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Pharm 2 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

Phase 0

A

Rapid Depolarization (ventricular contraction)

  • increased NA conductance (channels open) through FAST channels (-70 mV)
  • end w/ Na channels “inactive” @ +65 mV
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2
Q

Phase 1

A

Early Rapid Repolarization

  • Na channels closed, inactivated
  • K channels open, begin transient efflux of K to “reset” voltage. (rapidly inactivated)
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3
Q

Phase 2

A
  • Plateau
  • via calcium influx through SLOW channels (L & T type channels)
  • K channels still open, maintain plateau through K+ efflux
  • voltage = +10 to -20 mV
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4
Q

Phase 3

A

Rapid Repolarization

  • lots of K movement
  • No significant movement of Ca or Na
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5
Q

Phase 4

A

Spontaneous Depolarization

  • slow depol. characteristic of all pacemaker cells
  • interaction of outward Ca and inward K during diastole
  • ATP dependent pumps move ions to regain balance
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6
Q

Slow channels, calcium mediated

A
  • responsible for phase 0 in SA and AV noes (slow conduction velocity
  • contribute to phase 2 in ventricular contractile cells (prolongs refractory period)
  • affects phase 4 spont. depol
  • facilitates catecholamines (cAMP)
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7
Q

Fast channels, Na mediated

A
  • phase 0 (rapid, sharp upstroke in His-Purkinje and atrial and ventricular muscle
  • rapid conduction velocity
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8
Q

Automaticity

A

impulse generation

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9
Q

T/F: Cells that undergo spontaneous phase 4 depol are automantic anc capable of impulse generation

A

True,

Factors that reduce automaticity at the higher pacemaker sites will passively favor movement of pacemaker to lower site

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10
Q

Ectopic Foci result from…

A
  • enhanced automaticity at a site outside the SA node
  • SNS influences, hypercarbia, hypoxia, dig tox
  • ex.) A.Fib - little cells just firing on their own, increased clot risk
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11
Q

Re-Entry

A

-circles around pacemaker sites to generate new paths

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12
Q

Na Channel impulse generation…

A

Atria

Ventricles

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13
Q

Ca Channel impulses generate…

A

SA node

AV node

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14
Q

Amiodarone and anticoags

A

increase bleed risk, increased INR

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15
Q

Amiodarone and meds that prolong QT interval

A

Torsades de Pointes

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16
Q

Amiodarone and Digoxin

A

increased dig toxicity

17
Q

Amiodarone and lidocaine

A

increased lidocaine toxicity

18
Q

amiodarone and statins

A

increase myalgias

19
Q

amiodarone and midazolam

A

prolonged sedation, increased risk of resp depression

20
Q

amiodarone and suggamedex

A

increased risk of bradycardia, additive effect

21
Q

amiodarone and AV nodal blockers

A

increased risk of bradycardias, sinus arrest, AV block

22
Q

Prodysrhythmic Effects

A

brady or rachy that represent new cardiac dyrrhythmias associated w/ chronic antidysrhythmic tx

ex. torsades, increased ventric tachy’s, wide complex vent. rhythm

23
Q

Torsades de Pointes

A

K channel blockade may prolong QT interval and induce triggered activity in ventricle –> polymorphic VT or VF

-occurs in 1-8% of pts recieving QT prolonging drugs
will develop torsades

24
Q

Which class blocks potassium channels and prolongs QTc interval

A

Class 1A and Class 3

25
Q

QT Prolonging Meds

A 
Class 1A and Class 3 antiarrhythmics,
antipsychotics (haldol, geodon, risperdal),
diuretics, 
antifungals,
antibiotics (macrolides and FQ's), 
antidepressants,
antinausea, 
methadone, aricept, volatile anesthetics
26
Q

QT Prolonging States

A 
>65 y.o.
bradycardia, genetic predisposition
low K, Mg or Ca
female
heart dx
QTc > 60 ms compared to pretreat or > 500 ms
recent cardioversion
DM2, hypothyroid, low temp
27
Q

Tx of QT prolong brady

A

magnesium
chemical pacemaker - isoproterenol
lidocaine (ventric arrhythmia)

28
Q

Incessent V. Tach

A
  • precipitated by 1A and 1C - slow impulses to that ventricular reentry drives vtach (reentry)
  • more likely with poor LV fx
29
Q

Wide Complex V. Rhythms

A
  • flecainide (1C) use with structural heart disease

- usually from high levels or quick change

Pharm 2 (8 decks)

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