Supraventricular tachycardias are related disorders where the elevation in heart rate is driven by pathophysiology in the atria. This group falls under the larger umbrella of tachyarrhythmias and includes paroxysmal supraventricular tachycardias (PSVTs), ventricular pre-excitation syndromes (i.e. Wolff-Parkinson-White), atrial flutter, multifocal atrial tachycardia, and atrial fibrillation. Sinus tachycardia is not itself a pathologic arrhythmia. The diagnosis of these conditions can be made with an electrocardiogram (ECG), and treatment differs between conditions.

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Image: “SVT Lead II” by displaced user. License: Public Domain


Sinus Tachycardia

Etiology

  • Normal physiological response to exercise
  • Normal physiological response to a decrease in vagal tone (reflex tachycardia)
  • Sympathetic stimulation in pathological conditions: fever, pain, hyperthyroidism, hypovolemia, sepsis, anemia, pulmonary embolism, myocardial infarction
  • Exposure to stimulants (nicotine, caffeine, amphetamines), anticholinergic drugs, beta-blocker medication withdrawal, illicit drugs (cocaine)

Clinical presentation

  • Palpitations
  • Postural orthostasis: fatigue, lightheadedness, exercise intolerance

Diagnosis

tachycardia-ecg

Image : “Sinus tachycardia! DD atrial flutter.” CG of sinus tachycardia showing sinus rhythm (normal P wave and QRS morphology) with a rate > 100 beats per minute (around 150). By MoodyGroove. License: CC BY-SA 3.0

  • Heart rate greater than 100 beats per minute with normal P waves and QRS complexes observed via ECG
    • Rate of impulses arising from the sinoatrial node is elevated.
  • Sinus tachycardia is typically regular between 100 – 180 beats per minute.
  • Determine underlying cause
    • Volume depletion vs. infection vs. other medical conditions 
    • Via CBC, WBC, TSH, angiography, urine drug test, etc.

Treatment

  • Reverse the underlying cause
  • If reversible causes have been excluded, consider beta-blockers, then ivabradine, then catheter ablation.

Video Gallery

Tachycardia: For The Boards by Carlo Raj, MD

Paroxysmal Supraventricular Tachycardias (PSVTs)

Etiology

  • Presents in young adulthood
  • Prevalence is similar in males and females and increases progressively with age.
  • 60% of PSVT cases are due to atrioventricular nodal reentry tachycardia (AVNRT).
    • Two different electrical pathways in the atrioventricular (AV) node form a loop that continuously conducts impulses leading to tachycardia.
    • The two pathways form a “fast” and “slow” pathway.
      • Anterograde conduction along the “slow” pathway 
      • Retrograde conduction along the “fast” pathway
  • 30% of PSVT cases are due to atrioventricular reciprocating tachycardia (AVRT).
    • Reentry loop is formed by a normal AV node.
    • Abnormal presence of an accessory conduction pathway between the atria and the ventricles
    • Typified by Wolff-Parkinson-White syndrome
  • 10% of PSVT cases are due to atrial tachycardia (AT) and sinoatrial nodal reentrant tachycardia (SANRT).

Clinical Presentation

  • Palpitations
  • Syncope or presyncope
  • Lightheadedness or dizziness
  • Diaphoresis
  • Chest pain
  • Shortness of breath

Diagnosis

  • Sudden-onset episodes of heart rate greater than 100 bpm caused by reentry involving the atrium, AV node, or an accessory pathway
  • PSVTs are typically regular and between 140 – 250 bpm with narrow QRS complexes (<120 ms).
  • Evaluate for signs and symptoms of hemodynamic (in)stability.
  • Assess ECG for type of narrow QRS complex tachycardia present.
    • Regular vs. irregular → P wave identification → atrial rate, P wave morphology, RP relationship, and AV relationship

Image: “Lead II (2) ECG EKG tracing of Supraventricular tachycardia SVT in a 40-year-old male” Example of an ECG tracing of supraventricular tachycardia with a regular rhythm, hidden P wave morphology (most noticeable in the third beat), narrow complex QRS <120 ms, and a rate >150 bpm (around 188 bpm). By James Heilman, MD. License: Public Domain

Treatment

  • Treat hemodynamic instability via urgent DC cardioversion if present.
  • AVNRT and AVRT:
    • Attempt vagal maneuvers (Valsalva, carotid massage) to slow conduction through the AV node
    • If ineffective, IV adenosine is the first-line pharmacotherapy to terminate the rhythm.
    • IV calcium-channel blockers (e.g., verapamil), IV beta-blockers (e.g., propranolol), or digoxin may be used to slow conduction through the AV node in acute or preventative treatment if adenosine is not effective.
    •  If persistent, AVRT: Consider IV procainamide or IV amiodarone

Video Gallery

Paroxysmal Supraventricular Tachycardia (PSVT) by Julianna Jung, MD, FACEP

Wolff-Parkinson-White Syndrome (WPW)

Etiology

  • Atrial impulses pass to the ventricles through both the AV node and an accessory pathway (bundle of Kent).
    • Leads to ventricular pre-excitation
  • Accessory pathway is often congenital in origin
    • Failure of resorption of the myocardial syncytium at the annulus fibrosis during development
  • Characteristic ECG findings in WPW are observed due to the accessory pathway activating the ventricle slightly before the AV nodal pathway.
    • Shortened PR-interval (< 0.12 s)
    • Slurred QRS upstroke (delta wave)
    • Widened QRS (> 120 ms)

Clinical Presentation

  • Majority of patients are asymptomatic.
  • Patients can develop wide QRS-complex atrial fibrillation with rapid ventricular response (RVR) as part of the AVRT reentry tachyarrhythmia.
    • Accompanying palpitations, lightheadedness or dizziness, syncope or presyncope, chest pain, or sudden cardiac arrest

Diagnosis

  • Short PR interval (< 0.12 s) and a delta wave: confirm the diagnosis of the WPW pattern on ECG
  • Invasive electrophysiology testing: confirming the diagnosis in rare circumstances (e.g., short effective refractory periods in competitive athletes)

Treatment

  • Indicated in patients with symptomatic tachyarrhythmias to prevent the rapid ventricular response (RVR).
    • Do not use AV-blocking agents to treat the tachyarrhythmia as slowed conduction through the AV node will worsen conduction through the accessory pathway and can be fatal.
    • Drugs for aborting the arrhythmia:
      • Procainamide 
      • Amiodarone
    • Catheter ablation of the accessory pathway for long-term control
    • Digoxin and calcium channel blockers are dangerous in WPW because they block the normal AV node and force conduction in abnormal pathway

Image: “Wolff Parkinson White Syndrome” by Tom Lück. License: CC BY 3.0

characteristic delta wave seen in a patient with WPW

Image: “Delta Wave” A characteristic delta wave seen in a patient with WPW. Note short PR interval. By James Heilman, MD. License: CC BY-SA 3.0

Video Gallery

Tachycardia: Wolff-Parkinson White Syndrome: Definition and Pathogenesis by Carlo Raj, MD

Atrial Flutter and Atrial Fibrillation

Atrial flutter

  • Rapid, regular atrial activity at a rate of 180–300 bpm 
  • Varying degrees of conduction block at the AV node (due to the refractory period)
  • Generally caused by reentry over a circuit of tissue along the tricuspid valve annulus  →  depolarizes large amounts of the atria throughout the cycle
  • Diffuse atrial polarization leads to its characteristic “sawtooth” pattern on ECG

Image: “Sawtooth appearance on ECG” Sawtooth appearance on ECG is characteristic of atrial flutter. By Lecturio.

Atrial fibrillation

  • Irregular atrial rate so fast that there are no discernable P waves on ECG
  • Patients have an “irregularly irregular” ventricular rhythm.
  • Generally caused by reentry in random circuits around the atria caused by abnormal electrical discharges that originate in the pulmonary veins
  • The feared complication of atrial fibrillation is stroke secondary to thrombus formation in the left atria.

Image: “Esophageal cancer presenting with atrial fibrillation” Example of an ECG tracing showing atrial fibrillation with irregularly irregular RR intervals and loss of P waves. By Bayraktar UD, Dufresne A, Bayraktar S, Purcell RR, Ajah OI. License: CC BY 2.0 Edited by Lecturio.

Video Gallery

Tachycardia: Atrial Flutter by Carlo Raj, MD
Tachycardia: Atrial Fibrillation: Pathogenesis by Carlo Raj, MD

Multifocal Atrial Tachycardia (MAT)

Etiology

  • 60% of cases are associated with significant pulmonary disease
    • COPD > pneumonia, pulmonary embolism, etc. 
    • Associated cardiac disease: coronary, valvular, hypertensive
  • Can also be associated with hypokalemia, hypomagnesemia, medications (e.g., isoproterenol, aminophylline, theophylline), chronic renal failure
  • Multiple atrial origin sites cause different and unique P wave morphology

Clinical presentation

  • Symptoms predominantly relate to the underlying precipitating illness rather than the arrhythmia.
  • MAT can worsen systemic oxygenation in patients with advanced pulmonary disease and exacerbate heart disease.
    • Cardiac decompensation: angina, dyspnea, orthopnea

Diagnosis

  • Atrial rate >100 bpm
  • Three or more distinct P wave morphologies on ECG
    • Each unique P wave morphology indicates a different atrial origin site
    • P waves return to baseline, separated by isoelectric intervals
  • P-P intervals, P-R duration, and R-R intervals that vary
Multifocal atrial tachycardia

Image: “Multifocal atrial tachycardia” Black arrows indicate multiple distinct P wave morphologies on ECG indicating MAT. By Jer5150. License: CC BY-SA 3.0

Treatment

  • Aimed at underlying disease
    • Magnesium and potassium replacement
  • Calcium channel blockers (e.g. verapamil) and beta-blockers (e.g. metoprolol) can be used with caution related to the underlying disease.
    • Avoid beta-blockers in lung disease
  • Ablation: rarely required since episodes are brief and resolve with correction of underlying abnormality
    • Indicated in persistent symptomatic MAT if patient does not respond to or cannot tolerate pharmacotherapy

Video Gallery

Tachycardia: Multifocal Atrial Tachycardia: Pathogenesis by Carlo Raj, MD

Clinical Relevance

The following conditions may be associated with the development of tachyarrhythmias.

  • Hyperthyroidism: an excess of thyroid hormones T3 and T4. Can promote the development of tachyarrhythmias, particularly atrial fibrillation. 
  • Structural heart disease: structural heart disease can be arrhythmogenic, and patients should be evaluated with echocardiography. Structural abnormalities may be a consequence of congestive heart failure, myocardial infarction, valvular heart disease. 
  • COPD: a spectrum of conditions characterized by irreversible airflow limitation correlated to smoking. COPD is a result of obstructive inflammation of the small airways as well as changes in the lung parenchyma and pulmonary vasculature. Advanced pulmonary disease is associated with the development of multifocal atrial tachycardia. 
  • Intoxication/ingestion: there are numerous pharmacologic and illicit drugs that may lead to sinus tachycardia or promote arrhythmias. 
  • Electrolyte abnormalities: several abnormalities are associated with the development of ventricular tachyarrhythmias, including hypokalemia and hypomagnesemia.
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