ARRHYTHMIAS

• Sinus rhythm
- Depolarization starts in the SA node and it
goes from the rt side and toward the left side
of the heart, thus :
- Regular
- Each QRS complex preceded by p wave 1:1
ratio
- P wave is positive in lead II and negative in
aVR
 BRADYARRHYTHMIAS
• HR less than 60 bpm
• Fatigue , exertional intolerance , dyspnea , light
headedness , syncopy
• Pathology in SA node , AV node , his-purkinjie system
• Hemodynamic stability
• Exclude reversible causes (high ICP , hypothyroidism ,
hyperkalemia, lyme disease , medications )
• Careful hx , labs (e, tsh , digoxin level …), ECG, exersize
treadmil ((chronotropic competence ) , ambolatory
ECG , electrophysiology study )
 Sinus bradycardia
• Trained athletes, during sleep >> as low as 30
bpm
• Pathologic : intrinsic ; sinus node dysfunction
( age-related myocardial fibrosis >>> rt
coronary ischemia , intracranial htn,
postsurgical scarring , infiltrative like
sarcoidosis ) vs extrinsic ( medication effect )
• Stable vs unstable
• Eliminate the cause
• Iv atropine , temporary pacing ( cutaneous vs
venous ) , permanent pacing ( post infectious ,
sick sinus syndrome )
 st
1 degree AV block
• 1 degree : prolonged av conduction ,
st

prolonged PR interval > 200 msec

• All p waves are conducted to ventricles , not
true block
• Increased risk of a.fib , pacemaker
implantation , and all-cause mortality in long
term follow up
 etiology
• Intrinsic AVN disease
• Enhanced vagal tone( athletes and may have higher
degree block )
• Acute myocardial infarction (MI), particularly acute
inferior wall MI( rt coronary art in 90 % , left
circumflex 10% )
• Myocarditis
• Electrolyte disturbances (eg, hypokalemia,
hypomagnesemia)
• Drugs (especially those drugs that increase the
refractory time of the AVN, thereby slowing
conduction)
• Drugs that most commonly cause first-degree AV block
include the following:
• Class Ia antiarrhythmics (eg, quinidine, procainamide,
disopyramide)
• Class Ic antiarrhythmics (eg, flecainide, encainide,
propafenone)
• Class II antiarrhythmics (beta-blockers)
• Class III antiarrhythmics (eg, amiodarone, sotalol,
dofetilide, ibutilide)
• Class IV antiarrhythmics (calcium channel blockers)
• Digoxin or other cardiac glycosides
• Magnesium
• Stable vs unstable
• Reversible vs irreversible cause
 nd
2 degree AV block
• Wenckebach ( mobitz 1 ) : almost always
localized to AVN, benign , improves with
exercize or increased sympathetic tone
• Mobitz 2 : block lower in the conduction
system , risk of progression to complete heart
block
• Exclude reversible causes ( thyroid ,
electrolytes , MI, myocarditis ( lyme , HIV ,
adenovirus , enterovirus , chagas ), drugs
• Stable vs unstable
• Transcutaneous , transvenous pacemaker ,
atropine ( improve AV conduction , don’t use
if infranodal block ( mobitz II, wide QRS .
Worsens infranodal conduction and
dysrhythmias )
• Mobitz II : temporary pacemaker to all
patients even if asymptomatic due to high risk
of progression to complete block
 rd
3 degree or complete heart block
• AV dissociation ( other causes : VT )
• The ventricular escape mechanism can occur
anywhere from the AVN to the bundle-branch Purkinje
system ( QRS duration )
• Third-degree AV block is electrocardiographically
characterized by:
• Regular P-P interval
• Regular R-R interval
• Lack of an apparent relationship between the P waves
and QRS complexes
• More P waves are present than QRS complexes
• A common misconception : to gauge a patient’s
stability according to the heart rate and blood
pressure rather than according to the symptoms and
level of the block.
• An asymptomatic patient with inferior wall myocardial
infarction (MI) causing complete heart block at the AV
node (AVN) level and a heart rate of 35 beats/min is at
very little immediate risk. A patient in the acute phase
of an anterior wall MI with intermittent distal high-
grade block is at immediate danger of impending
asystole and requires immediate preparation for
pacing of some kind, even though the heart rate
between asystolic episodes may be 90 beats/min.
• Withdrwal of offending drugs
• Treat underlying cause
• Assess the need for temporary pacing
 Indications for permanent pacing
• Symptomatic bradycardia with no reversible
cause
• Asymptomatic bradycardia with significant
pauses ( > 3 seconds in sinus rhythm ) or
persistent HR < 40/min
• A.fib with 5 seconds pauses
• Asymptomatic complete block and mobitz II
AV block
• Alternating BBB
 TACHYARRHYTHMIAS
• HR > 100 bpm
• Sinus tachycardia ( always look for secondary
cause , e.g. PE )
• ECG , ECHO , TSH
• Narrow complex vs wide complex tachycardias
 Supraventricular tachycardias
• Arise in atrial tissue or AV node
• Narrow complex tachycardia ( normal
conduction )
• Could be wide complex in the presence of BBB ,
aberrancy , pacing , accessory pathway(
preexcitation syndrome)
• Arising in the atrium ( PACs , sinus tachycardia ,
fibrillation and flutter , MAT ) VS arising from AV
node ( junctional tachycardia , AVNRT , AVRT )
• All age groups but more in young adults
• F>m
• Usually no structural heart disease
• Episodes can often be terminated by valsalva
maneuvers , carotid sinus massage, facial
immersion in cold water
• Adenosine can help to diagnose the etiology ;
termination with adenosine suggests AV node
dependence , failure indicates atrial flutter and
atrial tachycardias.
 PACs
• Extremely common , increases with age
• Increased risk of atrial fibrillation
• Symptomatic : b blockers
 MAT
• Multiple , >= 3 p wave morphologies and a
heart rate > 100 bpm
• End-stage COPD and other pulmonary
diseases , electrolytes disturbances , drugs( e.
g.theophylline )
• Treat underlying cause
• Bblockers , NDP CCB also can help
 Atrioventricular nodal reentrant
tachycardia ( AVNRT )
• The most common type of SVT
• Reentrant conduction within the AV node
• Typical AVNRT : conduction goes down the slow
pathway and goes back up to the atrium over the
fast pathway( slow –fast ) >> short RP interval
with a retrograde p wave very close to QRS
complex ( may buried in the QRS complexes and
invisible OR may appear as a pseudo R’ wave in
V1 and pseudo s wave in inferior leads
• Atypical : fast-slow >> long RP interval
• Acute management : physical maneuvers , iv
adenosine
• To prevent recurrence : bblockers or NDP CCB
• Catheter ablation : high success rate
• 1% risk of AV node injury and pacemaker
implantation
 Atrioventricular reciprocating
tachycardia ( AVRT )
• Accessory pathway –mediated
• Orthodromic AVRT ( most common , conduction via
AV node so narrow complex )
• Antidromic AVRT ( conduction via the accessory
pathway , so wide complex )
• Adenosine is given in orthodromic , BUT
contraindicated in preexcited a.fib and antidromic
AVRT as well as all other av nodal blockers ( bb , ccb ,
digoxin )bcz will induce more rapid conduction via the
accessory pathway >> vent.fibrillation
• Patients with evidence of preexcitation on resting ECG
( delta wave ) and symptomatic svt >> WPW syndrome
 Atrial fibrillation
• Irregularly irregular , pulse defecit , variable intensity
of s1
• Most common sustained cardiac arrhythmias
• Risk increase with age
• Stasis and intracardial thrombus formation
• 5 fold increase risk of stroke , increase risk of HF and
dementia
• Can be due to reversible physiologic insult (
hyperthyroidism , cardiac surgery, PE
• More commonly ,due to longstanding disease
affecting the heart( htn , structural disease , OSA )
• 1 detected , paroxysmal( resolve
st

spontaneously , episodes last < 7 days ) ,

persistent( episodes > days , resolve by
cardioversion) , permanent ( persistent > 1
year duration )
• Management : rate control , rhythm control ,
stroke prevention
• Less than 48 hurs vs > 48 hours
• Chemical vs electrical cardioversion
• Amiodarone vs class 1c ( flecainide ,
propafenone ) and ibutilide
• Bb , ccb , digoxin vs procainamide in
preexcited a.fib
• CHA2DS2VASc score
• Warfarin , NOACs ( nonvalvular a.fib )
 Atrial flutter
• Sawtooth appearance
• Atrial rate 250-300 , with 2:1 ratio or variable
block
• Management : rate and rhyhm control , stroke
prevention
 Wide complex tachycardia
• Ddx : svt with abberant conduction,
preexcitation , paced rhythms , VT
 PVCs
• Frequent >10% of all beats : myopathy
• r/o structural heart disease
• Benign if without high risk features
• Treatment for symptomatic or high burden
• Bb , ccb , antiarrhythmic
 VENTRICULAR TACHYCARDIA
• Nonsustained vs sustained ( > 30 seconds )
• Structural heart disease vs idiopathic
• Regular , wide complex
• Monomorphic vs polymorphic
• Polymorphic ( normal vs prolonged QT )
• Management ( stable vs unstable , pulseless ?)
• Procainamide( avoid in structura disease ,
amiodarone , lidocaine )
• Synchronised dc vs defibrillation
 Ventricular fibrillation
• Bizzare rhythm
• Defibrillation and CPR