Pharmacology - Heart Flashcards

1
Q

Explain the conduction pathway in the heart

A

SA Node excitation

AV Node excitation

HIS Bundle and Branches

Purkinje Fibres

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2
Q

What does each part of an ECG mean?

A

P Wave –> Depolarisation of the atria

QRS Complex –> Depolarisation of the ventricles

T Wave –> Repolarisation of the ventricles

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3
Q

Why can the pacemaker of the heart undergo spontaneous depolarisation?

A

Because its 4th phase has no true baseline (creaps upwards)

This is due to sodium influx via hyperpolarisation-activated, cAMP-gated, non-selective channels (funny channel)

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4
Q

What occurs at the 4 (5) phases of the Cardiac Action Potential?

A

Phase 0 –> Rapid depolarisation

Due to rapid sodium influx via voltage-activated Na+ channels

Phase 1 –> Rapid repolarisation

Phase 2 –> Plateau

Due to slow Ca2+ influx via L-type channels, and efflux via K+ channels (both voltage-gated)

Phase 3 –> Repolarisation

Due to increased K+ efflux via voltage-gated K+ channels

Phase 4 –> Stable baseline

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5
Q

What’s the difference between an Absolute and an Relative refractory period?

A

Absolute/Effective –> When a second AP isn’t possible regardless of the strength of the stimuli (as phase 0 can’t be reached)

Relative –> If a very strong stimulus is created, then a second AP can be caused

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6
Q

How is the if ‘funny’ channel modulated?

And what drug inhibits it?

A

Stimulates –> Sympathetic NS via B1/2 receptors

Inhibits –> Parasympathetic (vagus nerve) NS via M2 receptors

Ivabradine

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7
Q

What are Channelopathies?

A

Cardiac ion channel genetic diseases

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8
Q

What are the classifications and types of Cardiac Arrhythmias?

A

Site of Origin in the Heart

Supraventricular (SAN/AVN/Atria)

Ventricular (HIS Bundles/Purkinje Fibres/Ventricles)

Effect on the Heart Rate

Bradycardia (below 60bpm)

Tachycardia/arrhythmia (above 100bpm)

Effect on the Heart Rhythm

Regular

Irregular

The type of QRS complex

Narrow

Broad (>120ms in duration of the ECG)

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9
Q

What can cause Cardiac Arrhythmias?

A

Existing heart diseases/myocardial iscaemia

Drugs –> eg, digoxin

Electrolyte disturbances (K+/Ca2+)

Hyper/hypothyroidism

Phenocrymocytoma (increased circulating catecholamines)

Genetic disorders –> eg, channelopathies

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10
Q

What different parts of the heart do Rate controlling and Rhythm controlling drugs act on?

A

Rate Controlling –> The Pacemaker AP

Rhythm Controlling –> The Cardiac AP

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11
Q

What is the Vaughan Williams Classification of antiarrhythimic drugs?

A

Class 1 –> Sodium channel blockers (preventing depolarisation….phase 0)

Class 2 –> Beta-Blockers (inhibits phase 2 and 4)

Class 3 –> Drugs that prolong the AP duration (inhibits repolarisation…..phase 3)

Class 4 –> Calcium Channel Blockers (inhibit the plateau….phase 2)

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12
Q

Explain Class I antiarrhythmic drugs

A

Sodium channel blockers –> so slow down depolarisation (phase 0)….and so the cardiac AP and AP conduction

There are 3 different types

1a (Disopyramide) –> Intermediate dissociation rate

Also block K+ channels, so prolong the QT interval (phase 3)

1b (Lidocaine) –> Fast dissociation rate

1c (Flecanide)–> Slow dissociation rate

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13
Q

How do Beta-Blockers (Class II) work?

A

Block B1-adrenoceptors

Slow conduction of at the AV node

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14
Q

How do class III drugs, like amiodarone, work?

A

Block voltage-activated K+ channels, preventing repolarisation in phase 3

So they prolong the duration of the cardiac AP and the QT interval –> Increasing the refractory period….so slowing the HR

Also blocks Na+, Ca2+ channels

Decreases expression of B1-adrenoceptors

A modest A-adrenergic receptor antagonist

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15
Q

What Beta-Blocker is also a Class III drug?

A

Sotalol

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16
Q

What is Sick Sinus Syndrome?

And what is the solution?

A

A group of heart rhythm disorders due to the misfunction of the SAN

  • Sinus pause
  • Sinus arrest (pause for over 3 seconds)
  • Bradycardia-Tachycardia syndrome

Solution = Implantable transcutaneous pacemaker (TCP)

17
Q

What’s The AV Block?

A

There are 3 degrees….

1st –> Slowed AV conduction

2nd –> Missed beats to the venticles

Split into Mobitz 1 (progressive prolongation of PR intervals) and Mobitz 2 (no pattern)

3rd –> Complete block, so no conduction to the ventricles

18
Q

What type of tachyarrhythmia is Atrial Fibrillation (AF)?

A

Supraventricular tachycardia (SVT)

19
Q

What are the 2 different mechanisms of tachyarrhythmias?

A

Automaticity –> Enhanced (sympathetic overactivity) or Abnormal (ectopic pacemaker)

Triggered –> Re-entry…..Early-after-depolarisation (EAD)…..Delayed after-depolarisation (DAD)

20
Q

What is caused by Atrioventricular Nodal Re-entrant Tachycardia (AVNRT)?

A

Paroxysmal SVT

21
Q

How does Ventricular Tachycardia (micro re-entry) occur?

A

Similar to AVNRT (re-entry), but occurs in the ventricular myocardium and Purkinje fibres

22
Q

What is Wolff-Parkinson-White Syndrome?

A

Macro re-entry

Atrioventricular Reciprocating Tachycardia (AVRT), which is where there is re-entry via accessory pathways

23
Q

What are the factors that can promote EAD (early after-depolarisations) and DAD (delayed after-depolarisations)

A
24
Q

What’s the difference between AF and an Atrial Flutter?

A

AF –> Fast irregulaly irregular heartbeat

Atrial Flutter –> Fast regular heartbeat