< CONDUCTIVE DISORDERS / ARRHYTHMIAS >

Lengkapi jenis EKG dan penjelasannya

Obat-obatan aritmia
RBBB & LBBB
EKG Basics !
Classical Approach Rate
to ECGs  Normal = 60-100 bpm (atrial rate; 150-250 bpm = paroxysmal tachycardia, 250-350 bpm = atrial flutter, > 350 bpm = AFib 
rate not discernible
 Regular rhythm (defined by equal R-R or P-P intervals between beats)
o To calculate  divide 300 by number of large squares between 2 QRS complexes
 Irregular rhythm
o Rate = 6 x number of R-R intervals in 10 s
 Atrial escape rhythm in case of sinus node failure = 60-80 bpm; junctional escape rhythm = 40-60 bpm; ventricular escape
rhythm = 20-40 bpm

Rhythm
 Regular : R-R interval is SAME
 Irregular : R-R interval VARIES
 Regularly irregular : repeating pattern of varying R-R intervals  Atrial flutter with variable block
 Irregularly irregular : R-R intervals vary erratically  AFib, VFib
 NSR ( Normal Sinus Rhythm )
o P wave precedes each QRS; QRS follows each P wave
o P wave axis is normal ( (+) in 2 in 3 following leads  I, II, aVF )
o Rate between 60-100 bpm

Axis
 Mean axis  direction of the mean vector
 Can be determined for any waveform  P, QRS, T
 Standard  QRS axis usually refers to the mean axis of the frontal plane – indicates the mean direction of ventricular
depolarization forces
 QRS axis in the frontal plane
o Normal : -30deg to 90deg  positive QRS in leads I and II
o LAD : axis < -30deg
o RAD : axis > 90dg
 QRS axis in the horizontal plane is not routinely calculated
o Transition from negative to positive is usually in lead V3

DDx for LAD DDx for RAD

 Left anterior hemiblock  RVH
 Inferior MI  Left posterior hemiblock
 WPW  COPD
 RV pacing  Lateral MI
 Normal variant  WPW
 Elevated diaphragm  Dextrocardia
 Lead misplacement  Septal defects
 Endocardial cushion defect

Conduction Abnormalities
Left Bundle Branch Block
Complete LBBB
 QRS duration > 120msec
 Broad notched R waves in leads V4, V5, and/or I,
aVL
 Deep broad S waves in lead V1-2
 Secondary ST-T changes ( (-) in leads with broad
notched R waves, (+) in V1-2) are usually present
 LBBB can mask ECG signs of MI
 LBBB : lead V1 negative, V6 positive and notched
Right Bundle Branch Block
Complete RBBB
 QRS duration > 120 msec
 Positive QRS in lead V1 (rSR’ or occasionally
broad R wave)
 Broad S waves in leads I, V5-6 (>40msec)
 Usually secondary T wave inversion in lead V1-2
 Frontal axis determination using only the first 60
msec
 RBBB : V1 (+) (rSR’); V6 has broad S wave

Left Anterior Fascicular Block
( LAFB)
(Left Anterior Hemiblock)
LAD
 Small q and prominent R in
leads I and aVL
 Small r and prominent S in
leads II, III, aVF
Left Posterior Fascicular Block
(LPFB)
(Left Posterior Hemiblock)
RAD
 Small r and prominent S in
leads I and aVL
 Small q and prominent R in
leads II, III, aVF
Bifascicular Block
RBBB Pattern
 Small q and prominent R
 The first 60 msec of the QRS
shows pattern of LAFB or
LPFB
 Bifascicular block 
impaired conduction in 2 of
the 3 fascicles  commonly
RBBB, or LAFB

Left Ventricular Hypertrophy (LVH) Right Ventricular Hypertrophy (RVH)

1
  S in V1 + R in V5 or V6 > 35 mm above age 40. (>40  RAD
mm for age 31-40, >45 mm for age 21-30)  R/S ratio > 1 or qR in lead V1
 R in aVL > 11 mm  RV strain pattern : ST segment depression and T wave
 R in I + S in III > 25 mm inversion in lead V1-2
 Additional criteria :
o LV strain pattern (asymmetric ST depression
and T wave inversion in leads I, aVL, V4-V6)
o LAE
The more criteria present, the more likely LVH is present.
If only 1 voltage criteria present, it is called minimal voltage
LVH which could be normal variant
Left Atrial Enlargement (LAE) Right Atrial Enlargement (RAE)
 Biphasic P wave with the negative terminal component  P wave > 2,5 mm in heaight in leads II, III, aVF  P
of the p wave in lead V1 > 1 mm wide and > 1 mm deep pulmonale
 P wave > 100 msec, could be notched in lead II  P
mitrale

Mechanisms Alterations in Impulse Formation

 Normal Automaticity
o Impulses from the SA node, caused by spontaneous depolarization, result in the basic cardiac pacemaker function
o “Downstream” cells in the AV node and Purkinje fibres also depolarize spontaneously, but at a slower rate.
o “Backup” pacemaking cells if the upstream rate is slower than the more distal spontaneous rate
o Normal automaticity is influenced by :
 Neurohormonal tone  sympathetic tone increases and parasympathetic tone decreases spontaneous firing
rate and thus heart rate
 Myocardial ischemia/infarction or other cardiac pathology (eg. heart failure) may alter heart rate via these
mechanisms
 Abnormal metabolic conditions  hypoxia, acidosis, hypothermia
 Electrolyte abnormalities  hyperkalemia,  HR
 Drugs  digitalis. Beta blockers, CCB
 Abnormal Automaticity d/t Triggered Activity ( d/t After Depolarizations )
o Early After Depolarizations
 During the terminal plateau or repolarization phases of action potential
 Consequence of the membrane potential transiently becoming ore positive during repolarization 
depolarization interrupting repolarization
 Called EADs and DADs
 May result in self-maintaining oscillations of depolarization, giving rise to action potentials  generating
a tachyarrhythmia  new baseline voltage >>> than threshold, which automatically triggers a new action
potential after refractory period ends
 EADs  basis for arrhythmias associated with QT prolongation, either congenital or acquired 
“Torsades de Pointes”
o Delayed After Depolarizations
 Occur after the action potential has fully repolarized, but before the next usual action potential
 Commonly occurs in situations of high intracellular calcium  digitalis intoxication, ischemia OR during
enhanced catecholamine stimulation  “twitchy” pacemaker cells

Alterations in Impulse Conduction

 Re-entry Circuits
o The presence of self-sustaining re-entry circuit causes rapid repeated depolarizations in a region of myocardium
o The conditions necessary for re-entry include block of an impulse into a region of the heart that is refractory (non-
excitable tissue or because of local functional block, where the impulse encounters tissue still in its refractory period),
followed by “re-entry” of the impulse around a region of block to the site of origin, forming a complete re-entry
circuit
 e.g. myocardium that is infarcted/ischemic will consist of non-excitable and partially excitable zones
which will promote the formation of re-entry circuits
 Conduction Block
o Ischemia, fibrosis, trauma and drugs can cause transient or permanent, unidirectional or bidirectional block
o most common cause of block is due to refractory myocardium (cardiomyocytes are in refractory period or zone of
myocardium unexcitable due to fibrosis)
o Cells in the conduction system distal to the block can assume pacemaking control if the block occurs along the
specialized conduction system
o Conduction block can lead to bradycardia
 Bypass Tracts
o Normally, the only electrical connection between atria and ventricles  AV node and penetrating Bundle of His
o An accessory bypass tract  direct connection between atrium and ventricle  similar to atrial tissue, through the
valve ring  impervious to electrical impulses

2
 Sinus bradycardia
Sinoatrial block
Sinus Arrest
Bradyarrhythmias
AV Block (2nd and 3rd degree)
Junctional Rhythm
Idioventricular Rhythm

Sinus Tachycardia
Atrial Tachycardia
Junctional Tachycardia
Narrow QRS
Arrhythmias AVNRT
AVRT (orthodromic)
Atrial Flutter
Regular

SVT w/ abberancy/BBB
Wide QRS Ventricular Tachycardia
AVRT (antidromic)

Tachyarrhythmias

Atrial Fibrillation
Atrial Flutter w/ variable block
Narrow QRS
Multifocal Atrial Tachycardia
Premature Atrial Contraction

Irregular
Atrial Fibrillation w/ BBB
Atrial Flutter w/ BBB and
variable block
Wide QRS
Polymoprhic VT
Premature Ventricular
Contraction

Atrial Fibrillation
(A-Fib)

 Irregularly irregular rhythm

 No P waves
 MOST COMMON CHRONIC ARRHYTHMIA
 Ashman’s Phenomenon  occasional aberrantly conducted beats (wide QRS) after short R-R cycles
Pathophysiology :
 Ineffective quivering  cause thrombi to form  ischemic stroke
Etiology :
 Cardiac disease
 Pulmonary disease
 Cardiomyopathies
 Electrolyte imbalances
 Thyroid disorders
Types :
 Paroxysmal  self terminating within 7 days +/- recurrent
 Persistent  fails to self-terminate
 Permanent  persistent > 1 year
 Lone  paroxysmal, persistent or permanent without evidence of heart disease
Tx :
 STABLE
o Rate control  initial management over rhythm control
3
  BB : metoprolol (caution if they have reactive airway disease)
 CCB : diltiazem
 Digoxin : preferred for px with hypotension or CHF
o Rhythm control  younger patients with lone a-fib
 Direct current cardioversion (DCC)
 Medicine : ibutilide, flecainide, sotalol, amiodarone
 Radio-freq ablation  perm pacemaker
 UNSTABLE : DCC
 ANTI-COAG : CHA2DS2-VASc or CHADS2 to determine risks for embolization

Drugs and Doses for Pharmacological Conversion of (Recent-Onset) AF

Drug Dose Follow Up Dose Risk

Phlebitis, hypotension. Will

slow the ventricular rate.
Amiodarone 5 mg/kg IV over 1 hour 50 mg/hr
Delayed AF conversion to
sinus rhythm
Not suitable for patients with
marked structural heart
disease; may prolong QRS
duration, and hence the QT
2 mg/kg IV over 10 mins, or interval; and may
Flecainide N/A
200-300 mg PO inadvertently increase the
ventricular rate due to
conversion to atrial flutter and
1:1 Conduction to the
ventricles
Can cause prolongation of the
QT interval and torsades de
1 mg IV over 10 mins after pointes; watch for abnormal
Ibutilide 1 mg IV over 10 mins
waiting for 10 mins T-U waves or QT
prolongation. Will slow the
ventricular rate.
Not suitable for patients with
marked structural heart
disease; may prolong QRS
duration; will slightly slow
2 mg/kg IV over 10 mins, or the ventricular rate, but may
Propafenone N/A
450-600 mg PO inadvertently increase the
ventricular rate due to
conversion to atrial flutter and
1:1 conduction to the
ventricles.
Second infusion of 2 mg/kg So far only evaluated in
Vernakalant 3 mg/kg IV over 10 mins IV over 10 mins after 15 mins clinical trials, recently
rest approved.

Drugs for Rate Control

Intravenous Administration Usual Oral Maintenance Dose

Beta-Blockers

Metoprolol CR/XL 2.5 – 5 mg 100 – 200 mg OD (ER)

Bisoprolol N/A 2.5 – 10 mg OD

Atenolol N/A 25 – 100 mg OD

Esmolol 10 mg N/A

Propranolol 1 mg 10 – 40 mg TID

Carvedilol N/A 3.125 – 25 mg BID

Non-Dihydropyridine Calcium Channel Antagonists

Verapamil 5 mg 40 mg BD to 360 mg (ER) OD

Diltiazem N/A 60 mg TDS to 360 mg (ER) OD

Digitalis Glycosides

4
 Digoxin 0.5 – 1 mg 0.125 mg – 0.5 mg OD

Digitoxin 0.4 – 0.6 mg 0.05 mg – 0.1 mg OD

Others

Amiodarone 5 mg/kg in 1 hr, an 50 mg/h maintenance 100 mg – 200 mg OD

Dronedarone N/A 400 mg BID

Atrial Flutter

 Flutter ( saw tooth ) waves

 Rate is regular
Tx :
 STABLE  Vagal, BB, CCB
 UNSTABLE  DCC
 DEFINITIVE MANAGEMENT  Radiofrequency ablation
Paroxysmal
Supraventricular
Tachycardia

 HR > 100 bpm

 Rhythm usually regular with narrow QRS complexes
 P wave is hard to see
Pathophysiology :
 Paroxysmal  sudden onset and termination (preceded by PAC)
 Supraventricular  rhythm originates above the ventricles
 Tachyarrhythmias  results of 3 main mechanisms :
o Re-entrant
 Repetitively following a revolving pathway comprising 2 limbs
 There must be an area of slow conduction
o Automaticity
 Spontaneous and often repetitive firing from a single focus  may either be ectopic or may originate in
the sinus node
 2 subcategories :
 Enhanced automaticity  focus that fires spontaneously and may originate in sinus node,
subsidiary pacemakers in the atrium including the Eustachian ridge, Bachmann bundle,
coronary sinus, AV valves, AV node, His-Purkinje system, and ventricles
 Abnormal automaticity  secondary to a disease  (+) alterations in ionic flow  9+) less
negative resting diastolic membrane potential  threshold potential more easily attained
o Triggered arrhythmias
 Depends on oscillation in the membrane potential

Types :
 AV Nodal Re-entry Tachycardia (AVNRT)  2 pathways both within the AV node  most common type
 AV Reciprocating Tachycardia (AVRT)  1 pathway within the AV node and 2nd outside the AV node

Conduction Pattern :
Orthodromic  impulses go  normal AV node and return leading to NARROW COMPLEX TACHYCARDIA
Antidromic  impulses go  accessory pathway fiest and return to the atria via N1 Pathyway  WIDE COMPLEX
TACHYCARDIA
Tx :
 Stable ( narrow complex ) : vagal maneuvers (stimulate acetylcholine   HR)  Adenosine is 1st line tx for SVT
 Stable ( wide complex ) : antiarrhythmics (amiodarone)  Procainamide in WPW
 Unstable  DCC
 Definitive management  Radiofrequency Ablation

Anti-Arrhythmic Drugs for SVTs

Agent Indication Intravenous Oral Dose Adverse Effects Drug Interaction

Dose

5
 Class I
Quinidine AF, AFL, 6-10 mg/kg over 200-400 mg 14- Hypotension (espc.  digitalis level
AVNRT, 20-30 min 6h; q8h with IV), ventricular  warfarin effect
AVRT long-acting proarrhythmia, GI  metoprolol,
preparations disturbance, propranolol,
thrombocytopenia propafenone levels
Procainamide AF, AFL, Bolus : 15 mg/kg 50 mg/kg/day GI disturbance,  procainamide level
AVNRT, given as 20 q3-4h; twice hypotension, SLE, with cimetidine,
AVRT mg/min daily dosage granulocytosis, FUO, quinidine, and
Infusion : 2-4 with long-acting haemolytic anemia, amiodarone
mg/min preparation myasthenia gravis
aggravation,
ventricular
proarrhythmia
Class 1C
Flecainide AF, AFL, AT, N/A 50-200 mg q12h Ventricular  digitalis level
AVNRT, proarrhythmia, CHF,  flecainide level with
AVRT GI disturbance, CNS amiodarone, cimetidine,
(dizziness, tremor, norpace, propranolol
light-headedness)  flecainide with
smoking
Propafenone AF, AFL, N/A 150-300 mg q8h GI disturbance, CNS Synergism with
AVNRT, or 225-425 mg (dizziness), metallic betablockers
AVRT bid (long-acting taste, CHF, 1st degree
form) AVB, IVCD, positive
ANA
Class II (IV)
Esmolol Ventricular rate Bolus : 500 N/A CHF, AVB,
control for AF, mcg/kg over 1-2 bradycardia,
AFL, ST, AT min bronchospasm
Infusion : 50-
200 mcg/kg/min
Propranolol Ventricular rate 1-5 mg at 1 20-320 mg/day CHF, AVB,
for AF, AFL, mg/min q6h, q8h, q12h bradycardia,
ST, AT or once daily, bronchospasm
depending on
preparation
Class III
Sotalol AF, AFL, N/A 80-160 mg q12h Dyspnea, fatigue, Synergism with Ca2+
AVNRT, dizziness, CHF, antagonists or
AVRT, AT bradycardia, betablockers
ventricular
proarrhythmia,
bronchospasm
Amiodarone AF, AFL, Bolus : 150 mg 100-400 mcg Pulmonary toxicity,  digoxin levels
AVNRT, over 10 min once daily CHF, tremor,  warfarin effects
AVRT, AT Infusion : 1 bradycardia,  LFTs,  quinidine,
mg/min x 6h, corneal deposits, skin procainamide/NAPA,
then 0,5 mg/min discoloration, GI flecainide
intolerance,  phenytoin level
hyper-/hypothyroidis
m
Ibutilide AF, AFL 1 mg bolus ovr N/A Ventricular
10 min; second proarrhythmia,
bolus, if needed, hypotension, GI
after 10-min disturbance
wait
Dofetilide AF, AFL N/A 125-500 mcg Ventricular Contraindicated with
twice daily proarrhythmia, verapamil, cimetidine,
modified by headache, chest pain, ketoconazole,
algorithm nausea, dizziness trimethoprim
Class IV
Diltiazem AF, AFL, Bolus : 0,25 90-360 mg/day Hypotension, Synergism with BB
AVNRT, mg/min over 2 in 1-4 divided bradycardia, CHF,
AVRT, AT, min then 0,35 doses, AVB
MAT mg/kg in 15 min depending on
if needed prep
Infusion : 5-15
mg/h
Verapamil AF, AFL, 2,5-20 mg over 40-120 mcg Hypotension, Synergism with BB
AVNRT, 20 min in q8h; 240-360 bradycardia, CHF,
AVRT, AT, divided doses mg once daily of AVB
MAT long-acting
preparation
Class V
Adenosine SVT dx, 6 mg IV rapid N/A Chest tightness, facial  activity by
AVNRT, bolus followed flushing, dyspnea, dipyridamole
AVRT, AT by 12 mg x 2 if AVB  activity by
6
 termination needed, half theophylline
dosage if
administered in
central line
Digoxin Ventricular rate Up to 1,0 mg 0,125-0,375 GI disturbance,  digoxin level :
control for AF, bolus in divided mg/day in single conduction defects,amiodarone, quinidine,
AFL, AT doses followed dose atrial/ventricular verapamil,
(generally not by 0,125-0,375 arrhythmias, indomethacin,
very effective mg/day headache, visual spironolactone,
in active disturbances alprazolam,
patients) erythromycin,
tetracycline
 digoxin level :
antacids,
cholestyramine,
rifampin, neomycin
 risk of digitalis
toxicity with potassium-
depleting diuretics
*) AF = Atrial Fibrillation, AFL = Atrial Flutter, AT = Atrial Tachycardia, AVB = Atrioventricular Block, MAT = Multifocal Atrial
Tachycardia, IVCD = Intraventricular Conduction Delay

Wandering Atrial
Pacemakers (WAP)

Multiple ectopic atrial foci generate impulses that are conducted to the ventricles
ECG : HR < 100 bpm and > 3 P Waves morphologies
Multifocal Arterial
Tachycardia
(MAT)

Same as WAP but HR > 100 bpm

MAT associated with COPD
Difficult to treat, CCB (verapamil) or BB used if LV function is preserved

Junctional
Dysrhythmias

AV node / junction becomes the dominant pacemaker of the heart in AV junctional rhythms
Etiologies :
 Sinus disease
 Coronary artery disease
7
  MC rhythm seen with digitalis toxicity
 Myocarditis
ECG : Regular rhythm, P waves inverted if present or are not seen
Associated with narrow QRS
Normal is 40-60 bpm (reflecting the intrinsic rate of the AV junction), accelerated is 60-100, and tachy > 100 bpm
Premature beats :
PVC

Premature beat originating from the ventricle : wide bizarre QRS occurring earlier than expected. With a PVC, T wave is in the
opposite direction of the QRS
Associated with a compensatory pause  overall rhythm is unchange
Potentially lethal because stroke volume and coronary flow are compromised
No tx needed, most ventricular arrhythmias occur after a PVC
Sinus Arrhythmias Same as normal sinus rhythm except the rhythm is irregular
HR  during inspiration
HR  during expiration
Normal variant, can be seen with bradycardia
If bradycardia and symptomatic  atropine
Torsades de
Pointes

V Tach that “twists” around baseline

MC due to hypomagnesemia, hypokalemia
Tx : IV magnesium
Ventricular
Fibrillation

Can be coarse or fine

Heart looks like it is quivering
Tx : Unsynchronized cardioversion (defibrillation) + CPR
Ventricular
Tachycardia

> 3 consecutive PVCs at a rate of > 100 bpm.

Must valuate pts if hemodynamically stable vs unstable and if it is sustained vs unsustained
Ventricular Tachycardia : prolonged QT interval is a common predisposing condition
Tx :
 Stable sustained VT  antiarrhythmics (amiodarone, lidocaine, procainamide)
 Unstable VT with a pulse  cardioversion synchronized
 VT (no pulse)  Defib + CPR  tx VF

CLINICAL ASPECTS OF CARDIAC ARRHYTHMIAS

8
 Sinus Bradycardia

Information :
 A slowing of the normal HR  result of  firing of the SA node, < 60 bpm
 At rest or during sleep  normal
 Results from several triggers :
o Intrinsic  aging, ischemic heart disease, cardiomyopathy
o Extrinsic  medications ( CCB, several beta-blockers), metabolic (hypothyroidism)
Sick Sinus
Bradycardia (SSB)

Information :
 Intrinsic SA node dysfunction  periods of inappropriate bradycardia
 Produces symptoms  dizziness, confusion or syncope
 Can be treated with IV anti-cholinergic drugs ( atropine ), beta-adrenergic agents (isoproterenol)  transiently  HR  for
acute
 Chronically  placement of permanent pacemaker is required  if not corrected by removal of aggravating factors
 Common in elderly patients  susceptible to SVTs
o Being combined will be known as bradycardia-tachycardia syndrome  results from atrial fibrosis  impairs
function of the SA node and predisposed to AF and flutter.
o Tx generally requires combination of anti-arrhythmic drug (  tachyarrhythmia ) and pacemaker ( to prevent
bradycardia )
First – Degree AV
Block

 Indicates prolongation of the normal delay between atrial and ventricular depolarization
 PR interval is lengthened > 0,2 secs
 P waves : QRS complex = 1 : 1
 Can be caused by a transient reversible influence or a structural defect
o Reversible : heightened vagal tone, transient AV nodal ischemia, drug that  conduction through AV node ( BB,
certain CCA, digitalis, other anti-arrhythmics)
o Structural : myocardial infarction, chronic degenerative disease of the conduction system (usually with aging)
 Generally, benign & asymptomatic condition  no treatment required

9
 Second – Degree
AV Block

 Characterized by intermittent failure of AV conduction  some P waves not followed by QRS complex
 Two types :
o Mobitz type I ( Weckenbach )
 Degree of AV delay gradually 
 ECG  progressive increase in the PR interval from one beat to the next until a single QRS complex is
absent
 Always results from impaired conduction in the AV node
 Benign  usually children, trained athletes, people with  vagal tone (particularly during sleep)
 Tx not necessary typically, but sometimes administration of IV atropine / isoproterenol usually improves
AV conduction transiently
 Pacemaker required for a symptomatic block
o Mobitz type II
 Sudden intermittent loss of AV conduction without preceding gradual lengthening of PR interval
 The block may persist for 2 or more beats  also known as high-grade AV block
 Usually caused by conduction block beyond the AV node ( bundle of His or distally in the Purkinje system
)
 May arise from extensive MI involving septum or chronic degeneration of His-Purkinje system
 Indicates severe disease and more dangerous than Mobitz type I.
 May progress to 3rd degree block without warning  the reason why pacemaker is required even if the pts
is asymptomatic
Third-Degree AV
Block

 Also termed complete heart block

 Present  complete failure of conduction between the atria and ventricles
 MC cause  MI, chronic degeneration of the conduction pathways with age  mostly adults
 Disconnects atria and ventricles  no relationship between P waves and QRS complex
o P waves marched out at a rate that is not related with QRS complex
 QRS complex may be of normal width and occur at 40 – 60 bpm or widened and occur at slower rates
 Pts frequently experiencing light-headedness and syncope
 Permanent pacemaker  almost always necessary

10
 Sinus Tachycardia

 Characterized by HR > 100 bpm with normal P waves and QRS complexes
 Results from  sympathetic and/or  vagal tone
 Appropriate physiologic response to exercise. May also result from sympathetic stimulation  fever, hypoxemia,
hyperthyroidism, hypovolemia, and anemia
Atrial Premature
Beats

 Common in healthy as well as diseased hearts

 Originate from automaticity or re-entry in atrial focus outside the SA node  exacerbated by sympathetic stimulation
 Usually asymptomatic but may cause palpitation
 Require treatment only if there are symptomatic  caffeine, alcohol, adrenergic stimulation can all predispose to APBs
 Beta-blockers  initial preferred pharmacologic treatment
Ventricular Pre-
Excitation
Syndrome 
Wolff-Parkinson-
White Syndrome

 Atrial impulses can pass in an anterograde direction to the ventricles through both the AV node and accessory pathway 
ventricles stimulated earlier than by normal conduction
 PR interval is short  ventricular stimulation begins earlier than normal
 QRS has a slurred rather than a sharp upstroke  known as delta wave
 QRS complex is widened  represents fusion of two excitation wave
 Pts are predisposed to PSVTs  accessory pathway provides a potential limb of a re-entrant loop.
o Most common PSVT  orthodromic AVRT
 An impulse travels anterogradely down the AV node to the ventricles and then retrogradely up the
accessory tract back to the atria
 Pharmacologic management requires greater caution.
o Preferred : sodium channel blockers ( specifically, class IA and IC antiarrhythmics) and some class III antiarrhythmic
drug
 Pts with symptomatic arrhythmias MUST GENERALLY UNDERGO an invasive electrophysiologic study and have RF catheter
ablation of the accessory pathway.

Clinical Usage Information For Anti-Arrhythmic Agents

Usual Dosage Ranges Time To Peak
Plasma Major Route Of Pregnancy
Drugs Intravenous (Mg) Oral (Mg)
Concentration Elimination Class
Loading Maintenance Loading Maintenance (Oral)
6-10 mg/kg at
Quinidine 0.3 to 0.5 - 800-1000 300-600 q 6 hr 1.5 – 3 hr Liver C
mg/kg/min
6-13 mg/kg at
250-1000 q 4-6
Procainamide 0.2-0.5 2-6 mg/min 500-1000 1 hr Kidneys C
hr
mg/kg/min
1-2 mg/kg over
Disopyramide 1 mg/kg/hr 100-300 q 6-8 hr 1 – 2 hr Kidneys C
15 to 45 min*
1-3 mg/kg at 20-
Lidocaine 1-4 mg/min N/A N/A N/A Liver B
50 mg/min
150-300 q 8-12
Mexiletine 500 mg* 0.5 – 1 g/24 hr 400-600 2 – 4 hr Liver C
hr
100 mg q 5 min 100-400 q 12-24
Phenytoin 1000 8-12 hr Liver D
for  1000 mg hr
Flecainide 2 mg/kg* 100-200 q 12 hr 50-200 q 12 hr 3-4 hr Kidneys C

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 150-300 q 8-12
Propafenone 1-2 mg/kg 1-3 hr Liver C
hr
0.25-0.5 mg q 5
Propranolol min to  0.20 10-200 q 6-8 hr 4 hr Liver C
mg/kg
15 mg/min for
10 min; 1
mg/min for 3
Amiodarone 1 mg/min 200-600 qd Kidneys D
min then 5
mg/min
thereafter
Dronedarone N/A N/A N/A 400 mg q 12 hr 3 – 4 hr Liver X
10 mg over 1-2
Sotalol 80-320 q 12 hr 2.5-4 hr Kidneys B
min*
Ibutilide 1 mg over 1 min N/A N/A N/A N/A Kidneys C
2-5 g/kg 0.125 – 0.5 q 12
Dofetilide N/A N/A Kidneys C
infusion hr
5-10 mg over 1- 0.005
Verapamil 80-120 q 6-8 r 1-2 hr Liver C
2 min mg/kg/min
6-18 mg
Adenosine N/A N/A N/A N/A C
(rapidly)
Digoxin 0.5-1 mg 0.125 – 0.25 qd 0.5-1.0 0.125 – 0.25 qd 2-6 hr Kidneys C

12