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Pharmacology Exam 2 > Anti-Arrhythmic > Flashcards

Anti-Arrhythmic Flashcards

1
Q

Cardiac Action Potential Phase 0

A
  • Rapid depolarization
  • Rapid Na entry; increases membrane potential
  • Negative to positive state
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2
Q

Cardiac Action Potential Phase 1

A
  • Inactivation/closing of Na channels

- K+, Cl- out

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3
Q

Cardiac Action Potential Phase 2

A
  • “Plateau” phase
  • Balance of Ca2+ in, K+ out– causes positive charge
  • Contraction of the heart
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4
Q

Cardiac Action Potential Phase 3

A
  • Rapid repolarization

- Ca2+ channels close, K+ channels stay open until membrane potential reaches -85 to-95 mV in cell

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5
Q

Cardiac Action Potential Phase 4

A
  • Resting membrane potential

- Heart is relaxed

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6
Q

Anti-Arrhythmic drugs: general

A
  • Alter membrane ion conduction
  • Increase or decrease conduction velocity
  • Change the duration of the refractory period
  • Suppress abnormal automaticity
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7
Q

Vaughn-Williams Classification

A
  • Class 1: Na channel blockers (1A, 1B, 1C)
  • Class 2: beta blockers
  • Class 3: K channel blockers
  • Class 4: Ca channel blockers
  • Misc. agents (digoxin, adenosine, magnesium, etc.)
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8
Q

Class 1: Na channel blockers

A
  • Reduce rate and rise of phase 0 and of the AP (slows conduction)
  • Oldest anti arrhythmic drug on market
  • Groups are broken down by their potency
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9
Q

1A

A
  • quinidine, procainamide, disopyramide
  • Moderately potent (also blocks K+)
  • Moderate time to take effect and stay bound to receptor for moderate amount of time
  • Increases AP duration and duration of refractory period
  • Treats both atrial and ventricular arrhythmias
  • Can precipitate new arrhythmias
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10
Q

1B

A
  • Lidocaine, mexilitene
  • Weak potency
  • Works very fast and offsets very fast
  • Doesn’t reduce AP duration but shortens refractory period
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11
Q

1C

A
  • Flecainide, propafenone
  • Strong potency
  • Strongest because they have the slowest time to take effect but stay bound the longest
  • Slows conduction velocity but little impact on AP duration and refractory period
  • Should NOT be used in those with structural heart disease (need a “normal” heart)
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12
Q

Procainamide

A
  • Class 1: 1A Na channel blocker
  • Moderately potent (also blocks K+)
  • Moderate time to take effect and stay bound to receptor for moderate amount of time
  • Increases AP duration and duration of refractory period
  • Treats both atrial and ventricular arrhythmias
  • Active metabolite that is cleared via kidney– would need to monitor renal function
  • ADR’s: hypotension (parenteral), lupus-like syndrome (30% get this, usually reversible unless have baseline autoimmune disorder), agranulocytosis, nausea, diarrhea
  • Can precipitate new arrhythmias
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13
Q

Quinidine

A
  • Class 1: 1A Na channel blocker
  • Moderately potent (also blocks K+)
  • Moderate time to take effect and stay bound to receptor for moderate amount of time
  • Increases AP duration and duration of refractory period
  • Treats both atrial and ventricular arrhythmias
  • Most toxic
  • ADR’s: HA vertigo, tinnitus, GI disturbances (significant- N/diarrhea), thrombocytopenia, hemolytic anemia, hepatitis
  • Can precipitate new arrhythmias
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14
Q

Disopyramide

A
  • Class 1: 1A Na channel blocker
  • Moderately potent (also blocks K+)
  • Moderate time to take effect and stay bound to receptor for moderate amount of time
  • Increases AP duration and duration of refractory period
  • Treats both atrial and ventricular arrhythmias
  • Negative inotrope
  • ADR’s: anticholinergic effects (tachy, etc.), exacerbates HF (don’t use in pt’s with HF), increases dig toxicity
  • Approved for ventricular arrhythmias
  • Can precipitate new arrhythmias
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15
Q

Lidocaine

A
  • Class 1: 1B Na channel blocker
  • Weak potency
  • Works very fast and offsets very fast
  • Doesn’t reduce AP duration but shortens refractory period
  • Therapeutic uses: treats ventricular arrhythmias only
  • Used IV or IM; never orally (high 1st pass effect)
  • Used for acute ventricular arrhythmias
  • ADR’s: CNS toxicity (paresthesia- numbness/tingling, confusion, seizure, tremor)
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16
Q

Mexiletine

A
  • Class 1: 1B Na channel blocker
  • Weak potency
  • Works very fast and offsets very fast
  • Doesn’t reduce AP duration but shortens refractory period
  • Therapeutic uses: treats ventricular arrhythmias only
  • Used PO never IV
  • Longer duration of activity (t1/2= 8-20 hours)
  • ADR’s: CNS toxicity (paresthesia- numbness/tingling, confusion, seizure, tremor), GI upset
17
Q

Flecainide

A
  • Class 1: 1C Na channel blocker
  • Strong potency
  • Strongest because they have the slowest time to take effect but stay bound the longest
  • Slows conduction velocity but little impact on AP duration and refractory period
  • Generally more well tolerated
  • Elimination via liver and kidney
  • ADR’s: can cause ophthalmic problems– need routine monitoring of eyes
  • Should NOT be used in those with structural heart disease (need a “normal” heart)
18
Q

Propafenone

A
  • Class 1: 1C Na channel blocker
  • Strong potency
  • Strongest because they have the slowest time to take effect but stay bound the longest
  • Slows conduction velocity but little impact on AP duration and refractory period
  • Generally more well tolerated
  • Mild beta-blocking properties (have similar structures to beta blockers)
  • ADR’s: proarrythmias/ conduction abnormalities, HF exacerbation, metallic taste/ constipation
  • Should NOT be used in those with structural heart disease (need a “normal” heart)
19
Q

Class 2: Beta blockers

A
  • Suppression of abnormal pacemaker activity by blocking sympathetic (beta1 receptor) activity in SA/AV node (used for rate control)
  • Used s/p MI as prophylaxis against sudden death and vfib (will treat both conditions with one drug)
  • Propranolol, metoprolol, esmolol
  • ADR’s: bronchospasm, cardiac depression, AV block, hypotension, exercise intolerance, sexual dysfunction
20
Q

Propranolol

A
  • Class 2: beta blockers
  • Suppression of abnormal pacemaker activity by blocking sympathetic (beta1 receptor) activity in SA/AV node (used for rate control)
  • Used s/p MI as prophylaxis against sudden death and vfib (will treat both conditions with one drug)
  • ADR’s: bronchospasm, cardiac depression, AV block, hypotension, exercise intolerance, sexual dysfunction
21
Q

Metroprolol

A
  • Class 2: beta blockers
  • Suppression of abnormal pacemaker activity by blocking sympathetic (beta1 receptor) activity in SA/AV node (used for rate control)
  • Used s/p MI as prophylaxis against sudden death and vfib (will treat both conditions with one drug)
  • ADR’s: bronchospasm, cardiac depression, AV block, hypotension, exercise intolerance, sexual dysfunction
22
Q

Esmolol

A
  • Class 2: beta blockers
  • Suppression of abnormal pacemaker activity by blocking sympathetic (beta1 receptor) activity in SA/AV node (used for rate control)
  • Used s/p MI as prophylaxis against sudden death and vfib (will treat both conditions with one drug)
  • ADR’s: bronchospasm, cardiac depression, AV block, hypotension, exercise intolerance, sexual dysfunction
  • Short acting for acute arrhythmias (often used in inpatient setting to get rid of arrhythmias in a short time frame)
23
Q

Class 3: K channel blockers

A
  • Mechanism of action: Block K channels to delay repolarization (phase 3)– increases AP and eRP
  • Treats both atrial and ventricular arrhythmias
  • Increase risk of subsequent arrhythmias (TdP)
  • Ibutilide, sotalol
24
Q

Ibutilide

A
  • Class 3: K channel blockers
  • Mechanism of action: Block K channels to delay repolarization (phase 3)– increases AP and eRP
  • Treats both atrial and ventricular arrhythmias
  • Increase risk of subsequent arrhythmias (TdP)
  • Blocks K, Na, and beta receptors, a good treatment for acute afib w/in 7 days
25
Q

Sotalol

A
  • Class 3: K channel blockers
  • Mechanism of action: Block K channels to delay repolarization (phase 3)– increases AP and eRP
  • Treats both atrial and ventricular arrhythmias
  • Increase risk of subsequent arrhythmias (TdP)
  • Blocks K and beta receptors, treatment for ventricular arrhythmias and afib
  • ADR’s: can cause brady and bronchospasm, cardiac depression, TdP
  • No significant DDI’s– good to use if pt is on a lot of meds
  • Do not use if LVEF <25%
  • Renally cleared
26
Q

Amiodarone

A
  • Class 3: K channel blockers
  • Mechanism of action: Block K channels to delay repolarization (phase 3)– increases AP and eRP
  • Treats both atrial and ventricular arrhythmias
  • Increase risk of subsequent arrhythmias (TdP)
  • Has class 1, 2, &4 electrophysiological properties– broad spectrum of therapeutic action (widely used)
  • t1/2= 1-10 weeks, takes long time to reach steady state
  • DDI’s: digoxin and warfarin + more!
  • ADR’s: pulmonary fibrosis, hepatic dysfunction, grey-blue skin, corneal deposits, hypo/hyperthryoidism (mainly composed of iodine)
  • Important to be diligent with monitoring (need to check thyroid/liver function tests and get CXR as baseline and check repeatedly), no skin or eye tests but looking for them and referring if comes up
27
Q

Dofetilide (Tikosyn)

A
  • Class 3: K channel blockers
  • Mechanism of action: Block K channels to delay repolarization (phase 3)– increases AP and eRP
  • Treats both atrial and ventricular arrhythmias
  • Increase risk of subsequent arrhythmias (TdP)
  • Blocks only K
  • Treatment and prophylaxis of afib
  • ADR’s: proarrhythmic: must be started inpatient; provider must be registered to prescribe and pharmacy to dispense (72 hr monitoring)
  • DDI: with HCTZ and verapamil
28
Q

Dronedarone

A
  • Class 3: K channel blockers
  • Mechanism of action: Block K channels to delay repolarization (phase 3)– increases AP and eRP
  • Treats both atrial and ventricular arrhythmias
  • Increase risk of subsequent arrhythmias (TdP)
  • May also block Ca, Na currents
  • Strong CYP 3A4 interactions
  • Lacks iodine atoms
  • ADR’s: GI intolerance, lacks pulmonary/thyroid/hepatic effects vs amiodarone
  • May be a little safer but can’t use in pt’s with decompensated HF
29
Q

Class 4: Ca Channel blockers

A
  • Mechanism of action: slows conduction in AV node by blocking Ca channels, used for rate control
  • Non-DHP’s only: benzothiazepine- diltiazem, and phenylalkylamine- verapamil
  • Good alternative to beta blockers in those with asthma/COPD
  • ADR’s: constipation, hypotension, heart block, exacerbation of HF
30
Q

Verapamil

A
  • Class 4: Ca channel blockers
  • Mechanism of action: slows conduction in AV node by blocking Ca channels, used for rate control
  • Good alternative to beta blockers in those with asthma/COPD
  • ADR’s: constipation, hypotension, heart block, exacerbation of HF
  • DDI’s: with digoxin, dofetilide, simvastatin, lovastatin
31
Q

Diltiazem

A
  • Class 4: Ca channel blockers
  • Mechanism of action: slows conduction in AV node by blocking Ca channels, used for rate control
  • Good alternative to beta blockers in those with asthma/COPD
  • ADR’s: constipation, hypotension, heart block, exacerbation of HF
32
Q

Digoxin

A
  • Misc. Group
  • Inhibits Na/K/ATPase transport system: increases intracellular Na/Ca (increases contractility)
  • Increase vagal efferent activity: reduces SA firing rate (decreased HR) and reduces conduction velocity
  • Requires therapeutic drug monitoring
  • DDI’s: multiple, watch for K and Mg levels

Pharmacology Exam 2 (6 decks)

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