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Clinical 2.0 > Arrythmias > Flashcards

Arrythmias Flashcards

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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
permanent AF
doesnt terminated even with cardioversion attempts
26
high adrenergic tone may cause temporary AF list some examples
``` thyrotoxicosis alcohol withdrawal sepsis post surgery excessive physical exertion sympathomimetic theophylline digoxin toxocity ```
27
artrial distention may cause permanent AF list some examples
``` ischemia hypertension valvular disorder congenital abnormalities cardiomyopathy pulmonary embolism pulmonary hypertension obesity ```
28
signs of AF
irregular pulse HR>100bpm hypotension EKG
29
symptomsof AF
``` asymptomatic palpitations dizziness syncope angina HF ```
30
serious complication of AF
tachycardia induced HF severe hypotension/HF embolic stoke
31
3 goals of therapy in AF
control of rapid ventricular response = ventricular rate control restoration of normal sinus rhythm = atrial rhythm control prevention of thromboembolic complication
32
what are the 3 rate control choices
beta blocker CCB digoxin
33
which rate control agents can you use in HF
beta blocker | digoxin
34
which rate control agent can you use in CAD
beta blocker CCB non DHP combo
35
what end results do you want from a rate control agent
HR<100 | minimize palpitations, dizziness, SOB
36
AE of diltiazem and verapamil
``` low Bp low HR CHF edema nausea constipation anorexia ```
37
diltiazem and verapamil interactions
3A4 and p-gp inhibitor | ex. statins, digoxin
38
beta blocker cautions
``` low BPlow HR CHF worsens: asthma, PVD, diabetes weakness fatigue abrupt discontinuation causes rebound tachycardia ```
39
digoxin AE
anorexia, nausea, vomiting, diarrhea headache, fatigue, confusion blurred vision, disturbed color vision, halos around bright objects arrhythmias
40
why do you want to watch out for potassium levels when usign digoxin
low potassium = more prone to digoxin toxicity
41
digoxin interactions
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
who should you start on early rhythm control
highly symptomatic multiple recurrences extreme impairment in QOL arrhythmia induced cardiomyopathuy
43
how effective is electrical cardioversion for rhythm contol
80-90%
44
new onset a fib in hospital treatment
amiodarone IV (potassium channel blocker)
45
what is pill in the pocket and when is it used
just take a single oral dose of flecainide or propafenone used in patients with on and off AF
46
what are the rhythm control choices in patients with no CHF and normal systolic function
dronedarone flecainide propafenone sotalol
47
rhythm control choices in patients with CHF of LV systolic dysfunction with EF>35%
amiodarone | sotalol - caution if at risk of torsades de pointes
48
rhythm control choice for patients wiht CHF or LV systolic dysfunction with EF<35%
amiodarone
49
why is amiodarone only first line rhythm control in patients with previous heart rpoblems
has a higher toxicity and effects outside of the heart | but lower toxicity in the heart
50
efficacy endpoints for rhythm control
maintain a normal sinus rhythm no palpitations, dizziness, SOB
51
sotalol interactions
QT prolonging meds
52
propafenone interactions
CYP450 3D6 substrate - inhibits digoxin elimination
53
flecainide interactions
QT prolonging meds | cyp450 2D6 substrate
54
things to monitor for amiodarone
``` pulmonary fubrosis hypo/hyperthyroidism optic neuropathy corneal microdeposits hepatotoxicity bradycardia tremoe photosensitivity - turn blue ```
55
amiodarone/dronedarone interactions *
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
oral anticoagulants
warfarin dabigatran rivaroxaban apixaban
57
who should recieve oral anticoagulation in AF
``` over 65 prior stroke hypertension heart failure diabetes ```
58
patients with AF that have CAD or arterial vascular disease should recieve what
asa
59
who may require a lower dose of OAC
low eGFR over 75 low body weight
60
what HAS-BLED score is high risk for cleed
>=3
61
why do we wait for cardioversion after AF
give time for the heart to get rid of any clots
62
how should anticoagulation be given >48 hours after AF
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
when would you consider long term anticoagulation
CHADS >= 1
64
when would NOAC be used over warfarin
non valvular AF
65
who should not use the new OAC
impaired renal function <25 over 75 without documented stable renal function rheumatic valvular heart disease prosthetic heart valves
66
warfarin interactions
substrate cyp450 2C9 strong 2C9 inhibitors = fluonazole, septra antibiotics kill off vit k producing bacteria
67
new OAC interactions
strong inhibitors of cyp450 3A4 and p-gp | aiodarone, dronedarone, propafenona, quinidine, verapamil, itraconazole, ketoconazole
68
what would you give a patient with acute CHF who is hemodynamiccaly unstable (SBP<90) *
electrical cardioversion | no anticoagulation
69
what would you give a patient with acute CHF that is hemodynamically stable *
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
first degree block bradycardia
PR:0.2 sec P:QRS 1:1
71
second degree block bradycardia
P:QRS <1:1
72
third degree block bradycardia
AV dissociation | no relation between P:QRS
73
name some factors that may precipitate bradyarrhythmias
``` class 1 antiarrythmic beta blockers amiodarone CCB digoxin clonidine adenosine ticagrelor lithium SSRI antipsychotics acetylcholinesterase inhibitors methadone ondansetron phenytoin high dose steroids ```
74
signs of bradyarrhythmias
HR<60 hypotension EKG
75
symptoms of bradyarrhythmias
``` dizziness syncope fatigue confusion CHF ```
76
therapeutic options for bradyarrhythmias
removal of bradycardic drugs atropine isoproterenol pacemaker - only can speed up a slow rate

Clinical 2.0 (24 decks)

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