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51 Cards in this Set
- Front
- Back
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What does the PR interval indicate?
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The conduction velocity from atria to ventricle.
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What is Long QT syndrome?
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As the name implies the QT interval is longer than normal. This longer than normal repolarization lends the person more susceptible to afterdepolarizations because the Na channels are more likely to reset and depolarize early.
Also referred to as "Torsades de pointes" |
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Atrial fibrillation and flutter are this type of arrhythmia.
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Supraventricular
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Ventricular tachycardia is due to this type of arrhythmia.
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Ventricular
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Name the 4 different types of anti-arrhythmic drug.
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Class I = Na channel blocker
Class II = Beta Blockers (B1) Class III = K channel blocker Class IV = Ca channel blocker |
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What is the effect of Na channel blockers on the SA and AV node?
What 2 effects does this have and where do the effects take place? |
They block open Na channels. This has a membrane stabilizing effect and decreases excitibility.
-Threshold is increased -Phase 4 slope is decreased Ultimately, this causes an increase in the duration of phase 4, decreased automaticity (SA firing) and decreased HR |
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What is the effect of Na channel blockers on the the ventricles (non-pacemaker cells)?
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Blocking Na channels in the ventricles decreases the phase 0 upstroke and therefore conduction velocity.
It also blocks re-entry |
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What is unique about Class IA drugs?
What is the consequence of this? |
They also block K channels. This decreases repolarization
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Describe the difference in Na channel blockage between the three classes of Na blocking drugs.
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Class I = moderate blockage
Class II = mild blockage Class III = marked blockage |
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Name the 2 main Class 1A drugs
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Quinidine
Procainamide |
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What is this class of drug indicated for?
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Supraventricular and Ventricular arrhythmia's
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What is the adverse effect of Quinidine? DDI?
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It also has anticholinergic effects which increase ventricular firing.
It's drug drug interaction is with Digoxin as they both compete for the same CYP liver enzyme. Digoxin has a low TI so this is very dangerous |
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What is the adverse effect of Procainamide?
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Hypotension (inhibits neurotransmission of sympathetic ganglia in the periphery)
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What is unique about Procainamide's metabolism?
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The population has varying degrees of enzyme efficiency in terms of metabolism. The enzyme produces a metabolite that effects only K channels.
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What is the main Class 1B drug?
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Lidocaine
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What is the major adverse effect of Lidocaine? DDI?
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CNS Na blockade that can cause seizures, dizziness
Metabolized by liver CYP enzymes. Other drugs metabolized by this process can increase Lidocaine's bioavailability |
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What is Lidocaine indicated for?
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Ventricular arrhythmia's
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What is the major Class 1C drug? What is it indicated for?
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Flecainide
Emergency supraventricular and ventricular arrhythmia's |
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What is the adverse effect of Flecainide?
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Can be pro-arrhythmic in some patients
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If a class I anti-arrhythmic decreases SA nodal automaticity too much, what adverse even tis likely to occur?
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Escape beat
Decrease Nodal firing too much and latent pacemakers may fire a beat |
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To avoid the development of torsades de pointes in a patient with QT syndrome, which class of drug should be avoided?
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Class IA?
Quinidine and Procainamide |
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What is the normal effect of the SNS in stimulating Beta 1 adrenoceptors on the SA and AV nodes??
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SA Node: stimulation leads to increased Na current and therefore increased slope of phase 4 and increased firing
AV Node: stimulation leads to increased Ca current which increased conduction velocity. It causes increased K current which decreases refractory period via faster repolarization |
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What are the 2 major actions of Beta Blockers on the SA and AV nodes?
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1. They decrease the slope of phase 4 via AV node (Na channels not phosphorylated)
2. They prolong repolarization via AV node (Ca and K channels not phosphorylated) |
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What are Beta Blockers indicated for?
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Supraventricular and ventricular arrhythmias precipitated by sympathetic stimulation.
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How are Beta Blockers helpful for these?
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Decrease automaticity (SA)
Increases refractory period (AV) - This decreases re-entry) |
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Name 4 beta blockers
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Bisoprolol (B1>>B2)
Atenolol, Metoprolol (B1>B2) Carvedilol (B1 > or = B2) |
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What are some potential adverse effects of Beta Blockers?
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Bronchospasm
Bradycardia Insomnia/Depression |
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The ability of a Beta Blocker to decrease re-entry is due to its action on this.
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The AV node
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What cells do K channel blockers effect?
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Pacemaker and Non-pacemaker cells
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What is the main effect of K channel blockers?
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They prolong repolarization which increases the refractory period and decreases re-entry
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What is the adverse effect associated with this outcome?
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Prolongation of APD increases the chance of developing an early after depolarization and torsades de pointes
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Name the 3 main K channel blockers
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Dofetilide
Sotalol Amiodarone |
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What is the advantage of Dofetilide?
What does it do? Adverse effect? What needs to be taken into consideration? |
It is pure, potent and selective (virtually no extracardiac pharmacological effects)
Prolongs repolarization and increases APD Torsades de pointes It is extensively cleared by the kidney |
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What is unique about Sotalol?
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It is a mixed II/III agent
The l-isomer inhibits Beta receptors The l and d isomers inhibit K channels |
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What are its main effects?
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Decreased automaticity (SA)
Decreased AV conduction Increased AV refractoriness |
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What are the major adverse effects
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Overdose effects: Bradycardia (Beta), torsades de pointes (K channel)
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What needs to be considered when giving this drug?
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Cleared extensively by the kidney
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What is unique about Amiodarones action?
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It is a mixed I-IV active agent due to it alteration of membrane lipids which contain the ion channels and receptors
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What are its effects?
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Decreased automaticity
Decreased conduction velocity Increased refractoriness ***Because you get extra class effects, it is effective at low doses and exhibits low incidence of torsades de pointes |
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What are the adverse effects of Amiodarone?
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Heart block, hypotension
Pulmonary Fibrosis Elevated liver enzymes (DDI interactions) Hypo/Hyperthyroidism due to structural similarity to thyroxine |
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What is Dronedarone?
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Similar agent to amiodarone but less toxic due to lack of iodine moieties and reduced lipophilicity. Newly approved
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In a patient with renal dysfunction, what arrhythmic event could occur with a Class III agent?
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Early after depolarization
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What cells do Calcium channel blockers have the most effect on?
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Pacemaker cells (SA and AV node)
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What is their effect?
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Decrease slope of phase 0 (upstroke)
This decreases conduction velocity through the AV node and blocks re-entry if the AV node is involved |
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What are Calcium channel blockers indicated for?
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Supraventricular arrhythmia's (SA, AV)
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What are the adverse events?
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AV block and hypotension in high doses.
***Vascular smooth muscle cells and cardiac cells display different calcium channels and respond differently to CCB's |
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What are 2 important DDI's with CCB's?
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CCB + Beta Blocker can lead to HF
CCB's can increase digoxin levels via competition for renal excretion |
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What other treatment is available for arrhythmia's?
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Adenosine - Promotes increased K channel opening and decreased Ca channel opening in SA and AV nodes
This leads to increased refractoriness, decreased APD and slowed automaticity. Given Intravenously for supraventricular arrhythmia's |
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What other treatment is available for arrhythmia's?
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K/dialysis - restores K levels for proper AP generation
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What does hypokalemia cause?
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Early and delayed depolarizations
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What does Hyperkalemia cause?
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Decreased conduction velocity
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