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CRRAB Week 4 - WLB > Calcium & Potassium Channel Blockers - Nordgren > Flashcards

Calcium & Potassium Channel Blockers - Nordgren Flashcards

1
Q

What are the three ways antiarrhythmic drugs achieve their goal of restoring normal sinus rhythm and conduction?

A
  1. Decrease or increase conduction velocity
    1. i.e. how fast the membrane depolarizes
  2. Alter the excitability of cardiac cells by changing the duration of the effective refractory period
    1. i.e. how long the action potential takes
  3. Suppress abnormal automaticity
    1. i.e. spontaneous depolarization, pacemaker potential
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2
Q

What are Class III Drugs?

A

K+ Channel Blockers

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3
Q

How does blocking K+ channels with Class III drugs alter the action potential?

A
  • 1° role of K+ = cell repolarization (phase 3)
  • Blocking these channels SLOWS repolarization
    • Increases AP duration
    • Increases AP refractory period
      • (prolong time that cell is “unexcitable”)
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4
Q

What effect do Class III Drugs have on EKG?

A
  • Lengthen the QT Interval
    • due to prolonged repolarization
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5
Q

What kind of arrhythmias are Class III Drugs useful for treating?

A

Useful in suppressing reentry arrhythmias.

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6
Q

What are the Class III Antiarrhythmic drugs we need to know?

A
  1. Amiodarone
  2. Dofetilide
  3. Ibutilide
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7
Q

What are the cardiac effects of Amiodarone?

A
  • Prolongs AP
  • Also a potent Na+ channel blocker, and weak blocker of beta receptors and Ca2+​ channels
    • slows HR and AV node conduction
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8
Q

What are the extracardiac effects of Amiodarone?

A

Causes peripheral vasodilation.

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9
Q

What are potential symptoms of Amiodarone toxicity?

A
  • Bradycardia + Heart block
    • in pts with preexisting SA or AV node disease
  • Drug accumulation in tissues:
    • Heart, lung, liver, skin, tears
    • Dose related pulmonary toxicity
    • Abnormal liver function and hypersensitivity hepatitis
    • Photodermatitis (gray-blue skin discoloration in sun-exposed areas)
    • Corneal microdeposits (halos develop in peripheral visual fields)
    • Hypo- and Hyperthyroidism
  • Blocks peripheral conversion of thyroxine (T4) → triiodothyronine (T3)
    • source of inorganic iodine
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10
Q

What are the important pharmacokinetics of Amiodarone?

A
  • Hepatic Metabolism (CYP3A4)
  • Metabolite is bioactive
  • Half life is complex → effects last 1-3 months past cessation of use
  • Can also inhibit many Cyp enzymes causing increased levels of Statins, digoxin and warfarin
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11
Q

What are the therapeutic uses of Amiodarone?

A
  • V-tach
  • V-fib
  • A-fib
  • A-flutter
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12
Q

What are the cardiac effects of Dofetilide?

A
  • Very selective K+ channel blocker
  • Prolongs AP
  • Increases QT interval
    • prolonged refractory period in His-Purkinje system & ventricles
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13
Q

What are the extracardiac effects of Dofetilide?

A
  • Hypokalemia
  • Hypomagnesemia
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14
Q

What are potential symptoms of Dofetilide toxicity?

A
  • life threatening Ventricular Arrhythmias
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15
Q

What are the important pharmacokinetics of Dofetilide?

A
  • Hepatic metabolism via CYP 3A4
  • 100% bioavailable
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16
Q

What are the therapeutic uses of Dofetilide?

A
  • Maintain and restore normal sinus rhythm in a-fib.
  • DO NOT USE IN:
    • long QT
    • Bradycardia
    • Hypokalemia
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17
Q

What are the cardiac effects of Ibutilide?

A
  • Prolongs AP
  • ALSO slow inward Na+ activator
    • delays repolarization → inhibits Na+ channel inactivation → increases effective refractory period
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18
Q

What are the extracardiac effects of Ibutilide?

A
  • Minimal
  • Hypokalemia
  • Hypomagnesemia
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19
Q

What are the potential symptoms of Ibutilide toxicity?

A
  • Excessive QT-interval prolongation and torsades de pointes
  • Can cause life-threatening ventricular arrhythmias
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20
Q

What are the important pharmacokinetics of Ibutilide?

A
  • Hepatic Metabolism
  • Mainly renally excreted but also some fecal elimination
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21
Q

What are the therapeutic uses of Ibutilide?

A
  • Acute conversion of Atrial Flutter and a-fib to normal sinus rhythm
    • More effective in flutter (mean time to termination = 20 min)
22
Q

How do Class III Anti-arrhythmic drugs affect the QRS complex?

A

No change!

(only slow the REpolarization, not depolarization)

23
Q

What do Class IV Drugs do?

A
  • Bind to L-type Ca2+ channels located on:
    • vascular smooth muscle
    • cardiac myocytes
    • SA/AV nodes
24
Q

What is the result of blocking L-type Ca2+ channels in smooth muscle?

A
  • Vasodilation
    • vascular smooth muscle relaxation
      • due to decreased influx of Ca2+
25
Q

What is the result of blocking L-type Ca2+ channels in cardiac myocytes?

A
  • Shorten plateau phase in fast-response AP’s (phase 2)
  • Reduce force of contraction
    • less Ca2+ available to bind troponin
26
Q

What is the result of blocking L-type Ca2+ channels in cardiac nodal cells?

A
  • Slowed rise of AP (phase 0)
    • causes prolonged repolarization at AV node
  • Decreased HR
  • Decreased conduction velocity of AV node
    • Increased effective refractory period of AV node
27
Q

What are the Class IV Drugs that we need to know?

A
  1. Dihydropyridines (“-pine”) : vascular L-type
  2. Non-Dihydropyridines: cardiac L-type
    1. Verapamil
    2. Diltiazem
28
Q

What are the cardiac effects of Dihydropyridines?

A
  • Block L type Ca2+ channels on vascular smooth muscle
    • vasodilation
    • decreases systemic vascular resistance (TPR) through smooth muscle relaxation
    • lowers arterial blood pressure (1° affects arterial vessels)
  • Decreased contractility
  • Shortened Phase 2 of AP
29
Q

What are the potential symptoms of Dihydropyridine toxicity?

A
  • Flushing, HA, excessive hypotension
  • Edema
  • Reflex tachycardia
  • Activation of sympathetic reflexes and lack of direct cardiac effects make these a poor choice for angina
    • ​long-acting dihydropyridines = safer anti-hypertensives, reduced reflex responses
30
Q

What are the therapeutic uses of Dihydropyridines?

A

Hypertension

31
Q

What are the cardiac effects of Verapamil?

A
  • Blocks both activated and inactivated L-type Ca2+ channels
    • Greater affect in:
      • tissues that fire frequently
      • tissues less polarized
      • nodal tissue
  • Decreased conduction velocity in AV node
32
Q

What are the extracardiac effects of Verapamil?

A

Peripheral vasodilation

33
Q

What are the potential symptoms of Verapamil toxicity?

A
  • AV block in large doses
  • AV block if AV node disease
  • Constipation, lassitude, nervousness, peripheral edema
  • Hypotension and V-fib
34
Q

What are the pharmacokinetics of Verapamil?

A

Hepatic Metabolism (significant 1st pass)

35
Q

What are the therapeutic uses of Verapamil?

A
  • Supraventricular Tachycardia
  • A-fib
  • Atrial Flutter
    • ***REDUCES ventricular rate, does not convert back to normal sinus rhythm***

***DO NOT use in Wolff-Parkinson-White Syndrome***

36
Q

What are the cardiac effects of Diltiazem?

A
  • Blocks both activated and inactivated L-type Ca2+ channels
    • Greater affect in:
    • tissues that fire frequently
    • tissues less polarized
    • nodal tissue
  • Decreased conduction velocity in AV node
  • Similar to Verapamil, but with more smooth muscle-relaxing effect
    • produces less bradycardia
37
Q

What are the extracardiac effects of Diltiazem?

A

Vasodilation

38
Q

What are the pharmacokinetics of Diltiazem?

A

significant first pass hepatic metabolism

39
Q

What are the potential symptoms of Diltiazem toxicity?

A
  • Hypotension
  • V-fib
40
Q

What are the therapeutic uses of Diltiazem?

A
  • Supraventricular Tachycardia
  • A-fib
41
Q

Which cell types are most susceptible to altered calcium currents?

A

Sinus and AV nodes

(slow response/pacemaker cardiac cells)

42
Q

What is the MOA of Adenosine?

A
  • Activation of K+ channels and inhibition of L-type Ca2+ channels
  • Results in hyperpolarization and suppression of Ca2+-dependent AP (nodal tissue)
    • suppresses AV conduction
    • increases AV refractory period
43
Q

What are the cardiac effects of Adenosine?

A
  • Suppresses AV conduction
  • Increases AV refractory period
44
Q

What are the extracardiac effects of Adenosine?

A

Vasodilation

45
Q

What are the therapeutic uses of Adenosine?

A
  • SVTs
    • Prompt conversion of Paroxysmal Supraventricular Tachycardia (PSVT)
  • Not effective for a-flutter or a-fib
46
Q

What are the potential side effects of Adenosine?

A
  • Flushing and headache
  • Rapid arterial hypotension
    • (short lasting w/cessation of drug)
  • Methylxanthines (caffeine) competitively antagonize binding of adenosine at the receptor
  • AV block
    • DO NOT use in patients with 2° or 3° degree AV block
47
Q

What are the therapeutic uses of Digitalis/Digoxin?

A
  • 1° use = Heart Failure
  • Also useful for reducing ventricular rate when it is being driven by a high arterial rate
    • a-fib & a-flutter
48
Q

What is the MOA of Digoxin?

A
  • Inhibits Na+/K+/ATPase Pump
    • increases intracellular [Na+] → reverses action on Na+/Ca2+ exchanger → more Ca2+ into cell → more Ca2+ to bind troponin
      • increased cardiac contractility
49
Q

What are the cardiac effects of Digoxin?

A
  • Increased cardiac contractility
    • Increased SV → Increased CO → Decreased HR!
  • Decreased intracellular K+ and increased intracellular Na+ levels contribute to depolarization of the resting membrane potential
    • afterdepolarization at high doses
50
Q

What are the extracardiac effects of Digoxin?

A
  • Activation of vagal efferent nerves to the heart
    • Slows SA rate and AV conduction
    • Increases refractory period
      • Leads to partial AV block
        • fewer impulses reach the ventricles
        • ventricular rate falls
51
Q

What are the side effects of Digoxin?

A
  • Extreme AV block
  • GI distress
  • Hyperkalemia
  • Life threatening arrhythmias
    • increased automaticity, decreased AV conduction
    • increased PR, flatttened T waves and decreased QT

***DO NOT USE if Hypokalemic, WPW or AV block***

52
Q

What are the important pharmacokinetics of Digoxin?

A
  • Renally excreted
    • impaired renal function leads to enhanced plasma levels of digoxin
    • narrow therapeutic index

CRRAB Week 4 - WLB (5 decks)

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