Nursing Students General Students
Published Jul 9, 2008
bsquared
12 Posts
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!
Daytonite, BSN, RN
1 Article; 14,604 Posts
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.
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?
[*]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:
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.