Arrhythmia Flashcards
1
Q
What are the two common atrial arrhythmias?
A
atrial fibrillation
atrial flutter
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
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
4
Q
What is the most common sustained cardiac arrhythmia?
A
atrial fibrillation
5
Q
What kind of arrhythmia is atrial fibrillation?
A
supraventricular arrhythmia
-results from continuous and chaotic atrial activity
6
Q
Is atrial fibrillation life-threatening?
A
rarely
-associated with impaired QoL and increases risk for stroke and left ventricular dysfunction
7
Q
Describe the irregular rhythm associated with atrial fibrillation.
A
atrial rate: 350-600bpm
ventricular rate: 120-180bpm
pulse: irregular
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
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
10
Q
What are the symptoms of atrial fibrillation?
A
fatigue
palpitations
chest pain
dyspnea
dizziness
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
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
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
14
Q
What should be identified during an investigation for atrial fibrillation?
A
- risk factors/comorbidities
-HTN, HFrEF, male, tobacco, alcohol, valvular disease - triggers for AF episodes
-alcohol, stimulants, sleep deprivation, stress - 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
15
Q
What are the routine investigations for atrial fibrillation?
A
12 lead ECG
ECHO
laboratory investigations
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
17
Q
What is the leading cause of preventable stroke?
A
atrial fibrillation
-severe strokes
18
Q
Which classifications of atrial fibrillation have the highest risk of stroke?
A
persistent
permanent
paroxysmal
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)
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
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
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
23
Q
Describe CHADS2.
A
C=recent CHF, +1
H=hypertension, +1
A=age 75, +1
D= diabetes, +1
S2=stroke or TIA, +2
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
25
Describe stroke prevention in the frail elderly with atrial fibrillation.
OAC recommended
-frail elderly are at higher risk of stroke=benefit from OAC
-DOACS favoured over warfarin
26
What is the impact of obesity on stroke rates and bleeding rates?
lower stroke rates
higher bleeding rates
27
Describe DOAC use in obese patients.
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
28
What is the rule of 3 for reducing the dose of apixaban?
consider 2.5mg BID if:
- > 80yrs
- <60kg
-SCr > 133umol/L
29
Describe dosing of OACs for stroke prevention when CrCl> 50ml/min.
warfarin: dose adjusted for INR 2.0
dabigatran: 150mg BID
rivaroxaban: 20mg daily
apixaban: 5mg BID
edoxaban: 60mg daily
30
Describe dosing of OACs for stroke prevention when CrCl 30-49ml/min.
warfarin: dose adjusted for INR 2.0-3.0
dabigatran: consider 110mg BID
rivaroxaban: 15mg daily
apixaban: 5mg BID
edoxaban: 30mg daily
31
Describe dosing of OACs for stroke prevention when CrCl 15-29ml/min or <15ml/min.
warfarin: no data
dabigatran: no data
rivaroxaban: no data
apixaban: no data
edoxaban: no data
32
What are the practical differences among DOACs?
bioavailability
drug-drug interactions
availability of an antidote
dosing
33
Describe the bioavailability difference amongst the DOACs.
dabigatran: specific formulation
rivaroxaban: food for complete absorption
34
Describe the drug interaction differences amongst the DOACs.
dabigatran and edoxaban:
-avoid strong P-gp inhibitors and inducers
apixaban and rivaroxaban:
-avoid strong P-gp and 3A4 inhibitors and inducers
35
What are the antidotes for DOACs?
dabigatran-->idarucizumab
Xa inhibitors-->andexanet alpha
36
Which DOACs are dosed BID?
dabigatran
apixaban
37
Which DOACs are dosed daily?
edoxaban
rivaroxaban (BID in triple therapy)
38
What are some areas where DOACs dont fit as well or further research is required and clinical judgement is required?
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
39
What are some characteristics that increase bleeding risk?
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*
40
What are some strategies to minimize bleeding risk?
co-prescribe PPI
measure and monitor renal function
alcohol abstinence
control BP
correct anemia
discontinue ASA and NSAIDs
provide mobility aids
41
Do we withhold anticoagulation in stroke prevention based on bleeding risk?
no
-only if bleeding is active or risk is extreme
42
What are the monitoring parameters for anticoagulation?
adherence
frequency of adverse effects
signs and symptoms of bleeding and bleed risk factors
regular SCr, CrCl, HbB
43
Describe the acute management for arrhythmia management in atrial fibrillation.
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
44
Differentiate between rate control and rhythm control.
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
45
Describe the approach to rate and rhythm management of paroxysmal AF.
low recurrence burden:
-->observation
-->pill in pocket (AAD)
high recurrence burden:
-->maintenance AAD therapy
46
Describe the approach to rate and rhythm management of persistent AF.
see slide 50
47
Describe the theory behind rate control.
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
48
Is there evidence that rate control or rhythm control are superior to one another?
little to none (until recently)
-rate control preferred in permanent AF
-both are recommended initial strategies
49
What is the general goal of rate control?
reduction in HR >20% with control of symptoms
targets:
-resting HR < 100bpm
50
What are the first line agents for rate control?
beta blockers or non-DHP CCB
-selection based on comorbidities, contraindications, and side effects
51
What are the odds of rate control at rest/exercise with beta-blockers and CCBs for rate control?
rest/exercise
75/85% with beta blockers
66/72% with non-DHP CCBs
52
Describe the approach to therapy for hemodynamically stable acute AF.
see slide 53
53
What are the treatment choices for ventricular rate control?
digoxin
CCB
beta-blockers
*choice depends on patient*
54
Describe the approach to therapy for long-term rate control.
see slide 55
55
Describe acute rhythm control.
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
What are the objectives of rhythm control?
relief of symptoms like palpitations, dyspnea and fatigue
improve CO and exercise tolerance
prevent tachycardia induced myocardial remodeling and HF
57
What are the options for restoration of normal sinus rhythm in AF?
rate control & await spontaneous conversion
electrical direct current cardioversion
pharmacologic
58
What is the greatest concern with conversion to sinus rhythm?
risk of thromboembolism if clot in atria
-anticoagulate if AF>48h (therapeutic INR 3wks before and 4wks post conversion)
59
Which patients are most likely to maintain normal sinus rhythm?
short duration of AF and absence of left atrial dilation
should be attempted:
-angina
-hypotension
-HF
-recent onset of AF
60
In general, which therapy is most effective for restoration of NSR?
electrical cardioversion
61
Provide a summary of AF treatment for arrhythmia management.
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
What is the historical standard for cardioversion?
OAC x 3wks before and 4wks after for pts with valvular AF or NVAF >48h
63
Describe cardioversion management.
see slide 66
64
Which agents are of choice for pharmacologic cardioversion?
sodium channel blockers
-propafenone
-flecainide
amiodarone
*digoxin, BB, CCB are not effective for cardioversion*
65
What are the conversion rates of pharmacologic cardioversion?
~75% when AF < 48h
-drops to 10-20% in AF of longer duration
66
What are the side effects associated with the drugs used for pharmacologic cardioversion?
GI
left ventricular depression
pro-arrhythmia
67
What should be combined with a drug used for pharmacologic cardioversion?
concurrent rate control agent
68
Describe the efficacy of different drugs in achieving sinus rhythm.
good efficacy:
-ibutelide IV
-procainamide IV
-propafenone
-flecainide
less:
-oral long term amiodarone
-dofetilide
not effective:
-acute IV amiodarone
-sotalol
69
Do antiarrhythmic drugs completely suppress AF?
may not completely suppress
-therefore focus should be on symptom relief, improving functional capacity, QoL and decreasing HC utilization
70
Describe normal cardiac functioning.
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
What is an arrhythmia?
abnormal contraction and changes to rate and rhythm
-disturbances occurred with the electrical impulse
72
What is the primary pacemaker?
SA node
73
What are the conduction fibers?
bundles of His
bundle branches
Purkinje fibers
74
Describe conduction through the SA node and AV node.
slow conductors (allows filling)
activated by calcium
75
Describe conduction through the conduction fibers and atrial & ventricular cells.
fast conductors
activated by sodium
76
What are the two general types of cardiac action potentials?
pacemaker cells
non-pacemaker cells
77
Describe action potentials at non-pacemaker cells.
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
Describe action potentials at pacemaker cells.
gated calcium channels open and cause influx of Ca2+
calcium channels close, potassium channels open
efflux of K+ repolarizes membrane
79
Differentiate between an absolute refractory period and relative refractory period.
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
What is an ECG? What are the normal findings?
visual translation of the voltage changes during action potentials
-P wave=atrial depolarization
-QRS complex=ventricular depolarization
-T wave=ventricular repolarization
81
What are the two types of disturbances that can cause arrhythmia?
disturbance in impulse generation
-automaticity (spontaneous impulse generation in latent pacemaker cells)
disturbance in impulse conduction
-re-entrant arrhythmias
82
What is automaticity?
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
What are the requirements for re-entry arrhythmia to occur?
1. two pathways for impulse conduction
2. an area of unidirectional block
3. slow conduction in the other pathway
84
What is the general MOA of antiarrhythmic medications?
blocking ion channels by binding to a site on the ion channel proteins thereby modifying action potential
85
Describe the Vaughan Williams classification of antiarrhythmics.
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
Describe the MOA of the class I antiarrhythmics.
*Na+channel blockers*
quinidine and procainamide:
-prolong QRS and QT
lidocaine and mexilitene:
-shorten the QT
propafenone and flecainide:
-really prolong QRS
87
Describe the MOA of the class II antiarrhythmics.
beta-blockers
-block beta-adrenergic stimulation
=blocking increased conduction velocity, shortened refractoriness, and increased automaticity
88
Describe the MOA of the class III antiarrhythmics.
block potassium channels thereby prolonging the refractory period
-delayed repolarization
89
Describe the MOA of amiodarone.
works on many areas
-Na+, K+, Ca2+ and B blockade
90
Describe the MOA of the class IV antiarrhythmic medications.
slow conduction, prolong refractoriness, and decrease automaticity of calcium dependent cells in the SA and AV nodes
91
Describe the MOA of digoxin.
inhibitor of Na+/K+-ATPase
increases vagal tone, which reduces conduction velocity
increases AV node refractoriness
92
What are the general classifications of arrhythmias?
bradyarrhythmia
tachyarrhythmia
supraventricular (above ventricles=atria)
ventricular
93
What is bradyarrhythmia?
HR < 60bpm
94
When do patients with bradyarrhythmia's typically get symptoms? What are some of these symptoms?
when HR < 50bpm
fatigue, lightheadedness, palpitations, syncope
95
What is the cause of bradyarrhythmia?
conduction delay or block in AV conduction system
can be caused by reversible factors (myocarditis, BB, CCB) or irreversible (acute MI, congenital disease)
96
What are the different degrees of AV block?
first degree (least severe-prolonged PR interval)
second degree
third degree (most severe-absence of AV conduction)
97
What is the treatment for chronic symptomatic AV block?
pacemaker
*leave it alone unless symptomatic*
98
What is tachyarrhythmia?
HR > 100bpm
99
What is the usual cause of supraventricular tachyarrhythmia?
usually caused by re-entry mechanisms
100
What are the typical symptoms of supraventricular tachyarrhythmia?
palpitations
fatigue
lightheadedness
neck fullness
chest pain
101
What is the treatment for tachyarrhythmia for narrow QRS complex?
vagal maneuvers
102
What is second line for narrow QRS complex?
adenosine or IV BB or CCB
103
What are the classifications of supraventricular tachyarrhythmias?
atrial fibrillation/flutter
multifocal atrial tachycardia
AV nodal re-entrant tachycardia
AV re-entrant tachycardia
104
What are examples of ventricular tachyarrhythmia?
premature ventricular complexes (PVCs)
-benign, common
ventricular tachycardia (VT)
-potentially fatal, life threatening
ventricular fibrillation (VF)
-fatal, medical emergency
105
Describe PVCs.
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
Describe ventricular tachycardia.
can be acutely caused by metabolic abmormalities, ischemia, or drug toxicity or can be chronic and recur in paroxsymal form
107
What is the treatment for acute VT?
sustained VT, unstable pt:
-first line=DC cardioversion
stable patient: medication can be used
-IV procainamide, amiodarone, lidocaine
108
What is the treatment to prevent VT recurrence?
amiodarone: most effective as maintenance therapy
sotalol also an option
109
Which patient population is more likely to experience ventricular fibrillation?
acute MI
drug overdose
hypoxemia
110
True or false: VF is a terminal event unless corrected
true
111
What is the treatment for VF?
1st line: DC cardioversion
IV amiodarone if unsuccessful
112
What is TdP?
Torsades de Pointes
-life threatening form of VT
-associated with long QT interval
113
What is the treatment for TdP?
IV magnesium sulfate 2g
DC cardioversion
114
What is the use of an implantable cardioverter defibrillator?
option for secondary prevention of spontaneous coronary death secondary to life threatening arrhythmia
115
What are some monitoring parameters for amiodarone?
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
Which body system is not impacted by amiodarone?
kidneys
117
Which medications are used first line for long term prevention or treatment of ventricular arrhythmias?
beta blockers
118
What is the QT interval?
the ventricular depolarization and repolarization
119
What can occur when the QT interval is prolonged?
delay in repolarization
can lead to TdP
120
Which medications pose the highest risk of QT prolongation?
antiarrhythmic medications
-due to their potassium channel blocking properties
-sotalol risk around 4%
121
What is the definition of a prolonged QTc interval?
*QTc=corrected QT interval*
females: > 480msec
males: >470msec
*become worried if >500msec*
122
What can we use to identify patient risk and modifiable risk factors for QT prolongation?
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
What should be done if a patient has an arrhythmia according to their Smart Watch?
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
