Supernormal conduction


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Electrocardiographic manifestation of "supernormal" conduction is defined as conduction that is more rapid than expected or presence of conduction when block is anticipated. It is not supernormal in the sense or being more rapid than normal. Therefore, the term relative supernormality or "supernormality" is more appropriate. The mechanism of "supernormal" conduction is conduction during a period of supernormal excitability and conduction associated with altered membrane potential. Some of the more common phenomena that are not dependent on conduction during the supernormal period but manifest better than expected conduction, thus simulating "supernormal" conduction, include dual AV nodal conduction, the "gap" phenomenon, "peeling back" of the refractory period, summation of subthreshold responses, diastolic phase 4 depolarization, and phasic autonomic influences.

Supernormal conduction

  1. 1. Supernormal ConduCtion Dr. VIKAS MEDEP
  2. 2.     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. 3.     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.
  4. 4.    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
  5. 5.   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.
  6. 6.    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).
  7. 7.    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
  8. 8. Supernormal Conduction    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.
  9. 9.    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.
  10. 10.  Effects of Membrane Potential on Supernormal Excitability and Conduction.   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.
  11. 11.   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.
  12. 12.   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,.
  13. 13.    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
  14. 14.    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
  15. 15.  During this supemormal phase of excitability, there also is a corresponding decrease in conduction time
  16. 16.      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.
  17. 17. 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.
  18. 18. 7. The Wenckebach phenomenon in the bundle branches. 8. Summation of sub threshold impulses. 9. Wendensky facilitation. 10. Bradycardia-dependent blocks.
  19. 19. 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.
  20. 20.  2.   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.
  21. 21. 3. The Gap Phenomenon   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.
  22. 22.   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.
  23. 23.    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
  24. 24.     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
  25. 25.  4.   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 .
  26. 26.  This demonstration of fast pathway conduction during slow pathway conduction adds strong evidence for the existence of dual A-V nodal pathways.
  27. 27. 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
  28. 28. 6. The shortening of refractoriness by changing the preceding CL.  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
  29. 29. 7. The wenckebach phenomenon in the bundle branches
  30. 30. 8. Summation of Subthreshold Responses   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
  31. 31. These experiments demonstrated that Summation of two subthreshold events in Purkinje fibers can elicit Propagated responses
  32. 32.  9. WENDENSKY FACILITATION  Depressed segment of PF / Mus fibers  Keep the impulses reaching this site blocked at this site  Block is overcome  Multiple stimuli reach the distal site  Suprathreshold stimulus results  Conduction
  33. 33. BRADYCARDIA-DEPENDENT,   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
  34. 34.   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.
  35. 35.   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.