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PBL PY2 Fall > Arrhythmias Therapeutic Lecture > Flashcards

Arrhythmias Therapeutic Lecture Flashcards

1
Q

what are the class 1a antiarrhythmics under the Vaugh-Williams classification?

A

Na channel blockers procainamide, quinidine, disopyramide

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2
Q

what are the class 1b antiarrhythmic drugs under the Vaughn-Williams classification?

A

Na channel blockers like lidocaine and mexiletine

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3
Q

what are class 1c antiarrhythmic drugs under the vaughn williams classification?

A

Na channel blockers like flecainide and propafenone

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4
Q

what are the class 2 antiarrhythmic drugs under the waughn-williams classification?

A

B blockers like metoprolol and bisoprolol

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5
Q

B blockers decrease the conduction of signals through the ___ node

A

AV

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6
Q

what are the class 3 antiarrhythmics under the vaign-williams classification?

A

K channel blockers like amiodarone, dronedarone, sotalol, ibutilide

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7
Q

what are the class 4 antiarrhythmics under the vaughn williams classification?

A

Ca channel blockers like diltiazem and verapamil

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8
Q

Ca channel blockers decrease signal conduction through the ___ node

A

AV

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9
Q

which antiarrhythmic drug has properties of all 4 classes?

A

amiodarone

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10
Q

in normal sinus rhythm the HR is between ____

A

60-100 bpm

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11
Q

in normal sinuz rhythm, the p wave is ____

A

present before each QRS wave and is identical each time

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12
Q

in normal sinus rhythm, the PR interval is _____ seconds

A

0.12 to 0.20

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13
Q

in normal sinus rhythm, the QRS wave lasts ___ seconds

A

<1.2

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14
Q

define arrhythmia

A

refers to any change from the normal sequence of electrical impulses (may be too slow, too fast, or erratic)

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15
Q

an arrhythmia occurs in what three cases?

A
  1. when the heart’s natural pacemaker develops an abnormal rate or rhythm
  2. when the normal conduction pathway is interrupted
  3. when another part of the heart takes over as pacemaker
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16
Q

if an arrhythmia is occurring and the HR is <60bpm, it is defined as a ___ arrhythmia

A

bradycardia

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17
Q

what are the 2 reasons for bradycardia arrhythmia?

A
  1. sinus bradycardia

2. heart blocks

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18
Q

if an arrhythmia is happening and the HR is >100 bpm, it is defined as ____ arrhythmia

A

tachycardia

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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

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20
Q

what are the possible supraventricular arrhythmias?

A

Afib, A flutter, PSVT, sinus tachycardia

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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)

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22
Q

which type of supraventricular arrhythmias has an irregular pattern?

A

A fib

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23
Q

which 2 classes of supraventricular arrhythmias have regualr patterns?

A

atrial flutter and PSVT

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24
Q

describe the ECG findings that suggest A fib

A
  1. no P waves
  2. irregular
  3. narow QRS
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25
Q

what is A fib?

A

an irregularly irregular supraventricular arrhythmia with atrial rates of 350-450 bpm

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26
Q

in A fib, ____ may cause hemodynamic compromise and symptoms

A

rapid ventricular response

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27
Q

what is the most common arrhythmia?

A

A fib

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28
Q

A fid occurs in __% of the general population

A

1-2%

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29
Q

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)

A

55

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30
Q

A fib has increased mortality risk due to what 2 things?

A
  1. thomboembolic events

2. ventricular dysfunction

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31
Q

A fib tends to increase stroke risk by ___%

A

3-5

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32
Q

strokes that occur as a result of Afib tend to be ____(more or less) severe

A

more

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33
Q

a fib used to be thought of as _____, now it is recognized as a conseqeunce or manifestation of ______

A

isolated electrophysiological disorder; other cardiac or noncardiac pathologies

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34
Q

t/f HTN is one of the most important risk factors for A fib

A

t

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35
Q

what are some examples of cardiac causes of afib?

A

HTN, CAD with prior MI, LV dysfunction, heart failure, etc.

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36
Q

what are some examples of non-cardiac causes of Afib?

A

obesity, excessive alcohol, pulmonary disease, hyperthyroidism etc.

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37
Q

what are the symptoms of Afib?

A

weakness, fatigue, dizziness, lightheadedness, SOB, palpitations, chest pain, syncope, reduced exercise tolerance

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38
Q

describe the morbidity of Afib

A

decreased cardiac output, heart failure, hypotension, stroke

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39
Q

define paroxysmal Afib

A

lasts >30sec but not greater than 7 days

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40
Q

define persistent A fib

A

lasts more than 7 days, but less than 1 year

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41
Q

define longstanding persistent a fib

A

a fib greater than a year where rhythm control is being pursued

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42
Q

define permanent a fib

A

continuous a fib in which therapeautic decision has been made to not pursue rhythm control

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43
Q

define primary a fib

A

due to an established pathophysiologic process

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44
Q

define secondary a fib

A

caused by self-limited or acute reversible precipitant like surgery or acute pulmnary disease

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45
Q

what is valvular AF?

A

AF in the presence of mechanical heart valve or moderate to severe mitral valve stenosis

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46
Q

if a patient presents with a fib and is hemodynamically unstable, what needs to be done immediately?

A

acute cardioveriosn

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47
Q

what qualifies as an “unstable” patient?

A

hemodynamic instability with hypotension, acute coronary syndrome or pulmonary edema

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48
Q

what type of cardioversion is recommened for the management of unstable patients?

A

immediate electrical conversion

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49
Q

when can an elective electrial cardioversion be performed?

A

if th epatient is very symptomatic, rate of rhythm control agents are ineffective/not tolerated

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50
Q

t/f slowing the heart rate, typically results in significant improvemnt or resolution of symptoms

A

t

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51
Q

what is the acute rate control dosing of diltiazem?

A

0.25mg\kg IV bolus over 10 mins (some sources say 2 min); repeat 0.35 mg\kg IV

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52
Q

what is the acute rate control dosing of verapamil?

A

0.075-0.15mg\kg over 2 minutes

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53
Q

CCBs like diltiazem and verapamil should be avoided in what cases?

A

avoid in: heart failure, decreased ejection fraction (has been some evidence that diltiazem is a thing)

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54
Q

what is the acute rate control dosing for metoprolol?

A

2.5-5mg IV q5min x3

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55
Q

caution should be used in what patient population for metoprolol in a fib?

A

caution if patient has HF

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56
Q

what is the dosing for acute rate control by digoxin?

A

0.5mg IV then 0.25 mg IV q24h x 2

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57
Q

which rate control drug is the last line option?

A

digoxin

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58
Q

what is the dosing of digoxin for acute rate control?

A

0.5mg IV then 0.25mg iV q4h x2

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59
Q

digoxin is useful in the setting of what condition?

A

heart failure and reduced ejection fraction

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60
Q

the onset of digoxin is ____ (slow or fast)

A

slow

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61
Q

explain the general pathophysiololgy of wolf-parkinson white (WPW) syndrome

A

formation of an accessory electrical pathway between the atria and the ventricles

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62
Q

what type of drugs need to be avoided in patients with WPW syndrome? why?

A

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

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63
Q

what is the 1st line option to manage symptomsof rapid ventricular tachycardia in WPW patients?

A

ablation of the accessory pathway

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64
Q

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

A

rate or rhythm

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65
Q

about 50% of a fib patients will spontaneously cardiovert after ___ hours

A

24

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66
Q

describe the findings of the RACE 7 ACWAS trial

A

no significant difference early or delayed cardioversion

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67
Q

most antiarrhythmic drugs act in ___ tissue

A

non-nodal

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68
Q

what are the major side effects of procainamide?

A

hypotension, bradycardia, ventricular proarrhythmia

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69
Q

what are the major side effects of flecainide and propafenone?

A

hypotension, bradycardia, conversion pauses, 1:1 conduction of AFL, ventricular proarrhythmia

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70
Q

what are the major side effects of ibutilide?

A

prolonged QT, torsades de pointes, hypotension

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71
Q

what are the major side effects of vernakalent?

A

bradycardia, hypotension, ventricular proarrhythmia

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72
Q

what are the mjor side effcets of amiodarone?

A

hypotension, bradycardia, atrioventricular block, torsades de pointes, phlebitis, TELLS

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73
Q

class 1c antiarrhythmic drugs must be combined with a ____ agent. Why?

A

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

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74
Q

is amiodarone good for acute afib conversion?

A

it wont do it quickly (will take 12-24 hours), but high dose IV or oral doses can convert it eventually

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75
Q

which K channel blocker is NOT for acute a fib conversion?

A

sotolol

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76
Q

what is the goal of rate control for a fib?

A

to reduce the HR to <100bpm at rest

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77
Q

what things would indicate a patient would need at least 3 weeks of anticoagulation before cardioversion?

A
  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
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78
Q

what things would indicate that a patient should be started on OAC, but is a candiatdate for immediate cardioversion if needed?

A
  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
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79
Q

how long should patients be on OAC after cardioversion?

A

at least 4 weeks, then assess for long-term use based on CHADS-65 score

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80
Q

based on the CHADS-65 algorithm, all patients will be on OAC if they have 1 of what 2 factors?

A
  1. age 65+

2. at least 1 point on CHADS2

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81
Q

based on the CHADS-65 algorith, what makes you a candidate for antiplatelet therapy rather than OAC?

A

not over 65, no CHADS2 points AND they have coronary artery disease or peripheral artery disease

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82
Q

compare rate vs rhytm control in patients with established AF (what does current evidence suggest?). Is this different for newly diagnosed patients?

A

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

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83
Q

rhythm control is recommended in what 3 cases?

A
  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
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84
Q

without an antiarhythmic drug, the recurrence of AF is ____%

A

75

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85
Q

the efficacy of maintaining NSR at 1 year with flecainide, propafenone or sotalol is between _____%

A

30-50

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86
Q

the efficacy for maintenance of NSR at 1 year for amiodarone is between ___%

A

60-70

87
Q

the efficacy for maintenance of NSR at 1 year for dronedarone is ___%

A

40

88
Q

for rhythm control in a patient with EF <35% or heart failure, what is the drug option?

A

amiodarone

89
Q

for rhythm control in patients with CAD with normal LV function, what are the drug options?

A

amiodarone and sotalol (presuming sotalol is not c/i)

90
Q

for rhythm control in patients with normal heart function (other than arrhythmia), what are the drug options?

A

propafenone, flecainide, sotalol, amiodarone, dronedarone

91
Q

what are the c/i for sotalol?

A

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
Q

what is the “pill in pocket” method for rhythm control?

A

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
Q

what agents are used for the “pill in pocket” method?

A

class Ic antiarrhythmic drugs and an AV block (BB or CCB)

94
Q

what are the doses of diltizem, verapamil, and metoprolol when used as “pill in pocket” therapy?

A

diltizem 60mg, verapamil 80mg, metoprolol tartrate 25mg (all of the options need to be taken 30 min before taking the class 1c antiarrhythmic)

95
Q

what class of drug is propafenone?

A

class 1c Na channel blocker

96
Q

what are the doses for flecainide and propafenone for “pill in pocket”?

A

if 70+ kg: F 300mg po or P 600mg PO

if <70kg: F 200mg PO or P 450mg

97
Q

can popafenone be used for both acute conversion and maintenance if NSR?

A

yes

98
Q

what is the propafenone dosing for acute arrhythmia conversion?

A

600mg PO x1

99
Q

what is the maintenance dose of propafenone?

A

150-300mg PO TID

100
Q

what are the adverse effects of propafenone?

A

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
Q

what monitoring needs to be done for propafenone?

A

vitals (BP & HR), ECG, electrolytes, CBC, LFTs

102
Q

propafenone has many drug interactions and should be avoided in combo with what drugs?

A
  1. drugs that prolong QT

2. digoxin

103
Q

if you need to use digoxin while on propafenone, how should you adjust the dose of the digoxin?

A

reduce digoxin dose by 25%

104
Q

what is the drug class of flecainide?

A

class 1c Na channel blocker

105
Q

can flecainide be used for both acute conversion and maintenance of arrhytmia?

A

yes

106
Q

what is the acute dosing of flecainide?

A

300mg po x1

107
Q

what is the acute dosing of flecainide?

A

300mg po x1

108
Q

what is the maintenance dose of flecainide?

A

100-200mg PO BID

109
Q

what are the ADR of flecainide?

A

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
Q

what should be monitored on flecainide?

A

symptoms, vitals (BP, HR), ECG, electrolytes, LFTs, CBC

111
Q

what drugs interact with flecainide that need to be cautioned?

A
  1. drugs that prolong QT

2. digoxin (increased levels of digoxin due by this interaction)

112
Q

what is the drug class of sotalol?

A

class 2 and class 3 (beta blocker and K channel blocker)

113
Q

can sotalol be used for acute conversion and maintenance on NSR?

A

NO! only for maintenance

114
Q

what is the maintenance dose of sotalol?

A

80-160mg PO BID

115
Q

what are the ADRs of sotalol?

A

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
Q

what needs to be monitored on sotalol?

A

symptoms, vitals (BP, HR), ECG, electrolytes, SCr

117
Q

avoid sotalol if patient is taking drugs that have what effect?

A

drugs that prolong QT interval

118
Q

avoid sotalol in patients with what conditions?

A
  1. Hx of prolonged QT
  2. heart failure
  3. asthma
  4. heart block
119
Q

what is the drug class of amiodarone?

A

broad spectrum

120
Q

Can amiodarone be used for both ventricular and supraventricular tachyarrhythmias?

A

yes

121
Q

amiodarone is appropriate regardless of the function of ___

A

left ventricle

122
Q

what is the dosing of amiodarone for AF?

A

600-800mg in divided doses for 2-4 weeks (with a 10-12 gram load), then 100-200mg daily

123
Q

what are some important PK characteristics of amiodarone?

A
  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
Q

amiodarone is metabolized by which CYP enzymes?

A

CYP3A4 and CYP2C8

125
Q

what CYP are inhibited by amiodarone?

A

CYP2D6, CYP1A2, CYP2C9, CYP3A4

126
Q

what are the CNS ADR of amiodarone?

A

ataxia, parethesia, peripheral neuropathy, insomnia, tremor

127
Q

the CNS ADR of amiodarone are ___dependent

A

dose

128
Q

what are the eye ADR of amiodarone?

A

cornial microdeposits, halo/blurred vision, optic neuritis

129
Q

what monitoring should be done on the eyes while on amiodarone?

A

eye exam at baseline and yearly

130
Q

can you use amiodarone if you have prexisting optic neuritis or if optic neuritis occurs while taking?

A

no

131
Q

what are the respiratory ADR of amiodarone?

A

cough, pulmonary fibrosis

132
Q

what monitoring should be done for respiratory while on amiodarone?

A

PFT/CXR at baseline and CXR every year

133
Q

how should amiodarone treatment be adjusted if pulmonary infiltration occurs?

A

should discontinue amiodarone

134
Q

what are the CV ADR of amiodarone?

A

bradycardia, prolonged QT, TdP

135
Q

what CV monitoring should be done while on amiodarone?

A

ECG, vitals at baseline and yearly

136
Q

how should the loading dose be adjusted in elderly?

A

decrease

137
Q

amiodarone should have the dose decreased or the drug discontinued if the patient’s QT interval is greater than ___msec

A

550

138
Q

what are the GO ADR of amiodarone?

A

nausea, anorexia, constipation, hepatitis, crrhosis

139
Q

what GI monitoring should be done while on amiodarone?

A

AST/ALT at baseline the q 6 months

140
Q

how shouls amiodarone therapy be adjusted if hepatitis or cirrhosis develops?

A

discontinue amiodarone

141
Q

what are the endocrine ADRs of amiodarone?

A

hypothyroidism, hyperthyroidism

142
Q

what endocrine monitoring should be done while on amiodarone?

A

TFT at baseline then q 6 months

143
Q

what drug can be given if a patient develops hypothyroidism while on amiodarone?

A

synthroid

144
Q

what are the skin ADRs of amiodarone?

A

blue-grey discoloration and photosensitivity

145
Q

t/f amiodarone patients should be using a high SPF sunscreen

A

t

146
Q

dronedarone is intended for the use in what situations?

A

nonpermanent (predominantly paroxysmal) AF with minimal structural heart disease

147
Q

which is more effective, amiodarone or dronedarone?

A

amiodarone

148
Q

which has fewer ADR, amiodarone or dronedarone?

A

dronedarone

149
Q

what is teh dose of dronedarone?

A

400mg BID

150
Q

what are the ADR of dronedarone?

A

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
Q

what needs to be monitored while on dronedarone?

A

symptoms, vitals (BP & HR), ECG, electrolytes, SCr, liver enzymes

152
Q

caution should be used when taking dronedarone if the patient has what conditions?

A

CAD, electrolye imbalance

153
Q

dronedarone use should be avoided in what conditions?

A

permanent AF, Hx of or current heart failure, heart block, unstable hemodynamics, lung/liver toxicity form past amiodarone use

154
Q

avoid dronedarone use if patients are taking what types of drugs?

A

strong CYP3A4 inhibitors, drugs that induce TdP

155
Q

what are ideal rate control options in patients with heart failure>

A

B blocker with or without digoxin

156
Q

what are the ideal drugs for rate control in patients with CAD?

A

beta blockers, CCBs, or a combination

157
Q

what are the ideal rate control drugs for patients that do not have CAD or heart failure?

A

B blocker, CCB, digoxin, or a combination

158
Q

digoxin may be considered as monotherapy only in particulary ___ patients

A

sedentary

159
Q

digoxin should not be 1st line for rate control and should be reserved for patients who are ____ or who have ____ dysfunction

A

sedentary, left ventricular systolic

160
Q

when should amiodarone be used for rate control?

A

reserved for exceptional cases in which other means are not feasible or are not enough

161
Q

what is the target HR for rate control?

A

100bpm

162
Q

what does CHADS stand for?

A

congestive heart failure, HTN, Age 75+, diabetes, stroke/TIA

163
Q

based on the CHADS-65 algorithm, what criteria dictate OAC use?

A

age 65+ or any one of: stroke/TIA, HTN, heart failure, diabetes

164
Q

according to the CHADS-65 algorithm, what dictates use of antiplatelet therapy?

A

CAD or PAD and none of the CHAD or 65 age criteria

165
Q

what are the potential anticoagulants for A fib?

A 
ASA
ASA & clopidogrel
warfarin
apixaban
rivaroxaban
edoxaban
dabigatran
IV heparin
LMWH
166
Q

when is dabigatran a good option?

A

age 80+ pr 75+ with other bleeding risk including CrCl 30-50mL/min

167
Q

apixaban is recommended if 2 of the 3 criteria are present:

A
  1. age 80+
  2. weight 60kg or less
  3. SCr 133 umol/L or more
168
Q

when should edoxaban 30mg be considered?

A

if weight 60kg or less or PgP inhitor EXCEPT amiodarone or verapamil

169
Q

when should OAC NOT be used??

A
  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
Q

during depolarization, there is an influx of ___ions

A

Na

171
Q

SA node action potentials are dependent on the influx of ___ions

A

Ca

172
Q

pacemaker cells are found in the ____

A

SA node

173
Q

t/f the AP in the SA node is automatic

A

t

174
Q

why can the SA node override the AV node and purkinjee?

A

bc the SA node acts faster

175
Q

when the SA node is impaired, the ____ will take over, but at a much slower rate

A

AV

176
Q

what is represented by the P wave?

A

atrial depolarization

177
Q

what is represented by the QRS wave?

A

ventricular depolarization

178
Q

what is represented by the T wave?

A

ventricular repolarization

179
Q

why cant you see atrial repolarization in the ECG?

A

bc it is hidden by the QRS complex

180
Q

AP travels from the ___ node, then the ___ node, the to the ___, ___ and ___

A

SA node, AV node, bundle branches, purkinjee and then the ventricles

181
Q

t/f anything that alters the action potential causes a change in ECG

A

true

182
Q

what ECG change will we see if Na channels are blocked?

A

prolonged depolarization

183
Q

what ECG changes will we see if K channel is blocked?

A

prolonged repolarization

184
Q

K channel blockers cause a prolonged ___interval

A

QT

185
Q

what is the issue with prolonging QT interval?

A

can cause dangerous arrhythmias

186
Q

how do beta blockers affect rate control?

A

by slowing the conduction through the AV node

187
Q

what is measured by the PR node?

A

how long it takes AP to go from the atria to the ventricle

188
Q

what classes of drugs will prolong the PR wave?

A

CCB and B blockers

189
Q

t/f MI can interupt the normal transduction pathway by scar tissue

A

t

190
Q

does a fast or slow heart rate necessarily mean pathology?

A

no

191
Q

what is the cause for sinus bradycardia and sinus tachycardia?

A

SA node firing more or less than usual

192
Q

what are PVS? When do they typically occur?

A

abnormal beats from the ventricle; typically after an MI

193
Q

t/f it is unlikely that a patient ONLY has A fib, there is typically something else going on that is causing it

A

t

194
Q

anything that irritates the ___ can cause A fib

A

atria

195
Q

why may patients feel tired when they are in a fib?

A

the cardiac input is not normal and may result in not enough blood getting to organs, leading to fatigue

196
Q

should you try to achieve rhythm control in permanent A fib?

A

no, should just try to bring down HR, prevent stroke and manage symptoms

197
Q

which has a higher risk for stroke, valvular or non-valvular?

A

valvular

198
Q

t/f the more persistent A fib is, the harder it is to get back to NSR

A

t

199
Q

electrical cardioversion targets what wave?

A

R

200
Q

how does electrical cardioversion work?

A

stuns the cells to stop them and hoefully when they reset, they go back into repolarization and SA node will kick in again

201
Q

do patients need to be sedated for electric cardioversion?

A

yes

202
Q

all drugs for acute rate control block the ___ node to prevent impulses going to the ventricles

A

AV

203
Q

digoxin is excreted by what way?

A

renally

204
Q

do patients with WPW syndrome have higher or lower rate of A fib?

A

higher

205
Q

t/f patients who are of advanced age will be less likely to spontaneously convert

A

t

206
Q

torsades de points

A
207
Q

what is torsades de pointes (TdP)?

A

a rapid polymorphic form of ventricuar tachycardia

208
Q

is torasdes de pointes life-threatening?

A

yes

209
Q

torsades de pointes may terminate spontaneously, or may degenerate into _____

A

ventricaulr fibrilation and sudden cardiac death

210
Q

the symptoms of torsades de pointes result from the compromised cardiac out put and HR of _____ to ____bpm

A

160-240

211
Q

the incidence of torsades de pointes is likely ____ (high/low)

A

low

212
Q

what causes qt prolongation?

A
  1. prolonged depolarization (activation of late stage Na)
  2. prolonged repolarization (delayed K)
  3. combination of both
213
Q

how long does a QT wave need to be for i to be concerning?

A

> 500ms

214
Q

what are the normal QT lengths in healthy mean and women?

A

men: 470ms or lower
women: 480ms or lower

PBL PY2 Fall (21 decks)

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