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101 Cards in this Set
- Front
- Back
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Class IA, IB, IC drugs are
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Na channel blockers
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Class II are
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Bblockers
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Class III are
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K channel blockers or others that prolong repolarization
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Class IV are
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Ca channel blockers
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What happens during phase 0 in the myocardium/His-purkinje system?
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Fast Na channels open
(Na influx) |
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What happens in phase 2 in the myocardium/His-purkinje system?
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-Fast Na channels inactivate
-K channels opeing -Slow Ca channels opening -Slow Na channels opening (Ca influx) |
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What happens in phase 3 in the myocardium/His-purkinje system?
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-Fast Na channels REactivating
-K channels fully open -Slow Ca channels closing -Slow Na channels closing (K efflux, repolarization) |
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What happens in phase 4 in the myocardium/His-purkinje system?
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K channels open
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What would happen if you blocked the fast Na channels?
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-decrease slope of phase 0
-decrease conduction velocity ie the speed of conduction is dependent on phase 0 |
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What would happen if you blocked K channels?
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-prolong phase 2
-increase refractory period |
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What is phase 4 due to in the SA and AV nodes?
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due to the I(sub)f pacemaker current channel, which lets Na (and other cations through), so Na is going in, causing depolarization
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What is phase 0 due to in the SA and AV nodes?
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slow Ca channel opening and Ca influx
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What is phase 3 due to in the SA/AV nodes?
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Ca channels inactive, K channels open, and there's K efflux
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What are mechanisms for cardiac arrhythmias
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abnormal automaticity (latent pacemaker or AV myocytes), triggered automaticity, or reentry
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How can abnormal automaticity happen?
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-ischemia causes a steeper slop for phase 4 of the AP in purkinje (reach threshold faster with steeper slope, picking up the pace of that latent pacemaker)
- ventricular myocytes are damaged and develop diastolic depolarization (don't normally have diastolic depol, but ischemia is a way to damage and develop this ectopic pacemaker) |
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Summarize abnormal automaticity
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when a latent pacemaker speeds up and takes control of the cardiac rhythm (AV node, His-Purkinje, or damaged myocyte can make a nonpacemaker cell depolarize spontaneously)
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Ways to eliminate arrhythmias due to increased automaticity...
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1.decrease phase 4 slope
2. make the diastolic potential more negative 3. make the threshold more positive *this will reduce or extinguish the abnormally high rate of firing |
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What do Na channel blockers do that helps?
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they decrease phase 4 slope and decrease excitability (increase threshold)
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What causes afterdepolarizations?
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interruptions in repolarization of a heart cell.
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How does an EAD (Early Afterdepolarization) occur?
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nprolonged phase 2. which means a prolonged depolarization. this can cause torsades de pointes
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What ion might be useful in tx of torsades because it suppresses EADs?
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magnesium. If you block Ca fluxing in, phase 2 will shorten. So one of the txs for torsades is Mg because it will shorter the AP duration and help eliminate the EAD
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What can prolong the plateau of the AP?
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anything that will increase the net inward current during repolarization. An example is a K channel blocker (phase 3 is K efflux, where repolarization occurs)
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If someone with recurrent VTach is taking an Na channel blocker, and he develops torsades, this is because the drug also blocked which channel?
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K channels. Prevents repolarization.
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One of the big side effects of K channel blockers is
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torsades.
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Requirements for reentry
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-two pathways for impulse conduction
-unidirectional block in one pathway -slow conduction through the loop of tissue |
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How do you stop reentry?
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-convert the unidirectional block to a bidirectional block. You do this by slowing conduction velocity or by increasing the effective refractory period.
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How do you decrease conduction velocity of fast response tissue (AV myocytes)?
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Effect phase 0, so block the Na channels. This will make phase 0 slope less steep, but it won't change the other phases. The conduction velocity will decrease.
end result is the impulse dies out, stopping reentry |
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What happens if you increase the effective refractory period?
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the propagating impulse finds tissue within the loop that is unexcitable and the impulse stops
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How do you increase the effective refractory period in the fast response tissue?
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block the K channels in the reentry circuit, which prolongs repolarization, increasing effective refractory period, propagating impulse encounters refractory tissue, and stopping reentry
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name 2 types of reentry arrhythmias
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afib and aflutter. These are txed by rate control (slow AV node conduction) and rhythm control (stop reentry, convert back to NSR)
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What types of drugs will slow AV conduction?
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-digoxin
-non DHP CCBs -Bblockers *use these for rate control |
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Blocking what channels will stop reentry to convert atrial fibrillation to NSR?
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Na channels and K channels. use these for rhythm control
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How do you prevent vtach/vfib?
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eliminate reentry with drugs. if there's pulseless VT or VF, you gotta shock em
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Blocking which channels wills top reentry to help treat/prevent VT or VF?
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Na (phase 0) and K channels (phase 3)
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What are the causes of PSVT (paroxysmal supraventricular tachy)
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1.AV nodal reentrant tachy (AVNRT)
-60% 2. AV Reentrant Tachy (AVRT) -WPW -Accessory pathway reentry -30% |
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How can you eliminate AV nodal reentry?
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prevent the premature atrial impulse or break the reentrant circuit in the AV node.
so use an AV nodal blocker for the slow pathway or a Na or K channel blocker for the fast pathway. |
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How can a person with WPW get AV reentrant tachy?
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a critically timed premature atrial impulse. It's either orthodromic AVRT where the effective refractory period is longer than the AV node (more common, impulse down AV node and up ERP), or Antidromic AVRT, where the ERP is shorter than the AV node (down ERP and up AV).
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How do you tell the difference between the two on an EKG?
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The wide QRS will be seen in the impulse that goes down the accessory pathway (antidromic), and the QRS is narrow when the antegrade goes down the AV node.
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How do you prevent orthodromic AVRT (WPW with narrow QRS)
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1. stop the premature atrial impulse
2. slow conduction or increase the ERP in the accessory pathway (to break the reentry circuit) 3. Slow down the AV node (break the circuit) AV blocker for the accessory pathway, and AV blocker for the AV. |
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What do you do if you have WPW and Afib?
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you would want to block Na or K channels, or block AV node, however blocking AV node is bad, so you want to block the accessory pathway.
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Why dont you want to block the AV node?
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if you block the AV node, that does not stop impulses from going to the ventricle because of the second pathway. If you use a Ca channel blocker, phase 2 will be shorter, meaning the ERP is also shorter, so more impulses will go through. Blocking the accessory tract may cardiovert to NSR, but blocking the AV node will make things worse.
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biggest problem with antiarrhythmic drugs is...
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cause you death from the pro-arrhythmic effect
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What are the Class I antiarrhythmic drugs and what are they used to do?
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Na Channel blockers, and they block fast Na channels (phase 0) in the open and/or inactivated (phase 2) state. NO affinity for Na channel blockers when Na channels are in the closed state
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What's the advantage of the lack of affinity for Na channels in the closed state?
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Work better in depolarized/damaged tissue and faster heart rates
this means recovery from block is slower and less complete, which increases stead state blocking. you are targeting the unidirectional block and trying to convert it to a bidirectional block. |
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What happens if you have a high steady state block of fast Na channels in normal tissue?
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this is how you get cardiac arrhythmias from Na channel blockers. conduction velocity is messed up.
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What are the classes of Na channel blockers?
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based on rate of recovery from block (how fast they come off the channel when it's in the closed configuration)
1A- intermediate 1B- very fast 1C- very slow |
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What does this mean
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The longer the rate of recovery, the higher the chance of affecting 'normal tissue' and the higher the chance in precipitating an arrhythmia.
1B least pro-arrhythmic, 1C most proarrhythmic effect |
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Name the class 1A Na channel blockers
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-quinidine
-procainamide -disopryamide -moricizine |
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MoA of Quinidine
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If you block Na channels, you decrease conduction velocity. Also blocks K channels.
With a moderate Na channel block, there is a decrease in phase 0 upstroke velocity, decrease conduction velocity and decrease reentry. when you prolong the repol, the ERP increases, also decreasing reentry |
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Effects of 1A on ectopic foci
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it will increase the threshold and decrease the phase 4 slope, all decreasing the rate of firing of ectopic foci
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So summarize Quinidine's effect on Na channel blockade...
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-decrease conduction velocity
-decrease excitability -decrease pacemaker --esp in ectopic pacemakers -prolong ERP |
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If you have Vtach or Afib, and you give quinidine, what does that do?
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decreases conduction velocity, prolongs effective refractory period, thus terminating/preventing arrhythmias.
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For narrow QRS (going down AV node) in WPW, what does quinidine do?
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In accessory pathway: decrease conduction velocity and prolong ERP (terminates/prevent arrhythmia)
In ectopic foci: decrease phase 4 slope (prevents arrhythmia only) |
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Clinical use of Quinidine
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-Afib/flutter
-Ventricular arrhythmias -WPW -AVNRT |
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Side effects of Quinidine
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-lots of GI problems
-initial increase in ventricular rate when tx afib/flutter ->inhibits vagal effect of the heart *to prevent this from quinidine is used for afib/flutter, give an AV blocker (since the goal is to slow the AV node down) -gives you torsades from K blockade |
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What happens to the QT interval if you prolong the AP duration?
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prolonged QT if the AP is prolonged
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Quinidine and blood vessels
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gives you hyotension because of the blocked alpha receptors (what normally vasoconstricts will now vasodilate) esp when used IV. that's why you only use this drug orally.
by the way, another adverse effect of quinidine is cinchonism, which will give you CNS toxicity |
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What does Procainamaide block? and other things
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Na, K, ganglionic blocker (causing hypotension)
halflife 3-5 hrs, so chronic use you may get lupus like problems IV use |
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Disopyramide info
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blocks Na, K, antimuscarinic
negative ionotropic (don't use on people with HF!!) oral |
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Go ahead and name some Class 1B Na channel blockers
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Lidocaine and mexiletine
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MoA of Lidocaine
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-blocks fast Na channels in open or inactivated state
-very fast recovery from block, thus a minimal effect on normal tissue (best on bad tissue) -best effect on depolarized and/or rapidly driven tissue -mild Na channel block (decrease phase 0 upstroke velocity), shorten AP duration (decrease conduction velocity) and decrease reentry. there is also a decrease in phase 4 slope (allow SA to take over as the pacemaker) |
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Which chamber does lidocaine work best in?
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works mainly in the ventricles. not effective for atrial arrhythmias or supraventricular arrhythmias. only good for ventricular arrhythmias.
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Comparing lidocaine to quinidine?
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lidocaine doesnt cause torsades (not a K channel blocker)
lidocaine doesnt work for afib **quinidine is good for any arrhythmia, while lidocaine is just good for ventricular arrhythmias |
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Do you use lidocaine for PVCs?
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no. because lidocaine is a pro-arrhythmic drug
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Adverse lidocaine effects
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-AV block
-Sinus Brady -decreased contractility -vent. arrhythmia -CNS and GI problems *whats good about lidocaine is that it has a very low pro-arrhythmic effect, so when you have vfib and defib them, you hang a lidocaine drip |
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Difference between Mexiletine and Lidocaine
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basically the same except Mexiletine is an oral drug. DOn't use this for afib, but use for vtach/fib
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What are the Class 1C drugs?
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-Flecainide
-Propafenone *both oral **long recovery from blockade (higher chance of affecting normal tissue than the other classes) |
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Class 1C effects in fast response tissue
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marked Na channel block, decreasing phase 0 upstroke velocity, decreasing conduction velocity, decreasing reentry
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Compare the proarrhythmic effect of class 1C to lidocaine and quinidine
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higher proarrhythmic effect compared to lidocaine.
Since quinidine can cause arrhythmia by 2 mechanisms (block Na and block K channels), so blocking Na is reduced with flecainide, but it's not a K channel blocker and WON'T cause torsades (and quinidine can cause it) |
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Which type of pts uses flecainide?
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those pts without structural heart disease since they're less prone to proarrhythmic effects of the drug.
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Adverse Flecainide effects
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Cardiad: proarrhythmic effect for those with structural heart disease
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Propafenone
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similar to flecainide, blocking beta receptors.
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What are the Class II drugs?
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Beta Blockers, selective and non selective. Blocking b1 receptors on the heart. The end result is a negative chronotropic effect on the SA node, decreased conduction velocity and increased ERP on the AV node. This can prevent arrhythmias triggered by excess catacholamines.
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Remind me, what is a clinical use for bblockers?
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reduce sudden death in post MI pts. since an increase in circulating catecholamine is correlated with the development of arrhythmias. The ventricular rate is controlled for pts with aflutter/fib, and can be used for AV nodal reentry or WPW.
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What are bblockers doing for afib?
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in the AV node, they prolong AV nodal conduction and refractoriness, which slows the ventricular rate. The pt will still have afib/flutter, but the heart rate is much slower, which is safer. Bblockers also do the same thing for WPWs (narrow QRS ie go through AV node) in order to terminate the arrhythmia. This is accomplished by shutting down the AV node, cardioverting the person, and terminating/preventing the arrhythmia.
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Would you use bblocker alone in a pt with atrial fib and WPW?
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NO. will not cardiovert afib because although the AV node is slowed down, you will not affect the accessory pathway.
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Long QT Syndrome
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Mutations in many genes, esp HERG, which includes the major subunit of I sub-kr, which is responsible for phase 3 K channel. If this isn't working, the AP duration is prolonged (not repolarizing), and long QT. This is why kids drop dead unexpectedly (esp from torsardes). This can be prevented by using a Bblocker to stop from getting that arrhythmia.
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Can you name the Class III drugs?
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-Amiodarone
-Drenedarone -Sotalol -Ibutilide -Dofetilide |
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MoA of Class III drugs
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-prolong the AP duration
-increase effective refractory period *by blocking K channels |
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MoA of Amiodarone
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Weak Ca channel blocker
-decrease phase 4 slope in SA node -coronary and peripheral vasodilation non competitive alpha and beta blocker blocks K, Na also (does everything, so used to treat all arrhythmias) |
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End result of Amiodarone
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-inhibits abnormal automaticity (by blocking Na channels)
-increases atrial, AV node, and ventricular ERP (by blocking K channels) -decrease AV conduction (blocking Ca and beta receptors and conduction in atria and ventricles (by blocking Na channels) |
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Big thing about amiodarone
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humungously long half life is 13-103 days. It's very lipid soluble so gets into the fat and takes a while to leave the system. So side effect may persist for mad long.
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How does it prevent reentry?
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by decreasing conduction velocity (block Na channels) and increasing ERP (block K channels).
used for AV Nodal Reentrat Tachy working on normal tissue or the fast pathway to break the circuit also used on AV Reentrant Tachy and WPW |
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What are the good things about Amioderone?
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Advantages are that it has a very low proarrhythmic effect (won't cause torsades) and no negative iontropic effect (can be used for heart failure).
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What are the bad things about Amioderone?
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Disadvantages are dose-related (deposits in tissue like cornea and skin sensitivity, bluish-gray coloration). also, since it's an analog of thyroid hormone, you can get hypo or hyperthyroidism
-pneumonitis leading to pulmonary fibrosis (starts with cough) -peripheral neuropathy -bradycardia/ AV Block |
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Drug interactions with amioderone
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with digoxin and warfarin, it's effects are increased. may need to adjust the dose.
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Comparing amioderone and dronedarone
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both block Na, K, Ca, beta receptors. low proarrhythmic effect.
the only thing dronedarone is used for so far is afib. They differ that dronedarone doesnt have iodine, and iodine is lipophilic, so the half-life is 1-2 days (only) so less toxic. |
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So who do you want to use dronedarone on.
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people will less severe heart failure. don't give it to people with more severe heart failure because they can be more dead.
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Sotalol
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K and beta blocker
-wont use to treat arrhythmia in pt with HF (bc neg. ionotropic) -high incidence of torsades -not used for HF |
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Ibutilide
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K channel blocker
IV only (KNOW THIS!!) can be used for HF high torsades |
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Dofetilide
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K channel blocker
Oral only can be used for HF high torsades |
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What effect will sotalol have on conduction velocity in fast response tissue?
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no effect. it's not a sodium channel blocker so it does not effect conduction velocity in fast response tissue.
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How does sotalol stop reentry in atria or ventricles?
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this is because it can block K channels (nothing about the beta receptor effect).
blocking K channels is going to prolong the AP duration and prolong the refractory period |
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What are the Class IV drugs?
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The calcium channel blockers, verapamil and diltiazam
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What causes phase 0 in the SA/AV nodes?
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Calcium influx. So this is where the CCBs will take their effect.
Conduction velocity will slow down and the ERP will be prolonged. |
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Clinical use of CCBs
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-terminate (IV) or prevent (oral) AV Nodal reentry
-slow ventricular rate in pts with atrial fib/flutter -narrow QRS AV Reentrant Tachy (WPW) |
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Would you use verapamil alone in a pt with atrial fib and WPW?
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No, it may shorten the ERP in the accessory pathway, enhance antegrade conduction and worsen the arrhythmia
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Contraindications of CCBs
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-ventricular arrhythmias because it's not effective. CCBs can also cause hypotension, hemodynamic collapse, activation of sympathetic NS and vfib
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Adenosine
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causes AV node block. this stops AV nodal reentry
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Pharmacokinetics of Adenosine
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very short half life (10 seconds) so you use as a rapid IV bolus, otherwise it won't get to the heart.
this is used to terminate AV nodal entry or WPW |
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What's an advantage of using adenosine?
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side effects last less than a minute
side effects: transient asystole, dyspnea (bronchoconstriction), chest pain/fullness, facial flushing |
