Tachyarrhythmia

Always consider the rhythm in the context of the clinical state of the patient. Any element of haemodynamic compromise necessitates immediate action.

Arrhythmias generally, and tachyarrhythmias specifically, are distinguished, on the basis of the QRS complex, into wide- and narrow-complex arrhythmias, respectively. This reflects a pragmatic approach, one based on differences in management between wide and narrow complex tachyarrhythmias,, because a wide complex suggests an arrhythmia of ventricular origin, and ventricular arrhythmias are associated with a more malign pathophysiology (structural heart disease) and poorer prognosis.

Treat any underlying cause or provoking factor for the arrhythmia:

• Hypoxia
• AMI (cardiac ischaemia)
• Electrolyte disturbance
• Drugs – incl. ethanol, nicotine, and caffeine
• Acid–base disturbance
• Fever
• Hypothermia [1]

Wide-complex tachycardia:

A wide-complex regular tachycardia (rate > 120-150+) is VT until proven otherwise, and demands immediate treatment to prevent VF ( wide complex and irregular) cardiac arrest. Occasionally, a person with a sustained VT will have little haemodynamic compromise (syncope, angina, left ventricular failure), in which case amiodarone can immediately be instituted. Amiodarone is a safe drug in the acute setting; most of its deleterious effects come with chronic use. Sometimes, a tachycardia with a wide complex is of supra-ventricular (and, there fore, of less malign) origin, and the wide complex courtesy of His-bundle disease–e.g. left bundle branch block.

Narrow-complex tachycardia

A tachycardia arising from the atria include atrial fibrillation (and flutter) and other tachycardias of supra ventricular origin, including the supraventricular tachycardia (SVT), paroxysmal atrial tachycardia, or the re-entry tachycardias that actually arise from the A-V node (junctional tachycardias). In these settings, the haemodynamic status of the patient is often determined by the ventricular rate transmitted across the A-V node such that some level of aberrance, i.e. a delay in conduction across the A-V node, affords a more modest ventricular rate, one conducive to haemodynamic stability. That is why patients with atrial fibrillation or flutter may have ventricular rates of about 150 bpm and be doing rather well. Often, that is all that is needed in managing atrial fibrillation, a touch of beta blocker to assist in A-V nodal conduction delay to give the ventricle a chance to refill after each systole. (Beta-blocker is contraindicated in the presence of significant pre-existing A-V nodal disease, as it can push these patients into complete heart block. But such patients will have declared themselves beforehand, as most will have evidence of second-degree heart block and be bradycardic rather than tachycardia).

• magnesium bolus +/- infusion
• amiodarone 150 mg bolus + 150 mg bolus +/- 150 mg bolus
  • long half-life and may prolong QT
  • more long-term adverse effects; may be best used acutely, then weaned after starting beta-blockers
• +/- beta-blocker vs. calcium-channel blocker: probably prefer beta-blockers, start low and go slow, but definitely avoid the combination of beta-blocker and calcium-channel blocker
  • sotalol (non-selective beta-blocker)
    • can cause prolonged Q-T / torsade: watch for ECG prolongation QT in first week
    • exacerbation LVF / bradycardia / COPD
  • metoprolol (cardioselective beta-blocker)
    • can exacerbate LVF / bradycardia / asthma
• +/- long-term digoxin, especially with heart failure
  • watch for digoxin toxicity [2]

An irregular narrow-complex ventricular rate of 150 bpm is AF with 2:1 block and a regular narrow-complex ventricular rate of 150 bpm (150-250) is SVT.

After assessing the nature of the QRS complex, wide or narrow, look at the ventricular rate (as guide to haemodynamic efficiency), are there any P-waves and, if so, what is the P-wave rate and rhythmicity and what, also, is the nature of the relationship, if any, between P waves and QRS complexes,.

4 steps in evaluating a tacchyarrthymia:

1. wide (> 12 ms or 3 small squares) or narrow complex?
2. what is the ventricular rate (and is it regular)?
   1. irregular:
      1. Atrial fibrillation (with aberrant conduction)
      2. Ventricular ectopic beats.
      3. VF
3. are there regular P waves?
   1. Sinus tachycardia (SVT or atrial flutter with 2:1 block and rate 150 can look like sinus tachycardia)
   2. absent:
      1. Atrial fibrillation / flutter
      2. Paroxysmal SVT
      3. VT
4. what is the relationship between P waves and the QRS complexes; or are the atria and ventricles, in fact, acting independent of one another (A-V dissociation)?

Pathophysiological mechanisms of tachyarrhythmias:

• re-entry: dual conduction pathways allow anterograde and retrograde conduction, respectively, affording the development, and sustainment, of a re-entry circuit; begin maximally, and with a fixed rate (no beat-to-beat variation), and cease just as abruptly
• automaticity enhanced: precipitated by adrenergic stimulation and medications such as digoxin, these arrhythmias show warm-up and slow-down periods and beat-to-beat variability
• triggered after-depolarisation: often caused by conditions that increase the QT interval, affording (early and late) after-depolarisation and more likely in the setting of a slow sinus rate and with digoxin therapy ³

Reference:

1. Australian College of Rural & Remote Medicine. Rural Emergency Skills Training Handbook. 3rd Edn. Brisbane: ACRRM, 2016: 66-71.
2. Farkas, Josh. “Atrial Fibrillation (AF) & Flutter complicating critical illness.” The Internet Book of Critical Care. Jan 6, 2017. Available at https://emcrit.org/ibcc/af/#digoxin. Accessed Aug 4, 2021.
3. Schwab, Theresa M. and Ross, Christopher H. “Narrow Complex Tachycardias.” In (Eds.) Amal Mattu, Jeffrey A. Tabas and Robert A. Barish. Electrocardiography in Emergency Medicine. Dallas, Texas: American College of Emergency Physicians, 2007: 45-58.

Further reading:

Sundhu, Murtaza et al. “Narrow Complex Ventricular Tachycardia.” Cureus vol. 9,7 e1423. 4 Jul. 2017, doi:10.7759/cureus.1423.