the
existence of dual A-V nodal
pathways.

30. 5. Peeling back refractoriness

Pre-excitation of the AV node by a ventricular or junctional
beat shortens the absolute refractory period of the AV or
the His-purkinje system and allows conduction of a
supraventricular impulse

33. 6. The shortening of refractoriness by changing the
preceding CL.
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The duration of refractory period is directly proportional
to length of preceding R-R interval.
300ms
480ms
300ms
480ms
300ms
300ms
480ms
480ms
300ms 270ms
450ms

34. 7. The wenckebach phenomenon in the bundle branches

35. 8. Summation of Subthreshold Responses
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If the controlled
subthreshold stimulus is
applied intracellularly at
times A or C excitation did
not cause depolarization.
However, if that same
Stimulus was delivered at
time B depolarization
occured

36. These experiments demonstrated that Summation of two subthreshold events in
Purkinje fibers can elicit Propagated responses

37.  9.
WENDENSKY FACILITATION
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Depressed segment of PF / Mus fibers
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Keep the impulses reaching this site blocked at this site
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Block is overcome
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Multiple stimuli reach the distal site
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Suprathreshold stimulus results

Conduction

38. BRADYCARDIA-DEPENDENT,
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Occurrence of impaired intraventricular conduction after
long pauses or slowing of the heart to a critical rate
Due to a gradual loss transmembrane resting potential
during a prolonged diastole with excitation from a less
negative take-off potenial

39. 
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In patients with bradycardia dependent aberrancy, the
beat at the end of a lengthened cycle is aberrated.
It is generally unexpected since there should be
sufficient time for the bundles to recover and conduction
to be normal after a long cycle.

40. 
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One explanation for its occurrence is that the bundles
are serving as pacemaker tissue and manifest
spontaneous phase 4 depolarization.
This pacemaker tissue is no longer suppressed by
stimuli from upper pacemakers when the cycle length is
very prolonged, leading to generation of an impulse
which will be conducted via the bundle and hence
aberrantly.