Unit 4 - Anti Arrhythmics Flashcards
(59 cards)
1
Q
what kinds of arrhythmias occur when there is normal automaticity?
A
sinus rhythm problems
- bradycardia
- tachycardia
ectopic activity/focus
-Purkinje > atrium/ventricle
2
Q
what kinds of arrhythmias occur when there is abnormal automaticity?
A
“triggered” activity
- early afterdepolarizations (EADs)
- -develop during phase 3 repolarization
- -decreased K+ currents (blocking repolarization)
- -increased Ca,L and Na+
- delayed afterdepolarizations (DADs)
- -develop during phase 4 (resting, diastole)
- -decreased K1 currents
- -increased diastolic Na+, Ca++ influx
- –decreased NCX and Na/K-ATPase, increased Ca++
3
Q
what happens when there is re-entrant arrhythmias? what favors it?
A
3 prerequisite conditions
- unidirectional block
- slow conduction
- conduction time > refractory time
favored by:
- tissue heterogeneity (refractory period, gap junction coupling, fibrosis)
- extrasystoles in atria and ventricle
4
Q
what are major determinants of conduction velocity, and how they change in arrhythmias?
A
- cardiac Na current decreases (increases threshold)
- length constant decreases (decreases membrane resistance; increases gap junction and extracellular resistance)
- fibrosis increases
- cell size (membrane capacitance)
5
Q
what is bradycardia? its causes?
A
abnormally slow HR (<60 bpm)
- depressed impulse formation
- impaired impulse conduction (block)
- excessive vagal tone
- hyperkalemia (severe may cause block)
- hypothyroidism, sleep apnea
- Rx (BB, CCA, ACh, adenosine)
6
Q
what is sick sinus syndrome? what is it associated with?
A
occurs in elderly > 65 yo
- disease of SA node, unknown origin
- sometimes occlusion of SA artery
- SA block not uncommon with SA bradycardia
7
Q
what are treatments for sinus bradycardia/block?
A
- treatment of causative medical condition
- alter medications
- artificial pacemaker if refractory
8
Q
what are the degrees of atrio-ventricular nodal blocks? treatments? associations? severity?
A
1st: prolonged PR interval, but normal 1:1 P wave to QRS complex (transmission of atria to ventricles)
2nd: dropped beats (not every P wave followed by QRS complex)
- Mobitz I: PR interval progressively prolongs until beat is dropped (Wenckebach)
- -excess vagal tone; responds to atropine but not sympathetic stimulation
- Mobitz II: PR interval constant in a P:QRS association pattern (more serious, may progress to full block)
3rd: complete AV block (most severe)
- no consistent PR itnerval, requires ventricular pacemaker (no activation)
- associated with trifascicular blocks
9
Q
what are fascicular blocks? ECG traits?
A
hemiblocks
- left anterior fascicle (left axis deviation)
- left posterior fascicle (right axis deviation)
10
Q
what do atrial premature systoles look like?
A
early occurance of a P-wave that may:
- be followed by normal QRS complex
- be blocked by AV node if too early
- block in bundle branches
- reset sinus rhythm (phase resetting)
11
Q
what do junctional premature systoles look like?
A
premature and/or inverted P wave
- originate from AV node/bundle
- may be preceded by inverted P wave (retrograde conduction)
- may be followed by normal QRS complex
- may block sinus beat
- -compensatory pause is delay until next normal sinus rhythm
12
Q
what do ventricular vextrasystoles look like?
A
abnormal QRS complex
- originate below bifurcation of His bundle (not preceded by P wave)
- asynchronous ventricular activation (prolonged QRS)
- may produce compensatory pause (block normal SAN impulse thru AVN)
13
Q
what are mechanisms for tachycardias?
A
- accelerated automaticity
- triggered activity (EAD, DAD)
- abnormal conduction
- AP inhomogeneity
- -depolarization (phase 0)
- -repolarization and refractoriness (phases 1-3)
- -resting potential (phase 4)
- abnormal conduction structures
- -accessory pathways
- -dual AV node pathways
14
Q
for the following types of tachycardia, what are the P-wave, PR interval, and onset of termination?
A
sinus: normal P wave, normal/prolonged PR interval, and gradual onset/termination
atrial: abnormal (not conducting) P wave, normal/prolonged PR interval, and paroxysmal onset/termination
junctional: retrograde (inverted) P wave, short/absent PR interval, and paroxysmal onset/termination
15
Q
what is sinus tachycardia? causes? treatment?
A
abnormally rapid HR > 100 bpm
- excessive symapthetic tone, pheochromocytoma
- sinus node re-entry
- hypotension (postural, blood volume)
- anemia, sepsis, shock
- anxiety, fever
- cardiac ischemia/infarction, heart failure
- pulmonary embolism or COPD
- stimulants (nicotine, caffeine, cocaine)
treated w/ carotid massage, Ach, B-blockers, AVn blocking agents, catheter ablation (may need pacemaker), If blocker
16
Q
what is SAN reentry? mechanism? prevalence? treatment?
A
due to SAN reentrant conduction
- rare
- paroxysmal
- terminate by electrical stimulus
17
Q
what is automatic atrial tachycardia? mechanism? prevalence?
A
due to ectopic atrial pacemaker
- rare
- non-paroxysmal, ectopic foci
- may precede flutter or fibrillation
18
Q
what is atrial reentry? mechanism? prevalence? treatment
A
due to atrial reentrant conduction
- rare
- paroxysmal, extrasystole trigger (140 bpm)
- terminated by electrical stimulation, but not responsive to vagal tone
19
Q
what is automatic AV junctional tachycardia? mechanism? prevalence? treatment?
A
due to ectopic His bundle pacemaker
- rare
- non-paroxysmal, ectopic foci
- variable rate (brady or tachy)
- no retrograde P waves, short PR interval, QRS
- slowed, not terminated, by vagal stimulation, adenosite
- commonly caused by cardiac glycoside toxicity
20
Q
what is AV node reentry? mechanism? prevalence? treatment?
A
due to dual AVN conduction pathways
- most common (2/3)
- dual conduction pathways, paroxysmal, extrasystole trigger
- -depends on Ca,L
- terminated by vagal tone, adenosine, BBs, CCBs
21
Q
what is bypass tract reentry? mechanism? prevalence?
A
due to AVN and bypass tract reentry
-second most common (20%)
22
Q
what is paroxysmal supraventricular tachycardia? mechanism? treatment?
A
paroxysmal atrial tachycardia
- typically AVN reentry accessory pathway
- initiated by extrasystole
- responds to vagal stimulation (carotid sinus massage)
- adenosine, beta-blockers, CCBs
23
Q
what is Wolff-Parkinson-White syndrome?
A
“fast” accessory pathway (outside nodes)
- typically atrial origin, bundle of Kent
- initiated by extrasystole
- shortened PR interval
- pre-excitation, delta-wave, wide QRS
- not responsive to vagal tone
- AVN blockers contraindicated
- treat with amiodarone, procainamide, cardioversion, ablation
- hi risk for sudden death
24
Q
what are types of ventricular tachycardia?
A
monomorphic (uniform)
- spontaneous extrasystoles (>3 PVCs)
- sustained (>30 seconds)
- -fusion beat has fused PVC and normal impulse
polymorphic (non-uniform)
- Torsades de Pointes (TdP), long QT syndrome
- -14 genes, drug induced, EADs
- catecholamine-induced polymorphic VT (CPVT)
- DAD mechanism, extrasystoles (glycosides)
- deficient Ca++ cycling
- exercise-induced
- beta-blockers
- ICD
- sympathectomy (left cardiac)
25
what is long QT syndrome 1? channel affected? induced by? treatment?
50% of them
- associated with Ks channel
- induced by exercise or emotion
- treated with B-blockers, L cardiac nerve denervation
26
what is long QT syndrome 2? channel affected? induced by? treatment?
40% of them
- associated with Kr channel
- induced by sleep, auditory, or post-partum
- treated with [K+]o therapy (BB less effective)
27
what is long QT syndrome 3? channel affected? induced by? treatment?
10% of them
- associated with Na channel
- induced by rest, sleep, bradycardia
- BB are less effective, so must block late Na "window" current
28
what does atrial flutter look like? treatment? severity?
rapid atrial rate (250 to 350 bpm)
- sawtooth F-wave pattern
- -QRS normal
- -AV dissociation (regular pattern)
- vagal stimulation and CCBs not effective
- not life-threatening unless transmitted to ventriclesapid rate (WPW)
29
what does atrial fibrillation look like? treatment? severity?
most common cardiac arrythmias
- leading cause of stroke (thrombosis)
- irregular atrial rate (400-500 bpm)
- anticoagulants, rate control, and anti-arrythmics are necessary for the rest of life if chronic and sustained
- -ablation therapy is inexact
- increased risk of stroke, HF, and SCD if gets to ventricles
30
what does ventricular flutter look like? treatment? severity?
lethal arrythmia if not treated
- no effective ventricular contraction
- cardioversion required
- no QRS or T waves
- rapid reentrant rhythm
- ICD
- DON'T give antiarrythmic drugs, as they could be proarrhythmic
31
what does ventricular fibrillation look like? treatment? severity?
lethal arrythmia if not treated
- no effective ventricular contraction
- cardioversion required
- no QRS or T waves
- rapid reentrant rhythm
- ICD
- DON'T give antiarrythmic drugs, as they could be proarrhythmic
32
what is parasystole?
slow automatic ventricular rhythm
- ectopic ventricular pacemaker origin
- abnormal QRS
33
what is bigeminy?
PVC after every sinus beat
34
what is trigeminy?
PVC after every 2nd sinus beat
35
what is overdrive suppression?
rapid stimulation suppression of normal pacemaker activity
36
what is syncope?
sudden loss of consciousness due to lack of blood the brain
37
what is the mechanism of action for class Ia antiarrhythmic drugs? names?
fast (open) Na+ channel block (oldest ones)
- prolongs effective refractory period
- prolongs action potential duration
- depress phase 0
quinidine, procainamide, disopyramide
38
what is quinidine? uses? toxicities? drug interactions?
class 1a antiarrythmic drugs
- use: chronic treatment of atrial flutter, fibrillation, SVT
- -alpha-adrenergic and M2 blockade, vagal inhibition
- -hypotension, sinus tachycardia
- toxicities: diarrhea, nausea, fever, hepatitis, thrombocytopenia, cinchonism, QT prolongation (TdP)
- -may increase AVN transmission
- drug interactionsL digoxin (plasma binding to albumin), CYP2D6 inhibition
- -metabolism induced by phenobarbital, phenytoin
39
what is procainamide? uses? toxicities?
class 1a antiarrythmic drugs
- use: chronic treatment of atrial flutter, fibrillation, SVT, ventricular fibrillation
- -local anesthetic properties, but no alpha-adrenergic or M2 blockade
- toxicity: drug-induced lupus syndrome (slow acetylators), QT prolongation (TdP), active metabolite, hypotension (ganglionic blockade)
40
what is disopyramide? toxicities?
class 1a antiarrythmic drugs
- no alpha-adrenergic blockade
- prominent anticholinergic action (constpiation, dry mouth, glaucoma)
- QT prolongation (TdP)
41
what is the mechanism of action for class Ib antiarrhythmic drugs? names?
Na+ channel block (open, inactivated); better at treating ischemia
- prefers depolarized (ischemic) tissue Na+ channel blockade
- prefers inactivated Na+ channels, rapidly unbinds at rest
- depress phase 0 in abnormal fibers
- shorten repolarization
- little effect on phase 0 in normal tissue
- lidocaine, mexiletine
42
what is lidocaine? uses? toxicities?
class 1b antiarrythmic drugs (NOT for atrial arrythmias)
- use: acute suppression of VF
- -local anesthetic (IV only; first pass metabolism)
- -emergency VT/VF, cardioversion, digitalis toxicity
- toxicities: tremor, nausea, seizures
- -no QT prolongation, may shorten APD slightly
- -late Na+ channel blockade
43
what is mexiletine?
```
class 1b antiarrythmic drug
oral lidocaine, but severe GI toxicity (not used anymore)
-metabolism induced by phenytoin
```
44
what is tocainide?
class 1b antiarrhythmic drug
- causes fatal bone marrow aplasia, pulmonrosis
- not in US
45
what is the mechanism of action for class Ic antiarrhythmic drugs? names?
1. Na+ channel block (slow unbinding, greatly prolongs Na recovery
2. K+ channel blockade (prolongs APD preferentially at faster rates)
- prolongs PR, QRS, QT interval, but no EA or TdP
flecainide, propafenone, moricizine
46
what is the use of class 1c antiarrythmic drugs? metabolism?
acute management of atrial fibrillation, SVT, but NEVER for ventricular arrythmias (strongest blockers)
- primary maintenance of sinus rhythm in chronic AF, SVT in patients w/o structural heart disease
- renal and CYP2D6 elmination
47
what is special about propafenone?
1c antiarrythmic drug that has beta-blocking activity (S-(+))
- 5-hydroxy metabolite lacks B-blocker activity, butll blocks Na
- -formed by CYPD2D6 first pass metabolism
48
what are toxicities of class Ic antiarrythmic drugs?
- may increase ventricular response to atrial flutter
- -contraindicated in heart failure, VT
- increased mortality in patients with acute MI (would kill pt)
- flecainide: blurred vision
- propafenone: sinus bradycardia, bronchospasm (due to beta-blocking properties)
49
what are class II antiarrythmic drugs? contraindications? names?
B1 adrenergic selective receptor blockers
- metoprolol: lipophilic, membrane stabilizing
- -improves mortality in CHF patients
- acebutolol: same, but with intrinsic sympathomimetic activity
- esmolol: IV, short half-life, used in acute emergency treSVTs when short duration desired
contraindicated in WPW syndrome, and sudden withdrawal in angina patient may cause MI
50
what is the mechanism of class III antiarrythmic drugs? major toxicity?
K+ channel blockade to prolong refractoriness
- major toxicity is risk of TdP arrythmias (strongly pro-arrythmic, not to treat ventricular arrythmias)
- sotalol, ibutilide, dofetilide, amiodarone, dronedarone
51
what is sotalol? side effects?
class III antiarrythmic drug
- blocks Ks, non-selective B-blocker
- preferred over quinidine for control of chronic AF
- ASE: EADs, TdP, decreased HR, decreased AV conduction
52
what is ibutilide?
class III antiarrythmic drug
- IV for termination of atrial flutter or fibrillation
- first pass metabolism renders oral dose ineffective
- for emergency settings
53
what is dofetilide?
class III antiarrythmic drug
- Kr blocker "restricted distribution", oral
- maintain sinus rhythm after cardioversion, convert chronic AF
- NOT for ventricular arrythmias or paroxysmal AF
54
what is amiodarone? uses? side effects?
class III antiarrythmic drug, thyroxine analog (although mixed action mimic all classes)
- decreases Na+, Ca++, and K+ currents
- alpha/beta adrenergic blocking effect
- prolongs ERP, APD
- useful against most all arrythmias, but NOT digitalis toxicity, and not during pregnancy
ASE: QT prolongation (TdP rare), pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, corneaicrodeposits, numerous drug interactions, photosensitivity (blue-gray skin)
55
what is dronedarone?
class III antiarrythmic drug
- benzofurane (not used as often)
- less effective but fewer side effects than amiodarone
- QT prolongation, nausea, diarrhea
56
what are class IV antiarryhmic drugs?
L-type Ca++ channel blockade
- slow SA, AV node activity
- prolong AV refractoriness
57
what do verapamil and diltiazem do?
slow ventricular rate during atrial flutter or a-fib
- prevent or terminate reentrant SVTs, contraindicated in WPW
- IV use hypotension, bradycardia, constpiation, diz
- will increase serum digoxin levels, AV block effects additive oxin, beta-blockers
58
what is adenosine?
natural nucleoside, IV bolus only
- GPCR-mediated decrease in cAMP
- beta-gamma mediated increase in K,ACh
- decrease SA, AV node activity
- increase AV refractoriness
- will terminate PSVT, AVN reentrant arrythmias
- -NOT atrial flutter, a-fib, multifocal atrial tachycardia, or WPW
- antagonized by methyl xanthines, sedationea, hypotension
- -may cause reflex sympathetic activation
59
how is Mg used in arrythmias?
MgSO4
- prevent recurrent TdP and some digitalis-induced arrythmias
- alternative to amiodarone for shock-refractoy cardiac arrest
