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PHAR253 > Arrhythmia > Flashcards

Arrhythmia Flashcards

1
Q

What are the two common atrial arrhythmias?

A

atrial fibrillation
atrial flutter

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2
Q

Describe atrial fibrillation.

A

electrical impulses generated from multiple locations
electrical activity is chaotic
atrial walls quiver rather than contract
EF is reduced
without treatment ventricular rate is elevated

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3
Q

Describe atrial flutter.

A

electrical activity in atria is coordinated
atria contract but at very rapid rate (250-350x/min)
rate is too fast to allow each impulse to conduct through AV node
generally about every 2nd beat gets through

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4
Q

What is the most common sustained cardiac arrhythmia?

A

atrial fibrillation

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5
Q

What kind of arrhythmia is atrial fibrillation?

A

supraventricular arrhythmia
-results from continuous and chaotic atrial activity

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6
Q

Is atrial fibrillation life-threatening?

A

rarely
-associated with impaired QoL and increases risk for stroke and left ventricular dysfunction

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7
Q

Describe the irregular rhythm associated with atrial fibrillation.

A

atrial rate: 350-600bpm
ventricular rate: 120-180bpm
pulse: irregular

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8
Q

Describe the incidence of atrial fibrillation.

A

most common sustained rhythm disturbance
prevalence increases with age:
-0.4% of adults <60yrs
-2-5% of adults >60yrs
->6% of adults >80yrs
greater in men
10-30% of HF patients have afib
5% of hospital admissions for cardiac disease are for afib

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9
Q

Describe the morbidity and mortality of atrial fibrillation.

A

rare acutely life-threatening
impairs functional and HRQOL
1.5-4x increased risk of mortality
-thromboembolic events and ventricular dysfunction
non-anticoagulated pts have 3-5x increased risk of stroke

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10
Q

What are the symptoms of atrial fibrillation?

A

fatigue
palpitations
chest pain
dyspnea
dizziness

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11
Q

Describe the pathogenesis of atrial fibrillation.

A

ectopic foci generate electrical impulses
rapid irregular and uncoordinated contractions
because impulses reach the AV node erratically=irregular ventricular rhythm

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12
Q

What are the classifications of atrial fibrillation?

A

valvular: presence of structural heart disease
non-valvular: absence of mitral valve repair, prosthetic valve or rheumatic mitral valve disease
lone AF: absence of clinical or ECHO findings of other CVD, pulmonary disease, cardiac abnormalities, <60yrs
paroxysmal: >30s but self-terminating within 7 days
persistent: continuous AF >7d but <1yr
longstanding persistent: continuous AF >1yr pursuing rhythm control
permanent: continuous AF not pursuing sinus rhythm control

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13
Q

Differentiate between an AF trigger and AF substrate.

A

trigger=cause arrhythmia to occur
substrate=make it more likely to occur
-ex: HTN, obesity, age, sex, genetics, remodeling

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14
Q

What should be identified during an investigation for atrial fibrillation?

A
  1. risk factors/comorbidities
    -HTN, HFrEF, male, tobacco, alcohol, valvular disease
  2. triggers for AF episodes
    -alcohol, stimulants, sleep deprivation, stress
  3. reversible causes/AF secondary to
    -infection, surgery, alcohol, pharmacologic agents
    review family history, prior pharm and non-pharm interventions
    date of first attack, duration and frequency, symptoms
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15
Q

What are the routine investigations for atrial fibrillation?

A

12 lead ECG
ECHO
laboratory investigations

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16
Q

What are some risk factors for atrial fibrillation?

A

alcohol and tobacco
-limit <1 drink/day, abstinence of both
sleep apnea
-CPAP for mod-severe
weight
-target >10% loss, BMI < 27kg/m2
diabetes
-A1C target < 7%
blood pressure
-target < 130/80, ACEI/ARB preferred
initiate exercise

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17
Q

What is the leading cause of preventable stroke?

A

atrial fibrillation
-severe strokes

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18
Q

Which classifications of atrial fibrillation have the highest risk of stroke?

A

persistent
permanent
paroxysmal

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19
Q

What are the goals of therapy in atrial fibrillation?

A

prevent stroke or systemic thromboembolism
cardiovascular risk reduction
improve symptoms, functional capacity and quality of life
prevent complications (LV dysfunction, falls)

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20
Q

What are the anticipated outcomes when the goals of therapy for atrial fibrillation are achieved?

A

improvement in survival
reduction in healthcare utilization

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21
Q

Describe the general overview of atrial fibrillation management.

A

diagnosis
–>identify + treat reversible precipitants
–>assessment of thromboembolic risk (CHADS-65)
–>management of arrhythmia
=risk factor modification
=OAC if at risk of stroke
=rate control or rhythm control

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22
Q

What are stroke risk stratifications such as CHADS used for?

A

determine the degree of antithrombotic therapy required based on an individuals risk of developing stroke

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23
Q

Describe CHADS2.

A

C=recent CHF, +1
H=hypertension, +1
A=age 75, +1
D= diabetes, +1
S2=stroke or TIA, +2

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24
Q

Describe CHADS-65.

A

stroke prevention in non-valvular AF
age > 65 –> OAC
prior stroke/TIA or HTN or HF or DM –> OAC
CAD or PAD –> antiplatelet
none of the above –> no antithrombotic
DOAC preferred over warfarin

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25
Q

Describe stroke prevention in the frail elderly with atrial fibrillation.

A

OAC recommended
-frail elderly are at higher risk of stroke=benefit from OAC
-DOACS favoured over warfarin

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26
Q

What is the impact of obesity on stroke rates and bleeding rates?

A

lower stroke rates
higher bleeding rates

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27
Q

Describe DOAC use in obese patients.

A

BMI < 30:
-use any DOAC as per guidelines
BMI 30-40:
-use any DOAC as per guidelines
BMI 40-49 or weight >120kg:
-use with caution: edoxaban, apixaban
BMI > 50:
-use warfarin

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28
Q

What is the rule of 3 for reducing the dose of apixaban?

A

consider 2.5mg BID if:
- > 80yrs
- <60kg
-SCr > 133umol/L

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29
Q

Describe dosing of OACs for stroke prevention when CrCl> 50ml/min.

A

warfarin: dose adjusted for INR 2.0
dabigatran: 150mg BID
rivaroxaban: 20mg daily
apixaban: 5mg BID
edoxaban: 60mg daily

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30
Q

Describe dosing of OACs for stroke prevention when CrCl 30-49ml/min.

A

warfarin: dose adjusted for INR 2.0-3.0
dabigatran: consider 110mg BID
rivaroxaban: 15mg daily
apixaban: 5mg BID
edoxaban: 30mg daily

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31
Q

Describe dosing of OACs for stroke prevention when CrCl 15-29ml/min or <15ml/min.

A

warfarin: no data
dabigatran: no data
rivaroxaban: no data
apixaban: no data
edoxaban: no data

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32
Q

What are the practical differences among DOACs?

A

bioavailability
drug-drug interactions
availability of an antidote
dosing

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33
Q

Describe the bioavailability difference amongst the DOACs.

A

dabigatran: specific formulation
rivaroxaban: food for complete absorption

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34
Q

Describe the drug interaction differences amongst the DOACs.

A

dabigatran and edoxaban:
-avoid strong P-gp inhibitors and inducers
apixaban and rivaroxaban:
-avoid strong P-gp and 3A4 inhibitors and inducers

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35
Q

What are the antidotes for DOACs?

A

dabigatran–>idarucizumab
Xa inhibitors–>andexanet alpha

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36
Q

Which DOACs are dosed BID?

A

dabigatran
apixaban

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37
Q

Which DOACs are dosed daily?

A

edoxaban
rivaroxaban (BID in triple therapy)

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38
Q

What are some areas where DOACs dont fit as well or further research is required and clinical judgement is required?

A

mechanical heart valves and mitral valve stenosis
use of strong P-gp and 3A4 inhibitors/inducers
pregnancy and lactation
extremes of body weight (>120kg, <50kg)
pediatrics

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39
Q

What are some characteristics that increase bleeding risk?

A

older age
uncontrolled HTN
DM
CrCl < 85ml/min
prior stroke
history of bleeding
anemia
ASA or NSAID use
SSRI/SNRI
benefit of DOAC for stroke prevention>bleeding risk in most cases

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40
Q

What are some strategies to minimize bleeding risk?

A

co-prescribe PPI
measure and monitor renal function
alcohol abstinence
control BP
correct anemia
discontinue ASA and NSAIDs
provide mobility aids

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41
Q

Do we withhold anticoagulation in stroke prevention based on bleeding risk?

A

no
-only if bleeding is active or risk is extreme

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42
Q

What are the monitoring parameters for anticoagulation?

A

adherence
frequency of adverse effects
signs and symptoms of bleeding and bleed risk factors
regular SCr, CrCl, HbB

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43
Q

Describe the acute management for arrhythmia management in atrial fibrillation.

A

determine if AF is primary or secondary
consider hemodynamic stability
determine whether rate vs rhythm control is appropriate
-no difference in CV outcomes
-new diagnosed AF–>rhythm control decreases CV death and stroke
determine need for hospitalization
determine need for OAC

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44
Q

Differentiate between rate control and rhythm control.

A

rate control:
-patient remains in atrial fibrillation
-slowing ventricular rate to minimize negative outcomes
rhythm control:
-used in stable patients with recent-onset AF
-early rhythm control can lower risk of stroke and CV death

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45
Q

Describe the approach to rate and rhythm management of paroxysmal AF.

A

low recurrence burden:
–>observation
–>pill in pocket (AAD)
high recurrence burden:
–>maintenance AAD therapy

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46
Q

Describe the approach to rate and rhythm management of persistent AF.

A

see slide 50

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47
Q

Describe the theory behind rate control.

A

AF symptoms due to loss of atrial kick or rapid ventricular rate
if NRS not attainable: control resting and exercise HR
CO and exercise capacity decreased when resting HR >90 & exercise >140

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48
Q

Is there evidence that rate control or rhythm control are superior to one another?

A

little to none (until recently)
-rate control preferred in permanent AF
-both are recommended initial strategies

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49
Q

What is the general goal of rate control?

A

reduction in HR >20% with control of symptoms
targets:
-resting HR < 100bpm

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50
Q

What are the first line agents for rate control?

A

beta blockers or non-DHP CCB
-selection based on comorbidities, contraindications, and side effects

51
Q

What are the odds of rate control at rest/exercise with beta-blockers and CCBs for rate control?

A

rest/exercise
75/85% with beta blockers
66/72% with non-DHP CCBs

52
Q

Describe the approach to therapy for hemodynamically stable acute AF.

A

see slide 53

53
Q

What are the treatment choices for ventricular rate control?

A

digoxin
CCB
beta-blockers
choice depends on patient

54
Q

Describe the approach to therapy for long-term rate control.

A

see slide 55

55
Q

Describe acute rhythm control.

A

stable pts with recent-onset AF who are eligible for cardioversion
cardioversion increases risk for systemic embolism so its important to anticoagulate as time allows

56
Q

What are the objectives of rhythm control?

A

relief of symptoms like palpitations, dyspnea and fatigue
improve CO and exercise tolerance
prevent tachycardia induced myocardial remodeling and HF

57
Q

What are the options for restoration of normal sinus rhythm in AF?

A

rate control & await spontaneous conversion
electrical direct current cardioversion
pharmacologic

58
Q

What is the greatest concern with conversion to sinus rhythm?

A

risk of thromboembolism if clot in atria
-anticoagulate if AF>48h (therapeutic INR 3wks before and 4wks post conversion)

59
Q

Which patients are most likely to maintain normal sinus rhythm?

A

short duration of AF and absence of left atrial dilation
should be attempted:
-angina
-hypotension
-HF
-recent onset of AF

60
Q

In general, which therapy is most effective for restoration of NSR?

A

electrical cardioversion

61
Q

Provide a summary of AF treatment for arrhythmia management.

A

rate control:
-indication: asymptomatic and rhythm control not favoured (elderly, longstanding AF, enlarged left atrium)
-CI: avoid CCB in HF
electrical cardioversion:
-indication: symptomatic AF, new onset with low risk of thromboembolism (<48h since onset or 3wks of anticoag)
-CI: no anticoag or inability to obtain TEE
antiarrhythmic medication:
-indication: younger pts, high CV risk, HF, failure of rate control
-CI: avoid propafenone and flecainide in structural or ischemic heart disease
catheter ablation:
-indication: younger pts, symptomatic AF, refractory in medical therapy, consider in HF
-CI: marked left atrial dilation

62
Q

What is the historical standard for cardioversion?

A

OAC x 3wks before and 4wks after for pts with valvular AF or NVAF >48h

63
Q

Describe cardioversion management.

A

see slide 66

64
Q

Which agents are of choice for pharmacologic cardioversion?

A

sodium channel blockers
-propafenone
-flecainide
amiodarone
digoxin, BB, CCB are not effective for cardioversion

65
Q

What are the conversion rates of pharmacologic cardioversion?

A

~75% when AF < 48h
-drops to 10-20% in AF of longer duration

66
Q

What are the side effects associated with the drugs used for pharmacologic cardioversion?

A

GI
left ventricular depression
pro-arrhythmia

67
Q

What should be combined with a drug used for pharmacologic cardioversion?

A

concurrent rate control agent

68
Q

Describe the efficacy of different drugs in achieving sinus rhythm.

A

good efficacy:
-ibutelide IV
-procainamide IV
-propafenone
-flecainide
less:
-oral long term amiodarone
-dofetilide
not effective:
-acute IV amiodarone
-sotalol

69
Q

Do antiarrhythmic drugs completely suppress AF?

A

may not completely suppress
-therefore focus should be on symptom relief, improving functional capacity, QoL and decreasing HC utilization

70
Q

Describe normal cardiac functioning.

A

function of the heart is to pump blood
-to do this, it must coordinate electrical impulses through cardiac tissue to cause contraction
SA node generates an electrical impulse which travels through the heart causing depolarization

71
Q

What is an arrhythmia?

A

abnormal contraction and changes to rate and rhythm
-disturbances occurred with the electrical impulse

72
Q

What is the primary pacemaker?

A

SA node

73
Q

What are the conduction fibers?

A

bundles of His
bundle branches
Purkinje fibers

74
Q

Describe conduction through the SA node and AV node.

A

slow conductors (allows filling)
activated by calcium

75
Q

Describe conduction through the conduction fibers and atrial & ventricular cells.

A

fast conductors
activated by sodium

76
Q

What are the two general types of cardiac action potentials?

A

pacemaker cells
non-pacemaker cells

77
Q

Describe action potentials at non-pacemaker cells.

A

Na+ influx causes rapid depolarization
K+ efflux beings initial repolarization
Ca2+ influx balances K+ efflux, causing slow depolarization
K+ efflux continues, resulting in repolarization

78
Q

Describe action potentials at pacemaker cells.

A

gated calcium channels open and cause influx of Ca2+
calcium channels close, potassium channels open
efflux of K+ repolarizes membrane

79
Q

Differentiate between an absolute refractory period and relative refractory period.

A

absolute
-time when the cell cannot be re-excited
-time it takes for the Na+ gates to fully reset
relative
-time immediately after the absolute refractory period, when the cell can be re-excited but requires a higher voltage than the usual threshold
-K+ channels still open and efflux still occurring, making the intracellular space more negative

80
Q

What is an ECG? What are the normal findings?

A

visual translation of the voltage changes during action potentials
-P wave=atrial depolarization
-QRS complex=ventricular depolarization
-T wave=ventricular repolarization

81
Q

What are the two types of disturbances that can cause arrhythmia?

A

disturbance in impulse generation
-automaticity (spontaneous impulse generation in latent pacemaker cells)
disturbance in impulse conduction
-re-entrant arrhythmias

82
Q

What is automaticity?

A

cells other than the SA node depolarize faster than the SA nodal cells and take control as the pacemaker
triggered automaticity:
-transient membrane depolarizations that occur during repolarization
-early after depolarizations or delayed after depolarizations prior to phase 4 of the action potential
-ex: multifocal atrial tachycardia (underlying cause of TdP)

83
Q

What are the requirements for re-entry arrhythmia to occur?

A
  1. two pathways for impulse conduction
  2. an area of unidirectional block
  3. slow conduction in the other pathway
84
Q

What is the general MOA of antiarrhythmic medications?

A

blocking ion channels by binding to a site on the ion channel proteins thereby modifying action potential

85
Q

Describe the Vaughan Williams classification of antiarrhythmics.

A

class Ia
-quinidine, procainamide, disopyramide
class Ib:
-lidocaine, mexiletine
class Ic:
-flecainide, propafenone
class II:
-beta blockers
class III:
-amiodarone, dofetilide, dronedarone, sotalol, ibutilide
class IV:
-verapamil, diltiazem

86
Q

Describe the MOA of the class I antiarrhythmics.

A

Na+channel blockers
quinidine and procainamide:
-prolong QRS and QT
lidocaine and mexilitene:
-shorten the QT
propafenone and flecainide:
-really prolong QRS

87
Q

Describe the MOA of the class II antiarrhythmics.

A

beta-blockers
-block beta-adrenergic stimulation
=blocking increased conduction velocity, shortened refractoriness, and increased automaticity

88
Q

Describe the MOA of the class III antiarrhythmics.

A

block potassium channels thereby prolonging the refractory period
-delayed repolarization

89
Q

Describe the MOA of amiodarone.

A

works on many areas
-Na+, K+, Ca2+ and B blockade

90
Q

Describe the MOA of the class IV antiarrhythmic medications.

A

slow conduction, prolong refractoriness, and decrease automaticity of calcium dependent cells in the SA and AV nodes

91
Q

Describe the MOA of digoxin.

A

inhibitor of Na+/K+-ATPase
increases vagal tone, which reduces conduction velocity
increases AV node refractoriness

92
Q

What are the general classifications of arrhythmias?

A

bradyarrhythmia
tachyarrhythmia
supraventricular (above ventricles=atria)
ventricular

93
Q

What is bradyarrhythmia?

A

HR < 60bpm

94
Q

When do patients with bradyarrhythmia’s typically get symptoms? What are some of these symptoms?

A

when HR < 50bpm
fatigue, lightheadedness, palpitations, syncope

95
Q

What is the cause of bradyarrhythmia?

A

conduction delay or block in AV conduction system
can be caused by reversible factors (myocarditis, BB, CCB) or irreversible (acute MI, congenital disease)

96
Q

What are the different degrees of AV block?

A

first degree (least severe-prolonged PR interval)
second degree
third degree (most severe-absence of AV conduction)

97
Q

What is the treatment for chronic symptomatic AV block?

A

pacemaker
leave it alone unless symptomatic

98
Q

What is tachyarrhythmia?

A

HR > 100bpm

99
Q

What is the usual cause of supraventricular tachyarrhythmia?

A

usually caused by re-entry mechanisms

100
Q

What are the typical symptoms of supraventricular tachyarrhythmia?

A

palpitations
fatigue
lightheadedness
neck fullness
chest pain

101
Q

What is the treatment for tachyarrhythmia for narrow QRS complex?

A

vagal maneuvers

102
Q

What is second line for narrow QRS complex?

A

adenosine or IV BB or CCB

103
Q

What are the classifications of supraventricular tachyarrhythmias?

A

atrial fibrillation/flutter
multifocal atrial tachycardia
AV nodal re-entrant tachycardia
AV re-entrant tachycardia

104
Q

What are examples of ventricular tachyarrhythmia?

A

premature ventricular complexes (PVCs)
-benign, common
ventricular tachycardia (VT)
-potentially fatal, life threatening
ventricular fibrillation (VF)
-fatal, medical emergency

105
Q

Describe PVCs.

A

often asymptomatic, can occur in healthy individuals
usually doesn’t require treatment
PVCs occurring after an MI can be a risk factor for sudden cardiac death
-studies show AAD to suppress PVC after MI doesn’t improve survival
-treat for sx: BB

106
Q

Describe ventricular tachycardia.

A

can be acutely caused by metabolic abmormalities, ischemia, or drug toxicity or can be chronic and recur in paroxsymal form

107
Q

What is the treatment for acute VT?

A

sustained VT, unstable pt:
-first line=DC cardioversion
stable patient: medication can be used
-IV procainamide, amiodarone, lidocaine

108
Q

What is the treatment to prevent VT recurrence?

A

amiodarone: most effective as maintenance therapy
sotalol also an option

109
Q

Which patient population is more likely to experience ventricular fibrillation?

A

acute MI
drug overdose
hypoxemia

110
Q

True or false: VF is a terminal event unless corrected

A

true

111
Q

What is the treatment for VF?

A

1st line: DC cardioversion
IV amiodarone if unsuccessful

112
Q

What is TdP?

A

Torsades de Pointes
-life threatening form of VT
-associated with long QT interval

113
Q

What is the treatment for TdP?

A

IV magnesium sulfate 2g
DC cardioversion

114
Q

What is the use of an implantable cardioverter defibrillator?

A

option for secondary prevention of spontaneous coronary death secondary to life threatening arrhythmia

115
Q

What are some monitoring parameters for amiodarone?

A

cardiac
-ECG (possible QT prolongation, TdP)
dermatologic
-photosensitive, blue-gray skin discolouration
endocrine
-can cause hyper/hypothyroid
hepatic
-can elevate liver enzymes
neurologic
ophthalmologic
-can cause optic neuropathy
pulmonary
-can cause dyspnea, cough, fever

116
Q

Which body system is not impacted by amiodarone?

A

kidneys

117
Q

Which medications are used first line for long term prevention or treatment of ventricular arrhythmias?

A

beta blockers

118
Q

What is the QT interval?

A

the ventricular depolarization and repolarization

119
Q

What can occur when the QT interval is prolonged?

A

delay in repolarization
can lead to TdP

120
Q

Which medications pose the highest risk of QT prolongation?

A

antiarrhythmic medications
-due to their potassium channel blocking properties
-sotalol risk around 4%

121
Q

What is the definition of a prolonged QTc interval?

A

QTc=corrected QT interval
females: > 480msec
males: >470msec
become worried if >500msec

122
Q

What can we use to identify patient risk and modifiable risk factors for QT prolongation?

A

Tisdale score
-age > 68: +1
-female: +1
-loop diuretic: +1
-K+ < 3.5mmol/L: +2
-presenting QTc interval >450msec: +2
-acute MI: +2
-HFrEF: +3
-1 QTc prolonging drug: +3
->2 QTc prolonging drugs: +3
-sepsis: +3
low risk=<7, moderate risk=7-10, high risk=>11

123
Q

What should be done if a patient has an arrhythmia according to their Smart Watch?

A

gather more information
-time frame, medical conditions, symptoms
assess the patients risk
-use CHADS-65 for afib patient
inform other HCP and refer patients as needed
reassure patient while watches are fun, they dont replace diagnostic testing

PHAR253 (16 decks)

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