Arrythmias

Physiology of Normal Rhythm Generation

Automatic Rhythms

pacemaker cells: undergo spontaneous phase 4 depolarization to threshold Þ set the automatic rhythm of the heart

SA node: the dominant pacemaker under normal conditions; fires at 60-100 bpm
escape pacemakers: other areas of the heart are capable of spontaneous depolarization

AV Node and Junction, specialized fibers of the atria, His-Purkinje system (40-60 bpm)
bundle branches and other areas (< 40 bpm)
normal rate of these pacemakers is lower than the normal rate of the main pacemaker (SA node)
they are normally suppressed by the sinus node (overdrive suppression), but when the sinus node fails, they take over and fire spontaneously, setting the pace of the heart

Potential Pacemakers of the Heart

SA Node – normal: 60-100 BPM (kept in this range by the Vagus Nerve).

SA node function during exercise:

Early Exercise – Vagus stops influencing node (moderate increase in HR)

Late Exercise – Catecholamines (more significant increase in HR)

AV Junction – this region includes the AV node and Bundle of His. Inherent automaticity: 40-60 BPM.

Ventricular Myocardium – Inherent automaticity: 15-20 BPM.

3 Parts of AV Conduction:

Intra-atrial (0.02 sec)
AV nodal (0.10 sec) – bulk of PR interval
His-Purkinje (0.04 sec)

Normal PR interval = 0.12-0.20 sec

Normal QRS = 0.06-0.10 sec

P wave = 100 msec

QRS wave = 100 msec

PR interval = 200 msec

Vagal Stimulus

5 ways to Ý vagal stimulus: Carotid sinus massage, valsalva maneuver, diver’s reflex (cold water on the face), eyeball pressure, adenosine.

Response to vagal stimulus: Prolongs AV node refractoriness and conduction, prolongs SA node firing.

Arrhythmias which have an obligatory circuit via the AV node (AVNRT, AVRT) will be extinguished by Ý vagal tone! Arrhythmias which do not have a circuit or are not dependent on the AV node will not be affected by Ý vagal tone (atrial flutter, etc).

Overview of Arrhythmias

Sinus Node

Sinus Arrhythmia

Sinus Bradycardia – HR < 60

Sinus Tachycardia – HR > 100

"Sick Sinus Syndrome" – Results in symptomatic bradycardia. Patients can’t Ý their HR with exercise.

Atria

Premature Atrial Complex (PAC) – most common cause of refractory pause between two normal beats.

Atrial Tachycardia

Atrial Flutter – Circuit goes at 300 BPM but only half the beats conduct through the AV node (2:1).

Atrial Fibrillation – Unorganized, chaotic circuits. 400-600 BPM. Irregularly Irregular.

Ventricles

Premature Ventricular Complex (PVC) – Caused by an ectopic site in the ventricle. Only a single beat.

Ventricular Tachycardia – Ectopic site in ventricle. Need 3 or more beats at a rate ³ 100.

Ventricular Fibrillation – Like atrial fibrillation but in ventricles. Fatal.

Supraventricular Tachycardia

AV Nodal Reentrant Tachycardia (AVNRT) – Fast but normal looking QRS complexes. P waves not seen because are buried in the QRS complex. A circuit forms in the AV node thus firing both into atria and ventricles almost simultaneously.

Accessory Pathway – most common is AVRT

AV Reentrant Tachycardia (AVRT) – Anterograde conduction through AV node and back up to atria via an accessory pathway. P waves will be visible and inverted, located after the QRS. The most important example of this is the Wolff-Parkinsons-White Syndrome (WPW).

Arrhythmia due to Normal or Abnormal Pulse Initiation – these are all very RARE

(1) Arrhythmias due to Normal Mechanism

Sinus Arrythmia:sinus rhythm >100 or <60, but sinus node is still dominant pacemaker; not necessarily pathologic (exercise can easily push you into tachycardia; a well-trained athlete can have bradycardia as low as 35)

tachycardia is always secondary to some extrinsic factor (exercise, fever, hypotension, etc)
bradycardia can be caused by intrinsic abnormality of pacemakers, parasympathetic dysautonomia, or extrinsic suppression (drugs); bradycardia also reflects abnormality in escape nodes (they were supposed to kick in!)
beat-to-beat irregularities in cycle length are also considered arrhythmias, even if the overall rate is normal

Ectopic Automatic Rhythms: occurs when site of dominant pacemaker shifts away from SA node; some etiologies:

sinus node dysfunction causes the rate to slow so that an escape pacemaker takes over
enhanced automaticity of the ectopic pacemaker causes its rate to increase so that it takes over the sinus node
the normal sinus node is prevented from being the dominant pacemaker:

sinus node exit block, or sinoatrial block (impulse never leaves the node)
AV block (AV node, His bundle, or bundle branches)

(2) Arrythmias due to Abnormal Mechanism

normal, working atrial and ventricular myocytes do not have automaticity (no phase 4 depolarization, but they can develop an abnormal type of automatic firing usually due to intrinsic cardiac disease
this abnormal current is NOT due to the normal pacemaker current (i.e. the "funny" Na⁺ channels)
occurs when cells are less hyperpolaized (Na⁺ channels close); current may be due to slow L-type Ca⁺⁺ channels
this automaticity will not be evident unless the rate is faster than that of the dominant pacemaker
MI often causes automaticity in Purkinje cells in the damaged region

(3) Arrythmias due to Afterdepolarizations

a normal action potential can trigger additional depolarizations that lead to extra beats or arrythmias

Early Afterdepolarizations (EAD): spontaneous depolarization during phase 2 or phase 3 (i.e. before repolarization is complete); the cell may then continue to repolarize, or it may lead to self-perpetuating depolarizations

Delayed Afterdepolarizations (DAD): occur after repolarization is complete, early in phase 4

usually, this is due to digitalis toxicity in which intracellular Ca⁺⁺ is very high

Arrhythmias due to Abnormal Pulse Conduction – most common mechanism of arrhythmias

(1) Prolongation of Conduction Time

can occur anywhere in the heart; may be general or localized (i.e. part of AV conduction system, or locus of MI)
may be due to slower transduction or farther path; can therefore occur in abnormally long but normally conducting tissue (i.e. in a septal defect where the impulse must take a long route around)
prolongation is most important in its contribution to ordered reentry (see below)

(2) Conduction Block:

can occur when:

(1) impulse encounters inexcitable tissue (abnormally depolarized or still in refractory period);
(2) strength of the impulse is too weak to propagate through normal tissue; or
(3) impulse encounters tissue that is not excitable (i.e. scar tissue)

if sinus node exit block or sinoatrial block Þ a latent or "escape" pacemaker will take over (e.g., if the AV conduction system is blocked, a pacemaker distal to the block will usually emerge); problems occur when a pacemaker does not emerge, or emerges too late, or results in bradycardia

types of AV node conduction block:

1^st degree: slow conduction through AV Þ prolonged P-R interval, 1:1 conduction

2^nd degree: some impulses are conducted, but not all

Type I (Wenkebach, or Mobits Type I): P-R interval prolongs progressively, then a beat drops; usually results in 2:1 or 3:1 or 4:1 conduction, etc.; Type I is usually due to AV block

Type II (Mobits type II): P-R interval is constant, but every few beats are dropped; usually due to block of the His system; Type II block is high risk, and absolute indication for a pacemaker

3^rd degree: no atrial beats go to ventricle; results in atrial and ventricular rates that are both constant (atrial is faster)

AV dissociation: any situation where the atria and ventricles are beating independantly

usually, there is a retrograde conduction block so that the ventricles cannot excite atria; anterograde conduction is maintained, so atrial impulse can override ventricular pulse depending on state of ventricular refractoriness
note: tissue in its relative refractory period can still conduct, but conduction is slower than normal
bundle branch blocks are seldom clinically significant unless both are blocked

(3) Unidirectional Block and Reentry: the cause of almost all clinically important tachyarrythmias

conditions for reentry:

(1) excitable substrate – cardiac tissue able to support reentry must be present
(2) central area of block (anatomic or functional) around which the impulse can travel
(3) unidirectional block that the excitation wavefront must encounter

also, the wavelength (Effective Refractory Period x Conduction Velocity) must be shorter than the path length, so that by the time the impulse gets back to the original point, the tissue is no longer refractory
an area of slow conduction shortens wavelength; although not necessary if path is long enough, most reentry circuits are quite short, so slow conduction exists in almost all clinically relevant reentry circuits

a simple example (Mayer’s 1966 jellyfish experiment):

if you stimulate a loop, the wave will propagate around both directions and cancel on the other side

if you stimulate again, and place a unidirectional block on one side, the unblocked side will continue to travel until it reaches the block; it will chase its tail through the block and continue around the loop only if the tissue in the tail has cleared its refractory period Þ this situation occurs if conduction is slow enough, or the path is long enough to allow repolarization to occur before the wavefront comes around again

clinically, this results in classical circus movement (reentrant excitation)

(a) Ordered Reentry: impulse travels in same circuit over and over; usually, circuit is a well-defined anatomic pathway

example: Wolff-Parkinson-White (WPW) arrhythmia – impulse travels from AV node, through the His-Purkinje system, down bundle branch, then retrograde through an accessory AV junction to get back to AV node

normally, the impulse travels anterograde through the accessory junction, but a premature beat can cause a block at that junction, as well as a slowing of the impulse Þ the ingredients for reentry!

this occurs in atrial flutter, AV Reentry Tachycardia (AVRT), AV Nodal Rentry Tachycardia (AVNRT)

also may occur in the ventricle, usually secondary to MI (slow conduction, conduction blocks, etc)

Persistent AV Junctional Reentry Tachycardia: similar to the WPW arrhythmia, but the circuit is contained in the AV node; there is a fast conducting segment and a slow conducting segment to the node; a premature beat may block the fast segment, and further slow the slow segment, setting up the conditions for reentry

Treatment: ablation of a part of the circuit

(b) Random Reentry: many impulses and reentrant pathways present; impulses propagate willy-nilly, NOT in a circle

this is the cause of myocardial fibrillations, both atrial ("A-fib") and ventricular (lethal)

(4) Reflection: a form of reentry that occurs in a linear bundle with an area of slow conduction in the middle

usually occurs in bundle of His or one of the bundle branches
if one of the legs of the bundle transmits slower, the faster signal from the other leg can propagate back up the slower leg to send a signal in the opposite direction

Simultaneous Abnormalities of Impulse Generation and Conduction

(1) Parasystole: caused by a stimulus (usually an ectopic pacemaker) that is protected from the dominant pacemaker by a unidirectional conduction block; because the block is unidirectional, the ectopic pacemaker can cause premature beats or tachycardia provided its impulse hits tissue that is not refractory

(2) Phase 4 Block: block can occur if an impulse arrives at tissue that is partially depolarized due to sub-threshold spontaneous phase 4 depolarization; this sub-threshold depolarization may be enough to inactivate enough Na⁺ channels to provide a conduction block

Tachycardias: Characteristics and Mechanisms

Tachycardia	Mechanism	Location	Rate Range	AV or Va Conduction
Sinus Tachycardia	Automatic	Sinus Node	³ 100 bpm	1:1
Atrial Fibrillation	Random Reentry	Atria; usu. >300 bpm	260-450 bpm,	Variable
Atrial Flutter	Ordered Reentry	R.Atrium; 300± 20 bpm	240-350 bpm,	2:1 or variable
Atrial Variable Tachycardia	i.Reentry ii.Automatic iii.Triggered	Atria Atria Atria	150-240 bpm ? 150-240 bpm	1:1, 2:1,or ? 1:1,2:1, or
Variable	DAD (caused by digitalis)
AV Nodal Tachycardia	Ordered Reentry	AV node usually	120-250 bpm	1:1
AV Reentry (WPW or concealed)	Ordered Reentry	Circuit (accessory AV connection, atria, AV node, His, Purkinje system, ventricles)	140-250 bpm,	1:1
Accelerated AV junctional tachycardia	Automatic or ? Triggered	AV junction (AV node and His bundle)	61-200 bpm, usu. 80-130 bpm	1:1 or variable
Accelerated idio- ventricular rhythm	Abnormal automaticity	Purkinje fibers	>60 - ? bpm	Variable, 1:1, or AV dissociation
Ventricular tachycardia	Reentry Automatic (rare)	Ventricles Ventricles	120-300 bpm	AV dissoc., variable, or 1:1 AV dissoc., variable, or 1:1
Bundle Branch Reentrant Tachycardia	Reentry	Bundle branches and ventricular septum	160-250 bpm, usu. 195-240 bpm	AV dissoc., variable, or 1:1
Right Ventricular outflow tract tachycardia	? Triggered (DAD)	Right Ventricular outflow tract	120-220 bpm	AV dissoc., variable, or 1:1
Torsade de pointes	? Triggered (EAD)	Ventricles	>200 bpm	AV dissociation
Sinus Node Reentry	Reentry	Sinus node and R.atrium	?110-180 bpm	1:1 or variable

Arrythmias in Detail

Bradyarrhythmias

Definition: heart rate < 60bpm

ECG Differentiation:

Are P waves present?
What is the relationship between the P waves and the QRS complexes?

SA Node

Sinus Bradycardia

Definition: slowing of the normal heart rhythm as a result of decreased firing of the SA node (rate < 60bpm)

Epidemiology: trained athletes, elderly

Clinical course: Benign, can be pathologic (decided by physician on basis of patient’s age, underlying heart disease, whether the HR Ý appropriately to exercise

Etiology:

abnormally Ý vagal tone

ß intrinsic automaticity of the SA node

Can occur:

Normal Þ well trained athletes, elderly

Drugs Þ b -blockers, verapamil, diltiazem

Disease Þ hypothermia, hypothyroidism

Treatment: only if patient is symptomatic

IV anticholinergic (atropine)

b-adrenergic agents (isoproteronol)

pacemaker

Sick Sinus Syndrome

Definition: markedly variable rate of impulse formation of the SA node

Symptoms:

paroxysmal dizzines
confusion
syncope

Bradycardia-tachydardia syndrome: periods of sinus node slowing transiently follow atrial tachyarrhythmias (atrial flutter or fibrillation)

Treatment:

combination antiarrhythmic drugs Þ suppress tachyarrhythmias

permanent pacemaker Þ bradyarrhythmias

Escape Rhythms

Definition: suppression of SA node activity or blockade within conduction pathway can lead to escape rhythms by more distal latent pacemakers.

Purpose: protective mechanism that maintains a HR during periods of ß SA node firing or AV conduction blocks

Symptoms:

slow pulse rate

ß Cardiac Output (headaches, syncope)

Treatment:

IV atropine (quickly)
pacemaker

Junctional Escape beats

Definition: arise at the junction of the AV node and the bundle of His

ECG:

normal, narrow QRS complex
rate – 40-60bpm
retrogade P waves (follow the QRS complex and inverted on inferior leads – II, III, aVF)

Ventricular Escape Beats

ECG:
slow rate – 30-40bpm
widened QRS complex (impulses are conducted outside normal conducting Purkinje system – ventricular conduction)

Atrioventricular Node – Conduction Block

First Degree Conduction Block

Definition: prolongation of the normal delay between atrial and ventricular depolarization

ECG: PR interval > 0.2s (> 5 small boxes (sb) or > 1 big box)

Etiology: transient influence or structural defects of the conduction pathway through AV node

Reversible:

Ý vagal tone

transient AV nodal ischemia

digitalis

b blocker

Ca⁺⁺ channel antagonist

Structural:

MI
chronic degenerative diseases

Clinical Course: benign, asymptomatic

Treatment: NONE

Second Degree Conduction Block

Definition: intermittent failure of AV conduction – not every P wave is followed by a QRS complex. 2 flavors:

(1) Mobitz Type I (Wenckebach): conduction defect becomes progressively more pronounced with each beat until an impulse is completely blocked, such that ventricular stimulation does not follow a P wave for a single beat.

ECG: Progressive Ý in PR interval until a singly QRS complex is absent, and then the cycle starts anew.

Block:

AV node (rather than Bundle of HIS)
acute inferior wall MI

Clinical Course: benign

Epidemiology:

children

trained athletes

individuals with Ý vagal tone

Treatment: not necessary unless symptomatic Þ atropine

(2) Mobitz Type II: AV conduction intermittently ceases, WITHOUT the warning of progressive PR prolongation

High-grade block: block persists > 2 or more beats

Block: HIS-Purkinje system

Etiology:

infarction
chronic degeneration

ECG: QRS abnormally wide (stimulates right and left bundle branches)

Clinical Course: severe – rhythm may progress to type III without warning Þ Adam Stokes seizures

Treatment: Pacemaker (ABSOLUTE indication)

(3) Third Degree Conduction Block – Atrioventricular Dissociation (AV dissociation)

Definition: complete failure of conduction between the artria and ventrices Þ divides the heart into 2 unconnected zones

Etiology:

acute MI
digitalis
chronic degeneration

ECG:

NO relationship between P waves and QRS complexes
escape rhythm drives ventricles independently-rate 30-55bpm

Symptoms:

lightheadedness
syncope

Treatment: Permanent pacemaker

Tachyarrhythmias

Definition: heart rate >100bpm

Etiology: Ý firing rate. Include enhanced cellular automaticity, triggered activity, and reentry

Two flavors:

supraventricular- arise above the ventricles
arise within the ventricle

ECG differentiation:

Width of the QRS complex ?

Normal: Supraventricular tachycardia
Wide: Ventricular Tachycardia

Morphology and rate of the P waves
Relationship between the P waves and the QRS complex
Response of the rhythm to vagal maneuvers (carotid sinus massage, adenosine)

Supraventricular Arrhythmias

(1) Sinus Tacyhcardia

Definition: SA node discharge rate of 100-180 bpm, normal P waves and QRS complexes

Etiology: Ý sympathetic stimulation of SA node Þ enhanced automaticity

Normal physiologic response: exercise

Pathologic:

fever
hyperthyroidism
hypoxemia

Treatment: treat underlying cause

(2) Atrial Premature Beats (PAC = paroxysmal atrial contraction)

Definition: an earlier than expcted P wave

Etiology: impulse arising from somewhere other than SA node

ECG:

an earlier-than-expected P wave with an ABNORMAL shape – impulse doesn’t arise from SA node (therefore conduction through the atria is abnormal)
followed by a normal QRS complex – ventricular conduction is not impaired
"blocked" APB – P wave with abnormal morphology NOT followed by a QRS complex – abnormal focus fires while surrounding atrial tissue is still refractory

Treatment: only if symptomatic:

reduce predisposing factors: ß caffeine/EtOH, ß adrenergic stimulation (stress)

b-blockers

(3) Atrial flutter

Definition: Impulses traveling in a circular course in atria, setting up regular, rapid flutter waves without any isoelectric baseline. The atrial rate is so fast that an AV node block occurs (typically 2:1 block if atrial rate is 300 bpm) because each alternate atrial impulse finds the AV node refractory

ECG: "sawtooth" appearing atrial activity at a rate of 250-350bpm

Workup: Vagal maneuver: ß AV nodal conduction thus slowing ventricular activity and allowing better visualization of underlying atrial activity

Etiology: Reentry within the right atrium around the SVC

Epidemiology: patients with preexisting heart disease

Clinical Course:

lasts for weeks or longer

degenerates into atrial fibrillation

can become MORE dangerous if atrial rate slows (conduction block disappearsÞ fast AV node conducts at 1:1 with ventricles, accelerating ventricle rate)

Treatment:

elecrical cardioversion

rapid atrial stimulation (break reentry circuit)

b-blockers, Ca⁺⁺ channel blockers (ß ventricular rate by Ý AV block)

Antiarrythmic drugs (convert back to normal sinus rhythm)

ablation–destroy reentry circuit

(4) Atrial Fibrillation

Definition: chaotic rhythm that results in an atrial rate of 350-600 discharges/min

AV block occurs (Ý sinus rate encounters refractory AV node)

ECG:

discrete atrial P waves are not discernible
baseline shows low amplitude undulations punctuated by QRS complexes and T waves
rhythm repetitively shifts between fibrillation and atrial flutter

Etiology: multiple micro-reentrant circuits within the atria

Precipitated by

right or left atrial enlargement (mitral valve stenosis or regurg)
HTN
Coronary Artery Disease
thyrotoxicosis
pulmonary embolism

Clinical Course: dangerous because:

rapid ventricular rates ß CO

no organized atrial contraction Þ blood stasis Þ thrombus formation Þ thromboemboli Þ stroke

Treatment:

Chronic Afib Þ long term anticoagulation treatment

b blockers, verapamil Þ ß ventricular rate by ß AV conduction

antiarryhthmics Þ conversion to sinus rhythm

electrical cardioversion

(5) Paroxysmal Supraventricular Tachycardias (PSVT’s)

Definition: sudden onset and termination atrial rates of 140 – 250bpm with narrow (normal) QRS complexes

Mechanisms:

reentry
enhanced automaticity
triggered activity

Reentrant Tachydardias: 2 flavors

Atrioventricular Nodal Reentrant Tachycardia (AVNRT): most common form of PSVT

Definition: Reentrant loop is within or near the AV node

There are 2 pathways:

a – slow-acting fast refractory path

b – fast-acting long refractory path Þ sets up for reentry

Note: current goes anterograde (never retrograde) through a loop; contrast to "Bypass tract" (accessory pathway)

ECG: P waves may be "hidden" in QRS complex (retrograde depol. occurs simultaneously with ventricular depolarization)

if not hidden they are inverted – in inferior leads

Clinical Course:

syncope
angina
pulmonary edema

Treatment:

vagal maneuvers

IV adenosine Þ terminate arrhythmia by ß AV conduction

Digitalis

b-blockers, verapamil

antiarrhythmics (IA or IC)

ablation

Atrioventricular Reentrant Tachycardias (AVRT):

Definition: Reentrant loop uses an accessory pathway "bypass tract" setting up a large reentrant loop

Accessory pathway: congenital abnormality where an additional conduction pathway from SA node exists. This pathway is capable of anterograde AND retrograde conduction (25% are only capable of retrograde)
2 flavors:

Orthodromic AVRT: impulses travel anterograde down AV node, then retrograde up accessory tract and back to atrium

ECG: NORMAL QRS width

retrograde P waves AFTER QRS complex
NO delta wave (see below)

Antidromic AVRT: impulses travel anterograde down accessory pathway, than retrograde up the AV node

ECG: Widened QRS complex (ventricles are activated from anterograde conduction over the accessory pathway)

Treatment:

Na⁺ channel blockers (IA, IC)–slow conduction and prolong the refractory period of accessry pathways
ablation

Non-reentrant supaventricular tachycardias

Definition: wandering atrial pacemaker – impulses originate from varying points in atria (ectopic atrial focus)

Etiology: Ý automaticity or triggered activity (DAD’s)

ECG: P wave is upright and precedes the QRS (abnormal shape)

Cause: Digitalis toxicity

Treatment: withdrawal of dig and correction of hyokalemia

vagal maneuvers have NO effect

(6) Multifocal Atrial Tachycardia

Definition: Ý automaticity in atria results in abnormal discharges from several ectopic foci

Clinical Course: occurs in the setting of pulmonary disease and hypoxemia

ECG: irregular rhythm with multiple P wave morphologies with average atrial rate > 100

Treatment: treat underlying disease, also verapamil

(7) Wolf–Parkinson-White Syndrome – Preexcitation Syndrome – Antidromic AVRT

Definition: abnormal connection between atria and ventricles through an accessory "bypass tract" – Bundle of Kent

ECG: PR interval is shortened (ventricles are stimulated via bundle of Kent NOT AV node – no delay)

Delta wave – slurred sharp upstroke of QRS complex
Widening of QRS complex – fusion of impulses arriving at ventricles by 2 separate routes

Clinical Course: May be asymptomatic but serious arrhythmias may occur

Ventricular Arrhythmias

(1) Ventricular Premature Beats (VPB) – PVC: Paroxysmal ventricular contraction)

Definition: Ventricular beat earlier then expected

Etiology: ectopic ventricular focus triggers an action potential

ECG: widened QRS complex (AP travels cell to cell through ventricle instead of via fast conduction system)

QRS NOT related to any preceding P wave

Treatment: asymptomatic patients: do nothing

b-blockers

(2) Ventricular Tachycardia

Definition: series of 3 or more VPB’s in a row. 2 flavors:

Sustained VT: > 30 sec or requiring termination of activity because of severe symptoms

Nonsustained VT

Etiology: Reentry. Associated with structural heart disease

Clinical Course: hypotension and loss of consciousness (because of low CO)

ECG: QRS complex wide and occur at rate of 100-200bpm

No consistent relationship between P waves and QRS complex
Can be mimicked by atrial tachycardias with bundle branch block

Treatment: Acute treatment – electrical cardioversion

antiarrhythmic drugs

(3) Torsades De Pointes ("twisting of the points")

Definition: form of ventricular tachycardia typified by varying amplitudes of QRS

Etiology: Early afterdepolarizations (trigered activity) – prolonged QT interval.

Cause:

Quinidone
hypkalemia
hypomagnesemia
congenital

Clinical Course: Symptomatic and self-limiting but can degenerate into ventricular fibrillation

Treatment: Treat underlying cause

IV magnesium (stabilize rhthym)

IV isopoterenol (shorten QT interval)

b-blockers (congenital causes because sympathetic stimulation aggravates symptoms)

(4) Ventricular Fibrillation

Definition: disordered rapid stimulation of the ventricles preventing them from contracting in a coordinated fashion

Clinical Course: MOST life threatening arrrhythmia. Drop in CO Þ death

Etiology: Multiple small wavelets of reentry. Associated with severe heart disease and acute MI

ECG: chaotic irregular with complexes of varying amplitude and mophology without discrete QRS waveforms

Treatment: Electrical Defibrillation