Treatment of Cardiac Arrhythmias Flashcards

1
Q

due to abnormal electrical activity in the heart

  • cardiac: HTN, abnormal heart valve function, CAD, CHF
  • non cardio: hyperthyroidism, autonomically mediated, alcoholism, sleep apnea, obesity
A

cardiac arrhythmias

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2
Q
  • most common type of mainly harmless arrhythmias, no need for treatment
  • fluttering or skipped beat, PACs or PVCs
  • too much exercise, caffeine, nicotine
A

premature (Extra) beats

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3
Q
  • tachycardias that start in atria or SA node

- a.fib, a flutter, PSVT, WPW syndrome

A

supraventricular arrhythmias

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4
Q
  • most common type of serious arrhythmia
  • electrical signals do not begin in SA node but other parts of atria or pulmonary vein, results in irregular fast heart beat
  • blood pools in atria and can form clots, causing stroke
A

atrial fibrillation

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5
Q
  • similar to Afib but regular fast heart beat, 250-350 bom
  • atria beat faster than the ventricles
  • if ventricular rate is less than 120 bpm people normally have no symptoms, much less common
A

atrial flutter

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6
Q
  • regular heart rate at 150-250 bpm, begins and ends suddenly
  • signals beginning in atria travel to ventricles can reenter the atria, resulting in extra heartbeats
  • more common in young people
  • due to alcohol, caffeine, vigorous activity, WPW syndrome
A

PSVT

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7
Q

tachycardia that start in the ventricles, can be very dangerous, usually require medical care immediately

A

ventricular arrhythmias (v.tach and v.fib)

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8
Q

fast but regular beat of ventricles that may last only for a few seconds or much longer, longer episodes can turn into v.fib

A

ventricular tachycardia

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9
Q
  • most serious arryhthmia
  • uncontrolled irregular beats up to 300bpm
  • chaotic, little blood pumped
  • if not converted to normal rhythm with electric shock death will occur in minutes
  • can occur during or after heart attack or due to weakened heart
A

ventricular fibrillation

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10
Q

heart rate <60 bpm, impulse not formed by SA node or not conducted properly to ventricles

  • mainly in elderly
  • CNS might not signal properly, SA node might be damaged, could be due to drug use
A

bradycardia

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11
Q

all arrhythmias result from disturbance of ________ (automaticity) or _________, or both

A

impulse formation

impulse conduction

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12
Q

distubance in impulse formation:

  • pacemaker rate depends on _______ and duration of diastolic interval
  • diastolic interval depends on slope of phase _____ depolarization
A

AP duration

4

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13
Q

EADs interrupt phase _____ usually at slow heart rates, can contribute to _______ related arrhythmias

A

phase 3

long QT

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14
Q

DADs interrupt phase ____ usually at fast heart rates

A

4

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15
Q

disturbances in impulse conduction can be due to ________, a common conduction abnormality

  • conduction has to be blocked and the block must be _______
  • conduction time around block must exceed ______
A

reentry

unidirectional

refractory period

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16
Q

antiarrhythmic drugs can either

  • slow _____
  • change abnormal to normal rhythm
  • cannot reliably speed up heart rate (bradycardia needs to be treated with _____)
A

heart rate

pacemaker

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17
Q

beta blockers, calcium channel blockers and digoxin provide ______ control

A

rate

18
Q

sodium channel blockers (procainamide, quinidine, disopyramide, flecainide) or potassium channels blockers (amiodarone, ibutilide, sotalol, dofetilide) provide _______ control

A

rhythm

19
Q

-decrease HR by elevating threshold for excitation, decreasing slope of phase 4 depolarization in SA node

A

class 1 Na+ channel blocker

20
Q
  • procainamide, quinidine, disopyramide
  • increase effective refractory period of atria and ventricles, can directly depress SA and AV nodes, prolong APD by nonspecific blocking K+ channels (QT prolongation)
  • has ganglion blocking activity which reduces peripheral vascular resistance, can lead to hypotension
A

class Ia sodium blockers

21
Q
  • excessive AP prolongation, QT prolongation, torsades, syncope, new arrythmias
  • reversible lupus like syndrome, n/d, hepatitis, agranulocytosis
  • does not elevate digoxin levels
A

procainamide

22
Q

-effective against most atrial and ventricular arrythmias, short half life

A

procainamide

23
Q
  • similar effects as procainamide, slows upstroke of AP, slows conduction
  • QT prolongation due to K+ channel blocking
  • modest antimuscarinic effect
  • blocks alpha receptors to cause vasodilation
  • precipitates digoxin toxicity, thrombocytopenia, cinchonism
  • rarely used
A

quinidine (class 1a)

24
Q

1a with more antimuscarinic effects

  • pronounced atropine like activity - urinary retention, dry mouth, blurred vision, constipation, worsening of glaucoma
  • may induce CHF, only approved to treat ventricular arrhythmias
A

disopyramide

25
Q
  • blocks activated and inactivated sodium channels with rapid kinetics
  • blocks channels in Purkinje fibers and ventricular cells to elevate excitation threshold and reduce automaticity
  • suppress electrical activity of depolarized diseased tissue, has minimal effect on normal or atrial tissues
  • does not affect K+ channels
A

lidocaine, class Ib

26
Q
  • least cardiotoxic of currently used sodium blockers
  • larger doses can depress myocardial contractility
  • neuro: parasthesias, tremor, slurred speech, convulsion
  • seizures after IV admin in elderly
  • must be given IV, ineffective in atrial flutter/fib
  • agent of choice for termination of ventricular tachycardia and to prevent v.fib after cardioversion
A

lidocaine, Ib

27
Q
  • lidocaine analog, resistant to first pass - oral
  • neurlogic side effects
  • used for ventricular arrythmias
  • relief of chronic pain (diabetic neuropathy, nerve injury)
A

mexiletine

28
Q

-all oral, increase mortality from cardiac arrest or arrythmic sudden death in patients with recent MI

A

class Ic

29
Q
  • blocks sodium and potassium channels, no QT prolongation
  • no antimuscarinic
  • treats supraventricular arrhythmias
  • effective in suppressing premature ventricular contractions
A

flecainide: class Ic

30
Q
  • blocks sodium channels, structurally similar to propranolol, weak beta blocking activity
  • metallic taste
  • may exacerbate arrythmias and cause constipation
  • suppress PVCs
A

Ic: propafenone

31
Q
  • propanolol (nonselective) and acebutolol (B1 selective) are most frequently used
  • for supraventricular and ventricular arrhytmias caused by symapthetic stimulation
  • to prevent ventricular fibrillation
  • esmolol (b1) is short acting, used for acute arrythmias during surgery
  • can be used for rate control
A

Class II beta blockers

32
Q
  • beneficial effects due to diminished sympathetic activation of heart and blood vessels
  • reduced cardiac activity, reduced vasoconstriction
  • diminished cardiac workload leads to reduced myocardial oxygen demand
  • prevent recurrent infarction and sudden death in patients with acute MI
  • averse: negative inotrop, may indue or worsen HF, CNS penetration
A

Class II: beta blockers

33
Q
  • oral or IV to maintain normal sinus rhythm in patients with a.fib or prevent recurrent v.tach
  • prolongs AP duration and QT interval by blocking K channels
  • decreases rate of firing in pacemaker cells by blocking inactivated Na channels
  • blocks alpha and beta adrenergic receptors and Ca2+ channels and inhibits AV node conduction to produce bradycardia
  • causes peripheral vasodilation after IV admin
A

class III: potassium blockers, amiodarone

34
Q
  • toxicity:
  • asymptomatic bradycardia and AV block in patients with SA/AV node disease
  • respiratory –> fatal pulm fibrosis
  • hepatitis
  • photodermatitis, gray blue skin discoloration
  • corneal microeposits, optic neuritis
  • blocks T4 to T3 conversion
  • hypo or hyper thyroidism
  • long half life, toxicity long after discontinuation
  • metabolized by CYP3a4
A

amiodarone toxicity

35
Q
  • structural analog of amiodarone but no iodines
  • blocks K and Na channels
  • no thyroid dysfunction or pulmonary toxicity, but there is liver toxicity
  • black box: increased risk of stroke, death, heart failure in patients with decompensated heart failure or permanent a. fib
A

dronedarone

36
Q
  • non selective B-blocker that prolongs APD and has antiarrhythmic properties
  • may cause prolonged repolarization resulting in torsades
  • treates life threatening ventricular arrhythmias, maintains sinus in a.fib, treat supraventricular and ventricular arrhythmias in pediatrics
A

sotalol

37
Q
  • block rapid component of delayed rectifier K current to slow cardiac repolarization
  • good to restore normal sinus rhythm in a fib or flutter
  • prolonged QT and torsades
A

dofetilide (oral), ibutilide (IV)

38
Q

-orally active, block L-type calcium channels in myocardium and vascular smooth muscles
-depress SA and AV nodes directly to decrease contractility, reduce SA node automaticity, slow AV node conduction
-orally use for treament of supraventricular arrythmias and for rate control in a.fib
-

A

class IV: CCBs (verapamil, diltiazem)

39
Q
  • opens inward rectifier K+ channels, causing hyperpolarization
  • inhibits L type calcium channels, inhibits calcium entry and conduction velocity in AV node
  • inhibits pacemaker current, decreases HR
  • mainly affects AV node
  • by IV injection to convert PSVTs to sinus rhythm
  • adverse: flushing, SOB, headache, hypotension, paresthesia
A

adenosine

40
Q

-potent and selective inhibitor of Na/K ATPase, increased calcium, positive inotrope
-stimulate vagus nerve and decreases HR, can be used in a.fib
-narrow therapeutic window: quinidine, amiodarone, captopril, verapemil, diltiazem, and cyclosporine enhance toxicity
-K competes for binding to Na/K ATPase, so drugs that produce hypokalemia (thiazide and loop diuretics) will enhance toxicity
-toxicity: GI, can cause almost all arrhythmias
-

A

digoxin

41
Q
  • has been used to prevent torsades and for digoxin induced arrhythmias
  • MOA unknown
A

magnesium

42
Q

contraindications:
- prostatism for _______, causes urinary retention due to anticholinergic activity
- chronic arthritis for _______, causes lupus like syndrome
- advaned lung disease for ________, causes pulmonary fibrosis

A

disopyramide

procainamide

amiodarone