1. abnormalities in automaticity that give rise to abnormal sites of pacemaker activity
2. "triggered" arrhythmias due to electrical instability
3. abnormalities in conduction, particularly re-entry (most common)

damaged tissue acquires abnormally fast rate of spontaneous depolarization, thus becoming the pacemaker

• Atrial focus causes supraventricular tachycardia
• ventricular cause V-tachycardia

To treat: increase AV node refractoriness or suppress ectopic focus

transient depolarization triggers extra cardiac beats, most often in cells overloaded with Ca++

1. "Delayed" after-depolarization (DAD) - occurs after repolarization; most common w/ catcholamine stimulation and give rise to coupled ventricular extra-beats
2. "Early" after-depolarization (EAD) - occurs during repolarization; most common when repolarization is delayed and can cause Toursades

minimal damage simply delays conduction through AV node

Prolongation of PR-interval

common w/ drugs taht suppress AV conduction (b-blockers, digitalis)

"dropped beats" when node fails to recover in time for next beat

ventricular rate is slower than atrial rate

complete block when there is no conduction of atrial beats to the ventricle

can be due to infarction of nodes

medical emergency

damage to conduction system in a non-critical region

abnormal route of conduction but no arrhythmia

circular currents repetitively stimulate the tissue

damage to segment of contuction system blocks anterograde conduction

slow retrograde conduction delivers an AP into excitable tissue, triggering depolarization and generating a new AP

1. suppress retrograde conduction
2. increase the refractoriness of normal tissue

causes v-tach or v-fib

requires therapy

treate v-tach w/ amiodarone, beta-blockers or class I anti-arrhythmics

causes atrial flutter or a-fib

ventricular response rate determines treatment

can use procainamide, dofetilide, dilitiazem

Paroxysmal atrial tachycardia

use physical maneuvers or suppress AV node conduction

1. if hemodynamic instability - cardioversion
2. if stable - IV antiarrhythmics

1. implantable cardiac defibrillators
2. can use anti-arrhythmic therapy

selective for the damaged tissues b/c:

1. damaged tissues tend to be depolarized more often
2. damaged tissues are more acidic
3. damaged Na channels are more frequently cycling through inactivation/repolarization

induction of arrhythmias, particularly in ischemic heart disease; used only in short-term

1. unmasking of re-entrant circuits in ischemic tissue
2. suppression of SA and AV nodal activity
3. inhibition of K channels and induction of arrhythmias associated w/ delayed repolarization

Detected by broad QRS complex

very specific for Na+ channels; does not affect vagal activity

tends to shorten the duration of the action potential but increases effective refractory period

generally mild and rapidly reversible

overdosage- CNS suppression w/ sedation, hallucinations and convulsions

Rapidly inactivated by liver (t1/2 of 60 min)

IV infusion

Metabolism depends on hepatic blood flow

1. binds to both Na and K channels
2. slowing phase 0 depolarization and prolonging AP due to slowing repolarization rate
3. slows conductino and extends refractory period
4. suppresses phase 4 depolarization (good for ectopic pacemaker activity)

1. acute V-tach
2. acute atrial flutter/fib
3. PAT with WPWS
4. long-term suppression of ventricular and supraventricular arrhythmias

1. cardiac arrhythmias: bradycardia, blocks, tachycardia
2. hypotension and decreased contractility (ganglionic blocking activity)
3. hypersensitivity: lupus-like syndrome (skin rash, arthritis and serositis --> at greatest risk if there is defect in acetylation

1. IV or ORAL
2. T1/2 of 3-4 hours
3. metabolized by acetylation --> NAPA formed, also an active anti-arrythmic w/ longer half life
4. NAPA inhibits K+ channels

Inhibit effects of endogenous catchols, and is useful for long-term suppression of ventricular arrhythmias in patients at risk of "sudden death"

meoprolol and d,l-sotalol

1. endogenous catechols activate Ca channel via cAMP
2. b-blockers compete w/ catechols for B1-adrenergic receptors

• decreased contractility, HR, conduction through AV node, and myocardial excitability

treat patients w/ increased adrenergic activity and elevated catechols

1. stress - surgical or anesthetic stress
2. CHF and ischemic heart disease
3. hyperthyroidism

Patients at risk for "sudden" cardiac death (post MI)

1. cardiac arrhythmias by suppressing nodes
2. worsening of CHF by decreasing CO and contractility
3. bronchospasm if B2 receptor blocked

1. d,l-sotalol - beta blocker + class III
2. metoprolol - beta1 selective

1. l-sotalol - non-selective beta blocker
2. d-sotalol - class III inhibitor of K+ channel

1. long-term suppression of ventricular arrythmias and those at risk of sudden death
2. adjunct to ICD, decreasing # of electrical events that require defibrillation
3. people at risk for supraventricular tachycardias

1. lower doses: beta blocker predominates and get expected side-effects
2. higher doses: K+ blocker is manifest and can get v-tach

non-selective b1,b2 antagonist

long t1/2 of 20 hours

block cardiac K+ channels (I_kr)

suppress many arrhythmias associated w/ re-entry

amiodarone is prototype

Class III: inhibits both K and Na channels as well as beta-adrenergic receptors

used extensively for acute suppression of ventricular arrhythmias b/c it has little cardiac toxicity

Is also used fro chronic suppression

very similar to thyroxine (has iodine)

1. acutely: IV inhibits K+ channel
2. chronic: ORAL for long-term alterations that decrease both Na and K activity as well as beta-adrenergics

1. IV - suppress V-tach/fib
2. IV - suppress atrial fib
3. Oral - suppress refractory ventricular arrhythmias (unresponsive to other treatments)

very few cardiac side effects, but precipitates in extracardiac tissues

1. pulmonary fibrosis - depostis in lungs causing irreversible damage
2. corneal deposits
3. rash - bluish discoloration and photodermatitis

Also can lead to thyroid dysfunction

1. Poor oral availability
2. very lipophilic so extensively partitioned
3. IV for acute effects that last for hours
4. Oral has very slow onset (takes 3-15 weeks)
5. clearance takes months after therapy terminated

polymorphic ventricular tachycardia (toursades) has impaired K+ channel activity

Responds well to IV Magnesium

1. tachycardia due to rapid ventricular response
2. thrombo-embolic stroke
3. CHF

1. control of ventricular response rate
2. cardioversion (to prevent thromboembolism)
3. suppression

1. beta blocker - IV propanolol (acute) or oral metoprolol (chronic)
2. Ca channel blocker - IV verapamil or oral diltiazem
3. Digitalis - increases vagal tone - can be oral or IV

Always accomplished in combination with a rate control drug to prevent increased condution of atrial beats

Used Class I (procainamide) or class III (amiodarone or dofetilide)

done w/ long-term suppression

1. class I flecainide - blocks both Na and K channels only if they do not have IHD
2. Class II beta blockers
3. Class III
4. Digitalis

caused by re-entry through AV node

1. Use physical maneuvers
2. Adenosine - transient use, binds to purinergic receptors, extremely effective for this use
3. Verapamil - ca channel blocker - longer half life - dont use in WPWS
4. Beta blocker
5. digitalis

due to SA node or AV node disease

best handled w/ a pacemaker

if due to inc vagal tone, treat w/ IV atropine