Arrythmias Flashcards
breifly describe the action potential
negative resting potential (4) influx of sodium causes depol (0) calcium influx (1) potassium efflux causes repol (2) large repol (3) completely repolarized (4)
p wave
depol of atrium
qrs complex
ventricle depol
repol of atrium happening at the same time
t wave
ventricle repol
cause of tachyarrythmias
- automaticity: abnormal impulse generation starts the arrhythmia
- re-entry: abnormal impulse conduction maintains the arrhythmia
conduction of an impulse
SA node - primary pacemaker
AV node - escape pacemaker
bundle of his
purkinje network
why is the av node the escape pacemake
prevents too many extra beats from firing. only lets a certain amount through
takes over if primary fails
which will be the primary pacemaker
the fastest rhythm takes over
normally SA 60-100rate/min
describe how reentry occurs
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
class 1a
sodium blocker medium
blocks depol
procainamide
class 1b
sodium blocker fast
lidocaine
class 1c
sodium blocker slow
flecainide
class 2 how do they help
beta blockers
reduced adrenergic stimulation of sa and av nodes
class 3
potassium channel blocker
prolongs refractory period
class 4 and how do they help
CCB non DHP
decreased calcium influx - decreased contractility
relaxation of aterial smooth muscle
how digoxin helps
increased na and Ca in the myocyte and decreased K
results in high contractility but slows down the sa/av node
how do sodium channel blockers reduce re entry
decrease conduction velocity to reentry loop loses steam and sa node takes over
how do potassium channel blockers reduce reentry
prolong the refractory period so the area is still refractory when the loop comes around
SA node takes over
what HR is considered tachycardia
over 100
what HR is considered bradycardia
below 60
what is atrial fibrillation
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
acute AF
48 hours
only seen in a hospitalized patient who already has an ekg on them
paroxysmal AF
terminates spontaneously within 7 days
persistent AF
continues for greater than 7 days
permanent AF
doesnt terminated even with cardioversion attempts
high adrenergic tone may cause temporary AF list some examples
thyrotoxicosis alcohol withdrawal sepsis post surgery excessive physical exertion sympathomimetic theophylline digoxin toxocity
artrial distention may cause permanent AF list some examples
ischemia hypertension valvular disorder congenital abnormalities cardiomyopathy pulmonary embolism pulmonary hypertension obesity
signs of AF
irregular pulse
HR>100bpm
hypotension
EKG
symptomsof AF
asymptomatic palpitations dizziness syncope angina HF
serious complication of AF
tachycardia induced HF
severe hypotension/HF
embolic stoke
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
what are the 3 rate control choices
beta blocker
CCB
digoxin
which rate control agents can you use in HF
beta blocker
digoxin
which rate control agent can you use in CAD
beta blocker
CCB non DHP
combo
what end results do you want from a rate control agent
HR<100
minimize palpitations, dizziness, SOB
AE of diltiazem and verapamil
low Bp low HR CHF edema nausea constipation anorexia
diltiazem and verapamil interactions
3A4 and p-gp inhibitor
ex. statins, digoxin
beta blocker cautions
low BPlow HR CHF worsens: asthma, PVD, diabetes weakness fatigue abrupt discontinuation causes rebound tachycardia
digoxin AE
anorexia, nausea, vomiting, diarrhea
headache, fatigue, confusion
blurred vision, disturbed color vision, halos around bright objects
arrhythmias
why do you want to watch out for potassium levels when usign digoxin
low potassium = more prone to digoxin toxicity
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
who should you start on early rhythm control
highly symptomatic
multiple recurrences
extreme impairment in QOL
arrhythmia induced cardiomyopathuy
how effective is electrical cardioversion for rhythm contol
80-90%
new onset a fib in hospital treatment
amiodarone IV (potassium channel blocker)
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
what are the rhythm control choices in patients with no CHF and normal systolic function
dronedarone
flecainide
propafenone
sotalol
rhythm control choices in patients with CHF of LV systolic dysfunction with EF>35%
amiodarone
sotalol - caution if at risk of torsades de pointes
rhythm control choice for patients wiht CHF or LV systolic dysfunction with EF<35%
amiodarone
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
efficacy endpoints for rhythm control
maintain a normal sinus rhythm no palpitations, dizziness, SOB
sotalol interactions
QT prolonging meds
propafenone interactions
CYP450 3D6 substrate - inhibits digoxin elimination
flecainide interactions
QT prolonging meds
cyp450 2D6 substrate
things to monitor for amiodarone
pulmonary fubrosis hypo/hyperthyroidism optic neuropathy corneal microdeposits hepatotoxicity bradycardia tremoe photosensitivity - turn blue
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
oral anticoagulants
warfarin
dabigatran
rivaroxaban
apixaban
who should recieve oral anticoagulation in AF
over 65 prior stroke hypertension heart failure diabetes
patients with AF that have CAD or arterial vascular disease should recieve what
asa
who may require a lower dose of OAC
low eGFR
over 75
low body weight
what HAS-BLED score is high risk for cleed
> =3
why do we wait for cardioversion after AF
give time for the heart to get rid of any clots
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
when would you consider long term anticoagulation
CHADS >= 1
when would NOAC be used over warfarin
non valvular AF
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
warfarin interactions
substrate cyp450 2C9
strong 2C9 inhibitors = fluonazole, septra
antibiotics kill off vit k producing bacteria
new OAC interactions
strong inhibitors of cyp450 3A4 and p-gp
aiodarone, dronedarone, propafenona, quinidine, verapamil, itraconazole, ketoconazole
what would you give a patient with acute CHF who is hemodynamiccaly unstable (SBP<90) *
electrical cardioversion
no anticoagulation
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
first degree block bradycardia
PR:0.2 sec
P:QRS 1:1
second degree block bradycardia
P:QRS <1:1
third degree block bradycardia
AV dissociation
no relation between P:QRS
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
signs of bradyarrhythmias
HR<60
hypotension
EKG
symptoms of bradyarrhythmias
dizziness syncope fatigue confusion CHF
therapeutic options for bradyarrhythmias
removal of bradycardic drugs
atropine
isoproterenol
pacemaker - only can speed up a slow rate
