ARRHYTHMIA

DR. Iyas J. Alwaheidi

EMERGENCY MEDICINE BOARD
ALSHIFA HOSPITAL 2016
 Arrhythmia
Objectives:

1- Mechanisms of arrhythmia
2- General approach
3- Bradydysrhthmia
4- Tachycardia
5- SVT vs Sinus tach (Both narrow complex and regular)
6- SVT with aberrancy vs VT ( Both wide complex and
regular)
7- Conduction abnormalities
• SA Node and AV node cells are slow conductors
activated by calcium, thus blocked by calcium
channel blockers such as verapamil

• Atrium, Bundle of His, and ventricle cells are

fast conducting and activated by sodium, thus
blocked by sodium channel blockers (class 1
anti-arrhythmics) such as quinidine, lidocaine
and propafenone
 Tachycardia Mechanisms:
1- Reentrance (impulse goes repetitively in pathway with two limbs one takes impulse away from
and one that carries it back to the site of origin, one of them have slow conduction )
1- Via AV node eg AVNRT
2- Via Accessory pathway (eg AVRT =in WPW syndrome, a congenital bundle of kent between
atrium and ventricle)
3- Sinus node Reentry

2- Automaticity
Enhanced Automaticity (focus fires spontaneously and repetitively, this focus can be in sinus
node, pacemakers in atrium, coronary sinus, AV valves, His-Purkinje, or the ventricles)
Abnormal Automaticity (secondary to disease causing lower resting membrane potential )
eg , MAT, AT, AF , Ectopic atrial tachycardia or multifocal tachycardia in patients with chronic lung
disease OR ventricular ectopy after MI
• Factors that enhance automaticity include:
 SANS,  PANS,  CO2,  O2,  H+,  stretch, hypokalemia and hypocalcaemia

3- Triggering (in long QT followed by Torsade de point), and in digoxin toxicity

Bradycardia Mechanims:
1- impulse generation problem
2- impulse conduction problem
 General Approach
• KEY WORD : ORGAN PERFUSION
• Patients may be asymptomatic, or complaining
of palpitation, dizziness, syncope or sudden
death
1- Is the patient in CARDIAC ARREST? VF, pulseless VT, PEA,
ASYSTOLE
2- Is the patient stable or unstable?
3- Is the rhythm tachycardia (>100b/min), or bradycardia
(<60b/min)?
===================
4- Is the rhythm regular or irregular?
5- Is the rhythm wide or narrow complex?
WIDE >0.12sec causes: SVT with preexisting or rate related BBB,
Ventricular arrhythmia, a pacemaker, or the presence of metabolic
abnormality (k) or toxins (TCA toxicity)
NARROW : conducted through normal pathways, and almost
always begin above or within AV node
6- Are P wave present? If so, are they associated with QRS
complexes? These two keys direct us to origin of rhythm
 Bradydysrhythmia
1- Sick sinus syndrome 2- Sinus Arrest
3- Idioventricular rhythm
4- AV blocks
Tachycardia
 ST vs SVT
• Gradual onset and termination
• HR= 220-age
• P wave : Identical to normal sinus rhythm P wave
• R-P Relationship: long
A physiologic response, when body increase HR to
meet metabolic demands or maintain blood pressure
Cardiac Output = HR * Stroke volume
BP= Cardiac output * SVR
Treat the cause
 AF
• Can be due to HTN, cardiomyopathy, valvular
heart desease, sick sinus, WPW, thyrotoxicosis
or ETOH
• Therapy is either rate control via slowing AV
node conduction with stroke prophylaxis or
rhythm control
 AF rate control
• Beta-blockers
Good for hyperthyroid or post-MI patients with a-
fib
Esmolol is good for acute management

• Digoxin increases vagal tone, thus indirectly

slowing AV node conduction. But it is used
essentially only in patients with LV dysfunction
because it’s inotropic.
• Calcium Channel Blockers
Nondihydropyridines (verapamil or dilitiazem)
block AV node conduction but also have negative
inotropy, so don’t use in CHF.
Dihydropyridines (nifedipine, amlodipine,
felodipine) have no effect on AV node conduction
• Adenosine is too short acting to be of any use
in a-fib
 Rhythm control
• Rhythm control does not decrease thromboembolic risk and may
be proarrhythmic
Class 1A (quinidine, procainamide, disopyramide) slows conduction
through HIS can cause torsades de pointes during conversion. They
also enhance AV node conduction, so they should be used only after
rate is controlled

Class 1C (propafenone, and flecainide) slow conduction through HIS

are good first choice.

• Amiodarone is good if patient is post-MI or has systolic dysfunction

 When to cardiovert in AF?
• Cardiovert if symptomatic
• Patients with a-fib for more than 2 days should
be receive 3 weeks of anticoagulation before
electrical cardioversion.
• Give coumadin for 4 weeks after cardioversion
SVT with aberrancy vs VT
 CONDUCTION ABNORMALITIES
• Above AV node, supranodal
(sinu-atrial block=exit block), intra-atrial block

• At level of AV node, nodal (1st ,2nd,3rd degree AV blocks)

• Below AV node, (infranodal, intraventricular block)

2nd, 3rd degree AV BLOCK
LBBB,LAFB, LPFB, Bifasciular, Trifascular
RBBB,