Arrhythmia Drugs Flashcards by M Njm

Why do arrhythmias from?

Defects in impulse formation

Defects in impulse conduction

How well did you know this?

Not at all

Perfectly

What are some defects in impulse formation?

Altered automacity

Triggered activity

How well did you know this?

Not at all

Perfectly

What is physiological altered automacity?

Regulation of SA node activity by autonomic nevrous system

How well did you know this?

Not at all

Perfectly

What is pathological altered automacity?

Latent pacemaker establishes HB instead of SA node (ectopic heart beat)

How well did you know this?

Not at all

Perfectly

What are some causes of establishment of latent pacemaking?

If latent pacemaker fires at rate faster than SA node

If SA node firing frequency is pathologically low

How well did you know this?

Not at all

Perfectly

What are some causes of latent pacemaker firing at rate FASTER than SA node?

Increased sympathetic acitvity, hypokalaemia and ischaemia trigger compensatory mechanisms in potential latent pacemakers i.e. cardiac myocytes

How well did you know this?

Not at all

Perfectly

What are some causes of SA node firing frequency is pathologically low?

Ischaemia i.e. right coronary artery - no blood supply to SA node
Circulatory hormones i.e. hypothyroidism
Hypokalemia

How well did you know this?

Not at all

Perfectly

What is triggered activity?

Afterdepolarizations triggered by normal action potential, two types
Early after depolarizations
Delayed after depolarizations

How well did you know this?

Not at all

Perfectly

When do early after depolarisation occur?

Phase 2 (terminal plateau) - AD mediated by Ca2+ L type channels 
Phase 3 (repolarization) - AD mediated by K+ channel opening (usually closed at this stage)

How well did you know this?

Not at all

Perfectly

TRUE/FALSE

Delayed after depolarizations are associated with drugs such as sotalol

FALSE

EADs associated with sotalol - drugs that lengthen QT interval (Ventricular systole) and prolonging AP

How well did you know this?

Not at all

Perfectly

When do delayed after depolarisation occur?

Occurs after complete repolarization

Caused by transient inward current involving Na+ channels

How well did you know this?

Not at all

Perfectly

TRUE/FALSE

Delayed after depolarizations are associated with drugs such as digoxin

TRUE
Digoxin reverses action of Na+/K+ pump, allowing Na+ to enter cell. This results in activation of Ca2+ channels which provokes DADs

How well did you know this?

Not at all

Perfectly

What are some causes of defects in impulse CONDUCTION?

Re-entry
Conduction block
Accessory tracts

How well did you know this?

Not at all

Perfectly

What is a re-entry circuit?

Defect in self sustaining electric circuit with parallel conduction, resulting in cyclical stimulation of myocardium.
Caused by unidirectional block or slowed retrograde conduction velocity

How well did you know this?

Not at all

Perfectly

What is heart block?

Fault in heart’s natural pacemaker due to block in electrical conduction (can be due to ischaemia , fibrosis etc)

How well did you know this?

Not at all

Perfectly

What is partial block?

Tissue conducts all impulses, but more slowly than usual. Example is first degree AV block

How well did you know this?

Not at all

Perfectly

What is intermittent block?

Tissue conducts some impulses but not others. Example is second degree AV block

How well did you know this?

Not at all

Perfectly

What is Mobitz T1?

Type of second degree heart block.
PR interval (atrial systole) lengthens from cycle to cycle until AV node fails and VENTRICULAR beat is missed.

How well did you know this?

Not at all

Perfectly

What is Mobitz T11?

Type of second degree heart block.

PR interval is CONSTANT but every nth ventricular depolarization missing

How well did you know this?

Not at all

Perfectly

What is complete block?

No impulses are conducted through affected area. Example is third degree AV block.
Atria and ventricles beat independently, governed by separate pacemakers.

What is the significance of accessory tract pathways

Impulse conducted faster through accessory pathway than through AV node
predispose to reentrant loops and tachyarrhythmia

What is disopyramide?

Class IA anti-arrhythmic drug

What is lignocaine?

Class IB antiarrhythmic drug

What is flecainide

Class IC antiarrhythmic drug

What is the Vaughn Williams classification of antiarrhythmic drugs?

``` Class 1 stimulates Na+ channels Class 2 inhibits B-adrenoreceptors Class 3 stimulates K+ channels class 4 stimulates Ca2+ channels ```

What does Class IA anti-arrhythmic drug do?

Associates with disassociates with Na+ channels at MODERATE rate. Slow rise of AP (velocity) PROLONGS refractory period. This works to PREVENT REENTRY

What does Class IB anti-arrhythmic drug do?

Associates with and disassociates with Na+ channels at FAST rate. Depresses conduction velocity This works to PREVENT PREMATURE BEATS and treat ventricular tachycardia

What does Class IC anti-arrhythmic drug do?

Associates with and disassociates with Na+ channels at SLOW rate. STRONGLY depresses conduction velocity (phase 0) This leads to -ve chrono and inotropic effects

TRUE/FALSE | Class I drugs bind preferentially to areas of the myocardium where AP firing frequency is highest

TRUE | During tachyarrhythmias Na+ channel spends most time in OPEN and ABSOLUTE inactivated state.

How does adenosine work?

Stimulates A1 (adenosine) receptors in AVN Opens GIRK channels (G protein coupled inwardly rectifying K+ channels) in the atrioventricular node This HYPERPOLARIZES cells and slows conduction in the AVN.

TRUE/FALSE | Adenosine is not used to terminate paroxysmal supraventricular tachycardia

FALSE | it is, slows conduction in AV node

TRUE/FALSE | Paroxysmal supraventricular tachycardia is caused by reentry

TRUE

What is the action of the Na+/K+ pump?

3 na+ pumped out of cell | 2 K+ pumped into cell

What is the mechanism of digoxin?

Inhibits Na+/K+ pump which results in more intracellular sodium This activates the Ca2+/Na+ exchanger which increases intracellular Ca2+ levels SOMEHOW indirectly causes inc. vagal activity

TRUE/FALSE | Digoxin increases sympathetic activity to the heart and Is therefore contraindicated in the treatment of AF

FALSE Digoxin actually increases vagal activity to the heart, the mechanism is unknown. It IS used to treat AF

TRUE/FALSE | Adenosine and Digoxin BOTH slow conduction in the AVN node

TRUE Digoxin through stimulating vagal activity Adenosine due to stimulation of A1 receptors (adenosine receptors) and GIRK (causing efflux K+ and hyperpolarizing cell)

Why is digoxin used to treat atrial fibrillation & atrial flutter?

In AF&AF atria beats at such high rates that ventricles can only irregularily follow (chaotic reentry impulse) Slowing the conduction of this impulse, slows and strengthens ventricular beat

What is the mechanism of Verapamil?

blocks L-type voltage-activated Ca2+ channels Slows conduction and prolongs refractory period in AV node and bundle of His

TRUE/FALSE | Verapamil should be used with great caution in combination with other drugs that have a negative ionotropic effect

TRUE can cause heart block in high dose - POWERFUL effect on AVN node conduction and already has negative inotropic effect - CAUTION with cumulative inotropic effects

Why has adenosine replaced verapamil in treatment of supraventricular arrhythmias ?

Its safer, adenosine used for acute treatment, but verapamil used for prophylaxis

What is lignocaine mainly used to treat?

Ventricular arrhythmias and premature beats - IV admin

What is flecainide mainly used for?

prophylaxis of paroxysmal atrial fibrillation

What is the main difference in pharm. use of disopyramide and procainamide?

Disopyramide is used (orally) to prevent recurrent ventricular arrhythmias, procainamide (IV) to treat ventricular arrhythmias following myocardial infarction

What are some problems associated with beta blockers?

excessive supression sympathetic drive that may trigger VT

How do beta blockers work?

Control SVT by suppressing impulse conduction through the AV node

TRUE/FALSE | Sotolol is a beta blocker

FALSE | it is a Type 3 agent (K+ blocker)

How do class 3 drugs work?

block of voltage-activated K+ channels slow repolarization of the AP =increase action potential inc. duration the effective refractory period

``` TRUE/FALSE Amiodarone has class IA, II and IV actions and also blocks β-adrenoceptors ```

``` True it is a class 3 drug but does other stuff 2 ```

Amiodarone is WAY more effective than other drugs, why is it not used in the long term?

``` Long term use side effects pulmonary fibrosis thyroid disorders photosensitivity reactions peripheral neuropathy ```