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Cardio 1 > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

Types of Afib

A

Paroxysmal - Episodes end spontaneously
Persistent - requires med intervention
Permanent - cannot be terminant

Chronic remodels the atrial sturcture and function

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2
Q

Afib consequences and Afib goals

A

Rapid ventricular rate causes fall in cardiac output and syncope

Atrial thrombi form and can dislodge…leading to embolic strokes

Rhythm control - completely normal HB

Rate - slow ventricles and improve cardiac output but atria still fibrillate

Anticoag also used

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3
Q

Ventricular tachycardias

A

Emergency so only suitable goal is rhythm control

Monomorphipc ventricular tachycardia and torsades de pointes have diff causes and diff txs

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4
Q

Prodcainamide
Lidocain
Felcainide

A

All rhythym control

Pro - blocks both cardiac Na and K channels
Lido - weakest Na blockers
Fl - storngest Na channel blockers

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5
Q

Metoprologl
Amiodarone/sotalol
Diltiazem/verapamil
Adenosine

A

Beta blocker - rate
K blocker - rhythm
Ca blocker - rate
Adenosine agonist—-AV-RT (av nodal reentry tachycardia)_

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6
Q

Rhythm control drugs

A

Mostly target cardiac voltage gated K and Na channels

Na blockers Slow generation of ventricular and atrial APs, slowing AP conduction

K blockers slow repolarization and prolong cardiac action potentials

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7
Q

Rate control drugs

A

Inhibit the AV node and thus slow conduction from atria to ventricles

Metoprolol - blocks AV node beta adrenergic receptors

Verapamil and diltiazem - block AV node Ca channels

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8
Q

Effects of anti-arrhythmics on noraml ECG

A

Ia - Widen QRS, prolong QT

IC - Widen QRS (strong)

II - Prolong PR

III - Prolong QT

IV - prolong PR

QRS wide - slowed conduction in ventricle

Prolonged QT - slowed ventricular repolarization

Prolong PR - slowed conduction in AV node

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9
Q

EADS and DADs

A

EADs

  • caused by abnormally long APs
  • Can leads to otorsade de pointes
  • Tx is shorten APs

DADs

  • Caused by toxic cytosolic Ca levels
  • Cause PVCs or monomorphic ventricular tachycardia
  • tx to relieve Ca overload if possible
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10
Q

Reentry circuits

A

APs loops around small region of the heart

Spread from reenetry circuit and repeatedly stimulate ventricles or atira

Often occurs following infarct, hypertrophic, or fibrotic hearts

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11
Q

Lidocaine dosage, how its used

A

Rhythm control

Injection

Rapidly metabolized os short term…prevent recurence of cardiac arrest in pts resuscitated following ventricular fibrillation or pulseless ventricular tachycardia

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12
Q

Na blocker mech

A

Slow generation of atrial and ventrciular APs and slow conduction velocity

Affect rapidly beating arrhythmic cells more than normal myocytes

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13
Q

Reentry circuits only generate tachycaridas if

and Na channel blocker effect

A

They can loop AND

reenter noraml tissue after it recovers form refractory period but before next normal HB arrives

Na blocks inactive since conduiton slow enough that next HB arrives before banormal wave finishes the loop

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14
Q

Na channel blocker and DADs

A

Prevent generation of unusually rapid APs

DADs persist but extra APs gone

Abnormailty generating DADs unaffected but Na blockers revent them from generating extrasystoles and runs of tachy

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15
Q

Lidocaine SE

A

Neurotoxicity

Can trigger a new ventricular tachycardia

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16
Q

WHen can Na blockers cause proarrythmias

A

Strucutaly damaged

Fibrotic regions where heartbeat is slower already

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17
Q

Na channel blocker and dorment reetry circuits

A

Dormant circuit - APs travel the circuit too quickly so point 1 is still refractory when stimulus arrive from point 3

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18
Q

IC Na blockers

A

Flecainide

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19
Q

Flecainide contraindications

and use

A

Pts with tructural HD - high risk of proarrhythmias

Pts with unstable hemodynamics like depressed CO - may widen QRS interval…HB spreads slowly so contraction is less forceful

“Pill in pocket” - immediate termination of sudden episdoes of paroxysaml A fib by self-admin in carefully selected, low risk pts

20
Q

Procainamide dosase and comments

A

Injection

Dual mixed Na and K blocker

Terminating monomorphic ventricular tachy

N-acetyl procainamide is major active metab

21
Q

K channel block effect

A

Prolongs AP and refractory period

22
Q

Reentry cirucit and K blocker

A

Prolongs te AP and refractory period so that cells do not respond when stimulus arrives from point 3

23
Q

Procainamide SE

A

Proarrythmic - torsade de pointes - due to K channel block

Negative inotropic effect - moderate iwdeing of the QRS interval

24
Q

K blocker toxicity

A

Excessively prolongs ventricular APs (and QT), induceing EADs and torsades

25
Q

Amiodarone and sotalol doage

A

O/I

26
Q

Sotalol ECG

A 
Prolonged QT (K block)
Prolong PR (Beta-adrenergic block)
Slower HR (beta-adrenergic block)
27
Q

USe and SE of sotalol

A

Co-existing ischemic HD - beta-blocker may help

Unstable hemodyanmcs - exaerbated by sotalol’s neg inotropic effects

Negative inotropy - beta blockade also causes inhibitory effects on HR and AV node

Proarrhythmia - Torsade de pointes due to K channel block

28
Q

Amiodarone indciations

A

Suppression of recurrent ventricular tachy - IV amiodarone an be used to prevent recurrence of cardiac arrest following resuscitation…oral for long term

Prophylaxis and tx of Afib…preferred with left vent hypertrophy or HF

Main effect is inhibiton of K channels
Weak of Na and Ca channels

Weak non-comp antagonist of alpha and beta receptors

29
Q

Amiodarone long term toxocity

A

Pulm toxocity - reversible

Thyrotoxicosis

Hypothyroidism - more common…inhibits conversion of T4 to T3

LOW risk of proarrhtymia

30
Q

Amiodarone metab

A

Large Vd, requires loading dose

Early detection of adverse effects important due to long T1/2…slowly metabolized

Can increased blood levels of digoxin and warfarin

Digoxin - inhibit P=glycoprotein involved in elim

Warfarin - CYP450 inhiibtor

31
Q

Metoprolo dosage nad mech

A

Oral, oral-ER, injection

Slow AP conduction across the AV node

Reverse acceleration of AV node APs by symp tone, returnign them to baseline

32
Q

Beta-blocker use

A

Choice for rate control of Afib…each AP takes longer so fewer beats per minute

Prolong diastolic period which allows more blood to enter ventricles and improve cardiac output

33
Q

Beta-blocker other use

A

Ventricular tachycardias

Negative inotropic effect so block increased calcium IC…dec in DADs and VT

34
Q

Diltiazem and verapamil dosing and tx

A

Injection for acute, oral for LT

Angina, HTN, or arrhtymias

35
Q

Diltiazem and verapamil mech

A

Slow generation of AV nodal APs

Takes longer to get across

Main control in pts who cannot tolerate B-blockers

36
Q

CCB vaso effect

A

Peripheral and coronary vasodilators

37
Q

Verapamil and diltizem effect on myocytes

A

Directly inhibit SA, AV, and cardiac contractility

Direct effect is opposed by indirect inc in sym tone caused by vasodilation and dec BP

38
Q

SE of verap and diltia

A

Dep APs - bradycardia or AV block

Dec ventricular contract - HF

Vasodilation - hypotension

39
Q

Diltiazem and verap intx

A

Beta-adrenergic blockers…can cause severe AV blocks

Digoxin levels - P-glycoprotein

Erythromycin - blood levels increased by verapamil CYP3A inhibiton…can cause fatal ventricular arrhythmias

40
Q

Benefit and risks of rhythm and rate control

A

Rhythm - better hemodynamics and dec thrombo risk…BUT more toxic anti-arrhtymics

Rate - better success rate…effective iwht perm A fib…prolonged anticoag use

41
Q

AV nodal reentry tachycardia

A

For AV nodal renetry tachycardia

Slow pathway conducts HB from atria to Vent

Fast conducts HB back to atria where it reenter slow one

42
Q

Mech of adenosine

A

Hyperpolarizes and blocks the AV node to stop reentry

Both pathways resynchronied and ready when next nromal HB arrives

Adenosine rapidly removed by ENT 1

43
Q

Clinical effects of adenosine and receptor

A

A1 - SA and AV node expression…lead to slow HR and slowed AV node conduction

44
Q

Adenosine inhibt effect on SA and AV nodes

A

Due to K channel activation…hyperpolarization

45
Q

Adenosine limitations and contraind

A 
Cardiac arrest (due to node inhibition)
Flushing due to vasodilation

Ashtmoa - can induce bronchoconstrictions

Cardio 1 (30 decks)

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