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MSII Pharmacology > Unit 4 - Anti Arrhythmics > Flashcards

Unit 4 - Anti Arrhythmics Flashcards

1
Q

what kinds of arrhythmias occur when there is normal automaticity?

A

sinus rhythm problems

  • bradycardia
  • tachycardia

ectopic activity/focus
-Purkinje > atrium/ventricle

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2
Q

what kinds of arrhythmias occur when there is abnormal automaticity?

A

“triggered” activity

  • early afterdepolarizations (EADs)
  • -develop during phase 3 repolarization
  • -decreased K+ currents (blocking repolarization)
  • -increased Ca,L and Na+
  • delayed afterdepolarizations (DADs)
  • -develop during phase 4 (resting, diastole)
  • -decreased K1 currents
  • -increased diastolic Na+, Ca++ influx
  • –decreased NCX and Na/K-ATPase, increased Ca++
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3
Q

what happens when there is re-entrant arrhythmias? what favors it?

A

3 prerequisite conditions

  • unidirectional block
  • slow conduction
  • conduction time > refractory time

favored by:

  • tissue heterogeneity (refractory period, gap junction coupling, fibrosis)
  • extrasystoles in atria and ventricle
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4
Q

what are major determinants of conduction velocity, and how they change in arrhythmias?

A
  • cardiac Na current decreases (increases threshold)
  • length constant decreases (decreases membrane resistance; increases gap junction and extracellular resistance)
  • fibrosis increases
  • cell size (membrane capacitance)
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5
Q

what is bradycardia? its causes?

A

abnormally slow HR (<60 bpm)

  • depressed impulse formation
  • impaired impulse conduction (block)
  • excessive vagal tone
  • hyperkalemia (severe may cause block)
  • hypothyroidism, sleep apnea
  • Rx (BB, CCA, ACh, adenosine)
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6
Q

what is sick sinus syndrome? what is it associated with?

A

occurs in elderly > 65 yo

  • disease of SA node, unknown origin
  • sometimes occlusion of SA artery
  • SA block not uncommon with SA bradycardia
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7
Q

what are treatments for sinus bradycardia/block?

A
  • treatment of causative medical condition
  • alter medications
  • artificial pacemaker if refractory
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8
Q

what are the degrees of atrio-ventricular nodal blocks? treatments? associations? severity?

A

1st: prolonged PR interval, but normal 1:1 P wave to QRS complex (transmission of atria to ventricles)
2nd: dropped beats (not every P wave followed by QRS complex)
- Mobitz I: PR interval progressively prolongs until beat is dropped (Wenckebach)
- -excess vagal tone; responds to atropine but not sympathetic stimulation
- Mobitz II: PR interval constant in a P:QRS association pattern (more serious, may progress to full block)
3rd: complete AV block (most severe)
- no consistent PR itnerval, requires ventricular pacemaker (no activation)
- associated with trifascicular blocks

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9
Q

what are fascicular blocks? ECG traits?

A

hemiblocks

  • left anterior fascicle (left axis deviation)
  • left posterior fascicle (right axis deviation)
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10
Q

what do atrial premature systoles look like?

A

early occurance of a P-wave that may:

  • be followed by normal QRS complex
  • be blocked by AV node if too early
  • block in bundle branches
  • reset sinus rhythm (phase resetting)
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11
Q

what do junctional premature systoles look like?

A

premature and/or inverted P wave

  • originate from AV node/bundle
  • may be preceded by inverted P wave (retrograde conduction)
  • may be followed by normal QRS complex
  • may block sinus beat
  • -compensatory pause is delay until next normal sinus rhythm
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12
Q

what do ventricular vextrasystoles look like?

A

abnormal QRS complex

  • originate below bifurcation of His bundle (not preceded by P wave)
  • asynchronous ventricular activation (prolonged QRS)
  • may produce compensatory pause (block normal SAN impulse thru AVN)
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13
Q

what are mechanisms for tachycardias?

A
  • accelerated automaticity
  • triggered activity (EAD, DAD)
  • abnormal conduction
  • AP inhomogeneity
  • -depolarization (phase 0)
  • -repolarization and refractoriness (phases 1-3)
  • -resting potential (phase 4)
  • abnormal conduction structures
  • -accessory pathways
  • -dual AV node pathways
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14
Q

for the following types of tachycardia, what are the P-wave, PR interval, and onset of termination?

A

sinus: normal P wave, normal/prolonged PR interval, and gradual onset/termination
atrial: abnormal (not conducting) P wave, normal/prolonged PR interval, and paroxysmal onset/termination
junctional: retrograde (inverted) P wave, short/absent PR interval, and paroxysmal onset/termination

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15
Q

what is sinus tachycardia? causes? treatment?

A

abnormally rapid HR > 100 bpm

  • excessive symapthetic tone, pheochromocytoma
  • sinus node re-entry
  • hypotension (postural, blood volume)
  • anemia, sepsis, shock
  • anxiety, fever
  • cardiac ischemia/infarction, heart failure
  • pulmonary embolism or COPD
  • stimulants (nicotine, caffeine, cocaine)

treated w/ carotid massage, Ach, B-blockers, AVn blocking agents, catheter ablation (may need pacemaker), If blocker

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16
Q

what is SAN reentry? mechanism? prevalence? treatment?

A

due to SAN reentrant conduction

  • rare
  • paroxysmal
  • terminate by electrical stimulus
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17
Q

what is automatic atrial tachycardia? mechanism? prevalence?

A

due to ectopic atrial pacemaker

  • rare
  • non-paroxysmal, ectopic foci
  • may precede flutter or fibrillation
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18
Q

what is atrial reentry? mechanism? prevalence? treatment

A

due to atrial reentrant conduction

  • rare
  • paroxysmal, extrasystole trigger (140 bpm)
  • terminated by electrical stimulation, but not responsive to vagal tone
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19
Q

what is automatic AV junctional tachycardia? mechanism? prevalence? treatment?

A

due to ectopic His bundle pacemaker

  • rare
  • non-paroxysmal, ectopic foci
  • variable rate (brady or tachy)
  • no retrograde P waves, short PR interval, QRS
  • slowed, not terminated, by vagal stimulation, adenosite
  • commonly caused by cardiac glycoside toxicity
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20
Q

what is AV node reentry? mechanism? prevalence? treatment?

A

due to dual AVN conduction pathways

  • most common (2/3)
  • dual conduction pathways, paroxysmal, extrasystole trigger
  • -depends on Ca,L
  • terminated by vagal tone, adenosine, BBs, CCBs
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21
Q

what is bypass tract reentry? mechanism? prevalence?

A

due to AVN and bypass tract reentry

-second most common (20%)

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22
Q

what is paroxysmal supraventricular tachycardia? mechanism? treatment?

A

paroxysmal atrial tachycardia

  • typically AVN reentry accessory pathway
  • initiated by extrasystole
  • responds to vagal stimulation (carotid sinus massage)
  • adenosine, beta-blockers, CCBs
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23
Q

what is Wolff-Parkinson-White syndrome?

A

“fast” accessory pathway (outside nodes)

  • typically atrial origin, bundle of Kent
  • initiated by extrasystole
  • shortened PR interval
  • pre-excitation, delta-wave, wide QRS
  • not responsive to vagal tone
  • AVN blockers contraindicated
  • treat with amiodarone, procainamide, cardioversion, ablation
  • hi risk for sudden death
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24
Q

what are types of ventricular tachycardia?

A

monomorphic (uniform)

  • spontaneous extrasystoles (>3 PVCs)
  • sustained (>30 seconds)
  • -fusion beat has fused PVC and normal impulse

polymorphic (non-uniform)

  • Torsades de Pointes (TdP), long QT syndrome
  • -14 genes, drug induced, EADs
  • catecholamine-induced polymorphic VT (CPVT)
  • DAD mechanism, extrasystoles (glycosides)
  • deficient Ca++ cycling
  • exercise-induced
  • beta-blockers
  • ICD
  • sympathectomy (left cardiac)
25
Q

what is long QT syndrome 1? channel affected? induced by? treatment?

A

50% of them

  • associated with Ks channel
  • induced by exercise or emotion
  • treated with B-blockers, L cardiac nerve denervation
26
Q

what is long QT syndrome 2? channel affected? induced by? treatment?

A

40% of them

  • associated with Kr channel
  • induced by sleep, auditory, or post-partum
  • treated with [K+]o therapy (BB less effective)
27
Q

what is long QT syndrome 3? channel affected? induced by? treatment?

A

10% of them

  • associated with Na channel
  • induced by rest, sleep, bradycardia
  • BB are less effective, so must block late Na “window” current
28
Q

what does atrial flutter look like? treatment? severity?

A

rapid atrial rate (250 to 350 bpm)

  • sawtooth F-wave pattern
  • -QRS normal
  • -AV dissociation (regular pattern)
  • vagal stimulation and CCBs not effective
  • not life-threatening unless transmitted to ventriclesapid rate (WPW)
29
Q

what does atrial fibrillation look like? treatment? severity?

A

most common cardiac arrythmias

  • leading cause of stroke (thrombosis)
  • irregular atrial rate (400-500 bpm)
  • anticoagulants, rate control, and anti-arrythmics are necessary for the rest of life if chronic and sustained
  • -ablation therapy is inexact
  • increased risk of stroke, HF, and SCD if gets to ventricles
30
Q

what does ventricular flutter look like? treatment? severity?

A

lethal arrythmia if not treated

  • no effective ventricular contraction
  • cardioversion required
  • no QRS or T waves
  • rapid reentrant rhythm
  • ICD
  • DON’T give antiarrythmic drugs, as they could be proarrhythmic
31
Q

what does ventricular fibrillation look like? treatment? severity?

A

lethal arrythmia if not treated

  • no effective ventricular contraction
  • cardioversion required
  • no QRS or T waves
  • rapid reentrant rhythm
  • ICD
  • DON’T give antiarrythmic drugs, as they could be proarrhythmic
32
Q

what is parasystole?

A

slow automatic ventricular rhythm

  • ectopic ventricular pacemaker origin
  • abnormal QRS
33
Q

what is bigeminy?

A

PVC after every sinus beat

34
Q

what is trigeminy?

A

PVC after every 2nd sinus beat

35
Q

what is overdrive suppression?

A

rapid stimulation suppression of normal pacemaker activity

36
Q

what is syncope?

A

sudden loss of consciousness due to lack of blood the brain

37
Q

what is the mechanism of action for class Ia antiarrhythmic drugs? names?

A

fast (open) Na+ channel block (oldest ones)

  • prolongs effective refractory period
  • prolongs action potential duration
  • depress phase 0

quinidine, procainamide, disopyramide

38
Q

what is quinidine? uses? toxicities? drug interactions?

A

class 1a antiarrythmic drugs

  • use: chronic treatment of atrial flutter, fibrillation, SVT
  • -alpha-adrenergic and M2 blockade, vagal inhibition
  • -hypotension, sinus tachycardia
  • toxicities: diarrhea, nausea, fever, hepatitis, thrombocytopenia, cinchonism, QT prolongation (TdP)
  • -may increase AVN transmission
  • drug interactionsL digoxin (plasma binding to albumin), CYP2D6 inhibition
  • -metabolism induced by phenobarbital, phenytoin
39
Q

what is procainamide? uses? toxicities?

A

class 1a antiarrythmic drugs

  • use: chronic treatment of atrial flutter, fibrillation, SVT, ventricular fibrillation
  • -local anesthetic properties, but no alpha-adrenergic or M2 blockade
  • toxicity: drug-induced lupus syndrome (slow acetylators), QT prolongation (TdP), active metabolite, hypotension (ganglionic blockade)
40
Q

what is disopyramide? toxicities?

A

class 1a antiarrythmic drugs

  • no alpha-adrenergic blockade
  • prominent anticholinergic action (constpiation, dry mouth, glaucoma)
  • QT prolongation (TdP)
41
Q

what is the mechanism of action for class Ib antiarrhythmic drugs? names?

A

Na+ channel block (open, inactivated); better at treating ischemia

  • prefers depolarized (ischemic) tissue Na+ channel blockade
  • prefers inactivated Na+ channels, rapidly unbinds at rest
  • depress phase 0 in abnormal fibers
  • shorten repolarization
  • little effect on phase 0 in normal tissue
  • lidocaine, mexiletine
42
Q

what is lidocaine? uses? toxicities?

A

class 1b antiarrythmic drugs (NOT for atrial arrythmias)

  • use: acute suppression of VF
  • -local anesthetic (IV only; first pass metabolism)
  • -emergency VT/VF, cardioversion, digitalis toxicity
  • toxicities: tremor, nausea, seizures
  • -no QT prolongation, may shorten APD slightly
  • -late Na+ channel blockade
43
Q

what is mexiletine?

A 
class 1b antiarrythmic drug
oral lidocaine, but severe GI toxicity (not used anymore)
-metabolism induced by phenytoin
44
Q

what is tocainide?

A

class 1b antiarrhythmic drug

  • causes fatal bone marrow aplasia, pulmonrosis
  • not in US
45
Q

what is the mechanism of action for class Ic antiarrhythmic drugs? names?

A
  1. Na+ channel block (slow unbinding, greatly prolongs Na recovery
  2. K+ channel blockade (prolongs APD preferentially at faster rates)
    - prolongs PR, QRS, QT interval, but no EA or TdP

flecainide, propafenone, moricizine

46
Q

what is the use of class 1c antiarrythmic drugs? metabolism?

A

acute management of atrial fibrillation, SVT, but NEVER for ventricular arrythmias (strongest blockers)

  • primary maintenance of sinus rhythm in chronic AF, SVT in patients w/o structural heart disease
  • renal and CYP2D6 elmination
47
Q

what is special about propafenone?

A

1c antiarrythmic drug that has beta-blocking activity (S-(+))

  • 5-hydroxy metabolite lacks B-blocker activity, butll blocks Na
  • -formed by CYPD2D6 first pass metabolism
48
Q

what are toxicities of class Ic antiarrythmic drugs?

A
  • may increase ventricular response to atrial flutter
  • -contraindicated in heart failure, VT
  • increased mortality in patients with acute MI (would kill pt)
  • flecainide: blurred vision
  • propafenone: sinus bradycardia, bronchospasm (due to beta-blocking properties)
49
Q

what are class II antiarrythmic drugs? contraindications? names?

A

B1 adrenergic selective receptor blockers

  • metoprolol: lipophilic, membrane stabilizing
  • -improves mortality in CHF patients
  • acebutolol: same, but with intrinsic sympathomimetic activity
  • esmolol: IV, short half-life, used in acute emergency treSVTs when short duration desired

contraindicated in WPW syndrome, and sudden withdrawal in angina patient may cause MI

50
Q

what is the mechanism of class III antiarrythmic drugs? major toxicity?

A

K+ channel blockade to prolong refractoriness

  • major toxicity is risk of TdP arrythmias (strongly pro-arrythmic, not to treat ventricular arrythmias)
  • sotalol, ibutilide, dofetilide, amiodarone, dronedarone
51
Q

what is sotalol? side effects?

A

class III antiarrythmic drug

  • blocks Ks, non-selective B-blocker
  • preferred over quinidine for control of chronic AF
  • ASE: EADs, TdP, decreased HR, decreased AV conduction
52
Q

what is ibutilide?

A

class III antiarrythmic drug

  • IV for termination of atrial flutter or fibrillation
  • first pass metabolism renders oral dose ineffective
  • for emergency settings
53
Q

what is dofetilide?

A

class III antiarrythmic drug

  • Kr blocker “restricted distribution”, oral
  • maintain sinus rhythm after cardioversion, convert chronic AF
  • NOT for ventricular arrythmias or paroxysmal AF
54
Q

what is amiodarone? uses? side effects?

A

class III antiarrythmic drug, thyroxine analog (although mixed action mimic all classes)

  • decreases Na+, Ca++, and K+ currents
  • alpha/beta adrenergic blocking effect
  • prolongs ERP, APD
  • useful against most all arrythmias, but NOT digitalis toxicity, and not during pregnancy

ASE: QT prolongation (TdP rare), pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, corneaicrodeposits, numerous drug interactions, photosensitivity (blue-gray skin)

55
Q

what is dronedarone?

A

class III antiarrythmic drug

  • benzofurane (not used as often)
  • less effective but fewer side effects than amiodarone
  • QT prolongation, nausea, diarrhea
56
Q

what are class IV antiarryhmic drugs?

A

L-type Ca++ channel blockade

  • slow SA, AV node activity
  • prolong AV refractoriness
57
Q

what do verapamil and diltiazem do?

A

slow ventricular rate during atrial flutter or a-fib

  • prevent or terminate reentrant SVTs, contraindicated in WPW
  • IV use hypotension, bradycardia, constpiation, diz
  • will increase serum digoxin levels, AV block effects additive oxin, beta-blockers
58
Q

what is adenosine?

A

natural nucleoside, IV bolus only

  • GPCR-mediated decrease in cAMP
  • beta-gamma mediated increase in K,ACh
  • decrease SA, AV node activity
  • increase AV refractoriness
  • will terminate PSVT, AVN reentrant arrythmias
  • -NOT atrial flutter, a-fib, multifocal atrial tachycardia, or WPW
  • antagonized by methyl xanthines, sedationea, hypotension
  • -may cause reflex sympathetic activation
59
Q

how is Mg used in arrythmias?

A

MgSO4

  • prevent recurrent TdP and some digitalis-induced arrythmias
  • alternative to amiodarone for shock-refractoy cardiac arrest

MSII Pharmacology (43 decks)

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