Arrythmias Flashcards
1
Q
What is the refractory period?
A
Brief period during which cell can’t again be excited
2
Q
What is normal SA node rhythm?
A
60-100bpm
3
Q
What normal AV node and bundle of his rhythm?
A
40bpm
4
Q
What is the function of purkinje system?
A
Innervates the mechanical myocardium and serves to initiate excitation → contraction coupling and contractile process
5
Q
What is this rhythm and what electrolytes are involved?
A
SA node
6
Q
What is this rhythm and what electrolytes are involved?
A
Myocardium contraction
7
Q
What are the types of bradyarrythmias?
A
- Sinus node dysfunction
- AV block
- Conduction tissue disease
8
Q
What are the types of SND?
A
Sinus bradycrdia
9
Q
What are the types of AV block?
A
1st, 2nd, 3rd
10
Q
What are the types of conduction tissue disease?
A
Left bundle branch block
RBBB
11
Q
What is considered bradyarrythmias?
A
<60bpm
12
Q
What are the types of tachyarrhythmias?
A
- Impulse generation problem
- Impulse conduction problem
13
Q
What is automatic tachycardia?
A
Where impulse generation exceeds the SA node activity
14
Q
What are the potential causes of tachycardia?
A
- Digoxin or catecholamines
- Hypoxia, electrolyte abnormalities and fiber stretch
15
Q
What are the transient membrane depolarizations of triggered automaticity?
A
- EAD (early after depolarizations)
- DAD (delayed after depolarizations)
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
17
Q
What is triggered automaticity?
A
Multifocal atrial tachycardia, digoxin induced tachycardia, exercise provoked VT
18
Q
What is reentrant tachycardia?
A
Indefinite propagation of the impulse and continued activation of previously refractory tissue
19
Q
What are the requirements for viable reentrant focus?
A
- 2 pathways for impulse conduction
- Area of unidirectional block (prolonged refractoriness) in one of these pathways
- Slow conduction in the other pathway
20
Q
What are the types of reentry?
A
Anatomically defined
Functionally defined
21
Q
What is anatomical reentry?
A
Electrical current is disrupted by an accessory pathway rerouting the current
WPW, PSVT, ventricular tachycardia, a flutter
22
Q
What is considered tachyarrythmia?
A
100bpm
23
Q
What is functional reentry?
A
Multiple places are firing at the same time so there no consistency
A fib and ventricular fib
24
Q
What are the rhythm drugs?
A
Class 1 and 3
25
The SA node set the ___?
Rate
26
What helps your heart rate stay between 60-100?
cholinergic and sympathetic inntervation
27
What are the presentations of arrhythmia?
1. Palpitations or heart racing
2. Chest pain
3. Dyspnea
4. DZ
5. Fatigue
6. Syncope
28
What labs are we looking at for arrhythmia
1. BP, HR, height, weight
2. Electrolytes (K+ and Mg2+), bleeding
3. 12 lead ECG (function) and echocardiogram (structure)
29
What are the different kinds of rhythm-based arrhythmia?
Regularly irregular
Irregular irregular
30
What are the different kinds of rate-based arrhythmia?
Fast (tachycardia) and slow (bradycardia)
31
What are the different kinds of origin-based arrhythmia?
Supraventricular (atrial)
Ventricular
32
What is the overall target for antiarrhythmics?
Directly alter electrical conductions
33
In what ways can we directly alter electrical conductions?
1. Depress the autonomic properties
2. Alter the conduction (reentrant loop)
3. Facilitate conduction
4. Depress conduction
5. Stop reentry
34
What is the Vaughan Williams Classification of drugs?
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
35
Drugs in C1a?
Quinidine
Procainamide
disopyramide
36
MOA of C1a? Indication?
Na and K block: intermediate on-off
1. Slow conduction velocity
2. Prolong RP
3. Decrease automaticity
supra ventricular and ventricular arrhythmias
37
Drugs in C1b?
Lidocaine and mexiletine
38
MOA of C1b? Indication?
Na block: fast on-off
1. Shorten RP
2. Little to no effect on conduction
3. Decrease automaticity
Ventricular arrythmias
39
MOA of C1c? Indication?
Na block: slow on-off
1. Slow conduction
2. Little to no effect on RP
3. Decrease automaticity
Supraventricular arrhythmias
40
Drugs in C1c?
Flecainide and propafenone
41
What is the MOA of Class 2? Indications?
Ca2+ block
1. Increased conduction
2. Shorten RP
3. Increased automaticity
Tachycardia w/ reentry loops or highly automatic nodal tissue
42
How does beta blockers increase automaticity?
interfere with calcium entry into the cell by altering catecholamine-dependent channel
43
What are the class 3 drugs?
Amiodarone
Dronedarone
Sotalol
Ibutilide
Dofetilide
44
MOA of Class 3?
Delay repolarizations by blocking K+ channels
1. Increase RP
May be proarrythmia in form of TdP by provoking EADs
45
What are the true potassium class 3 drugs? Indication?
Ibutilide IV and dofetilide PO
Supraventricular arrhythmia
46
Indication of sotalol?
Supraventricular and ventricular arrhythmias
Inhibitors outward K+ movement during repolarization and nonselective b-blockade
47
Indication of dronedarone?
Supraventricular arrhythmias
Less effective than amiodarone
48
Indication of amiodarone?
Supraventricular and ventricular arrhythmias
All classes with nonselective b-block
Highly effective with low pro-arrythmic effects
49
What is the commonly prescribe AAD?
Amiodarone
50
Metabolism of amiodarone?
Substrate of CYP3A4, moderate inhibitor of CYPs (2C9, 2D6, 3A4) and PgP
51
ADRs of amiodarone?
Bradycardia, hyper/hypothyroidism, photosensitivity, TdP, blindness
52
MOA of Class IV? Indication?
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
Drugs of Class IV?
Verapamil and diltiazem
54
Conversion of IV and PO dose of digoxin?
IV is 75% of PO dose
55
Drugs of Class 5?
Digoxin, atropine, adenosine, magnesium sulfate
56
Indications of digoxin? Toxicity?
A fib
Neurological symptoms, yellow vision, hyperkalemia
57
How do you monitor digoxin?
Trough levels
Therapeutic level: 0.5-2 ng/mL
58
Antidote for digoxin?
Digifab
59
Indication when to use digifab
1. Life-threatening arrhythmia, asystole, symptomatic bradycardia
2. End-organ dysfunction
3. Serum K >5.5
60
What is adenosine indicated for? ADRs?
Slows conduction through AV node
Causes cardiac arrest and conversion to other arrhythmias (feeling of impending doom)
61
What medications are CI with HFrEF?
Class 1A, C
Dronedarone and sotalol
Class IV
62
What are the types of SVA?
1. A fib and flutter
2. PSVT
3. Automatic atrial tachycardia
4. Premature atrial complexes
5. Sinus tachycardia
63
DDI of amiodarone?
CYP3A4 substrate
64
DDI of diltazem?
CYP3A4 substrate
65
DDI of verapamil?
CYP3A4 substrate
66
What is acute A fib?
Onset within 48
67
What is paroxysmal A fib?
terminates spontaneously in <7 days
68
What is recurrent A fib?
2+ episodes
69
What is persistent A fib?
>7 days; doesn't terminate spontaneously
70
What is long standing persistant A fib?
>12 months
71
What is permanent A fib?
Patient and provider jointly decide to stop SR restoration/maintenance
72
What is nonvalvular A fib?
Absence of mitral stenosis, mechanical or bio prosthetic valves, or mitral repair
73
What is A fib?
Extremely rapid and disorganized atrial activation having an irregular pulse
74
What are the symptoms of AFib?
1. Rapid HR/palpitation
2. Fatigue, dyspnea, DZ
Affects both sides of atrium
ECG: No decernable P wave (rate 120-180)
75
How does flutter differ from A fib?
Atrial activity more organized and effects only the left
ECG: Sawtooth pattern and rate 300 bpm
76
A fib better care components?
Anticoagulation/avoid stroke
Better symptom management
Cardiovascular and comorbidity optimization
77
Causes and Risk factors of A fib and flutter?
1. Infection
2. Cormodidities
78
Pharm and non pharms to avoid stroke?
Anticoags and watchman device
79
When would you use rate control drugs?
1. No or minimal symptoms
2. Treatment of choice for permanent AF
80
When would you use rhythm control drugs?
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
What is the management after watchman placement?
Anticoagulant and ASA → 45 days later change from anticoagulant to P2Y12i (DAT) → after 6 months peel of P2Y12i and continue ASA indefinitely
82
What are the rate goals for A fib?
<110bpm for asymptomatic patients with HFpEF (>50%)
<80 bpm for symptomatic or HFrEF (<40%)
83
Describe rate control A fib algorithm?
Avoid nonselective B-block in COPD
Digoxin is add on
84
What are the goals of rhythm control?
Restore sinus rhythm → cardioversion
85
What are the methods for cardioversion?
DCCV (electrical)
1. Class III pure IK blockers (ibutilide and dofetilide)
2. Class Ic AADs (flecainide and propafenone)
3. Amiodarone (oral or IV)
86
What do you do is cardioversion increases risk for thromboembolism?
>48 hr duration or unknown duration anticoagulation prior to cardioversion (3 weeks) & 4 weeks after
< 48 hr duration no anticoagulation
87
How should you do maintain sinus rhythm?
Class Ic or III AADs or Amiodarone (most common)
Ablation: cut off abnormal electrical pathway
88
A fib and flutter algorithm?
89
What are your types of PSVT?
1. AV nodal reentry (AVNRT)
2. AV reentry incorporating an accessory pathway (AVRT)
3. SA nodal reentry
4. Intra atrial reentry
90
What is AVNRT?
AV nodal reentry
Symptomatic but hemodynamically stable
Middle aged
91
What is AVRT?
AV reentry incorporating an accessory pathway
Young adults
Well tolerated but can lead to syncope
92
What are the acute treatments for PSVT?
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
What is the preventative treatment for PSVT?
First line option: ablation
Second line: nodal AADs or Class Ic
94
Indications for PSVT prophylaxis?
1. Frequent episodes that require therapeutic intervention → interfering with life style
2. Infrequent episodes causing severe symptoms
95
What are the vagal maneuvers?
1. Bearing down
2. Face in ice cold water
3. Carotid massage
4. Blowing into folded straw
5. Coughing
6. Gagging
96
PSVT treatment algorithm?
97
What are the types of ventricular arrhythmias?
1. Premature ventricular complexes (PVC)
2. Ventricular tachycardia
3. Ventricular fib
98
What are PVCs?
Elicited by abnormal automaticity, triggered activity, or reentrant mechanisms → sudden cardiac death
Commonly in healthy individuals
99
What is the PVC treatment for healthy patient w/o SHD?
1. Norisk of VT or SCD
2. No drug therapy needed
100
What is the PVC treatment for patient w underlying SHD?
1. Higher mortality
2. AADs increase risk of lethal arrhythmias
3. Give beta blockers, antiplatelets, statins, 4. ACEIs/ARBs, aldosterone antagonists as appropriate
5. ICD indicated in HFrEF
101
What is considered ventricular tachycardia?
1. 3 or more consecutive PVCs
2. HR >100 bpm
3. wide QRS, regular pattern
102
What is non-sustained VT (NSVT)?
Episode lasts <30 seconds
103
What is sustained VT (NSVT)?
Lasts >30 seconds
104
What is monomorphic VT?
QRS complexes are similar in morphologic characteristics from beat to beat
105
What is polymorphic VT?
QRS complexes vary in shape and/or size between beats
106
What might amplify VT?
1. Severe electrolyte abnormalities (hypoK+ and Mg2+)
2. Hypoxia
3. Digoxin toxicity
4. Acute MI or myocardial ischemia from HF
107
What is the VT algorithms?
108
What is TdP?
QT prolongation → cardiac arrest
109
What is the therapy of TdP?
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
ADRs associated with TdP?
1. Caution when baseline QTc is > 450 msec in men; >470 msec in women
2. Discontinue drug when QTc is > 500 msec
111
Drugs that are CI with TdP?
1. AAD
2. Chemo
3. Antipsychotics and TCA
4. Fluoroquinolones and macrolides
5. Voriconazole
6. Methadone
112
What is VFib?
Medical emergency requiring CPR
Results in absence of CO and CV collapse
113
What are the ACLA guidelines rec for VFib?
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
Types of badyarrhythmias?
1. Sinus bradycardia
2. AV block
115
What is considered Sinus Bradycardia? Causes?
HR <60
MI, hypothyroidism, (beta blockers, digoxin, CCBs, amiodarone), hyperkalemia
116
Who are susceptible to sinus bradycardia?
1. Common in young, athletic individuals (asymptomatic)
2. Elderly
117
How do you manage sinus bradycardia?
Acute symptomatic: Atropine 0.5-1 mg IV push; up to 3 mg
Long term or unresponsive to atropine: Pacemaker
118
Where do AV block occur?
1. AV node
2. Bundle of HIs
3. Bundle branches
119
What causes AV block?
AV nodal disease, acute MI, myocarditis, increased vagal tone, drugs, hyperkalemia
120
What are the treatment goals for AV blocks?
Restore sinus rhythm if symptomatic
121
What is the treatment for AV block?
D/C drugs slowing AV node conduction
Reversible: temporary pacemaker or atropine, dopamine, epinephrine, isoproterenol
Chronic: permanent pacemaker
122
What do we monitor and follow up?
1. Mortality
2. Signs and symptoms
3. Surrogate markers for efficacy
4. Quality of life
5. Economics
6. Arrhythmia specific
123
Signs and symptoms to look for when following up with arrythmias
1. Recurrences documented by electrocardiogram
2. Time to recurrence
3. Frequency of recurrences
4 .Exercise tolerance
5. Lightheadedness
6. Blood pressure
7. Heart rate
