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S4 Pharma CPT > Arrhythmia Drugs > Flashcards

Arrhythmia Drugs Flashcards

1
Q

What are the four classes of arrhythmia drugs?

A

1 - Na channel blocker
2 - beta blocker
3 - potassium blocker
4 - Ca blocker

‘No boys kick constantly’

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2
Q

What can calcium channel blockers be divided into? Give examples, boths mechanism of action and uses

A

Dihydropyridines:
E.g. amlodipine, felodipine
Acts selectively on vascular smooth muscle -> reduces systemic resistance and arterial pressures
Used in HTN (hypertension)

Non-dihydropyridines:
E.g. verapamil, diltiazem 
-ve inotrophic/ chronotrophic/ dromotrophic (force, rate, cardiac conduction velocity) 
Used in HTN, angina, arrhythmias
Don’t use with beta b (-> ❤️block)
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3
Q

What does each part of the ECG represent?

A 
P - contraction of atria 
PR segment (end of P to start Q) - through AVN 
QRS - contraction ventricles 
ST segment (end S to start T) - break 
T wave - depolarisation ventricles 
Also have PR interval (start of P to start Qj
QT interval (start Q to end of T)
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4
Q

What is an arrhythmia?

A

Heart condition where disturbances in pacemaker impulse formation &/or contraction impulse conduction -> rate &/or timing of contraction may be insufficient to maintain normal CO

E.g. bradycardia, tachycardia, atrial fibrillation, atrial flutter, PSVT, ventricular fibrillation, V-tachycardia, long QT syndrome, sinus node dysfunction, ❤️block

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5
Q

How is a transmembrane electric gradient maintained within the cardiac cells in which the interior of the cell is negative with respect to the outside of the cell?

A
  • Na+ higher outside
  • Ca2+ much higher outside
  • K+ higher INSIDE

(Salty caramelised banana)

-90mV resting potential

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6
Q

How is the ventricular/ cardiac action potential achieved?

A

RMP -90mV (mostly due to background Na/ K ATPase (3Na out, 2K in)

  1. V-gated Na+ channels open upstroke
  2. Transient outward K+ current
  3. V-gated Ca2+ channels open plateau (L-type)
  4. Ca2+ channels inactive, V-gated K+ channels open repolarisation
  5. Na/ K ATPase (3Na out, 2K in) -> RMP
  • Na influx
  • K+ efflux
  • Ca efflux
  • more K efflux

See slide 11

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7
Q

How is the SA node action potential achieved?

A

If funny current/ pacemaker potential activated at membrane potentials more negative than -50mv (more negative = more activates)
HCN channels:
1. Influx Na+ depolarises cell
2. V- gated Ca2+ channels influx upstroke
3. V- gated K+ channels efflux downstroke repolarisation

See slide 11

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8
Q

How does the SAN action potential lead to the ventricular/ cardiac action potential?

A

SAN APs -> increase in cytosol Ca2+ -> actin and myosin interaction -> contraction

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9
Q

How do class 1 anti arrhythmia drugs work?

A

Block Na channels in cardiac action potential so no influx of Na+ and

Marked slowing conduction in tissue (upstroke shifted right) - slide 13

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10
Q

How do class 2 antiarrhythmia drugs work?

A

Beta blockers

Decrease sympathetic drive -> reduces SAN/ AVN firing -> decrease Ca2+ influx into ❤️-> increase plateau duration & diminishes phase 4 depolarisation & automaticity

Slide 15

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11
Q

How do class 3 antiaarrhythmia drugs work?

A

Block K+ channels so extend refractory period (QT interval longer)
Increase AP duration (APD)

Slide 16

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12
Q

How do class 4 anti arrhythmia drugs work?

A

Calcium channel blockers

Decrease inward Ca currents -> decrease phase 4 spontaneous depolarisation (plateau phase lasts longer)

Slide 17

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13
Q

Mechanisms of arrhythmogenesis

A

Slide 22/ 23

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14
Q

How is Wolf- Parkinson white caused?

A

Heart beats abnormally fast for periods of time

Accessory pathway called bundle of Kent connects atria to ventricles so AP can re-enter (down purkinje fibres -> BOK -> atria)

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15
Q

Where can re-entry occur in everyone?

A

At the AVnode
50% of people have a fast and slow pathway, 50% just a fast pathway

Ectopic beat travels down part pathway -> refractory -> pushes rhythm back up other way -> creating circuit constant loop -> tachycardia

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16
Q

How can we get micro- reentries?

A

If patient has MI -> damaged imperfect tissue -> localised rentry within scar tissue -> ventricular tachycardia

17
Q

Which classes of drugs are used for abnormal generation and which for abnormal conduction and why?

A

Abnormal generation:
Decrease of phase 4 slope (in pacemaker cells) - reduces SAN/ AVN firing/ spontaneous depolarisation
E.g. class 2 beta blockers & class 4 Ca blockers

Abnormal conduction:
Decrease conduction velocity e.g. class 1 Na channel blockers slow depolarisation

Or increase effective refractory period so the cell won’t be reexcited again e.g. class 3 K channel blockers

18
Q

What is Vaughan-Williams classification? Give examples in each class

A

All 1 block Na
1a - moderate phase 0 e.g. Quinidine, procainamide
1b - no change in phase 0 e.g. lidocaine
1c - marked phase 0 e.g. Flecainide, propafenone

2 beta adrenergic blockers e.g. bisoprolol, metoprolol, propranolol

3 prolong repolarisation e.g. amiodarone, sotalol

4 Ca channel blockers e.g. Varepamil, diltiazem

19
Q

Class 1A agents, absorption and elimination, effects on cardiac activity, effects on ECG, uses, side effects

A

Procainamide, quinidine, disopyramide

Oral or IV

Decreased conduction (decreased phase 0 of AP) and automaticity (slope phase 4)

Increased refractory period and threshold

Quinidine - anticholinergic to speed up AV conduction used with digitalis, beta blocker or CCB

ECG: increased QRS, +/- PR, increased QT

Uses: quinidine - atrial fibrillation/ flutter, brugada syndrome

Procainamide - supraventricular/ ventricular arrhythmias

Side effects: hypotension, proarrhythmia, insomnia, GI, lupus like syndrome

20
Q

Class 1B agents, absorption and elimination, effects on cardiac activity, effects on ECG, uses, side effects

A

Lidocaine - IV
mexiletine - oral

Fast binding offset kinetics
No change phase 0 normal tissue
APD slightly decreased
Increased threshold

Decrease phase 0 conduction in fast beating/ ischaemic tissue

ECG: none in normal, in fast/ ischaemic increased width QRS

Uses: acute ventricular tachycardia

Side effects: less proarrhythmic, abdo upset

21
Q

Class 1C agents, absorption and elimination, effects on cardiac activity, effects on ECG, uses, side effects

A

Flecainide and propafenone

Oral or IV

Very slow binding offset kinetics

Decreased phase 0 normal tissue/ automaticity

Increased APD and refractory period

ECG: increased PR/ QRS/ QT

Uses: supraventricular arrhythmias, premature ventricular contractions, Wolff Parkinson white syndrome

Side effects: proarrhythmia, sudden death with chronic use, structural/ ischaemic heart disease increased ventricular response to supraventricular arrhythmias

22
Q

Investigations for atrial fibrillation pneumonic and causes

A

ATRIAL BP

Alcoholic liver disease - LFTs
Thyroid disease - T3/T4 
Rheumatic HD - Hx 
Ischaemic HD - Hx
Atrial myxoma - cancer 
Lung disease
BP 
Pherocromcytoma
23
Q

How to remember the names of cardioselective beta blockers

A

MANBABE

Beta 1

Metoprolol
Atenolol
Nebivolol
Bisoprolol
Acebutolol
Betaxolol
Esmolol

Mixed alpha beta - doesn’t end in olol e.g. carvediol, labetalol

Non selective: propranolol, nadolol

24
Q

Class 2 agents, absorption and elimination, effects on cardiac activity, effects on ECG, uses, side effects

A

Propranolol oral/ IV, bisoprolol oral, metoprolol IV/ oral, esmolol IV

Increased APD/ refractory period in AVN

Decreased phase 4 depolarisation

ECG: increased PR, decreased HR

Uses: sinus and catecholamine dependent tachycardia, reentrant arrhythmias, slow AV conduction in atrial fibrillation/ flutter

Side effects: bronchospasm, hypotension, don’t use partial av block or acute heart failure

25
Q

Class 3 amiadorone absorption and elimination, effects on cardiac activity, effects on ECG, uses, side effects

A

Amiodarone (sotalol)

Oral or IV

Increased refractory period and APD/ threshold

Decreased phase 0 and conduction/ phase 4/ speed of AV conduction

ECG: increased PR/ QRS/ QT, decreased HR

Uses: most arrhythmias

Side effects: pulmonary fibrosis, hepatic injury, increased LDL cholesterol, thyroid disease, photosesnsiitvy, optic neuritis

May need reduce digoxin and monitor warfarin

26
Q

Class 3 sotalol, absorption and elimination, effects on cardiac activity, effects on ECG, uses, side effects

A

Sotalol

Oral

Increased APD/ refractory period

Slow phase 4/ AV conduction

ECG: increased QT, decreased HR

Uses: supraventricular and ventricular tachycardia

Side effects: proarrhythmia, insomnia

27
Q

Class 4 agents, absorption and elimination, effects on cardiac activity, effects on ECG, uses, side effects

A

Verapamil - oral or IV
Diltiazem - oral

Slow conduction through AV
Increased refractory period AVN/ slope phase 4

ECG: increased PR, increased or decreased HR depending on blood pressure response

Uses: supraventricular tachycardia

Side effects: caution partial AV block can get asystole if beta blocker on board, hypotension, GI

28
Q

What’s Adenosines mechanism of action?

A

Natural nucleoside binds alpha 1 R activates K+ currents in AV/ SAN, increases APD, hyperpolarosation -> decreases HR Bc decrease CA currents more of an effect (increases refractory period AVN)

Slows AV conduction

29
Q

What’s vernakalants mechanism of action?

A

Blocks atrial specific K+ channels, slows atrial conduction, increases potency with higher heart rates

30
Q

Ivabradine mechanism of action

A

Blocks If ion current highly expressed in sinus node, slows sinus node but does not affect BP

31
Q

Digoxin mechanism of action

A

Enhances vagal activity increases K+ currents, decreases Ca currents, increases refractory period, slows AV conduction and HR

32
Q

Atropine mechanism of action

A

Selective muscarinic antagonist, blocks vagal activity to speed AV conduction and increase HR

S4 Pharma CPT (22 decks)

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