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Pharmacology > Cardiac Arrhythmia Drugs > Flashcards

Cardiac Arrhythmia Drugs Flashcards

1
Q

Draw and label the cardiac action potential and the SAN potential. Where do each class of anti-arrhythmias act?

A

–

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2
Q

What do you want to do if there if abnormal conduction?

A
  • Decrease conduction velocity (beta blockers etc.)

* Increase effective refractory period (potassium channel blocker)

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3
Q

Describe how arrhythmias occur

A

Abnormal impulse generation:
Automatic rhythms - sinus tachycardia (enhanced normal automaticity increased AP from SA node), ectopics )AP arises from site other than SA node)
–> beta blockers of CCBs that affect automaticity
Triggered rhythms
- Delayed after depolarisation - arising from the resting potential
- Early after depolarisation - prolonged plateau - arises from plateau

Abnormal impulse conduction
Conduction block
Re-entry
Abnormal anatomic conduction -WPW

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4
Q

What are atria arrhythmias?

A
  • Atrial fibrillation – chaotic re-entrant impulse conduction through the atrium leads to fibrillation rather than coordinated contraction of the atria, and irregular conduction to the ventricles.
  • Atrial flutter – not all impulses are conducted to the ventricles as they arrive during the refractory period – conduction ratio is 2:1 (atrial rate is 280-300 bpm)
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5
Q

What is paroxysmal SVT?

A

atrial firing rates of 140-250 beats per minute due to re-entry circuits

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6
Q

What is ventricular fibrillation

A

chaotic re-entrant impulse conduction through the ventricle which is invariably fatal if not converted back

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7
Q

What is ventricular tachycardia?

A

Ventricular tachycardia is ventricular extrasystoles at a rate of 100-250 beats per minute

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8
Q

What is Torsades de pointes?

A

Torsades de Pointes is generated by afterdepolarisations in people with long QT syndrome, leads to QRS complexes of varying amplitudes.

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9
Q

What is re-entry?

A

Impulses travel one way and are blocked by scar tissue and so backfire creatine a secondary depolarisation

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10
Q

What are the classes of anti-arrhythmic drugs? Examples

A

1: Na channel blockers (A Quinidine/B Lidocaine/C Flecanide)
2: Beta blockers (propanolol, atenolol)
3: Potassium channel blockers (amiodarone)
4: Calcium channel blockers (verapamil, diltiazem)

Not Beating Properly Cardio

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11
Q

What are class 1 anti-arrhythmias? How do they work?

A

Sodium Channel blockers

• Decrease automaticity in the SAN
o Decrease the slope of the funny current in the SAN
o Make the threshold more positive in the SAN

• Decrease re-entry circuits in ventricular myocytes
o Decreasing the upstroke velocity in phase 0 (slows conduction velocity)
o Prolongs repolarisation (minor effect)

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12
Q

What are the subtypes of Na channel blockers?

A

There are three subtypes of sodium channel blockers based on the effect they have on phase 0 of the ventricular action potential

1A: Moderate effect on upstroke
1B: No effect on upstroke
1C: marked effect on upstroke

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13
Q

Examples, MOA, Uses, ADRs of class 1A? ECG changes?

A

Na channel blcokers
Quinidine, procainamide

Moderate affect on phase 0
Decrease conduction and increase refractory period whilst also decreasing automaticity
Increases with of QRS and QT interval

Uses:
o Quinidine is used to:
• maintain sinus rhythm in AF and flutter
• prevent recurrent tachycardia and fibrillation
o Procainamide
• Acute treatment of supraventricular and ventricular arrthymias

ADRs:
Hypotension, 
Torsades de pointes because of long QT
Dizziness
Confusion 
Seizures
GI disturbance
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14
Q

Examples, MOA, Uses, ADRs of class 1B? ECG changes?

A

Lidocaine (IV only)

Increase threshold but no change on phase 0
No change to ECG

Uses: use dependent blockade so more useful in diseased tissue
• Ventricular tachycardia and fibrillation (especially post MI)
• NOT USED in atrial arrthymias

ADRs: Dizziness and drowsiness

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15
Q

Examples, MOA, Uses, ADRs of class 1C? ECG changes?

A

Flecanide
Reduces phase 0 and automaticity whilst increasing refractory period
Increases PR, QRS, QT on ECG

Uses: Supraventircular arrhythmias ( AF, flutter) WPW, premature ventricular contraction

ADRs:
• Proarrthymia and sudden death – don’t use in MI or ischaemia (Shown by CAST trial)
• Increase ventricular response to supraventricular arrthymias
• CNS and GI effects

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16
Q

Examples, MOA, Uses, ADRs of class 2? ECG changes?

A

Propanolol, atenolol, esmolol

Block B1 receptors
• Decrease automaticity in the SAN
o Decreases the slope of the funny current
• Decreases conduction velocity and increases refractory period at the SAN
o By reducing potassium and calcium currents

Increase PR interval and decrease HR

o Uses:
• Sinus tachyarrthymias
• Catecholamine dependent tachyarrthymia
• Converting re-entrant arrthymias in the AV node
• Protecting the ventricles from high atrial rates

o ADRs:
• Bronchospasm
• Hypotension
• Don’t use in AV block or acute heart failure!

17
Q

Examples, MOA, Uses, ADRs of class 3? ECG changes?

A

Amiodarone, sotalol

Block K channel to increase refractory period, raise threshold and decrease speed of AV conduction.
• Increases duration of action potential + prolonged repolarisation

PR, QRS and QT prolong, HR slows

o Uses:
• Amiodarone does everything (classes 1-4 + alpha blocker) – so is very broad spectrum

o	ADRs (increase with time)
•	Pulmonary fibrosis
•	Hepatic injury (leads to DDIs – take care with warfarin and class 1)
•	Increased LDLs
•	Thyroid disease
•	Photosensitivity

o Sotalol
• Wide spectrum – SVT and ventricular tachycardia
• ADRs: proarrthymia, fatigue, insomnia

18
Q

Examples, MOA, Uses, ADRs of class 4? ECG changes?

A

Verapamil, Diltiazem

Blocking Ca channels increase refractory period in AV node and changes slow in SAN to slow heart rate

PR increase on ECG

o Uses:
• Control ventricles during SVT + convert SVT

o	ADRs:
•	Caution with partial AV block
•	Asystole if given with beta blocker
•	Not good with hypotension or reduced cardiac output
•	GI disturbance
19
Q

What is adenosine? MOA, use?

A

Given as a rapid IV bolus – binds A1 receptors and activated potassium channels, activates K channels in SAN and AVN and leads to hyperpolarisation.
Increases refractory period, which slows AV conduction.

It terminates re-entrant rhythms by stopping ventricular contraction and slows AV conduction.

Used to convert re-entrant supraventricular arrthymias and hypotension during surgery

20
Q

Digoxin MOA, uses?

A

Enhances vagal activity which slows AV conduction and slows heart rate. Used to treat AF and atrial flutter

21
Q

Atropine MOA/use?

A

Selective muscarinic antagonist – blocks vagal activity and increases heart rate, treats vagal bradycardia

Pharmacology (24 decks)

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