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ZCP302 > Arrhythimias > Flashcards

Arrhythimias Flashcards

1
Q

What are the electrical properites of cardiac cells?

A
  1. Automaticity. 2. Excitability. 3 Conductivity. 4. Refractoriness
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2
Q

Define chronotropic, inotropic, dromotropic and bathmotropic

A

C - frequency of the heartbeat
I - force of contraction of the heart
D - conduction of impulse through heart
B - excitability of cardiac muscle

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3
Q

Describe in detail the action potential of the heart

A

Upstroke. Then there is rapid depolarization, which means an opening of calcium channels. Then rapid repolarization, seen by the notch. Potassium moves out and calcium moves in. The plateau signifies the muscle still being depolarized. Calcium channels close. Final repolarization takes place and potassium channels close. The cell is slowly depolarized.

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4
Q

What do the diffrent points on the ECG represent?

A

P wave: atrial depolarization
QRS complex: ventricular depolarization
T wave: ventricular repolarization
PR interval: AV conduction
QT interval: ventricular action potential
ST interval: plateau portion of ventricular action potential

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5
Q

What is the function of the SA node?

A

The SA node is the pacemaker in the heart, governed by the autonomic nervous system

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6
Q

What are the 3 criteria for excitation?

A

Atrial excitation and contraction should be complete before the onset of ventricular contraction
Excitation of cardiac muscle fibres should be coordinated to ensure that each heart chamber contracts as a unit.
Both the atria and ventricles should contract simultaneously

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7
Q

What is delayed after depolarizations?

A

Elevated Ca, which can delay repolarization. This results in QT interval prolongation and can cause ventricular arrythmia

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8
Q

What are supraventricular arrythmias and give 3 examples?

A

All arrythmias that originate above the bundle of His. Examples are sinus bradycardia, sinus tachycardia, atrial flutter and atrial fibrillation

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9
Q

What is a sinoatrial block?

A

Its the failure of an inpulse being transmitted from the SA node to the AV node

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10
Q

What is an atrial flutter?

A

Charaterised by rapid ineffective atrial contractions where the rate is about 250 to 350 beats per minute

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11
Q

Why is ventricular fibrillation so dangerous?

A

This is a dangerous form of arrythmia because the ventricles cannot pump blood effectively and can lead to death

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12
Q

What is Torsades de Pointes?

A

It is a polymorphic ventricular tachycardia which is associated wtih twisting of QRE complexes and prolonged QT interval

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13
Q

What is the classification of antiarrhythmic drugs

A

Type 1 - target your sodium ions and your potassium ions
Type 2 - Calcium ions
Type 3 - Potassium ions
Type 4 - Calcium ions

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14
Q

List the main actions of AADs

A

Supress abnormal impulse formation and conduction. Drugs that block Na/Ca channels can reduce abnormal automaticity and slow conduction of cardiac muscle. Drugs that block K channels can prolong repolarization and the AP duration.

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15
Q

What is the mechanism of action of Class Ia drugs?

A

Block fast Na channels and delayed potassium channels. Slow phase 0 depolarization and phase 3 repolarization in ventricular tissue

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16
Q

What are the main adverse effects of quinidine?

A

Nausea, vomiting and lengthens QT interval

17
Q

What is the MOA of procainamide?

A

Use and state dependent block of Na channels, slowed conduction velocity and pacemaker activity

18
Q

What is the MOA of Class 1B drugs and give an example of one?

A

Blocks INa channels predominately in open/inactivated state. Not effective against SVAs. Lidocaine is an example

19
Q

What is the MOA of class 1C and give an example?

A

Potent blocker of sodium and potassium channels. It reduces Vmax. Flecainide is an example.

20
Q

What is the MOA of Class II agents?

A

Selective for B1 cardiac receptors. They slow ventricular response in atrial flutter and fibrillation. They also slow the heart rate. Beta-blockers are an example

21
Q

What is the MOA of class III drugs

A

They prolong the action potential by blocking K channels in cardiac muscles. Also prolongs the ventricular action potential duration.

22
Q

What is the MOA of amiodarone? And name two adverse effects?

A

Decreases SA node automaticity and decreases AV node conduction velocity. Bradycardia and blue-grey discolouration.

23
Q

What is the MOA of Ibutilide and Dofetilide?

A

Block outward potassium channels selectively. These channels repolarise myocardial tissue during phase 3 of the action potential

24
Q

What is the MOA of Class IV drugs and give an example?

A

NDHP block slow inward calcium current during phase 0 and 2 of the cardiac cycle. They mostly target the L-type calcium channels.

25
Q

List 3 adverse effects of Class IV drugs

A

Cardiac depression, constipation and hypotension

ZCP302 (7 decks)

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