EKGs

Question 1

what are the Supraventric tachycardias? (6)

Answer 1

• sinus tach
• multifocal atrial tach
• atrial flutter
• a fib
• Atrioventric nodal reentrant tachy (AVNRT)
• AV reentrant tachy (AVRT)
• junctional tach

Question 2

what are the paroxysmal supraventric tachycardias? (4)

Answer 2

• atrioventricular nodal reentrant tachycardia (AVNRT)
• Atrioventricular reentrant tach (AVRT)
• atrial tach
• junctional tach

Question 3

what to do in cases of hemodynamically stable SVT?

Answer 3

1. figure out which type of SVT by either:
   - vagal maneuvers (carotid sinus massage, valsalva, eyeball pressure)
   - Adenosine
   - -> slow conduction at AP node (figure out if there are hidden p waves for atrial flutter/tach, cause transient AV node block –> stop AV-node dependent arrhythmias (AVNRT and AVRT))

Question 4

how do you treat hemodynamically stable patients with wide QRS-complex tach (ventric tach)?

Answer 4

amiodarone or lidocaine

Question 5

how do class I antiarrythmics work?

Answer 5

block NA channels– inhib initial depolarizatin phase (phase 0)

Question 6

flecainide and propafenon are what class antiarrhythmic?

Answer 6

IC– block NA channels– inhib initial depolarizatin phase (phase 0)

Question 7

what is different about flecainide and propafenon (class Ic antiarrhythmic) compared to other class I drugs? how does this effect people with faster heart rates

Answer 7

slowest rate of drug binding/dissociation from Na channel receptor —> in pts with faster heart rates, they have less time to dissociate from Na channels –> more blocked channels –> progressive decrease in impulse conduction —> widened QRS (termed “use dependence”). this is the mechanism behind their efficacy agst SV arrhythmias (and therefore can be used to fight afib in people with structurally normal hearts)

Question 8

how does digoxin work/what is it used for?

Answer 8

inhibs ATPase- dependent Na-K pump –> increases intracellular ca –> decreases Na-Ca exchanger activity –> increase intracellular Ca.
- enhances vagal tone
- slows conduction through AV node
==> causes bradyarrhythmias (younger, healthier pts) or enhance automaticity and delayed after-depolarizations leading to ventricular ectopy and tachyarrythmias (more common in older pts with underlying cardiac activity)

Question 9

how can digoxin’s enhancement of vagal tone/slowing conduction through AV node effect young/healthy pts? older pts?

Answer 9

==> causes bradyarrhythmias (younger, healthier pts) or enhance automaticity and delayed after-depolarizations leading to ventricular ectopy and tachyarrythmias (more common in older pts with underlying cardiac activity)

Question 10

how do CCBs (class IV) work?

Answer 10

calcium channel blockade –> use dependence (in pts with increased ventricular activation, they have less time to dissociate from Ca channels –> more blocked channels –> progressive decrease in impulse conduction) —> progressive prolongation of refractory period in AV node –> increased PR interval

Question 11

Pts on flecainaide or propafenon (class IC antiarrythmics) would see what change in the EKG at faster heart rates?

Answer 11

widened QRS

Question 12

pts on CCBs (verapamil/dilt) would see what EKG change with faster heart rates?

Answer 12

prolonged PR interval

Question 13

twave inversion in V1-V =

Answer 13

rt heart strain (ie in setting of PE)