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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

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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

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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)

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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

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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)

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6
Q

class I antiarrhythmic drugs

A

*sodium channel blockers

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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

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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)

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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

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10
Q

class IA antiarrhythmic drugs - examples

A

*disopyramide
*quinidine
*procainamide

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

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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

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12
Q

class IA antiarrhythmic drugs - action potential impact

A

*slows phase 0
*widens action potential (AP)

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13
Q

class IA antiarrhythmic drugs - EKG impact

A

*widened QRS
*prolonged QT interval

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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

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15
Q

quinidine

A

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

-anti-malarial
-ADE: GI upset

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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

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17
Q

class IB antiarrhythmic drugs - examples

A

*lidocaine
*mexiletine

“Lettuce and Mayonnaise make you skinny”

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18
Q

class IB antiarrhythmic drugs - MOA

A

*weak Na+ channel blockade
*decrease action potential duration

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19
Q

class IB antiarrhythmic drugs - action potential impact

A

*weakly slows phase 0
*shortens action potential

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20
Q

class IB antiarrhythmic drugs - EKG impact

A

*normal/baseline QRS
*shortened QT interval!

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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)

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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

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23
Q

class IC antiarrhythmic drugs - examples

A

*flecainide
*propafenone

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

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24
Q

class IC antiarrhythmic drugs - MOA

A

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

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25
class IC antiarrhythmic drugs - action potential impact
*strongly slows phase 0
26
class IC antiarrhythmic drugs - EKG impact
*widened QRS *no impact on QT interval
27
flecainide
*class IC antiarrhythmic (SODIUM CHANNEL BLOCKER - strongly slows phase 0) -avoid in patients with LV dysfunction or coronary artery disease
28
propafenone
*class IC antiarrhythmic (SODIUM CHANNEL BLOCKER - strongly slows phase 0) -avoid in patients with LV dysfunction or coronary artery disease
29
summary of class I antiarrhythmic drug effects
*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
class II antiarrhythmic drugs
beta blockers
31
beta blockers (class II antiarrhythmics) - MOA
*decrease SA & AV node activity by decreasing cAMP → decreased Ca2+ currents *suppress abnormal pacemakers by decreasing the slope of phase 4
32
beta blockers (class II antiarrhythmics) - indications
*supraventricular tachycardia (SVT) *ventricular tachycardia
33
beta blockers (class II antiarrhythmics) - action potential impact
*strongly slows phase 4 (of the pacemaker cells - SA and AV node) to slow down heart rate
34
beta blockers (class II antiarrhythmics) - overview
*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
beta blockers (class II antiarrhythmics) - EKG impact
*decrease heart rate *no impact on QRS or QT interval *may prolong PR interval (b/c they slow conduction at the AV node)
36
beta blockers (class II antiarrhythmics) - ADEs
*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
beta blockers (class II antiarrhythmics) - examples
*metoprolol *propranolol *esmolol *atenolol *timolol *carvedilol
38
class III antiarrhythmic drugs
potassium channel blockers
39
potassium channel blockers (class III antiarrhythmics) - examples
*amiodarone *ibutilide *dofetilide *dronedarone *sotalol
40
potassium channel blockers (class III antiarrhythmics) - overview
*work by blocking the potassium channels *mainly target fast response tissues (tissues with a cardiac action potential - ventricles)
41
potassium channel blockers (class III antiarrhythmics) - action potential impact
*prolongs phase 3 (of ventricular cells) to increase absolute refractory period
42
potassium channel blockers (class III antiarrhythmics) - EKG impact
*QRS unchanged *WIDENING OF QT INTERVAL
43
ibutilide
*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
dofetilide
*class III antiarrhythmic (POTASSIUM CHANNEL BLOCKER - prolongs phase 3/refractory period) -admit to hospital for first 5 doses due to risk of Torsades
45
sotalol
*class III antiarrhythmic (POTASSIUM CHANNEL BLOCKER - prolongs phase 3/refractory period) -admit to hospital for first 5 doses due to risk of Torsades
46
dronedarone
*class III antiarrhythmic (POTASSIUM CHANNEL BLOCKER - prolongs phase 3/refractory period) -amiodarone without the iodine -increases mortality in those with heart failure
47
amiodarone
*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
QT prolongation increases risk for ?
QT prolongation increases risk for Torsades de Pointes
49
class IV antiarrhythmic drugs
calcium channel blockers
50
calcium channel blockers (class IV antiarrhythmics) - overview
*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
calcium channel blockers (class IV antiarrhythmics) - MOA
*decrease conduction velocity *increase effective refractory period (ERP) *increase PR interval *decrease HR
52
calcium channel blockers (class IV antiarrhythmics) - action potential impact
*prolongs phase 0
53
calcium channel blockers (class IV antiarrhythmics) - EKG impact
*INCREASE IN PR INTERVAL *QRS unchanged *QT interval unchanged
54
calcium channel blockers (class IV antiarrhythmics) - examples
*verapamil *diltiazem note - dihydropyridine calcium channel blockers (amlodipine, other -dipines) do not act on the heart, just the blood vessels
55
calcium channel blockers (class IV antiarrhythmics) - ADEs
*constipation
56
verapimil
*class IV antiarrhythmic (CALCIUM CHANNEL BLOCKER - prolongs phase 0 of pacemaker cells, increases PR interval)
57
diltiazem
*class IV antiarrhythmic (CALCIUM CHANNEL BLOCKER - prolongs phase 0 of pacemaker cells, increases PR interval)
58
digoxin - overview
*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
digoxin - MOA
*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
digoxin - toxic rhythm effects
*can cause: -sinus bradycardia -AV block -accelerated junctional rhythm -premature ventricular beats
61
digoxin - ADE: hyperkalemia
*due to inhibition of Na+/K+ ATPase, it is difficult to get potassium back into the intra-cellular environment
62
digoxin - acute toxicities
*GI: N/V, abdominal pain *CV: dysrhythmias *CNS: lethargy, confusion, weakness
63
digoxin & vision
*causes BLURRY YELLOW VISION
64
digoxin ADEs - summary
*hyperkalemia *blurry yellow vision *toxic heart rhythms *N/V, abdominal pain
65
adenosine - overview
*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
atropine - MOA
*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
ivabradine - MOA & info
*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
what is the real risk of Afib/Aflutter?
*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
anticoagulation in Afib/Aflutter
*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
rate control in Afib/Aflutter
*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
emergency medication therapy for ventricular tachycardia
1st. amiodarone 2nd. lidocaine 3rd. ventricular tachycardia ablation
72
long-term/outpatient medication therapy for ventricular tachycardia
1st. amiodarone 2nd. mexiletine 3rd. ventricular tachycardia ablation

Cardiology Exam (52 decks)

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