Treatment of Cardiac Arrhythmias Flashcards
due to abnormal electrical activity in the heart
- cardiac: HTN, abnormal heart valve function, CAD, CHF
- non cardio: hyperthyroidism, autonomically mediated, alcoholism, sleep apnea, obesity
cardiac arrhythmias
- most common type of mainly harmless arrhythmias, no need for treatment
- fluttering or skipped beat, PACs or PVCs
- too much exercise, caffeine, nicotine
premature (Extra) beats
- tachycardias that start in atria or SA node
- a.fib, a flutter, PSVT, WPW syndrome
supraventricular arrhythmias
- most common type of serious arrhythmia
- electrical signals do not begin in SA node but other parts of atria or pulmonary vein, results in irregular fast heart beat
- blood pools in atria and can form clots, causing stroke
atrial fibrillation
- similar to Afib but regular fast heart beat, 250-350 bom
- atria beat faster than the ventricles
- if ventricular rate is less than 120 bpm people normally have no symptoms, much less common
atrial flutter
- regular heart rate at 150-250 bpm, begins and ends suddenly
- signals beginning in atria travel to ventricles can reenter the atria, resulting in extra heartbeats
- more common in young people
- due to alcohol, caffeine, vigorous activity, WPW syndrome
PSVT
tachycardia that start in the ventricles, can be very dangerous, usually require medical care immediately
ventricular arrhythmias (v.tach and v.fib)
fast but regular beat of ventricles that may last only for a few seconds or much longer, longer episodes can turn into v.fib
ventricular tachycardia
- most serious arryhthmia
- uncontrolled irregular beats up to 300bpm
- chaotic, little blood pumped
- if not converted to normal rhythm with electric shock death will occur in minutes
- can occur during or after heart attack or due to weakened heart
ventricular fibrillation
heart rate <60 bpm, impulse not formed by SA node or not conducted properly to ventricles
- mainly in elderly
- CNS might not signal properly, SA node might be damaged, could be due to drug use
bradycardia
all arrhythmias result from disturbance of ________ (automaticity) or _________, or both
impulse formation
impulse conduction
distubance in impulse formation:
- pacemaker rate depends on _______ and duration of diastolic interval
- diastolic interval depends on slope of phase _____ depolarization
AP duration
4
EADs interrupt phase _____ usually at slow heart rates, can contribute to _______ related arrhythmias
phase 3
long QT
DADs interrupt phase ____ usually at fast heart rates
4
disturbances in impulse conduction can be due to ________, a common conduction abnormality
- conduction has to be blocked and the block must be _______
- conduction time around block must exceed ______
reentry
unidirectional
refractory period
antiarrhythmic drugs can either
- slow _____
- change abnormal to normal rhythm
- cannot reliably speed up heart rate (bradycardia needs to be treated with _____)
heart rate
pacemaker
beta blockers, calcium channel blockers and digoxin provide ______ control
rate
sodium channel blockers (procainamide, quinidine, disopyramide, flecainide) or potassium channels blockers (amiodarone, ibutilide, sotalol, dofetilide) provide _______ control
rhythm
-decrease HR by elevating threshold for excitation, decreasing slope of phase 4 depolarization in SA node
class 1 Na+ channel blocker
- procainamide, quinidine, disopyramide
- increase effective refractory period of atria and ventricles, can directly depress SA and AV nodes, prolong APD by nonspecific blocking K+ channels (QT prolongation)
- has ganglion blocking activity which reduces peripheral vascular resistance, can lead to hypotension
class Ia sodium blockers
- excessive AP prolongation, QT prolongation, torsades, syncope, new arrythmias
- reversible lupus like syndrome, n/d, hepatitis, agranulocytosis
- does not elevate digoxin levels
procainamide
-effective against most atrial and ventricular arrythmias, short half life
procainamide
- similar effects as procainamide, slows upstroke of AP, slows conduction
- QT prolongation due to K+ channel blocking
- modest antimuscarinic effect
- blocks alpha receptors to cause vasodilation
- precipitates digoxin toxicity, thrombocytopenia, cinchonism
- rarely used
quinidine (class 1a)
1a with more antimuscarinic effects
- pronounced atropine like activity - urinary retention, dry mouth, blurred vision, constipation, worsening of glaucoma
- may induce CHF, only approved to treat ventricular arrhythmias
disopyramide
- blocks activated and inactivated sodium channels with rapid kinetics
- blocks channels in Purkinje fibers and ventricular cells to elevate excitation threshold and reduce automaticity
- suppress electrical activity of depolarized diseased tissue, has minimal effect on normal or atrial tissues
- does not affect K+ channels
lidocaine, class Ib
- least cardiotoxic of currently used sodium blockers
- larger doses can depress myocardial contractility
- neuro: parasthesias, tremor, slurred speech, convulsion
- seizures after IV admin in elderly
- must be given IV, ineffective in atrial flutter/fib
- agent of choice for termination of ventricular tachycardia and to prevent v.fib after cardioversion
lidocaine, Ib
- lidocaine analog, resistant to first pass - oral
- neurlogic side effects
- used for ventricular arrythmias
- relief of chronic pain (diabetic neuropathy, nerve injury)
mexiletine
-all oral, increase mortality from cardiac arrest or arrythmic sudden death in patients with recent MI
class Ic
- blocks sodium and potassium channels, no QT prolongation
- no antimuscarinic
- treats supraventricular arrhythmias
- effective in suppressing premature ventricular contractions
flecainide: class Ic
- blocks sodium channels, structurally similar to propranolol, weak beta blocking activity
- metallic taste
- may exacerbate arrythmias and cause constipation
- suppress PVCs
Ic: propafenone
- propanolol (nonselective) and acebutolol (B1 selective) are most frequently used
- for supraventricular and ventricular arrhytmias caused by symapthetic stimulation
- to prevent ventricular fibrillation
- esmolol (b1) is short acting, used for acute arrythmias during surgery
- can be used for rate control
Class II beta blockers
- beneficial effects due to diminished sympathetic activation of heart and blood vessels
- reduced cardiac activity, reduced vasoconstriction
- diminished cardiac workload leads to reduced myocardial oxygen demand
- prevent recurrent infarction and sudden death in patients with acute MI
- averse: negative inotrop, may indue or worsen HF, CNS penetration
Class II: beta blockers
- oral or IV to maintain normal sinus rhythm in patients with a.fib or prevent recurrent v.tach
- prolongs AP duration and QT interval by blocking K channels
- decreases rate of firing in pacemaker cells by blocking inactivated Na channels
- blocks alpha and beta adrenergic receptors and Ca2+ channels and inhibits AV node conduction to produce bradycardia
- causes peripheral vasodilation after IV admin
class III: potassium blockers, amiodarone
- toxicity:
- asymptomatic bradycardia and AV block in patients with SA/AV node disease
- respiratory –> fatal pulm fibrosis
- hepatitis
- photodermatitis, gray blue skin discoloration
- corneal microeposits, optic neuritis
- blocks T4 to T3 conversion
- hypo or hyper thyroidism
- long half life, toxicity long after discontinuation
- metabolized by CYP3a4
amiodarone toxicity
- structural analog of amiodarone but no iodines
- blocks K and Na channels
- no thyroid dysfunction or pulmonary toxicity, but there is liver toxicity
- black box: increased risk of stroke, death, heart failure in patients with decompensated heart failure or permanent a. fib
dronedarone
- non selective B-blocker that prolongs APD and has antiarrhythmic properties
- may cause prolonged repolarization resulting in torsades
- treates life threatening ventricular arrhythmias, maintains sinus in a.fib, treat supraventricular and ventricular arrhythmias in pediatrics
sotalol
- block rapid component of delayed rectifier K current to slow cardiac repolarization
- good to restore normal sinus rhythm in a fib or flutter
- prolonged QT and torsades
dofetilide (oral), ibutilide (IV)
-orally active, block L-type calcium channels in myocardium and vascular smooth muscles
-depress SA and AV nodes directly to decrease contractility, reduce SA node automaticity, slow AV node conduction
-orally use for treament of supraventricular arrythmias and for rate control in a.fib
-
class IV: CCBs (verapamil, diltiazem)
- opens inward rectifier K+ channels, causing hyperpolarization
- inhibits L type calcium channels, inhibits calcium entry and conduction velocity in AV node
- inhibits pacemaker current, decreases HR
- mainly affects AV node
- by IV injection to convert PSVTs to sinus rhythm
- adverse: flushing, SOB, headache, hypotension, paresthesia
adenosine
-potent and selective inhibitor of Na/K ATPase, increased calcium, positive inotrope
-stimulate vagus nerve and decreases HR, can be used in a.fib
-narrow therapeutic window: quinidine, amiodarone, captopril, verapemil, diltiazem, and cyclosporine enhance toxicity
-K competes for binding to Na/K ATPase, so drugs that produce hypokalemia (thiazide and loop diuretics) will enhance toxicity
-toxicity: GI, can cause almost all arrhythmias
-
digoxin
- has been used to prevent torsades and for digoxin induced arrhythmias
- MOA unknown
magnesium
contraindications:
- prostatism for _______, causes urinary retention due to anticholinergic activity
- chronic arthritis for _______, causes lupus like syndrome
- advaned lung disease for ________, causes pulmonary fibrosis
disopyramide
procainamide
amiodarone
