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Pharmacology (Fall) > Antiarrhythmic Drugs (part 2) > Flashcards

Antiarrhythmic Drugs (part 2) Flashcards

1
Q

Arrhythmia =

A

any rhythm that is not a normal sinus rhythm with normal atrioventricular (AV) conduction

any rhythm that is not a normal sinus rhythm with normal atrioventricular (AV) conduction

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2
Q

Bradyarrhythmias:

A

HR < 50-60 bpm
- Sick sinus syndrome
- Atrio-ventricular conduction block

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3
Q

Tachyarrhythmias:

A

HR > 100 bpm

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4
Q

Supraventricular tachyarrhythmias

A

due to abnormal electrical signals originating above the ventricles

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5
Q

Paroxysmal tachycardia :

A

HR 150-250 bpm

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6
Q

Atrial Flutter:

A

atria beat at 250-350 bpm, regular heart rhythm

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7
Q

Atrial Fibrillation:

A

atria beat up to 500 bpm, irregular rhythm, uncoordinated contraction

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8
Q

Ventricular tachyarrhythmias

A

due to abnormal electrical signal originating in ventricles

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9
Q

Ventricular Tachycardia:

A

> 120 bpm, regular heart rhythm

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10
Q

Ventricular Fibrillation:

A

irregular rhythm with uncoordinated contraction, immediate cause of death

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11
Q

Arrhythmia caused by:

A

Alteration in the movement of ions responsible for the action potentials in the pacemaker cells, conduction system and/or muscle.

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12
Q

What are the important ions in the action potential?

A
  1. Pacemaker (slow) cells (SA node, AV node)
    - Ca and K are most important.
  2. Conduction and muscle (fast) cells (atria, purkinje fibers, ventricles)
    - Na, Ca and K are most important
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13
Q

What are the causes of cardiac arrhythmias?

A
  • Insufficient OXYGEN to myocardial cells
  • ACIDOSIS or accumulation of waste products
  • ELECTROLYTE disturbances
  • STRUCTUAL DAMAGE of the conduction pathway
  • DRUGS (e.g. antiarrhythmics, psychotropics and antihistamines)
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14
Q

What are the mechanisms of cardiac arrhythmias?

A
  1. Abnormal impulse formation
    aka: ECTOPIC FOCI = pacemaker of abnormal origin
    A) Abnormal automaticity
    - SA node (altered regular pacemaker activity) enhanced activity of spontaneous pacemakers
    B) Triggered activity
    • disturbances in repolarization triggers EARLY AFTERDEPOLARIZATIONS (EADs) in ATRIA or VENTRICLES
      –> long QT/torsade de points
  2. Abnormal conduction
    - impaired AV node (heart block) leads to bradyarrhythmias
    - RE-ENTRY (circus) conduction leads to tachyarrhythmias
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15
Q

Describe where ACh is

A
  • neurotransmitter
  • released from parasympathetic nerves
  • acts on muscarinic receptors

phase 4 - slows depolarization rate
- decreases automaticity (SA node),

  • slowed conduction (AV node)
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16
Q

Describe where Norepinephrine/Epinephrine is

A
  • neurotransmitter
  • released from sympathetic nerves
  • acts on β1-adrenergic receptors
  • phase 4 - increases depolarization rate and reduces AP firing threshold
  • increases automaticity (SA node), increased conduction (AV node)
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17
Q

What may trigger Torsade de pointes?

A

Early Afterdepolarizations (EADs)

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18
Q

What is Torsade de pointes?

A

twisting of the points (looks like a party streamer)

conditions/drugs which PROLONG the QT interval may precipitate these

19
Q

Torsade de pointes

A

characterized by twisting of isoelectric points on ECG and
prolonged QT interval

inherited and/or DRUG INDUCED (increased QT interval)

can lead to ventricular fibrillation and sudden death

responds to MAGNESIUM

20
Q

What do drug induced increase in QT interval include?

A

include:
- antiarrhythmics (Class Ia and III)
- antihistamines (e.g. seldane)
- anti-psychotics
- antibiotics (e.g. erythromycin)

  • can cause sudden death
  • hERG assays now routine during drug development
21
Q

What does re-entry require?

A
  • available circuit (closed conduction loop)
  • unidirectional block
  • different conduction speed in limbs of circuit: conduction time (CT) > effective refractory period (ERP)
22
Q

Where does re-entry occur?

A

can occur in any part of the heart
- within a small region of the atria or ventricles
- within the AV node
- between atria and ventricles, etc
- accounts for most tachyarrhythmias in cardiac patients

23
Q

What happens when re-entry is localized to atria/ventricles?

A

when localized to atria/ventricles, re-entry can be stopped by converting the UNIDIRECTIONAL block INTO BI-directional block
- In NON-PACEMAKER (FAST) cells; this can be done with drugs that BLOCK Na+ CHANNELS DIRECTLY (Class I drugs) or by drugs that REDUCE Na+ CHANNEL ACTIVITY INDIRECTLY (Class III drugs; they delay repolarization which slows recovery of Na+ channels from inactivation)

24
Q

A special case of reentry in the AV node:

A
  • paroxysmal supraventricular tachycardia (PSVT)
    – cause not clear and is often short lasting
25
Q

What is the re-entry in the AV node (special case) controlled by?

A

controlled by drugs that depress AV conduction, causing bidirectional block
- calcium channel blockers (Class IV)
- β-adrenergic receptor blockers (Class II)
- Adenosine (Class V)

26
Q

Wolff-Parkinson-White Syndrome

A

in some cases an abnormal electrical pathway connecting the atria and ventricles may be present

27
Q

What is Wolff-Parkinson-White Syndrome?

A
  • alternative conduction pathway
    – ventricles back to atria (bundle of Kent)
  • incidence is less than 3% population
    – often asymptomatic and rarely fatal
  • catheter ablation of abnormal electrical pathway is the preferred long-term approach
28
Q

What should you avoid if patient has Wolff-Parkinson-White Syndrome?

A

Avoid AV node blockers if atrial fibrillation or flutter
- β-adrenergic receptor blocker , calcium antagonist, adenosine or digoxin

29
Q

What are the Mechanisms of Action of Antiarrhythmic Drugs?

A
  1. Reducing Automaticity
  2. Blocking Re-entry Mechanisms
  3. Normalize Ventricular Rate (SUPRA-VENTRICULAR tachycardia)
    –> by slowing conduction through the AV node
30
Q

Mechanisms of Action of Antiarrhythmic Drugs

1) Reducing Automaticity

A) Abnormal automaticity

B) Triggered activity

A

A) slow the rate of spontaneous Phase 4 depolarization by blocking B1 receptors or Ca2+ channels –> reduced pacemaker activity

B) by blocking open & inactivated Na+ or Ca2+ channels in depolarized tissues –> reduced triggered activity

31
Q

Mechanisms of Action of Antiarrhythmic Drugs

2) Blocking Re-entry Mechanisms

A

1) Reduce Phase 0 depolarization
(CLASS I, II or IV)

Slows conduction in the ischemia area

converts region of UNIDIRECTIONAL BLOCK TO BIDIRECTIONAL BLOCK

2) prolong the action potential repolarization
(CLASS III K channel blockers)

increases the effective refractory period (ERP)

conduction time < ERP = re-entry blocked

32
Q

Mechanisms of Action of Antiarrhythmic Drugs

3) Normalize Ventricular Rate (SUPRA-VENTRICULAR tachycardia)

A

slowing AV nodal conduction
beta-blockers (Class II), calcium channel blockers (Class IV), adenosine and digoxin
–>
reduces ventricular rate
–>
increasing time for ventricular filling from atrium
–>
improves stroke volume (SV)
–>
increases cardiac output (CO = HR x ↑↑SV)
–>
improved hemodynamics

33
Q

What are the Class I antiarrhythmia drugs?

A

(procainamide, lidocaine, flecainide)
- primarily block Na channels

34
Q

What are the Class II antiarrhythmia drugs?

A

(propranolol, metoprolol, esmolol)
- primarily block B-adrenergic receptors

35
Q

What are the Class III antiarrhythmia drugs?

A

(amiodarone, sotalol)
- primarily block K channels

36
Q

What are the Class IV antiarrhythmia drugs?

A

(verapamil)
- primarily block Ca channels

37
Q

What are the Class V antiarrhythmia drugs?

A

(magnesium, adenosine, digoxin)
- other mechanisms

38
Q

What are the 3 subclasses of Na+ channel blockers?

A

IA - procainamide
moderate Na+ channel blockade; dissociates from the channel with intermediate kinetics

IB - lidocaine
weak Na+ channel blockade; dissociates from the channel with rapid kinetics

IC – flecainide
strong Na+ channel blockade; dissociates from the channel with slow kinetics

39
Q

What is the treatment of Bradycardia?

A

symptomatic bradycardia (< 50-60 bpm) – PACEMAKER

40
Q

What is the treatment of Tachycardia?

A
  • isolated ectopic beats or short runs of tachycardia
    – if Asymptomatic - no treatment
  • Symptomatic/severe tachycardia – IMMEDIATE CARDIOVERSION (ELECTRICAL/PHARMACOLOGICAL)
41
Q

What is the treatment of Atrial Fibrillation?

A
  • anticoagulation (prior to cardioversion, if possible)
  • antiarrhythmics:

1) ventricular rate control (BY TARGETING AV NODE)
- verapamil, beta-blocker, digoxin: target AV node to reduce ventricular rate

2) conversion to sinus rhythm – in highly symptomatic patients (BY TARGETING ECTOPIC FOCI/RE-ENTRY):
- procainamide, flecainamide, amiodarone or sotalol

42
Q

What is the treatment of Ventricular Fibrillation?

A

irregular rhythm with uncoordinated contraction, IMMEDIATE CAUSE OF DEATH

REQUIRES IMMEDIATE CARDIOVERSION:
- ELECTRICAL: transthoracic defibrillation
and/or
- PHARMACOLOGICAL: IV amiodarone, lidocaine or magnesium may be used as an adjunct

43
Q

What is the treatment of Ventricular Tachycardia?

A

to terminate an episode
- in patients unconscious and hypotensive (mean arterial pulse <60 mm Hg): cardioversion (synchronized DC shock)
- in patients with stable hemodynamics: IV lidocaine, flecainide patients without structural heart disease), amiodarone, sotalol

special cases
- torsade de pointes: IV magnesium is the treatment of choice
arrhythmias after acute myocardial infarction: IV lidocaine often used as a first line agent

for chronic therapy of VT:
- implantable cardioverter defibrillators (ICD) is preferred over antiarrhythmic drugs for initial therapy

44
Q

What are the Implantable Cardioverter Defibrillators (ICD) side effects?

A
  • anxiety, depression, post-traumatic stress disorder (b/c shocks are uncomfortable)
  • amiodarone may be used in conjunction to reduce risk of ICD shocks

*Electrical stimulus will disrupt activity & maintain a normal sinus rhythm

Pharmacology (Fall) (28 decks)

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