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Clinical 2.0 > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

breifly describe the action potential

A 
negative resting potential (4)
influx of sodium causes depol (0)
calcium influx (1)
potassium efflux causes repol (2) 
large repol (3) 
completely repolarized (4)
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2
Q

p wave

A

depol of atrium

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3
Q

qrs complex

A

ventricle depol

repol of atrium happening at the same time

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4
Q

t wave

A

ventricle repol

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5
Q

cause of tachyarrythmias

A
  1. automaticity: abnormal impulse generation starts the arrhythmia
  2. re-entry: abnormal impulse conduction maintains the arrhythmia
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6
Q

conduction of an impulse

A

SA node - primary pacemaker
AV node - escape pacemaker
bundle of his
purkinje network

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7
Q

why is the av node the escape pacemake

A

prevents too many extra beats from firing. only lets a certain amount through
takes over if primary fails

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8
Q

which will be the primary pacemaker

A

the fastest rhythm takes over

normally SA 60-100rate/min

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9
Q

describe how reentry occurs

A

area that has a longer refractory period takes long to turn back to repol state
when impulse enters this area conducting is stopped so goes around through the area that is already repolled then when gets back to the area that was original refractory it will be repolarized again and can conduct through

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10
Q

class 1a

A

sodium blocker medium
blocks depol
procainamide

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11
Q

class 1b

A

sodium blocker fast

lidocaine

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12
Q

class 1c

A

sodium blocker slow

flecainide

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13
Q

class 2 how do they help

A

beta blockers

reduced adrenergic stimulation of sa and av nodes

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14
Q

class 3

A

potassium channel blocker

prolongs refractory period

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15
Q

class 4 and how do they help

A

CCB non DHP
decreased calcium influx - decreased contractility
relaxation of aterial smooth muscle

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16
Q

how digoxin helps

A

increased na and Ca in the myocyte and decreased K

results in high contractility but slows down the sa/av node

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17
Q

how do sodium channel blockers reduce re entry

A

decrease conduction velocity to reentry loop loses steam and sa node takes over

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18
Q

how do potassium channel blockers reduce reentry

A

prolong the refractory period so the area is still refractory when the loop comes around
SA node takes over

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19
Q

what HR is considered tachycardia

A

over 100

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20
Q

what HR is considered bradycardia

A

below 60

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21
Q

what is atrial fibrillation

A

reentry loops firing faster than SA so take over
extremely fast and disorganized atrial rhythm causes atrium to quiver heart not filled efficiently
faster ventricular rate as well

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22
Q

acute AF

A

48 hours

only seen in a hospitalized patient who already has an ekg on them

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23
Q

paroxysmal AF

A

terminates spontaneously within 7 days

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24
Q

persistent AF

A

continues for greater than 7 days

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25
Q

permanent AF

A

doesnt terminated even with cardioversion attempts

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26
Q

high adrenergic tone may cause temporary AF list some examples

A 
thyrotoxicosis
alcohol withdrawal 
sepsis 
post surgery 
excessive physical exertion 
sympathomimetic 
theophylline
digoxin toxocity
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27
Q

artrial distention may cause permanent AF list some examples

A 
ischemia 
hypertension
valvular disorder
congenital abnormalities
cardiomyopathy 
pulmonary embolism 
pulmonary hypertension 
obesity
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28
Q

signs of AF

A

irregular pulse
HR>100bpm
hypotension
EKG

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29
Q

symptomsof AF

A 
asymptomatic 
palpitations
dizziness
syncope
angina
HF
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30
Q

serious complication of AF

A

tachycardia induced HF
severe hypotension/HF
embolic stoke

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31
Q

3 goals of therapy in AF

A

control of rapid ventricular response = ventricular rate control
restoration of normal sinus rhythm = atrial rhythm control
prevention of thromboembolic complication

32
Q

what are the 3 rate control choices

A

beta blocker
CCB
digoxin

33
Q

which rate control agents can you use in HF

A

beta blocker

digoxin

34
Q

which rate control agent can you use in CAD

A

beta blocker
CCB non DHP
combo

35
Q

what end results do you want from a rate control agent

A

HR<100

minimize palpitations, dizziness, SOB

36
Q

AE of diltiazem and verapamil

A 
low Bp 
low HR 
CHF
edema
nausea
constipation 
anorexia
37
Q

diltiazem and verapamil interactions

A

3A4 and p-gp inhibitor

ex. statins, digoxin

38
Q

beta blocker cautions

A 
low BPlow HR
CHF
worsens: asthma, PVD, diabetes
weakness
fatigue 
abrupt discontinuation causes rebound tachycardia
39
Q

digoxin AE

A

anorexia, nausea, vomiting, diarrhea
headache, fatigue, confusion
blurred vision, disturbed color vision, halos around bright objects
arrhythmias

40
Q

why do you want to watch out for potassium levels when usign digoxin

A

low potassium = more prone to digoxin toxicity

41
Q

digoxin interactions

A

due to inhibition of p-gp and p450: amiodarone, dronedarone, propefenone, quinidine, duinine, verapamil, itraconazole– recommended reducing digoxin dose by 50%
macrolides kill bacteria that break down digoxin
cholestyramine, Al/Mg antacids, kaolin-oectin, dietary fibre, sucralfate – 2 hour interval
beta blocker, non DHP CCB – doing the same thing
calcium rapid IV — causes arrhythmias
diuretics, amphotericin B, laxatives – indirect via hypokalemia

42
Q

who should you start on early rhythm control

A

highly symptomatic
multiple recurrences
extreme impairment in QOL
arrhythmia induced cardiomyopathuy

43
Q

how effective is electrical cardioversion for rhythm contol

A

80-90%

44
Q

new onset a fib in hospital treatment

A

amiodarone IV (potassium channel blocker)

45
Q

what is pill in the pocket and when is it used

A

just take a single oral dose of flecainide or propafenone used in patients with on and off AF

46
Q

what are the rhythm control choices in patients with no CHF and normal systolic function

A

dronedarone
flecainide
propafenone
sotalol

47
Q

rhythm control choices in patients with CHF of LV systolic dysfunction with EF>35%

A

amiodarone

sotalol - caution if at risk of torsades de pointes

48
Q

rhythm control choice for patients wiht CHF or LV systolic dysfunction with EF<35%

A

amiodarone

49
Q

why is amiodarone only first line rhythm control in patients with previous heart rpoblems

A

has a higher toxicity and effects outside of the heart

but lower toxicity in the heart

50
Q

efficacy endpoints for rhythm control

A

maintain a normal sinus rhythm no palpitations, dizziness, SOB

51
Q

sotalol interactions

A

QT prolonging meds

52
Q

propafenone interactions

A

CYP450 3D6 substrate - inhibits digoxin elimination

53
Q

flecainide interactions

A

QT prolonging meds

cyp450 2D6 substrate

54
Q

things to monitor for amiodarone

A 
pulmonary fubrosis
hypo/hyperthyroidism 
optic neuropathy 
corneal microdeposits
hepatotoxicity 
bradycardia 
tremoe 
photosensitivity - turn blue
55
Q

amiodarone/dronedarone interactions *

A

inhibitor of cyp450 1A2, 2C9, 2D6, 3A4 and p-gp
lower dose if on: digoxin, warfarin, flecainide, quinidine, atrovastatin, simvastatin
additive effects wiht rate slowing agents and QT prolonging agents

56
Q

oral anticoagulants

A

warfarin
dabigatran
rivaroxaban
apixaban

57
Q

who should recieve oral anticoagulation in AF

A 
over 65 
prior stroke 
hypertension
heart failure 
diabetes
58
Q

patients with AF that have CAD or arterial vascular disease should recieve what

A

asa

59
Q

who may require a lower dose of OAC

A

low eGFR
over 75
low body weight

60
Q

what HAS-BLED score is high risk for cleed

A

> =3

61
Q

why do we wait for cardioversion after AF

A

give time for the heart to get rid of any clots

62
Q

how should anticoagulation be given >48 hours after AF

A

3 weeks of anticoagulants pre cardioversion and 4 weeks post
unless thrombus already ruled out just cardiovert right away and anticoagulants for four weeks after

63
Q

when would you consider long term anticoagulation

A

CHADS >= 1

64
Q

when would NOAC be used over warfarin

A

non valvular AF

65
Q

who should not use the new OAC

A

impaired renal function <25
over 75 without documented stable renal function
rheumatic valvular heart disease
prosthetic heart valves

66
Q

warfarin interactions

A

substrate cyp450 2C9
strong 2C9 inhibitors = fluonazole, septra
antibiotics kill off vit k producing bacteria

67
Q

new OAC interactions

A

strong inhibitors of cyp450 3A4 and p-gp

aiodarone, dronedarone, propafenona, quinidine, verapamil, itraconazole, ketoconazole

68
Q

what would you give a patient with acute CHF who is hemodynamiccaly unstable (SBP<90) *

A

electrical cardioversion

no anticoagulation

69
Q

what would you give a patient with acute CHF that is hemodynamically stable *

A

if HR>100 rate control with digoxin
consider electrical cardioversion given severity of symptoms
anticoagulants 3 weeks before and 4 weeks after
consider long term amiodarone

70
Q

first degree block bradycardia

A

PR:0.2 sec
P:QRS 1:1

71
Q

second degree block bradycardia

A

P:QRS <1:1

72
Q

third degree block bradycardia

A

AV dissociation

no relation between P:QRS

73
Q

name some factors that may precipitate bradyarrhythmias

A 
class 1 antiarrythmic
beta blockers
amiodarone
CCB
digoxin 
clonidine
adenosine 
ticagrelor
lithium 
SSRI
antipsychotics
acetylcholinesterase inhibitors
methadone
ondansetron
phenytoin 
high dose steroids
74
Q

signs of bradyarrhythmias

A

HR<60
hypotension
EKG

75
Q

symptoms of bradyarrhythmias

A 
dizziness 
syncope
fatigue
confusion 
CHF
76
Q

therapeutic options for bradyarrhythmias

A

removal of bradycardic drugs
atropine
isoproterenol
pacemaker - only can speed up a slow rate

Clinical 2.0 (24 decks)

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