Narrow-Complex Supraventricular Tachycardia Lecture Review

Treatment and Management Strategies for Supraventricular Tachycardia (SVT)

• Two-Tier Level of Treatment: Clinicians should approach SVT management in two distinct phases:

  • Emergent and Acute Phase: Treatment of SVTs should be handled as a whole group when the patient is unstable. This is because it is often difficult or impossible to differentiate specific rhythms when seconds count in an emergency.

  • Focused Treatment: Once the patient is hemodynamically stable, focused treatment of the individual rhythm can be instituted after isolation and further study of the specific arrhythmia.

• 2015 ACC/AHA/HRS Guideline Strategy: A new unified strategy was adopted to treat SVTs as a whole, providing a higher safety profile. This approach allows clinicians of all training levels to provide emergent treatment without requiring absolute certainty in an exact diagnosis.

• Terminology Note: The term "Paroxysmal SVT," previously used to identify rhythms with rapid onset and termination, is no longer in use.

Definitions and Overview of Supraventricular Tachycardias

• Definition of SVT: A supraventricular tachycardia is a rhythm with a ventricular rate greater than or equal to $100\,\text{beats per minute (BPM)}$ where the rhythm originates or is maintained by tissue in the sinus node, atria, atrioventricular (AV) node, the bundle of His, or a combination of these sites.

• Mechanisms of Tachycardia:

  • Reentry Circuit Loop: The most common mechanism where an individual loop triggers the rhythm.

  • Individual Focus: Influenced by increased automaticity.

• Classification by QRS Width:

  • Narrow-Complex SVT: QRS complexes are < 0.12\,\text{seconds} wide. These are narrow because the depolarization wave utilizes the normal electrical conduction system of the ventricles.

  • Wide-Complex Tachycardia (WCT): QRS complexes are $\ge 0.12\,\text{seconds}$ wide. These occur when waves travel through aberrant pathways or by direct cell-to-cell transmission.

• Prevalence Statistics (Common Narrow-Complex SVTs):

  • AV Nodal Reentry Tachycardia (AVNRT): Most common; responsible for approximately $60\%$ of cases.

  • AV Reentry Tachycardia (AVRT): Accounts for approximately $30\%$ of cases.

  • Atrial Tachycardia: Accounts for approximately $10\%$ of cases.

  • Note: Atrial fibrillation and atrial flutter are excluded from these specific statistics as they are in a class by themselves; however, atrial fibrillation is the most common pathologic arrhythmia seen clinically.

Detailed Review of Specific Narrow-Complex SVTs

• 1. Physiologic Sinus Tachycardia:

  • Development: A normal response to stressors like exercise, fever, dehydration, anxiety, hyperthyroidism, or caffeine.

  • Pacer Site: Sinus node.

  • Characteristics: Sinus P waves precede every QRS. Heart rates are typically between $100\,\text{BPM}$ and the maximum heart rate calculated as $220 - \text{patient's age} = \text{Max HR}$.

  • Onset/Termination: Not paroxysmal; shows a "warm-up" period of gradual increase and a "cool-down" period of gradual slowing.

• 2. Inappropriate Sinus Tachycardia:

  • Definition: Sinus tachycardia in the absence of a physiological cause.

  • Subtypes: Resting HR > 100\,\text{BPM} or exaggerated HR responses to minor exertion.

  • Limits: Sinus rates rarely reach $200\,\text{BPM}$ in these patients; no known cause is identified, and it typically causes no structural dysfunction.

• 3. Focal Atrial Tachycardia (Focal AT):

  • Mechanism: Increased automaticity at a single ectopic atrial focus. In rare diseased cases, microreentry circuits are used.

  • ECG Features: Flat baseline between P waves (unlike undulating sawtooth flutter). Most common atrial rates are $150-250\,\text{BPM}$, though documentation shows rare cases up to $400\,\text{BPM}$.

  • Conduction: Most common ratio is $2:1$, though $1:1$ is possible.

  • Clinical Warning: Focal AT with a $2:1$ block should trigger an immediate search for digoxin toxicity.

  • Progression: It is a risk factor for Atrial Fibrillation due to the formation of isolated tissue islands with different refractory periods.

• 4. Multifocal Atrial Tachycardia (MAT):

  • Incidence: Comprises < 1\% of SVTs.

  • Cause: Firing of at least 3 different pacemakers. Rate is typically $100-150\,\text{BPM}$ but can reach $250\,\text{BPM}$.

  • ECG Features: Variable P-wave morphologies and PR intervals. Flat baseline segments exist between complexes, though they become hard to see at high rates.

  • Clinical Association: Strongly associated with severe Chronic Obstructive Pulmonary Disease (COPD); treatment focuses on hypoxemia and respiratory compromise.

• 5. AV Nodal Reentry Tachycardia (AVNRT):

  • Demographics: More common in women; typically occurs in the 30s and 40s.

  • Rates: Typically $170-220\,\text{BPM}$, but can range $150-250\,\text{BPM}$.

  • Mechanism: Dual pathways in the AV node. The fast pathway has a long refractory period; the slow pathway has a short refractory period. Initiation is often triggered by PACs.

  • ECG Features: Retrograde P waves (negative in II, III, aVF) often buried in the QRS or peeking out as pseudo-S waves (leads II, III, aVF) or pseudo-R waves (lead V1).

• 6. Orthodromic AV Reentry Tachycardia (AVRT):

  • Mechanism: Reentry loop between the AV node and an accessory bypass tract. Impulses travel down the AV node normally (orthodromic) and return to the atria via the accessory pathway.

  • ECG Features: Narrow QRS complejos. Rate is usually $150-250\,\text{BPM}$. Better tolerated than antidromic AVRT because the AV node provides a physiologic block safeguard.

  • Preexcitation: Visible outside of tachycardia as delta waves and short PR intervals (Wolff-Parkinson-White pattern).

• 7. Junctional Tachycardia:

  • Mechanism: Increased automaticity at the AV node. Rates typically $100-200\,\text{BPM}$.

  • ECG Features: Inverted P waves occurring before, after, or buried in the QRS. Normally narrow complexes unless rate-related aberrancy occurs.

  • Clinical Context: Often seen post-AMI, in digoxin toxicity, acute myocarditis, or following cardiac surgery due to node irritation.

• 8. Atrial Flutter:

  • Mechanism: Atrial macroreentry circuit firing at $250-350\,\text{BPM}$.

  • ECG Features: Continuous undulating "sawtooth" baseline (F waves). Classic pattern is an atrial rate of $300\,\text{BPM}$ with a $2:1$ conduction, resulting in a ventricular response of $150\,\text{BPM}$.

• 9. Atrial Fibrillation:

  • Mechanism: Irregularly irregular rhythm with no observable P waves.

  • ECG Features: Random oscillations (f waves) best seen in lead V1, with rates between $400-600\,\text{BPM}$. Rapid uncontrolled Afib may appear regular at first glance, but any consistent irregularity indicates AF until proven otherwise.

Clinical Presentation and Historical Evaluation

• Primary Determinant: The clinical manifestation depends on how the ventricles perform. Young, healthy patients tolerate SVT well; older patients or those with CAD may not.

• Assessment Goals:

  1. Determine hemodynamic stability (Signs of instability require emergent action).

  2. Diagnose the specific rhythm (secondary goal).

• Symptoms: Palpitations (most common), anxiety, chest pain, light-headedness, diaphoresis, shortness of breath, polyuria (due to increased atrial natriuretic factor), and rarely syncope.

• Palpitation Patterns:

  • Sudden and regular: Reentrant SVTs (AVNRT, AVRT, Atrial Flutter).

  • Gradual and regular: Sinus or Junctional tachycardia (warm-up/cool-down).

  • Irregular: Premature complexes, MAT, or Atrial Fibrillation.

• Physical Examination Clues:

  • Unstable Signs: Mental confusion, pallor, cyanosis, diaphoresis, cool/clammy skin, poor capillary refill, rapid shallow breathing, hypotension.

  • Cannon A Waves: Large jugular venous pressure spikes occurring when the right atrium contracts against a closed tricuspid valve. Frequently reported by AVNRT patients as "pounding in the neck."

Diagnostic Procedures and ECG Analysis

• The Multi-Lead Necessity: Single leads often lead to misdiagnosis. The isoelectric P-wave lead (often lead II) may make P waves invisible, whereas lead V1 (placed at the right anterior chest) can see them clearly.

• Isoelectric Segments: Segments at the start or end of a QRS that cannot be distinguished from the baseline. Clinicians must measure the widest interval across multiple leads to avoid false low QRS width measurements.

• AV Node Dependence:

  • Dependent Rhythms: AVNRT, AVRT, Junctional Tachycardia. These respond well to vagal maneuvers and adenosine.

  • Independent Rhythms: Sinus tachycardia, Atrial tachycardia, Atrial Flutter, Atrial Fibrillation.

• Vagal Maneuvers: Valsalva maneuvers, carotid sinus massage, and cold-water immersion. Carotid sinus massage requires auscultation for bruits and checking for history of TIAs/stroke before performance.

• AV Dissociation: Pathognomonic for ventricular tachycardia (VTach). Its presence in a narrow-complex SVT rules out AVNRT and AVRT.

• Electrical Alternans: Variation in R-wave amplitude. Ominous sign of cardiac tamponade if paired with distended neck veins and hypotension, but otherwise often a benign finding related to respiratory pressure changes.

Pharmaceutical Intervention: Adenosine

• Profile: Ultra-short-acting agent; slows sinus node automaticity and AV conduction for < 5\,\text{seconds}.

• Diagnostic Trial: Used to slow AV conduction to reveal underlying P or F waves.

• Success Rates: $6\,\text{mg}$ IV push offers $60-80\%$ success; a subsequent $12\,\text{mg}$ dose offers $90-95\%$.

• Administration Guidelines: Must be a very rapid IV push followed by a normal saline flush, then raising the arm above heart level. For central lines, initial dose should be reduced to $3\,\text{mg}$.

• Contraindications: Methylxanthines (theophylline, caffeine) block its effects. Contraindicated in asthma/active wheezing, second or third-degree AV block, sick sinus syndrome, and known hypersensitivity.

• Side Effects: Facial flushing, anxiety, chest pain (feeling of "dying"), and brief asystole.

Hemodynamic Consequences of Tachycardia

• Cardiac Output ($\text{CO}$): Determined by stroke volume ($\text{SV}$) and heart rate ($\text{HR}$). $\text{CO} = \text{SV} \times \text{HR}$.

• Relative Ischemia: Faster heart rates increase myocardial oxygen demand. If demand exceeds supply, the tissue becomes ischemic and fails to contract properly, leading to shock.

• Impact on Diastole: Rapid rates shorten the diastolic phase significantly more than the systolic phase. Since ventricles fill during diastole, filling time and end-diastolic volume decrease, lowering blood pressure.

• Loss of Atrial Kick: Atrial contraction normally adds an extra stretch/overfill to the ventricles to maximize contraction. Loss of this kick (e.g., in Afib or retrograde conduction) reduces stroke volume.

• Synchronized vs. Unsynchronized Contraction: SVTs are generally better tolerated because the ventricles contract symmetrically using the normal conduction system. WCTs are more dangerous due to the lack of synchronized ventricular activation.