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STEP Pathology > deck_5062812 > Flashcards

deck_5062812 Flashcards

1
Q

What is the electrophysiologic effect of Procainamide?

A

suppresses ectopic pacemaker activity in partially depolarized cells. reduces conduction velocity (reduced phase O APD). Also prolongs ActionPotential Duration (Class III activity).

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2
Q

When is Procainamide indicated?

A

Effective in atrial and ventricular conductive arrhythmias or for short-term treatment (i.e. postoperative atrial fibrillation). Little effect on normal SA, AV node automaticity

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3
Q

Side effects of Procainamide?

A

-drug induced lupus, (arthralgia, skin rash, pleural and pericardial effusions),-Torsades de Pointes. Prominent side effects limit long-term use. Only available acute IV

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4
Q

How is Procainamide metabolized?

A

undergoes hepatic metabolism (acetylation) and renal excretion of active metabolite (N-acetyl procainamide). 50% of population are slow acetylators (more likelyto develop lupus).

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5
Q

How is Procainamide given?

A

Available for IV use only (due to risk of lupus with prolonged PO use)  

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6
Q

What is Quinidine used for?

A

atrial, ventricular arrhythmias Dose-dependent QT prolongation/ Torsades de Pointe (blocks Ikr) and Ventricular Tachycardia /Fibrillation Quinidine   syncope (Class III activity)

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7
Q

Side effects of Quindine?

A

diarrhea, autoimmune thrombocytopenia.high incidence of side effects, concerns over pro arrhythmia have markedly limited its use (Orphan Drug)

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8
Q

Note about Disopyramide.

A

prominent vagolytic (atropine-like) effect leads to urinary retention, dry mouth, blurred vision) also negative inotropic effect may precipitate heart failure. Also rarely used.

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9
Q

What is the electrophysiologic effect of Lidocaine?

A

Binds to open and inactivated Na+ channels with rapid on-off kinetics (T/2 less than 1sec). Preferentially binds to Na+ channels in partially depolarized cells to suppress abnormal automaticity. won’t affect normal HR, only tachycardias

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10
Q

When is Lidocaine indicated?

A

Highly effective insuppressing acute ventricular tachycardia. NOT effective for atrial arrhythmias.  

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11
Q

How is Lidocaine metabolized?

A

orally absorbed but undergoes extensive first pass hepatic metabolism so only effective intravenously. Eliminated by hepaticbiotransformation.  

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12
Q

Side effects of Lidocaine?

A

CNS, agitation, confusion, seizures (easily missed in CCU).

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13
Q

What is Mexilitine?

A

Class IB AA like Lidocaine that is an orally effective analogue, but causes frequent GI distress, limiting use.

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14
Q

What is the electrophysiologic effect of Flecainide?

A

Potent, long-acting Na+ channel blocker (T/2 > 10seconds). Suppresses automaticity, increases effective refractory period in atria and ventricles. 

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15
Q

When is Flecainide contraindicated?

A

Contraindicated in patients with structural heart disease (i.e. CHF, valvular disease, etc.)! Proarrhythmic effect in patients with LV dysfunction, CHD, sustained VT.Increased Mortality post-MI in Coronary Arrhythmia Suppression Trial (CAST)

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16
Q

When is Flecainide indicated?

A

Mortality not increased in patients with supraventricular arrhythmias (afib, aflutter, PSVT) and no structural heart disease

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17
Q

What is Propafenone?

A

class IC agent with BBproperties. Also sees limited use in Afib, Aflutter in patients without structural heart disease. 

18
Q

What arrhythmias is propanolol used for?

A

Used to suppress VPBs related to sympathetic activity.lipid soluble, non-selective

19
Q

What arrhythmias is metoprolol used for?

A

Cardioselective (β1), Lipid soluble.Used to slow heart rate in supraventricular arrhythmias by blocking AV node.

20
Q

What arrhythmias is acebutolol used for?

A

Cardioselective, Intrinsic Sympathomimeticactivity (ISA). Used to suppress ventricular premature beats related to sympathetic activity.

21
Q

What arrhythmias is esmolol used for?

A

Cardioselective, ultra-short acting.Administered intravenously to slow AV node conductionfor acute treatment of supraventricular arrhythmias.

22
Q

What arrhythmias is atenolol used for?

A

Cardioselective, long acting, water soluble.Used for rate control in atrial flutter and atrial fibrillation and to prevent recurrence of PSVT.

23
Q

What is Amiodarine?

A

Class III AA consisting of iodine containing structural analogue of thyroid hormone. Interacts with nuclear thyroid hormone receptors

24
Q

MOA of Amiodarone?

A

– Primary: K+ channel blockade – Secondary: Na+ (IA), Ca2+ channel blockade, and β-adrenergic blocking properties.  

25
Q

What id Amiodarone useful for?

A

Highly effective in treatment of atrial, ventricular arrhythmias. IV amiodarone used for acute treatment of life-threatening arrhythmias (Ventricular Tachycardia, Ventricular Fibrillation). has replaced lidocaine as drug of choice in cardiac rescuscitation (ACLS).

26
Q

How is Amiodarone metabolized?

A

highly lipophilic, eliminated very slowly (T/2 20-100 days).Oral or IV loading dose needed for rapid onset of action. Metabolized by CYP3A4 (inhibits also) 

27
Q

Side effects of Amiodarone?

A

very common-Pulmonary fibrosis (5% incidence, fatal in 1 in 400 -treated with higher doses recommended for VT.  Photosensitivity Dermatitis (gray-blue skin) Corneal microdeposits (visual halos) hypothyroidism or hyperthyroidism  proximal muscle weakness, hepatitis

28
Q

What is Dronedarone?

A

a non-iodinated congener of Amiodarone has been approved for treatment of paroxysmal atrial fibrillation or maintenance of sinus rhythm following cardioversion.

29
Q

When is Dronedarone contraindicated?

A

It is contraindicated in patients with decompensatedcongestive heart failure.

30
Q

What is Sotalol?

A

K+ channel blocker and nonselective β-blocker (1/3 as strong as propranolol) with action potential prolongingcharacteristics (class III).

31
Q

What is sotalol used for?

A

treatment of atrial, ventricular, AV nodal reentrant arrhythmias including ventricular tachycardia.

32
Q

How is Sotalol metabolized?

A

excreted by kidney (dose adjustment needed for renal disease)

33
Q

When is Sotalol contraindicated?

A

QT interval >450 msec (baseline) or >500 msec (on treatment) Advanced renal insufficiency (CrCl less than 40 ml/min) Asthma or COPD decompensated CHF second or third degree AV block sinus bradycardia 

34
Q

Side effect of Sotalol?

A

Torsade de Pointe can occur in up to 3.1% of patients treated with Sotalol.

35
Q

What are the “pure” K+ channel blockers?

A

Dofetilide and Ibutilide

36
Q

Uses of the “pure” K+ channel blockers?

A

They do not have Class I, II or IV activity. Although they are likely effective in treatment of ventricular arrhythmias, they are primarily used to treat atrial arrhythmias (a fib).

37
Q

What is the major adverse effect of Dofetilide?

A

Polymorphic Ventricular  Tachycardia (Torsade de Pointe)

38
Q

When is Dofetilide contraindicated?

A

contraindicated in patients with long QT interval (>440 msec)

39
Q

What is Ibutilide used for?

A

IV Only. Indicated for acute termination ofatrial fibrillation or atrial flutter. Torsades de Pointes occurs in 3-8% of patients.  

40
Q

What is Torsades de Pointes caused by?

A

initiated by early after depolarization (EAD) in setting of prolonged QT

41
Q

Which drugs cause Torsades de Pointes?

A

Seen with K+ channel blocking antiarrhythmics (Class III)  [Sotolol, Ibutilide, Dofetilide, Amiodarone (rarely)] • Other drugs can also induce torsades (IKr blocking properties): – Tricyclic Antidepressants [Imiprimine (Tofranil®)] – Na+ channel blockers (Class 1: Quinidine, Procaineamide) – non-sedating antihistamines (Terfenidine) (withdrawn from market) • These drugs all have class III activity

STEP Pathology (80 decks)

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