ventricular arrhythmias

who do ventricular arrythmias usually occur in

who do ventricular arrythmias usually occur in

pts with structural heart disease (ex: ACS esp STEMI, CAD, LV dysfunction)

may be precipitated by electrolyte abnormalities (decreased K or Mg), hypoxia, or acidosis

drug causes include (but not limited to): digoxin, sympathetic amines, antiarrythmic agents

premature ventricular contractions (PVC)

ectopic beats arising within ventricular tissue

also referred to as ventricular premature depolarizations (VPD) or ventricular premature beats (VPB)

ventricular tachycardia (VT)

a series of atleast PVC’s at a rate of >100bpm

unsustained VT

VT lasting <30s and terminates spontaneously

sustained VT

VT lasting >30s and requires therapeutic intervention for termination (may lead to VF)

ventricular fibrillation (VF)

the absence of organized ventricular rhythm, resulting in no cardiac output

manifested by absence of pulse and palpable BP

PVC symptoms

asymptomatic

VT (with pulse) symptoms

depends on duration and HR

palpitations, dizziness, SOB, chest pain (if underlying CAD), syncope

VF/pulseless VT symptoms

immediate lack of consciousness

PVC prognosis

little prognostic significance (benign),except in pts with CAD or history of MI (prognostically significant)

VT (with pulse) prognosis

may progress to VF

VF /pulseless VT prognosis

death within mins if no resuscitation

sudden cardiac death

benign PVC treatment

none

prognostically significant asymptomatic PVC treatment

no tx

prognostically significant symptomatic PVC treatment

B blockers (most pts have CAD so BB preferred)

meds to avoid in PVC

Class IC agents

nonsustained VT with pulse Tx

none

prevention Tx of VT with pulse

ICD to prevent VT if history of VT and at risk of sudden cardiac death

may use AAD with ICD (ex: BB + amiodarone) to reduce frequency of ICD shocks

VF/pulseless VT Tx

defibrillation- drug therapy used only as adjunct (epinephrine, amiodarone, lidocaine)

prevention of pulseless VT/VF

implantable cardioverter-defibrillator (ICD) may be used to prevent recurrent VT/VF

if someone has sustained monomorphic VT and is hemodynamically unstable what to do

DCCV and ACLS

if someone has sustained monomorphic VT and stable heart disease what drugs and steps are next in algorithm

cardioversion, procainamide, IV amiodarone or sotolol

if no termination reassess AADs, repeat DCCV

if no termination = ablation

if someone has sustained monomorphic VT and is hemodynamically stable without stable heart disease what drugs and steps are next in algorithm

verapamil or BB

if no termination = cardioversion

definition of proarrhythmia

capacity of a cardiac or noncardiac drug to aggravate an existing arrhythmia or provoke a new arrythmia at therapeutic or sub therapeutic levels

proarrythmias include:

torsades de pointes

sustained or nonsustained VT

what is torsades de pointes

paroxysmal, polymorphic VT that can degenerate into VF

produces HR of 160-240bpm

is associated with evidence of delayed ventricular repolarization (long QT interval or prominent U waves) on ECG

as HR increases, QT interval _______

shortens

main factor associated with TdP

prolonged QT interval (risk greatest when QTc >500ms, or if it has increased more than 60ms from baseline)

TdP risk factors

QTc interval >500ms

increase in QTc interval >60ms compared w/ pretreatment value

advanced age

female sex

acute MI

I HFrEF

hypokalemia/magnesia/calcemia

bradycardia

diuretic Tx

concurrent administration of >1 QTc prolonging drug

elevated plasma conc of QTc interval prolonging drugs

• inadequate dose adjustment of renally eliminated drugs in pts w/ AKI/CKD

• rapid IV infusion of QTc prolonging drug

• drug int

possible genetic predisopostion

how do drugs cause TdP

usually delay ventricular repolarization in an inhomeogenous way which facilitates formation of multiple reentrant loops in the ventricle

examples of drug causes of TdP

macrolide abx

quinolone abx

antidepressants (Citalopram/escitalopram - many others possible risk)

antipsychotics (haloperidol, chlorpromazine - several atypical are possible risk)

antiarrythmcis- all esp sotolol

antiemetics- ondansetron, droperidol

methadone

pharmacist action if mod-high risk of TdP

contact physician to discuss:

maintain normal Mg, K, Ca

ECG monitoring- where appropriate and feasible

consider an alternate non QTc prolonging drug for pts with high risk

if pt TdP risk score is >/= 7 and pt is taking high risk drug int med what to do (if therapy can’t be altered)

obtain ECG when plasma conc of QTc prolonging drug is at steady state

what to do for hospitalized pts receiving Tx with QTc prolonging drugs

document QTc prior to initiation of Tx, and every 8-12hr following initiation of Tx or dosage increase, increase monitoring if QTc prolongation is observed

ECG monitoring for methadone pts

baseline and repeat at 30 days, annually

first step in algorithm for managing TdP

d/c QT prolonging drugs and correct hypokalemia/hypomagnesia

after you d/c QT prolonging drug and correct electrolytes in TdP what is next for hemodynamically unstable pt

defibrillation

after you d/c QT prolonging drug and correct electrolytes in TdP what is next for hemodynamically stable pts

magnesium sulfate 1-2g IV administered over 15min

treatment for TdP w/ bradycardia (after magnesium sulfate given)

isoproterenol 2-10mcg/min continuous IV infusion

or

rapid pacing via temporary pacemaker

treatment for TdP without bradycardia (after magnesium sulfate)

defibrillation