Arrhythmias Therapeutic Lecture Flashcards
1
Q
what are the class 1a antiarrhythmics under the Vaugh-Williams classification?
A
Na channel blockers procainamide, quinidine, disopyramide
2
Q
what are the class 1b antiarrhythmic drugs under the Vaughn-Williams classification?
A
Na channel blockers like lidocaine and mexiletine
3
Q
what are class 1c antiarrhythmic drugs under the vaughn williams classification?
A
Na channel blockers like flecainide and propafenone
4
Q
what are the class 2 antiarrhythmic drugs under the waughn-williams classification?
A
B blockers like metoprolol and bisoprolol
5
Q
B blockers decrease the conduction of signals through the ___ node
A
AV
6
Q
what are the class 3 antiarrhythmics under the vaign-williams classification?
A
K channel blockers like amiodarone, dronedarone, sotalol, ibutilide
7
Q
what are the class 4 antiarrhythmics under the vaughn williams classification?
A
Ca channel blockers like diltiazem and verapamil
8
Q
Ca channel blockers decrease signal conduction through the ___ node
A
AV
9
Q
which antiarrhythmic drug has properties of all 4 classes?
A
amiodarone
10
Q
in normal sinus rhythm the HR is between ____
A
60-100 bpm
11
Q
in normal sinuz rhythm, the p wave is ____
A
present before each QRS wave and is identical each time
12
Q
in normal sinus rhythm, the PR interval is _____ seconds
A
0.12 to 0.20
13
Q
in normal sinus rhythm, the QRS wave lasts ___ seconds
A
<1.2
14
Q
define arrhythmia
A
refers to any change from the normal sequence of electrical impulses (may be too slow, too fast, or erratic)
15
Q
an arrhythmia occurs in what three cases?
A
- when the heart’s natural pacemaker develops an abnormal rate or rhythm
- when the normal conduction pathway is interrupted
- when another part of the heart takes over as pacemaker
16
Q
if an arrhythmia is occurring and the HR is <60bpm, it is defined as a ___ arrhythmia
A
bradycardia
17
Q
what are the 2 reasons for bradycardia arrhythmia?
A
- sinus bradycardia
2. heart blocks
18
Q
if an arrhythmia is happening and the HR is >100 bpm, it is defined as ____ arrhythmia
A
tachycardia
19
Q
what does it mean if a tachycardic arrhythmia has a QRS <0.12 (narrow)?
A
means its a supraventricular above the ventricle arrhythmia
20
Q
what are the possible supraventricular arrhythmias?
A
Afib, A flutter, PSVT, sinus tachycardia
21
Q
if tachycardic arrhytmia and the QRS is >0.12 (wide), where is the arrhythmia occuring? What type of arrhythmias are possible causes?
A
in the ventricle; V fib, ventricular tacchycardia, premature ventricular complexes (PVCs)
22
Q
which type of supraventricular arrhythmias has an irregular pattern?
A
A fib
23
Q
which 2 classes of supraventricular arrhythmias have regualr patterns?
A
atrial flutter and PSVT
24
Q
describe the ECG findings that suggest A fib
A
- no P waves
- irregular
- narow QRS
25
what is A fib?
an irregularly irregular supraventricular arrhythmia with atrial rates of 350-450 bpm
26
in A fib, ____ may cause hemodynamic compromise and symptoms
rapid ventricular response
27
what is the most common arrhythmia?
A fib
28
A fid occurs in __% of the general population
1-2%
29
after age ___, the incidence of A fib doubles with each decade of life and with other risk factors for heart disease and stroke (like HTN, DM, HF & valvular heart disease)
55
30
A fib has increased mortality risk due to what 2 things?
1. thomboembolic events
| 2. ventricular dysfunction
31
A fib tends to increase stroke risk by ___%
3-5
32
strokes that occur as a result of Afib tend to be ____(more or less) severe
more
33
a fib used to be thought of as _____, now it is recognized as a conseqeunce or manifestation of ______
isolated electrophysiological disorder; other cardiac or noncardiac pathologies
34
t/f HTN is one of the most important risk factors for A fib
t
35
what are some examples of cardiac causes of afib?
HTN, CAD with prior MI, LV dysfunction, heart failure, etc.
36
what are some examples of non-cardiac causes of Afib?
obesity, excessive alcohol, pulmonary disease, hyperthyroidism etc.
37
what are the symptoms of Afib?
weakness, fatigue, dizziness, lightheadedness, SOB, palpitations, chest pain, syncope, reduced exercise tolerance
38
describe the morbidity of Afib
decreased cardiac output, heart failure, hypotension, stroke
39
define paroxysmal Afib
lasts >30sec but not greater than 7 days
40
define persistent A fib
lasts more than 7 days, but less than 1 year
41
define longstanding persistent a fib
a fib greater than a year where rhythm control is being pursued
42
define permanent a fib
continuous a fib in which therapeautic decision has been made to not pursue rhythm control
43
define primary a fib
due to an established pathophysiologic process
44
define secondary a fib
caused by self-limited or acute reversible precipitant like surgery or acute pulmnary disease
45
what is valvular AF?
AF in the presence of mechanical heart valve or moderate to severe mitral valve stenosis
46
if a patient presents with a fib and is hemodynamically unstable, what needs to be done immediately?
acute cardioveriosn
47
what qualifies as an "unstable" patient?
hemodynamic instability with hypotension, acute coronary syndrome or pulmonary edema
48
what type of cardioversion is recommened for the management of unstable patients?
immediate electrical conversion
49
when can an elective electrial cardioversion be performed?
if th epatient is very symptomatic, rate of rhythm control agents are ineffective/not tolerated
50
t/f slowing the heart rate, typically results in significant improvemnt or resolution of symptoms
t
51
what is the acute rate control dosing of diltiazem?
0.25mg\kg IV bolus over 10 mins (some sources say 2 min); repeat 0.35 mg\kg IV
52
what is the acute rate control dosing of verapamil?
0.075-0.15mg\kg over 2 minutes
53
CCBs like diltiazem and verapamil should be avoided in what cases?
avoid in: heart failure, decreased ejection fraction (has been some evidence that diltiazem is a thing)
54
what is the acute rate control dosing for metoprolol?
2.5-5mg IV q5min x3
55
caution should be used in what patient population for metoprolol in a fib?
caution if patient has HF
56
what is the dosing for acute rate control by digoxin?
0.5mg IV then 0.25 mg IV q24h x 2
57
which rate control drug is the last line option?
digoxin
58
what is the dosing of digoxin for acute rate control?
0.5mg IV then 0.25mg iV q4h x2
59
digoxin is useful in the setting of what condition?
heart failure and reduced ejection fraction
60
the onset of digoxin is ____ (slow or fast)
slow
61
explain the general pathophysiololgy of wolf-parkinson white (WPW) syndrome
formation of an accessory electrical pathway between the atria and the ventricles
62
what type of drugs need to be avoided in patients with WPW syndrome? why?
AV nodal blocking drugs like B blockers and CCB bc blocking the AV node will cause even more electrical impulses to be channeled to the pathological accessory pathway of WPW
63
what is the 1st line option to manage symptomsof rapid ventricular tachycardia in WPW patients?
ablation of the accessory pathway
64
in a hemodynamically stable patient with recent onset a fib presenting to the ER within 48 hours of onset and low stroke risk, evidence equally supports ___ or ___ control
rate or rhythm
65
about 50% of a fib patients will spontaneously cardiovert after ___ hours
24
66
describe the findings of the RACE 7 ACWAS trial
no significant difference early or delayed cardioversion
67
most antiarrhythmic drugs act in ___ tissue
non-nodal
68
what are the major side effects of procainamide?
hypotension, bradycardia, ventricular proarrhythmia
69
what are the major side effects of flecainide and propafenone?
hypotension, bradycardia, conversion pauses, 1:1 conduction of AFL, ventricular proarrhythmia
70
what are the major side effects of ibutilide?
prolonged QT, torsades de pointes, hypotension
71
what are the major side effects of vernakalent?
bradycardia, hypotension, ventricular proarrhythmia
72
what are the mjor side effcets of amiodarone?
hypotension, bradycardia, atrioventricular block, torsades de pointes, phlebitis, TELLS
73
class 1c antiarrhythmic drugs must be combined with a ____ agent. Why?
AV nodal blocking agent (like B blocker or CCB) bc class 1c drugs have a paradoxical increase in HR effect, so BB or CCB will help combat this
74
is amiodarone good for acute afib conversion?
it wont do it quickly (will take 12-24 hours), but high dose IV or oral doses can convert it eventually
75
which K channel blocker is NOT for acute a fib conversion?
sotolol
76
what is the goal of rate control for a fib?
to reduce the HR to <100bpm at rest
77
what things would indicate a patient would need at least 3 weeks of anticoagulation before cardioversion?
1. valvular arrhythmia
2. if they have had a recent stroke or TIA
3. if the arrhythmia has been happening for 12-48 hours and they have a CHADS2 score of 2+
4. if its been 48 hours or greater since onset of arrhythmia
78
what things would indicate that a patient should be started on OAC, but is a candiatdate for immediate cardioversion if needed?
1. if they are hemodinyamically unstable
2. it has lasted less than 12 hours and have not had a recent stroke or TIA
3. it started 12-48 hours ago and their CHADS2 score is between 0-1
79
how long should patients be on OAC after cardioversion?
at least 4 weeks, then assess for long-term use based on CHADS-65 score
80
based on the CHADS-65 algorithm, all patients will be on OAC if they have 1 of what 2 factors?
1. age 65+
| 2. at least 1 point on CHADS2
81
based on the CHADS-65 algorith, what makes you a candidate for antiplatelet therapy rather than OAC?
not over 65, no CHADS2 points AND they have coronary artery disease or peripheral artery disease
82
compare rate vs rhytm control in patients with established AF (what does current evidence suggest?). Is this different for newly diagnosed patients?
for established AF, multiple RCT have shown no significant difference in CV outcomes
For newly diagnosed patients (within 1 year), an initial strategy of rhythm control has been associated with reduced CV death and stroke rates
83
rhythm control is recommended in what 3 cases?
1. newly diagnosed patients
2. patients who remain symptomatic with rate control
3. patients who are not likely to have rate control manage their symptoms
84
without an antiarhythmic drug, the recurrence of AF is ____%
75
85
the efficacy of maintaining NSR at 1 year with flecainide, propafenone or sotalol is between _____%
30-50
86
the efficacy for maintenance of NSR at 1 year for amiodarone is between ___%
60-70
87
the efficacy for maintenance of NSR at 1 year for dronedarone is ___%
40
88
for rhythm control in a patient with EF <35% or heart failure, what is the drug option?
amiodarone
89
for rhythm control in patients with CAD with normal LV function, what are the drug options?
amiodarone and sotalol (presuming sotalol is not c/i)
90
for rhythm control in patients with normal heart function (other than arrhythmia), what are the drug options?
propafenone, flecainide, sotalol, amiodarone, dronedarone
91
what are the c/i for sotalol?
patients at high risk for torsades de pointes (low weight, women, age >65 recieving diuretics (low K will increase the incidence for torsades and death)
92
what is the "pill in pocket" method for rhythm control?
for symptomatic patients with infrequent, longer-lasting (2 hours or more) episodes of AF or AFL as an alternative to daily therapy (to reduce side effects of drugs)
93
what agents are used for the "pill in pocket" method?
class Ic antiarrhythmic drugs and an AV block (BB or CCB)
94
what are the doses of diltizem, verapamil, and metoprolol when used as "pill in pocket" therapy?
diltizem 60mg, verapamil 80mg, metoprolol tartrate 25mg (all of the options need to be taken 30 min before taking the class 1c antiarrhythmic)
95
what class of drug is propafenone?
class 1c Na channel blocker
96
what are the doses for flecainide and propafenone for "pill in pocket"?
if 70+ kg: F 300mg po or P 600mg PO
| if <70kg: F 200mg PO or P 450mg
97
can popafenone be used for both acute conversion and maintenance if NSR?
yes
98
what is the propafenone dosing for acute arrhythmia conversion?
600mg PO x1
99
what is the maintenance dose of propafenone?
150-300mg PO TID
100
what are the adverse effects of propafenone?
agranulocytosis, dysrhythmia (bradycardia, heart block, ventricular tachycardia), hypotension, exacerbation of heart failure & asthma, fatigue, headache, anxiety, dizziness, blurred vision, nausea, vomiting, diarrhea, peripheral neuropathy
101
what monitoring needs to be done for propafenone?
vitals (BP & HR), ECG, electrolytes, CBC, LFTs
102
propafenone has many drug interactions and should be avoided in combo with what drugs?
1. drugs that prolong QT
| 2. digoxin
103
if you need to use digoxin while on propafenone, how should you adjust the dose of the digoxin?
reduce digoxin dose by 25%
104
what is the drug class of flecainide?
class 1c Na channel blocker
105
can flecainide be used for both acute conversion and maintenance of arrhytmia?
yes
106
what is the acute dosing of flecainide?
300mg po x1
107
what is the acute dosing of flecainide?
300mg po x1
108
what is the maintenance dose of flecainide?
100-200mg PO BID
109
what are the ADR of flecainide?
agranulocytosis, dysrrhymia (bradycardia, heart block, ventricular tachycardia), hypotension, exacerbation of heart failure & asthma, fatigue, headache, anxiety, dizziness, blurred vision, nausea, vomiting, diarrhea, metallic taste
110
what should be monitored on flecainide?
symptoms, vitals (BP, HR), ECG, electrolytes, LFTs, CBC
111
what drugs interact with flecainide that need to be cautioned?
1. drugs that prolong QT
| 2. digoxin (increased levels of digoxin due by this interaction)
112
what is the drug class of sotalol?
class 2 and class 3 (beta blocker and K channel blocker)
113
can sotalol be used for acute conversion and maintenance on NSR?
NO! only for maintenance
114
what is the maintenance dose of sotalol?
80-160mg PO BID
115
what are the ADRs of sotalol?
fatigue, depression, insomnia, headache, dizziness, blurred vision, hypotension, dysrrhythmia (bradycardia, heart block, TdP), exacerbation of heart failure/asthma, nausea, vomiting, diarrhea, masks hypoglycemia, Raynauds
116
what needs to be monitored on sotalol?
symptoms, vitals (BP, HR), ECG, electrolytes, SCr
117
avoid sotalol if patient is taking drugs that have what effect?
drugs that prolong QT interval
118
avoid sotalol in patients with what conditions?
1. Hx of prolonged QT
2. heart failure
3. asthma
4. heart block
119
what is the drug class of amiodarone?
broad spectrum
120
Can amiodarone be used for both ventricular and supraventricular tachyarrhythmias?
yes
121
amiodarone is appropriate regardless of the function of ___
left ventricle
122
what is the dosing of amiodarone for AF?
600-800mg in divided doses for 2-4 weeks (with a 10-12 gram load), then 100-200mg daily
123
what are some important PK characteristics of amiodarone?
1. high Vd
2. takes a long time to onset and long half-life
3. inhibits PgP
4. metabolized and inhibits CYP3A4 and others
124
amiodarone is metabolized by which CYP enzymes?
CYP3A4 and CYP2C8
125
what CYP are inhibited by amiodarone?
CYP2D6, CYP1A2, CYP2C9, CYP3A4
126
what are the CNS ADR of amiodarone?
ataxia, parethesia, peripheral neuropathy, insomnia, tremor
127
the CNS ADR of amiodarone are ___dependent
dose
128
what are the eye ADR of amiodarone?
cornial microdeposits, halo/blurred vision, optic neuritis
129
what monitoring should be done on the eyes while on amiodarone?
eye exam at baseline and yearly
130
can you use amiodarone if you have prexisting optic neuritis or if optic neuritis occurs while taking?
no
131
what are the respiratory ADR of amiodarone?
cough, pulmonary fibrosis
132
what monitoring should be done for respiratory while on amiodarone?
PFT/CXR at baseline and CXR every year
133
how should amiodarone treatment be adjusted if pulmonary infiltration occurs?
should discontinue amiodarone
134
what are the CV ADR of amiodarone?
bradycardia, prolonged QT, TdP
135
what CV monitoring should be done while on amiodarone?
ECG, vitals at baseline and yearly
136
how should the loading dose be adjusted in elderly?
decrease
137
amiodarone should have the dose decreased or the drug discontinued if the patient's QT interval is greater than ___msec
550
138
what are the GO ADR of amiodarone?
nausea, anorexia, constipation, hepatitis, crrhosis
139
what GI monitoring should be done while on amiodarone?
AST/ALT at baseline the q 6 months
140
how shouls amiodarone therapy be adjusted if hepatitis or cirrhosis develops?
discontinue amiodarone
141
what are the endocrine ADRs of amiodarone?
hypothyroidism, hyperthyroidism
142
what endocrine monitoring should be done while on amiodarone?
TFT at baseline then q 6 months
143
what drug can be given if a patient develops hypothyroidism while on amiodarone?
synthroid
144
what are the skin ADRs of amiodarone?
blue-grey discoloration and photosensitivity
145
t/f amiodarone patients should be using a high SPF sunscreen
t
146
dronedarone is intended for the use in what situations?
nonpermanent (predominantly paroxysmal) AF with minimal structural heart disease
147
which is more effective, amiodarone or dronedarone?
amiodarone
148
which has fewer ADR, amiodarone or dronedarone?
dronedarone
149
what is teh dose of dronedarone?
400mg BID
150
what are the ADR of dronedarone?
nausea, vomiting, diarrhea, athenia, fatigue, bradycardia, rash, SCr (temporary increase by 10-20 umol/L), SOB, cough, interstitial lung disease, increased serum transaminases, bilirubin
151
what needs to be monitored while on dronedarone?
symptoms, vitals (BP & HR), ECG, electrolytes, SCr, liver enzymes
152
caution should be used when taking dronedarone if the patient has what conditions?
CAD, electrolye imbalance
153
dronedarone use should be avoided in what conditions?
permanent AF, Hx of or current heart failure, heart block, unstable hemodynamics, lung/liver toxicity form past amiodarone use
154
avoid dronedarone use if patients are taking what types of drugs?
strong CYP3A4 inhibitors, drugs that induce TdP
155
what are ideal rate control options in patients with heart failure>
B blocker with or without digoxin
156
what are the ideal drugs for rate control in patients with CAD?
beta blockers, CCBs, or a combination
157
what are the ideal rate control drugs for patients that do not have CAD or heart failure?
B blocker, CCB, digoxin, or a combination
158
digoxin may be considered as monotherapy only in particulary ___ patients
sedentary
159
digoxin should not be 1st line for rate control and should be reserved for patients who are ____ or who have ____ dysfunction
sedentary, left ventricular systolic
160
when should amiodarone be used for rate control?
reserved for exceptional cases in which other means are not feasible or are not enough
161
what is the target HR for rate control?
100bpm
162
what does CHADS stand for?
congestive heart failure, HTN, Age 75+, diabetes, stroke/TIA
163
based on the CHADS-65 algorithm, what criteria dictate OAC use?
age 65+ or any one of: stroke/TIA, HTN, heart failure, diabetes
164
according to the CHADS-65 algorithm, what dictates use of antiplatelet therapy?
CAD or PAD and none of the CHAD or 65 age criteria
165
what are the potential anticoagulants for A fib?
```
ASA
ASA & clopidogrel
warfarin
apixaban
rivaroxaban
edoxaban
dabigatran
IV heparin
LMWH
```
166
when is dabigatran a good option?
age 80+ pr 75+ with other bleeding risk including CrCl 30-50mL/min
167
apixaban is recommended if 2 of the 3 criteria are present:
1. age 80+
2. weight 60kg or less
3. SCr 133 umol/L or more
168
when should edoxaban 30mg be considered?
if weight 60kg or less or PgP inhitor EXCEPT amiodarone or verapamil
169
when should OAC NOT be used??
1. mechanical or bioprosthetic heart valves
2. mitral stenosis
3. rheumatic heart disease
4. severe or end-stage renal disease
5. unstable renal function
6. certain drug interaction
170
during depolarization, there is an influx of ___ions
Na
171
SA node action potentials are dependent on the influx of ___ions
Ca
172
pacemaker cells are found in the ____
SA node
173
t/f the AP in the SA node is automatic
t
174
why can the SA node override the AV node and purkinjee?
bc the SA node acts faster
175
when the SA node is impaired, the ____ will take over, but at a much slower rate
AV
176
what is represented by the P wave?
atrial depolarization
177
what is represented by the QRS wave?
ventricular depolarization
178
what is represented by the T wave?
ventricular repolarization
179
why cant you see atrial repolarization in the ECG?
bc it is hidden by the QRS complex
180
AP travels from the ___ node, then the ___ node, the to the ___, ___ and ___
SA node, AV node, bundle branches, purkinjee and then the ventricles
181
t/f anything that alters the action potential causes a change in ECG
true
182
what ECG change will we see if Na channels are blocked?
prolonged depolarization
183
what ECG changes will we see if K channel is blocked?
prolonged repolarization
184
K channel blockers cause a prolonged ___interval
QT
185
what is the issue with prolonging QT interval?
can cause dangerous arrhythmias
186
how do beta blockers affect rate control?
by slowing the conduction through the AV node
187
what is measured by the PR node?
how long it takes AP to go from the atria to the ventricle
188
what classes of drugs will prolong the PR wave?
CCB and B blockers
189
t/f MI can interupt the normal transduction pathway by scar tissue
t
190
does a fast or slow heart rate necessarily mean pathology?
no
191
what is the cause for sinus bradycardia and sinus tachycardia?
SA node firing more or less than usual
192
what are PVS? When do they typically occur?
abnormal beats from the ventricle; typically after an MI
193
t/f it is unlikely that a patient ONLY has A fib, there is typically something else going on that is causing it
t
194
anything that irritates the ___ can cause A fib
atria
195
why may patients feel tired when they are in a fib?
the cardiac input is not normal and may result in not enough blood getting to organs, leading to fatigue
196
should you try to achieve rhythm control in permanent A fib?
no, should just try to bring down HR, prevent stroke and manage symptoms
197
which has a higher risk for stroke, valvular or non-valvular?
valvular
198
t/f the more persistent A fib is, the harder it is to get back to NSR
t
199
electrical cardioversion targets what wave?
R
200
how does electrical cardioversion work?
stuns the cells to stop them and hoefully when they reset, they go back into repolarization and SA node will kick in again
201
do patients need to be sedated for electric cardioversion?
yes
202
all drugs for acute rate control block the ___ node to prevent impulses going to the ventricles
AV
203
digoxin is excreted by what way?
renally
204
do patients with WPW syndrome have higher or lower rate of A fib?
higher
205
t/f patients who are of advanced age will be less likely to spontaneously convert
t
206
torsades de points
207
what is torsades de pointes (TdP)?
a rapid polymorphic form of ventricuar tachycardia
208
is torasdes de pointes life-threatening?
yes
209
torsades de pointes may terminate spontaneously, or may degenerate into _____
ventricaulr fibrilation and sudden cardiac death
210
the symptoms of torsades de pointes result from the compromised cardiac out put and HR of _____ to ____bpm
160-240
211
the incidence of torsades de pointes is likely ____ (high/low)
low
212
what causes qt prolongation?
1. prolonged depolarization (activation of late stage Na)
2. prolonged repolarization (delayed K)
3. combination of both
213
how long does a QT wave need to be for i to be concerning?
>500ms
214
what are the normal QT lengths in healthy mean and women?
men: 470ms or lower
women: 480ms or lower
