V-tach

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I need help with pathogenesis of Ventricular tachycardia. I found two from my textbooks but those don't go to the cellular level. Any suggestions where I can find a good one?

Thank you in advance!

Specializes in med/surg, telemetry, IV therapy, mgmt.

the pathophysiology of the cardiac arrhythmias, of which ventricular tachycardia is one, is always due to abnormal electrical conduction that disrupts how the electrical signal is being generated or conducted through the normal electrical pathway. with ventricular tachycardia a very fast ventricular pacemaker sets a pace of 100 to 200 beats per minute to override higher sites for control of the heart so that the ventricles are always dissociated from the atria and in control of the pacing of the heartbeats. the danger is that multiple foci in the ventricles become irritable and generate uncoordinated, chaotic electrical impulses that cause the heart to fibrillate rather than contract. this can quickly progress to ventricular fibrillation and death.

the electrical conduction system of the heart is a specialized collection of cells that coordinate the bioelectrical activity of the heart. they are involved in initiating (pacemaking) and conducting each electrical impulse. they also coordinate the sequencing of the atrial and ventricular contractions to allow the efficient pumping of blood.

http://texasheart.org/hic/anatomy/conduct.cfm
- has information on the normal sequence of electrical conduction

pacemaking function is usually performed by the cells of the electrical conduction system, although
any
myocardial cell can perform this function.

the cells of the sa node will create action potentials (electrical firings) and discharge an electrical impulse on an average of 70 times a minute. for a pacemaker cell or other cardiac cells to initiate, receive and react to an electrical impulse sent their way, this cyclical process must occur:

  • polarization - a cell becomes more negative, moving toward disequilibrium with the extracellular fluid

  • refractory state - the short period of time immediately after depolarization when the cell is unable to fire or conduct an impulse.

  • depolarization - a cell becomes more positive, moving toward equilibrium with the extracellular fluid

  • threshold potential - the state during which an action potential (electrical firing) is triggered

the normal sequence is that the electrical impulse travels through the heart tissue exciting myocardial cells to contract in a unified manner which results in muscular activity (a heartbeat) :

  1. begins at the sa node (the main pacemaker)
    • through the atria along bachman's bundle (part of the electrical conduction system that transmits the impulses through the interatrial septum)

    • through the interrnodal pathways (three pathways of the electrical conduction system found in the atria that transmit the impulse from the sa node to the av node)

[*]goes through the av node (responsible for slowing down conduction from the atria to the ventricles just long enough for atrial contraction to occur. this slowing allows the atria to "overfill" the ventricles and helps maintain the output of the heart at a maximum level)

[*]and proceeds down through the ventricles

  • down the bundle of his (originates in the av node)

  • along the bundle branches (there are two: the left bundle branch and the right bundle branch which originate in the bundle of his and end at the purkinje system)

  • and then down the perkinje fibers where

  • the impulses from the right and left perkinje fibers finally meet up again and cancel each other out at their terminus

these electrical causes the myocardium of the atria and ventricles to contract and relax. normally, this proceeds at a regular rate. however, as in any pathological condition, any break in the pathway results in an impaired ability of the cardiac muscle to contract. so, dysrhythmias can be caused by an abnormal rate of pulse generation by the sa node or the abnormal conduction of impulses through the heart's conduction system which includes the myocardial cells themselves.

ventricular tachycardia is due to the premature conduction of a pulse that starts outside (ectopic) the sa node. keep in mind from physiology that the sa node is the heart's pacemaker. why are ectopic cells able to act as the pacemaker and fire off a "spark" that begins the electrical conduction pathway that ends in the heart muscle responding by beating?

  1. enhanced automaticity - automaticity is one of the unique properties of cardiac tissue that allow it to contract without nervous stimulation (nerves). the beating of our hearts relies on an electrical impulse, but it cannot distinguish where the impulse is coming from--it only knows "electrical impulse". there are a number of factors that can increase, or intensify, this automaticity property of the other cardiac cells (they are called latent pacemakers) to reach threshold and depolarize (fire off an electrical spark):
    • drugs such as epinephrine, atropine, digoxin
    • conditions like acidosis, alkalosis, hypoxia, mi, hypokalemia, hypocalcemia

[*]reentry - the way i understand re-entry is to go back to the normal conduction pathway of an electrical impulse. after the impulse completes its run through the perkinje fibers (keep in mind that the impulse has to spilt into two in order to proceed through the perkinje fibers of each ventricle) they once again join together where they kind of fizzle out. with re-entry problems this "join up and snuff out" after proceeding through the ventricles doesn't happen because there has been something in one of the ventricles to block or disrupt the electrical conduction through the perkinje fibers on one side. what happens is the impulse that is able to continue down the perkinje fibers of the ventricle that has a clear pathway has no way to fizzle out, so what does it do? it just keeps its charge going as long as it can. if this lone electrical charge which is now meandering around in the ventricle happens to run into a charged myocardial cell(s) that is (are) at its threshold potential (excited and waiting to fire off) [remember that automaticity factor of cardiac cells] they are going to "jump the gun" and fire off which will start an ectopic ventricular event. this happens when:

  • there has been ischemia (no oxygen causes the inability to depolarize which is what sets off the firing of an electrical impulse) or infarction (nonviable tissue that no longer functions) that physically blocks electrical impulses.
  • conditions such as hyperkalemia, some antiarrhythmic drugs

some links that might be helpful:

Thank you so much, Daytonite. All of the info that you posted here helped me a lot and the links that you included as well. Again, thank you very much.

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