Much of the information below comes from Emergency Medicine Cases:

https://emergencymedicinecases.com/tachydysrhythmias/

tachyarrhythmias

We had a great case with VT in the 200's which the team successfully cardioverted to a NSR. So I thought this would be a good review for all of us. There are a lot of notes on this page but just three things to bring your attention to: 

1. When do we use procainmide vs amiodarone 

Procainamide is currently considered to be the first line medication for sustained monomorphic VT in stable patients.  

Use amiodarone: 

1. Polymorphic VT related to cardiac ischemia

2. ICD patient with VT above detect rate (usually >175 bpm)

3. VT in the cardiac arrest patient

Why do we use amiodarone instead of procainamide in pt's with ischemia? I don't know the answer to this...if someone does please explain... or Dr. Toe since your cardiology, can you find out?

*** The consensus to this is that: due to benefit of the beta blocker activity and procainamide a potent calcium channel blocker should be avoided in ischemia because it can be proarrhythmic ***

 

2. When do we use Calcium Channel Blocker vs Adenosine for SVT? 

Diltiazem is at least as effective as adenosine for conversion of SVT and has the advantage of lasting longer and not inducing an uncomfortable experience (often described as a feeling of near death) for the patient as observed with adenosine.

Use Adenosine in hypotensive pt's!

3.What do we shock at when doing electrical cardioversion? 

Make sure to sedate the pt and shock high! Go 200, if it's going to work it's going to work higher. There is actually not much cardiac injury from the shock it self, so go big and fix the problem. 

Podcast: 

https://emergencymedicinecases.com/tachydysrhythmias/

Episode Notes: 

General Approach to Tachydysrhythmias

Asking these three questions will help classify any tachydysrhythmia in most cases.

1.     Regular or irregular?

2.     Narrow or wide QRS?

3.     Are there P waves? P-QRS relationship? How many P waves for each QRS?

Tachydysrhythmias1.JPG

Wide & regular tachydysrhythmias

Ventricular Tachycardia (VT) vs SVT with aberrancy: Assume VT

Wide & regular = ventricular tachycardia until proven otherwise. Clinical stability does not differentiate between VT and SVT with aberrancy. Despite multiple ECG algorithms and rules to distinguish VT from SVT with aberrancy (Brugada, Wellens, Vereckei, R wave peak time) none are better than 90% specific to identify SVT with aberrancy. No feature or combination of ECG features is 100% specific for SVT with aberrancy. Hence, using an algorithm/rule, there is a 10% chance that you will label VT as SVT with aberrancy erroneously and if you treat the patient with AV nodal blockers, cardiovascular collapse may result.

 

There are several factors that make VT very likely:

1.     Prior MI, heart failure, recent angina and advanced age.

2.     AV dissociation (P and QRS complexes at different rates) and fusion complexes (sinus and ventricular beat coincide to produce a hybrid complex of intermediate morphology) on ECG (see images below)

3.     Pave Criteria – R-wave peak time >50ms in Lead ll

4.     Presence of 1st degree heart block on previous ECG

Tachydysrhythmias3.JPG

Arrows show AV dissociation (from Life in the Fast Lane blog)

Tachydysrhythmias4.JPG

The first narrow complex is a fusion complex

Remember that although advanced age makes a wide complex tachycardia VT much more likely than SVT with aberrancy, up to 50% of patients under 40 years of age who present with a wide complex regular tachycardia with have VT. In addition, response to adenosine does not rule out VT.

As per ACLS guidelines, If any tachydysrhythmia presents as unstable, the treatment of choice is synchronized electrical cardioversion.

For many stable patients, electrical cardioversion may be the preferred treatment of choice for VT. For example, electrical cardioversion should be considered in all patients with known heart disease and VT regardless of clinical stability, as the risks of antidysrhythmic medication are probably higher than those of electrical cardioversion in this patient population. Many patients with known heart disease and VT may not be considered “unstable” according to ACLS guidelines (those with hypotension, decreased LOA, acute heart failure or ischemic chest pain), but nonetheless may have poor cardiac output and be unable to tolerate antidysrhthmic medications. In patients with known LV dysfunction and VT, even with normal BP, consider incipient shock and immediate cardioversion. Remember that cardiac output can be dangerously low while the patient maintains a “normal” BP. Blood pressure ≠ cardiac output. 

Avoid the “verapamil death test”! Do not give a calcium channel blockers to a patient with a wide complex tachycardia.

For wide and irregular tachycardia consider other diagnoses (especially when standard treatments are not effective at restoring normal sinus rhythm) such as:

  • Hyperkalemia (HR usually < 120 bpm)

  • Sodium channel blocker toxicity (often very wide QRS > 200 ms)

  • Accelerated Idioventricular Rhythm (AIVR). This is a reperfusion rhythm often seen post-lytics for STEMI; Think of “slow VT”. The treatment is observation, not medication.

Tachydysrhythmias5.JPG

Accelrated Idioventricular Rhythm (AIVR) From Life in the Fast Lane blog

Pitfall: Mistaking AIVR (post-lytics for STEMI) for VT and treating with lidocaine may cause cardiovascular collapse.

 

VT is not a single entity

There are 4 types of VT that EM providers need to be aware of:

1. Scar mediated monomorphic VT – the classic VT we see in older patients with a cardiac history

->Rx: procainamide, as per the PROCAMIO study.

2. Polymorphic VT – usually related to a cardiac ischemic event

->Rx: amiodarone

3. Exercise induced non-sustained monomorphic VT – in young patients (e.g. 20’s)

->Rx: no ED treatment required; outpatient beta blockers

4. Catecholaminergic Polymorphic VT (CPVT): Heritable VT in young patients (teens/20’s) presenting as polymorphic or bidirectional with a LBBB pattern and inferior axis.

->Rx: IV beta blocker, AVOID amio and procainamide

Tachydysrhythmias6.JPG

CPVT with bidirectional VT

Management of Stable Ventricular Tachycardia

The 2016 PROCAMIO RCT trial compared IV procainamide and amiodarone for the treatment of acute but stable sustained monomorphic VT. Procainamide was associated with less major cardiac adverse events and a higher proportion of tachycardia termination within 40 minutes. Procainamide is currently considered to be the first line medication for sustained monomorphic VT in stable patients.

Indications for amiodarone in VT

While procainamide is currently considered to be the first line medication for stable sustained VT, there remain three important indications for amiodarone in the setting of VT:

1. Polymorphic VT related to cardiac ischemia

2. ICD patient with VT above detect rate (usually >175 bpm)

3. VT in the cardiac arrest patient

 

VT in the ICD patient

VT below detect (usually <175 bpm)

VT is too slow for ICD to recognize. Treat as you would any VT.

VT above detect (usually >175 bpm)

Recurrent episodes of VT. Treatment involves prevention, which is usually a combination of IV amiodarone, beta blockade and sedation. Consider causes such as ICD malfunction, electrolyte imbalance and severe CHF.

Magnet? If an ICD patient is not in VT but their ICD is delivering shocks, place a magnet on the ICD to put it into VVI mode (pacing preserved, shocking disabled).

Narrow Complex Tachydysrhythmias

 

How to distinguish Atrial Flutter from SVT

1. Bix rule: a P wave seen halfway between two QRS complexes implies there is likely another P buried in the QRS, suggesting flutter (see image below)

2. Examine all 12 leads: look for signs like a sawtooth pattern or 2:1 conduction to suggest flutter.

3. Continuous atrial activity: in flutter, there is usually no isoelectric baseline compared to SVT.

4. SVT is regular, like clockwork.

Tachydysrhythmias7.JPG

Bix rule: a P wave seen halfway between two QRS complexes implies there is likely another P buried in the QRS, suggesting flutter

 

How to distinguish Sinus Tachycardia from SVT

1. SVT is regular while sinus tachycardia shows some variability with respiration

2. Sinus tachycardia maximum = (220 bpm – age)

 

SVT Treatment

Vagal maneuvers 

The REVERT trial that compared the effectiveness of a modified vs. “standard” Valsalva to convert SVT to sinus rhythm showed a NNT = 3, however real world experience does not seem as promising. This difference may be due to the study control group being seated in the “standard” Valsalva group as apposed to supine.

What is the preferred medication for conversion of SVT to sinus rhythm, Adenosine or Calcium Channel Blockers (CCBs)?

Diltiazem is at least as effective as adenosine for conversion of SVT and has the advantage of lasting longer and not inducing an uncomfortable experience (often described as a feeling of near death) for the patient as observed with adenosine.

  

Atrial fibrillation with Wolff Parkinson White (WPW)

  • Irregularly irregular tachycardia

  • Changing QRS morphologies (as opposed to AF with a bundle branch block, which will be monomorphic)

  • Rate 250-300 bpm

Tachydysrhythmias8.JPG

WPW with atrial fibrillation – Avoid all AV nodal blockers including amiodarone! From Life in the Fast Lane blog

 

Avoid all AV nodal blockers including amiodarone. Blocking the AV node may precipitate a fatal ventricular tachydysrhythmia as conduction will preferentially travel through the accessory pathway. Treat with electrical cardioversion or procainamide.

 

Clinical features of Atrial fibrillation vs. Atrial Flutter

 Atrial Flutter is easier to electrically cardiovert, but more difficult to chemically cardiovert or rate control compared to Atrial Fibrillation.

 

Tachydysrhythmias2.JPG

 

Refer patients with new atrial flutter to an electrophyiologist as it is almost always responsive to ablation while difficult to chemically cardiovert or rate control.

Disposition & Patient Education for Atrial Fibrillation

A recent study by Stiell et al. in the Annals of Emergency Medicine looked at 30-day outcomes for patients presenting to the ED with AF or flutter.

  • Oral anticoagulants were under-prescribed by ED physicians – approximately 50% didn’t receive them

  • 10% had “adverse outcomes” which included recurrent presentations, hospitalization and 1 stroke but no deaths

ED patients are often told on discharge from the ED to return if they have recurrent symptoms of AF resulting in a high bounce back rate. Many of these patients are young and otherwise healthy. In these patients, isolated AF is almost always a benign entity. Educate otherwise healthy patients with paroxysmal AF that their disease is not life threatening and that it usually resolves on it’s own or with outpatient treatment. Teaching patients to fear AF results in needless visits to the ED and increased patient anxiety.