Webinar # 16 Lecture: AVRT and AVNRT: Breaking the Circuit of Supraventricular Tachycardia

Clinical Scenario

            A previously healthy 11 year-old female presented to the emergency department with a “fast heart rate” that started about 2 hours prior to presentation. She was reportedly a healthy child and active in several sports. She had a fairly active day and had been swimming in a pool when her symptoms started. Her mother thought that she was just anxious, so took her home and had her try some deep breathing exercises. Persistence of symptoms prompted consult to the ED.

            She was seen anxious and coherent. Her height and weight were both on the 50^th percentile for age. She had a faint regular pulse of 210 beats per minute and her blood pressure was 100/70 mmHg. Cardiovascular examination revealed no murmur nor any signs of heart failure. The rest of the physical examination was unremarkable.

            The ECG of the patient is as follows:

Questions:

1. What is the diagnosis?
2. Management for the condition?

I. Normal Conduction System of the Heart

• Start in the sinoatrial (SA) node
• Through RA and LA
  • Atrial Contraction
• Through the atrioventricular (AV) node
  • Conduction is slowed down
• To the his bundle, right and left bundle branches, and purkinje system
  • Ventricular contraction

II. Mechanisms of Arrhythmia

• Reentry
  • Occurs when a propagating impulse fails to terminate after normal activation of the heart
  • The impulse persists and propagates as a continuous circuit around an anatomic obstacle leading to reexcitation of the heart
• Enhanced Automaticity
  • Accelerated generation of an action potential by abnormal tissues within the myocardium
  • The cells with enhanced automaticity exhibit increased firing rate compared with pacemaker cells
  • If the firing rate exceeds that of the SA node, the ectopic focus can be the dominant pacemaker of the heart

• Triggered Activity
  • Disturbances with recovery or repolarization
  • Interruption in repolarization (called afterdepolarization) can have sufficient magnitude that may reach threshold and trigger another action potential during repolarization

III. Classification of Tachyarrhythmia

IV. Supraventricular Tachycardia

• Abnormally rapid rhythm (tachycardia) that originates proximal to the bundle of His (supraventricular) caused by an abnormal mechanism
  • Typically narrow QRS complex
  • REGULAR rapid rhythm
  • Abrupt onset and termination
• Most common sustained arrhythmia in children
• Estimated incidence of 1 in 25,000 to 1 in 250 children
• Twice as common in females

AVRT versus AVNRT

A. Atrioventricular Reentry Tachycardia (AVRT)

• Accessory pathway is present
  • Can conduct electrical impulse antegradely, retrogradely, or both
• When an extra beat happens and the impulse is conducted through the ventricular myocardium, the impulse may be conducted back to the atria through the AP, and stimulates the atria, AV node and the ventricular conduction system again
• A loop of continuous, self-propagating impulse is formed and each turn will have corresponding ventricular contraction -> TACHYCARDIA

ECG Features

• Narrow complex
• Regular rhythm
• Rate is fixed
• P wave likely visible on ECG and displaced/retrograde to QRS complex (may not be present at all times)

B. Atrioventricular Nodal Reentry Tachycardia (AVNRT)

• No accessory pathway
• Abnormality is located in the AV node
• When an atrial extrasystole happens and the Fast Pathway is still refractory, the impulse will travel through the slow pathway and will result in ventricular systole
• When the slow pathway reaches the distal arm of Fast pathway, it is no longer refractory and impulse is transmitted retrogradely through it
• A continuous loop is formed and each turn will have its corresponding atrial and ventricular contractions -> TACHYCARDIA

ECG Features

• Narrow complex
• Regular rhythm
• Rate is fixed
• No P waves prior to QRS complexes because P waves are usually buried within QRS complex (not always the case)
• Difficult to differentiate AVRT versus AVNRT based on ECG alone
• Definitive diagnosis with electrophysiologic studies

V. Supraventricular Tachycardia in Emergency Setting

A. Common presenting symptoms:

• Palpitations
• Fatigue
• Lightheadedness
• Chest discomfort
• Dyspnea
• Presyncope, rarely syncope

B. History

• Symptoms
• Frequency and length of episode
• Onset and triggers
• Any underlying disease
• Medications
  • Triggering factors
• Used for underlying heart disease

C. Work-up

• Electrocardiogram during SVT
  • Narrow QRS complex
  • Regular rhythm, rate is fixed
  • AVRT – P waves may be visible
  • AVNRT – P waves are usually not visible
• Electrocardiogram during Sinus Rhythm
  • To look for signs of pre-excitation or presence of accessory pathway
• Echocardiogram
  • For those with sustained SVT to exclude possibility of structural heart disease
• Ambulatory 24-hour Holter monitoring
• Exercise stress testing

D. Management of SVT

1. Vagal Maneuvers

Valsalva Maneuver

• Forced expiration in a closed glottis
• Aortic pressure is transiently increased resulting in reflex slowing of heart rate

Carotid Massage

• Performed to transiently increase pressure in the carotid sinus resulting reflex slowing of heart rate
• Only one side should be massaged at a time
• Pressure is applied underneath the angle of the jaw in gentle circular motion for about 10 seconds

2. Adenosine

• Preferred agent because of its rapid onset and short half-life
• Blocks AV conduction, hence terminating the re-entry circuit in both AVRT and AVNRT
  • Hyperpolarizes the cells in the AV node – requires higher threshold to generate an action potential
  • Dose: 0.1 – 0.2 mg/kg
• Dose is given as rapid IV bolus followed by a saline flush
• Side effects: chest discomfort, flushing, acute bronchospasm, hypotension
• Documentation of response to adenosine provides an important diagnostic information

Responses to Adenosine and Differentials

3. Calcium Channel Blocker

• Verapamil (0.1 mg/kg) and Diltiazem (5 mkday)
• Inhibits L-type calcium channels in the SA and AV nodes resulting in decreased firing and slowed conduction, respectively
• Relatively contraindicated in <1 year old

4. Beta Blockers

• Block adrenergic receptors
• Causing decreased sympathetic tone
• Slowing of heart rate
• Metoprolol, atenolol, propranolol, and esmolol are effective in acute termination of SVT
• IV Esmolol dose: 200-400 ug/kg over 10 minutes
• Side effects: Bronchospasm, hypoglycemia, constipation, fatigue, insomnia, and nightmares

5. Amiodarone

• Blocks potassium channels
• Increases action potential duration by prolonging refractoriness
• LD 5 mg/kg over 20-60 minutes, followed by continuous infusion of 10-15 mg/kg/day
• Side effects: Photosensitivity, thyroid dysfunction, liver failure, weakness, peripheral neuropathy, and pulmonary fibrosis

6. Digoxin

• Increases vagal tone
  • Slowing AV conduction
  • Prolonging refractoriness
• Excreted primarily by the kidneys and must be used with caution in patients with renal failure
• Increased toxicity in hypokalemia, hypomagnesemia, hypocalcemia, myocardial ischemia, myocarditis

7. Cardioversion

• Electrical conversion of an organized tachycardia into a normal rhythm
• Energy should be delivered  using a shock SYNCHRONIZED to the QRS complex
• Dose initially at 0.5-1 J/kg and may be increased until 2 J/kg

E. Long-Term Management

• Referral to arrhythmia specialist is a must
• Educate the patient on performing vagal maneuvers if the tachycardia recurs
• Choice of long term therapy depends on type of tachyarrhythmia, frequency and duration of episodes, symptoms, and risks
• Medical management is a good option for many
  • Typical first line medications: Calcium channel blockers, beta blockers, digoxin
• Ablating the crucial component of the arrhythmia mechanism with RFA or cryoablation
  • High success rate (>90%)
  • Low complication rate (1-3%)

VI. Summary

• SVT is one of the most common rhythm disturbances presenting in the ED
• Reentry is the main mechanism of arrhythmia in SVT
• P waves may or may not be apparent in SVT
• SVT is generally a narrow QRS complex and regular tachycardia but may also present with wide QRS complex in some conditions
• Treatment options in the ED: vagal maneuvers, pharmacologic agents, and cardioversion
• Always do rhythm strip documentation when giving interventions
• Adenosine should be given and flushed rapidly
• Defibrillator should be switched to SYNC mode when doing cardioversion
• Wait for at least three seconds before lifting the paddles off the chest

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