Pharmacotherapy of Dysrhythmias Flashcards
symptoms of dysrhythmias
palpitations, chest pain, fatigue, dyspnea, lightheadedness, syncope, CHF exacerbation, embolic complication
types of supraventricular arrhythmias
AFib, AFL, atrial tachycardia, AVNRT/SVT
pathophysiology of AFib
multiple small reentrant atrial circuits, automaticity, atrial remodeling, irregularly irregular HR/rhythm, loss of atrial contribution to ventricular filling
risk factors for AFib
drugs (caffeine, stimulants), alcohol, smoking, obesity, MI, diabetes, HTN, age, etc etc etc
complications of AFib
stroke, heart failure, mortality
_____ AFib terminates spontaneously of with intervention within 7 days of onset
paroxysmal
____ AFib is continuous AFib sustained > 7 days
persistent
______ AFib lasts greater than 12 months
long-standing persistant
____ AFib involves a joint decision btwn patient and clinician to stop further attempts to restore/maintain normal sinus rhythm
permanent
_____ AFib is AFib in the absence of rheumatic mitral stenosis, mechanical or biprosthetic heart valve, mitral valve repair
non-valvular
AFib treatment goals
prevent thromboembolism, control ventricular rate, convert to and maintain NSR
how do you consider rate vs rhythm control
consider patient-specific factors: age, activity level, severity of symptoms: if AFib identified early, pursue rhythm control
consider rhythm control when…
patient preference, HFrEF, recent AFib diagnosis, high burden AFib, younger, failed rate control, worsening HF symptoms with AFib
consider rate control when…
patient preference, longstanding AFib, low burden AFib, severe LA dilation, NYHA III-IV, failed previous rhythm control
is there a difference in outcome between lenient and strict rate control
no
when to use lenient rate goal
asymptomatic or LVEF >40%
what is the lenient rate goal
<110 bpm
when to use strict rate goal
symptomatic or LVEF<40%
what is the strict rate goal
<80 bpm
agents to use for rate control
beta blockers/ verapamil/ diltiazem preferred, digoxin, amio (caution potential for cardioversion, stroke risk if pt is not anticoagulated)
when would digoxin or amio be preferred for rate control
in decompensated heart failure (LVEF <40%)
metoprolol dosing for rate control
2.5-5 mg IV bolus, up to 3 doses
diltiazem dosing for rate control
0.25 mg/kg IV bolus, 5-15 mg/hr infusion
amio dosing for rate control
150 mg IV bolus, 0.5-1 mg/kg infusion
what is DCCV
direct current cardioversion
meds used to enhance success of conversion by shock, and prevent immediate recurrence
flecainide, propafenone, amiodarone, ibutilide, dofetilide
echo-guided cardioversion
ensure no clot !!! can’t pursue rhythm control until you know there’s no clot–> clots can embolize if you shock and do rhythm control
pharmacologic agents for cardioversion
flecainide, propafenone, amiodarone, sotalol, dofetilide, ibutilide
flecainide dosing for cardioversion
200-300 mg PO
propafenone dosing for cardioversion
600 mg PO
amio dosing for cardioversion
IV bolus 150 mg over 1 hr. then cont infusion @ 1 mg/min x 6 hours. then infusion of 0.5 mg/min x 18 hours. then convert to PO: 400 mg bid or tid (7-10 days) until total loading dose of 10 grams reached
what agents are used for the “pill in the pocket” method
flecainide, propafenone
pearls for “pill in the pocket” method
low-access, rural areas, clearly symptomatic AFib, must be trialed in monitored setting first
pharmacologic agents for maintenance of NSR
flecainide, propafenone, amiodarone, sotalol, dronedarone, dofetilide
amio dosing for maintenance of NSR
200 mg daily
dronedarone dosing for maintenance of NSR
400 mg bid
dofetilide dosing for maintenance of NSR
125-500 mcg bid
flecainide dosing for maintenance of NSR
50-150 mg bid
propafenone dosing for maintenance of NSR
150-300 mg tid or 225-425 mg bid
sotalol dosing for maintenance of NSR
80-160 mg bid
general monitoring for antiarrhythmics
proarrhythmias (any antiarrhythmic can be proarrhythmic), QTc (class IA, III), potassium, magnesium, kidney function (sotalol, dofetilide, DOACs), left ventricular function
special considerations for dofetilide
must be initiated in-patient: monitor QTc, kidney function (CrCL), adjust dose accordingly, monitor for minimum of 3 days
dofetilide drug interactions
CYP3A4: verapamil, ketoconazole, trimethoprim, HCTZ
contraindications with dofetilide
CrCL <20 mL/min, QTc > 440 msec
what to monitor with amio
chest xray, pulmonary function, liver function, thyroid function (T4, TSH), opthalmologic, ECG
drug interactions with amiodarone and dronedarone
digoxin and warfarin (cut dose in half), other anti-dysrhythmics, beta blockers, calcium channel blockers, statins (dose cap w/ simva and lova), QTc prolonging drugs, CYP3A substrates/inhibitors/inducers
special considerations for digoxin
not first line, narrow therapeutic window, risk of toxicity (age, frailty, renal insufficiency), monitor serum drug concentrations
therapeutic anticoagulation is required for ___ before and ___ after cardioversion
3 weeks before and 4 weeks after. exception: can perform cardioversion sooner if echo is performed to rule out presence of clot
left atrial occlusion device
for patients with contraindications to anticoagulation (traps the clot so it can’t escape)
ventricular dysrhythmias originate from where
below bundle of His
ventricular dysrhythmias are characterized by ___
abnormal QRS, abnormal QT interval
non-sustained ventricular tachycardia
less than 3 beats, terminates spontaneously
sustained ventricular tachycardia
30 s or requiring termination in < 30 s due to hemodynamic compromise
monomorphic ventricular tachycardia
stable, single QRS morphology with each beat
polymorphic ventricular tachycardia
changing/multiform QRS morphology with each beat
clinical presentation of PVCs
non life-threatening, typically asymptomatic, associated w/ increased risk of mortality
clinical presentation of VT
symptoms vary from asymptomatic to pulseless + hemodynamic collapse. faster HR, longer duration, LV dysfunction= more symptoms
clinical presentation of VF
hemodynamic collapse, syncope, cardiac arrest
how do you know it’s torsades
polymorphic ventricular tachycardia characterized by prolongation of QT interval
risk factors for drug-induced torsades
bradycardia, using >1 QT prolonging drug, digoxin therapy, female, heart failure, high drug levels, hypokalemia, impaired hepatic drug metabolism, left ventricular hypertrophy, rapid infusion by IV, recent conversion from AFib, QTc > 500 msec, severe hypomagnesemia, treatment w/ diuretics
drugs that may cause TdP
antiarrhythmics: quinidine, procainamide, disopyramide, sotalol, dofetilide, ibutilide. anti-infectives (clarithromycin), antiemetics (droperidol), antipsychotics (haloperidol), antidepressants (sertraline), methadone
what agents to use for monomorphic VT with no structural heart disease
verapamil or beta blocker
what agents to use for monomorphic VT with structural heart disease
procainamide, sotalol, amiodarone
what agents to use for polymorphic VT with normal QTc
amiodarone, beta blockers, lidocaine
what agents to use for polymorphic VT with long QTc
d/c offending agents, correct lytes, magnesium, lidocaine, pacing, isoproterenol
amio dosing for VT
150 mg IV, then infusion (1 mg/min for 6 hours, then 0.5 mg/min for 18 hours), monitor for hypotension/bradycardia/AV block
lidocaine dosing for VT
1-1.5 mg/kg IV load, repeat 5-10 min later with 0.5-0.75 mg/kg then maintenance infusion of 1-4 mg/min. monitor for bradycardia and CNS changes
procainamide dosing for VT
10-17 mg/kg IV load given as continuous infusion (20 mg/min) then maintenance infusion of 1-4 mg/min. monitor for QRS widening > 50%
magnesium sulfate dosing for VT
1-2 gm IV over 15 min, may repeat as needed, may follow w/ infusion of 0.5-1 gm/hr. monitor for hypotension, vasodilation
