This week in morning report we discussed a case of a woman presenting with palpitations leading to syncope with an ultimate diagnosis of AV-nodal re-entrant tachycardia. We started our discussion by reviewing an approach to palpitations which can include several etiologies including non-cardiac causes. We focused in on supraventricular tachycardias (SVT) and defined some of them and reviewed pathophysiology. See below for the highlights!

Our fictional patient case in Morning Report is a woman with two episodes in the past month of palpitations leading to syncope. Each episode has no clear trigger

1. Differential Diagnosis of Palpitations

Cardiac causes	Arrhythmias – Atrial fibrillation – Atrial fibrillation – AV re-entrant tachycardia – AV-nodal re-entrant tachycardia – Multifocal atrial tachycardia – Wolff-Parkinson White or pre-excitation syndromes – Brugada (sodium channel gene mutation, can lead to sudden cardiac death) – Ventricular tachycardias / Ventricular fibrillation – QT prolongation –> leading to Torsades de Pointes (think about medications such as anti-emetics – ondansetron, metoclopramide, domperidone), anti-psychotics such as haloperidol, quetiapine, antibiotics such as fluoroquinolones, TCAs such as amitriptyline or nortriptyline Valvular heart disease Autonomic dysfunction Sick sinus syndrome Atrial or ventricular premature contractions
Endocrine Causes	Pheochromocytoma (palpitations, flushing, labile blood pressure, diaphoresis) –> testing with 24 hour urine metanephrines Thyroid disease Hypoglycemia
Malignancy	Carcinoid syndrome
Pulmonary	Pulmonary embolism – look for S1Q3T3 on ECG, often sinus tachycardia
Drug-related	Caffeine Withdrawal from alcohol Beta-blocker withdrawal Cocaine use Pregnancy Nicotine
Hematologic	Anemia
Psychiatric	Panic disorder, anxiety
Infectious	Fever

In our case, the person had associated syncope and thus we reviewed that neurologic causes of syncope should be entertained including epilepsy, stroke/TIA, as well as other causes such as orthostatic hypotension.

2. Categorization of Arrhythmias

Our patient was having recordings of HR in the 170s on her Fit Bit device and episodes of palpitations were leading to syncope. We discussed an approach to cardiac arrhythmias and then focused specifically on SVT.

The supraventricular tachycardias are summarized below. Of note, supraventricular tachcardia with “aberrancy” refers to usually SVT with a bundle branch block. SVT with aberrancy demonstrates a wider QRS and the way to differentiate SVT from VT is summarized in section # 5 below.

3. SVTs – What are They?

The main SVTs to know about are summarized below:

a) Atrial Fibrillation

• The rhythm is IRREGULAR
• P waves not clearly seen
• “Fibrillatory waves” are often seen – they can either fine (amplitude < 0.5mm) or coarse (amplitude > 0.5mm)

b) Atrial Flutter

• Classic “saw tooth” pattern on ECG, best seen in leads II, III, aVF
• Rate is often 150 BPM
• Loss of isoelectric baseline
• AV block can be 2:1, 3:1, 4:1 which is the ratio of “saw tooth waves” to R complexes
• Usually the rhythm is regular except in situations of variable block

c) Multifocal atrial tachycardia

• At least three different P wave morphologies
• Rate 100 to 180 BPM
• Irregular
• Etiology: Usually seen in the setting of chronic obstrutive pulmonary disease (COPD), hypoxia, pulmonary hypertension

d) Atrio-ventricular re-entrant tachycardia

• Presence of accessory pathway (left free ventricular wall, posteroseptal, right free ventricular wall, anteroseptal)
• Antidromic versus orthodromic
• Orthodromic: Re-entry impulse circulates in antegrade direction through the AV node
• Antidromic: Impulse travels in retrograde direction through the AV node

Pre-excitation means that there is an accessory pathway between the atria and ventricles and the electrical impulse can therefore bypass the AV node. Ventricular depolarization starts earlier than expected (it starts where the accessory pathway inserts in the ventricular tachycardia). Wolff-Parkinson White (WPW) is when there is evidence of pre-excitation on resting ECG and also if the patient has recurrent tachyarrhythmias.

e) AV nodal reentrant tachycardia (AVNRT)

• Onset is sudden, termination also abrupt
• Usually initiated by a premature supra-ventricular beat (atrial or junctional)
• Retrograde P waves may sometimes be seen in leads II or III, best to look in V1 for pseudo R’
• P wave is not visible in most cases because it is buried in the QRS complex, but in some cases the P wave will be visible before or after the QRS complex. Either way, they are retrograde because of the direct atrial activation.

For patients with suspected supraventricular tachycardia, aside from ECG, investigations may include: ambulatory ECG monitoring such as Holter monitor may, exercise stress testing (for patients with exercise-associated arrhythmias), or stress testing (exercise or pharmacologic) for underlying myocardial ischemia (for those with symptoms of angina and risk factors for coronary artery disease.

4. Management of AV-nodal re-entrant tachycardia

Management is included below from the guidelines for acute AVNRT versus chronic/long-term management (first and second figures respectively). In the acute setting, Valsalva (modified) or carotid massage and/or adenosine is the first choice (no negtative inotropy). If ineffective and the patient is hemodynamically stable can consider IV beta blockers or diltiazem. If patients are unstable, then electrical cardioversion should be performed.

To determine the approach for chronic management, it is important to assess the following:
– Frequency of episodes
– Severity of symptoms
– Comorbid conditions
– Medication compliance
– Medication side effects
In some patients you may do pill in pocket approach or vagal maneuvers as needed

Catheter ablation is considered for patients with episodes of AVNRT that are either:
– Frequently occurring
– Refractory to medical therapy
– Poorly tolerated (eg, associated with near-syncope or syncope, angina, or severe dyspnea)
– Or result in admission to the hospital

5. Differentiating SVT from Ventricular Tachycardia (VT)

To differentiate SVT from VT, there are a few tricks listed in the table below. Below the table is an example fusion and capture beat that might be seen in VT. Fusion beat is a “superimposition” of a native QRS beat and the VT rhythm, while capture beat is a clear “capture” of a native QRS beat. These both point towards VT.

	Ventricular Tachycardia	Supraventricular Tachycardia
Clinical History	Underlying heart disease	Usually no underlying heart disease
Carotid massage	No response	May terminate
Cannon A waves	May be present	Not seen
AV dissociation	May be seen	Not seen
Fusion or Capture beats	May be seen	Not seen
Initial QRS deflection	May differ from normal QRS complex	Same as normal QRS complex

References:

1. Life in the Fast Lane (LITFL) is a great reference for key points on different rhythms and ECG examples – https://litfl.com/atrial-flutter-ecg-library/
2. Guidelines for SVT management – https://www.ahajournals.org/doi/epub/10.1161/CIR.0000000000000311
3. AVNRT, AVRT, Pre-excitation – https://ecgwaves.com/topic/pre-excitation-avrt-wolff-parkinson-white-wpw-syndrome/

Please feel free to forward any questions or comments to cmr@wchospital.ca!