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Therapeutics I > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

What is the refractory period?

A

Brief period during which cell can’t again be excited

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2
Q

What is normal SA node rhythm?

A

60-100bpm

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3
Q

What normal AV node and bundle of his rhythm?

A

40bpm

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4
Q

What is the function of purkinje system?

A

Innervates the mechanical myocardium and serves to initiate excitation → contraction coupling and contractile process

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5
Q

What is this rhythm and what electrolytes are involved?

A

SA node

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6
Q

What is this rhythm and what electrolytes are involved?

A

Myocardium contraction

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7
Q

What are the types of bradyarrythmias?

A
  1. Sinus node dysfunction
  2. AV block
  3. Conduction tissue disease
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8
Q

What are the types of SND?

A

Sinus bradycrdia

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9
Q

What are the types of AV block?

A

1st, 2nd, 3rd

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10
Q

What are the types of conduction tissue disease?

A

Left bundle branch block
RBBB

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11
Q

What is considered bradyarrythmias?

A

<60bpm

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12
Q

What are the types of tachyarrhythmias?

A
  1. Impulse generation problem
  2. Impulse conduction problem
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13
Q

What is automatic tachycardia?

A

Where impulse generation exceeds the SA node activity

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14
Q

What are the potential causes of tachycardia?

A
  1. Digoxin or catecholamines
  2. Hypoxia, electrolyte abnormalities and fiber stretch
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15
Q

What are the transient membrane depolarizations of triggered automaticity?

A
  1. EAD (early after depolarizations)
  2. DAD (delayed after depolarizations)
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16
Q

What is the difference between EAD and DAD?

A

EAD: Any factor that blocks the ion channels responsible for cellular depolarization

DAD: precipitated by digoxin or catecholamines and suppressed by non DHP CCB

DAD and EAD

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17
Q

What is triggered automaticity?

A

Multifocal atrial tachycardia, digoxin induced tachycardia, exercise provoked VT

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18
Q

What is reentrant tachycardia?

A

Indefinite propagation of the impulse and continued activation of previously refractory tissue

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19
Q

What are the requirements for viable reentrant focus?

A
  1. 2 pathways for impulse conduction
  2. Area of unidirectional block (prolonged refractoriness) in one of these pathways
  3. Slow conduction in the other pathway
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20
Q

What are the types of reentry?

A

Anatomically defined
Functionally defined

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21
Q

What is anatomical reentry?

A

Electrical current is disrupted by an accessory pathway rerouting the current

WPW, PSVT, ventricular tachycardia, a flutter

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22
Q

What is considered tachyarrythmia?

A

100bpm

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23
Q

What is functional reentry?

A

Multiple places are firing at the same time so there no consistency

A fib and ventricular fib

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24
Q

What are the rhythm drugs?

A

Class 1 and 3

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25
Q

The SA node set the ___?

A

Rate

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26
Q

What helps your heart rate stay between 60-100?

A

cholinergic and sympathetic inntervation

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27
Q

What are the presentations of arrhythmia?

A
  1. Palpitations or heart racing
  2. Chest pain
  3. Dyspnea
  4. DZ
  5. Fatigue
  6. Syncope
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28
Q

What labs are we looking at for arrhythmia

A
  1. BP, HR, height, weight
  2. Electrolytes (K+ and Mg2+), bleeding
  3. 12 lead ECG (function) and echocardiogram (structure)
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29
Q

What are the different kinds of rhythm-based arrhythmia?

A

Regularly irregular
Irregular irregular

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30
Q

What are the different kinds of rate-based arrhythmia?

A

Fast (tachycardia) and slow (bradycardia)

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31
Q

What are the different kinds of origin-based arrhythmia?

A

Supraventricular (atrial)
Ventricular

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32
Q

What is the overall target for antiarrhythmics?

A

Directly alter electrical conductions

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33
Q

In what ways can we directly alter electrical conductions?

A
  1. Depress the autonomic properties
  2. Alter the conduction (reentrant loop)
  3. Facilitate conduction
  4. Depress conduction
  5. Stop reentry
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34
Q

What is the Vaughan Williams Classification of drugs?

A

Class I: Sodium channel blockers
Class II: Beta-blockers
Class III: Potassium channel blockers
Class IV: Non-dihydropyridine CCBs
Other (Class V): Digoxin, Atropine, Adenosine, Magnesium sulfate

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35
Q

Drugs in C1a?

A

Quinidine
Procainamide
disopyramide

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36
Q

MOA of C1a? Indication?

A

Na and K block: intermediate on-off
1. Slow conduction velocity
2. Prolong RP
3. Decrease automaticity

supra ventricular and ventricular arrhythmias

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37
Q

Drugs in C1b?

A

Lidocaine and mexiletine

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38
Q

MOA of C1b? Indication?

A

Na block: fast on-off
1. Shorten RP
2. Little to no effect on conduction
3. Decrease automaticity

Ventricular arrythmias

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39
Q

MOA of C1c? Indication?

A

Na block: slow on-off
1. Slow conduction
2. Little to no effect on RP
3. Decrease automaticity

Supraventricular arrhythmias

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40
Q

Drugs in C1c?

A

Flecainide and propafenone

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41
Q

What is the MOA of Class 2? Indications?

A

Ca2+ block
1. Increased conduction
2. Shorten RP
3. Increased automaticity

Tachycardia w/ reentry loops or highly automatic nodal tissue

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42
Q

How does beta blockers increase automaticity?

A

interfere with calcium entry into the cell by altering catecholamine-dependent channel

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43
Q

What are the class 3 drugs?

A

Amiodarone
Dronedarone
Sotalol
Ibutilide
Dofetilide

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44
Q

MOA of Class 3?

A

Delay repolarizations by blocking K+ channels
1. Increase RP

May be proarrythmia in form of TdP by provoking EADs

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45
Q

What are the true potassium class 3 drugs? Indication?

A

Ibutilide IV and dofetilide PO

Supraventricular arrhythmia

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46
Q

Indication of sotalol?

A

Supraventricular and ventricular arrhythmias

Inhibitors outward K+ movement during repolarization and nonselective b-blockade

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47
Q

Indication of dronedarone?

A

Supraventricular arrhythmias

Less effective than amiodarone

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48
Q

Indication of amiodarone?

A

Supraventricular and ventricular arrhythmias

All classes with nonselective b-block

Highly effective with low pro-arrythmic effects

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49
Q

What is the commonly prescribe AAD?

A

Amiodarone

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50
Q

Metabolism of amiodarone?

A

Substrate of CYP3A4, moderate inhibitor of CYPs (2C9, 2D6, 3A4) and PgP

51
Q

ADRs of amiodarone?

A

Bradycardia, hyper/hypothyroidism, photosensitivity, TdP, blindness

52
Q

MOA of Class IV? Indication?

A

Blocks L-type CC in SA and AV nodal tissue
1. Slow conduction
2. Prolong RP
3. Decrease automaticity

Automatic or reentrant tachycardia from SA or AV nodes

53
Q

Drugs of Class IV?

A

Verapamil and diltiazem

54
Q

Conversion of IV and PO dose of digoxin?

A

IV is 75% of PO dose

55
Q

Drugs of Class 5?

A

Digoxin, atropine, adenosine, magnesium sulfate

56
Q

Indications of digoxin? Toxicity?

A

A fib

Neurological symptoms, yellow vision, hyperkalemia

57
Q

How do you monitor digoxin?

A

Trough levels
Therapeutic level: 0.5-2 ng/mL

58
Q

Antidote for digoxin?

A

Digifab

59
Q

Indication when to use digifab

A
  1. Life-threatening arrhythmia, asystole, symptomatic bradycardia
  2. End-organ dysfunction
  3. Serum K >5.5
60
Q

What is adenosine indicated for? ADRs?

A

Slows conduction through AV node

Causes cardiac arrest and conversion to other arrhythmias (feeling of impending doom)

61
Q

What medications are CI with HFrEF?

A

Class 1A, C
Dronedarone and sotalol
Class IV

62
Q

What are the types of SVA?

A
  1. A fib and flutter
  2. PSVT
  3. Automatic atrial tachycardia
  4. Premature atrial complexes
  5. Sinus tachycardia
63
Q

DDI of amiodarone?

A

CYP3A4 substrate

64
Q

DDI of diltazem?

A

CYP3A4 substrate

65
Q

DDI of verapamil?

A

CYP3A4 substrate

66
Q

What is acute A fib?

A

Onset within 48

67
Q

What is paroxysmal A fib?

A

terminates spontaneously in <7 days

68
Q

What is recurrent A fib?

A

2+ episodes

69
Q

What is persistent A fib?

A

> 7 days; doesn’t terminate spontaneously

70
Q

What is long standing persistant A fib?

A

> 12 months

71
Q

What is permanent A fib?

A

Patient and provider jointly decide to stop SR restoration/maintenance

72
Q

What is nonvalvular A fib?

A

Absence of mitral stenosis, mechanical or bio prosthetic valves, or mitral repair

73
Q

What is A fib?

A

Extremely rapid and disorganized atrial activation having an irregular pulse

74
Q

What are the symptoms of AFib?

A
  1. Rapid HR/palpitation
  2. Fatigue, dyspnea, DZ
    Affects both sides of atrium

ECG: No decernable P wave (rate 120-180)

75
Q

How does flutter differ from A fib?

A

Atrial activity more organized and effects only the left

ECG: Sawtooth pattern and rate 300 bpm

76
Q

A fib better care components?

A

Anticoagulation/avoid stroke
Better symptom management
Cardiovascular and comorbidity optimization

77
Q

Causes and Risk factors of A fib and flutter?

A
  1. Infection
  2. Cormodidities
78
Q

Pharm and non pharms to avoid stroke?

A

Anticoags and watchman device

79
Q

When would you use rate control drugs?

A
  1. No or minimal symptoms
  2. Treatment of choice for permanent AF
80
Q

When would you use rhythm control drugs?

A
  1. Paroxysmal or persistent AF
  2. Symptomatic despite adequate rate control
  3. Hemodynamically unstable
  4. HF
  5. Tachycardia-mediated cardiomyopathy
  6. Young, first AF episode, preference
81
Q

What is the management after watchman placement?

A

Anticoagulant and ASA → 45 days later change from anticoagulant to P2Y12i (DAT) → after 6 months peel of P2Y12i and continue ASA indefinitely

82
Q

What are the rate goals for A fib?

A

<110bpm for asymptomatic patients with HFpEF (>50%)

<80 bpm for symptomatic or HFrEF (<40%)

83
Q

Describe rate control A fib algorithm?

A

Avoid nonselective B-block in COPD

Digoxin is add on

84
Q

What are the goals of rhythm control?

A

Restore sinus rhythm → cardioversion

85
Q

What are the methods for cardioversion?

A

DCCV (electrical)

  1. Class III pure IK blockers (ibutilide and dofetilide)
  2. Class Ic AADs (flecainide and propafenone)
  3. Amiodarone (oral or IV)
86
Q

What do you do is cardioversion increases risk for thromboembolism?

A

> 48 hr duration or unknown duration  anticoagulation prior to cardioversion (3 weeks) & 4 weeks after

< 48 hr duration  no anticoagulation

87
Q

How should you do maintain sinus rhythm?

A

Class Ic or III AADs or Amiodarone (most common)

Ablation: cut off abnormal electrical pathway

88
Q

A fib and flutter algorithm?

A
89
Q

What are your types of PSVT?

A
  1. AV nodal reentry (AVNRT)
  2. AV reentry incorporating an accessory pathway (AVRT)
  3. SA nodal reentry
  4. Intra atrial reentry
90
Q

What is AVNRT?

A

AV nodal reentry
Symptomatic but hemodynamically stable

Middle aged

91
Q

What is AVRT?

A

AV reentry incorporating an accessory pathway

Young adults

Well tolerated but can lead to syncope

92
Q

What are the acute treatments for PSVT?

A
  1. Directly or indirectly increase vagal tone to AV node
  2. Depress conduction through Ca2+ dependent tissue
  3. Depress conduction through fast, sodium-dependent tissue
93
Q

What is the preventative treatment for PSVT?

A

First line option: ablation
Second line: nodal AADs or Class Ic

94
Q

Indications for PSVT prophylaxis?

A
  1. Frequent episodes that require therapeutic intervention → interfering with life style
  2. Infrequent episodes causing severe symptoms
95
Q

What are the vagal maneuvers?

A
  1. Bearing down
  2. Face in ice cold water
  3. Carotid massage
  4. Blowing into folded straw
  5. Coughing
  6. Gagging
96
Q

PSVT treatment algorithm?

A
97
Q

What are the types of ventricular arrhythmias?

A
  1. Premature ventricular complexes (PVC)
  2. Ventricular tachycardia
  3. Ventricular fib
98
Q

What are PVCs?

A

Elicited by abnormal automaticity, triggered activity, or reentrant mechanisms → sudden cardiac death

Commonly in healthy individuals

99
Q

What is the PVC treatment for healthy patient w/o SHD?

A
  1. Norisk of VT or SCD
  2. No drug therapy needed
100
Q

What is the PVC treatment for patient w underlying SHD?

A
  1. Higher mortality
  2. AADs increase risk of lethal arrhythmias
  3. Give beta blockers, antiplatelets, statins, 4. ACEIs/ARBs, aldosterone antagonists as appropriate
  4. ICD indicated in HFrEF
101
Q

What is considered ventricular tachycardia?

A
  1. 3 or more consecutive PVCs
  2. HR >100 bpm
  3. wide QRS, regular pattern
102
Q

What is non-sustained VT (NSVT)?

A

Episode lasts <30 seconds

103
Q

What is sustained VT (NSVT)?

A

Lasts >30 seconds

104
Q

What is monomorphic VT?

A

QRS complexes are similar in morphologic characteristics from beat to beat

105
Q

What is polymorphic VT?

A

QRS complexes vary in shape and/or size between beats

106
Q

What might amplify VT?

A
  1. Severe electrolyte abnormalities (hypoK+ and Mg2+)
  2. Hypoxia
  3. Digoxin toxicity
  4. Acute MI or myocardial ischemia from HF
107
Q

What is the VT algorithms?

A
108
Q

What is TdP?

A

QT prolongation → cardiac arrest

109
Q

What is the therapy of TdP?

A
  1. DCC
  2. 2 g IV magnesium sulfate over 1 minute – suppresses EADs
  3. If IV magnesium ineffective,transvenous or pharmacologic pacing with isoproterenol or epinephrine is indicate
110
Q

ADRs associated with TdP?

A
  1. Caution when baseline QTc is > 450 msec in men; >470 msec in women
  2. Discontinue drug when QTc is > 500 msec
111
Q

Drugs that are CI with TdP?

A
  1. AAD
  2. Chemo
  3. Antipsychotics and TCA
  4. Fluoroquinolones and macrolides
  5. Voriconazole
  6. Methadone
112
Q

What is VFib?

A

Medical emergency requiring CPR

Results in absence of CO and CV collapse

113
Q

What are the ACLA guidelines rec for VFib?

A
  1. High quality CPR
  2. Prompt defibrillation
  3. Epinephrine 1 mg IV push Q3-5 minutes
  4. Amiodarone 300 mg IV bolus after 3 shocks; may repeat 150 mg
  5. Lidocaine as alternative to amiodarone
114
Q

Types of badyarrhythmias?

A
  1. Sinus bradycardia
  2. AV block
115
Q

What is considered Sinus Bradycardia? Causes?

A

HR <60

MI, hypothyroidism, (beta blockers, digoxin, CCBs, amiodarone), hyperkalemia

116
Q

Who are susceptible to sinus bradycardia?

A
  1. Common in young, athletic individuals (asymptomatic)
  2. Elderly
117
Q

How do you manage sinus bradycardia?

A

Acute symptomatic: Atropine 0.5-1 mg IV push; up to 3 mg

Long term or unresponsive to atropine: Pacemaker

118
Q

Where do AV block occur?

A
  1. AV node
  2. Bundle of HIs
  3. Bundle branches
119
Q

What causes AV block?

A

AV nodal disease, acute MI, myocarditis, increased vagal tone, drugs, hyperkalemia

120
Q

What are the treatment goals for AV blocks?

A

Restore sinus rhythm if symptomatic

121
Q

What is the treatment for AV block?

A

D/C drugs slowing AV node conduction

Reversible: temporary pacemaker or atropine, dopamine, epinephrine, isoproterenol

Chronic: permanent pacemaker

122
Q

What do we monitor and follow up?

A
  1. Mortality
  2. Signs and symptoms
  3. Surrogate markers for efficacy
  4. Quality of life
  5. Economics
  6. Arrhythmia specific
123
Q

Signs and symptoms to look for when following up with arrythmias

A
  1. Recurrences documented by electrocardiogram
  2. Time to recurrence
  3. Frequency of recurrences
    4 .Exercise tolerance
  4. Lightheadedness
  5. Blood pressure
  6. Heart rate

Therapeutics I (32 decks)

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