Treatment of Cardiac Arrhythmias Flashcards
1
Q
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
A
cardiac arrhythmias
2
Q
- most common type of mainly harmless arrhythmias, no need for treatment
- fluttering or skipped beat, PACs or PVCs
- too much exercise, caffeine, nicotine
A
premature (Extra) beats
3
Q
- tachycardias that start in atria or SA node
- a.fib, a flutter, PSVT, WPW syndrome
A
supraventricular arrhythmias
4
Q
- 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
A
atrial fibrillation
5
Q
- 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
A
atrial flutter
6
Q
- 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
A
PSVT
7
Q
tachycardia that start in the ventricles, can be very dangerous, usually require medical care immediately
A
ventricular arrhythmias (v.tach and v.fib)
8
Q
fast but regular beat of ventricles that may last only for a few seconds or much longer, longer episodes can turn into v.fib
A
ventricular tachycardia
9
Q
- 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
A
ventricular fibrillation
10
Q
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
A
bradycardia
11
Q
all arrhythmias result from disturbance of ________ (automaticity) or _________, or both
A
impulse formation
impulse conduction
12
Q
distubance in impulse formation:
- pacemaker rate depends on _______ and duration of diastolic interval
- diastolic interval depends on slope of phase _____ depolarization
A
AP duration
4
13
Q
EADs interrupt phase _____ usually at slow heart rates, can contribute to _______ related arrhythmias
A
phase 3
long QT
14
Q
DADs interrupt phase ____ usually at fast heart rates
A
4
15
Q
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 ______
A
reentry
unidirectional
refractory period
16
Q
antiarrhythmic drugs can either
- slow _____
- change abnormal to normal rhythm
- cannot reliably speed up heart rate (bradycardia needs to be treated with _____)
A
heart rate
pacemaker
17
Q
beta blockers, calcium channel blockers and digoxin provide ______ control
A
rate
18
Q
sodium channel blockers (procainamide, quinidine, disopyramide, flecainide) or potassium channels blockers (amiodarone, ibutilide, sotalol, dofetilide) provide _______ control
A
rhythm
19
Q
-decrease HR by elevating threshold for excitation, decreasing slope of phase 4 depolarization in SA node
A
class 1 Na+ channel blocker
20
Q
- 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
A
class Ia sodium blockers
21
Q
- excessive AP prolongation, QT prolongation, torsades, syncope, new arrythmias
- reversible lupus like syndrome, n/d, hepatitis, agranulocytosis
- does not elevate digoxin levels
A
procainamide
22
Q
-effective against most atrial and ventricular arrythmias, short half life
A
procainamide
23
Q
- 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
A
quinidine (class 1a)
24
Q
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
A
disopyramide
25
- 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
26
- 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
27
- lidocaine analog, resistant to first pass - oral
- neurlogic side effects
- used for ventricular arrythmias
- relief of chronic pain (diabetic neuropathy, nerve injury)
mexiletine
28
-all oral, increase mortality from cardiac arrest or arrythmic sudden death in patients with recent MI
class Ic
29
- blocks sodium and potassium channels, no QT prolongation
- no antimuscarinic
- treats supraventricular arrhythmias
- effective in suppressing premature ventricular contractions
flecainide: class Ic
30
- blocks sodium channels, structurally similar to propranolol, weak beta blocking activity
- metallic taste
- may exacerbate arrythmias and cause constipation
- suppress PVCs
Ic: propafenone
31
- 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
32
- 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
33
- 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
34
- 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
35
- 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
36
- 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
37
- 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)
38
-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)
39
- 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
40
-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
41
- has been used to prevent torsades and for digoxin induced arrhythmias
- MOA unknown
magnesium
42
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
