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Pharmacology B > Lecture 5 - Antiarrhythmics 2 > Flashcards

Lecture 5 - Antiarrhythmics 2 Flashcards

1
Q

Bradyarrhythmias: HR = ?

A

< 50-60 bpm

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2
Q

Types of Bradyarrhythmias

A
  • Sick sinus syndrome

- Atrio-ventricular conduction block

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3
Q

Tachyarrhythmias: HR = ?

A

> 100 bpm

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4
Q

Types of Tachyarrhythmias

A
  • Supraventricular

- Ventricular

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5
Q

List and describe 3 types of Supraventricular arrhythmias

A

1) Paroxysmal Tachycardia: HR 150-250 bpm
2) Atrial Flutter: atria beat at 250-350 bpm, regular heart rhythm
3) Atrial Fibrillation: atria beat up to 500 bpm, irregular rhythm, uncoordinated contraction

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6
Q

List and describe 3 types of Ventricular arrhythmias

A

1) Ventricular Tachycardia: >120 bpm, regular heart rhythm
2) Ventricular Fibrillation: irregular rhythm with uncoordinated contraction, immediate cause of death
3) Torsade de pointes: long QT syndrome

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7
Q

What is an 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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8
Q

What are the most important ions in Pacemaker (slow) cells?

SA node, AV node

A

Ca2+

K+

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9
Q

What are the most important ions in Non-Pacemaker (fast) cells?
(atria, purkinje fibres, ventricles)

A

Na+
Ca2+
K+

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10
Q

List a few causes of cardiac arrhythmias

A
  • Insufficient oxygen to myocardial cells
  • Acidosis or accumulation of waste products
  • Electrolyte disturbances
  • Structural damage of the conduction pathway
  • Drugs
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11
Q

What are the 2 mechanisms of cardiac arrhythmias?

A

1) Abnormal impulse formation
A) Abnormal automaticity
B) Triggered Activity

2) Abnormal conduction

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12
Q

Describe:

1A) Abnormal automaticity

A
  • SA node (altered regular pacemaker activity)
  • ectopic foci (pacemaker of abnormal origin)
  • decrease in phase 4 K+ conductance (hypokalemia) - increases spontaneous depolarization
  • inactivation of Na+ channels in depolarized cells (ischema) - converts fast cells into ectopic pacemakers
  • localized super sensitivity to catecholamines following ischema
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13
Q

What would cause a change in phase 4 slope?

A
  • increase rate of depolarization

- decrease rate of depolarization

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14
Q

increase rate of depolarization = ?

A

increased HR

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15
Q

decrease rate of depolarization

A

decreased HR

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16
Q

More depolarized RMP = ?

A

increased HR

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17
Q

More hyperpolarized RMP = ?

A

decreased HR

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18
Q

More negative AP threshold = ?

A

increased HR

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19
Q

More positive AP threshold = ?

A

decreased HR

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20
Q

SNS _______ HR

A

increases

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21
Q

PNS _______ HR

A

decreases

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22
Q

ACh is released from _____ nerves

A

parasympathetic

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23
Q

ACh acts on _____ receptors

A

muscarinic

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24
Q

How does ACh affect the heart?

A
  • phase 4 - slows depolarization rate
  • decreases automaticity (SA node)
  • slows conduction (AV node)
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25
Q

NE/E is released from ______ nerves

A

sympathetic

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26
Q

NE/E acts on ______ receptors

A

B-adrenergic

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27
Q

How does NE/E affect the heart?

A
  • phase 4 - increases depolarization rate and reduces AP firing threshold
  • increases automaticity (SA node)
  • increases conduction (AV node)
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28
Q

Describe:

1B) Triggered activity

A

-slow and poorly conducted action potential in atria or ventricle

  • cells depolarize before complete repolarization has occurred
  • non-automatic myocardial cells (atria, ventricles)
    • repolarization is required to change Na channels from inactive to resting
    • Ca channel availability is based on time
  • may be caused by prolonged duration of action potential - prolonged QT interval?
  • with increased action potential duration (QT interval) calcium channels may be ready before the sodium channels
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29
Q

EAD = ?

A

early after depolarization

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30
Q

EAD is due to ?

A

opening of Ca channels

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31
Q

EADs may trigger ________

A

Torsade de Pointes

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32
Q

Torsade de Pointes = ??

A

twisting of the points

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33
Q

Why type of conditions or drugs may precipitate Torsade de Pointes?

A

conditions or drugs which prolong the QT interval

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34
Q

Torsade de Pointes:

Characterized by ??

A

twisting of isoelectric points on ECG and prolonged QT interval

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35
Q

Torsade de Pointes:

Can be ____ or drug-induced

A

inherited

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36
Q

Torsade de Pointes:

Can lead to ??

A

ventricular fibrillation and sudden death

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37
Q

Torsade de Pointes:

Responds to _____

A

magnesium (Class 5 anti arrhythmic)

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38
Q

What drugs can increase QT interval?

A
  • aniarrhythmics (Class 1a and 3)
  • antihistamines
  • anti-psychotics
  • antibiotics (ex. erythromycin)
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39
Q

Describe:

2) Abnormal conduction

A
  • impaired AV node (heart block) leads to bradyarrhythmias
  • re-entry (circus) conduction leads to tachyarrhythmias
  • local differences in conduction velocity and membrane characteristics lead to development of electrical circuits (circus conduction)
  • re-routing of the normal electrical circuitry results in multiple beats before the next sinus beat is generated resulting in tachycardia
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40
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)
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41
Q

See slides 20-22 about a unidirectional block

A

cool beans

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42
Q

List some causes of re-entry

A
  • ischemia
  • congenital
  • hyperkalemia
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43
Q

Re-entry can occur in what parts of the heart?

A

In any part of the heart:

  • AV node
  • between SA node and atria
  • between atria and ventricles
  • accounts for most tachyarrhythmias in cardiac patients
44
Q

How can re-entry be stopped?

A

by converting the unidirectional block tissue to bi-directional block

**In non-pacemaker (fast) cells, this can be done with drugs that block Na+ channels directly (Class 1 drugs)

45
Q

A special case of re-entry in the AV node can cause what?

A

paroxysmal supra ventricular tachycardia (PSVT)

-cause is not clear and is often short lasting

46
Q

Re-entry in the AV node is controlled by what kind of drugs?

A

Drugs that depress AV conduction, causing bidirectional block:

  • calcium channel blockers (Class 4)
  • B blockers (Class 2)
  • Adenosine (Class 5)
47
Q

In some cases an abnormal electrical pathway may be present. Ex. _______

A

wolff-parkinson-white syndrome

48
Q

Describe 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
  • Treated by catheter ablation of abnormal electrical pathway
  • Amiodarone is first choice agent used to stabilize heart rate
49
Q

______ = first first choice agent used to stabilize heart rate in Wolff-Parkinson-White syndrome

A

Amiodarone

50
Q

When would you want to avoid AV node blockers?

A

If atrial fibrillation or flutter

-B blocker, Ca2+ blocker, adenosine or digoxin

51
Q

What are the 3 mechanisms of action of antiarrhythmic drugs?

A

1) Reducing Automaticity
2) Blocking re-entry mechanisms
3) Normalizing ventricular rate (supraventricular tachycardia)

52
Q

Describe ways we can reduce automaticity

A

1) blocking inactivated Na or Ca channels in depolarized tissues (preventing conversion to “resting” state)
- will reduce triggered activity

2) hyper polarize RMP (more negative RMP)
- will reduce pacemaker activity

3) increase membrane threshold potential for activation of NA (fast cells) of CA channels (slow cells)
- will reduce pacemaker activity

53
Q

Describe ways we can block re-entry mechanisms

A

1) -Reduce phase 0 depolarization
- Slows conduction in the ischemia area
- Converts region of unidirectional block to bidirectional block

2) -Prolong the action potential repolarization
- Increases the effective refractory period (ERP)
- Conduction time < ERP = re-entry blocked

54
Q

Describe how we can normalize ventricular rate (supraventricular tachycardia)

A

-slowing AV nodal conduction
(B blockers - Class 2)
(Ca blockers - Class 5)
(Digoxin)

  • reduces ventricular rate
  • increasing time for ventricular filling from atrium
  • improves stroke volume (SV)
  • increases cardiac output (CO = HR X increased SV)
  • improved hemodynamics
55
Q

Class 1 drugs block ___ channels

A

Na+

56
Q

Examples of Class 1 drugs

A

procainamide
lidocaine
flecainide

57
Q

Class 2 drugs block __

A

B receptors

58
Q

Examples of Class 2 drugs

A

propranolol
metoprolol
esmolol

59
Q

Class 3 drugs block __ channels

A

K+

60
Q

Examples of Class 3 drugs

A

amiodarome

sotalol

61
Q

Class 4 drugs block __ channels

A

Ca2+

62
Q

Examples of Class 4 drugs

A

verapamil

63
Q

Class 5 drugs have other mechanisms: Give some examples of class 5 drugs

A

magnesium
adenosine
digoxin

64
Q

Describe Class 1A sodium channel blockers

A

Procainamide:

  • Moderate phase 0 depression and slow conduction
  • Usually prolong repolarization

Also blocks K+ channels in phase 3

  • prolongs duration of action potential (QT interval)
  • increases effective refractory period

slowed conduction + increased refractory = block reentry

Also decreases phase 4 slope = reduced automaticity of ectopic pacemakers (ventricular muscle and purkinje fibres)

65
Q

Describe Class 1B sodium channel blockers

A

Lidocaine:

  • Minimal phase 0 depression and slow conduction
  • Usually shorten repolarization
  • modest effect in normal tissue -especially atria because the AP duration is so short
  • block is increased in depolarized tissue (ex. ischemic) - selective depression of conduction in depolarized cells
66
Q

Describe Class 1C sodium channel blockers

A

Flecainide:

  • Strong phase 0 depression and slow conduction
  • Little effect on repolarization
  • Modest K channel block but no increased QT interval
  • Slight to no effect on the refractory period
67
Q

Why is the use of procainamide limited?

A
  • depresses hemodynamics
  • blockade of K channels
    • prolongation of QT interval
    • may cause Torsade de points
  • may cause Lupus like Syndrome
    • reversible, occurs in1/3 of patients
  • chronic treatment doesn’t appear to reduce mortality rate
68
Q

Class 1B - Lidocaine:

Usually given __

A

IV

69
Q

Class 1B - Lidocaine:

Has no value in treating _______ ________, due to lack of effect on the atria (because AP duration is too short)

A

supra ventricular tachyarrhythmias

70
Q

Class 1B - Lidocaine:

Toxicity ?

A
  • Low incidence of toxicity and hemodynamic side effects

- Neurologic effects: tremor, nausea, lightheadedness, hearing disturbances, slurred speech and convulsions

71
Q

Class 1C - Flecainide:

Contraindicated in ??

A

patients with previous myocardial infarction, highly arrhythmogenic

72
Q

Class 1C - Flecainide:

Used to treat what?

A

supra ventricular (atrial fibrillation and flutter) and life-threatening ventricular arrhythmias, particularly where benefits outweigh pro arrhythmic risk (life-threatening sustained VT) but only in patients with structurally normal hearts

73
Q

_____ = non-specific B blocker

A

Propranolol

74
Q

____ and ____ = B1 selective blockers

A

Metoprolol

Esmolol

75
Q

B blockers ____ HR

A

decrease

76
Q

How do B-blockers decrease HR?

A
  • reduced phase 4 slope in pacemaker cells by reducing the pacemaker current (funny current - If)
  • reduced AV conduction velocity by reducing the voltage-gated Ca2+ current
  • prolonged refractory period in nodal tissues
77
Q

B-blockers are mainly used to control ??

A

ventricular rate in supra ventricular tachycardias (atrial fibrillation and flutter)

78
Q

B-blockers reduce short and long term mortality after ??

A

acute MIs

  • counters increased sympathetic activity in patients with AMI
  • anti-hypertensive and anti-ischemic effect is beneficial
79
Q

Contraindications of B-blockers?

A
  • bradycardia and heart block
  • patients with pulmonary problems: cardioselective beta blockers may be used with caution, but non-selective B-blockers CI.
  • decompensated congestive heart failure (due to negative inotropic effects)
  • in diabetics, may mask tachycardia occurring with insulin-induced hypoglycaemia (risk of diabetic shock/coma)
  • CI in Wolff-Parkinson-White Syndrome (may increase re-entry)
80
Q

Because esmolol has a very short __________ it may be used inc cases where B-blockers would normally be CI.

A

duration of action (t1/2 = 10 min)

81
Q

Describe:

Class 3 agents (amiodarone and sotalol)

A
  • K+ channel blockade in phase 3 prolongs the cardiac AP duration (increased QT interval)
  • increased refractory period
82
Q

Describe Amiodarone (Class 3)

A

Wide Spectrum anti arrhythmic

  • block inactivated Na channels (Class 1)
  • block Ca channels (Class 4)
  • modest B-blocker (Class 2)
83
Q

Sotalol is also a _____

A

B-blocker

84
Q

Class 3 agents (amiodarone and sotalol) are generally well tolerated hemodynamically, can be used in patients with ??

A

structural heart disease

85
Q

Risk with Class 3 agents (amiodarone and sotalol) ?

A

by prolonging AP duration, they prolong QT interval - may predispose pt to torsade de pointes

86
Q

Amiodarone is used for?

A

Both supra ventricular and ventricular tachycardia:

For supra ventricular tachycardia - maintains sinus rhythm in patients with recurrent atrial fibrillation

For ventricular tachycardia - effective, with less risk of pro-arrhythmic effect compared to other drugs

87
Q

Shit ton of adverse effects with amiodarone - see slides 46 and 47

A

prob won’t but ok :)

88
Q

Why kind of arrhythmias is sotalol effective against?

A

Supraventricular tachycardia (equally effective as amiodarone) - maintains sinus rhythm in patients with recurrent atrial fibrillation

Ventricular tachycardia: less effective than amiodarone, but may be preferred when amiodarone toxicity is a concern since it has fewer non-cardiac effects

89
Q

Adverse effects of sotalol

A
  • Excreted exclusively by kidneys - may accumulate in patients with renal disease
  • Bradycardia (13%) - CI in patients with sick sinus syndrome
  • Bronchospasm - due to non-selective block of B-blockers
  • Greater risk of torsade de pointes than amiodarone (due to AP prolongation)
90
Q

Describe Class 4 drug - Verapamil

A
  • Blocks Ca channels in plasma membrane (open and inactivated)
  • Slow conduction in AV node due to Ca channel blockade
  • Used to reduce ventricular rate in supra-ventricular tachycardias (atrial fibrillation and flutter)
    • Increased ventricular filling - increased CO
  • Verapamil used in acute paroxysmal supra ventricular tachycardia (reentry through the AV node)
  • CI in Wolff-Parkinson-White syndrome
91
Q

Magnesium (Class 5) useful in ??

A

Torsade de Pointes, even when magnesium levels are normal - first-line agent

92
Q

Where else is magnesium valuable in?

A

Ventricular arrhythmias in ischemic cells, associated with loss of cellular magnesium.

93
Q

Describe the mechanism of magnesium

A

Mechanism unknown, but may involve regulating calcium accumulation

  • reduces sodium and calcium currents
  • reduces calcium release from the SR
  • cofactor of the Na+/K+ ATPase pump
94
Q

Very fucking briefly describe Adenosine (Class 5) - this lecture needs to END

A

-Acts on purine (A1) receptors of SA and AV nodes

Mode of action:

  • increases K+ conductance (hyperpolarizes)
  • depresses slow inward Ca2+ current
  • slows the phase 4 of AV pacemaker action potential
  • slows sinus rate and decreases AV node conduction
  • used for supra ventricular tachycardia due to AV node re-entry

kay sorry that wasn’t that brief

95
Q

Adenosine is given ___

A

IV

96
Q

Drug interactions with Adenosine ?

A

methylxanthines (caffeine/theophylline) block adenosine receptors

97
Q

Describe Digoxin (Class 5)

A
  • decreases AV node conduction
  • simulates vagus nerve and releases ACh
  • inhibits calcium currents and activates K+ currents
  • useful in atrial fibrillation, atrial flutter, and supra ventricular tachycardia with a rapid ventricular response
  • reduces the ventricular rate - increases stroke volume - increases CO
  • can lead to delayed afterdepolarizations
  • should not be used in wolf-parkinson-white syndrome - may cause death
98
Q

Treatment of bradycardia

A

symptomatic bradycardia (<50-60 bpm) = pacemaker

99
Q

Treatment of tachycardia

A
  • isolated ectopic beats or short runs of tachycardia
  • if asymptomatic - no treatment

-symptomatic/severe tachycardia - immediate cardioversion (electrical/pharmacological)

100
Q

Treatment of paroxysmal tachycardia

A
  • vagal maneuvers (valsalva, carotid massage)
  • IV adenosine or verapamil or beta-blockers; target AV node to reduce ventricular rate

For WPW: has to be treated with procainamide, flecainide or amiodarone

If area of tissue responsible for the arrhythmia can be identified (ectopic site, accessory pathway), then radio frequency ablation is preferred: highly effective, life-long cure. Avoids unwanted side effects of arrhythmic drugs

101
Q

How do you treat atrial fibrillation?

A
  • anticoagulation
  • antiarrhythmics:
    1) ventricular rate control
    2) maintain sinus rhythm

1) Rate control:
- Verapamil, beta-blocker, digoxin; target AV node to reduce ventricular rate
- Amiodarone

2) Rhythm control - in highly symptomatic patients:
- Procainamide, flecainamide, amiodarone or sotalol

102
Q

How do you treat ventricular fibrillation?

A

Irregular rhythm with uncoordinated contraction, immediate cause of death

- transthroacic defribrillation    - IV amiodarone, lidocaine or magnesium may be used as an adjunct
103
Q

How do you treat ventricular tachycardia to terminate an episode

A

In patients unconscious and hypotensive (mean arterial pulse <60 mmHG): cardioversion (synchronized DC shock)

In patients with stable hemodynamics: IV lidocaine, flecainide patients without structural heart disease), amiodarone, sotalol

104
Q

How do you treat ventricular tachycardia (special cases)

A

Torsade de pointes: IV magnesium is the treatment of choice

-Arrhythmias after acute MI: IV lidocaine often used as a first line agent

105
Q

How do you treat ventricular tachycardia (for chronic therapy for VT)

A

implantable cardioverter defibrillators (ICD) is preferred over anti arrhythmic drugs for initial therapy

106
Q

Side effects of implantable cardioverter defibrillators (ICD)?

A
  • anxiety, depression, post-traumatic stress disorder

- amiodarone may be used in conjunction to reduce risk of ICD shocks

Pharmacology B (21 decks)

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