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S2B3: Pharm > Antiarrhythmic Agents II > Flashcards

Antiarrhythmic Agents II Flashcards

1
Q

Describe the effect of beta-adrenergic stiumlation of the atria & ventricles?

stimulation of the SA & AV nodes?

A
  • Atria & ventricles (stronger)
    • B stimulation of ICa-L via
      • cAMP –> PKA –> phosphorylation of CaL-type channels
      • increases the size of the action potential & plateau phase is lager b/c more calcium coming in
  • SA & AV nodes (faster)
    • B stimulatin of If & ICa-L
      • via CAMP –> PKA –> phosphorylation of funny & CaL-type channels
      • action potential becomes more frequent, the interval between the action potentials becomes more shorter, its easier to generate an action potential & the action potential is steeper
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2
Q

What is the general response of B-adrenergic receptor blockers in the AV node & the atria and venricles?

A
  • Slow AP conduction through AV node
    • SA & AV node: reduce B-stimulation of If to decrease HR
    • reduce B-stimulation of ICa-L to increase AP threshold in AV node
  • Reduce B-stimulation of cardiac contraction
    • reduce B-stimulation of ICa-L (phase 2) to reduce cardiac contraction
  • Other cardiac benefits
    • normalized Ca2+ handling, reduced SERCA phosphorylation to reduce Ca2+i overload
  • ** shown to reduce mortality in HF patients !!
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3
Q

What are the Antiarrhythmic Class I drugs?

A
  • Esmolol (IV only)
  • Metoprolol
  • Atenolol
  • Propranolol
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4
Q

What is is the mechism of action of beta-blockers?

A
  • Cardiac effect
    • Inhibit B-adrenergic receptor stimulation by SNS
  • This results in:
    • reduced If to slow SA node AP rate (HR)
    • reduced ICa-L to slow AV conduction velocity
    • suuppression of automaticity - suppress EADs (early after depolarizations)
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5
Q

What are the clinical uses for beta blockers?

A
  • Uses: most commonly prescribed drug class for CV disease
    • sinus tachycardia
    • supraventricular and ventricular tachyarrhythmias
    • atrial fibrillation: rate control
    • stable angina, hypertension, heart failure
    • reduces mortality following acute MI in HF
  • All patients with either HF or post MI will be on a B-blocker, if they can tolerate it
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6
Q

What are the physiologic responses to activation of B1 and B2 adrenergic receptors?

A
  • B1
    • Cardiac cells: increased heart rate adn contraction strength
    • juxtaglomerular cells (kidney): increase blood pressure
  • B2
    • Vasculat: dilate vessels
    • Bronchial: dilate bronchial tubes to open the airway
  • B-receptor agonists are commonly used to treat patients suffering from diseases that close the airway, namely asthma & COPD (chronic obstructive pulmonary disease)
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7
Q

What are the nonselective B-blockers?

What are the cardioselective B-blockers? What receptor are they selective for?

A
  • Nonselective B-blockers
    • both B1 and B2-adrenergic receptors
      • propranolol
  • Cardioselective B-blockers
    • more selective for B1-adrenergic receptors
      • Atenolol
      • Metoprolol
      • Esmolol
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8
Q

What are the common adverse effects of B-blockers?

A
  • Both cardioselective & nonselective
    • CV: bradycardia, heart block, hypotension, exercise intolerance
  • More common nonselective due to B2-blockers
    • Pulmonary: bronchospasm
    • Vascular: cold extremities, Raynaud’s phenomenon, claudication, and erectile dysfunction
    • Metabolic: excerbation of hypoglycemia in patients taking oral hypoglycemic agents or insulin, new onset diabetes
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9
Q

What type of drug is Propranolol?

Phamacokinetics?

Adverse effects?

A

Propranolol (nonselective B-blocker)

  • Pharmacokinetics
    • stron 1st pass metaboism, CYP2D6
    • Propranolol levels strongly increased by CYP2D6 blockers (e.g. quinidine, terbinafine)
    • Lipophilic: enters the bran well
  • Adverse effects: (additional)
    • CNS: nightmares, fatigue, depression
    • Pulmonary: bronchospasm (B2-receptor block)
    • Contraindicated in asthma & COPD patients
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10
Q

What type of drug is Metoprolol?

Phamacokinetics?

Adverse effects?

A

Metoprolol

Cardioselective - B1- adrenergic receptors

  • Pharmacokinetics
    • Metabolized by CYP2D6
    • plasma levels increase by CYP2D6 blockers (e.g. quinidine)
    • less lipophilic than propranolol
  • Adverse effects
    • less pulmonary effects due to low B2-receptors block
    • less metabolic & vascular effects dur to low B2-block
    • less CNS effects due to lower CNS penetration
    • Cardiac adverse effects due to bock of B1-receptors block
      • bradycardia, heart block, hypotension, exercise intoerance
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11
Q

What type of drug is Atenolol?

Phamacokinetics?

Adverse effects?

A

Atenolol

(cardioselective - B1-adrenergic receptors)

  • Pharmacokinetics
    • excreted by the kidney unchanged
    • less potential drug-drug interaction than metoprolol
    • Plasma levels increased in patients with renal disease
    • Hydrophilic - little or no CNS penetration
  • Adverse effects
    • less pulmonary effects due to low B2-receptors block
    • less metabolic & vascular effects due to low B2-block
    • No CNS effects due to poor CNS penetration
    • Cardiac adverse effects due to block of B1-receptors block
      • bradycardia, heart block, hypotension, exercise intolerance
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12
Q

What type of drug is Esmolol?

Phamacokinetics?

Adverse effects?

A

Esmolol (IV only)

Cardioselective - B1-adrenergic receptors

  • Use:
    • intraoperative arrhythmias, constant infusion
  • pharmacokinetics
    • very short plasma lifetime T1/2 = 10 minutes
    • metabolized by plasma esterases
  • adverse effects
    • cardiac: hypotension
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13
Q

How do Class III anti-arrhythmia drugs work?

A
  • Block K+ currents during repolarization (phase 3)
    • longer action potential which generates the longer effective refractory period
  • this prolongs refractoriness (ERP) by prolonging AP duration
  • Amiodarone also inhibits INa, ICa and B-receptors
  • trying to maintain the heart in sinus rhythm
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14
Q

What are the antiarrhythmic class III drugs?

A
  • Amiodarone
  • Dronedarone
  • Dofetilide
  • Ibutilide (IV only)
  • Sotalol
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15
Q

What are the common uses of Class III: Potassium Channel Blockers?

Drug-drug interactions?

A
  • Common effect
    • All block IKr
  • Uses
    • Convert an arrhythmia back to sinus rhythm (IV) Or maintain the heart in sinus rhythm (oral)
      • ventricular tachycardia
      • supraventricular tachycardia - Rhythm control
  • Drug-drug interactions
    • avoid prescribing other drugs that block IKr
      • Macrolides (clarithromycin, erythromycin)
      • fluoroquinolones (levofloxacin, moxifloxacin)
      • lefamulin
      • telavancin
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16
Q

What type of drug is Amiodarone?

Phamacokinetics?

Adverse effects?

Drug-drug interactions?

A

Amiodarone

most commonly used class III agent- Potassium channel blocker

Also blocks INa, ICa, and B-adrenergic receptors

  • Uses
    • IV: convert arrhythmia back to sinus rhythm
      • termination of ventricular tachycardia
      • termination of supraventricular tachycardia
    • oral: maintain sinus rhythm
      • supraventricular tachyarrhythmias
        • atrial fibrillation - rhythm control
      • ventricular tachyarrhythmias
      • redue shock frequency in patients with ICD
    • _Safe in patients with structural heart disease (_MI)
  • Pharmacokinetics
    • active metabolite, desethylamiodarone
    • hepatic metabolism: CYP3A4
    • Inhibitor of CYP3A4, CYP2C9, and P-glycoprotein (not potent)
    • T1/2 40-55 days - Hepatic excretion
      • several weeks in required to reach full effect
      • loading dose (400-1200 mg/day) for 10-20 days
        • Taper to maintenance dose (typically 200 mg/day)
  • Adverse effects
    • Hepatic - liver function - test before & monitor during
    • GI: Stomach upset, constipation
    • CV: LQT, but low risk of Torsades de Pointes
      • also block INa, ICa, and B-receptors (mechanism you get Torsades)
    • Pulmonary fibrosis - not used with lung disease
      • potentially fatal
    • Thyroid dysfunction (either hypo or hyper)
    • Tissue deposition
    • Skin reactions - photodermatitis
  • Drug-drug interactions
    • moderate inhibitor of
      • CYP2C9: most NSAIDs, Celecoxib, ARBs
      • CYP3A4: statins, calcium channel blockers
    • inhibits P-glycoprotein - digoxin transport
17
Q

What type of drug is Dronedarone?

uses?

Phamacokinetics?

Adverse effects?

A

Dronedarone- amiodarone analog w/o iodine

potassium channel blocker

  • Uses
    • atrial flutter/fibrillation after conversion
  • Pharmacokinetics
    • T1/2: 13-19 hrs (,uch shorter than amiodarone)
    • hepatic metabolism by CYP3A4
      • inhibits CYP2D6, CYP3A4, and P-glycoprotein
  • Adverse effects: No iodine = no thyroid problems
    • hepatic toxicity - avoid in patients with liver disease
    • contraindicated in patients with (increased mortality)
      • permanant atrial fibrillation
      • severe heart failure
      • conduction problems
18
Q

What type of drug is Dofetilide?

Uses?

Phamacokinetics?

Adverse effects?

Drug-drug interactions?

A

Dofetilide

pure IKr-channel blocker (oral)

  • Uses
    • maintain sinus rhythm
      • atrial flutter/fibrillation (rhythm control)
      • ventricular tachyarrhythmia
  • pharmacokinetics
    • 20% of drug metabolized by CYP3A4
    • 80% renal excretion unchanged
  • Adverse effects: Narrow therapeutic index
    • ​Torsades de Pointes - problem at treatment start
    • Required: treatment must be initiation in-hospital to monitory for Torsades de Pointes over a 3-day period
  • Drug-drug interactions: drugs to avoid
    • plasma levels increased by verapamil, ketoconazole, trimethoprims/sulfamethoxazole, hydrochlorothiazide, and cimetidine (OTC)
19
Q

What type of drug is Ibutilide?

Phamacokinetics?

Adverse effects?

A

Ibutilide (IV only) - potassium channel blocker

also increase slow inward Na+ current

  • Uses
    • pharmacologically conert atrial flutter or fibrillation into sinus rhythm
  • Pharmacokinetics
    • rapid hepatic metabolism with T1/2 2-6 hours
  • Adverse effects: Torsades de Pointes
    • patients must be monitored for several hours following termination of ibutilide treatment to monitor for Torsades de Pointes
20
Q

What type of drug is Sotalol?

Uses?

Phamacokinetics?

Adverse effects?

A

Sotalol - Potassium channel blocker

also a nonselective B-blocker (Class II)

  • Uses
    • maintain sinus rhythm
      • atrial flutter/fibrillation (Rhythm control)
      • ventricular arrhythmias
  • Pharmacokinetics
    • renal excretion: unchanged (fewer drug-drug interaction problems)
  • Adverse effects
    • torsades de pointes
    • recommended to initiate treatment in-hospital setting, but many cardilogists do not follow this recommendation
    • bronchospasm - due to B2-receptor block
21
Q

What are the 2 classes of calcium channel blockers?

What do they do?

Uses?

A
  • Dihydropyridine
    • selectively inhibits smooth muscle ICa-L current
      • smooth muscle relaxation
        • antihypertensive drugs
        • antianginal drugs
  • Non-dihydropyridine (Class IV antiarrhythmic drugs)
    • more selectively inhibits cardiac muscle ICa-L current
      • slows heart rate (SA & AV nodes) and decreases cardiac contraction strength (ventricular myocytes)
        • antiarrhythmic drugs
        • antianginal drugs
22
Q

How do Class IV drugs work?

A
  • SA node: decrease AP rate (HR)
  • AV node: slow conduction velocity
  • myocytes: decrease EADs & DADs
23
Q

Describe the mechanism of action for the calcium channel blockers

A
  • Block cardiac ICa-L indirectly reduce NCX activity
    • increases AP threhold in SA & AV nodes
      • reduced heart rate - SA node
      • Reduced maximum AV node rate
      • slowed conduction through AV node - rate control
    • reduce plateau depolarization of AP (phase 2, ICa-L )
    • Suppress ectopic excitability
      • suppress EADs - block ICa-L
      • Suppress DADs – suppress NCX action by ICa-L block
24
Q

What are th Antiarrhythmic Class IV drugs?

A
  • Diltiazen
  • Verapamil
25
Q

Clinical uses of Class IV drugs?

Common adverse effects?

A
  • Clinical uses
    • supraventricular and ventricular tachycardias
    • atrial flutter/fibrillation: rate control
    • other uses: angina, occasionally hypertension
  • Common adverse effects
    • GI: constipation
    • CV: heart block, heart failure, hypotension, bradycardia, and asystole (esp. rapid IV)
    • Contraindicated: heart failure with low ejection fraction, slow heart rate, low blood pressure
    • contraindicated: Wolff-Parkinson-White syndrome
26
Q

Pharmacokinetics of Verapamil & Diltiazem?

Drug-drug interactions?

A
  • Pharmacokinetics
    • both metabolized by CYP3A4
    • both also moderate blockers of CYP3A4
    • both inhibit P-glycoprotein
    • potential drug-drug interactions
      • e.g. statins (CYP3A4)
      • e.g. dofetilide (p-glycoprotein & CYP3A4) – AVOID
27
Q

What is the mechanism of action of adenosine?

Use?

Pharmacokinetics?

Adverse Effects?

A
  • MOA: activation of adenosin receptors
    • adenosine receptors - GPCR: activates Gi
    • reduces intracellular cAMP
    • slows heart rate
      • reduced ICa-L - decreased cAMP to decreased PKA
      • reduced If - decreased cAMP to decreased PKA
      • activates G-protein-activated inward rectifier K+ (GIRK) channels
    • slows conduction velocity
      • inhibits ICa-L - decrease cAMP to decrease PKA
    • increases ERP in AV node
    • Dialates coronary and peripheral vessels
      • inhibits ICa-L - decrease cAMP to decrease to PKA activity
  • Use
    • acute termination of paroxysmal supraventricular tachycardia (PSVT)
  • Pharmacokinetics (IV only)
    • rapid onset, short duration of action - T1/2 - 10
  • Adverse effects
    • flushing, dyspnea
    • cheest pain, transient heart block, bronchoconstriction
28
Q

What is the mechanism of action of Cardiac glycoside?

Use?

Pharmacokinetics?

Adverse Effects?

A
  • MOA
    • enhanced vagal tone: increased muscarinic receptor activation of GIRK
      • slows HR (SA node)
    • Afib
      • slows conduction through AV node - Rate control
    • Inhibits Na+/K+ ATPase (pump)
      • positive inotropic agent (HF)
      • indirect inhibition of NCX to increase intracellular Ca2+
  • ​Uses
    • Atrial flutter/fibrillation ONLY: Rate control
    • heart failure: inotropic agent
  • Pharmacokinetics
    • P-glycoprotein transport
    • Hepatic metabolism
    • Rena excretion: 50-70% unchanged
  • Adverse effects
    • Arrhythmias
    • Bradycardia - vagomimetic effect
    • ventricular tachycardia
      • excessive [Ca2+]I runs NCX backwards
      • high NCX activity generates DADs
      • DADs can produce ectopic activity
  • Drug-drug interactions
    • P-glycoprotein inhibitors
    • Amiodarone, dronedarone, diltiazem, verapamil, propranolol
    • Can increase plasma digoxin levels ot increase toxicity
29
Q

Uses for Magnesium sulfate?

A
  • Corrects hypomagnesemia
  • may suppress EADs
  • uses:
    • refractory ventricular arrhythmias, and drug-induced torsades de pointes arrhythmias
30
Q

use for potassium chloride?

A
  • corrects hypokalemia, which may suppress ectopic pacemakers and prevent or terminate some arrhythmias
31
Q

Fill out the provided flow chart

A
32
Q

Answer the blanks indicated on the provided flow chart

A
33
Q

Identify the blanks in the provided flow chart

A

S2B3: Pharm (3 decks)

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