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Pharm Unit 4 > Anti-arryhthmics > Flashcards

Anti-arryhthmics Flashcards

1
Q

Quinidine, procainamide, disopyramide (NEVER USED FOR VENTRICULAR ARRHYTHMIA!!)

A

Class: Class IA anti-arrhythmics
Mech: Block inward potassium rectifying channel (slow rate) at normal concentrations; blocks sodium channels (fast rate) at high concentrations; depress phase 0, slow conduction and prolong repol (prolong ERP and APD)
Thera: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
Important SE’s: quinidine with nausea/diarrhea, fever, hepatitis, thrombocytopenia, QT prolongation; drug interactions (displaces digoxin), inhibits Cyp2D6, metabolism induced by phenytoin, phenobarbital;
procainamide: no alpha-adrenergic blockade or M2 blockade; drug-induced lupus syndrome, QT prolongation, active metabolite that is NAPA, hypotension;
disopyramide: no alpha-adr blockade, prominent ACh action, QT prolongation!!!

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2
Q

Lidocaine, mexiletine, tocainide

A

Class: Class IB anti-arrhythmics
Mech: Block sodium channels in inactivated state mostly (late Na channel blockade); no action on atrial tissue
Thera: Digitalis toxicity, cardioversion, emergency VT/VF
SE’s: lidocaine with tremor, nausea, seizures; mexiletine with GI toxicity
Misc: lidocaine with no QT prolongation, could shorten APD slightly; mexiletine given orally, lidocaine IV

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3
Q

Flecainide, propafenone, moricizine

A

Class: Class IC anti-arrhythmics
Mech: Sodium channel blockers (most potent in class I), acting as negative ionotrope; IKr blockade; s+-propafenone with beta-blocking activity, 5-hydroxy metabolite without beta-blocker activity;
Thera: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
Important SE’s: Worsened heart failure and VT, proarrhythmia in ischemic tissue, increased mortality; they can prolong APD preferentially at faster heart rates and prolong PR, QRS, QT interval; Flecainide with blurred vision as SE and betablocking of s+-propafenone could cause sinus tachy and bronchospasm

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4
Q

Propanolol, carvedilol.

A

Class: Class II anti-arrhythmics - beta blockers
Mech: Blocks beta-adrenergic receptors; decrease SA, AV node activity (phase 4 depolarization); propanolol is membrane stabilizing and highly lipophilic and suppresses exercise-induced tachy, digitalis-induced tachyarrhythmias, MI; carvedilol and metoprolol to decrease CHF mortality; acebutolol similar to metoprolol but some intrinsic sympathomimetic activity
Thera: Control of ventricular rate in atrial fibrillation/flutter; prevent or terminate SVTs
Important SE’s: Hypotension, brochospasm, bradycardia
Misc: Decreases mortality in CHF; contraindicated in WPW and sudden withdrawal of beta blocker in angina patient could cause MI
esmolol given IV and useful in acute emergency treatment of SVTs where short duration is desired

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5
Q

Sotalol, amiodarone, dofetilide, ibutelide, dronedarone

A

Class: Class III anti-arrhythmics
Mech: K channel blockade = prolongs refractoriness; amiodarone can decrease Na, Ca, K currents and has alpha and beta adrenergic blocking effect and prolongs ERP and APD; dofetilide an IKr blocker
Thera: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
ibutilide IV for atrial F or F;
dofetilide: convert chronic AF, paroxysmal AF, maintain sinus rhythm after cardioversion
amiodarone: chronic AF, SVTs, acute VF, prophylaxis (cardiac surgery)
Important SE’s: Torsades de Pointes; QT prolongation, pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction
Other SE’s: Photosensitivity (blue-gray skin; numerous drug interactions;
dronedarone with QT prolongation, nausea, diarrhea
sotalol with EADs, TdP, decreased HR, decreased AV conduction

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6
Q

Nifedipine, amlodipine, felopidine, isradipine, veapamil, diltiazam.

A

Class: Class IV anti-arrhythmics - calcium chanel blockers
Mech: Blockade of L-type calcium channels: slow SA & AV node activity; prolong AV refractoriness
Thera: Prevent or terminate reentrant SVTs (verapamil and diltiazem for acute afib or flutter)
Important SE’s: IV use Hypotension, bradycardia, constipation, dizziness
Other SE’s: Increased serum digoxin levels
Misc: Contraindicated in WPW

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7
Q

Adenosine

A

Class: Anti-arrhythmic
Mech: decreases SA, AV node activity; increases AV refractoriness;
Thera: terminates PSVT, AVN reentrant arrhythmias, NOT atrial flutter, a fib, multifocal atrial tachy, WPW;
Important SE’s: Sedation, dyspnea, hypotension; antagonized by methylxanthines (caffeine, theophylline)

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8
Q

Digoxin

A

Class: Anti-arrhythmic
Mech: Na/K pump inhibitor; slows AVN activity and conduction, indirect atrial
Thera: Atrial fibrillation/flutter; chronic SVT
Important SE’s: Nausea, cognitive dysfunction, blurred or yellow vision
Other SE’s: May cause DAD arrhythmias
Misc: Low therapeutic index; drug interactions; hypokalemia will exacerbate effect

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9
Q

Magnesium sulfate

A

Class: Anti-arrhythmic
Thera: Prevents recurrent TdP and some digitalis-induced arrhythmias
Misc: Alternative to amiodarone for shock-refractory cardiac arrest.

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10
Q

Mechanisms of arrhythmias:

A
  1. Automaticity (normal automaticity with bradycardia and tachycardia involving If and ICa, L; also ectopic activity/focus in atria/ventricle; also ABNORMAL automaticity with triggered activity, EADs occuring after phase 3 and DADs in phase 4)
  2. Conduction (conduction block with SAN, AVN types I, II, III; and BBB, like RBBB, LBBB, hemiblocks; also RENTRANT ARRHYTHMIAS, like unidirectional block, slow conduction, and a conduction time greater than the refractory period)
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11
Q

Ectopic activity more likely to happen in; what would we see in accelerated normal automaticity of your atria/ventricles? What about SA node?

A

Purkingje fibers (some pacemaker activity) more so than the atria and ventricles;
If and ICa,L increase, in times of ischemia, catecholamine usage, depol moderate;
maybe decreased funny current and see HCN at SA node

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12
Q

EADs develop during; DADS develop during

A 
phase 3 repol, with blockade of Ikr and Iks and increase of INa late, ICa,L;
phase 4 (resting, diastole) with decreased IK1 and increased Na, Ca influx (the Na/K ATPase isn't working, NCX not working, and IC Ca goes up)
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13
Q

Major determinants of conduction velocity are mostly

A
  1. decreased cardiac Na current
  2. Increased gap junction resistance (less voltage travels downstream of AP, meaning less conduction and potential ischemia)
  3. Increased fibrosis (secondary to the other two; look for hypertrophy
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14
Q

Reentry involves:

A
  1. unidirectional block (asymmetric excitability: impulse conducted in one direction and not another)
  2. Slow conduction (decremental conduction)
  3. Conduction time is greater than the refractory period (might need to treat with complete block and block smaller branch to prevent reentry); look at SHEET!!;
    Reentry favored by refractory period, gap junction coupling, fibrosis; as well as extrasystoles
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15
Q

Sinus bradycardia may be caused by; how to treat?:

A
  1. depressed impulse FORMATION
  2. impaired impulse CONDUCTION
  3. Excess VAGAL tone
  4. Hyperkalemia
  5. Hypothyroidism, sleep apnea
  6. Meds (BB, CCblockers, ACh, adenosine);
    think sick sinus syndrome with disease of the SA node and in elderly greater than 65 yrs of age; also occlusion of SA artery;
    treat causative medical condition, alter meds, may require artificial pacemaker
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16
Q

AV nodal block:

A
  1. First degree (prolonged PR interval: 1:1 P:QRS)
  2. 2nd degree (not every P wave followed by QRS, aka dropped beat): can be Mobitz type 1 with PR getting longer until beat is dropped or Wenckebach; Mobitz type 2 with PR interval contsant but patterns are 2:1, 3:2, 4:3, 3:1 P:QRS pattern
  3. 3rd degree: complete AV block (no consistnet PR interval; rely on ventricular pacemaker)
17
Q

Which AV nodal blocks require electronic pacemakers?

A

Mobitz type II (ventricular rate is half of atrial rate in e.g. 2:1 P:QRS), 3rd degree (complete block)

18
Q

BBB: if either left anterior or posterior fascicle block, what is that?

A

hemiblock!! (former is LA deviation; latter is RA deviation)

19
Q

Atrial premature systoles:

A

Early occurrence of a P wave:

  1. could be followed by normal QRS
  2. could be blocked by AV node if too early
  3. Could block in bundle branches
  4. Could reset sinus rhythm “phase resetting”
20
Q

Junctional premature systoles:

A

premature, or inverted P wave:

  1. originates from AV node (or AV bundle)
  2. could be preceded by an inverte P wave (retrograde conduction)
  3. Could be followed by normal QRS complex
  4. Could block a sinus beat (compensatory pause; a delay seen until next normal sinus rhythm)
21
Q

Ventricular extrasystoles:

A

abnormal QRS complex:

  1. originates below His bundle bifurcation (not preceded by P wave)
  2. asynchronous ventricular activation (prolonged QRS)
  3. could produce compensatory pause (blocks normal SAN impulse through AVN)
22
Q

Mechs for Tachycardia:

A
  1. accelerated automaticity
  2. triggered activity (EADs, DADs)
  3. abnormal conduction
23
Q

Characteristics of the 3 different tachys regarding P wave, PR interval, onset and termination; most prevalent ones?

A

Sinus with normal P wave, normal and prolonged PR, gradual onset and termination; atrial with abnormal P wave, normal and prolonged PR, paroxysmal; junctional with retrograde P waves, short or absent PR, paroxysmal;
AV node reentry most prevalent of all SVTs, bypass tract reentry less prevalent

24
Q

Sinus tach: causes and treatments

A
  1. excess symp tone 2. rarely sinus node reentry
  2. hypotention (reflex tachy) 4. hyperthyroidism
  3. COPD
  4. Stimulants (nicotine, caffeine, cocaine);
    treat:
  5. carotid massage, ACh mostly
  6. beta blockers
  7. AVN blocking agents (verapamil, adenosine)
  8. may need catheter ablation and pacemaker!!!
25
Q

Automatic atrial tachy and paroxysmal SVT:

A
  1. Non-paroxysmal, ectopic foci; could precede flutter or fibrillation;
  2. aka PAT; usually AVN reentry
  3. initiated by extrasystole
  4. responds to vagal stimulation (carotid sinus massage)
  5. give adenosine, beta blockers, CCBs
26
Q

Automatic AV Junctional Tachy:

A
  1. Non-paroxysmal, ectopic foci (usually His bundle)
  2. variable rate (50-60 b/m, or rapid)
  3. Either no or retrograd P waves, short PR, QRS
  4. Typically caused by cardiac glycoside toxicity
27
Q

Reentrant SVT’s:

A
  1. Sinus node reentry (paroxysmal, terminate by electrical stimulus)
  2. Atrial reentry (paroxysmal, extrasystole trigger; terminated by electrical stim, but NOT responsive to vagal tone)
  3. AV node reentry: dual conduction pathways, paroxysmal, extrasystole trigger, depends on ICa,L;
    terminate by vagal tone, adenosine, BBs, CCBs
28
Q

WPW:

A

Think “fast” AV accessory pathway:

  1. usually atrial origin
  2. initiated by extrasystole: short PR interval
  3. Not responsive to vagal tone
  4. AVN blockers contraindicated; amiodarone and procainamide indicated here
  5. HIGHER RISK for sudden death!!!
29
Q

Types of ventricular tachy:

A
  1. Monomorphic (uniform): spontaneous extrasystoles with >3 PVCs and originates in ventricular tissue; sustained is >30 sec and can lead to vfib and flutter
  2. Polymorphic (non-uniform): think of Torsades de Pointes and Long QT syndrome (etiology of 14 genes, drug-induced, EADs);
    LQT1: IKs channel with beta blockers and left cardiac nerve denervation for treatment (due to exercise and emotion)
    LQT2: beta blockers less effective against IKr channel and potassium levels outside too low (due to sleep, auditory, post-partum)
    LQT3: beta blockers less effective, and need to block late INa window current (rest, sleep, bradycardia)
30
Q

Ventricular tachy for polymorphic:

A
  1. Catecholamine-induced polymorphic VT (CPVT)
  2. DAD mechanism, with extrasystoles
  3. Deficient IC Ca cycling with RYR2 issues
  4. Exercise-induced;
    Treat:
  5. beta-blockers for LQT1
  6. ICD (defibrillator)
  7. Sympathectomy: left cardiac nerve
31
Q

Atrial flutter

A

Rapid atrial rate (250-350 b/m); sawtooth F-wave pattern;

  1. normal QRS
  2. AV dissociation
  3. Vagal stim and CCBs not effective; not life-threatening UNLESS transmitted to ventricles at rapid rate (WPW)
32
Q

Atrial fibrillation:

A

MOST COMMON CARDIAC ARRHYTHMIA; irregular atrial rate 400-600 b/m;
1. anticoagulants, rate control, anti-arrhythmics for rest of like to prevent risk of stroke, HF, sudden cardiac death
2. ablation therapy?;
irregular F waves, QRS complex, RR interval; no real P waves

33
Q

V flutter (similar to V fib)

A

Lethal arrhythmia if not terminated:

  1. No effective ventricular contraction
  2. Cardioversion required
  3. No QRS or T waves
  4. Rapid reentrant rhythm
  5. ICD
  6. Antiarrhythmic drugs maybe proarrhythmic

Pharm Unit 4 (13 decks)

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