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Clinical 2 (Sam) > 8 - Arrhythmias > Flashcards

8 - Arrhythmias Flashcards

1
Q

Although there are pure forms, most common arrhythmias are combinations of both _________ and ________.

A

automaticity

re-entry

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2
Q

Describe an arrhythmia of automaticity

A
  • Abnormality in impulse generation

- Often starts the arrhythmia

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3
Q

Describe an arrhythmia of re-entry

A
  • Abnormality in impulse conduction

- Often maintains the arrhythmia

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4
Q

What is the primary pacemaker?

A

SA node

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5
Q

What is the escape pacemaker(s)?

A 
-AV node
then
-bundle of His
then 
-Bundle branches
then 
-Purkinje network
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6
Q

What is the rate of the SA node?

A

60 - 100 beats/min

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7
Q

What is the rate of the AV node?

A

40 - 60 beats/min

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8
Q

What is the rate of the ventricles (bundle branches & purkinje network) ?

A

20 - 40 beats/min

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9
Q

Describe what is happening in a re-entry arrhythmia

A
  • Different conduction velocity

- Different refractoriness

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10
Q

Type 1a AAD (anti-arrhythmic drug):
Sodium channel blockers (med)

Give examples

A

Quindine

Procainamide

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11
Q

Type 1b AAD (anti-arrhythmic drug):
Sodium channel blockers (fast)

Give examples

A

Lidocaine

Mexilintine

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12
Q

Type 1c AAD (anti-arrhythmic drug):
Sodium channel blockers (slow)

Give examples

A

Flecainide

Propafenone

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13
Q

Type 2 AAD (anti-arrhythmic drug):
Beta blockers

Give examples

A

Metoprolol

Atenolol

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14
Q

Type 3 AAD (anti-arrhythmic drug):
K+ channel blockers

Give examples

A

Amiodarone
Sotalol
Ibutilide

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15
Q

Type 4 AAD (anti-arrhythmic drug):
Calcium Channel blockers

Give examples

A

Diltiazem

Verapamil

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16
Q

Type __ = Sodium channel blockers

A

1

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17
Q

Type __ = K+ channel blockers

A

3

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18
Q

Type __ = calcium channel blockers

A

4

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19
Q

Type __ = beta blockers

A

2

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20
Q

AAD (anti-arrhythmic drugs) either control the _______ or the _______

A

rate or the rhythm

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21
Q

How do rate control agents work?

A

Reduce automaticity: prevent or slow arrhythmias

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22
Q

How do rhythm control agents work?

A

Reduce re-entry: prevent or stop arrhythmias

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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)

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24
Q

Which types of AADs control rhythm ?

A

Type 1 - Sodium channel blockers

Type 3 - K+ channel blockers

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25
Q

MOA of Type 2 (Beta Blockers)

A
  • Reduced adrenergic stimulation of SA/AV nodes

- Decreased adrenergic stimulation of myocardial contractility

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26
Q

MOA of Type 4 (Non-DBP Calcium Channel Blockers)

A
  • Reduced calcium current and recovery in SA/AV nodes
  • Decreased calcium influx in myocytes, decreased myocardial contractility
  • Relaxation of arterial smooth muscles
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27
Q

MOA of Digoxin (Na+/K+ ATPase Blocker)

A

-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
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28
Q

MOA of Class 1 (sodium channel blockers)

A
  • Decrease in conduction velocity

- Re-entry loop loses “steam”, SA node takes over

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29
Q

MOA of Class 2 (K+ channel blockers)

A
  • Prolonged refractory period

- Re-entry loop “catches its tail”, SA node takes over

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30
Q

What is the idea behind anti-arrhythmic therapy?

A

to slow down the AV node and allow SA node to take over again

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31
Q

List the few pure rhythm control agents

A 
Quinidine
Sotalol
Amiodarone
Propafenone
Flecainide
Ibutilide/Dofetilide
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32
Q

What type is Quinidine?

A

Class 1a and K+ blocker

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33
Q

What type is Sotalol?

A

Class 3 and BB

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34
Q

What type is Amiodarone?

A

Class 3 and Na-channel blocker, CCB, BB

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35
Q

What type is Propafenone?

A

Class 1c and BB

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36
Q

What type is Flecainaide?

A

Pure Class 1c

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37
Q

What type of patients is Class 1c contraindicated in?

A

patients with previous heart issues?

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38
Q

What type is Ibutilide/Dofetilide?

A

Pure class 3

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39
Q

What does Ibutilide/Dofetilide have a high risk of?

A

Torsades de Pointes

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40
Q

> ____ bpm = tachycardic

A

100

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41
Q

< ____ bpm = bradycardic

A

60

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42
Q

Normal respiratory rate (RR) ?

A

12 - 20

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43
Q

What is atrial fibrillation?

A
  • 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
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44
Q

Categories of atrial fib:

Acute = ?

A

48 hours

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45
Q

Categories of atrial fib:

Paroxysmal = ?

A

terminates spontaneously within 7 days

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46
Q

Categories of atrial fib:

Persistent = ?

A

continues for greater than 7 days

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47
Q

Categories of atrial fib:

Permanent = ?

A

does not terminate even with cardioversion attempts

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48
Q

What are some temporary factors that may precipitate atrial fibrillation?

A

Things that cause high adrenergic tone:

  • alcohol withdrawl
  • sepsis
  • post surgery
  • more on slide 18
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49
Q

What are some permanent factors that may precipitate atrial fibrillation?

A

Things that cause atrial distension:

  • ischemia
  • hypertension
  • obesity
  • more on slide 18
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50
Q

Signs of A fib?

A

-Irregular pulse
-HR > 100 bpm
-Hypotension
EKG

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51
Q

Symptoms of A fib?

A
  • Asymptomatic
  • Palpitations
  • Dizziness
  • Syncope
  • Angina
  • Heart Failure
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52
Q

Serious complications of A fib?

A
  • Tachycardia induced HF
  • Severe hypotension/HF
  • Embolic stroke
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53
Q

What are the 3 major goals of therapy for arrhythmias ?

A

1) Control of rapid ventricular response = ventricular rate control
2) Restoration of normal sinus rhythm = atrial rhythm control
3) Prevention of thromboembolic complications

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54
Q

Once A Fib is detected, must assess patients for their risk of having a ______

A

stroke

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55
Q

If no risk of stroke, pick either ______ or ______ control

A

rate or rhythm

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56
Q

If risk of stroke, add _____ or _____

A

ASA or OAC (oral anticoagulant)

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57
Q

If a patient has no heart failure or CAD:

What rate control options are there?

A
  • BB
  • CCB (non-DHP)
  • Digoxin
  • Combination Rx
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58
Q

If a patient has CAD:

What rate control options do we have?

A
  • BB
  • CCB
  • Combination Rx
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59
Q

If a patient has heart failure:

What rate control options do we have?

A

BB +/- digoxin

60
Q

When is digoxin as mono therapy considered?

A

only in particularly sedentary individuals

61
Q

What are the efficacy endpoints of using a rate control agent?

A

HR < 100 bpm

Minimize symptoms (palpitations, dizziness, SOB)

62
Q

What safety endpoints do we monitor for rate control agents?

A

bradycardia, AV block

63
Q

What safety endpoints do we monitor for diltiazem/verapamil?

A 
BP < 100/60
CHF
edema
nausea
constipation
anorexia
64
Q

What does diltiazem/verapamil interact with?

A

These are 3A4 and P-GP inhibitor so:

  • watch out with 3A4 substrates (statins) or
  • P-GP substrates (digoxin)
65
Q

What safety endpoints do we monitor for metoprolol/atenolol?

A 
BP < 100/60
HR < 60
CHF
asthma
diabetes
weakness
fatigue
PVD
abrupt D/C
66
Q

What safety endpoints do we monitor for digoxin?

A

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
Q

What does digoxin interact with??

A

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
Q

What do rate control agents do?

A

control contraction of ventricle (i.e. control AV node)

69
Q

What do rhythm control agents do?

A

affect the atria

70
Q

What are some options for restoring normal sinus rhythm (to stop a. fib)

A
  • electrical cardioversion
  • IV amiodarone
  • pill in the pocket (must be rate controlled first)
71
Q

What is the safest rhythm control agent for patients with a Hx of CHF or left ventricular systolic dysfunction?

A
  • amiodarone

- sotalol (can be used if EF > 35%)

72
Q

What are the options for rhythm control agents if a patient has no history of CHF?

A
  • dronedarone
  • flecainide
  • propafenone
  • sotalol
  • amiodarone
73
Q

What are the efficacy endpoints for rhythm control agents?

A
  • Maintain NSR (normal sinus rhythm)

- No palpitations, dizziness, SOB

74
Q

Safety end points for sotalol?

A 
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
Q

Safety end points for propafenone?

A 
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
Q

Safety end points with flecainide?

A 
blurred vision
dizziness
dyspnea
headache
tremor
nausea
worsening HF
conduction disturbances
QT prolongation
ventricular arrhythmias (high risk with CAD)
CrCl < 50
77
Q

What interacts with sotalol?

A

QT prolonging medications

78
Q

What interacts with propafenone?

A
  • this is a CYP450 2D6 substrate.

- it will inhibit digoxin elimination

79
Q

What interacts with flecainide?

A

QT prolonging meds

this is a CYP450 2D6

80
Q

What are strong CYP 2D6 inhibitors?

A

bupropion, paroxetine, quinidine, cinacalcet

81
Q

Amiodarone side effects:

Monitoring recommendation fo pulmonary fibrosis?

A
  • Chest radiograph (baseline, then every 12 months)

- Pulmonary function tests (if symptoms develop)

82
Q

Amiodarone side effects:

Management of pulmonary fibrosis

A
  • Discontinue amiodarone immediately

- Initiate corticosteroid therapy

83
Q

Amiodarone side effects:

Monitoring recommendations for Hypothyroidism

A

TFTs (thyroid function tests ?)(baseline then every 6 months)

84
Q

Amiodarone side effects:

Management of Hypothryoidism

A

Thyroid hormone supplementation (ex. levothyroxine)

85
Q

Amiodarone side effects:

Monitoring recommendations for Hyperthyroidism

A

TFTs (thyroid function tests ?)(baseline then every 6 months)

86
Q

Amiodarone side effects:

Management of Hyperthryoidism

A

Antithyroid drugs (ex. methimazole)

87
Q

Amiodarone side effects:

Monitoring recommendations for optic neuritis/neuropathy

A

Opthalmologic examination (baseline [only if significant visual abnormalities present] then if symptoms develop)

88
Q

Amiodarone side effects:

Management for optic neuritis/neuropathy?

A

Discontinue amiodarone immediately

89
Q

Amiodarone side effects:

Monitoring recommendations for corneal micro deposits?

A

slit-lamp examination (routine monitoring not necessary)

90
Q

Amiodarone side effects:

Management for corneal micro deposits?

A

no treatment necessary

91
Q

Amiodarone side effects:

Monitoring recommendations for hepatotoxicity?

A

LFTs (liver function tests) (baseline, then every 6 months)

92
Q

Amiodarone side effects:

Management of hepatotoxicity ?

A

Lower the dose or discontinue amiodarone if LFTs > 3x the upper limit of normal

93
Q

Amiodarone side effects:

Monitoring recommendations for bradycardia/heart block?

A

ECG (baseline, then every 3-6 months)

94
Q

Amiodarone side effects:

Management for bradycardia/heart block?

A

lower the dose if possible or D/C amiodarone if severe

95
Q

Amiodarone side effects:

Monitoring recommendations for tremor, ataxia, peripheral neuropathy

A

History/physical examination (each office visit)

96
Q

Amiodarone side effects:

Management for tremor, ataxia, peripheral neuropathy

A

lower the dose if possible or D/C amiodarone if severe

97
Q

Amiodarone side effects:

Monitoring recommendations for photosensitivity/blue-gray skin discolouration

A

History/physical examination (each office visit)

98
Q

Amiodarone side effects:

Management for photosensitivity/blue-gray skin discolouration

A

advise patients to wear sunblock while outdoors

99
Q

What medications are recommended to have a dose decrease of up to 50% when starting amiodarone/dronedarone?

A
  • digoxin
  • warfarin
  • flecainide
  • quinidine
  • atorvastatin
  • simvistatin
100
Q

What agents have an additive effect with amiodarone/dronedarone?

A

1) rate-slowing agents: HR < 60 bpm

2) QT prolonging agents: QTc > 500 msec

101
Q

Give examples of oral anticoagulants

A
  • warfarin
  • dabigatran
  • rivaroxaban
  • apixaban
102
Q

Age > ___ = OAC

A

65

*see slide 42

103
Q

History of what would indicate a patient should be on OAC?

A 
prior stroke
HTN
HF
DM
*see slide 42
104
Q

History of what would indicate a patient should be on ASA?

A

CAD
arterial vascular disease
*see slide 42

105
Q

If a fib < ____ hours then no anticoagulation

106
Q

If a fib > 48 hours, then ?

A

3 weeks of anticoagulation pre-cardioversion and at least 4 weeks post op

107
Q

If thrombus is ruled out on TEE then what?

A

Give IV heparin and cardiovert, then anticoagulation at least 4 weeks post op.

108
Q

Who is apixaban indicated for?

A

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
Q

Who is apixaban NOT indicated for?

A
  • Patients with impaired renal function
  • Patients > 75 yrs old
  • Patients with valvular heart disease
  • Patients with prosthetic heart valves
110
Q

What are some toxicity endpoints of anticoagulants?

A
  • signs of bleeding

- Hgb < 100 or drop of 20%

111
Q

What are some toxicity endpoints for warfarin?

A
  • 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
Q

What are some toxicity endpoints for new oral anticoagulants?

A
  • CrCl < 30
  • Interact with strong Cyp 3A4 & P-GP inhibitors: (amiodarone/dronedarone, propafenone, quinidine/quinine, verapamil, intraconazole, ketoconazole)
113
Q

What do you recommend for a hemodynamically unstable (SBP < 90) patient with acute CHF?

A

electrical cardioversion

*consider long term amiodarone to prevent reoccurrence of A. fib

114
Q

What do you recommend for a hemodynamically stable patient with acute CHF?

A
  • 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
Q

Monitoring endpoints for OAC?

A
  • 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
Q

Describe a 1st degree block

A

Usually AV node

  • PR > 0.2 sec
  • P:QRS 1:1
117
Q

Describe a 2nd degree block

A
  • P:QRS < 1:1
  • Dropped QRS’s
  • Mobitz type 1 (wenkebacke): AV node
  • Mobitz type 2: below AV node
118
Q

Describe a 3rd degree block

A

(AV node or below)

-AV dissociation, no relation between P:QRS

119
Q

List 3 factors that may precipitate bradyarrhythmias

A
  • lithium
  • class 1 AAD
  • digoxin
  • more on slide 53
120
Q

Signs of bradyarrhythmias

A
  • HR < 60 bpm
  • Hypotension
  • EKG
121
Q

Symptoms of bradyarrhythmias

A
  • dizziness
  • syncope
  • fatigue
  • confusion
  • CHF
122
Q

What are the therapeutic options for bradyarrhythmias ?

A
  • removal of bradycardia drugs
  • atropine
  • isoproterenol
  • pacemaker
123
Q

What is tachy-brady syndrome?

A

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
Q

What is defined as ventricular tachycardia (VT) ?

A

3 or more repetitive PVC’s (extra beats coming from the ventricle) occurring at a rate > 100 bpm

125
Q

_________ VT: < 30 seconds

A

Nonsustained

126
Q

__________ VT: > 30 seconds

127
Q

______ VT: More frequent than NSR

128
Q

_________ VT: High sympathetic tone

A

Exercise-induced

129
Q

________ VT: consistent QRS

A

Monomorphic

130
Q

________ VT: varying QRS

A

Polymorphic

131
Q

What is the classic polymorphic VT?

A

Torsade de points

132
Q

Temporary factors that may precipitate ventricular tachycardia

A
  • metabolic abnormalities (low K or Mg)
  • drug toxicities (digoxin, TCA’s)
  • MI within 24 hrs
133
Q

Permanent factors that may precipitate ventricular tachycardia

A
  • CHF
  • Remote MI with left ventricular aneurysm
  • genetics (ex. Brugada syndrome)
134
Q

Signs of VT

A
  • HR > 100 bpm
  • EKG
  • hypotension
135
Q

Symptoms of VT

A
  • Palpitations
  • Angina
  • Syncope
136
Q

What are the potential consequences of an arrhythmia if left untreated?

A

-Progression to ventricular fibrillation (VF) and then asystole (cardiac arrest/sudden cardiac death)

137
Q

What are the options for primary prevention of SVT/VF?

*SVT = sustained ventricular tachycardia

A

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
Q

What are the options for acute treatment of SVT/VF?

*SVT = sustained ventricular tachycardia

A
  • electrical cardioversion
  • amiodarone IV
  • lidocaine (rare)
  • procainamide (rare)
139
Q

What are the options for secondary prevention of SVT/VF?

*SVT = sustained ventricular tachycardia

A

ICD (implantable cardioverter defibrillator)

  • for VF
  • for SVT: MI/CHF or low BP during SVT

+/-

  • BB
  • Sotalol
  • Amiodarone
  • Ventricular ablation
140
Q

Why are anti-arrhythmic agents used in addition to ICD (implantable cardioverter defibrillators)?

A
  • Decrease (appropriate) shocks for VT/VF
  • Decrease (inappropriate) shocks for A. Fib/flutter
  • Decrease rate of VT for overdrive pacing
141
Q

What is the definition of Torsade de points?

A

-rapid form of polymorphic ventricular tachycardia, with preexistent prolonged QTc

142
Q

List a few of the factors that precipitate Torsade de pointes?

A
  • Antibiotics
  • Methadone
  • Antidepressants (ex. citalopram)

**more on slide 74

143
Q

**We need to know 1 anti-cancer med with possible risk for TdP (tornado de points).

A

Dasatinib

*slide 75

144
Q

What are the 3 mechanisms of drug-induced QT prolongation and TdP ?

A
  • Block of repolarizing K+ currents
  • Stimulation of I-Ca-1
  • Stimulation of I-Na
145
Q

What is the Cordarone Paradox? (Coradrone is brand name of Amiodarone)

A 
QT prolongation
Low TdP risk
Multichannel blockade:
-Both Kr &amp; Ks: minimize QT dispersion
-Na, Ca, Beta: minimize EAD
146
Q

What are risk factors for TdP?

A
  • history of TdP
  • QTc > 500 msec

High risk = > 11
Medium risk = 7-10
Low Risk = <7

147
Q

What are the options for acute treatment of Torsades de Pointes?

A
  • Magnesium IV
  • Overdrive pacing
  • DCC ????
  • Isoproterneol
  • Stop all QT prolonging drugs
  • Potassium supplementation

Clinical 2 (Sam) (18 decks)

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