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Narrow Complex Tachycardia

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Sinus Tachycardia

Only Rate !

Every P wave is followed by a QRS

Every QRS is preceded by a P wave

Regularly regular

Rate >100

Treat the underlying cause !

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AVNRT :AtrioVentricular NODAL Reentrant Tachycardia

Start in or around the AV node hence, Atrial origin (narrow complex )
Occurs with a Premature beat (PAC)
SA node cannot depolarize the myocytes due to refractory period created by this ectopic origin
Namely SVT most common in young adults

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Characteristics

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Treatment

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Failed?

If vagal maneuvers fail, then medication it is !
Adenosine : first choice in AVNRT
Onset : 5-20 sec
Duration : 30-45 sec
Technique : Start adenosine by using rapid IV bolus (large, non– distal vein followed by a rapid flush) key is the rapid bolus technique with higher success noted after training to adhere to that tenet of delivery.
Or you can mix the drug with the flush in one syringe and give it rapidly !
First dose 6mg , second dose 12mg another 12mg if failed
Talk to the patient ! This is what will happen ! Do you want this ?

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Failed?

Reanalyze the rhythm if still SVT consider BB or calcium channel blockers

Esmolol

Metoprolol

Diltiazem

Last resort cardioversion with 100-200 j and expert opinion

Work up :

ECG , if recurrent Cardiology follow up

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AVRT : AtrioVentricular Reentrant Tachycardia

It’s a form of preexcitation where an AVNRT develop with a coexistent accessory pathway (WPW)
Can be narrow complex (Orhodromic) or wide complex (Antidromic) depending on the direction of the currant

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WPW in sinus rhythm

Sinus rhythm with a very short PR interval (< 120 ms)

Broad QRS complexes with a slurred upstroke to the QRS complex — the delta wave

Dominant R wave in V1 — this pattern is known as “Type A” WPW and is associated with a left-sided accessory pathway

Tall R waves and inverted T waves in V1-3 mimicking right ventricular hypertrophy — these changes are due to WPW and do not indicate underlying RVH

Negative delta wave in aVL simulating the Q waves of lateral infarction — this is referred to as the “pseudo-infarction” pattern

A delta wave is slurring of the upstroke of the QRS complex. This occurs because the action potential from the sinoatrial node is able to conduct to the ventricles very quickly through the accessory pathway, and thus the QRS occurs immediately after the P wave, making the delta wave.

Delta wave : some of the impulse already transmitted so part of the ventricle is starting to depolarize before the impulse transmit through the AV node given the Delta wave

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Characteristics

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Atrial Tachycardia

Usually regular

Atrial rate > 100 bpm

Abnormal P wave morphology and axis (e.g. inverted in inferior leads) due to ectopic origin

Unifocal, identical P waves

Isoelectric baseline Normal QRS morphology

An atrial rhythm with more than 100 QRS complexes/min arising from a non–sinus node site(s) within the left or right atrium.

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Atrial tachycardia

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Atrial fibrillation

Chaotic atrial discharge

No unifocal organized atrial depolarization

120-170 BPM (ventricular rate)

Multiple risk factors

No Distinct P wave

Irregularly irregular

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Atrial fibrillation

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Atrial flutter

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Atrial flutter

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Treatment

Treatment of AF and Aflutter depends on several factors

Hemodynamic Stability ?
Onset ?
Duration?
Precipitating factors ?
Comorbidity ?
CHAD-VASC

Treatment option are :

Rhythm control : chemical vs electrical
Rate control
Anticoagulation

Don’t assume the duration

Don’t convert >48 hrs

In longstanding AF cardioversion is less likely to succeed and start resuscitation and rate control

Rate control with goal of <120 ventricular rhythm

Diltiazem is the best in rate control

Healthy patient with new onset AF is more likely to convert in the next 48 hrs

IV calcium channel blockers (eg, diltiazem, verapamil)

or beta blockers (eg, metoprolol) are easily titrated and can be

followed by an oral agent.

Nodal agents should not be used for

rate control in the setting of accessory pathway conduction

because AV conduction—with retrograde conduction into the

accessory pathway—may be the only thing preventing the ventricular

rate from accelerating and degenerating into ventricular

fibrillation.

Consider pharmacological and/or electrical rhythm control for people with atrial fibrillation whose symptoms continue after heart rate has been controlled or for whom a rate-control strategy has not been successful.

100- 200 j in a fib

Start with 50 j in Aflutter

For stable patients with new-onset or newly recurrent atrial

fibrillation—defined as having a duration of 48 hours or less—or

in those with therapeutic anticoagulation, ED cardioversion is an

option unless valve disease, hypokalemia, or digitalis toxicity exist;

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A fib with WPW

Treat like a Vtach
Procainamide is first line , second line is amiodarone
AV nodal blocking agent is contraindication , why ?
Unstable patient or failure of pharmacological therapy :

Shock with 100-200J

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Multifocal Atrial Tachycardia (MAT)

Result from three different focus competing to pace the heart

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AF + low ejection fraction

AF can be a cause or a result of heart failure as both causes similar cellular changes
Treat both based on the acuity of the situation
Treat HF with standard therapy and treat AF initially with rate control to be then evaluated for rhythm conversion or implantable defibrillator
Find whether the AF is causing the HF (possibly reversible) or the HF causing AF and treat accordingly
Only two drugs has been tested and recommended to control the rhythm in AF with HFrEF :
Amiodarone
Dofetilide

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A fib with WPW

Treat like a Vtach
Procainamide is first line , second line is amiodarone
AV nodal blocking agent is contraindication , why ?
Unstable patient or failure of pharmacological therapy :

Shock with 100-200J

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Best of luck !