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Cardio-respiratory Physiology And Pharmacology > Anti-dysrhythmic Drugs > Flashcards

Anti-dysrhythmic Drugs Flashcards

0
Q

How is dysrhythmia classified ?

A

Site of origin - atria/ventricles

Types of rhythmic disturbance - increased/decreased and regular/irregular

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1
Q

What is dysthymia ?

A

Disturbance of cardiac rhythm

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2
Q

Define atrial tachycardia ?

A

Heart rate of 150-240 bpm

Regular beating

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3
Q

Define atrial flutter

A

Heart rate 240-350bpm

Regular beating

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4
Q

Define atrial fibrillation

A

Irregular beating
Tachycardia and flutter often lead to this
Some people are asymptotic while others have pain, palpitations and dizziness

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5
Q

Define ventricular tachycardia

A

120-300bpm heart rate

Regular beating

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6
Q

Define ventricular fibrillation

A

Irregular beating that can be fatal in minutes

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7
Q

Why do dysrhythmias arise ?

A

Caused by changes in generation or conduction of electrical impulses

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8
Q

Explain abnormal impulse generation ?

A

AUTOMATICITY- increased pacemaker activity

TRIGGERED ACTIVITY- when an ectopic beat arises after a normal beat

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9
Q

Explain abnormal impulse conduction

A

HEART BLOCK - when impulses don’t travel through SAN to AVN properly
REENTRY - propagating impulse fails to die out

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10
Q

Explain automaticity

A

Also called ectopic pacemaker activity
It results from increased sympathetic stimulation and by partial depolarisation that can occur during ischaemia due to increased extracellular potassium levels
Causes increase phase 4 depolarisation and it can also cause normally quiescent tissue to undergo spontaneous rhythms

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11
Q

Explain triggered activity

A

EARLY AFTER DEPOLARISATION
- an extra AP before previous one reaches baseline caused by deactivation of L-type calcium channels
-results from sympathetic stimulation and heart failure
DELAYED AFTER DEPOLARISATION
- an extra AP after previous ap has returned to baseline
- caused by increased intracellular calcium levels which activate sodium/calcium exchanger which pumps out a calcium for 3 sodium in so a net increase of +1 causing depolarisation
Results scroll, sympathetic stimulation, heart.failure and cardiac glycosides

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12
Q

Explain re-entry

A

When an electrical impulse re-excites regions of the myocardium
- normally an impulse propagates in both directions and once they meet they die out but if a damaged area cause either a transient block or a unidirectional block continuous circulation of this impulse occurs

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13
Q

What are the 4 classes of anti-dysrhythmic drugs ?

A 
1-sodium channel blockers 
2-beta blockers 
3- potassium channel blockers 
4- calcium channel blockers 
Also cardiac glycosides
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14
Q

What is the aim of anti-dysrhythmic drugs ?

A

They affect electrical impulse formation/propagation through the effects of ion channels, receptors and ionic pumps

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15
Q

What is the main function of the sodium channels blockers ?

A

the atrial/ventricular tissue depolarisation is caused by sodium influx so these drugs block these channels reducing the upstroke

16
Q

What do the potassium channels blockers affects ?

A

They affect the repolarisation phase of both aps in the pacemaker cells and atrial/ventricular tissue
Increase the refractory period

17
Q

What are the aims of the beta blockers ?

A

Reduce funny current at phase 4 depolarisation of pacemaker cells
Reduce calcium current in the upstroke of pacemaker potential and plateau phase of atrial/ventricular tissue

18
Q

What is the aim of the calcium channel blockers ?

A

Reduce the calcium current in the upstroke of the pacemaker potential and the plateau phase of the atrial/ventricular potential

19
Q

What are the 4 main mechanisms by which anti-dysrhythmic drugs work ?

A

1- reduce funny current
2- slow conduction of sodium and calcium currents by beta- blockers
3- increase refractory period by blocking potassium channels
4- reducing intracellular calcium by blocking calcium channels

20
Q

What are the sodium channel blockers divided into and how do each of them work ?

A

A, b, c
All three work on the activated state of sodium channels
Only b is able to block the inactivated state

21
Q

What is an important characteristic of class 1 drugs ?

A

Use dependence

So he faster the heart beats the more effective these drugs block

22
Q

Explain the association/dissociation, ap effects, use, side effects and examples of 1a….

A

Medium - only bind in activated state so reduce upstroke
Slow the conduction of sodium ions and they also have class 3 effects by increasing refractory period
Used for ventricular and supraventricular dysrythmias
Forsake de pointed, polymorphic dysrythmias, anti cholinergic effects
Quinidine, procainamide

23
Q

Explain the association/dissociation, use, side effects and examples of 1b…

A

Fast
Little effect on conduction as it unwinds quickly but it’s good at preventing premature beats
Used for ventricular dysrythmia after heart attack
Bolus lidocaine can cause seizures and coma
Lidocaine , mexiletine

24
Q

Explain the association/dissociation, use, side effects and examples of 1c….

A

Slow
Slows conduction and is bound through ap so generally reduce excitability
Ventricular and supraventricular tachycardias
Well tolerated
Flecainide

25
Q

Give examples of beta blockers and explain effects …

A

Propranolol and atenolol
Used to treat ventricular dysrythmias because they can reduce sympathetic activity
Increas refractory period at AVN
Suppress non sustained ventricular arrhythmias
Reduce ectopic pacemaker activity -1b
Exacerbate heart failure by reducing CO
Propranolol can cross BBB and cause nightmares

26
Q

Give examples of class 3 drugs and explain their effects….

A

Soltalol (+2activity)and amiodarone(+1,2,4 activity)
Prolong refractory period in atria and ventricles
Reverse use dependence
Used in atrial fibrillation
Can’t be used on people with long Q-T syndrome

27
Q

Give examples of class 4 drugs and explain there effects…

A

Verapamil and dilitazem
Slow conduction at AVN and reduce triggered activity
Used in supraventricular arrhythmias to slow ventricular rate

28
Q

What are cardiac glycosides ?

A

Digoxin
They enhance vagal activity which slows automaticity and prolongs av conduction and refractoriness
Control ventricular rate in atrial fibrillation
Prevent re-entrant arrhythmias involving AVN

Cardio-respiratory Physiology And Pharmacology (33 decks)

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