Flashcards in Heart 3: Cardiac Refractory Periods Deck (19):
What determines refractory periods?
voltage and time dependence of Na (fast response) and Ca (slow response) channels
Why can relative refractory periods be dangerous? Describe the mechanism and implications.
mechanism the same as in neural tissue- has to do w inactivation of Na channel. if voltage of cell rel. positive then h gate closed. Na channel in inactive state. during rel. refractory period starting to recover so do have percentage of Na channels available and can get AP but these AP during rel. refr. period are not normal bc not fully restored. if you do stimulate during rel. ref. the AP upstroke dep. on number of Na channels available at that moment. refractory periods all due to to voltage and time dep. of Na channel. Ca slow response AP in AV node also have refractory period which gets into post- repolarization refractory bc kinetics of Ca slower than Na it has slightly longer ref. which has filtering affect.
if you stimulate at place more positive voltage then you have less Na channels available and so AP that will be generated will have slower upstroke and less A and will conduct more slowly- implications can kill you. abnormal AP can generate arrhythmias
Describe the difference between fast and slow response in regards to refractory periods.
Fast Response = primarily voltage-dependent refractoriness. As soon as it is repolarized it’s ready to go again.
Slow Response (L type channels) = primarily time-dependent refractoriness. Even after repolarization, it’s still refractory.
Describe the refractory period in ventricular/atrial muscle vs AV node.
What do anti-arrhythmic drugs do?
in ventricular muscle/atrial refractory period is length of AP bc once AP repolarizes it allows Na channel to instantly recover… instant change in gating char. from inactive to resting..so means heart is available again for another full AP. allows tachycardias to occur. can go v rapidly. just has to be at cycle length which is longer that refractory period.
at AV node situation diff. slow response. v slow char. compared to Na channel, activates and inactivates slowly. even tho cell has repolarized. refractory period is extended… bc inactivation gate of Ca channel even tho cell is REpolarized takes longer to go from inactive state back to resting state. anti-arhythmic drugs change refractory char. of tissue to prevent tachycardias.
What is ventricular tachycardia and how is it treated?
as soon as AP over can get another AP and heart could go at cycle length of 300 milliseconds. (rate of 200 beats per minute) so give anti-a drugs to lengthen refractory characteristics and lengthen tachycardia.
What is a premature beat in heart and what are the implications of this?
premature beat in heart… beat that comes earlier than supposed to. when get aberrant beat-during diastole or between beats thats a premature beat. 99 percent are benign. but if premature beat comes v early in cycle then contraction of heart, long pause where heart fills then another AP where beats again. premature beat during diastole not problem but if it comes so early and hits repol. of previous beat, hits rel. ref. period of previous beat then bc of more positive voltage at being activated the upstroke will be slow bc Na channels haven't recovered yet. this AP generated at that moment … can see the more positive the membrane potential, the slower will be upstroke and more abnormal will be conduction
premature beat will try to stimulate heart but bc of slow char. if there's anything wrong w your heart then this weak AP can block at that point and then conducts in abnormal pattern and causes reentry of excitation and throw heart into arrhythmia..vulnerable period of heart.
What is R on T phenomenon? What could result?
premature beat (R wave) that occurs during relative refractory period (T wave) of previous beat.
(R-ventricular depolarization. T is ventricular repolarization)
...could create premature ventricular contractions (PVCs)
nonsustained ventricular tachycardia- spontaneous 3 beats in a row...
What is commotio cordis?
critical time is the repolarization of the AP (the T wave) ... causes cardiac arrest (fibrillation)
if baseball or object hits heart during cycle of vulnerable period on repolarization of AP, generating abnormal AP that can throw heart into VF
It is a form of ventricular fibrillation (V-Fib), not mechanical damage to the heart muscle or surrounding organs, and not the result of heart disease. The fatality rate is about 65%. It can sometimes, but not always, be reversed by defibrillation.
Decribe post-repolarization refractoriness.
in slow responses- refractoriness outlasts AP duration.
The refractory period of a slow response is significantly longer than the AV node action potential duration. In other words, even though the voltage of the action potential fully repolarizes, the cell is still refractory. This is because the refractory period of slow Ca2+ channels is more dependent on time than on voltage.
This mechanism is responsible for the fact that conduction through the AV node slows when stimulated at higher rates (short cycle lengths).
This mechanism also prevents rapid ventricular activation during atrial tachy-dysrhythmias such as atrial fibrillation or flutter.
Cardiologists might do a stress test to uncover arrhythmias that have been suppressed by vagal stimulation. Why/how?
if doing stress test, receives some inhibitory input of Vagus nerve, get increased sympathetic tone and do the things that sympathetic does on the heart to increase HR and shortening of PR interval..so if AV node had been filtering out atrial impulses now with a shorter refractory period now may be able to see that...what it had been filtering out
What happens in atrial fibrillation?
-ventricular rate is too rapid (greater than 100 beats/min)
-ventricular rhythm is irregularly irregular.
In atrial fibrillation, what is determining the rate and rhythm of the ventricular activation?
What happens in exercise?
the AV node refractory period
in exercise -relieves parasympathetic inhibition and gives sympathetic stimulation and so you get shorter refractory period and more of irregular heart beats
How do you slow ventricular rate in patient with atrial fibrillation?
give anti-a drug which is lengthen the refractory period of the AV node while will filter out even more impulses and let them through less frequently. slow HR
could also Na or K channel blockers, beta blockers, Ca channel blocker to slow down ventricular rate by lengthening ref. period
to slow down AV node give beta blocker. it blocks beta receptors on AV node and slows conduction though AV node and lengthens ref. period preventing or lowering ventricular rate.
What causes the irregularly irregular ventricular rhythm in atrial fibrillation?
atrial hitting AV at diff intervals and AV node filtering in abnormal way trying to prevent them getting into ventricle.
ventricular beat is due to conduction from the atria.. its not a ventricular pacemaker (don't confuse with 3rd degree heart block- where ventricle is being generated by a pacemaker in ventricle)
What would result from a drug that blocked Ca channels?
Drugs that block slow inward calcium channels are used to reduce pacemaker firing rate by slowing the rate of rise of depolarizing pacemaker potentials (phase 4 depolarization). These drugs also reduce conduction velocity at the AV node, because those cells, like SA nodal cells, depend on the inward movement of calcium ions to depolarize.
As heart rate increases what happens to systole?
What phase of the cardiac cycle shortens more with increased HR, systole or diastole?
systole= AP duration/when heart contracts ...
as HR increases systole decreases
diastole= how long between beats (period of time when heart resting and filling with blood)
-as HR goes up AP duration shortens automatically
-as HR slows, AP duration lengthens
diastole shortens much more than systole (heart shortens AP and brings back some diastolic filling time. by shortening systole conserving some diastole. always lose more diastole than systole during increase in HR but shortening systole helps preserve some diastole.)
Describe what a prolonged QT syndrome is and what could cause it.
prolonged QT syndrome - abnormal prolongation of the QT interval
-acquired: bradycardia, hypokalemia, drugs (quinidine)
-congenital: due to genetic lesions in Na (h gate doesn't close properly or channel flows longer than it should) and/or K channels (don't turn on on time and repolarization is delayed and AP prolonged)
How can hypokalemia lead to prolonged QT syndrome?
low K decreases K permeability..if decrease K permeability its more difficult for K to leave cell and it prolongs AP