8 - Arrhythmias Flashcards
(147 cards)
1
Q
Although there are pure forms, most common arrhythmias are combinations of both _________ and ________.
A
automaticity
re-entry
2
Q
Describe an arrhythmia of automaticity
A
- Abnormality in impulse generation
- Often starts the arrhythmia
3
Q
Describe an arrhythmia of re-entry
A
- Abnormality in impulse conduction
- Often maintains the arrhythmia
4
Q
What is the primary pacemaker?
A
SA node
5
Q
What is the escape pacemaker(s)?
A
-AV node then -bundle of His then -Bundle branches then -Purkinje network
6
Q
What is the rate of the SA node?
A
60 - 100 beats/min
7
Q
What is the rate of the AV node?
A
40 - 60 beats/min
8
Q
What is the rate of the ventricles (bundle branches & purkinje network) ?
A
20 - 40 beats/min
9
Q
Describe what is happening in a re-entry arrhythmia
A
- Different conduction velocity
- Different refractoriness
10
Q
Type 1a AAD (anti-arrhythmic drug):
Sodium channel blockers (med)
Give examples
A
Quindine
Procainamide
11
Q
Type 1b AAD (anti-arrhythmic drug):
Sodium channel blockers (fast)
Give examples
A
Lidocaine
Mexilintine
12
Q
Type 1c AAD (anti-arrhythmic drug):
Sodium channel blockers (slow)
Give examples
A
Flecainide
Propafenone
13
Q
Type 2 AAD (anti-arrhythmic drug):
Beta blockers
Give examples
A
Metoprolol
Atenolol
14
Q
Type 3 AAD (anti-arrhythmic drug):
K+ channel blockers
Give examples
A
Amiodarone
Sotalol
Ibutilide
15
Q
Type 4 AAD (anti-arrhythmic drug):
Calcium Channel blockers
Give examples
A
Diltiazem
Verapamil
16
Q
Type __ = Sodium channel blockers
A
1
17
Q
Type __ = K+ channel blockers
A
3
18
Q
Type __ = calcium channel blockers
A
4
19
Q
Type __ = beta blockers
A
2
20
Q
AAD (anti-arrhythmic drugs) either control the _______ or the _______
A
rate or the rhythm
21
Q
How do rate control agents work?
A
Reduce automaticity: prevent or slow arrhythmias
22
Q
How do rhythm control agents work?
A
Reduce re-entry: prevent or stop arrhythmias
23
Q
Which types of AADs control rate?
A
Type 2 - Beta blockers
Type 4 - Non-DBP Calcium channel blockers
Digoxin (Na+/K+ ATPase Blocker)
24
Q
Which types of AADs control rhythm ?
A
Type 1 - Sodium channel blockers
Type 3 - K+ channel blockers
25
MOA of Type 2 (Beta Blockers)
- Reduced adrenergic stimulation of SA/AV nodes
| - Decreased adrenergic stimulation of myocardial contractility
26
MOA of Type 4 (Non-DBP Calcium Channel Blockers)
- Reduced calcium current and recovery in SA/AV nodes
- Decreased calcium influx in myocytes, decreased myocardial contractility
- Relaxation of arterial smooth muscles
27
MOA of Digoxin (Na+/K+ ATPase Blocker)
-Increased myocyte Na+/Ca2+ causing decreased K+, increasing AV node refractory period
- Increased vagal tone, decreased SA/AV activity
- Increased intracellular Na, exchanged for Ca2+, increased contractility
28
MOA of Class 1 (sodium channel blockers)
- Decrease in conduction velocity
| - Re-entry loop loses "steam", SA node takes over
29
MOA of Class 2 (K+ channel blockers)
- Prolonged refractory period
| - Re-entry loop "catches its tail", SA node takes over
30
What is the idea behind anti-arrhythmic therapy?
to slow down the AV node and allow SA node to take over again
31
List the few pure rhythm control agents
```
Quinidine
Sotalol
Amiodarone
Propafenone
Flecainide
Ibutilide/Dofetilide
```
32
What type is Quinidine?
Class 1a and K+ blocker
33
What type is Sotalol?
Class 3 and BB
34
What type is Amiodarone?
Class 3 and Na-channel blocker, CCB, BB
35
What type is Propafenone?
Class 1c and BB
36
What type is Flecainaide?
Pure Class 1c
37
What type of patients is Class 1c contraindicated in?
patients with previous heart issues?
38
What type is Ibutilide/Dofetilide?
Pure class 3
39
What does Ibutilide/Dofetilide have a high risk of?
Torsades de Pointes
40
> ____ bpm = tachycardic
100
41
< ____ bpm = bradycardic
60
42
Normal respiratory rate (RR) ?
12 - 20
43
What is atrial fibrillation?
- Atria beat really fast (400-600 atrial beats per minute) and disorganized rhythm (irregularly irregular)
- Loss of atrial kick = heart is not filled as efficiently
- Extremely fast atrial rhythm results in fast ventricular rate
44
Categories of atrial fib:
| Acute = ?
48 hours
45
Categories of atrial fib:
| Paroxysmal = ?
terminates spontaneously within 7 days
46
Categories of atrial fib:
| Persistent = ?
continues for greater than 7 days
47
Categories of atrial fib:
| Permanent = ?
does not terminate even with cardioversion attempts
48
What are some temporary factors that may precipitate atrial fibrillation?
Things that cause high adrenergic tone:
- alcohol withdrawl
- sepsis
- post surgery
* more on slide 18
49
What are some permanent factors that may precipitate atrial fibrillation?
Things that cause atrial distension:
- ischemia
- hypertension
- obesity
* more on slide 18
50
Signs of A fib?
-Irregular pulse
-HR > 100 bpm
-Hypotension
EKG
51
Symptoms of A fib?
- Asymptomatic
- Palpitations
- Dizziness
- Syncope
- Angina
- Heart Failure
52
Serious complications of A fib?
- Tachycardia induced HF
- Severe hypotension/HF
- Embolic stroke
53
What are the 3 major goals of therapy for arrhythmias ?
1) Control of rapid ventricular response = ventricular rate control
2) Restoration of normal sinus rhythm = atrial rhythm control
3) Prevention of thromboembolic complications
54
Once A Fib is detected, must assess patients for their risk of having a ______
stroke
55
If no risk of stroke, pick either ______ or ______ control
rate or rhythm
56
If risk of stroke, add _____ or _____
ASA or OAC (oral anticoagulant)
57
If a patient has no heart failure or CAD:
| What rate control options are there?
- BB
- CCB (non-DHP)
- Digoxin
* Combination Rx
58
If a patient has CAD:
| What rate control options do we have?
- BB
- CCB
* Combination Rx
59
If a patient has heart failure:
| What rate control options do we have?
BB +/- digoxin
60
When is digoxin as mono therapy considered?
only in particularly sedentary individuals
61
What are the efficacy endpoints of using a rate control agent?
HR < 100 bpm
Minimize symptoms (palpitations, dizziness, SOB)
62
What safety endpoints do we monitor for rate control agents?
bradycardia, AV block
63
What safety endpoints do we monitor for diltiazem/verapamil?
```
BP < 100/60
CHF
edema
nausea
constipation
anorexia
```
64
What does diltiazem/verapamil interact with?
These are 3A4 and P-GP inhibitor so:
- watch out with 3A4 substrates (statins) or
- P-GP substrates (digoxin)
65
What safety endpoints do we monitor for metoprolol/atenolol?
```
BP < 100/60
HR < 60
CHF
asthma
diabetes
weakness
fatigue
PVD
abrupt D/C
```
66
What safety endpoints do we monitor for digoxin?
GI: anorexia, n/v/d
Neurological: headache, fatigue, confusion
Visual: blurred vision, disturbed color vision, halos around bright objects
Cardiac: arrhythmias
Digoxin trough levels 1-2 mcg/L
K < 3.5 mmol/L
67
What does digoxin interact with??
LOTS OF STUFF:
- amiodarone/dronedarone
- propafenone
- quinidine/quinine
- verapamil
- intraconazole
* these reduce digoxin dose by 50%
- macrolide
* incrased levels via P-GP/P450
- cholestyramine, Al-Mg antacids, kaolin-pectin, dietary fibre, sucralfate: 2 hour interval between administration
- BB, non-DHP CCB
- calcium, rapid IV: arrhythmias
- diuretics, amphotericin B, laxatives: indirect via hypokalemia
68
What do rate control agents do?
control contraction of ventricle (i.e. control AV node)
69
What do rhythm control agents do?
affect the atria
70
What are some options for restoring normal sinus rhythm (to stop a. fib)
- electrical cardioversion
- IV amiodarone
- pill in the pocket (must be rate controlled first)
71
What is the safest rhythm control agent for patients with a Hx of CHF or left ventricular systolic dysfunction?
- amiodarone
| - sotalol (can be used if EF > 35%)
72
What are the options for rhythm control agents if a patient has no history of CHF?
- dronedarone
- flecainide
- propafenone
- sotalol
- amiodarone
73
What are the efficacy endpoints for rhythm control agents?
- Maintain NSR (normal sinus rhythm)
| - No palpitations, dizziness, SOB
74
Safety end points for sotalol?
```
BP < 100/60
HR < 60
CHF
asthma
diabetes
weakness
fatigue
PVD
abrupt D/C
```
plus n/v/d
QT prolongation
torsade de points
CrCl < 60 mL/min
75
Safety end points for propafenone?
```
BP < 100/60
HR < 60
CHF
asthma
diabetes
weakness
fatigue
PVD
abrupt D/C
```
```
plus headache
taste disturbances
nausea
vomiting
lupus
ventricular arrhythmias (high risk with CAD)
```
76
Safety end points with flecainide?
```
blurred vision
dizziness
dyspnea
headache
tremor
nausea
worsening HF
conduction disturbances
QT prolongation
ventricular arrhythmias (high risk with CAD)
CrCl < 50
```
77
What interacts with sotalol?
QT prolonging medications
78
What interacts with propafenone?
- this is a CYP450 2D6 substrate.
| - it will inhibit digoxin elimination
79
What interacts with flecainide?
QT prolonging meds
| this is a CYP450 2D6
80
What are strong CYP 2D6 inhibitors?
bupropion, paroxetine, quinidine, cinacalcet
81
Amiodarone side effects:
| Monitoring recommendation fo pulmonary fibrosis?
- Chest radiograph (baseline, then every 12 months)
| - Pulmonary function tests (if symptoms develop)
82
Amiodarone side effects:
| Management of pulmonary fibrosis
- Discontinue amiodarone immediately
| - Initiate corticosteroid therapy
83
Amiodarone side effects:
| Monitoring recommendations for Hypothyroidism
TFTs (thyroid function tests ?)(baseline then every 6 months)
84
Amiodarone side effects:
| Management of Hypothryoidism
Thyroid hormone supplementation (ex. levothyroxine)
85
Amiodarone side effects:
| Monitoring recommendations for Hyperthyroidism
TFTs (thyroid function tests ?)(baseline then every 6 months)
86
Amiodarone side effects:
| Management of Hyperthryoidism
Antithyroid drugs (ex. methimazole)
87
Amiodarone side effects:
| Monitoring recommendations for optic neuritis/neuropathy
Opthalmologic examination (baseline [only if significant visual abnormalities present] then if symptoms develop)
88
Amiodarone side effects:
| Management for optic neuritis/neuropathy?
Discontinue amiodarone immediately
89
Amiodarone side effects:
| Monitoring recommendations for corneal micro deposits?
slit-lamp examination (routine monitoring not necessary)
90
Amiodarone side effects:
| Management for corneal micro deposits?
no treatment necessary
91
Amiodarone side effects:
| Monitoring recommendations for hepatotoxicity?
LFTs (liver function tests) (baseline, then every 6 months)
92
Amiodarone side effects:
| Management of hepatotoxicity ?
Lower the dose or discontinue amiodarone if LFTs > 3x the upper limit of normal
93
Amiodarone side effects:
| Monitoring recommendations for bradycardia/heart block?
ECG (baseline, then every 3-6 months)
94
Amiodarone side effects:
| Management for bradycardia/heart block?
lower the dose if possible or D/C amiodarone if severe
95
Amiodarone side effects:
| Monitoring recommendations for tremor, ataxia, peripheral neuropathy
History/physical examination (each office visit)
96
Amiodarone side effects:
| Management for tremor, ataxia, peripheral neuropathy
lower the dose if possible or D/C amiodarone if severe
97
Amiodarone side effects:
| Monitoring recommendations for photosensitivity/blue-gray skin discolouration
History/physical examination (each office visit)
98
Amiodarone side effects:
| Management for photosensitivity/blue-gray skin discolouration
advise patients to wear sunblock while outdoors
99
What medications are recommended to have a dose decrease of up to 50% when starting amiodarone/dronedarone?
- digoxin
- warfarin
- flecainide
- quinidine
- atorvastatin
- simvistatin
100
What agents have an additive effect with amiodarone/dronedarone?
1) rate-slowing agents: HR < 60 bpm
| 2) QT prolonging agents: QTc > 500 msec
101
Give examples of oral anticoagulants
- warfarin
- dabigatran
- rivaroxaban
- apixaban
102
Age > ___ = OAC
65
| *see slide 42
103
History of what would indicate a patient should be on OAC?
```
prior stroke
HTN
HF
DM
*see slide 42
```
104
History of what would indicate a patient should be on ASA?
CAD
arterial vascular disease
*see slide 42
105
If a fib < ____ hours then no anticoagulation
48
106
If a fib > 48 hours, then ?
3 weeks of anticoagulation pre-cardioversion and at least 4 weeks post op
107
If thrombus is ruled out on TEE then what?
Give IV heparin and cardiovert, then anticoagulation at least 4 weeks post op.
108
Who is apixaban indicated for?
The treatment of non-valvular a. fib for prevention of stroke and systemic embolism AND whom:
1) anticoagulation is inadequate following at least a 2-month trial of warfarin OR
2) anticoagulation using warfarin is CI or not possible due to inability to regularly monitor INR
109
Who is apixaban NOT indicated for?
- Patients with impaired renal function
- Patients > 75 yrs old
- Patients with valvular heart disease
- Patients with prosthetic heart valves
110
What are some toxicity endpoints of anticoagulants?
- signs of bleeding
| - Hgb < 100 or drop of 20%
111
What are some toxicity endpoints for warfarin?
- INR > 3 (high risk of bleeding)
- Lots of interactions with Strong 2C9 inhibitors (fluconazole, septa)
- Caution with all ANTIBIOTICS; They kill off Vitamin K producing bacteria in the gut - increases risk of bleeding
112
What are some toxicity endpoints for new oral anticoagulants?
- CrCl < 30
- Interact with strong Cyp 3A4 & P-GP inhibitors: (amiodarone/dronedarone, propafenone, quinidine/quinine, verapamil, intraconazole, ketoconazole)
113
What do you recommend for a hemodynamically unstable (SBP < 90) patient with acute CHF?
electrical cardioversion
*consider long term amiodarone to prevent reoccurrence of A. fib
114
What do you recommend for a hemodynamically stable patient with acute CHF?
- If HR > 100 ppm, rate control with digoxin 0.5 mg then 0.25 mg q6h IV then 0.25 mg daily
- Consider electrical cardioversion given the severity of his symptoms with a fib
- Anticoagulation for 3 weeks pre cardioversion (unless TEE rules out atrial thrombus)
- Anticoagulation at least 4 weeks post cardioversion
*consider long term amiodarone to prevent reoccurrence of A. fib
115
Monitoring endpoints for OAC?
- no focal or neurological deficit, headache, sudden change in vision, one-sided weakness, slurred speech, loss of balance
- warfarin INR = 2-3
- newer agents: no target levels
116
Describe a 1st degree block
Usually AV node
- PR > 0.2 sec
- P:QRS 1:1
117
Describe a 2nd degree block
- P:QRS < 1:1
- Dropped QRS's
- Mobitz type 1 (wenkebacke): AV node
- Mobitz type 2: below AV node
118
Describe a 3rd degree block
(AV node or below)
| -AV dissociation, no relation between P:QRS
119
List 3 factors that may precipitate bradyarrhythmias
- lithium
- class 1 AAD
- digoxin
* more on slide 53
120
Signs of bradyarrhythmias
- HR < 60 bpm
- Hypotension
- EKG
121
Symptoms of bradyarrhythmias
- dizziness
- syncope
- fatigue
- confusion
- CHF
122
What are the therapeutic options for bradyarrhythmias ?
- removal of bradycardia drugs
- atropine
- isoproterenol
- pacemaker
123
What is tachy-brady syndrome?
Pt has A. fib but when they don't have A. fib, they have bradycardia.
i.e. they need a rate controlling agent for A. fib but also need a pacemaker to control bradycardia
124
What is defined as ventricular tachycardia (VT) ?
3 or more repetitive PVC's (extra beats coming from the ventricle) occurring at a rate > 100 bpm
125
_________ VT: < 30 seconds
Nonsustained
126
__________ VT: > 30 seconds
Sustained
127
______ VT: More frequent than NSR
Incessant
128
_________ VT: High sympathetic tone
Exercise-induced
129
________ VT: consistent QRS
Monomorphic
130
________ VT: varying QRS
Polymorphic
131
What is the classic polymorphic VT?
Torsade de points
132
Temporary factors that may precipitate ventricular tachycardia
- metabolic abnormalities (low K or Mg)
- drug toxicities (digoxin, TCA's)
- MI within 24 hrs
133
Permanent factors that may precipitate ventricular tachycardia
- CHF
- Remote MI with left ventricular aneurysm
- genetics (ex. Brugada syndrome)
134
Signs of VT
- HR > 100 bpm
- EKG
- hypotension
135
Symptoms of VT
- Palpitations
- Angina
- Syncope
136
What are the potential consequences of an arrhythmia if left untreated?
-Progression to ventricular fibrillation (VF) and then asystole (cardiac arrest/sudden cardiac death)
137
What are the options for primary prevention of SVT/VF?
*SVT = sustained ventricular tachycardia
Post MI/CHF:
- beta blockers
- ACEi
- aldosterone antagonist
- ICD (EF<35%) (implantable cardioverter defibrillator)
- NOT class 1/class 3 anti-arrhythmics: causes increased mortality (except amiodarone)
138
What are the options for acute treatment of SVT/VF?
*SVT = sustained ventricular tachycardia
- electrical cardioversion
- amiodarone IV
- lidocaine (rare)
- procainamide (rare)
139
What are the options for secondary prevention of SVT/VF?
*SVT = sustained ventricular tachycardia
ICD (implantable cardioverter defibrillator)
- for VF
- for SVT: MI/CHF or low BP during SVT
+/-
- BB
- Sotalol
- Amiodarone
- Ventricular ablation
140
Why are anti-arrhythmic agents used in addition to ICD (implantable cardioverter defibrillators)?
- Decrease (appropriate) shocks for VT/VF
- Decrease (inappropriate) shocks for A. Fib/flutter
- Decrease rate of VT for overdrive pacing
141
What is the definition of Torsade de points?
-rapid form of polymorphic ventricular tachycardia, with preexistent prolonged QTc
142
List a few of the factors that precipitate Torsade de pointes?
- Antibiotics
- Methadone
- Antidepressants (ex. citalopram)
**more on slide 74
143
**We need to know 1 anti-cancer med with possible risk for TdP (tornado de points).
Dasatinib
*slide 75
144
What are the 3 mechanisms of drug-induced QT prolongation and TdP ?
- Block of repolarizing K+ currents
- Stimulation of I-Ca-1
- Stimulation of I-Na
145
What is the Cordarone Paradox? (Coradrone is brand name of Amiodarone)
```
QT prolongation
Low TdP risk
Multichannel blockade:
-Both Kr & Ks: minimize QT dispersion
-Na, Ca, Beta: minimize EAD
```
146
What are risk factors for TdP?
- history of TdP
- QTc > 500 msec
High risk = > 11
Medium risk = 7-10
Low Risk = <7
147
What are the options for acute treatment of Torsades de Pointes?
- Magnesium IV
- Overdrive pacing
- DCC ????
- Isoproterneol
- Stop all QT prolonging drugs
- Potassium supplementation
