Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiology Exam > EP Drugs (Antiarrhythmics) > Flashcards

EP Drugs (Antiarrhythmics) Flashcards

1
Q

relationship between cardiac action potential & EKG

A

*phase 0 = sodium channels open = QRS complex
-prolongation → widened QRS

*phase 3 = repolarization (potassium channels open) = T wave
-prolongation → QT interval prolongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

relationship of pacemaker action potential (SA/AV node action potential) to automaticity, conduction velocity, and repolarization/refractory period

A

*phase 4 = sodium influx = AUTOMATICITY (intrinsic rate of the beat; steeper slope means faster rate)
*phase 0 = calcium influx = CONDUCTION VELOCITY (how fast the signal travels through the cells after firing)
*phase 3 = potassium efflux = REPOLARIZATION/refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

relationship of cardiac action potential to automaticity, conduction velocity, and repolarization/refractory period

A

*phase 0 = sodium influx = CONDUCTION VELOCITY (you can slow conduction velocity by blocking sodium channels)
*phase 1 = early potassium efflux (sodium channels close)
*phase 2 = plateau = balance between Ca2+ influx and K+ efflux
*phase 3 = repolarization = K+ efflux = REPOLARIZATION/refractory period (you can prolong the refractory period by blocking potassium channels)
*phase 4 = resting potential = AUTOMATICITY (not really any automaticity in the myocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ways to end a re-entrant pathway

A

*end the re-entrant pathway by:
1. increasing absolute refractory period
2. slowing down the conduction velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Vaughn-Williams Classification System for Antiarrhythmic drugs

A

*class I: sodium channel blockers
*class II: beta blockers
*class III: potassium channel blockers
*class IV: calcium channel blockers

*classes I and III target the fast response tissues (tissues with a “cardiac action potential” - specifically the ventricles)
*classes II and IV target the slow response tissues (tissues with a “pacemaker action potential” - specifically the SA and AV nodes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

class I antiarrhythmic drugs

A

*sodium channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

sodium channel blockers (class I) - overview

A

*slow or block conduction velocity (especially in depolarized cells)
*mainly target fast response tissues (tissues with a cardiac action potential; ventricles)
*decrease the slope of phase 0 depolarization → increased action at FASTER HR
*shift the curve to the left, causing fewer sodium channels to be available to fire, even at lower resting potentials, slowing conduction velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

the different states of sodium channels

A

*closed (resting) - able to be activated
*open (active) - open with Na+ ions passing through
*closed (inactive) - can’t be opened (in the refractory period)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

heart rate influence on states of sodium channels

A

*at higher heart rates, the sodium channel spends more time in open & inactive states
*at lower heart rates, the sodium channel spends more time in the resting state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

class IA antiarrhythmic drugs - examples

A

*disopyramide
*quinidine
*procainamide

“Double Quarter Pounders make you ‘slow’ and ‘fat’”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

class IA antiarrhythmic drugs - MOA

A

*moderate Na+ channel blockade
*increase action potential duration
*increase effective refractory period (ERP) in ventricular action potential
*increase QR interval
*some K+ channel blocking effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

class IA antiarrhythmic drugs - action potential impact

A

*slows phase 0
*widens action potential (AP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

class IA antiarrhythmic drugs - EKG impact

A

*widened QRS
*prolonged QT interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

disopyramide

A

*class IA antiarrhythmic (SODIUM CHANNEL BLOCKER - moderately slows phase 0 and widens AP)

-reduces contractility
-historically used to treat LVOT obstruction in hypertrophic cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

quinidine

A

*class IA antiarrhythmic (SODIUM CHANNEL BLOCKER - moderately slows phase 0 and widens AP)

-anti-malarial
-ADE: GI upset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

procainamide

A

*class IA antiarrhythmic (SODIUM CHANNEL BLOCKER - moderately slows phase 0 and widens AP)

-used for Wolff-Parkinson-White pts with Afib when cardioversion is not an option
-ADE: some patients who use it for 6+ months will develop a lupus-like syndrome and become ANA-positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

class IB antiarrhythmic drugs - examples

A

*lidocaine
*mexiletine

“Lettuce and Mayonnaise make you skinny”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

class IB antiarrhythmic drugs - MOA

A

*weak Na+ channel blockade
*decrease action potential duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

class IB antiarrhythmic drugs - action potential impact

A

*weakly slows phase 0
*shortens action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

class IB antiarrhythmic drugs - EKG impact

A

*normal/baseline QRS
*shortened QT interval!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

lidocaine

A

*class IB antiarrhythmic (SODIUM CHANNEL BLOCKER - weakly slows phase 0 and shortens AP)

-ADE: at high levels, pts experience confusion, paresthesias, and seizures (monitor levels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

mexiletine

A

*class IB antiarrhythmic (SODIUM CHANNEL BLOCKER - weakly slows phase 0 and shortens AP)

*ADE: may also cause dizziness, slurred speech, and GI upset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

class IC antiarrhythmic drugs - examples

A

*flecainide
*propafenone

“Fries Please!” - makes you slow but not fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

class IC antiarrhythmic drugs - MOA

A

*strong Na+ channel blockade
*strongly slows phase 0
*significantly prolongs effective refractory period (ERP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

class IC antiarrhythmic drugs - action potential impact

A

*strongly slows phase 0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

class IC antiarrhythmic drugs - EKG impact

A

*widened QRS
*no impact on QT interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

flecainide

A

*class IC antiarrhythmic (SODIUM CHANNEL BLOCKER - strongly slows phase 0)

-avoid in patients with LV dysfunction or coronary artery disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

propafenone

A

*class IC antiarrhythmic (SODIUM CHANNEL BLOCKER - strongly slows phase 0)

-avoid in patients with LV dysfunction or coronary artery disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

summary of class I antiarrhythmic drug effects

A

*strength of sodium blockade: class IC > IA > IB

*IA: widened QRS, QT interval prolongation
*IB: normal QRS, QT interval shortens
*IC: profound QRS widening

30
Q

class II antiarrhythmic drugs

A

beta blockers

31
Q

beta blockers (class II antiarrhythmics) - MOA

A

*decrease SA & AV node activity by decreasing cAMP → decreased Ca2+ currents
*suppress abnormal pacemakers by decreasing the slope of phase 4

32
Q

beta blockers (class II antiarrhythmics) - indications

A

*supraventricular tachycardia (SVT)
*ventricular tachycardia

33
Q

beta blockers (class II antiarrhythmics) - action potential impact

A

*strongly slows phase 4 (of the pacemaker cells - SA and AV node) to slow down heart rate

34
Q

beta blockers (class II antiarrhythmics) - overview

A

*work by blocking the effect of beta-1 stimulation by epi/norepi
*mainly target slow response tissues (tissues with a pacemaker action potential - SA and AV nodes)

35
Q

beta blockers (class II antiarrhythmics) - EKG impact

A

*decrease heart rate
*no impact on QRS or QT interval
*may prolong PR interval (b/c they slow conduction at the AV node)

36
Q

beta blockers (class II antiarrhythmics) - ADEs

A

*those that also block beta2 may cause bronchospasm
*may cause AV block or sinus bradycardia
*may precipitate arterial vasospasm in Raynaud’s
*slows conversion of thyroid hormone
*prevent symptoms associated with low blood sugar (be cautious in diabetic patients)

37
Q

beta blockers (class II antiarrhythmics) - examples

A

*metoprolol
*propranolol
*esmolol
*atenolol
*timolol
*carvedilol

38
Q

class III antiarrhythmic drugs

A

potassium channel blockers

39
Q

potassium channel blockers (class III antiarrhythmics) - examples

A

*amiodarone
*ibutilide
*dofetilide
*dronedarone
*sotalol

40
Q

potassium channel blockers (class III antiarrhythmics) - overview

A

*work by blocking the potassium channels
*mainly target fast response tissues (tissues with a cardiac action potential - ventricles)

41
Q

potassium channel blockers (class III antiarrhythmics) - action potential impact

A

*prolongs phase 3 (of ventricular cells) to increase absolute refractory period

42
Q

potassium channel blockers (class III antiarrhythmics) - EKG impact

A

*QRS unchanged
*WIDENING OF QT INTERVAL

43
Q

ibutilide

A

*class III antiarrhythmic (POTASSIUM CHANNEL BLOCKER - prolongs phase 3/refractory period)

-used for acute conversion of Afib
-high risk of Torsades (give Magnesium first)

44
Q

dofetilide

A

*class III antiarrhythmic (POTASSIUM CHANNEL BLOCKER - prolongs phase 3/refractory period)

-admit to hospital for first 5 doses due to risk of Torsades

45
Q

sotalol

A

*class III antiarrhythmic (POTASSIUM CHANNEL BLOCKER - prolongs phase 3/refractory period)

-admit to hospital for first 5 doses due to risk of Torsades

46
Q

dronedarone

A

*class III antiarrhythmic (POTASSIUM CHANNEL BLOCKER - prolongs phase 3/refractory period)

-amiodarone without the iodine
-increases mortality in those with heart failure

47
Q

amiodarone

A

*class III antiarrhythmic (POTASSIUM CHANNEL BLOCKER - prolongs phase 3/refractory period)

-many different effects
-drug of choice for VT/VF in setting of cardiac arrest
-significant ADEs: PULMONARY FIBROSIS, thyroid issues, liver issues (monitor PFTs, TFTs, and LFTs)
-note: amiodarone-induced pulmonary fibrosis is very bad

48
Q

QT prolongation increases risk for ?

A

QT prolongation increases risk for Torsades de Pointes

49
Q

class IV antiarrhythmic drugs

A

calcium channel blockers

50
Q

calcium channel blockers (class IV antiarrhythmics) - overview

A

*decrease conduction velocity by prolonging phase 0 of pacemaker cells
*mainly acts on slow response tissues (tissues with a pacemaker action potential - SA and AV nodes)

51
Q

calcium channel blockers (class IV antiarrhythmics) - MOA

A

*decrease conduction velocity
*increase effective refractory period (ERP)
*increase PR interval
*decrease HR

52
Q

calcium channel blockers (class IV antiarrhythmics) - action potential impact

A

*prolongs phase 0

53
Q

calcium channel blockers (class IV antiarrhythmics) - EKG impact

A

*INCREASE IN PR INTERVAL
*QRS unchanged
*QT interval unchanged

54
Q

calcium channel blockers (class IV antiarrhythmics) - examples

A

*verapamil
*diltiazem

note - dihydropyridine calcium channel blockers (amlodipine, other -dipines) do not act on the heart, just the blood vessels

55
Q

calcium channel blockers (class IV antiarrhythmics) - ADEs

A

*constipation

56
Q

verapimil

A

*class IV antiarrhythmic (CALCIUM CHANNEL BLOCKER - prolongs phase 0 of pacemaker cells, increases PR interval)

57
Q

diltiazem

A

*class IV antiarrhythmic (CALCIUM CHANNEL BLOCKER - prolongs phase 0 of pacemaker cells, increases PR interval)

58
Q

digoxin - overview

A

*derived from the Digitalis purpurea (Foxglove)
*SLOWS CONDUCTION THROUGH AV NODE BY INCREASING VAGAL ACTIVITY
*regarded as a positive inotropic agent because it increases contractility by increasing intracellular calcium

59
Q

digoxin - MOA

A

*direct inhibition of Na+/K+-ATPase → indirect inhibition of Na+/Ca2+ exchanger
*increased intracellular calcium → positive inotropy (increased contracility
*increases vagal tone → slow conduction through AV node → decrease HR

60
Q

digoxin - toxic rhythm effects

A

*can cause:
-sinus bradycardia
-AV block
-accelerated junctional rhythm
-premature ventricular beats

61
Q

digoxin - ADE: hyperkalemia

A

*due to inhibition of Na+/K+ ATPase, it is difficult to get potassium back into the intra-cellular environment

62
Q

digoxin - acute toxicities

A

*GI: N/V, abdominal pain
*CV: dysrhythmias
*CNS: lethargy, confusion, weakness

63
Q

digoxin & vision

A

*causes BLURRY YELLOW VISION

64
Q

digoxin ADEs - summary

A

*hyperkalemia
*blurry yellow vision
*toxic heart rhythms
*N/V, abdominal pain

65
Q

adenosine - overview

A

*adenosine has a VERY short half-life
*slows conduction through mechanisms by binding A2 receptor:
-hyperpolarizes cell by opening K+ channel
-blocks adenylate cyclase (decreased funny current & decreased calcium influx)
*by BLOCKING AV NODE, it gets people OUT OF SVT

66
Q

atropine - MOA

A

*atropine blocks the acetylcholine receptor
*takes away parasympathetic influence on heart rate:
-increases the slope of phase 4 in SA and AV node
-heart rate should increase
*if someone is bradycardia, often put atropine to bedside in case they become symptomatic

67
Q

ivabradine - MOA & info

A

*inhibitor of If (“funny current”
*used for rate control in heart failure if HR > 70 bpm
*side effects: bradycardia, AF
*interactions: metabolized by CYP3A4

68
Q

what is the real risk of Afib/Aflutter?

A

*thromboembolism (most likely from the left atrial appendace)
*if someone has Afib/flutter > 48h, we need a TEE (transesophageal echo) to assess for thrombus in left atrial appendage

69
Q

anticoagulation in Afib/Aflutter

A

*score 0 = no anticoagulation
*score 1+ = need anticoagulation wtih a direct oral anticoagulant or vitamin K antagonist

*things that contribute to CHADS2-VASc score:
-CHF, HTN, age 75+ (2 pts), diabetes, prior TIA or stroke (2 pts), vascular disease (MI, aortic plaque), age 65-74, female (1 pt)

70
Q

rate control in Afib/Aflutter

A

*aim for rate < 110 bpm for most of the day

1st. either metoprolol or diltiazem
2nd. digoxin
3rd. AV nodal ablation

note - do NOT use calcium channel blockers (ex. diltiazem) in heart failure

71
Q

emergency medication therapy for ventricular tachycardia

A

1st. amiodarone
2nd. lidocaine
3rd. ventricular tachycardia ablation

72
Q

long-term/outpatient medication therapy for ventricular tachycardia

A

1st. amiodarone
2nd. mexiletine
3rd. ventricular tachycardia ablation

Cardiology Exam (52 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions