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CPR Pharm > Anti Arrhythmic Drugs - Konorev > Flashcards

Anti Arrhythmic Drugs - Konorev Flashcards

1
Q

Fast action potential is seen in ?

A
  • Ventricular Contractile cardiomyocytes
  • Atrial Cardiomyocytes
  • Purkinje Fibers
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2
Q

Slow action potential is seen in…?

A
  • Sinoatrial Node

- Atrioventricular Node cells

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3
Q

What is the order of Action potential in Fast AP? What is Phase 0

A
  • 0, 1, 2, 3, 4
  • Phase 0 is the upstroke and is voltage-dependent fast Na+ channels opening from depolarization as Na+ enters the cell down its chemical gradient
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4
Q

What is the order of action potential in Slow AP? what is Phase 0?

A
  • Phase 4, 0, 1, 2, 3
  • Phase 0 is upstroke the Ca2+ influx throughout relatively slow L type (long acting) Ca 2+ channels
  • Phase 4 consists of poorly selective in flux of Na+ and K+ pacemaker current If that is activated by hyper polarization and slow Ca2+ influx through T type Ca2+ channels
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5
Q

What are the class 1A antiarrythmics? (3)

A
  • Quinidine
  • Procainamide
  • Disopyramide
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6
Q

What are the class 1B anti arrhythmic drugs?

A
  • Lidocaine

- Mexiletine

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7
Q

What are the class 1C antiarrythmic drugs

A
  • Flecainide

- Propafenone

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8
Q

What is the action of Class 1A antiarrhythmics?

A
  1. Block sodium channels (slow impulse conduction and reduce automatism of pace makers0 –> Reduce phase 0 and Prolong QRS in ECG
  2. Block potassium channels –> prolong action potential duration and prolong QT interval ECG
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9
Q

What does Procainamide do?

A
  • Class 1A
    1. Blocks Sodium Channels
    2. Antimuscarinic Activity
    3. Hypotension–> ganglion-blocking properties that reduce peripheral vascular resistance
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10
Q

Is Procainamide used frequently?

A

No, needs a frequent dose and has lupus-related side effects

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11
Q

What is the clinical use of procainamide?

A
  • not first choice

- used in sustained ventricular tachycardias and arrhythmias associated with myocardial Infarctions

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12
Q

What are the adverse effects of Procainamide?

A
  • QT interval prolongation –> induction of Tornado de pointes arrythmias
  • syncope
  • Lupus with Arthritis, pleuritic, pulmonary disease, hepatitis, fever
  • hypotension
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13
Q

What are the actions of quinidine?

A

Class 1A
-Sodium channel blocker

  • antimuscarinic effect on heart–> can enhance AV conductance
  • Hypotension–> Tachycardia
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14
Q

Is quinine used often?

A

no, there are better antiarrhythmics

- has cardiac and extracardiac adverse effects

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15
Q

What are the adverse effects of quinidine?

A
  • QT interval prolongation–> induction of torsade de pointes, arrhythmia, and syncope
  • GI side effects (diarrhea, nausea, vomiting)
  • Tinnitus, hearing loss, confusion, delirium, disturbances in vision, and psychosis (cinchonism)
  • Thrombocytopenia, hepatitis, fever
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16
Q

What is the action of Disopyramide?

A
  • Sodium channel block

- antimuscarinic on heart

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17
Q

What is the clinical use of Disopyramide

A

Recurrent ventricular arrhythmias

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18
Q

What are the adverse effects of Disopyramide?

A
  • Prolonged Qt, induction or torsades de pointes arrythmia and syncope
  • Negative inotropic effect –> may precipitate heart failure
  • Atropine-like symptoms - tachycardia, urinary retention, dry mouth, blurred vision, constipation, exacerbation of glaucoma
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19
Q

What is the mechanism of class 1B drugs

A
  • block sodium channels -> decreased phase 0 slope

- more specific and do not potassium channels –> do not prolong action potential or QT duration on ECG

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20
Q

How is class 1B lidocaine administered?

A

only IV because extensive first pass metabolism

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21
Q

What is the the clinical use of lidocaine?

A

termination of ventricular tachycardia in the setting of acute myocardial ischemia

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22
Q

What are the adverse effects of lidocaine

A
  • least toxic of class 1 drugs-> pro arrhythmic effects are uncommon
  • may cause hypotension in heart failure patients->inhibit cardiac contractility
  • Neuro side effects -> paresthesias, tremor, slurred speech, convulsions
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23
Q

What is the mechanism of mexiletine?

A

orally active congener of lidocaine

- has electrophysiological and antiarrhythmic effects similar to lidocaine

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24
Q

What are the adverse effects of mexiletine?

A
  • tremor
  • blurred vision
  • nausea
  • lethargy
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25
Q

What are the actions of Class 1 C drugs

A
  • block Sodium channels-> slow impulse conduction
  • block certain potassium channels
  • do not prolong Qt interval
  • Prolong QRS interval
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26
Q

What class is flecainide?

A

Class 1C

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27
Q

What are the clinical uses of Flecainide?

A
  • Normal patients that have supra ventricular arrhythmias

- Refractory ventricular arrhythmias that are life threatening

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28
Q

What are the adverse effects of Flecainide?

A

Ventricular arrhythmia exacerbation in paths with preexisting ventricular tachyarrhythmias

  • Patients with a previous MI
  • patinets with ventricular ectopic rhythms
  • contraindicated with hx of structural or ischemic heart disease (healthy hearts only)
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29
Q

What class is propafenone?

A
  • sodium channel blocking kinetics similar to flecainide

- possesses weak beta blocking activities

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30
Q

What is the clinical use of propafenone

A

supra ventricular arrhythmias in patients without structural disease

Healthy Hearts only

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31
Q

What are the adverse effects of Flecainide and propafenone?

A

exacerbation of ventricular arrhythmias

-esp pass with preexisting tachyarrhythmias, MI, or ventricular ectopic rhythms

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32
Q

What are the class 1C antiarrhtymic drugs?

A

Propafenone and Flecainide

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33
Q

What are class 2 anti arrhythmic drugs?

A

Beta Blockers

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34
Q

What are the antiarrhytmic actions of beta blockers?

A

SA node–> decrease HR and increase RR interval
AV node–>Decrease AV conductance and increase PR interval

There is a decreased response to polarization

  • increased threshold from the effect on L-type Ca2+ channels
  • decreased slope from the effects on Funny sodium and T-type Ca channels
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35
Q

What beta blocker is used for

  • arrhythmias from stress/thyroid storm
  • atrial fibrillation and flutter
  • paroxysmal supraventricular arrhythmias
  • arrhytmias associated with MI–> to decrease Motality in patients with MI
A

Propanolol

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36
Q

What are the properties of esmolol?

A

It is a short acting selective beta 1 blocker

  • has a short half life
  • used in IV form–> rapid onset followed by response termination
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37
Q

What are the clinical uses of esmolol?

A

IV Class 2 beta blocker

  • supraventricular arrhythmias
  • arrhythmias associated with thyrotoxicosis
  • myocardial ischemia or acute myocardial infarction with arrhythmias
  • Used with general anesthesia to control arrhythmias in preoperative period
38
Q

What are the adverse effects of Beta blockers

A
  1. Reduced Cardiac Output
  2. Bronchoconstriction
  3. Impaired glucose mobilization
  4. increased VLDL and decreased HDL (BAD)
  5. Sedation, depression,
  6. Withdrawal syndrome associated with sympathetic hyperresponsivness
39
Q

What are the contraindications of beta blockers?

A
  1. Asthma
  2. Peripheral vascular disease
  3. Raynauds
  4. Type 1 diabetics on insulin
  5. Bradyarrhythmias and AV conduction abnormalities
  6. Severe depression of Cardiac function
40
Q

What are the class 3 Antiarrhytmic drugs?

A
  1. Amiodarone
  2. Sotalol
  3. Dofetilide
  4. Ibutulide
41
Q

How do class 3 anti arrhythmic drugs affect action potential?

A
  1. block potassium channels
  2. prolong AP
  3. Prolong QT interval
  4. Prolong refractory period
42
Q

What is the clinical uses of Class 3 amiodarone?

A
  1. Recurrent ventricular tachycardia

2. Atrial fibrillation

43
Q

What are the pharmacodynamic properties of Class 3 Amiodarone

A
  • blocks potassium channels
  • prolongs QT interval and APD
  • blocks inactivated sodium channels
  • has adrenolytic activity
  • has calcium channel blocking activity
  • causes Brady cardia and slows AV conduction
44
Q

What are the adverse side effects of amiodarone?

A
  • AV block and bradycardia
  • incidence of torsades (lower risk than other class 3 drugs)
  • hepatits
  • fatal pumonary fibrosis
  • Photodermatits -> glue/grey skin discoloration
  • optical neuritis
  • blocks peripheral conversion of thyroid hormones–> hyper or hypothyroidism
45
Q

What class is sotalol?

A 
Class 2 non selective beta blocker
- class 3 agent--> prolongs action potential duration
46
Q

What is the clinical use of sotanlol?

A
  • life threatening ventricular arrhythmia

- maintenance of sinus rhythm in patients with afib

47
Q

What are the adverse side effects of sotalol

A
  • depression of cardiac function

- provoke torsades de pointes

48
Q

How do class 3 dofetilide and ibutilide work?

A

block there rapid component of delayed rectifier potassium current (repolarization)

49
Q

What is the clinical use of dofetilide

A

maintain sinus rhythm after cardio version in patients with Afib

50
Q

What are the adverse effects of Dofetilde and Ibutilide

A

QT interval prolongation and increased risk of ventricular arrhythmias

51
Q

What are the clinical uses of defetilide and ibutilide

A
  • restore sinus rhythm in patients with a fib
52
Q

What type of cells to class 4 drugs act on?

A

Cells that exhibit pacemaker potential –>

  • decrease slope of phase 0
  • increase L-type Ca2+ channel threshold potential
53
Q

How do Class 4 anti arrhythmic drugs work?

A
  • Block L type calcium channels
  • Slow sinoatrial node depolarization to reduce heart rate
  • prolong conduction and refractory period in the AV node
54
Q

What are the 2 class 4 drugs ?

A

Verapamil and diltiazem

55
Q

What are the clinical uses of class 4 verapamil and diltiazem?

A
  1. termination and prevention of paroxysmal supraventricular tachycardia cardia
  2. Ventricular rate control in A fib and flutter
56
Q

What are the Adverse effects of Verapamil and diltiazem?

A
  1. Cardiac–> Negative inotropy, Av block, sinoatrial node arrest, Bradyarrhythmias, hypotension
  2. constipation (verapamil)
57
Q

What anti arrhythmic is used to provide rapid relief of paroxysmal supraventricular tachycardia?

A

adenosine -> brings it to sinus rhythm rapidly and is given intravenously

58
Q

What are the adverse effects of adenosine?

A

-SOB
-Bronchoconstriction
-chest burning
-AV block
Hypotension

59
Q

How does adenosine work as an anti arrhythmic?

A

activates A1 adenosine receptor (GPCR Gi)

  • enhances potassium current and inhibits Ca2+ and funny currents–> causes hyperpolarization and suppression of pacemaker cell AP
  • Inhibits AV conduction and increases AV nodal refractory period
60
Q

What was the result of CAST (cardiac arrhythmia suppression trial) trial with Flecainide and other Class 1 C drugs

A

trial was stopped because it increased mortality by 2.5 fold

  • is a proarrhythmia because it induced a significant new arrhythmia or worsened an existing one
61
Q

What is a proarrhythmia?

A

drug induced siginificant new arrhythmia or worsening of an existing arrhythmia

62
Q

What is the clinical approach to treating arrhythmias?

A
  1. Eliminate the cause
  2. Make a firm diagnosis
  3. Consider underlying cardiac conditions and comorbidities
  4. Consider nonpharmacological therapy of arrhythmias
63
Q

What are non pharmacological approaches to cardiac Arrhythmia treatment?

A
  1. Catheter ablation
  2. implantable cardioverter-defibrillator
  3. artificial cardiac pace maker
  4. direct current cardioversion
64
Q

How can class 1A and class 3 drugs trigger fatal arrhythmias?

A

Class 1A and Class 3 excessively slow repolarization–> can cause torsades de pointes

65
Q

How do class 1A and 1C drugs trigger fatal arrhythmias?

A

cause excessive conduction slowing–> persistent ventricular tachycardias

66
Q

When should pharmacotherapy be used for cardiac arrhythmias?

A
  • alleviate weakness and fatigue–> improve quality of life
  • prevent deterioration of hemodynamics -> low cardiac output, hypotension, and syncope
  • minimize risk of sudden cardiac death associated with certain types of arrhythmias
67
Q

What is atrial fibrillation?

A

organized atrial contraction is lost–> reduced left ventricular filling

68
Q

What are the sx of Afib?

A
  • fatigue, weakness, decreased exercise tolerance
  • hypotension
  • pulmonary congestion
  • exacerbation of heart failure
69
Q

What is renentry?

A

type of arrhythmia in which one impulse enters and excites areas of the heart more than once

70
Q

How would you describe the electrical impulse conduction in Afib?

A

rapid irregular erratic rhythm with a disorganized atrial activation 350-600bpm
- ventricular rate is 120-180 bpm depending on AV conductivity

71
Q

What is rhythm control in A fib tx?

A

rhythm control is conversion to sinus rhythm through cardioversion (direct or chemical -Class 1C or 3)

72
Q

What drugs help to maintain sinus rhythm in AF patients with minimal heart disease

A
  1. Catheter ablation
  2. Sotalol
  3. Amiodarone
  4. Dofetilide
  5. Flecainide
  6. Propafenone

Class 1C and Class 3

73
Q

What tx maintains sinus rhythms in AF pts with structural disease

A
  1. Cateter ablation
  2. Sotalol
  3. Amiodarone
  4. Dofetilide

Class 3

74
Q

If a patient with AFib can not be treated with direct cardio conversion and has no HF and LVEF greater than 40%, what are the treatment options?

A
  1. Amiodarone
  2. Dofetilide
  3. Flecainide
  4. Ibutilide
  5. Propafenone
75
Q

If a patient with AFib can not be treated with direct cardio conversion and has HF and LVEF less than 40%, what are the treatment options?

A

Amiodarone
Dofetilide
Ibutilidte

76
Q

What is the tx strategy for someone with Paroxysmal/persistent AF without HF, and LVEF >40%

A
  1. CCB or beta blocker
  2. CCB and dioxin or beta blocker and digoxin
  3. Amiodarone
77
Q

What is the Tx strategy for pt with paroxysmal or persistent AF with HF and LVEF <40%

A
  1. beta blocker
  2. Beta blocker and digoxin
  3. Amiodarone
78
Q

What is Paroxysmal supraventricular tachycardia mechanism?

A
  • dual properties in AV node have heterogenous electrophysiologic properties (fast and slow conducting_ to allow for rentry circuit formation
79
Q

What are the symptoms of Paroxysmal supraventricular tachycardia?

A

abrupt onset of palpitations

  • dizziness
  • lightheadedness
  • dyspnea
  • chest pain
80
Q

What forms a reentry circuit?

A

Anterograde conduction through the slow pathways

retrograde conduction through the fast pathways

81
Q

What does the egg look like for Paroxysmal supraventricular tachycardia? (PSVT)

A

Narrow QRS complex tachycardia, P wave inverted or not seen because atrial depolarization occurs simultaneously with ventricular depolarization

82
Q

How do you treat Paroxysmal supraventricular tachycardia initially?

A
  1. vagal maneuvers

2. Adenosine

83
Q

How do you treat PSVT with LVEF > 40% or no hx of HF

A
  1. Diltiazem or verapamil
  2. Beta blocker
  3. Digoxin
84
Q

How do you treat PSVT with LVEF<40%/ HF

A
  1. Digoxin
  2. Amiodarone
  3. Diltiazem
85
Q

What is used to prevent PSVT episodes?

A
  1. Catheter ablation
  2. CCB ( Verapamil and Diltiazem)
  3. Betablocker (Metoprolol, Atenolol, Propanlol)
86
Q

What is Torsade de Pointes?

A

-Rapid for of polymorphic VT that occurs in setting of prolonged ventricular depolarization (long QT)

87
Q

What are the clinical manifestations of Torsades?

A

-HR 160-250
-Palpitations, dizzy, light headed
-hypotension, hemodynamic collapse, syncope
sudden cardia death
- egg looks like twisting of points

88
Q

What causes acquired long QT syndrome?

A
  1. Prolonged AP duration ( slow HR- sinus Brady or AV block and Electrolyte abnormalities hypokalemia and hypomagnesium)
  2. Drugs (especially 1A and 3
89
Q

What does QT interval represent?

A

The time it takes the ventricle to contract in systole

90
Q

What does PR interval represent?

A

The time between atrial and ventricular depolarizaiton

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