Exam 1 lecture 4 Flashcards
re-entry
when depolarization that does not die out, but keeps going along various branching or circular pathways within the myocardium, generated by wave of depolarization hitting areas that have already been repolarized, results in continuous wave of depolarization that encircles a region of heart.
conditions that favor re-entry
long pathway, reduced conduction velocity which has same effect as long pathway, shortened refractory period which accelerates muscle repolarization
ventricular or atrial fibrillation
many small waves spreading through micro-loops in different directions over the myocardial surface
re-entry can cause
ventricular tachycardia or atrial flutter
Long pathways
dilated atria and ventricles
variable conduction rates and regions of excitability
during normal repolarization, ischemia and injury which slows conduction and repolarization, hyperkalemia and cocaine can slow the conduction velocity
altered repolarization rates (short refractory period)
catecholamines
aberrant pathways or accessory anatomical pathways
AV nodal re-entry
ventricular tachycardia
current from an ectopic beat re-enters the focus, travels slowly through it and again emerges to find surrounding myocardium repolarized and vulnerable-> series of ectopic beats can be initiated .
aberrant pathways (AV nodal re-entry)
2 pathways develop in AV node. Slowly conducting pathway with a short refractory period, and a preferred alternate rapidly conducting pathway with a long refractory period
re-entrant supraventricular tachycardia
rapid heart rhythms at or above AV node
Wolff-parkinson white syndrome
short P-R and pre-excitation wave slurring the upstroke and the QRS. Aberrant muscular bridge (bundle of Kent) connects atria with ventricles and bypasses AV node. Can suddenly cause tachycardia at a rate that impairs ventricular filling, cardiac output drops, fall in mean arterial pressure, leading to dizziness, fainting and angina pectorsis due to inadequate perfusion of the coronary arteries
delta or pre-excitation wave
from WPW, rapid activation of some regions of the ventricle directly through the bypass before slower activation of other regions through the atrioventricular node produces delta wave on upstroke of QRS
paroxysmal supraventricular tachycardia
premature atrial depolarization occurs while accessory pathway is still in refractory period but AFTER AV node has recovered-> impulse passes anterogradly through excitable AV node into ventricles-> in meantime accessory pathway has recovered its excitabilty and impulse conducts retrogradely from ventricles back to atria. Causes inverted P wave after QRS, and if impulse arrives at atria at time when AV node has again recovered its excitability, whole circuit can repeat.
WPW
impulse conducts rapidly down Bundle of Kent directly into ventricular myocardium, and will see short P-R interval, pre-excitation wave (delta wave) and slurred QRS upstroke
Lown-Ganong-Levine (LGL) syndrome
short P-R interval and NORMAL WIDTH QRS. AV node re-entry involving fast and slow pathways or an AV node by pass are possible mechanisms
Triggered activity
premature ectopic foci occuring in atria or ventricles are sometimes “triggered events”, abnormal depolarization that are ALWAYS coupled to a preceding action potential
EAD (early after depolarization)
depolarizations that occur before the cell is fully repolarized , occur in congenital or acquired LQTS where repolarization has been slowed, (can be because of mutation or drug effects of Ikr)
