Narrow Complex Tachycardia - Approach

Narrow complex tachycardias are Supraventricular tachycardias, meaning only that they originate above the ventricles.

 

 

Approach to sinus tachycardia:

• Arises almost always as a physiologic response or compensation to an underlying trigger, and this must be identified
• Common causes:
  • Exercise
  • Catecholamine surge: pain, fear, anger, stress
    • MI
    • Fever
    • Anxiety
    • PE
  • Decreased effective circulating volume
  • Sepsis: to augment CO to compensate for low SVR
  • Systolic heart failure: to compensate for low stroke volume
  • Endocrine abnormalities: hyperthyroidism, pheochromocytoma
  • Hypoxia
  • Anemia
• Should not be treated unless underlying triggers have been ruled out, and it is deemed to be inappropriate
  • Inappropriate causes: impaired autonomic control, POTS
• Consequences: decreased cardiac output from reduced diastolic filling time, myocardial ischemia from increased oxygen demand and reduced coronary perfusion

 

 

Approach to narrow complex tachycardia:

• Narrow QRS indicates that depolarization of the ventricles is via the His-Purkinje system, and thus originates at or above the AV node
• First step is to evaluate the clinical status of the patient - if stability is at all a concern, proceed to emergent cardioversion
• Next step is evaluate the ECG for clues:
  • Onset: presence of PAC or PVC prior to arrhythmia, as well as sudden onset, suggest reentrant tachycardia
  • Termination: terminal P wave indicates that AV block terminated the arrhythmia, suggesting AV nodal dependence
  • Rate: Rate of 150 suggests atrial flutter, very fast rates suggest flutter or atrial tachycardia
    • Fixed rate also suggests flutter or SVT (AVNRT, AVRT, AT)
  • Rhythm:
    • Irregular: atrial fibrillation, flutter with variable conduction, MAT
    • Regular: sinus tachycardia, atrial flutter, atrial tachycardia, sinus node reentrant tachycardia, AVNRT, AVRT, junctional tachycardia
• Vagolytic maneuvers can help identify atrial activity, as well as provide information regarding AV nodal dependence if arrhythmia terminates
  • Maneuvers: carotid sinus massage (check for bruits, hx CVA), valsalva, cold water to face, adenosine
    • Adenosine has half-life of less than 10 seconds, and thus must be pushed rapidly followed immediately by flush (use two-way stopcock)
      • Adverse effects: nausea, flushing, chest tightness, hypotension, heart block, asystole
      • Avoid in patients with asthma, or post-heart transplant
  • Atrial activity
    • P wave morphology: all P waves are not sinus!
      • Sinus P waves are positive in inferior leads, I, and aVL, negative/biphasic in V1, and negative in aVR
    • RP interval: distance from R wave to P wave (see attached Mayo Clin Proc review)
      • Very short: suggests typical AVNRT, given rapid retrograde conduction
      • Short: suggests AVRT
      • Long: suggests atrial tachycardia or sinus tachycardia
  • AV nodal dependence: whether or not AV node is part of reentrant circuit
    • Independent: arrhythmia persists despite interruption of AV nodal conduction
      • Sinus tachycardia
      • Sinus node reentrant tachycardia
      • Atrial tachycardia
      • MAT
      • Atrial fibrillation
      • Atrial flutter
    • Dependent: arrhythmia terminates upon interruption of AV nodal conduction
      • AVRT
      • AVNRT
      • Junctional ectopic tachycardia

 

Overview of atrial flutter

• Pathophysiology: macroreentrant rhythm, typically involving tricuspid annulus
  • Electrically unstable, and often degenerates into atrial fibrillation or reverts to sinus rhythm
• Causes:
  • Pulmonary disease (e.g. PE)
  • Sympathetic tone (e.g. postop, pain)
  • Infection
  • Valvular disease
  • Post-cardiac surgery
  • Valvular disease
  • Atrial enlargement (e.g. secondary to hypertension)
  • Hyperthyroidism
• Management
  • Rate control: can be difficult, given that ventricular rate drops in fixed intervals (e.g. 150, 100, 75, etc)
    • In addition, AV node is less refractory than in atrial fibrillation, and thus high doses of AV nodal blocking agents can be required
    • Agents:
      • CCB (verapamil, diltiazem): negative inotropes, and cause peripheral vasodilation
      • BB (metoprolol, esmolol): also negative inotropes
        
      • Amiodarone: has some negative inotropic effects, and can also cause unintended cardioversion
        
      • Digoxin: slow onset of action, and dependent on vagal tone for effect; however, has positive inotropic effects
    • Remember that CO = HR x SV, and SV = contractility x preload
      
      • In atrial flutter, preload is impaired due to shortened diastolic filling time
        
      • Thus, negative inotropy can drop CO and BP
  • Restoration of NSR: improves hemodynamics, decreases oxygen demand, and alleviates symptoms
    • Options:
      • DCCV: requires conscious sedation, which may compromise hemodynamics
      • Pharmacologic: less effective, and agents carry some proarrhythmic risk
    • Anticoagulation:
      • As in atrial fibrillation, flutter >48h carries a risk of post-cardioversion embolism (~1% risk)
        • Thus, patients should be anticoagulated for 4 weeks prior to DCCV, or TEE performed to rule out LA clot (see attached NEJM paper)
      • In addition, even if no clot is present, there is a risk of embolism after cardioversion due to atrial stunning, which results in stasis within the LA
        • After cardioversion, patient should be anticoagulated for 4 weeks

 

Ddx can also be broken down by site of origin:

A. Atria
· SA nodal reentrant tachycardia - fairly rare, due to reentrant loop within the SA node.  Usually of little clinical consequence.  P-waves identical to sinus p-waves, but rapid onset and termination helps distinguish from sinus tachycardia.
· Atrial tachycardia – different p-wave morphology than with sinus rhythm.  Seen with CAD, COPD.
· Multifocal atrial tachycardia – 3 or more p wave morphologies, irregular, usually seen with severe lung disease (COPD)
· Atrial Flutter 
· Atrial Fibrillation

B. AV Node
· AV nodal reentrant tachycardia (AVNRT) – reentry from dual pathways within the AV node
· AV Reentrant Tachycardia (AVRT) – reentry with AV node and accessory pathway (includes Wolf-Parkinson White Syndrome)
· Junctional Tachycardia – due to increased automaticity at the AV junction

 

Major distinction is whether the rhythm is regular or not: 
Irregular Narrow Complex Tachycardia = 1) A-fib, 2) A-flutter with variable conduction, or 3) MAT

 

“Paroxysmal SVT” by convention excludes these three irregular rhythms, and includes:
1) AVNRT – 60% of cases
2) AVRT – 30%
3) Atrial tachycardia
4) SA node reentrant tachycardia

Clues that suggest AVNRT or AVRT are retrograde P-waves, or P-waves that are bured in the QRS, with characteristic abrupt onset and offset, with rates usually > 150. 

 

Immediate Management:
1) If unstable (i.e. hypotensive, altered mental status, chest pain) – immediate DC cardioversion
2) If stable – can try vagal maneuvers (i.e. carotid massage) although these are usually not very successful. 
3) Adenosine – given as a 6 mg IV push, followed immediately by saline flush (this is important, as half-life is around 5 seconds).

Effects on rhythms:
· Sinus tachy, Atrial tachy, MAT – will transiently slow the heart rate
· Atrial flutter – will increase the AV conduction ratio, which may “unmask” flutter waves
· AVNRT/AVRT – usually will abruptly terminate the rhythm, classically with a p-wave after the last QRS.

 

**Caution with adenosine in patients with active bronchospasm; other side effects include facial flushing, chest pain, palpitations, hypotension, and rarely asystole – so important to always have patient on monitor and crash cart nearby! **

 

(Christopher Woo MD, 10/9/10)

(Chanu Rhee MD, 2/11/11)