Arrhythmias and drugs Flashcards

1
Q

Four things drugs can alter?

A

TPR
Inotropy
Heart rate and rhythm
Blood volume

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2
Q

Five abnormalities in cardiac rhythm?

A
Bradycardia
Atrial flutter
Atrial fib
Tachycardia (Ventricular aand supraventricular tachycardia)
Ventricular fibrillation
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3
Q

Causes of Tachycardia? 4. explain them

A

Ectopic Pacemaker activity- Damaged area of myocardium becomes depolarised and fires spontaneously, dominating over the SA node

Afterdepolarisation- Abnormal depolarisation following the AP

Atrial flutter or atrial fib

Re-entry loop (Either a conduction delay or accessory pathway

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4
Q

2 causes of bradycardia? explain them , with possible causes for each (2 each)

A

Sinus bradycardia- Intrinsic SA node dysfunction or some extrinsic factor (drugs)
Conduction block- Problems at AV node or buyndle of his
Extrinsic factors- drugs

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5
Q

When are delayed after-polarisations more likely to happen?

A

with high intracellular Ca2+

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6
Q

When are early afterdepolarisations more likely?

A

prolonged AP

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7
Q

Describe why re-entry loops can lead to tachycardia

A

there’s a partial block
when the wave of depolarisation comes down, it can only pass down one of the two pathways.
however, when it passes down and rounds, it can pass back up the pathway witb the partial block
since the pathway has had time to repolarise, this means no refractory period, so action potenials can fire again

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8
Q

Three examples of re-entry loops

A

Atrial fibrillation (multiple reentry loops in the atria

AV node has a fast and slow pathway–> it depolarisaing it (ie not the SA node)–>supraventricular tachycardia

Accessory pathway from the atria to the ventricles that can send a signal to the ventricles, bypassing the atria–>ventricles contracting too early

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9
Q

what are the 4 classes of drugs that affect rate and heart rhythm

A

Drugs that block VG Na+ channels
Antagonists for β-adrenoceptorss
drugs that block K+ channels
drugs that block Ca2+ channels

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10
Q

Example of a drug that blocks Na+ channels?

A

Lidocaine (Local anaesthetic)

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11
Q

Explain how drugs that block Na+ channels work to prevent arrhythmias

A

block open or inactive Na+ channels
in damaged myocardium, more Na+ channels open
so can depolarise spontaneously sends off a wave of depolarisation across the myocardium
Blocks these Na+ channels, so prevents arrhythmias

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12
Q

Why don’t Na+ channel blockers bloick the Na+ channels of normal myocytes?

A

these channels dissociate too quickly

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13
Q

Two example of β-adrenoceptor antagonists?

A

Propranolol and atenolol

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14
Q

What do β-adrenoceptor agonists do and to what effect?

A

blocks sympatyhetic activty to the heart by acting at the β 1 adrenoceptor

so decreases the slope of the pacemaker potential in the SA node and slows conduction at the AV node

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15
Q

Explain why blocking the sympathetic activity to the SA node will decrease the slope of the pacemaker potential?

A

Normally, noradrenaline binds to the β 1 receptors
these are GPCRs
G alpha s
so increases cAMP
cAMP activates HCN channels
so more Na+ can enter–> increased slope of pacemaker potential

blocking the sympathetic nervous decreases this effect

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16
Q

What three problems can β blockers help with?

A

slow conduction at AV node, so can prevent supraventricular tachycardias

Used following an MI
Following an MI, you get increased sympathetic activity
can lead to arrhythmias
β blockers can prevent these

Reduces oxygen demand since heart isn’t working as hard, so recduces ischaemia

17
Q

What effect do drugs that block K+ channels have on the action potential?

A

Prolong the action potential

18
Q

Why are drugs the block the K+ channels generally not used

A

they’re pro arrhythmic

19
Q

What is the one exception drug to the drugs that block K+ channels and what is it used to treat?

A

amiodarone

Wolff-Parkinsonn-White syndrome (accessory pathway)

20
Q

Example of drugs that block a Ca2+ channel?

A

verapamil

21
Q

What is the effect of a drug that blocks the Ca2+ channel

A

decreases slope of AP
Decreases AV node conduction
decreases force of contraction

22
Q

What effect does administering adenosine have?

A

accts at β 1 receptors at the AV node
enhances K+ conductase so hyperpolarises cells so decreases the no of signals passing through the AV node (useful against supraventricular tachycardia)

its antiarrhythmic