Anti-Arrhythmic Drugs I + Ii - Baker

Front 1

The dominant pacemaker of the heart is the _______.

Back 1

SA node

Front 2

Stimulation from the _____________ branch of the autonomic nervous system is lacking in the ventricles.

Back 2

Parasympathetic

Front 3

Where are fast response action potentials found?

Back 3

Atrial tissue, the His-Purkinje system, and ventricular tissue

Front 4

What ion is responsible for phase 0/depolarization in fast response fibers?

Back 4

Na+

Front 5

The slope of phase 0 corresponds with what?

Back 5

Conduction velocity

Front 6

Phase 2, the plateau phase, corresponds with the opening of what channels?

Back 6

Ca2+ (and K+)

Front 7

What is the effective refractory period? What phases of the action potential does it correspond with?

Back 7

-period in which an action potential cannot be created regardless of stimulation
-phase 1-3

Front 8

What kinds of drugs increase the effective refractory period?

Back 8

K+ channel blockers (extend phase 3)

Front 9

Where are slow action potentials found?

Back 9

SA and AV nodes

Front 10

In slow action potentials, phase 0 or depolarization is mediated by what ion?

Back 10

Ca2+

Front 11

What phases are missing in the slow action potential?

Back 11

-Phase 1 and 2 (plateau)
- 4 --> 0 --> 3 --> 4

Front 12

The ability of slow response action potential to spontaneously depolarize is called what?

Back 12

Automaticity

Front 13

Autonomic inputs will alter the slope of what phase in the slow action potential?

Back 13

-Phase 4
-parasympathetic decreases slope
-sympathetic increases slope

Front 14

What kinds of drugs would slow conduction of slow response action potentials?

Back 14

Ca2+ channel blockers

Front 15

Name the two major mechanisms of arrhythmias

Back 15

-abnormal impulse formation
-altered impulse conduction

Front 16

Name 4 ways impulse formation can be altered.

Back 16

-altered normal - chronic change in firing rate of SA node
-latent pacemaker - SA node loses function so AV node or His-Purkinje system take over at slower rate
-abnormal automaticity - i.e. heart damage causes cells that are normally not automatic to become automatic
-After depolarizations (early or delayed)

Front 17

What is a delayed after depolarization? An early after depolarization?

Back 17

-DAD - depolarization out of sequence that occurs immediately upon reaching Phase 4/resting potential
-EAD - depolarization out of sequence that occurs mid phase 3

Front 18

What causes DAD?

Back 18

Elevated levels of intracellular Ca2+

Front 19

What drug can cause DAD?

Back 19

Digoxin (toxicity)

Front 20

What kind of drug could cause an Early After Depolarization?

Back 20

K+ channel blocker

Front 21

Multiple EADs in a row create what arrhythmia?

Back 21

Torsade de Pointe (polymorphic ventricular tachycardia)

Front 22

What happens when an excitatory action potential reaches another action potential?

Back 22

It extinguishes

Front 23

Rate of conduction in an ischemic zone is faster or slower?

Back 23

slower

Front 24

Describe how electrical impulses passing through an ischemic zone can cause an arrhythmia.

Back 24

1 - excites the tissue but conduction is slow
2 - signal from an adjacent purkinje fiber is able to re-excite the ischemic area via retrograde conduction
3 - get a self-propagating pathway (re-entrant pathway)

Front 25

What two kinds of agents can be used to block re-entrant pathways in ventricular or atrial muscle tissue?

Back 25

-K+ channel blockers (extends refractory period)
-Na+ channel blockers (slows conduction further)

Front 26

What is the treatment for ventricular fibrillation?

Back 26

Shock

Front 27

What class of drug would you use to treat a re-entrant pathway that involved the AV node? What is another name for an AV nodal reentry tachycardia?

Back 27

-Ca2+ channel blocker (would slow conduction rate)
-PSVT (Paroxysmal Supraventricular Tachycardia)

Front 28

Name 5 supraventricular arrhythmias.

Back 28

-sinus bradycardia (<60 bpm)
-sinus tachycardia (>100 bpm)
-atrial flutter (>300 bpm)
-atrial fibrillation (> 400 bpm)
-AV nodal Reentry tachycardia (PSVT)

Front 29

Increased _________ tone is responsible for sinus bradycardia.

Back 29

-vagal (parasympathetic)

(could treat with atropine)

Front 30

Increased ____________ tone is responsible for sinus tachycardia.

Back 30

sympathetic

(could treat with beta blockers)

Front 31

Atrial flutter is caused by _____________ re-entry while atrial fibrillation is caused by _____________ re-entry.

Back 31

-stable (only one); disorganized (multiple)

Front 32

Name 4 types of ventricular arrythmias

Back 32

-premature ventricular contraction
-ventricular tachycardia
-ventricular fibrillation
-Torsade de Pointe (Polymorphic VT)

Front 33

What two drugs are used to treat bradyarrythmias acutely? What intervention is done long-term to treat them?

Back 33

-Anticholinergics - atropine
-Beta agonists - isoproternol

-pacemaker

Front 34

To stop re-entrant pathways in tachyarrhythmias, you want to __________ conduction and ________________ refractory period.

Back 34

decrease; increase

Front 35

Ion channel blockers have a greater affinity for channels in the _____________ and ________________ states than for those in the ____________ state.

Back 35

-inactive and conducting; resting

Front 36

Lidocaine is ineffective against what kinds of arrhythmias?

Back 36

atrial arrhythymias

Front 37

Which drug has the highest affinity for Na+ channels?

Back 37

Flecainide