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Sketchy Pharmacology Notecards > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

What are the different phases of cardiac action potential?

A

Phase 0 - upstroke indicated by NaPhase 2 - plateau dictated by Ca2+Phase 3 - repolarization dictated by K+Phase 4 – resting membrane potential

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2
Q

What are the different classes of anti arrhythymatics.

A
  • Class I - Na channel blockers
  • Class II - Beta blockers
  • Class III - K channel blockers
  • Class IV - non dihydropyridine Ca channel blockers
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3
Q

What are the use of these different classes of antiarrythymics?

A

Class I and IIIare used for rhythym control and affect the cardiac AP at the atrias, ventricles and the His-Purkinje system whereas Class II and IV are for rate control at the SA and AV node.

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4
Q

How does Class I antiarrythymics exhibit their MOA?

A

Na channel blockers so they reduce the velocity of the upstroke of AP in atria and ventricles, hence slows the AP.This leads to decrease automaticity of ectopic pacemaker and reduce excitability of cardiac tissues.

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5
Q

What kind of Na channels do class I antiarrythymics bind to?

A

Open or inactivated Na channels, they dont bind well to resting Na channels, as result they have use dependence properties which meanswhich means tissues undergoing frequent depolarization are the most susceptible to blockage by them

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6
Q

What are the effects of class I on SA and AV nodes?

A

NONE, does not effect funny Na current

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7
Q

ECG changes of class I drugs?

A

Widened QRS due to decrease CV of AP

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8
Q

Binding strength of 1A, 1B and 1C

A

IC>IA>IB

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9
Q

Examples of Class IA

A

QuninidineProcainamideDisopyramide

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10
Q

Properties of 1A

A
  • Intermediate binding affinity and intermediate use dependence
  • Also block K channels, prolong duration of phase 2, 3 and AP duration
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11
Q

What is an additional use of 1A?

A

Treats WPW syndrome – Wolf Parkinson White syndrome, type of supraventricular tachycardia, consist of extra signals passing through outside the AV node, block arrhythmias thru accessory pathway

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12
Q

What are the adverse effects of Qunidine?

A

Cinchonism and thrombocytopenia

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13
Q

What are the adverse effects of procainamide?

A

Causes drug induced lupus, also causes a decrease in inotropy at high concentrations so it can exacerbate HF

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14
Q

What are the adverse effects of disopyramide?

A

Exacerbate heart failure, at toxic concentrations this drug has anti inotropic effects

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15
Q

Adverse effects of all 1A?

A

QT prolongation - precipitates torsades arrhythmia and syncope.Anything that blocks K channels prolongs QT intervalIronically most of the anti arrythymics are also arrythymogenic, they can lead to the development of arrhythmias!

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16
Q

What are the examples of Class IB?

A

Lidocaine

Phenytoin -anti-epileptic that shows antiarrythymic properties Mexiletine

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17
Q

What are the properties of 1B?What are they particularly useful against?

A
  • Lowest binding affinity, modest effect on upstroke of AP
  • Decreased AP duration by decreasing phase 2 and 3 duration, preferentially affect ischemic or depolarized purkinje and ventricular tissue
    As a result they are more selective to ventricle cells and HIS Purkinge system, makes them useful in treating ventricular arrythymias and ischemic dead tissue
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18
Q

What is the most common cause of death post MI?What drug should be used?

A

Ischemia induced ventricular arrythymias, class IB antiarrythymics

19
Q

What are the adverse effects of class 1B?

A

Neurological (paresthesia, tremor, convulsions)

20
Q

What are examples of 1C?

A

Propafenone Flecainide

21
Q

What are the properties of 1C?

A
  • Strong binding affinity for Na+ channel – strong use dependence, drastic slowing of phase 0 upstroke
  • Do not affect cardiac AP duration since K channels are untouched
  • QRS is significantly prolonged
    Can be used to treat atrial fibrillation, they can maintain and restore normal sinus rhythym. Can also be used in ventricular and supraventricular arrhythymias
22
Q

What are the adverse effects of 1C?

A

Contraindicated in pts with history of structural or ischemic heart disease (proarrythmic effects) since these drugs tight bindly it may delay conduction speed that is out of proportion of the prolongation of the refractory period, this can lead to arrhythmias due to reentrant loops.

23
Q

Compare and contrast AP duration as a result of administering 1A, 1B and 1C antiarrhythmics.

A

Class 1A inhibit K channels as well so they significantly prolong the duration of APClass 1B has the least binding tendency to Na channels, they prolong the duration of the APClass 1C has NO effect on duration of AP!

24
Q

What are examples of Class II anti arrhythymatics?

A

Since they are beta blockers their ending is “-olol”
Esmolol -this is given IV to treat intra operative rather acute arrhythmias)
Metoprolol -cardio specific beta 1 antagonists
Propranolol andTimolol -Non selective beta 1 and beta 2 antagonist
Carvedilol -Partial alpha antagonist properties

25
Q

Explain the use of beta blockers as anti arrhythymics.

A

Block arrhythmia promoting adrenergic stimuli in the SA node, beta blockers decrease heart rhythym.

  • First line of treatment to control atrial fibrillation and atrial flutter
  • Prevent acute supraventricular arrythymias
  • Prevent rapid ventricular response.
26
Q

What is rapid ventricular response and what specific drug is used to treat this?

A

Rapid ventricular responsehappens when there are too many signals coming from the atria to the AV node, in response to all these signals the AV node causes tachycardia, this process is called rapid ventricular response.A specific beta blocker that is used for this purpose is metoprolol – it prevents ventricular response to atrial fibrillation and flutter. However it is important to know that this does not fix the cause of atrial fibrillation, hence it is only used for rate control.

27
Q

What are the adverse effects of beta blockers?

A

Heart block and bradyarrhythmias

28
Q

Examples ofClass III Antiarrythymics.

A 
Potassium channel blockers, ends with"-tilide"	
Sotalol - also a beta blocker and also a Class III anti arrythymic	Dofetilide	Ibutilide	
Amiodarone* - shares properties of class I, II, III, and IV, it also blocks Na channels, it also has weak beta adrenergic and Ca channel blocking effects.
29
Q

What are the effects of class III?

A

Block K channels –> prolonging phase 2 and 3 of cardiac action potential –> prolonged refractory period

30
Q

What are class III used for?

A

Can be used for all three: atrial fibrillation/atrial flutter, ventricular arrhythymia and supraventricular arrhythymia

31
Q

What class does Amiodarone belong to?

A

Shares properties of class I, II, III, and IV, it also blocks Na channels, it also has weak beta adrenergic and Ca channel blocking effects

32
Q

What are the side effects of amiodarone?

A
  • Neurological - tremor, ataxia, peripheral neuropathy, sleep disturbances
  • Gray corneal microdeposits – theseusually asymptomatic Large amounts of iodine, this is because amiodarone is a iodine compound –> can cause hyper or hypothyroidism, needto do a thyroid test before starting patients on Amiodarone
  • Pulmonary fibrosis, can lead to restrictive lung disease, pulmonary fibrosis can be potentially fatal
  • Can cause heart block and heart failure
  • Hypersensitivity hepatitis – liver function tests have to be monitored
  • Gray-blue skin discoloration due to skin deposits
  • Photodermatitis
  • Inhibitor of CYP450 - increase concentrations of many drugs such as warfarin
  • Low incidence of Torsades* in contrast to others
33
Q

What are the side effects of sotalol, dofetilide, and ibutilide?

A

Induce torsades

34
Q

Examples ofClass IVAntiarrythymics.

A

DiltiazemVerapamil

35
Q

Examples ofClass VAntiarrythymics.

A
  • Digoxin
  • Magnesium
  • Adenosine
36
Q

Digoxin.

A
  • Digoxin - antiarrhythmic properties
  • Parasympathomimetic effects via direct stimulation of the vagus nerve –> AV nodal inhibition - similar to beta and calcium blockers
  • Treats atrial fibrillation (and flutter)
  • Prevents rapid ventricular response in atrial fib and flutter (rate control)
37
Q

Magnesium.

A

Magnesium - antiarrhythmics, treats torsades de pointes, even if the serum Mg levels are normal, Mg does this by interacting with a wide number of channels such as Na channels, K channels and Na-K ATPase

38
Q

Potassium

A

Potassium -Hyperkalemia - induces arrhythmias, ascending weakness and paralysis
* Peaked T waves with Shortened QT interval
Hypokalemia - induce arrhythmias,
* Severe muscle weakness, renal abnormalities, and glucose intolerance
* U waves at end of T wave
* Decreased T wave

39
Q

Where does adenosine exert its effect as an anti arrhythmic?

A

At A1 receptors found on myocardium and at SA and AV nodes, primary MOA is at the SA and AV nodes

40
Q

Explain adensoine’s MOA.

A

A1 receptor interaction -increases outward K+ current — Hyperpolarization, suppressed Ca2+ dependent AP at the SA and AV node.AV node is affected mostly, increases AV node refractory period.

41
Q

What is the main adverse effect of adenosine?

A

Can cause transient high grade heart block - direct AV node inhibiton - but short lived since t1/2 is only 10sDecreases AV conduction

42
Q

What is the no. 1 indication of adenosine?What is its other use?

A

TreatsSupraventricular arrhtymias – no.1 indication of adenosine is to treat Paroxysmal Supraventricular tachycardia to back to normal sinus rhythymVasodilator, increases coronary dilation (mediated by binding to A2 receptors) - helpful in cardiac testing

43
Q

What drugs strongly interfere with adenosine MOA?

A

Adenosine’s actions are inhibited by caffiene andtheophylline (methylxanthines)

44
Q

What are other side effects of adenosine?

A
  • Cutaneous flushing
  • Shortness of breath
  • Chest pain
  • Impending sense of doom
  • Headache
  • Hypotension

Sketchy Pharmacology Notecards (14 decks)

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